John Nicholson was a strict vegetarian for more than 20 years. But when he and his partner became ill, they had a carnivorous conversion and immediately felt better. Here is their story:

In 1979 I turned 18 and by then was a bit of a hippy. I was 10 years out of date; this was when punk was really big and I was just getting into Jefferson Airplane and The Grateful Dead. It was around then that I started to think differently about food. By 1982, I was living in the North of Scotland in a sort of croft with my partner, Dawn. Two years later, we decided to stop eating meat because we used to see all the cattle taken away to the slaughterhouse and we were growing a lot of our own food anyway. That’s where the adventure into vegetarianism, wholefoods and healthy eating started.

If you’ve read The Great Cholesterol Con, the name Brian Barker should ring a bell. Brian was featured in Chapter 9 of the book, where I described the life-changing events that took place after his doctor prescribed him a statin drug. Brian remains very ill to this day, and his experiences both sadden and infuriate me. I met Brian and his lovely wife Heather in Sydney in 2005, and it was dispiriting to see such truly nice folks have to suffer what they’ve been through, and it’s infuriating to realize they’re victims of a patently stupid medical mindset that often views toxic statin drugs as wonder pills that should be prescribed freely to everyone over fifty. Ironically, Brian had no personal history of heart disease whatsoever, but his doctor at the time – faithful believer of drug company and medical authority propaganda that he was – figured he’d throw Brian on simvastatin anyhow, “just as an extra precaution”. This flippantly prescribed and utterly unnecessary “extra precaution” transformed Brian from a healthy, active man into a chronically and seriously ill patient who now needs others to help him with the most basic of daily tasks.

In this article, Heather Barker describes their ordeal in full, from that fateful day in May 2002 when Brian was first prescribed a statin drug, to the present, where he continues to struggle not only with ill health but a callous New Zealand health bureaucracy that seems hellbent on denying Brian the financial compensation he is legally entitled to.

A statin is a lipid-lowering agent and although the mechanism is not fully understood or agreed upon by the medical professionals – statins do appear to lower cholesterol. However is the lowering of cholesterol beneficial in reducing heart mortality and what are some of the consequences of lowering cholesterol? This is my personal experience and I do not wish to contradict or undermine those people who tirelessly work towards lowering cardiovascular disease.

My husband Brian and I live in Auckland, New Zealand. Brian was an active person who enjoyed walking, swimming, writing and watching sport. He had solid computer skills in his job with a major airline and was responsible for paying about 700 staff. Brian was a good communicator and was extremely thorough and analytical in his work. He was able to do complex equations in his head and prided himself on accuracy. Honesty and confidentially were key to this job. He also contributed short stories to books held in the National Library and enjoyed looking forward to planned holidays.

That was until a weekend in June 2002 when our lives changed forever. On May 1st 2002 Brian started taking a statin prescribed by a cardiologist based on Brian’s family history and not his health. The cardiologist agreed he was physically fit and did not otherwise meet the criteria for a statin. No blood tests were taken.

Several weeks later Brian became seriously ill with a life threatening event we now know is called rhabdomyolysis which means his muscle tissue melted. This caused acute renal failure. Our GP did not recognize the symptoms which included severe pain in the right flank, frequent vomiting, nausea, no urine output, confusion and weakness.

The GP did not feel it was necessary to do blood tests until pressured by me to do so. When the test results showed Brian had renal failure the doctor’s response was to get Brian to drink a further 4 litres of water. This exacerbated the already dangerous situation. It was 5 days after the initial onset of these symptoms before Brian was hospitalized.

Caused by Simvastatin

Once hospitalised at North Shore Hospital the doctors examined Brian and confirmed the renal failure due to the statin. Neither of us understood most of what was said but were grateful for their help. Brian was transferred to the renal unit at Auckland Hospital and started dialysis. This was now 7 days after the onset of symptoms.

During the course of his treatment both in the hospital and as an outpatient, Brian and I mentioned his weakness, pain, nausea, tingling sensations in many of his muscles, fatigue and frequency in urinating once his kidneys started working again. The list also included urinary incontinence, impotence, confusion, tiredness, widespread discomfort, nightmares, anxiety, thumping headaches and an inability to seize and understand facts.

While he was on dialysis Brian had what we were told 3 years later was a stroke. Neurologists have told us this was due to the extreme stress his body was under in addition to the toxicity from the statin.

Reporting the Problem

Mandatory reporting of adverse reactions is not required in NZ, so I gave the information to the Centre for Adverse Reactions in Dunedin and it was also recorded at the WHO database by Merck Sharp and Dome.

Brian remained on dialysis for some time and eventually his kidney function returned but he remained very ill and was unable to do much without assistance.

Getting Compensated

In New Zealand we have a compulsory accident cover. It is called the Accident Compensation Corporation. ACC is the sole and compulsory provider of accident insurance for all work and non-work injuries. The ACC Scheme is administered on a no-fault basis, so that anyone, regardless of the way in which they incurred an injury, is eligible for coverage under the Scheme. Due to the Scheme’s no-fault basis, people who have suffered personal injury do not have the right to sue an at-fault party, except for exemplary damages.

ACC  accepted our claim that Brian had a medical misadventure and he was assured by his case manager at ACC that any future treatment relating to his injury – for the duration of his life would be covered by ACC. This was in 2002.

ACC provided support with speech language therapists, physiotherapists, psychologists and ongoing treatment from muscular skeletal specialists.

When Brian did not make a full recovery he was retired from his employment and I left my full time job to assisted Brian with day to day tasks like showering and getting dressed. Making decisions were now often difficult for him, he was easily confused about what was required of him and exhausted much of the day. Logging in to a computer was much too hard for him and driving was initially impossible. Brian had become very vulnerable and emotional often weeping with fear and frustration at his inability to move on with his life.

I read as much as I could about rhabdomyolysis and muscle damage. We changed our diet to include far more vegetables, eliminated processed foods and reduced carbohydrates and under medical advice from overseas doctors I included – CoQ10, Omega 3, and magnesium.

I was also really concerned to find thousands of others world wide had been damaged by statins. I had information from the Centre of Adverse Reactions in Dunedin in 2010 which said 11 people in NZ have died from simvastatin and there are over 30 reports of rhabdomyolysis  in their database. I didn’t ask about other statins. It is my belief that ACC and in general, the medical profession and pharmaceutical companies would prefer these statistics were not made public.

Compensation Quicksands

The first eight years after the adverse reaction were really hard for Brian and he has shown courage and determination to be the best he can. Many of the original symptoms from 2002 became more manageable but he still suffers from ongoing pain and is limited in his capacity to function fully in society. Until 2009 ACC was very supportive so we could concentrate on Brian’s rehabilitation.

However since 2009, ACC has continued to strive to ‘prove’ he didn’t have an adverse reaction to the statin or the symptoms from the statin injury are spent or most frustratingly that the symptoms are all age related or pre-existed 2002.

Over the next two years he was sent for assessment after assessment, in total around 15. Each assessment leaves him exhausted and traumatised. He was compelled to attend each appointment in order to preserve his entitlements with the ACC. Brian battled on and almost every specialist agreed with the original diagnosis. However it took just one report challenging the original diagnosis to determine that the effects of the injury were now spent. As a consequence Brian has now had his entitlements suspended.

This has directly impacted on our relationship and health. At times, both of us have felt we could not face one more day of this additional pressure. Brian’s nightmares and anxiety have become more regular and his speech and confidence in communicating with people has deteriorated as he has to endure the retelling of details of the original injury and subsequent illness to medical assessors contracted by ACC.

In 2012 we opted for Brian to have a muscle biopsy to ‘show’ he had long standing damage from the statin. The results did not show any mitochondrial damage but did show cell hypertrophy. The muscular skeletal specialist has explained that essentially the muscle cells which survived the rhabdomyolysis became super big and have contributed to the body wide discomfort.

Brian has also had a blood test to see if he had any genes that could predispose him to statin-induced myotoxicity. But he was negative for these tests.

Was it Needed?

To our knowledge Brian had no pre-existing health disorders, he didn’t have diabetes or any cardiovascular disease. But his father, mother and brother had all had heart attacks. So it is reasonable to assume that taking a statin to lower cholesterol would be just the thing for Brian. This is what the advertisements say. This is what the doctors say – at least the ones who haven’t read the impartial reports about cardiovascular disease and mortality.

It is strange then to think that Brian’s mother was on a statin but still had a heart attack.

His younger brother was on a statin for years and developed a heart problem and later had a heart attack and triple bypass and he is still on high doses of a statin. He has also developed diabetes.

Does Cholesterol Need to be Lowered?

Maybe lowering cholesterol isn’t the answer. Many well known doctors and researchers are bold enough to query the statistics provided by the pharmaceutical companies. And to their credit many doctors we have dealt with over the last 11 years have been very supportive and for that we would like to thank them.

Could it be that inflammation or other factors cause atherosclerosis? Is animal fat relevant? Does a diet full of processed foods affect our heart? Would we be better with a diet rich in olive oil and fish? Physicians, scientists and science writers are debating these issues. Having a debate about it is good. It’s a start. Our goal should be to reduce disease but not at the risk of damaging other parts of the body. Nobody should have to go through what we go through every day.

Persisting and unresolved damage from the statin injury has remained a problem for Brian, but we must also endure ongoing legal battles with ACC to ensure his Claimant Rights are being met.

There are still too many doctors and health professionals who are not willing to look at drug side effects, overall risk versus benefit and most importantly the need to remember the Hippocratic Oath: ‘I will prescribe regimens for the good of my patients according to my ability and my judgment and never do harm to anyone.’

–

Heather’s article originally appeared at RxISK.org. Clicking here will not only link to the original article but also comments by others who suffered serious health issues after being prescribed statin drugs.

You can also report a drug side effect and get a free RxISK Report here.

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Anthony Colpo is an independent researcher, physical conditioning specialist, and author of The Fat Loss Bible and The Great Cholesterol Con. For more information, visit TheFatLossBible.net or TheGreatCholesterolCon.com

Copyright © Anthony Colpo.

Disclaimer: All content on this web site is provided for information and education purposes only. Individuals wishing to make changes to their dietary, lifestyle, exercise or medication regimens should do so in conjunction with a competent, knowledgeable and empathetic medical professional. Anyone who chooses to apply the information on this web site does so of their own volition and their own risk. The owner and contributors to this site accept no responsibility or liability whatsoever for any harm, real or imagined, from the use or dissemination of information contained on this site. If these conditions are not agreeable to the reader, he/she is advised to leave this site immediately.

Several readers have asked me about a study published back in January claiming to show vegetarians have a 32% lower risk of cardiovascular disease than meat eaters. I’ve only just had a chance to sit down, read through the study, and digest the results.

My conclusion, in short: It’s a load of cobblers.

The study in question is the massive EPIC-Oxford study, from which sources who should know better are claiming “Vegetarianism Can Reduce Risk of Heart Disease by Up to a Third“!

Holy asparagus.

Before you fall for this kind of nonsense, there’s a few things about this study you should know.

Real Science versus Pretend Science

Firstly, it was not a clinical trial that took a large group of people and randomly assigned them to either a vegetarian or meat-containing diet then followed them for a specified period of time, and found the vegetarian group had a 32% lower risk of CVD. Instead, it was a study that falls into the category of epidemiology, a field of research which without question constitutes the most useless and bullshit-filled arena in all of the modern health sciences.

If that sounds harsh…it isn’t. I could be far more scathing, considering the immeasurable damage caused by the modern infatuation with epidemiology and the associated and widespread idiocy that insists on accepting its statistical associations as physiological fact, despite the fact that one of the most basic rules of science is association does not equal causation.

So what exactly is epidemiology, I hear some of you asking?

Nutritional epidemiology is where researchers study populations for relationships between dietary factors and certain diseases. There are several types of epidemiological studies, including cross-cultural or ecological ones, which compare the relationships between diet and disease among different countries. This is the least reliable form of epidemiology, as you are often comparing the proverbial apples with oranges. For example, do you think, just maybe, there might be other factors aside from diet affecting heart disease risk in a country undergoing major political, economic and/or social upheaval, when compared to peaceful, affluent countries?

If you answered “no” to that question, then rejoice, for a secure and lucrative career as a money-wasting epidemiologist who fills journals with useless papers that come to utterly unfounded conclusions awaits you!

For the rest of you whose brains remain intact, the obvious answer to the above question is yes. Average stress levels in countries experiencing upheaval tend to be higher, and stress is a major contributor to heart disease (take a look at Eastern Europe, for example). Other factors such as cigarette smoking, differences in medical diagnosis, and excessive Vodka consumption (if you think I’m joking, take a look at Eastern Europe again) may also differ greatly from that experienced by someone living in a peaceful country.

Cross-cultural epidemiology, by the way, is the very kind that gave us the idiotic and highly destructive cholesterol theory of heart disease. Thanks to Ancel Keys and the obsession with cholesterol and saturated fat spawned by his fraudulent epidemiology, modern medicine is still nowhere near to finding a cure for heart disease, and its preventive efforts revolve around toxic statin drugs of negligible efficacy. It’s an absolute disgrace, and for that we have epidemiology to thank.

Eat the Red Ones Last

So why not recruit people in the same country, and follow them instead, you ask? Well, someone just a little bit smarter than Ancel Keys once asked the same thing, and the phenomenon of prospective cohort studies was born. This is where you take a bunch of folks who live in the same country (preferably in the same area of that country) and follow them for a given period of time. You tally up the amount of people who succumbed to whatever disease you are studying, then examine their dietary habits to see if any relationships consistently stand out. For example, if heart attack victims in the large mid-Western town of Dumpsterville tended to eat more red M&Ms but healthy people tended to eat more of the yellow ones, and you had the one-dimensional mind that seems to predominate among modern epidemiologists, you would conclude that red M&Ms cause heart disease, while yellow M&Ms prevent heart disease. Easy!

If that sounds absolutely ridiculous to you, then congratulations – you’re well on your way to grasping the field of nutritional epidemiology!

The reality is that the above hypothetical study could never prove jack about jack. There could be a million reasons why people who ate more red M&Ms suffered more heart disease. Perhaps these people had more aggressive temperaments or handled stress poorly, perhaps they came from lower-socioeconomic backgrounds, perhaps they smoked more, drank more and consumed more recreational drugs, perhaps they had a higher rate of childhood undernutrition, perhaps they were more likely to be overweight, perhaps they spent less time out in the sun and hence had lower blood levels of vitamin D…the list of potential confounders goes on and on.

And on.

Multivariate Self-Flagellation

Sometimes epidemiologists attempt to ‘adjust’ for these confounders in a process typically known as multivariate analysis, but this is merely mathematical maneuvering that attempts to do after the fact what real studies (i.e. randomized clinical trials) do right from the outset. RCTs minimize the effect of confounding factors right from the word go; before the study has even started, the participants in an RCT have been randomly assigned to the treatment and control groups. This means that each group is likely to have the same average age and a similar number of males, females, overweight subjects, smokers, drinkers, drug takers, sun worshippers, exercisers, and supplement users. Randomization isn’t perfect; sometimes the role of chance dictates that a group in a study is burdened with a higher number of smokers, as happened in the LA Veterans study that compared high-saturate and polyunsaturate-rich diets.

Most of the time though, randomization works remarkably well, as anyone who has ever spent any meaningful amount of time poring through the baseline characteristic tables of published RCTs can attest.

There’s one other important benefit of randomization: It ensures that each group is also more likely to have an even distribution of factors that contribute to heart disease that we don’t know about, or that researchers typically overlook. This is especially pertinent because epidemiologists often fail to include factors in their multivariate analyses that we already do know to contribute to heart disease. For example, nutritional epidemiology studies examining heart disease rarely, if ever, inquire about – let alone adjust for – bodily iron stores, psychosocial stress, sunlight/vitamin D levels, and use of recreational drugs aside from alcohol – even though all the aforementioned have a significant volume of evidence linking them to heart disease.

RCTs minimize the effect of these confounders on the end result by maximizing the likelihood that treatment and control groups are evenly weighted with subjects sporting these characteristics. That way we can be pretty confident that if the treatment group in an RCT enjoyed a significantly lower rate of heart disease, it was in fact due to the treatment and not some unforeseen confounder that was more prevalent in one group.

Epdemiology, in contrast, makes no such effort whatsoever. Instead, epidemiologists fire up their calculators after the study has finished and attempt to weed out the influence of whatever select list of confounding factors they have compiled. There’s an astronomical difference between running a few calculations on paper and actually going back in time and physically removing all important non-dietary differences from the participants of an epidemiological study. And at any rate, the second option is impossible.

Epidemiology has its legitimate uses, but the fact remains it is a vastly inferior and often totally inadequate mode of research for studying relationships between diet and disease. It’s a sad, sad testament to the woeful state of nutritional science when so many researchers and so-called ‘experts’ hold epidemiology in the same esteem as data from randomized controlled clinical trials, when the typically inaccurate and confounder-prone data of the former cannot even begin to compare with the far more reliable data of the latter.

So, to reiterate, the EPIC-Oxford study is an epidemiological study. Which means that right from the outset it blows compared to properly conducted RCTs, and that it is not equipped to detect anything other than statistical associations. And I will repeat: The first rule of good science is that association does not equal causation. Sadly, the first rule of epidemiology these days seems to be association equals causation, baby!

So being an epidemiological study, those of you who subscribe to good science rather than pseudoscientific bollocks might expect it to have more than a few flaws.

Your expectations will be met quite lavishly.

An Epic Omission

The authors mention early on in the paper that a “recent analysis of the European Prospective Investigation into Cancer and Nutrition (EPIC)–Oxford cohort also showed a 17% lower risk (albeit nonsignificant) of fatal IHD in vegetarians than in nonvegetarians”.

In other words, the authors had already dredged the EPIC-Oxford data for CHD (essentially the same thing as IHD, if you’re wondering) relationships and were only able to come up with a non-significant relationship between vegetarianism and reduced CHD death. So they had another go, this time using a combined endpoint of non-fatal and fatal CHD. Combining endpoints is always a handy method for achieving statistical significance when your original sole endpoint failed to do so.

Before we discuss the results that ensued, it’s also worth mentioning something that the authors avoided mentioning: The previous EPIC-Oxford analysis they refer to found no overall mortality advantage to vegetarians whatsoever. Fish eaters and vegetarians had slightly lower rates of coronary heart disease than meat eaters, but higher rates of stroke. Total cancer incidence was significantly lower among fish eaters and borderline significantly lower among vegetarians than among meat eaters. In stark contrast to prevailing anti-meat dogma, the risk of colorectal cancer was significantly higher among vegetarians. For all causes of death combined, mortality in fish eaters was non-significantly lower than in meat eaters, while mortality in vegetarians was non-significantly higher.

Yet that study got relatively little attention – I certainly don’t recall “Vegetarian Diet Sucks for Improving Lifespan!” splashed across headlines all around the world. Why didn’t the EPIC-Oxford authors make a big ballyhoo about the distinctly uninspiring results of their 2008 paper which, if we are to take this epidemiology gig seriously, indicated that vegetarianism will do absolutely bugger all to extend life? Improved health and longevity is a big selling point of the vegetarian shills, yet here is the largest ever study on the subject showing otherwise. Why ignore the overall mortality result (not to mention the association between vegetarianism and higher stroke and colorectal cancer risk, the latter of which we are incessantly told is promoted by meat consumption) and instead make a big circus solely out of the CHD results, when most people really don’t fancy escaping CHD only to get struck down by some other form of premature death?

Well, if I wanted to play devil’s advocate, I could surmise that maybe some of the authors of this study had strong vegetarian leanings and therefore had a strong subconscious motivation to validate their beliefs.

I can’t speak for all the authors, but the paper itself mentions that one of the authors, Timothy J. Key is a member of the UK Vegetarian Society, which describes itself as “an educational charity working to support, represent and increase the number of vegetarians in the UK”. No other such affiliations are disclosed, yet a quick Google search reveals that one of his co-authors, Paul Appleby, is a member of the International Vegetarian Union, “an international non profit organization whose purpose is to promote vegetarianism”.

How sweet.

So at least 2 of the authors of this study belong to organizations whose stated goal is to convince more people to become vegetarians. Personally, I couldn’t give a rat’s rectum about furthering the vegetarian cause, especially if that cause is based on myth and pseudoscience. I just want at the facts, and the facts are that this study is severely lacking on several counts.

Pssst…Wanna Join a Study?

The EPIC-Oxford study began back in the early 90s and “aimed to recruit participants with a wide range of diets and targeted vegetarians and vegans as well as the UK general population.” Between 1993 and 1999, 57,446 men and women aged >20 were recruited to take part in the study and completed a baseline questionnaire.

The EPIC-Oxford participants were recruited through general practices in Oxfordshire, Buckinghamshire, and Greater Manchester and by post with the aim of attracting health-conscious people living throughout the UK. Participants were excluded from the analysis if they were over 90 years at recruitment, had no follow-up, had a prevalent registered or self-reported malignant cancer, were of unknown smoking category or unknown diet group, had unreliable nutrient data, or had a self-reported history of heart attack, stroke, or angina at baseline, which left a total of 46,694 participants available for the  analysis we are discussing today.

Along with answering questions about their education and socioeconomic status, smoking and exercise habits, oral contraceptive and hormone use (if female), and health history, participants also completed a food-frequency questionnaire that estimated the intake of 130 different food items over the past 12 months.

Participants were asked whether they ate any meat, fish, eggs, or dairy products and were categorized as nonvegetarians if they ate any meat or fish, and as vegetarians if they did not eat meat and fish. Time of adherence to a vegetarian diet was calculated by subtracting the age at which the participant last ate meat or fish from their age at the time of recruitment.

Around the time of recruitment, blood samples and blood pressure readings were also requested, and provided by 19,103 participants. Despite the numerous differences we could expect to find between the blood of meat eaters and vegetarians, the only thing examined was serum concentrations of lipids and apolipoproteins.

Take special note of all this folks: The subjects completed a single questionnaire at the start of the study, asking about diet and a limited number of confounding factors. A single blood pressure measurement was taken, and blood samples were obtained from less than half the participants, and then checked for an extremely limited number of markers. We’ll get back to how this could affect the results in a moment.

The Baseline Data

A look at the baseline data reveals a few interesting discrepancies.

It’s no big secret that CVD incidence is associated with age. The older you are, the more likely you are to suffer a stroke, heart attack or angina. Now, if this were a well-conducted RCT, randomization would usually ensure that the non-vegetarian and vegetarian groups had a similar mean age. But of course, this was an epidemiological study that contained no such safeguard. In both the male and female cohorts of the study, vegetarians on average were 8 years younger than their non-vegetarian counterparts. So the vegetarians had a rather significant advantage in terms of an average younger age.

Non-vegetarians had a slightly higher consumption of alcohol, but the study data tells us nothing about the actual pattern of alcohol consumption (i.e. did the non-vegetarians also engage in more binge-drinking, which also increases the risk of CVD?)

Non-vegetarian males were more likely to have ever smoked, and were more likely to be current smokers. Smoking habits were fairly similar between the two female groups, with the exception of a higher number of heavy smokers in the non-vegetarian female group. Needless to say, smoking is a pretty substantial risk factor for CVD, and the vegetarian cohort enjoyed a slight advantage in this respect.

Being male is also a pretty significant risk factor for CVD, and it’s interesting that this study was heavily weighted in favour of females; less than a quarter of the study participants were male. Given that most heart attack victims are male, especially at the average age of the participants in this study, it is not unreasonable to question the validity of generalizing whatever results were obtained from the study to both females and males.

Body mass index (BMI) was slightly but not significantly lower in vegetarians.

Slightly more of the non-vegetarians described themselves as “inactive” (around 4% in absolute numbers), and a similar proportion of the vegetarians described themselves as “active”, but no information is given about the type and total volume of exercise performed by each group. So the vegetarians also appear to have a slight advantage in terms of higher activity levels, which are also protective against CVD.

Interestingly, vegetarians were more likely to have higher educational status but more likely to be poor…hmmm, damn the cost of organic soy grits these days!

Non-vegetarians were more likely to have diabetes, were twice as likely to have hypertension, and significantly more likely to have been receiving long-term medical treatment.

Now why would this be?

There is no tightly controlled RCT in existence showing that animal foods cause diabetes or hypertension or predispose one to developing a higher rate of long-term medical problems. Yes, there is plenty of epidemiological slop claiming otherwise, but when these findings are subject to the bright light of randomized clinical scrutiny, they fall flat in a heap.

The real answer is simple: Vegetarians tend to be health conscious people, and engage in a number of activities aside from dietary change in order to improve their health. And that was indeed the case in the EPIC-Oxford study, where vegetarians were less likely to smoke and more likely to exercise. They were also significantly younger, which in itself proffered a significant CVD advantage.

Another thing worth mentioning: After 5 years, the researchers asked how many of the vegetarian participants were still following their meat-free way of life. They also asked the non-vegetarians if they had become vegetarians.

At 5 years, 10.6% of the male and 16.3% of the female vegetarians had abandoned their meatless ways, while only 2.8% and 2.6% of male and female meat eaters had switched to the herbivorous camp.

This was the only time the participants were asked about adherence to their original diets, yet mean follow-up in this study was 11.6 years! So how do we know exactly how many vegetarians remained that way by the time the final data were tallied up?

We don’t.

Personally, as a person who prefers his science to be of the randomized, controlled variety, this study has already lost me – it has more holes than a Swiss cheese factory, and the groups are too dissimilar in baseline factors for me to even begin to care about the results. However, I belong to a species known as Homo sapiens whose members believe in all manner of weird shit, including the notion that a food group (meat) that formed a staple of our diet for some 2.4 million years and enabled us to survive in often inhospitable conditions and outlive countless other species that went extinct (okay, we helped put more than a few of those species out of commission along the way but that was because we were vigorously hunting them for their meat..duh!) is somehow bad for us.

?!

And so here I am on a Saturday morning typing up this dissection which points out the bleeding obvious when really I should be out walking my dog, watching him sniff then pee against tree after tree, marveling at the seemingly limitless holding capacity of the canine bladder and wondering just why dogs have such a fascination for each other’s urinary output. Don’t laugh, if you own a dog then I know full well you’ve wondered the exact same thing. Sorry Ramone, I promise we’ll go for an extra long walk later, OK champion? I might even walk you past the university and let you eat an epidemiologist or two.

JUST KIDDING! I would never feed my dog such poor quality fare.

Um, anyway, back to the merde at hand…oops…I meant matter at hand. Truly.

After tallying up the data, and ‘adjusting’ for age, smoking, alcohol, physical activity, educational level, affluence level (and use of oral contraceptives or hormone therapy for menopause in women), the researchers claimed that after total follow-up of 517,960 person-years “Vegetarians had a 32% lower risk of IHD”.

Further adjustment for BMI reduced this number to 28%, but interestingly it’s the 32% number that seems to have made it’s way into all the press releases.

What would have been a far more accurate conclusion – albeit far less exciting for the Internationally United Promoters of Vegetarian Propaganda – is something like the following:

“Nominating one’s self as “vegetarian” at the start of the study was, after adjustment for a very limited number of confounding factors, statistically associated with a lower incidence of the combined endpoint of fatal and non-fatal CHD.”

Good science forbids us from claiming vegetarian diets lower CHD risk, because it is clear from this study that the vegetarians came into the study with several advantages, including younger age, lower smoking levels, and a lower incidence of long-term health problems that cannot reasonably and logically be blamed upon meat consumption.

Yes, we tried adjusting the results for several confounders, but this was an after-the-fact mathematical exercise that could never even begin to replicate the equalizing effects of randomization garnered in RCTs. Also, the number of confounders we considered was only a small sampling of the total number of potential factors affecting CHD and even those factors were anlaysed in the crudest sense possible (i.e., no consideration of drinking patterns or type or volume of exercise).

While a number of us are vegetarian ourselves, we are magnificently impartial individuals who place ethics and ruthlessly objective scientific scrutiny above any emotional attachment we may have to vegetarianism, and therefore would never ever be so crass as to claim that ‘Vegetarian Diets Reduce Heart Disease by 32%!’. The relative risk reduction found in our study was nothing more than a statistical association and does not even begin to infer causality. Before one could even begin to claim a causal association, the RR found in our study would need to be confirmed in the controlled, randomized clinical trial setting in which two similar diets varying only in their inclusion of meat (non-vegetarian group) or an isocaloric non-meat substitute (vegetarian group) were consumed for several years. This way, one would truly be comparing the effect of meat-containing and non-meat containing diets, with minimal or no interference from other unrelated dietary and lifestyle factors.”

Yeah, it’s a little more wordy, but gives a far more truthful picture of what really went on.

Out of Sight, Out of Mind

In the discussion section of the paper, the authors discuss the results of other epidemiological studies that appear to support their results, but nowhere do they discuss the complete lack of RCT evidence confirming a cardiovascular benefit for vegetarian diets.

Heck, they don’t even discuss the epidemiological evidence that contradicts their “Vegetarianism is Heart Healthy!” thesis.

Let’s take a look at another recent epidemiological study of similar size that examined the relationship of meat intake to CHD, stroke, and total CVD incidence. This study is interesting because it involves a population incessantly cited by the anti-meat/anti-cholesterol/anti-saturate/anti-everything tasty crowd – the Japanese.

The study was conducted by researchers from universities all around the country that gave us sushi, Nissan GTRs, Kazushi Sakuraba, and shy, demure girls who often turn out to be anything but shy and demure when you…uh, never mind, where was I…oh yeah, the big Japanese epidemiological study.

Yes, as part of the Japan Collaborative Cohort Study (JACC Study), researchers conducted a prospective cohort study of 51,683 Japanese (20,466 men and 31,217 women) aged 40-79 years living in all of Japan. Similar to EPIC-Oxford, a food frequency questionnaire was administered at baseline. The questionnaire included questions about consumption of meat, including beef, pork, poultry, liver and processed meat. Five choices were presented for each item with regard to consumption habits: rarely, 1–2 days a month, 1 –2 days a week, 3 –4 days a week and almost daily.

During 820,076 person-years of follow-up for 51,683 persons, the JACC researchers documented 537 deaths due to ischemic heart disease, 1209 due to stroke and 2685 total cardiovascular deaths.

For men, there were no associations between total meat consumption and age-adjusted mortality from stroke or total CVD. However, when one looks at the CHD data in isolation, as the EPIC-Oxford researchers chose to do for their latest analysis, there was an inverse trend with mortality from CHD. In other words, as meat consumption increased, CHD mortality decreased. After multivariable adjustment, the relative risk reduction for the highest versus lowest quintile of total meat consumption was 34% and remained statistically singificant.

For women, total meat consumption was not associated with mortality CHD or total CVD in either age-adjusted or multivariable models. Although there was an inverse trend with mortality from stroke in the age-adjusted model, the association was no longer statistically significant after multivariate analysis.

The inverse association with CHD was similarly observed for red and processed meat consumption among men, while no association existed for any subtype of meat consumption among women(Nagao 2012).

In other words, an even larger study than the EPIC-Oxford, in terms of both number of participants and person follow-up years, and conducted by researchers who to the best of my knowledge do not belong to any organizations dedicated to to furthering the vegetarian cause, found completely opposite results.

You see how this vegetarian promotion gig works, folks?

It’s a bit like choosing an outfit before a big date. You pick the clothes that flatter your physique and hide its flaws. If you’re female, you wear a wonder-bra, look in the mirror and frown, then stuff a few tissues either side of your fledgling cleavage to perk things up a little, until you’re confident that the object of your affections will see something that really isn’t there. If you’re a bloke, you douse yourself with poncey-sounding colognes to give the impression you’re a dapper dude who always smells like a subtle but enticingly masculine blend of wooded musk and cinnamon.

The whole point of this carry-on, of course, is to hide your numerous flaws and present only the side of yourself you wish for your target to see, in the hope of forming the most favourable possible impression.

Yep, sometimes researchers are a lot like dodgey pick-up artists. They have an end game, and often aren’t above engaging in illusory shenanigans to get to home base.

Show Me the RCTs!

I’ve talked a lot about RCTs, so the next question that begs asking is: Have any RCTs been conducted comparing omnivorous diets with vegetarian diets that ran long enough to establish a body count?

Despite the exuberant claims made by vegetarians, none of the long term dietary intervention RCTs examining the effect of diet on CHD incidence and mortality involved vegetarian diets.

There was a small trial that has been the subject of incessant vegetarian shilling, but a close examination of its results reveals a very different story to the hooplah. I’m talking, of course, about the Lifestyle Diet Heart Trial headed by one Dean Ornish.

Ornish has built a pretty lucrative career off the back of this trial, claiming his program has been “proven to reverse heart disease.”

The reality is that Ornish’s program has been shown to do no such thing.

Ornish’s program actually involves several interventions aside from the omission of meat. Participants are counseled to exercise, engage in stress reduction activities, and to cut all the refined and heavily processed crap from their diets. All these factors on their own could have an impact on CHD risk, but despite these confounding factors Ornish routinely cites his intervention as proof of the efficacy of meat-free and low-fat diets.

But just how effective is his program, anyway?

After one year of follow-up in the Lifestyle trial the researchers reported 82% of those in the experimental group experienced regression of arterial plaque, compared to only 42% of those in the control group. The experimental group subjects also experienced significantly less chest pain. But these factors could easily be due to exercise and stress reduction(Ornish 1990).

In 1998, the Journal of the American Medical Association published the five-year follow-up data for the Lifestyle Heart Trial. While the experimental group experienced a significantly reduced overall incidence of cardiac events (a classification that included angioplasty, bypass surgery, heart attack, and hospitalization for any cardiac cause), the treatment group actually experienced one more death than the control group (two people in the intervention group died compared to one person in the control group).

According to Ornish, one of the treatment group deaths was in a participant who had stopped following the intervention. Another intervention subject reportedly got a little too enthusiastic whilst exercising, exceeding his prescribed target heart rate with fatal consequences.

So maybe Lady Luck wasn’t looking out for Ornish in the first Lifestyle Trial. Maybe she was trying to send him some kind of message, like, “Oi! Yeah, you with the white coat and bean sprout sandwich! How about running a larger and longer trial before making all these dodgey claims?!?”

I’m not sure if this is what actually transpired, but at any rate Ornish did actually launch another trial. And I’m sure by now you know why few people have ever heard of the follow-up trial.

Yessirree, it was a certified fizzer.

The Multicenter Lifestyle Demonstration Project sought to apply the intervention in Ornish’s original trial to a larger group of patients recruited from clinics across the U.S.(Ornish 1998). Practitioners from eight medical centers around the country were trained in all aspects of the Lifestyle program, which they proceeded to administer to patients with coronary artery disease. The study was not a randomized, controlled trial; instead, outcomes in the 194 patients who completed the intervention were compared with 139 patients who did not take part in the Lifestyle program but had recently undergone revascularization procedures.

After three years, there were no significant differences in cardiac event rates nor mortality between patients in the intervention and control groups. The number of cardiac events per patient year of follow-up when comparing the experimental group with the control group was as follows: 0.012 versus 0.012 for myocardial infarction, 0.014 versus 0.006 for stroke, 0.006 versus 0.012 for non-cardiac deaths, and 0.014 versus 0.012 for cardiac deaths (none of the differences were statistically significant)(Ornish 1998).

This is despite the fact that the Lifestyle participants received dedicated counseling, lost weight and improved their exercise tolerance. No corresponding data were given for the control group, but given the absence of the intense counseling afforded to the intervention group, it is unlikely that the former would have experienced such changes – a contention supported by the original Lifestyle trial.

In his 1998 paper reporting on the MCLP results, though, Ornish writes as if these uninspiring results were a great success. His reasoning is that his program is cheaper than revascularization, yet produced similar coronary event and mortality rates. Because 150 of his 194 patients avoided revascularization (44 still had to be wheeled into the operating theater during the 3-year study), Ornish’s selling point in the paper is that his program is a cheaper alternative to revascularization.

That all sounds great, but if you’ve read The Great Cholesterol Con you’ll know that when revascularization is put to the test in RCTs, it has repeatedly failed to show any mortality advantage and some studies have actually shown a slight disadvantage, when compared to patients receiving standard non-invasive medical care. So, in effect, Ornish’s 1998 paper is boasting that his program is no more effective but at least cheaper than another largely ineffective option.

Woohoo…

Where the Tofu Hits the Road

So looking at the epidemiological data and the meager clinical data, we see absolutely no reduction in overall mortality among vegetarians, even when the vegetarian participants are afforded important baseline or peri-trial advantages. Despite the fact that most of these epidemiological studies show vegetarians to be slimmer, more active and less likely to smoke than omnivores, they enjoy no overall mortality advantage. Logically, this would indicate that something about the vegetarian diet counteracts lower levels of smoking, overweight, and inactivity to such a degree that mortality remains as high as that seen among omnivores with generally unhealthier lifestyles. It’s no secret that vegetarians (and especially vegans) are more likely to be deficient in B12, a critically important vitamin whose importance still isn’t fully appreciated by many medical and layfolk alike. Vegetarians, by avoiding fish, deprive themselves of long-chain omega-3 fatty acids, which have been shown in large clinical trials to reduce CHD mortality. Blood sampling often shows vegetarians to have higher blood levels of the omega-6 fat linoleic acid; a high blood n-6:n-3 ratio does not bode well for future CVD risk.

Meat is also rich in numerous critical nutrients such as creatine, carnosine, carnitine and taurine, all of which are either absent or found in negligible amounts in plants, and all of which are found in lower average amounts in vegetarians. Taurine has shown promise in helping patients with chronic heart failure, although studies to date have been small, short and scarce. Not so with carnitine, which has been shown by Italian researchers to reduce mortality from both heart failure and CHD. Creatine has also shown promise in patients with congestive heart failure and has even been shown in at least one trial to raise intelligence in vegetarians (no, I’m not kidding).

Carnosine, meanwhile, is a potent inhibitor of anti-glycosylation end products (aptly named AGEs), meaning it prevents the forming of protein-sugar cross-links in your body that quite literally cause you to age faster. No surprise then, that these same studies show that vegetarians have higher blood levels of AGEs.

AGEs, by the way, are a big reason why diabetics age much faster and suffer higher rates of just about every known health ailment, including CHD.

(References for all the above nutrient information can be found at the end of this article)

To turn around and claim in the face of all this contradictory evidence that vegetarian diets reduce heart disease is so stupid it defies comprehension.

Such a thesis can only be maintained by citing data from supportive confounder-prone epidemiological studies, and completely ignoring the non-supportive and often completely contradictory body of clinical evidence.

Suffice to say for now that the claimed heart-healthiness of vegetarianism is a complete and utter sham. The next time I find a few spare moments to knock out an article, I’ll discuss the kind of diet that has been shown to dramatically reduce CHD and overall mortality in randomized controlled clinical trials.

Here’s a clue: It contains meat.

Yep, that’s all I’m giving you for now

Until next time, adios amigos!

Disclosure Statement: The author of this article (in non-third person terms, that would be me, Anthony) has absolutely no relationship, financial or otherwise, with the meat, dairy, or egg industries. The author does, however, make a point of enjoying a bloody good steak on a very regular basis.

References:

Nagao M, et al. Meat consumption in relation to mortality from cardiovascular disease among Japanese men and women. European Journal of Clinical Nutrition, Jun, 2012; 66 (6): 687-693.

Ornish D, et al. Can lifestyle changes reverse coronary heart disease? The Lifestyle Heart Trial. Lancet, Jul 21, 1990; 336 (8708): 129-133.

Ornish D, et al. Intensive Lifestyle Changes For Reversal of Coronary Heart Disease. Journal of the American Medical Association, Dec 16, 1998; 280 (23): 2001-2007.

Ornish D, et al. Avoiding Revascularization with Lifestyle Changes: The Multicenter Lifestyle Demonstration Project. American Journal of Cardiology, Nov 26, 1998; 82 (10B): 72T-76T.

Antony AC. Vegetarianism and vitamin B-12 (cobalamin) deficiency. American Journal of Clinical Nutrition, 2003; 78: 3-6.

Chan KM, Decker EA. Endogenous skeletal muscle antioxidants. Critical Reviews in Food Science and Nutrition, 1994; 34 (4): 403-26.

Hipkiss AR. Carnosine. a protective, anti-ageing peptide? International Journal of Biochemistry & Cell Biology, 1998; 30: S63-868.

Price DL, et al. Chelating Activity of Advanced Glycation End-product Inhibitors. Journal of Biological Chemistry, 2001; 276 (52): 48967-48972.

Davini P, et al. Controlled study on L-carnitine therapeutic efficacy in post-infarction. Drugs Under Experimental and Clinical Research, 1992; 18: 355-365.

Sebekova K, et al. Plasma levels of advanced glycation end products in healthy, long-term vegetarians and subjects on a western mixed diet. European Journal of Nutrition, Dec, 2001; 40 (6): 275-281.

Rizos I. Three-year survival of patients with heart failure caused by dilated cardiomyopathy and L-carnitine administration. American Heart Journal, Feb, 2000; 139 (2, Pt 3): S120-123.

Iliceto S, et al. Effects of L-carnitine administration on left ventricular remodeling after acute anterior myocardial infarction: the L-Carnitine Ecocardiografia Digitalizzata Infarto Miocardico (CEDIM) Trial. Journal of the American College Of Cardiology, Aug, 1995; 26 (2): 380-387.

Kreider RB. Effects of creatine supplementation on performance and training adaptations. Molecular and Cellular Biochemistry, Feb, 2003; 244 (1-2): 89-94.

Andrews R, et al. The effect of dietary creatine supplementation on skeletal muscle metabolism in congestive heart failure. European Heart Journal, Apr, 1998; 19 (4): 617-622.

Gordon A, et al. Creatine supplementation in chronic heart failure increases skeletal muscle creatine phosphate and muscle performance. Cardiovascular Research,Sep, 1995; 30 (3): 413-418.

Lukaszuk JM, et al. Effect of creatine supplementation and a lacto-ovo-vegetarian diet on muscle creatine concentration. International Journal of Sport Nutrition & Exercise Metabolism, Sept, 2002; 12 (3): 336-348.

Harris RC, et al. Absorption of creatine supplied as a drink, in meat or in solid form. Journal of Sports Sciences, Feb, 2002; 20 (2): 147-151.

Laidlow SA, et al. The taurine content of common foodstuffs. Journal of Parenteral Enteral Nutrition, Mar-Apr, 1990; 14 (2): 183-188.

Pasantes-Morales H, et al. Taurine content in foods. Nutrition Reports International, 1989; 40: 793-801.

Schaffer SW, et al. Interaction between the actions of taurine and angiotensin II. Amino Acids, 2000; 18 (4): 305-318.

Azuma J, et al. Therapeutic effect of taurine in congestive heart failure: a double-blind crossover trial. Clinical Cardiology, May, 1985; 8 (5): 276-282.

Azuma J, et al. Double-blind randomized crossover trial of taurine in congestive heart failure. Current Therapeutic Research, Clinical and Experimental, 1983; 34 (4): 543-57.

Beyranvand MR, et al. Effect of taurine supplementation on exercise capacity of patients with heart failure. Journal of Cardiology, May, 2011; 57 (3): 333-337.

Laidlaw SA, et al. Plasma and urine taurine levels in vegans. American Journal of Clinical Nutrition, 1988; 47: 660-663.

Pasantes-Morales H, et al. Taurine content in breast milk of Mexican women from urban and rural areas. Archives of Medical Research, Spring, 1995; 26 (1): 47-52.

—

Anthony Colpo is an independent researcher, physical conditioning specialist, and author of The Fat Loss Bible and The Great Cholesterol Con. For more information, visit TheFatLossBible.net or TheGreatCholesterolCon.com

Copyright © Anthony Colpo.

Disclaimer: All content on this web site is provided for information and education purposes only. Individuals wishing to make changes to their dietary, lifestyle, exercise or medication regimens should do so in conjunction with a competent, knowledgeable and empathetic medical professional. Anyone who chooses to apply the information on this web site does so of their own volition and their own risk. The owner and contributors to this site accept no responsibility or liability whatsoever for any harm, real or imagined, from the use or dissemination of information contained on this site. If these conditions are not agreeable to the reader, he/she is advised to leave this site immediately.

Joe writes:

Anthony,
 
I just finished your book The Fat Loss Bible, and really enjoyed it. I learned a lot of diet and exercise techniques to help improve my current regimen.
 
Quick background on me. I went through a “transformation” about a year ago. I went from 183 to a ripped 155 at 5’8″. I experienced all the positive comments you talk about in your book, and even had fitness photos taken.   During this time I had a coach whom taught me much of what you write in your book.  Exercise, calories are king, concept of deficit, etc…. My technique was and still is to use weekly calories as a moving average, and shoot for a weekly deficit.   Furthermore, I would use intermittent fasting as a way to “fit” my calories into the week.  I did not pay attention to macros, only calories, no matter what it was (junk, sweets, etc)

So far, this has worked well with a few glitches.  
 
First, I had rebounded twice from last year.  Not completely, but enough to be upset and depressed about it.  Each time I dieted back down, and currently I am on my third come back.   My problem is I don’t know what to do to STAY lean once I get there.  Once I am there, I feel I am starving and it’s tough to maintain energy.  Also, I have trouble getting through to that very last push to ultimate leanness.  Instead I experience the fatigue, lack of motivation, no pump, feeling cold all the time, low sex drive…..   

Your concept of energy flux is interesting, although, I have always been afraid of raising calories in fear of fat gain.
 
1. At my level of leanness, should I be using energy flux too push to that last level leanness and maintain? ( I use a heart rate monitor as way to track calorie expenditure)
 
I usually use intermittent fasting as way to “save” calories for big eating events (dinner with friends, winery, etc). Some weeks I would even eat very low calories plus a fast to save for huge eating weekend, but I noticed that I would feel like a weak, unmotivated, sapling.  I do not use IF as my staple diet like you talk about in your book.  I eat in a deficit, then one day of week

I will fast, but only to “save” the calories for later in week.
 
 2. Is the one day fast (provided that my calories for the other days are higher, but still in deficit) detrimental to obtaining that last level of fat loss?  
 
Some gurus say one needs to be carb depleted to lose fat.  I have found that I probably am eating low carb even though I don’t count due to my diet regimen,  but I feel like crap and can’t train hard.  With that being said…….
 
3. By ensuring I’m in a deficit, aren’t I already carb depleted because my body will not be fully able to replenish glycogen stores?
 
4.  My primary form of “cardio” was walking.  I’m not saying I will give up walking, but I was always concerned with performing HIIT or any other activity (biking, MMA, etc) due to my interpretation, or misinterpretation that I will be burning mostly glycogen and or muscle given I was in a deficit.  I’ve been told that if I want to burn fat then do low intensities like walking.  Thoughts?   
 
Thank you.  Again, I really enjoyed your book and look forward to hearing from you.

Anthony replies:

Hi Joe,

first of all, congratulations on dropping around 30 pounds of chub – that’s a great result! Unfortunately, your celebration party has been gate-crashed by some very unwelcome guests. I reckon it’s time to step up and show them the door.

Reading through your email, it becomes clear that you need to drop both the intermittent fasting gig (even if it is on an irregular basis) and any kind of carb-restriction. Both of these are battering your already struggling adrenal-pituitary-thyroid axis.

“Some gurus say one needs to be carb depleted to lose fat.”

Here’s some free and very valuable advice: Many ‘gurus’ are full of shit, and you need to be very wary of what they claim. The claim that you need to be “carb-depleted” to lose fat is utter nonsense. I could start reciting the science showing as much, but you’ve already read my book in which I discuss this. Instead, I’ll employ here something known as commonsense: If one has to be “carb-depleted” to burn fat, why are so many athletes who eat mountains of carbohydrates so lean? Just look at any high level road cyclist or triathlon competitor – how do these guys get so lean if all the carbs they are eating ‘block’ fat-burning?

And I think it’s also fair to ask: If reducing or eliminating carbs is the key to opening the fat-burning floodgates, why are most of the prominent low-carb advocates such a bunch of flabsters?

The “walking/low-intensity cardio is best for fat loss” tenet is another long-disproved myth. This myth started because, yes, a higher proportion of the meager calorie burn you achieve will come from fat. Upping the intensity will cause your body to tap into proportionately higher amounts of glycogen. But what this theory overlooks is the fact that, compared to walking, your overall calorie burn will be so much higher doing things like fast cycling, boxing, skipping, etc, that regardless of the exact fat:glucose ratio being employed, the total amount of fat you burn will be much higher.

Female triathlete Lokelani McMichael. Tell me again how high carbs and vigorous exercise impede fat-burning?

More triathletes whose bodies stubbornly refuse to support the “carbs impede fat-burning” and “low intensity cardio is best for fat loss” nonsense.

Your problem in a nutshell is that your caloric and carbohydrate intakes are too low. And your body is now in an emergency, semi-starvation state as a result. That’s why you are experiencing low sex drive, perpetual low body temp, lack of motivation, low energy, etc. Your body isn’t stupid; it reacts to the insufficient food intake by slowing down all non-essential functions, so that essential stuff – like keeping your heart beating and your brain functioning – gets priority access to the meager pool of available energy.

Doing things like intermittent fasting and eating insufficient carbs – where you go for long intervals in a glucose-depleted state – only make matters worse. You would do well to read the following article:

Is a Low Carb Diet Bad For Your Thyroid?

I suggest you also have another read through The Fat Loss Bible, taking special note of the sections debunking the “carbs/insulin make you fat” sham, and the Appendix dealing with Intermittent fasting.

The solution to your problem lies with the Energy Flux approach, a scientifically documented option I present and explain in The Fat Loss Bible. You need to start eating more to lift your body out of its present semi-starvation state. You also need to start exercising more intensely. In other words, you need to stop eating like a bird and exercising like a baby boomer, and start eating and training like an ass-kicking athlete. I understand you have lingering fears that this will somehow make you fat – it won’t. Just raise your caloric and carbohydrate intake and exercise volume/intensity in an incremental fashion. As you begin to see and experience marked improvements, you’ll know you’re on the right track.

And for now, put your goal of becoming super-shredded aside and focus instead on nursing yourself back to optimal health. When your body temperature, energy levels and sex drive have fully returned to normal, then you can set about knocking off a few more percent body fat. Your immediate goal is to get back your mojo, without putting on any extra chub in the process. You describe yourself as “ripped”, so I highly doubt people are going to look, point and make fat jokes as you walk past simply because you’re in the midst of modifying your fat loss/maintenance strategy.

If you’ve been dieting and now feel tired and weak, it might be time to stop skimping on the carbs, bump up your calories, and start training like you mean it.

Also, I’m not sure what your supplementation routine is like at the moment, or if you even have one, but in addition to the recommendations in The Fat Loss Bible I’d suggest a good sublingual B complex formula (Source Naturals Coenzymate B
is a great product), an ionic mineral concentrate such as Trace Minerals Research ConcenTrace, and an iodine supplement (given your ‘adrenal fatigue’ symptoms, I’d avoid potassium iodide and go for a non-potassium-containing form of iodine, like TPCS Iosol Formula II. Make sure you are supplementing with selenium as recommended in The Fat Loss Bible.

In short, you’ve only just finished reading my book, which means you haven’t had a chance to test drive any of the recommendations I make in it. You’ve tried a partial intermittent fasting approach, and that left you feeling royally buggered, so I can only imagine what a full-time IF regimen would do to you. You’ve also listened to the carb-phobes and the low-intensity cardio crowd, and their advice has failed you. Now it’s time to try my approach, which definitely does not involve intermittent fasting, carbohydrate restriction, eating like a mouse, nor exercising like a senior citizen.

I know full well which approach will prove superior – now it’s your turn to find out.

I hope this helps push you in the right direction,

Kind regards,

Anthony.

—

Anthony Colpo is an independent researcher, physical conditioning specialist, and author of The Fat Loss Bible and The Great Cholesterol Con. For more information, visit TheFatLossBible.net or TheGreatCholesterolCon.com

Copyright © Anthony Colpo.

Disclaimer: All content on this web site is provided for information and education purposes only. Individuals wishing to make changes to their dietary, lifestyle, exercise or medication regimens should do so in conjunction with a competent, knowledgeable and empathetic medical professional. Anyone who chooses to apply the information on this web site does so of their own volition and their own risk. The owner and contributors to this site accept no responsibility or liability whatsoever for any harm, real or imagined, from the use or dissemination of information contained on this site. If these conditions are not agreeable to the reader, he/she is advised to leave this site immediately.

Warning: This article contains language some folks would consider naughty. If you are deeply offended by words that start with “Sh…” and rhyme with “git”, you should close this page immediately and go back to reading Better Homes and Gardens.

If ever you needed proof the world is heavily populated by utter morons, all you’d need to do is examine a recent study appearing in Nature Medicine, wonder how supposedly educated people could ever contrive such utter rubbish, then marvel at the ease with which this pseudoscientific slop has been uncritically soaked up by media outlets and individuals all around the world.

I’m talking, of course, about the current “Carnitine in Red Meat Causes Heart Disease!” nonsense doing the rounds in the mainstream media, that preeminent source of misinformation that plays a key role in keeping the general population as dumbed down, confused and distracted as possible.

The Plain Facts, Whether You Like Them or Not

Before I begin tearing apart this joke of a ‘study’, I want to make a couple of things perfectly clear:

–Carnitine does NOT cause heart disease.

–No-one -I repeat NO-ONE – has ever shown red meat nor supplemental carnitine to cause heart disease in human beings. Not the ‘researchers’ responsible for the appalling Nature Medicine paper, and not anyone else.

So what’s with this latest study? Where do the researchers get off making such idiotic claims?

If you earnestly believe this stuff causes heart disease, my condolences. Life must be tough without a brain.

How to Make Headlines With Complete and Utter Garbage in 3 Easy Steps

The only kind of study equipped to support a fantasmagorical claim like “Carnitine Causes Heart Disease!” is a randomized controlled trial (RCT) in which you take a bunch of volunteers, randomly assign them to two groups, then assign one group to take carnitine supplements and the other a placebo. You would then let the study run long enough for people to start dying from heart disease (if the participants had preexisting CVD, this will generally happen a lot sooner). After several years (or less if one group showed a huge advantage over the other, in which case you would be ethically obliged to end the trial early) you would tally up the data.

By the way, if this trial was intended to examine the effects of carnitine on CVD incidence and mortality in human beings – as opposed to rats, mice, pigs, or Mongolian Gerbils – then it must meet another absolutely essential requirement: The participants of the trial must be human beings.

“No shit Anthony!“, you say? Hey, you’d be amazed at how many highly-decorated researchers apparently can’t tell the fundamental differences between a rodent and an adult Homo sapien. And that includes the authors of the Nature Medicine paper, as we’ll discuss shortly.

If the data from your human RCT showed more people in the carnitine group died of heart disease and your trial was a meticulously conducted endeavour pretty much free of confounding factors, dodgey researcher behaviour, or untoward influence from parties with a vested financial interest in the results, then and only then could you justify the claim “Carnitine Causes Heart Disease!” Even then, for the finding to be accepted as gospel fact by the scientific community at large, your research would need to be replicated and validated by other researchers.

So conducting such a carefully controlled trial must be what the Nature Medicine paper authors did, right? After all, they sound pretty damn confident that “Carnitine Causes Heart Disease!”

They did nothing of the sort.

Instead, they engaged in an exercise known as PIM (Pseudoscientific Intellectual Masturbation).

To be a good PIM-artist really isn’t that difficult. All you need, along with seemingly impressive credentials, is to serve up the right mix of shady inferences, dodgey extrapolations and ridiculous but tantalizingly sensationalist conclusions. Write a good press release, and you can be assured the shocking ignorance of most health reporters and the public’s eternal gullibility and faith in authority will do the rest.

The title of the paper, which Nature Medicine posted on its website on April 7 ahead of print, is “Intestinal microbiota metabolism of l-carnitine, a nutrient in red meat, promotes atherosclerosis“. Again, we can see the authors aren’t mincing their words – as far as they’re concerned, they’ve conclusively established a causal role for carnitine in the pathogensis of heart disease.

In their dreams, baby.

Why This Study is a Load of Bollocks

The very first line of the study’s text reads:

“The high level of meat consumption in the developed world is linked to CVD risk, presumably owing to the large content of saturated fats and cholesterol in meat1,2. However, a recent meta-analysis of prospective cohort studies showed no association between dietary saturated fat intake and CVD, prompting the suggestion that other environmental exposures linked to increased meat consumption are responsible3.”

See the numbers “1″, “2″ and “3″ at the end of the first and second sentences? These are citation numbers referring to the studies allegedly confirming what those sentences are saying. So let’s take a look at these studies.

Sudy “1″ can be found here. It was the Nurses’ Health Study and, yes, the researchers claimed that red meat intake was associated with a higher risk of CVD and diabetes. This was not an RCT but an epidemiological study, which means it was a load of uncontrolled, confounder-prone slop. As I have explained many times before, epidemiological studies are hopelessly subject to innumerable confounding factors over which the researchers have absolutely no control (and don’t give me this bollocks about “multivariate analyses”, which is simply an abbreviated way of saying “sophisticated mathematical chicanery that convinces epidemiologists they have god-like powers and can endow their work the same kind of robust validity seen with carefully conducted RCTs”).

So what I want you all to do now is open the PDF for the NHS paper and scroll down to pages 11 and 12 to view Table 1, which contains the baseline characteristics of the participants (to avoid contorting your neck, right click on the table and select “Rotate Clockwise”). Remember what I said about these garbage epidemiological studies being hopelessly prone to confounders? The NHS is a textbook classic example – we can clearly see that as red meat consumption went up, so too did smoking rates, trans fat intake, and history of angina/diabetes/blood pressure. And as red meat intake increased, levels of physical activity decreased.

In other words, subjects in the higher red meat quintiles clearly lived unhealthier lives and possessed several other unhealthy traits totally unrelated to red meat intake.

Here’s a few facts for our red meat-hating brethren in the epidemiology community to ponder:

–The primary source of trans fats are refined vegetable fats (you know, the same fats our idiotic health authorities told us were “heart healthy”, then quietly backed away from when mounting evidence showed otherwise).

–Smoking, meanwhile, involves ingestion of noxious gases from nicotine-containing products, primarily cigarettes. In my four-plus decades on this crazy blue ball called Earth, I’ve yet to see someone roll a topside steak, light it up, and draw on it like a Marlboro. In other words, red meat has nothing to do with smoking, and to blame the effects of the latter on the former is sheer idiocy.

–Any claim that red meat intake causes physical inactivity is similarly absurd. In fact, given its high concentrations of B-vitamins, creatine, iron, and carnitine (critical for energy production, idiotic statements about CHD from clueless researchers notwithstanding), we would reasonably expect red meat intake to facilitate, rather than impede, strenuous exercise.

–There is no reliable evidence whatsoever to support any notion that angina, diabetes and high blood pressure are caused by red meat intake. They are, however, promoted by smoking, inactivity, and trans fat intake, all of which increased among the NHS subjects along with rising red meat intakes. These ailments are also strongly linked to such factors as high refined carbohydrate intakes, stress, ambient pollution, and high bodily iron stores – none of which were reported in Table 1.

So yes, in the NHS, red meat was indeed “associated” with higher rates of CHD, but in the same way a woman who unwittingly marries a serial killer is “associated” with violent crime. The latter is not responsible for her husband’s murderous behaviour, and the former is in no way responsible for the otherwise unhealthy behaviour of its most voracious consumers.

So why would people who consume more red meat exhibit generally unhealthier lifestyle and dietary habits?

It’s simple. People who care less about their health, and ignore exhortations to avoid trans fats/smoking/inactivity are also more likely to ignore recommendations to avoid or limit red meat consumption. And so red meat is eaten in higher amounts among these subjects, allowing dodgey epidemiologists who think health research is all about clever statistical shenanigans to create “associations” between red meat and all sorts of health ailments. They then pronounce these associations as causal rather than statistical, blatantly ignoring one of the most fundamental rules of good science:

ASSOCIATION DOES NOT EQUAL CAUSATION.

Health-conscious people, by the way, will also be more likely to eat poultry compared to red meat, which is why this source of animal flesh was associated with a lower risk of CVD in the NHS.

There’s one more thing I’d like to point out about the NHS paper. If you look at the “Body Mass Index” scores among the various quintiles of red meat consumption, they are pretty much identical. But scroll down to the “Calories” data, and you’ll see that as red meat intake increases, so too does the self-reported calorie intake. So what we are supposed to believe from this hogwash is that people who eat less red meat maintain the same level of overweight as people who eat higher amounts, despite eating 700 less calories per day!

You’d have to be Gary Taubes to believe bullshit like that.

So if the self-reported calorie intakes are way off the mark, what else in the NHS data is wildly inaccurate? Who knows. Like I said, it’s just a mass of totally uncontrolled, dubiously reported (a single dietary questionnaire every four years) and hopelessly confounder-prone data, ripe for dredging and misinterpretation by those happy to accept weak statistical odds ratios as physiological fact.

Anyway, let’s leave the bad joke that is the NHS red meat paper and move onto reference “2″. Before I discuss this paper, I want to reiterate that the Nature Medicine paper authors cite it in support of their claim “high level of meat consumption in the developed world is linked to CVD risk“.

The reality is it showed nothing of the sort, as you can see for yourself by clicking here. This paper was a meta-analysis examining the pooled data from not one, not two, but 20 epidemiological studies dealing with red meat and CVD and/or diabetes risk. Yessirree, a genuine all-you-can-eat epidemiological extravaganza encompassing data for some 1,218,380 individuals and 23,889 CHD, 2280 stroke, and 10,797 diabetes cases.

And what did it find? “Red meat intake was not associated with CHD…or diabetes mellitus”. Nor was it associated with stroke.

Processed meat intake was associated with a 1.42 and 1.19 increased risk of CHD and diabetes, respectively, but not stroke. Whether this is because of an unhealthy consumer phenomenon similar to the one we saw for red meat in the NHS, or a genuine detrimental effect of processed meat, or whether we should just ignore the results period because 1.42 and especially 1.19 are pathetically weak hazard scores considering the confounder-prone source, is an entirely different discussion. What matters here is that, despite the massive data-dredging opportunity it presented, the most massive analysis to date found no relationship between red meat and heart disease.

But the Nature Medicine authors cite it as showing that red meat is associated with CHD. Why would they say this when it is patently untrue? The NM paper has 23 listed contributors from a mix of institutions including Cleveland Clinic, University of California–Los Angeles, Cleveland State University, Perelman School of Medicine at the University of Pennsylvania, Wake Forest School of Medicine in North Carolina, Children’s Hospital Oakland Research Institute in Oakland, California.

Are we to seriously believe none of these 23 researchers read the meta-analysis in its entirety?

Are we to seriously believe none of them saw the words “Red meat intake was not associated with CHD“?

So why have they cited the meta-analysis in support of a statement patently at odds with its findings?

It gets worse.

Study “3″ can be found here. This study did not deal specifically with red meat intake; rather, it examined the relationship between CVD and saturated fats in general (i.e. not just from red meat, but other meats, dairy products, etc). This was also a meta-analysis, incorporating epidemiological data for 347,747 subjects, 11,006 of whom developed CHD or stroke. Contrary to decades of dedicated anti-saturate brainwashing, there was no relationship between saturated fat intake and CHD, stroke or CVD risk.

Now, I need you to re-read the first 2 sentences of the Nature Medicine paper – c’mon, humour me, it’s important:

“The high level of meat consumption in the developed world is linked to CVD risk, presumably owing to the large content of saturated fats and cholesterol in meat1,2. However, a recent meta-analysis of prospective cohort studies showed no association between dietary saturated fat intake and CVD, prompting the suggestion that other environmental exposures linked to increased meat consumption are responsible3.”

Did you notice the subtle but very dodgey sleight of hand performed by our anti-carnitine crew? The first sentence claims an association between meat intake and cardiovascular disease, but the second sentence claims this relationship is not explained by saturated fat intake. Despite having red meat squarely in their sights, they’ve also carefully slotted the word “meat” into the sentences rather than “red meat”, so they can technically claim study “2″ in support, even though it only found an association for processed meat (red meat by far is the richest source of carnitine; the carnitine content of processed meat varies widely due to its use of various meats, fillers and often high fat content; white meat contains negligible amounts).

So the reality is one of the studies allegedly showing a relationship between red meat intake and CVD was hopelessly confounded by other unrelated factors, while the much larger and all-encompassing meta-analysis showed no relationship of red meat – irrespective of its saturated fat content – with CVD. Yet the authors falsely claim otherwise, then lead into the saturated fat argument to pave the way for their carnitine hypothesis.

In other words, their carnitine hypothesis is based on a false premise. They go on to claim that carnitine may be the real explanation for the relationship between red meat and CVD, but there is no relationship between red meat and CVD!

So the underlying assumption upon which they build their carnitine theory is utter rubbish. I’m sure you guys don’t need me to remind you what happens to elaborate structures built on quicksand…

Up, Up and Away With TMA

Not to be deterred by the small matter of their thesis being built on a blatant falsehood, the Cleveland Clinic-led researchers then go searching for an alternative culprit to explain their mystical relationship between red meat and CVD.

They settle on a rather unusual choice, a substance known as trimethylamine, or TMA for short.

What the bleep is trimethylamine, I can hear you all asking?

Trimethylamine belongs to a group of organic compounds known as amines, and has a pungent, fishy, ammonia-like odor. TMA is formed naturally during the decomposition of plants, fish and animal products, and is ingested in foods such as fish, or from foods containing TMA precursors such as trimethylamine oxide (TMAO), choline, and L-carnitine, which are metabolized to TMA by enterobacteria.

TMA is the substance mainly responsible for the funky smell imparted by rotting fish. It is present in the plasma and urine of humans, and can also contribute to the less-than-pleasant aromas arising from some infections, bad breath and vaginal odors.

Sounds pretty gross, but TMA is present in every one of us after we eat foods containing TMA precursors. Conversion back to TMAO is the major fate of most TMA in our bodies, and considerable variability exists among humans in the efficiency of this process.

In a nutshell, what the authors of the Nature Medicine paper are saying is that when we eat red meat, the carnitine in that meat gets converted to TMA by microbes in our gut. That much is straightforward, concurs with what we already know about carnitine and TMA, and pretty much falls into the category of “Um, yeah, so what?”

It’s what the authors claim next that strains the boundaries of credulity. They claim that this newly formed TMA goes on to cause heart disease by promoting uptake of cholesterol into the artery walls.

For crying out loud…

CHOLESTEROL DOES NOT CAUSE HEART DISEASE.

The evidence absolving cholesterol of any causative role in atherosclerosis from heart disease is so abundant I was able to fill an entire book with it. And the best that any of my critics have been able to muster in response is to accuse me of being a money-hungry profiteer who resides out in left field (hi Dr Gholke, Pee Pee, Janet, et al!) In other words, they cannot even begin to factually refute the points I raise in the book.

Here are the facts:

–The campaign against saturated fats and cholesterol was born in 1953 after a shameless researcher by the name of Ancel Keys plotted the total fat intake and CHD mortality for six countries on a graph. By doing so, he was able to show a strong linear positive association between the two; as fat intake went up, so too did CHD mortality. But what he didn’t mention in his paper was that data for twenty-two countries was available at the time, and he’d simply chosen the six countries that best supported his thesis and flippantly ignored the rest. Depending on which six countries Keys chose, he could have shown fat intake was completely unrelated to CHD mortality, or he could even have shown that as fat intake went up, CHD mortality went down. Key’s research was patently fraudulent, but his driven, domineering manner and his position on the American Heart Association’s nutrition advisory panel saw to it that his shambolic findings eventually became official public policy. The anti-fat theory promptly morphed into the anti-cholesterol theory, and initially saw the heavy promotion of polyunsaturated fats as ‘healthier’ substitutes for saturated fats.

The above is now common knowledge, so why do so many researchers and health authorities keep up with the anti-cholesterol sham when from the very outset it was based on a fraud?

–Autopsy studies have repeatedly shown no relationship between blood cholesterol levels and atherosclerosis. Some of these studies observed recently deceased people with very low cholesterol levels but severely atherosclerotic arteries.

–Decades of dietary intervention trials have completely failed to lower coronary mortality, despite the fact that blood cholesterol levels were indeed lowered in the intervention groups.

–The most successful dietary intervention trial ever conducted, the Lyon Diet Heart Study, slashed mortality rates among those assigned to an omega-3, antioxidant-rich “Mediterranean” diet, even though cholesterol levels between the diet and control groups remained identical throughout the study.

–Statin drugs, those overhyped and inherently toxic agents that nonetheless have shown CHD mortality reductions in some population groups, only work because they possess a whole host of effects aside from mere cholesterol-lowering. This is why they’ve been able to deliver meager mortality reductions where their predecessors, the fibrates, were able to deliver none. In one particularly telling study- which, ironically, was published in Nature Medicine – researchers took the popular lovastatin and completely disabled its cholesterol-lowering abilities, then found it still possessed potent anti-inflammatory effects.

These are just a few of the contradictions to the untenable cholesterol hypothesis of heart disease that I discuss in The Great Cholesterol Con (you know, the book I allegedly wrote while residing out in “left field” and has since apparently made me millions of dollars, which of course is why I’m sitting here on a Saturday morning writing this article when I’d much rather be sipping Frangelico in the Caribbean or doing my darndest to destroy the gearbox on a brand new Lamborghini*).

I also debunked the “LDL Cholesterol is Bad Cholesterol!” bollockery in a Journal of American Physicians article that you can freely access here (for a Spanish version, click here).

I will repeat: Cholesterol does not cause heart disease. Cholesterol is an essential component of your cell membranes, and if someone were to suck all of the cholesterol out of your body you’d promptly collapse on the floor into a pile of mush, hair and bones.

Because of its key role in providing structural integrity to cell membranes, cholesterol constitutes an important repair substrate for our bodies. The lipid hypothesists wank on and on about how atherosclerotic plaques have been observed to contain cholesterol, but big deal. They’ve also been observed to contain white  blood cells, calcium, the allegedly heart-healthy omega-6 fatty acid linoleic acid, fibrous tissue, and more. Now, if someone came along and said we should all go on diets or take drugs that lower our white blood cell count in order to fight heart disease, they’d be roundly ridiculed and laughed at. Ditto if they said we should eat diets or take drugs that destroy fibrous tissue or deplete our body of calcium. But when someone comes along and makes the equally ridiculous claim that we should eat Spartan diets and take powerful drugs in order to lower our blood cholesterol, they make the cover of Time magazine, receive awards for their monumental contribution to furthering human ignorance cardiovascular science, take up lucrative positions at “lipid clinics” where they can further research the non-existent relationship between cholesterol and CHD while the rest of us work real jobs, and receive lucrative honoraria from drug companies to boot!

I just love the way this shit works. Not.

The bottom line is that cholesterol, just like most other components of atherosclerotic plaque, is in the plaque as part of the body’s attempt to repair a damaged section of artery. Cholesterol does not cause heart disease, no more than police officers and paramedics cause the accident scenes they attend – they’re there to deal with the mess after the accident already happened.

Cholesterol’s importance in the repair process may be a key reason why heart attack patients presenting to the emergency ward suffering heart attack and displaying high cholesterol levels are far more likely to survive the ordeal than those presenting with low cholesterol levels. Yeah, I know, you probably never heard this and it goes against all your anti-cholesterol brainwashing, but it’s true[1-4].

So as it turns out, the Nature Medicine anti-meat/anti-carnitine paper is now based on two utterly false premises. In addition to the “meat causes heart disease” fantasy, the researchers have also added the fairy tale about cholesterol causing heart disease to their repertoire of dodgey working assumptions.

Guys, can I stop here? Seriously, the idiocy is killing me!

Huh? What’s that? You want me to keep going? Something about never leaving a job half-done? And you want to hear more about this TMA charade?

Ah, bugger. Alright, on we go…

TMA = Too Many Assumptions [of a Most Untenable Nature]

Okay, so we’re now up to the bit where the researchers fed some volunteers carnitine supplements as part of their TMA gig. Before I describe what happened, I just have to share the following passage from p.2 of their paper with you:

“Given the similarity in structure between l-carnitine and choline (Fig. 1a), we hypothesized that dietary l-carnitine in humans, like choline and phosphatidylcholine, might be metabolized to produce TMA and TMAO in a gut microbiota–dependent fashion and be associated with atherosclerosis risk. To test this hypothesis, we initially examined data from our recently published unbiased small-molecule metabolomics analyses of plasma analytes and CVD risks.

An analyte with identical molecular weight and retention time to l-carnitine was not in the top tier of analytes that met the stringent P value cutoff for association with CVD. However, a hypothesis-driven examination of the data using less stringent criteria (no adjustment for multiple testing) revealed an analyte with the appropriate molecular weight and retention time for l-carnitine that was associated with cardiovascular event risk (P = 0.04).”

Due to the heavy use of gobbledegook, many of you won’t have a clue what all that means, but those of you familiar with both science-speak and the dodgey behaviour of statisticians are no doubt smiling one of those deep, knowing smiles right now. What they are essentially saying, in plain English, is this:

“We came up with this bright idea that carnitine might be converted to TMA and that this might increase CVD risk. So to see if this had any validity, we pulled out the data from a recent analysis we did linking itty bitty chemical substances to CVD risk. As it turns out, there were no substances with the same key characteristics as l-carnitine that were associated with CVD risk, which effectively sent our thesis down the toilet.

Damn.

However, we weren’t going to give up that easily, because if we could somehow support our thesis it could get us some kick-ass coverage in the media! Hey, nothing like another headline-grabbing paper to keep those research funds flowing in!

So what we then did was pretty much the research equivalent of donning beer goggles in order to make an ugly woman attractive enough to sleep with: We dramatically loosened up our criteria until we finally found a substance that had similar characteristics to l-carnitine and delivered us the statistically significant association we needed to proceed with our charade. Gotta love statistics! With enough TLC, you can massage and bend those numbers any way you want, baby!”

So after gettin’ jiggy with the “metabolomic” data and finding the flabby, dateless, gap-toothed association they were after – not with carnitine mind you, but with a substance that kinda sorta was a little bit like carnitine – they then proceeded with the clinical phase of their caper.

To get this phase rolling, they fed five omnivorous subjects an 8-ounce sirloin steak, corresponding to an estimated 180 mg of l-carnitine, together with a capsule containing 250 mg of isotope–labeled l-carnitine. They then observed modest post-meal increases in carnitine and TMAO.

Then, to examine the role of gut microbes in TMAO formation from dietary l-carnitine, they placed the same volunteers on oral broad-spectrum antibiotics to suppress intestinal microbiota and then performed a second l-carnitine “challenge”. After the week-long treatment with the antibiotics, they noted near complete suppression of detectable TMAO in the subjects’ blood and urine.

Nothing outlandish there.

Then they rounded up some more omnivores and also found themselves a bunch of vegans and vegetarians. They found fasting baseline TMAO levels were significantly lower among the vegans and vegetarians. In a subset of these individuals, they performed another carnitine challenge (but with no steak, only supplements) and found the vegans and vegetarians had a markedly reduced capacity to synthesize TMAO from the supplemental carnitine. Vegans and vegetarians also had significantly higher post-challenge plasma concentrations of carnitine compared to the omnivores, indicating they were unable to metabolize the carnitine as effectively. Given that carnitine plays a key role in cellular energy production, this is hardly worth bragging about, but as you’ll soon learn the researchers carry on like this is in fact a wonderful thing.

The next sections of the paper deal with the researchers fishing through some of the subjects’ faeces to determine the concentrations of choline, carnitine, TMAO and gut bacteria. This task, which I’m guessing they assigned to the junior members of the team, found certain types of bacteria were associated with plasma TMAO levels and being omnivorous or vegetarian/vegan. This in turn suggests that your usual diet will have an effect on both the bacterial composition of your gut and your ability to synthesize TMA and TMAO from dietary l-carnitine.

Again, nothing particularly outlandish.

Return of the Bollocks

It doesn’t take long, however, for things to start going downhill again. After some mice experiments which I’ll discuss later, the researchers put their epidemiological costumes back on and examined the relationship of fasting plasma concentrations of l-carnitine with CVD risk in 2,595 subjects undergoing elective cardiac evaluation. Among this sample, they observed a positive association with plasma carnitine and coronary artery disease, peripheral artery disease and overall CVD.

A look at the supplementary data soon reveals why: As plasma carnitine levels rose, so too did the patients’ age, rate of smoking, and pre-existing CAD and CVD. Yessir, the same old unhealthy-lifestyle-meets-red-meat phenomenon that has confounded so many other epidemiological studies is again at work here.

What a joke.

After the usual overrated adjustment for a limited range of “traditional CVD risk factors”, only the highest quartile of plasma carnitine showed an increased ‘risk’ of any note.

From this terribly slanted epidemiological study, they also examined the relationship between plasma carnitine and 3-year risk for composite of adverse cardiac events (death, myocardial infarction, stroke and revascularization). Again, only the highest quartile of carnitine concentration was associated with this composite endpoint, after adjustments for several CVD risk factors.

After further adjustment for plasma TMAO concentration and a larger number of accompanying comorbidities (e.g. extent of CAD, ejection fraction, medications and estimated renal function), the significant relationship between carnitine and the composite endpoint was completely abolished. For example, in patients exhibiting high plasma carnitine but low TMAO, the relative risk was actually reduced (0.80 adjusted hazard ratio) when compared to patients with low levels of both.

I guess that kinda got left out of the press release…

In patients with high levels of carnitine and TMAO, the HR was 2.1. But what does that prove? Absolutely nothing, except that high levels of carnitine and TMAO were associated with a higher risk of composite CVD endpoints in a sample of 3,000 patients. Exactly why they were associated with higher risk is anyone’s guess; Was it causal or, as per the situation with cholesterol, an after-the-fact association? This study is simply not equipped to tell us that, although I am here to tell you without a shadow of a doubt that carnitine does not cause heart disease. I’ll present the evidence for that assertion in uno momento, but for now let’s look at the next section of the study.

More Mouseshit

After the epidemiological entree, the researchers serve up their main course. Yep, this is where they roll out the mice and feed them either their usual chow diet or the same fare plus supplemental l-carnitine. The mice fed carnitine, of course, go on to develop more ‘atherosclerosis’ than those fed standard chow. I say “of course” because it hardly takes a brain surgeon to figure what is going to happen when researchers showing strong signs of a predetermined agenda take a special strain of a herbivorous animal and feed it large amounts of a substance it has never evolved to properly metabolize. Plant foods contain bugger all carnitine – the only meaningful source is animal flesh. So when you take an animal that has never developed the mechanisms to efficiently metabolize carnitine, it’s hardly surprising that pathological changes might occur after carnitine feeding.

This is the very same reason why feeding cholesterol – also found only in animal foods – has repeatedly produced ‘atherosclerosis’ in herbivorous lab animals over the years, but has completely failed to induce atherosclerosis in carnivorous animals. The former never evolved to efficiently metabolize cholesterol, while the latter did so on a daily basis. Dogs, for example, simply will not show any pathological changes in their arteries after being fed cholesterol unless you surgically remove their thyroids (again, I discuss this all in detail in The Great Cholesterol Con).

Now once again, let’s all stop and engage in one of those reflective moments where you angle your head slightly upwards and to the side and look like you’re deep in philosophical thought. But instead of pondering life’s deeper mysteries, I want you to simply ask yourself this:

If cholesterol feeding cannot induce atherosclerosis in meat-eating animals no matter how hard researchers try, why keep up the charade? Why the $#@% rip out the thyroid glands of man’s best friend? If they need to disfigure such beautiful and loyal creatures, shouldn’t that in itself tell them the cholesterol theory is utter bullshit? At what point do these researchers finally acknowledge reality, give up the cholesterol wank, and go searching for the real causes of heart disease?!

And you thought I was being overly misanthropic when I said the world was full of morons…

Anyways, back to our carnitine-fed mice. Did I mention that these were Apoe−/− mice?

What the bleep are Apoe−/− mice, I hear you asking?

Apoe−/− mice are specially bred mice that spontaneously develop ‘atherosclerotic lesions’ on a standard chow diet. If they develop arterial plaque like there’s no tomorrow on mice chow, what do you think is going to happen when they are supplemented an essentially foreign substance like carnitine?

Duh!

When the mice were given an oral antibiotic “cocktail” to wipe out their intestinal flora, in addition to l-carnitine, they showed marked reductions in plasma TMA and TMAO concentrations and no increase in atherosclerosis.

But so what? This still doesn’t change the fact that they are likely to metabolize carnitine very differently to humans. Proof of this comes from the researchers’ own initial studies with mice. This is where they gave them carnitine then cut them open to examine the bacterial compsition of their intestinal tract. They found “several bacterial taxa whose proportion was significantly associated (some positively, others inversely) with dietary l-carnitine and with plasma TMA or TMAO concentrations”.

However…

“…a direct comparison of taxa associated with plasma TMAO concentrations in humans versus in mice failed to identify common taxa. These results are consistent with prior reports that microbes identified from the distal gut of the mouse represent genera that are typically not detected in humans”.

In other words, my contention that this strain of mice metabolizes carnitine differently than humans is not just theoretical musing – it’s a plain fact.

Not fussed by yet another self-contradiction to their untenable anti-carnitine theory, the researchers continue on with their mice shenanigans. Rather than admitting their results have little real life applicability to humans, they instead seek to find a “mechanism” for the carnitine-induced atherosclerosis seen in the Apoe−/− mice.

They observed that both carnitine and choline inhibited what is known as reverse cholesterol transport, which basically refers to the removal of cholesterol from tissues into the bloodstream and back to the liver. To understand why this is significant, we have to ponder for a moment the grade-school mentality towards cholesterol that dominates the medical and science fields nowadays. When the cholesterol theory first started showing signs of self-contradiction many moons ago, researchers quickly went into salvage mode by claiming it wasn’t just total cholesterol that mattered, but the ratio of LDL:HDL. They labelled LDL the “bad” cholesterol because it took cholesterol to the tissues. I guess the fact that our tissues sorely need cholesterol and we’d be royally screwed if they didn’t get it never crossed their minds. Bottom line, appearing on the cover of Time magazine or receiving Nobel prizes in no way guarantees you have a clue what you’re on about. There is nothing “bad” about LDL – it serves a vital function in our bodies and we’d be in a really bad place without it.

But let’s continue on…

Next, they dubbed HDL the “good” cholesterol because that was the lipoprotein that carried cholesterol away from the tissues and back to the liver where it was broken down into bile.

And so was born the ridiculously simplistic good cholesterol/bad cholesterol charade, which like the total cholesterol theory is a complete and utter wank. Studies have repeatedly shown that LDL does not cause atherosclerosis nor heart disease, something I discuss at length in my LDL paper.

So researchers then latched onto the oxidized LDL theory, again using the childishly simplistic logic that the higher your LDL, the higher your oxidized LDL.

And again, it was complete nonsense. While oxidized LDL may indeed be harmful, it has no relationship with your levels of total or LDL cholesterol. Rather, poor antioxidant status and disordered blood sugar control are the main culprits. Again, I discuss this in my LDL paper which you can access free of charge thanks to the good folks at JPANDS right here.

Oh, and remember how the researchers also observed that the nutrient choline inhibited reverse cholesterol uptake? Well, notice how they remain silent about that, and focus their hate campaign on carnitine which, unlike choline, is found mainly in red meat?

What they would be well aware of, but have chosen to ignore, is that carnitine-containing red meat is hardly the only food that raises TMA levels nor does it even come close to being the food that causes the greatest spike in TMA levels.

Guess which food causes the greatest hike in TMA levels?

Fish.

Yep, heart-healthy fish.

Thanks to a condition known as trimethylaminuria, whose unfortunate sufferers experience ‘‘fish-odour syndrome’’, numerous researchers have investigated the potential TMA-raising effects of choline and choline precursors and, more recently, actual foods.

Some especially insightful findings come from scientists at the Imperial College in London, who examined the urine of healthy male volunteers fed 30 different foods. Not all at once, of course. Instead, on separate occasions the volunteers consumed a 227 g serving of the foodstuff under investigation along with a standardized breakfast.

Beef ingestion resulted in negligible amounts of urinary TMA: a mere 20µg trimethylamine/g food, less than that seen for bread, carrots, cauliflower, cabbage, mushroom, peas, and potatoes. Lamb, by far the richest dietary source of carnitine, returned a score of 16.4µg.

In stark contrast, prawns, mackeral and cod delivered urinary TMA levels of 948, 679, and 1335µg trimethylamine/g food, respectively!

A previous paper by the same researchers also reported combined urinary levels of TMA+TMAO and found similar results. Beef and lamb produced lower urine levels of TMA+TMAO than the overwhelming majority of vegetables, all fish and seafood products, cheese, and eggs.

This previous paper also reported the effect of oral ingestion of betaine (1.76 g), carnitine (2.97 g), choline (2.10 g), creatinine (1.70 g), lecithin (11.65 g) and TMAO (1.67 g) on six separate occasions. Betaine, creatinine, and lecithin all failed to raise urinary TMA+TMAO levels. TMAO, not surprisingly, produced the highest levels, followed by choline. Carnitine, meanwhile, was converted to TMA+TMAO at only half the rate of choline (30.6% vs 62.9%, respectively).

Now let’s get back to the Nature Medicine paper. The researchers wanked on and on about red meat, but made no effort to investigate other foods, even though many other foodstuffs have already been documented to produce much higher TMA and TMAO increases than red meat. Based on the results of previous research, if we are going to make the extraordinary claim that carnitine-rich red meat causes heart disease due to its effects on TMA/TMAO levels, then for the sake of consistency we also need to claim that a far higher risk is posed by choline, most vegetables and all seafood.

Such a claim, of course, would be ridiculous. So the researchers simply ignored the inconvenient choline, vegetable and seafood data, and went about constructing a case against red meat.

Can you say preconceived agenda?

Summing It All Up So Far

So what we have is a study which used misrepresented epidemiology, blatant cherry-picking and a singles bar attitude to metabolomics as a springboard to validate what strongly looks like a preconceived agenda to implicate red meat and carnitine in the pathogenesis of heart disease.

This validation rests heavily on studies with a genetically modified strain of a herbivorous creature that is 0.001 the size of adult humans who follow omnivorous diets and have done so for millions of years. Despite the stark differences between the two species, this idiotic comparison is now being used to claim carnitine causes heart disease and to scare people away from both red meat and carnitine.

In further justification of their absurd theory, the researchers cite the allegedly lower CVD risk enjoyed by vegetarians and vegans. I recently explained in detail why the claim vegetarian/vegan diets confer protection against heart disease is yet another example of anti-science at its finest, propagated by people with an anti-meat agenda:

Vegetarian Diets Reduce Heart Disease? Nonsense!

The researchers even cite the Lyon Diet Heart Study in support of their theory, noting the subjects were instructed to eat less red meat. Yes, but they were also instructed to eat more fruits and vegetables and supplied with a special omega-3-rich spread. Blood testing showed both their serum antioxidant and omega-3 levels were increased; no such information was available for carnitine or TMA/TMAO.

The sad reality is that the Nature Medicine paper is one of the most poorly conceived pieces of rot I’ve had the misfortune of reading in a long, long time.

Ah, the good old days. When men were men, worked real jobs instead of playing with their statistics, and beat fresh carcasses in their pursuit of physical excellence.

Why Carnitine is Your (Very Good) Friend

Okay, I think we’ve well established that the methodology and reasoning in the Nature Medicine paper is dodgier than a drug-dealing loan-shark who also dabbles in used car sales.

What we’re now going to do is examine even more evidence the Nature Medicine researchers blatantly ignored – evidence not only showing carnitine does not cause cardiovascular disease, but may in fact benefit it.

I must say, I was shocked when I first heard about the current anti-carnitine hate campaign. I’ve read a lot about this amino acid over the years and have only ever been able to discover good things about it. So why on Earth were they picking on this beautiful, energy-providing amino acid, I wondered?

Like cholesterol, there is nothing “bad” about carnitine. Like cholesterol, it performs crucial functions in the body and if someone were to shove a carnitine-specific vacuum up your keester and completely suck this crucial amino acid from your body, you’d find yourself in a whole heap of trouble, real quick.

Carnitine is found in nearly every cell in your body, and plays a critical role in energy production. And when I say critical, I really do mean critical. It transports fatty acids into the “engines” of your cells – the mitochondria – so they can be oxidized to produce energy. Some very unfortunate folks suffer from a condition known as primary carnitine deficiency, a genetic disorder that interferes with cellular carnitine transport. This condition usually manifests itself by five years of age, and common symptoms include cardiomyopathy (which in turn increases the risk of heart failure), skeletal-muscle weakness, and hypoglycemia.

Carnitine also transports toxic compounds generated during energy production out of the mitochondria to prevent their accumulation. Yep, carnitine is one hell of a compound; it fuels your cellular engines and cleans them at the same time. The physiological equivalent of BP Ultimate, if you will.

Thanks to its critical role in fat-derived energy production, carnitine is concentrated in tissues like skeletal and heart muscle where fatty acids constitute a vital fuel source.

While muscles also rely heavily on carbohydrate (save me the “fat adaptation” speech, oh ye flabby low-carbers who bonk ten minutes into a strenuous ride), the heart relies primarily on fatty acids even when you consume a high-carb diet.

Are you beginning to see why I hold the anti-carnitine authors and the screwball journalists who uncritically soaked up their nonsense with such contempt? If the world listens to these maniacs and embarks on an anti-carnitine campaign, we will much more likely see an increase  in heart disease, rather than a decrease. Not to mention a marked decline in overall health and well being.

Bold claim?

Not at all.

The Evidence they Ignored

We discussed how the researchers chose a specially bred strain of mice to prove their point that carnitine promotes atherosclerosis. Having obtained the results they were after, they then engage in some highly questionable extrapolation to incriminate carnitine as doing the same thing to humans.

Well, guess what? This was hardly the first time researchers had fed carnitine to herbivorous animals.

And guess what else? Yep, they obtained results starkly different to those reported in the Nature Medicine paper. Not surprisingly, that paper does not so much as mention these conflicting studies.

Here are just a few:

Spanish researchers took mice bred to be especially prone to obesity and fed them a high-fat diet for nine weeks, during which time they suffered reduced cardiac output, worsening arterial function, deteriorating glycemic control, and decreased tissue production of nitric oxide (the gas that helps keep your arteries supple and elastic). During the subsequent four weeks, they divided the mice into 2 groups. One group continued to receive plain water, while the other group’s drinking water was supplemented with carnitine (200 mg/kg/day). The carnitine-enhanced water improved cardiac output, arterial function, insulin resistance and increased nitric oxide levels. Plain water had no effect.

Egyptian researchers deliberately made rabbits hypercholesterolemic by feeding them cholesterol (again, unlike humans they aren’t equipped to properly process cholesterol, and dietary ingestion quickly raises their blood levels). They then made them carnitine deficient, and observed severe atherosclerotic lesions, intimal plaques and foam cell formation. Daily administration of L-carnitine (250 mg/kg), for 28 days, completely prevented the progression of atherosclerotic lesions in both aorta and coronary arteries.

Italian researchers similarly found that rabbits on a cholesterol-enriched diet who were supplemented with l-carnitine experienced a “decrease of plaque cell proliferation and severity of aortic atherosclerotic lesions.”[5]

So even in other strains of mice and in rabbits, other researchers have found no adverse effect of carnitine and in fact have found beneficial effects!

But that’s in animals. What cardiovascular effects does supplemental carnitine have in humans?

The Italians: Not Just Hot Curvy Babes and Hot Curvy Cars

The Italians have performed a lot of research on both l-carnitine and acetyl-l-carnitine, and their work is crying out to be replicated by other groups (of course, if carnitine were a patentable drug, this replication would have happened long ago). As far back as the 1970s and 1980s, they had reported l-carnitine improved exercise tolerance, reduced infarct size in heart attack patients, and reduced post-cardiac event mortality at one and six months.

Inspired by these early results, in 1992 Italian researchers published the results of a carnitine intervention trial involving 160 recent heart attack victims. This was a non-blinded trial in which patients were randomly assigned to 4 grams daily of carnitine in addition to their usual medication, or to a group which received their usual medication but no supplemental carnitine. After one year, there were ten deaths in the control group (8 due to cardiovascular causes) but only one in the carnitine group (due to thromboembolism).

In addition to greatly lowered mortality risk, the patients in the carnitine group also enjoyed improvements in heart rate and blood pressure, and a reduction of angina attacks, rhythm disorders, and signs of impaired heart muscle contractility[7].

Another group of Italian researchers took thirty-eight elderly patients suffering heart failure, and randomly assigned them to receive either l-carnitine or placebo in addition to their usual medical care. The dose was 1g twice daily, for 45 days. Those receiving carnitine experienced greater ECG improvements and a marked reduction in their daily digitalis requirement. No adverse reactions to carnitine were observed in any of the patients[8].

These were small, short studies; to see if they could be replicated in a larger, double-blind trial, a larger Italian study was commenced. This study, published in 2005, aimed to determine the effect of L-carnitine in patients presenting to cardiology units with heart attack. In those receiving carnitine, the amino acid was delivered at a dose of 9 grams intravenously for the first 5 days, then then 4 grams per day orally for the next 6 months. The researchers had originally planned to include 4,000 patients with acute anterior myocardial infarction, but lower than expected numbers of eligible patients meant only 2,330 patients participated.

During the first 5 days, patients receiving the high-dose IV carnitine enjoyed a significantly lower rate of mortality. During the remainder of the study, this advantage dissipated; at 6 months, the carnitine group showed a non-significant 14% relative reduction in the combined occurrence of death and heart failure, and a non-significant 12% lower overall mortality.

Disappointing, but hardly supportive of idiotic claims that “Carnitine Causes Heart Disease!”

Hopefully researchers will keep studying the cardiovascular effects of carnitine, and hopefully not in isolation but in conjunction with other critical and potentially synergistic nutrients such as taurine, CoQ10 and even creatine. All of which, by the way, are only found in animal products (hmmm, I wonder how long will it take for some nutty research crew to come out and claim they are also bad for your heart…)

There’s been a whole bunch of studies examining the effect of effect of carnitine on walking distance in patients with peripheral arterial disease. Researchers at Adelaide’s  Flinders University recently conducted a review of this research and found “Most trials demonstrated a small or modest improvement in walking performance with administration of PLC [propionyl-l-carnitine] or l-carnitine. These findings were largely independent of level or quality of evidence, while there was some evidence that intravenous administration was more effective than oral administration and those with severe claudication may achieve greater benefits than those with moderate claudication.”

They also noted in their conclusion, “Routine carnitine supplementation in the form of PLC may therefore be a useful adjunct therapy for management of intermittent claudication.”[9]

Carnitine has also been shown to benefit, of all things, erectile dysfunction. Yep, researchers recruited a bunch of aging Italian ex-Stallions and then randomized them to either 4 grams daily of carnitine (2g acetyl-l-carnitine + 2g propionyl-l-carnitine), 160mg testosterone undecanoate, or placebo for 6 months. During the six months of the study, the carnitine combo proved significantly more effective than testosterone undecanoate in improving “nocturnal penile tumescence“, which is science-speak for nighttime boners. Carnitine was also significantly more effective for improving scores on the International Index of Erectile Function (yes, they have an international index for this kind of thing).

A year later, the same researchers published the results of another study involving patients who underwent prostatectomy. They compared sildenafil, sildenafil plus the aforementioned carnitine mix, or placebo. The carnitine+sildenafil group scored significantly better than sildenafil-only patients for erectile function, sexual intercourse satisfaction, orgasm, and general sexual well-being. Only the carnitine+sildenafil group had a significantly increased percentage of patients with a positive intracavernous injection test (please don’t ask me to describe what that involves…)

A more recent Italian study examined supplementation with propionyl-L-carnitine, L-arginine and niacin and sexual performance among men presenting to an erectile dysfunction clinic. After three months of treatment, a small but statistically significant improvement in total and individual items of the International Index of Erectile Function was found. Analyses of global assessment questions answered by the patients revealed the nutrient trio improved erections in 40% of cases, with a partial response occurring in up to 77% of subjects enrolled.

L-carnitine: Critical for your ticker, good for your pecker too!

In Closing…

If I haven’t convinced you by now that the study behind the current carnitine hating is complete and utter horseshit, then nothing will. For the rest of you that haven’t recently undergone a lobotomy, it’s important you start standing up to this kind of rot. This is serious business folks. Googling around, I see this study has received immense worldwide coverage while very few rebuttals have been posted, despite the fact it is patently absurd nonsense.

In recent times there seems to be an intensifying of research efforts, no matter how ridiculous, aimed at vilifying perfectly natural and wholly nutritious animal foods (see my article on the atrocious anti-egg research of Canadian trio Spence et al here, and the recent claim that vegetarian diets reduce heart disease here).

I’m not sure what the endgame is here. Some folks out there are convinced this growing anti-animal food crusade is part of some wider conspiracy, something I’m simply not placed to endorse nor refute. And while some of you are no doubt snickering and making jokes about tin foil hats, I will point out the following: Anyone who’s read Marvin Harris’ truly brilliant Cannibals and Kings will know this would hardly be the first time in history the powers-that-be have instigated and nurtured efforts to vilify certain types of meat in order to fulfill ulterior motives.

Regardless of whether or not a bunch of wealthy oligarchical assholes are covertly trying to manipulate our perceptions of certain foods, I sincerely doubt garden-variety research teams are a knowing part of any such agenda. Far more likely and ubiquitous explanations are the power of conformity, the desire for recognition, and financial gain.

In the “Contributions” section of the Nature Medicine paper (which can be viewed by clicking here and scrolling down) we learn “S.L.H. [co-author Stanley Hazen] conceived of the idea, helped design the experiments, provided the funding for the study and helped draft and critically revise the manuscript”.

Scrolling further down and taking a quick look at the competing financial interests of the authors  reveals the usual links to drug companies and research outfits that profit handsomely from the cholesterol sham:

“Z.W. [Zeneng Wang] and B.S.L. [Bruce Levinson] are named as co-inventors on pending patents held by the Cleveland Clinic relating to cardiovascular diagnostics and have the right to receive royalty payments for inventions or discoveries related to cardiovascular diagnostics from Liposciences. W.H.W.T. received research grant support from Abbott Laboratories and served as a consultant for Medtronic and St. Jude Medical. S.L.H. [Stanley Hazen] and J.D.S. are named as co-inventors on pending and issued patents held by the Cleveland Clinic relating to cardiovascular diagnostics and therapeutics patents. S.L.H. has been paid as a consultant or speaker by the following companies: Cleveland Heart Lab., Esperion, Liposciences, Merck & Co. and Pfizer. He has received research funds from Abbott, Cleveland Heart Lab., Esperion and Liposciences and has the right to receive royalty payments for inventions or discoveries related to cardiovascular diagnostics from Abbott Laboratories, Cleveland Heart Lab., Frantz Biomarkers, Liposciences and Siemens.”

But my eyebrows were raised when I read about “patents” and “royalty payments…relating to cardiovascular diagnostics”. So I jumped onto Google and promptly discovered the following patent application: “TRIMETHYLAMINE-CONTAINING COMPOUNDS FOR DIAGNOSIS AND PREDICTION OF DISEASE”

The applicant is seeking a patent for TMA tests that will purportedly determine whether people are at risk of developing CVD, diabetes, insulin resistance, metabolic syndrome, or fatty liver.

The applicant/owner of the patent is none other than The Cleveland Clinic Foundation, and the listed inventors are, lo and behold, Stanley Hazen, Bruce Levison, and Zeneng Wang.

And so we now see a potentially very lucrative income stream for these researchers if their carnitine/red meat/TMA/heart disease charade gains traction. Again, this kind of information gets left out of the hyperbolic fanfare accompanying the release of these types of studies, and it’s left up to people like me – you know, living out here in “left field” sipping Dom Pérignon in our jaccuzzis, being pampered by half our supermodel harems while the other half washes our collection of exotic supercars out on our imported Italian marble driveways -  to point out the absurdities and blatant conflicts of interest in these intelligence-assaulting studies.

Folks, stand up to stupid…it really isn’t that hard.

Otherwise, in 20 years time, billions of your (and your children’s) taxpayer dollars are going to be handed over to clueless researchers attempting to uncover the ‘paradox’ of why red meat consumption has dramatically diminished yet heart disease still remains our number one killer, along with an ‘unexplained’ increase in anemia and chronic fatigue…

Related and Recommended Reading:

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*Please note AnthonyColpo.com does not condone reckless driving on public roads. If the author was wealthy enough to own and thrash a Lamborghini, he would most assuredly do it on a racetrack. Or in a muddy paddock. Now that would be fun. Or maybe the giant car park next to Bunnings at…uh, never mind.

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1. Onder G, et al. Serum cholesterol levels and in-hospital mortality in the elderly. American Journal of Medicine, Sep, 2003; 115 (4): 265-271.

2. Horwich TB, et al. Cholesterol levels and in-hospital mortality in patients with acute decompensated heart failure. American Heart Journal, Dec, 2008; 156 (6): 1170-1176.

3. Stachon A, et al. Prognostic Significance of Low Serum Cholesterol after Cardiothoracic Surgery. Clinical Chemistry, 2000; 46 (8): 1114–1120.

4. Spinar et al. Baseline characteristics and hospital mortality in the Acute Heart Failure Database (AHEAD) Main registry. Critical Care, 2011; 15: R291.

6. Spagnoli LG, et al. Propionyl-L-carnitine prevents the progression of atherosclerotic lesions in aged hyperlipemic rabbits. Atherosclerosis, Apr 7, 1995; 114 (1): 29-44.

7. Davini P, et al. Controlled study on L-carnitine therapeutic efficacy in post-infarction. Drugs Under Experimental And Clinical Research, 1992; 18: 355-365.

8. Ghidini O, et al. Evaluation of the therapeutic efficacy of L-carnitine in congestive heart failure.  International Journal of Clinical Pharmacology, Therapy and Toxicology, Apr, 1988; 26 (4): 217-220.

9. Delaney CL, et al. A systematic review to evaluate the effectiveness of carnitine supplementation in improving walking performance among individuals with intermittent claudication. Atherosclerosis. 2013 Mar 15. pii: S0021-9150(13)00179-2. doi: 10.1016/j.atherosclerosis.2013.03.004. [Epub ahead of print]

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Anthony Colpo is an independent researcher, physical conditioning specialist, and author of The Fat Loss Bible and The Great Cholesterol Con. For more information, visit TheFatLossBible.net or TheGreatCholesterolCon.com

Copyright © Anthony Colpo.

Disclaimer: All content on this web site is provided for information and education purposes only. Individuals wishing to make changes to their dietary, lifestyle, exercise or medication regimens should do so in conjunction with a competent, knowledgeable and empathetic medical professional. Anyone who chooses to apply the information on this web site does so of their own volition and their own risk. The owner and contributors to this site accept no responsibility or liability whatsoever for any harm, real or imagined, from the use or dissemination of information contained on this site. If these conditions are not agreeable to the reader, he/she is advised to leave this site immediately.

Dr. Stephen L. DeFelice is something of a quiet achiever in the world of medicine. While many folks have never heard of him, he recently won the annual UNICO Marconi Science Award for his efforts with carnitine and accelerating medical discovery.

Dr DeFeLice is the physician who brought carnitine into the U.S. in 1965 and has been involved in research on it ever since, including efforts to get it approved as an orphan drug back in the 80s.

In other words, if anyone knows a thing or two about carnitine, it’s Dr DeFelice. Like yours truly, he was aghast at the recent anti-carnitine beat-up that Nature Medicine, in a display of terribly poor judgement, posted on their website on April 7 ahead of print publication (seriously Nature Medicine, do you guys still have a peer review process? If so, how on Earth did such misleading and one-sided slop make it into your journal?)

In response, on April 18 Dr DeFelice issued a press release about carnitine, which I have reprinted in full below.

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Carnitine: A Highly Promising Biomarker and Proven Treatment for Cardiac Disease and a Case Against it as a Cause of Atherosclerosis

Stephen L. DeFelice, M.D., Founder and Chairman of FIM, The Foundation for Innovation in Medicine, who brought carnitine into the United States, speaks out on the current carnitine controversy.

WESTFIELD, N.J., April 18, 2013 /PRNewswire- US Newswire/ — L-carnitine is a natural substance found in high concentrations in the heart. It transports fatty acids into mitochondria, the furnaces of the cell, to be metabolized and produce energy. Because the heart requires high levels of energy it primarily uses fat which has more calories per unit than sugar.

I’m the physician who brought L-carnitine into the United States in 1965 to conduct the first clinical trial in patients with hyperthyroidism. Later on, I was stationed at WRAIR, the Walter Reed Army Institute of Research, and, for certain reasons, believed that L-carnitine could both prevent and treat myocardial ischemia, a lack of oxygen supply to the heart, even during a heart attack. At the institute I was fortunate to meet an expert cardiovascular pharmacologist, Major James Vick . Together we conducted a number of animal studies supporting my hypothesis. When hearts were made ischemic, arrthymias and cardiac arrest ensued. When given before, during or after the ischemic phase, L-carnitine dramatically prevented and reversed these events. We also found that L-carnitine reversed hearts that were in congestive failure.  Subsequent laboratory studies by other investigators confirmed these findings. In other animal studies, including monkeys, we showed that L-carnitine protects the heart against a number of toxins including the septicemia- producing bacterium, E.coli, and the anti-cancer drug, doxorubicin.

In an animal experiment, scientist Austin Shug of the University of Wisconsin, as a member of a research team, discovered, that L-carnitine leaks out from the ischemic portion of the myocardium. He and I then met with cardiologist James Thomsen of the same university and planned a clinical protocol in patients with coronary artery disease. The study was conducted and demonstrated that L-carnitine protects the human heart against myocardial ischemia (The American Journal of Cardiology in 1979). Then Dr. Shug teamed up with physician, Vera Regitz , at the German Heart Institute. In a series of clinical studies conducted in patients with congestive heart failure, cardiomyopathy and coronary artery disease they discovered that, in these conditions of cardiac stress, cardiac muscle levels of L-carnitine are very low while blood levels are significantly higher than normal. (The last publication is linked to this press release on www.fimdefelice.org). This indicates that the high blood levels are due to leakage from the myocardium or heart muscle. Elevated L-carnitine blood levels, therefore, is a highly promising biomarker for of serious cardiac distress and due to and not a cause of atherosclerosis as misinterpreted in the Clevelandclinical study. (This offers an interesting opportunity for an innovative medical device company). From a medical therapeutic point of view, high doses of L-carnitine should have been administered to these patients. In animal studies Vick and I first showed that much higher than normal blood levels of L-carnitine are needed to prevent and reverse ischemia as well as having other beneficial cardiac effects. This observation has been subsequently confirmed by other investigators in multiple animal and clinical studies.

On April 13 of this year- last week- the findings of a multicenter clinical study were published in Mayo Clinic Proceedings reporting that L-carnitine, when administered after a heart attack, significantly reduces death from all causes as well as causing a significant reduction of ventricular arrthymias and angina attacks when compared to placebo or a control group.

You may wonder with the abundance of published laboratory and clinical studies reporting the cardiac benefits of L- carnitine, why does it remain a “secret” to doctors particularly since it is approved for such uses in other countries. Generally speaking, doctors learn about pharmaceuticals after FDA approval which is followed by promotional-educational programs by pharmaceutical companies. In the early 70′s I did make an attempt to launch a clinical program with L-carnitine to obtain FDA approval for coronary artery disease. The Thomsen study was part of that effort. It was my first lesson of medical economics; L-carnitine lacked a patent. In addition, since it is a natural substance, it is difficult to obtain a strong patent. But based on  laboratory studies which I sponsored, I managed to obtain use or methods patents for a number of cardiac conditions. Though such patents are not strong ones, I did manage to obtain initial interest of support until D,L carnitine appeared in the health food stores freely available for purchase by the consumer. Understandably, the support was withdrawn. Later on L-carnitine distribution in these stores shortly followed which was the final nail in the coffin.

Because of the Orphan Drug Act, however, I teamed with the late Dr. Claudio Cavazza , the proprietor of Sigma tau, Inc. and a good man, to obtain two FDA approvals – Primary Carnitine Deficiency, a fatal disease in children and for patients undergoing renal dialysis. So both the intravenous and oral forms of pharmaceutical quality are now available to physicians by prescription to administer to patients for heart conditions.  But there is still that dilemma that no company is permitted to launch an educational program without FDA approval. On the other hand, doctors are permitted to prescribe without such approval. Bottom line, the cardiac promise of L-carnitine is too important to be withheld from the medical community.

(There is confusion regarding whether L-carnitine is a dietary supplement or FDA approved pharmaceutical. It’s both.)

Getting back to carnitine as a cause of atherosclerosis, children with Primary Carnitine Deficiency experience life-threatening heart failure which is reversed by L-carnitine which restores its cardiac levels. Many of these children have been on very high doses of L-carnitine for long periods of time without any signs of atherosclerosis. It is FDA approved as a drug and also in many other countries where long-term animal safety studies at high doses are required . These studies show no signs of atherosclerosis. The FDA approved package insert lists no serious side effect of L-carnitine.

Many parents of children who are being treated with L-carnitine are now legitimately concerned about the safety of carnitine. Hopefully, this brief review will lighten their burden. Its efficacy and safety have long been established.

This press release is posted online along with the Regitz study and more information on carnitine at www.fimdefelice.org.

Contact: Patricia Park
fimdefelice@aol.com, 908-233-2448
The Foundation for Innovation in Medicine
SOURCE FIM, The Foundation for Innovation in Medicine

RELATED LINKS
http://www.fimdefelice.org

See also:
Bullshit Study of the Year: “Carnitine Causes Heart Disease”

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Anthony Colpo is an independent researcher, physical conditioning specialist, and author of The Fat Loss Bible and The Great Cholesterol Con. For more information, visit TheFatLossBible.net or TheGreatCholesterolCon.com

Copyright © Anthony Colpo.

Disclaimer: All content on this web site is provided for information and education purposes only. Individuals wishing to make changes to their dietary, lifestyle, exercise or medication regimens should do so in conjunction with a competent, knowledgeable and empathetic medical professional. Anyone who chooses to apply the information on this web site does so of their own volition and their own risk. The owner and contributors to this site accept no responsibility or liability whatsoever for any harm, real or imagined, from the use or dissemination of information contained on this site. If these conditions are not agreeable to the reader, he/she is advised to leave this site immediately.

Please note: This article contains occasional use of words that rhyme with and sound a lot like phuck, phucktard, and bullschit. Do not continue if you are offended by such words.

And definitely do not continue if you’re the kind of dimwit who thinks it’s fine for others to launch unprovoked attacks on my persona, but a big sin for me to return in kind. If that’s you, the following article may trigger an aneurysm LOL

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Kate writes:

Anthony, I’d love to see your response to this guy calling you out:

http://primalnorth.blogspot.com/2013/05/sorry-anthony-colpo-truly-keto-athletes.html

Not a strong case at all in my opinion.

Anthony replies:

Well, well, what do we have here? Some very cocksure joker claiming I’ve got it all wrong when it comes to the well-established inferiority of low-carb diets for athletic performance.

The author, some bloke by the name of Danny Albers, uses the same entirely predictable method of attack favoured by virtually all my critics. It pretty much goes like this:

1. Read something by Anthony Colpo that destroys cherished beliefs;

2. Get angry! “How dare that Colpo asshole dispute something I staunchly believe in?!”

3. Pull out keyboard and type up long-winded blog post falsely accusing Colpo of cherry-picking and dishonesty. Include lots of smug, condescending insinuations and/or outright accusations that Colpo deliberately ignored or was too myopically dumb to include evidence refuting his argument!

4. To strengthen case against Colpo, employ lots of cherry-picking and dishonesty. Yeah, this is extremely hypocritical, but it’s for the good of the low-carb/vegan/intermittent fasting/[insert name of other beloved screwball diet] cause! Hey, all’s fair in hate and war!

5. When Colpo provides a spirited and uncomfortably sound refutation of this defamatory and totally unprovoked attack, accuse him of being nasty and vitriolic! Yes, this is ridiculously hypocritical, but refer back to #4.

We’ve seen this tired approach used by everyone from the lowliest Internet trolls to PhDs and MDs, all of whom have repeatedly and spectacularly failed to discredit my arguments. In fact, what they usually achieve is to both make themselves look like complete idiots and strengthen my own case even further.

Despite this well-established pattern, there’s still always some goofball out there who makes the mistake of assuming I’m as dumb as he/she is, who earnestly thinks he/she will be the one glorious pioneering troll to finally topple me with their patently transparent use of red herrings, misquotations and outright lies.

And so it is with poor Danny.

Danny Is as Danny Does

Albers doesn’t waste any time unleashing the bullshit – check out the heading to his post, for example:

“Sorry Anthony Colpo – Truly Keto Athletes Do Exist”

Sorry Danny, but I never said they didn’t.

What I did say was low-carb diets are distinctly inferior to high carb diets for athletic performance and that there are no athletes who have won world class athletic events while following truly low-carb diets. And I stand by both of these statements for the simple fact that they’re true, and will continue to stand by them until such time someone can provide me with factual evidence to the contrary, as opposed to smug, evasive, duplicitous, ad hominem Internet hogwash.

By the way, when I refer to athletic performance, I’m talking about strenuous glycogen-depleting activities in which you continually move your body through space, as opposed to standing on a stage in undies and flexing your muscles. Nonetheless, high-carb diets have scientifically and empirically documented advantages over low-carb diets for bodybuilders also, something we’ll discuss shortly.

So right from the outset, Danny’s article is based on a fraudulent statement, the claim that somewhere, sometime, in a galaxy far, far away, I made the assertion there are no keto athletes on Planet Earth, which is total bullshit.

Unfortunately, low-carbers revel in bullshit. They lather it up, joyfully rub it all over their skin with a near orgasmic expression on their faces– kind of like that sheila in the old Lux commercials, but with a triple chin – then lay back as it soaks deep into their eager pores, basking in the pungent radiance that only the freshest, sloppiest, nostril-pinching bovine poo-poo can emanate.

And, it must be said, Albers is no exception.

When trumpeting his fallacious “Colpo reckons there are no keto athletes!” red herring, Albers ignores a rather inconvenient fact. Namely, I’m no fan of vegetarian diets and I think vegan diets suck every bit as hard as low-carb diets, yet I’ve openly discussed the fact there are vegetarian and vegan athletes who – unlike low-carb athletes – have actually won world class athletic events. Why would I make this concession for vegan athletes, but not low-carb athletes, when I staunchly believe both dietary paradigms are a load of overhyped and pseudoscientific rubbish (as anyone who has ever spent more than four seconds at my website can readily attest)?

The answer to that is I make no such concession because there are no true low-carb athletes who have won a truly world class athletic event. But Albers needs to believe otherwise, because his mental capacity and strength of character simply do not allow him to consider the possibility that it is he – not me – who is wrong.

While Albers struggles to find endurance athletes who kinda-sorta-maybe-once-for-a-short-while followed low-carb diets, Dave Scott won the biggest triathlon event on the globe, the gruelling Hawaii Ironman, while following a strict vegan diet. And it was hardly a one-off fluke; while following his vegan diet, Dave repeated his win an amazing six times, a feat that has since been matched by only one other competitor (Mark Allen)!

Now, using the very same logic that underscores Danny’s own argument, this would mean that vegan diets are @#$%ing awesome for athletes, that there is absolutely no disadvantage to these diets, and that anyone who claims otherwise is a dopey, cherry-picking, conspiracy theorist dipshit! Hey, if anecdotal tales about people who allegedly train and even compete on low-carb diets are to be taken as ‘proof’ these diets are great for exercise, the experiences of people like Dave Scott should rightly be taken as proof that vegan diets are the most awesome of all.

If you’re a moron, that is.

Stop Telling Tales

Anecdotal stories, while useful, cannot be considered proof of a diet’s efficacy or superiority for a number of reasons. The main being that they are a highly uncontrolled example of evidence, one that does not take into account a virtually limitless array of potential confounders. In Dave Scott’s case, for example, we can reasonably ask if he would have done just as well or even better if he consumed animal products along with his plant foods. The answer, according to Dave himself, appears to be yes.

In 1994, he began eating fish, chicken and turkey and after doing so found his diet to be, in his own words, “much, much healthier”.  Which just goes to show that a gifted, hard-training athlete can follow an inferior diet and still kick ass; innate talent and hours upon hours of dedicated training can help an athlete succeed in spite of a less-than-optimal diet. Keep this in mind a little later when we discuss the list of athletes and non-competitive exercisers Danny has dredged up in his desperate attempt to support his limp low-carb thesis.

By the way, if you’re a reality-hating zealot who refuses to believe what I’ve just written, then fine, listen to Dave “The Man” Scott himself:

Refreshingly objective and non-religious dietary commentary from one of the greatest triathletes of all time.

The same year he began consuming animal flesh, Scott came out of competitive retirement at the age of 40 to take second place at the Hawaii Ironman World Championships, very nearly winning for a record-breaking seventh time. A pretty damn impressive performance after a long competitive lay-off, and especially impressive for someone whose age would qualify him as a master’s athlete in many sporting organizations. And that wasn’t the end of it – in 1996 at age 42, he returned again to place 5th, running the marathon in 2:45.

Anecdote versus Science

Obviously, relying solely on anecdotal tales can lead to all sorts of misleading assumptions. Therefore, the best way to determine whether a low-carb, vegan or whatever other diet is superior or even just plain equal when compared to the omnivorous high-carb diet typically recommended to athletes is not by cherry-picking examples of athletes and bodybuilders who allegedly follow your favoured diet. Rather than resorting to such selective, subjective and highly defective bollockery, the correct approach would be to defer to the scientific method and conduct a randomly controlled clinical trial (RCT) in which your favoured diet is compared to an omnivorous high-carb diet.

Which brings us to the second act of blatant dishonesty committed by Albers. He claims “My favorate [SIC] way to counter sweeping declaritions [SIC] of certainty is with a clinical trial that proves otherwise.”

He then provides links to two of these ‘clinical trials’, but one is not a trial at all – it’s simply a discussion paper by none other than Stephen Phinney:

http://www.nutritionandmetabolism.com/content/1/1/2

Phinney, as my regular readers will know, is a researcher who has ‘tested’ low-carb diets and erroneously claims they do not impair endurance performance. Phinney has participated in Atkins-funded research, sits on the Atkins Nutritionals “Science Advisory Board“, and has a further vested financial interest in the low-carb paradigm via his books The Art and Science of Low Carbohydrate Performance, The Art and Science of Low Carbohydrate Living and The New Atkins for a New You (all co-authored with Atkins-sponsored researchers Jeff Volek and Eric Westman).

Phinney is also the guy who caused an excited buzz in the low-carb community late last year when he publicly claimed ultra-endurance runner Timothy Olson won the Western State 100-mile race while following a low-carb diet. But when asked for further details about Olson’s diet, Phinney flatly refused to share them, stating:

“I wouldn’t tell you the details even if I knew because it’s confidential research information.”

What?!?

Phinney appeared to be admitting he didn’t even know the details of Olson’s diet! Which, of course, begs the question of why on Earth he felt qualified to publicly make grand statements about it?

Then he stated that even if he knew the details, he wouldn’t share them with us anyway, because they’re “confidential”.

Yeah, sure. They’re so ‘confidential’ that Tim himself has publicly described his eating habits, and they sure as heck ain’t low-carb. As I explained in this article about Tim, his so-called ‘low-carb’ diet included sweet potatoes and “lots of vegetables, fruits”, along with rice and corn tortillas. And while Phinney would have us all believe Tim was a ketogenic “fat-adapted” athlete who powered through his races relying solely on his body fat stores, the truth was Tim consumed ample amounts of in-race carbohydrate in the form of soft drinks, Gu gels, Cliff gels, honey stingers, the carbohydrate-rich EFS drink made by one of his sponsors, First Endurance, and even orange slices!

Low-carb athlete my foot.

I just checked Tim’s blog to get an idea of where he’s currently at with his diet and training, and this is what he wrote recently (April 10):

“I don’t like labels and would not call myself low-carb, paleo, etc. I would say that I follow a diet with more protein & fat and less carbs than most people and that it has helped me recover faster, reduce inflammation and overall just feel healthier. My diet consist [SIC] of mainly organic and local if possible grass-fed meats, vegetables, eggs, nuts, seeds, fruits, sweet potatoes and coconut oil.”[Bold emphasis added]

Despite this, Olson is the very first athlete Albers cites in his post as a shining example of low-carb athletic success! He writes:

“I thinks its [SIC] quite obvious Tim does not follow a ketogenic diet at all, but he does follow a “minimal carb approach” and mindfully times his carbs and eats in a way that promotes body fat as his primary fuel source. An earlier article by Anthony Colpo rightly points out that Tim Olson is not a VLC practitioner, however his carb consumption compared to others in his sport is incredibly lower in carbs.”

What you just witnessed was the red herring weasel-word approach to dietary argument. Faced with the uncomfortable fact Tim’s diet is not even remotely ketogenic, Albers nevertheless claims it still qualifies as low-carb because it is “incredibly lower” than the runners he competes against. What I would like to know is exactly what data Albers bases this grand claim upon? Does he know the actual carbohydrate intake of Olson’s competitors? Does he even know Olson’s actual carbohydrate intake?

I think we all know the answer to those questions.

Danny employs a rather sneaky tactic here, but thankfully most of my readers are of the non-lobotomized variety and will quickly see through his duplicity. But for the sake of Danny and his fellow fanatical low-carb ilk, I’ll point out the following:

Even if someone eats less carbs than their competitors, that in no way automatically means they eat low-carb. If, for example, your competitors average 600 grams of carb per day and you average 300, that doesn’t even begin to make you a low-carber. I love the glycogen-depleting sport of cycling, but even in the midst of summer when my cycling mileage is at its highest, I’d struggle to get more than 600 grams of carbs down my gullet, and my daily average would be closer to 500 grams. Pro cyclists competing in stage tours, meanwhile, have been documented by researchers (as opposed to semi-literate bloggers) to put away almost 1000 grams of carbs daily, and we’re talking guys who are 15-20kg lighter than me!

So using Danny’s logic…I’m a low-carber!

THUD!!

Excuse me while I pick myself of the floor, folks, I just fell off my chair laughing!

THUD!!

Godamnit Anthony, get it together!

Sorry everyone, he’s a funny guy, this Danny!

OK, OK…composure now regained. Which will allow me to ask another question of Mr Albers: Why, exactly, do you write Olson “mindfully times his carbs and eats in a way that promotes body fat as his primary fuel source” yet make absolutely no mention of the abundant in-race carbs Tim himself has acknowledged using to get through his races?

Let me answer that for you: Because it would oblige you to remove Olson from your collection of alleged low-carb athletes, thereby weakening your argument. So, like most duplicitous and dogmatic low-carb shills, you simply ignore the discomforting contradictory facts, acting as if they never existed.

And you then smugly turn around and repeatedly and condescendingly imply in your article I’m the one too dopey to acknowledge contradictory facts!

How utterly precious.

Back to the Trials …

Before I debunk the other trial Albers believes support his low-carb beliefs, I want to address the frequently-cited trial conducted by Stephen Phinney that supposedly showed no performance decrement among cyclists after four weeks on a zero-carb diet. If Albers wanted to cite Phinney, and believes so strongly in the primacy of clinical trials, he could easily have mentioned this study and its numerous flaws, but n-o-o-o-o, he instead links to what essentially constitutes an opinion piece by Phinney that wanks on about Eskimos, pemmicam and Arctic explorers.

Good on ya, Danny.

So let’s do the distinctly un-Danny thing and examine this trial in detail. It involved trained road cyclists who were placed by Phinney and co on a zero-carb diet for four weeks. Within seven to 10 days of eliminating carbs, the cyclists experienced the well-known transient energy crash many folks experience soon after starting a ketogenic diet. During this time, the cyclists felt like crap and had difficulty keeping up their training schedules. This passed, and after four weeks no decrease in endurance was allegedly noted when they were tested at 62-64% VO2max.

Phinney et al concluded “aerobic endurance exercise by well-trained cyclists was not compromised by four weeks of ketosis”, and low-carbers have been more than willing to readily accept this claim at face value.

Which is a pity, because it’s nonsense.

Here’s what you haven’t been told: While the performance of the cyclists at 62-64% VO2max was reportedly unaffected by the ketogenic diet, Phinney casually admitted years later in a throwaway comment that their ability to perform more intense activity (sprinting) deteriorated!

Where exactly did he admit this?

In the very article you can find when clicking the second link Albers provided at the start of his blog post. You know, the one Albers falsely claimed was a clinical trial. Danny is quick to post the link, but not so quick to mention this pivotal piece of information. Which means he either hasn’t read Phinney’s article, or he has read it but didn’t understand what he was reading, or he did understand but ignored its implications and went ahead and posted it on his website any old how knowing full well most of his readers are committed carbphobes who won’t even bother to open it.

Whichever of these possibilities actually transpired, the end result is the same: We have yet another example of misleading carry on by an individual who is quick to impugn the integrity and competency of others while he himself spews forth unbridled bullshit.

As for Phinney, rather than discuss the performance-killing implications of his findings, he simply described the sprinting performance of the ketogenic cyclists as “constrained”, then quickly moved on as if nothing ever happened.

Yep, nothing to see here, folks, move along!

Not so fast.

As I’ve previously pointed out, telling a competitive cyclist that a zero-carb diet won’t affect his ability to perform moderate endurance exercise but his sprinting ability will be “constrained” is a bit like telling a grown man that lopping off his willy won’t affect his general mobility but will “constrain” his sex life.

Yep, it would be an understatement of most prodigious proportions.

Given that most cycling races are won only after a frantic sprint to the finish, the correct conclusion from Phinney’s study would be:

“Zero-carb diets are bloody useless for competitive cyclists!”

In fact, they’d be pretty much useless for any sport that includes both an endurance component and short bouts of explosive activity which would be, um, almost every popular sport in the world.

It’s at this point that the low-carb shills will object that the cyclists’ poor sprint performance was due to insufficient fat adaptation. The cyclists needed longer to become fat adapted and then their performance would have been fine blah blah blah…

Sure thing. And if you lob off a guy’s willy, it will magically grow back if you wait long enough.

As we have already discussed, the subjects experienced the customary initial energy crash that frequently accompanies the fat adaptation process. This was accomplished within ten days, right at the start of the study. By the end of the four week study, the subjects were well and truly fat adapted, a fact confirmed by respiratory quotient (RQ) testing. Measuring RQ allows researchers to check how a person’s fat adaptation is coming along, and is typically expressed on a scale ranging from 1.0 (pure carbohydrate oxidation) to around 0.7 (pure fat oxidation). At the completion of the study, Phinney’s elite cyclists displayed a mean RQ during testing at 60-65% VO2max of 0.72, a bee’s cajone away from 0.7[1]. In other words, they were as ‘fat adapted’ as they were ever going to be.

Wait a Minute…their Aerobic Performance Sucked too!

Based on what we’ve discussed so far, you’d think it was only sprint performance that deteriorated among Phinney’s cyclists. Remember, Phinney claimed – and continues to claim – that the aerobic endurance of the cyclists was unaffected by the ketogenic diet.

But is that true? Is that what the results actually showed?

Nope.

Even at the low aerobic intensity used in this study, two of the cyclists did in fact experience significant declines in their time to exhaustion (-48 and -51 minutes)!

Another experienced a 3-minute increase, while two others experienced a 30-minute and a hefty 84-minute increase.

But you wouldn’t ever know this unless you scrupulously examined the individual data for yourself, because Phinney and his team simply combined the results of all five cyclists and calculated the mean time change, which gave the misleading impression of an unchanged time-to-exhaustion performance across the board, then presented that as their final result.

So most people who are told this study proves low-carb diets pose no threat to endurance performance are blissfully unaware that two of the 5 cyclists in fact experienced massive declines in performance. Another experienced little change, leaving the two remaining cyclists who experienced substantial increases in their time to exhaustion. Well, three out of five ain’t bad, right?

Actually, given the design of the study, it’s very poor. And here’s why: During the first week of the study, the cyclists consumed a high-carbohydrate diet supplying enough calories to keep their weight stable. The next four weeks were spent on an isocaloric zero-carb diet that also resulted in no weight change (hmmm, what happened to the “metabolic advantage”?) At the end of weeks one and four, the cyclists performed their endurance tests.

What’s wrong with that, you ask?

Everything.

The study, to be quite frank, was poorly conceived and conducted. Unlike other studies, there was no familiarization test and the before and after tests were not performed in random order.

While non-cyclists may assume they’re the same thing, stationary cycling and road cycling on a real bike involve very different dynamics, both mentally and physically. For one thing, stationary cycling at a set pace for hours on end while you remain in one spot is, let’s be perfectly honest, boring beyond batshit. In contrast, road cycling is a far more interesting and mentally engaging endeavour that involves continual input of sensory data from the environment, especially in a race situation. And rather than outwit competitors or complete a set distance in the quickest possible time, in a stationary bike ride-to-exhaustion test you’re simply pedalling at a set pace for as long as possible, until you feel too knackered to continue. If you’re not familiar with such a test, this ‘exhaustion’ may occur prematurely as result of psychological rather than physiological factors.

Then there are the physical differences. Riding a real bicycle allows you to use a lot of “body English” as you rhythmically bob from side to side. You simply can’t do this on a stationary bike. I’m sure every road cyclist who’s ever ridden an ergo will have experienced that moment where they wanted to pick up the pace and start throwing the damn thing from side to side, only to remember they’re on an immovable one-dimensional contraption that allows no lateral movement, only forward rotation of the cranks.

Now, I don’t know about the stationary cycling experience of the cyclists in Phinney’s study (and I’m guessing Phinney doesn’t either), but a good many road cyclists do not own stationary bikes. Even in the depths of winter, most of the serious roadies I know would rather get out and do battle with the elements on a real bike than sit indoors going nowhere for 90 minutes.

Which means if you are going to conduct a clinical trial in which the subjects will be subjected to unfamiliar tests – such as road cyclists being made to stationary cycle to exhaustion – good science dictates you allow the subjects to undergo familiarization tests before getting down to the nitty gritty. Some researchers use a single familiarization test, while others employ several to be doubly sure any changes in performance observed during the subsequent trial are genuine intervention effects and not simply an artefact of the subjects becoming familiar with the new activity.

Phinney and his team, for reasons known only to them, didn’t bother with any familiarization protocol. None whatsoever!

Nor did they bother to include an isocaloric four week high-carb phase, and randomly assign some cyclists to do that phase first and others to do the zero-carb phase first.

Instead, everyone performed the first test after only one week of the high-carb diet, then the second test after four weeks of the zero-carb diet. Therefore, the two significantly improved performances were in all likelihood simply an artefact of test familiarization. In other words, the increased time to exhaustion seen in two of the cyclists was most likely due to improved efficiency as a result of a learning effect after performing a formerly unfamiliar test for the second time. As Andrew R. Coggan, Ph.D, an exercise physiologist, multi-sport endurance athlete and prolific published researcher, noted: “in my opinion, and those of many others, such large changes in performance are not believeable, [SIC] suggesting that the pre-diet performance of [the cyclist who experienced an 84-minute increase] was greatly underestimated”[2].

If this is the case – and I firmly believe it is, given that far higher quality research involving carbohydrate restriction has failed to replicate the performance improvements claimed by Phinney – then the true implications of his study are very different to the ones he routinely claims.

Namely, if the increases in ‘endurance’ noted in two of the cyclists were an artefact of test familiarization, that means the zero-carb diet sucked so badly that despite this familiarization one of the subjects experienced no significant improvement and the remaining two experienced significant declines in performance!

Or to put it in even simpler terms, ketogenic diets are so bad that in 60% of cases they will negate the powerful improvements seen with test familiarization!

Or to put it another way, keto diets suck the big one for both aerobic and anaerobic performance!

Or in even simpler terms…ok, ok, I think you get the picture.

So What Happens When a Properly Conducted Study Examines Carb Restriction and Cycling Performance?

In 2000, Helge and colleagues from the University of Copenhagen published the results of a longer clinical trial. During the first seven weeks of this study, one group ate a high-carb diet, the other a low-carb/high fat diet. During the eighth week, both groups ate the high-carb diet. The subjects trained three times a week during the first 4 weeks, then 4 times a week during the last 4 weeks on stationary cycles, at a controlled exercise intensity that ranged between 60 and 85 percent. The workouts lasted 60-75 minutes.

So unlike Phinney’s study, in which all five cyclists were made to follow a high-carb diet for only one week and then a zero-carb diet for 4 weeks, this was a controlled parallel study in which the subjects were randomly assigned to follow low- or high-carb diets concurrently for a similar length of time.

An added bonus of this study is that in the final week, the low-carb group was also allowed to eat a high-carb diet, which helped examine the claim that “training low [-carb] and competing high [-carb]“ would produce a performance advantage thanks to super-duper glycogen supercompensation.

During the first seven weeks, the low-carb/high fat group ate 177 grams of carbs and 217 grams of fat per day. The high-carb group ate 546 grams of carbs and 75 grams of fat per day. Both groups ate similar amounts of protein.

While 177 grams of carbs may not typically be considered ‘low-carb’, keep in mind that exercise increases the carbohydrate threshold required to reach ketosis. Indeed, blood ketones rose markedly during the study in the low-carbohydrate group, and were far higher at seven weeks than in the high-carb group.

Also keep in mind I’m reporting this in response to the claims of one Danny Albers, who by his own criteria and appraisal of Tim Olson’s diet is logically required to consider a daily 177 grams of carbohydrate to be “incredibly lower” than that consumed by most serious cyclists…

Anyway, when time to exhaustion at 81% VO2max was tested at 7 weeks, the high-carb group improved their time by a mighty 191%. The poor low-carbers meanwhile, with their super cool wicked awesome “incredibly lower” carb intake, could only manage a meagre 68% improvement!

So much for ‘fat adaptation’…

After the eighth week, when both groups ate the high-carb diet, the low-carb group managed to improve their time by another 18%, but their average time to exhaustion was still much shorter than that of the high-carbers[3].

So much for super-duper-train-low-compete-high-glycogen-recompensation…

Bottom line: Both zero-carb and supposedly “non-ketogenic” low-carb diets are woefully inferior to high-carb diets when it comes to fuelling athletic activity.

That’s what the controlled research shows, Danny! I don’t make this stuff up, I simply relay what researchers did and what they reported with ruthless indifference to anyone’s pet dietary beliefs.

But Danny and his low-carb compatriots simply refuse to believe what the research shows. Rather than read the research in its entirety with their own eyes, and acknowledge the majority of athletes use high carbohydrate diets because they have been proven in tightly controlled research to be superior, they prefer to believe high-carb diets are favoured simply because that’s what athletes have been brainwashed into following. Yep, the only reason pro athletes don’t rock the field on low-carb diets is because, in Danny’s words, they’ve been repeatedly told it’s “IMPOSSIBLE”!

Yep, the real problem here, according to our budding expert, is a lack of enlightenment among pro athletes and their advisors! These poor sods need to open their minds, and their newly-ketogenic asses will follow!

Thankfully, people like Albers haven’t even begun to be taken seriously by professional athletes and their coaches. Otherwise, we’d have the sad spectacle of professional athletes who look like they’ve been doping with Valium instead of EPO and testosterone…

Needless to say, there has never been any brainwashing campaign to hide the alleged benefits of low-carb diets from athletes. The reality of the matter is that researchers have in fact repeatedly tried to find an ergogenic effect of carbohydrate restriction and ‘fat loading’, and their efforts have been a disappointing failure. After reviewing this research, fellow Aussie and exercise physiologist Louise Burke and her colleague Bente Kiens noted, “those at the coal-face of sports nutrition can delete fat loading and high-fat diets from their list of genuine ergogenic aids for conventional endurance and ultraendurance sports.”

Regular readers know I generally couldn’t give two turds about so-called decorated credentials, but Louise Burke is the real deal: An individual who works with elite Australian athletes, who truly knows her stuff when it comes to athletic nutrition, whose work I greatly admire, and whose knowledge would absolutely cock its leg and pee all over the fanciful, nonsensical slop offered by any low-carb shill. When Louise speaks on the topic of sports nutrition, anyone who’s not a brain-damaged low-carber should listen carefully, which is why I highly recommend her book Practical Sports Nutrition. No, it’s not the cheapest book at Amazon but its contents are truly worth thousands of times the cover price of your typical popular format Atkins-Protein-Power-Skinny-Bitch-China-Study-type garbage. Seriously, Burke’s book should be on the shelf of every single trainer and nutritionist who has to deal with competitive and serious recreational athletes.

Anyway, back to the matter at hand…

The Other Trial

I’m delighted Albers cited a recent trial involving Italian gymnasts in his first hyperlink, as I’m including a discussion of this very study in my upcoming book Why Carbs are Absolutely Bloody Awesome! (relax, that’s just the working title). So Danny has saved me some valuable time – so nice of him!

You can access the full text of this study here (Albers provides a link to the abstract only, which again leads me to suspect he hasn’t even read the actual study).

The paper is titled “Ketogenic diet does not affect strength performance in elite artistic gymnasts” and was conducted by Paoli et al at the University of Padova in Italy. In true dimwit fashion, I’m guessing most of the folks who cite this paper in support of low-carb diets barely made it past the title, and few if any have carefully read the actual study.

The study was partially funded by Gianluca Mech SpA, an Italian food company that produced the high-protein, zero-carb supplements used in the study. Antonio Paoli, the main researcher responsible for the study’s conception, design, statistical analysis and interpretation of data and draft of manuscript, has been a consultant for and has received grant/research support from Gianluca Mech. Another of the researchers, Lorenzo Cenci, is a paid scientific consultant for Gianluca Mech.

Not that that would ever influence the design and results of the study, no sir.

Or would it? Let’s take a look…

The first important thing to point out about this study is that it was not a study in which two diets identical in every respect except for their fat and carbohydrate intake were compared head to head. Instead, the subjects were compared while following their usual diet for 30 days, and while following a 30-day intervention diet that included not just carbohydrate restriction, but a number of other key changes.

Read that last sentence again folks.

This was a study in which the test diet involved multiple interventions, only one of which was carbohydrate restriction. As noted earlier, at no point did the subjects follow a high-carb diet that incorporated these other interventions, leading us to the first major problem with this study: The results are being used to claim ketogenic diets do not harm physical performance, when in fact the alleged lack of harm in this study may have stemmed from other factors. Regrettably, this study does not tell us what would happen if these confounding factors were removed and a ketogenic carbohydrate intake was examined in isolation.

Just what kind of factors am I talking about?

Well, when following their everyday diet, the subjects’ average (self-reported) daily protein intake was a meagre 83.5 grams. During the ketogenic intervention diet, this more than doubled to 200.8 grams per day!

The nine subjects in this study were elite Italian gymnasts, two of whom belonged to the Italian national team. So the first question that begs to be asked is why the heck are elite Italian gymnasts eating a poncey protein intake of only 83 grams per day?

The second question that must be asked is why is this study being used in support of carbohydrate restriction when it in fact also included a dramatic increase in protein intake? Protein intake is a variable independent of carbohydrate intake, ie, one can just as easily consume diets that are high-protein/high-carbohydrate, high-protein/low-carbohydrate, low-protein/high-carbohydrate, and so forth. Which means that if this study was truly intended to examine the effect of ketosis upon performance, it should have examined two diets with identical protein contents, varying only in their fat/carbohydrate ratios.

Needless to say athletes of all stripes have been consuming high-protein/high-carbohydrate diets for years, and have done so with great success. High-protein/low-carbohydrate diets?

Not so much.

In fact, in the endurance world, not at all.

The second glaring inequity in this study is the fact that while following their usual diets the subjects were not provided with any nutritional supplements. During the ketogenic phase, however, the subjects were supplied with protein supplements, a daily multivitamin-mineral supplement, and were also given four different herbal formulas containing a wide variety of herbs! All supplied, of course, by Gianluca Mech.

The herbal formulas, it should be noted, included ginseng, miura puama and guarana – the latter containing caffeine.

So what we now have is a study comparing a low-protein/high-carbohydrate diet devoid of nutritional supplements with a high-protein/low-carbohydrate diet featuring extra vitamins, minerals and an array of herbal extracts – some with potential ergogenic effects.

Looks like the low-carb crowd has taken a leaf out of the Ornish/Esselstyn low-fat book: Conduct a trial using a multifaceted intervention, then automatically ascribe any observed benefit to the feature you wish to glorify. In the case of Ornish/Esselstyn, that feature is a highly restrictive fat intake; in the case of low-carbers, it’s a highly restrictive carbohydrate intake.

Either way, this kind of duplicity has no place in science.

If you conduct a multifaceted intervention, then when discussing the results be perfectly clear that they arose from a multifaceted intervention, rather than floating off into fairyland and pretending they were due to your pet aspect of that intervention.

So what did the results of the Italian study show, exactly?

Before I answer that, remember that the argument put forth by myself is that low-carb diets are vastly inferior for sports performance, while Albers claims not only are they are A-OK but that they in fact confer a “competitive advantage”. And he cites this study in support of his stance.

Which is most interesting given that while this was a study with gymnasts, their performance in actual gymnastic events was not assessed at any point during the study. I repeat: This study did not examine performance in a glycogen-depleting sport activity.

Instead, the researchers simply got the gymnasts to perform a bunch of bodyweight exercises before and after each 30-day diet period. These tests consisted of doing as many repetitions as possible of push-ups, reverse grip chin-ups, hanging leg raises, and parallel bar dips. The subjects were also tested for maximal height achieved in the squat jump and counter movement jump,

When the data were tallied up, there was no difference in performance on these tests before and after either the standard or ketogenic diet phases.

The only change of any note was a mean 1.9kg loss of fat and 1.6kg overall weight loss in the ketogenic group, a consequence of the lower caloric intake (-300 cals/day) consumed during this phase. The researchers reported “a non-significant increase in muscle mass”: 300g during the keto phase, 200g during the standard diet phase.

So even with what our boy Danny would call an “incredibly higher” protein intake and a bunch of extra supplements, the ketogenic diet did nothing that any other diet providing the same level of caloric restriction couldn’t do.

As for Albers’ claim this study disproves my assertion that ketogenic diets impair athletic performance in glycogen-depleting sports, my suspicion he hasn’t even read the study appears to have been spot on. The study didn’t even look at athletic performance – the only tests involved were brief jump tests, which literally lasted a split second each, and four single sets of various bodyweight exercises each performed for 15-43 reps.

These tests, in other words, were about as glycogen-depleting as mowing your lawn.

What does this study tell us about the performance impact of a low-carb diet during cycling or running or boxing or swimming or even gymnastic events?

Absolutely nothing.

Danny, I hate to break this to you, but you done fucked up, son! You publicly called me out, acted like a patronizing little smart ass, but forgot one small but absolutely crucial detail – you didn’t even read the studies you cited! I have stated the plain facts: LOW-CARB DIETS ARE VASTLY INFERIOR FOR ATHLETES PARTAKING IN GLYCOGEN-DEPENDANT SPORTS. And you figured you could disprove this scientifically established fact by posting links to two papers, the contents of which you hadn’t even examined. Like so many of your low-carb compatriots over the years, you figured an alluring title and a supportive-sounding abstract constituted all the evidence you need to smugly attack me.

You silly, silly boy.

Now folks, please excuse me while I scramble for a photo of Sara Varone or Marco Pantani or Cristina Buccino or something else Italian, high-carb, and red-bloodedly magnifico in order to recover from the shameful display of disgracefully unItalian behaviour that was the aforementioned keto study! I mean, Italian researchers trying to make ketogenic diets look good? WTF?! Is nothing sacred??

Anthony’s Super-Effective Italian-Based, Four-Course, Testosterone Restoration Protocol (stare at each of the following images for a minimum of 3 seconds each, then bask in the resultant dopamine surge. If no such surge ensues, my condolences on your eunuch status):

The Appetizer:

Entrée

Main Course

And let’s not forget Desert

OK, the nobility and pride of my Mediterranean forebears has been restored  Let us continue on…

A Guide to Dealing with Severe Ownage for Impulsive, Regret-Prone Low-Carbers

I can just picture a very red-faced Danny sitting at his computer right now, one hand on the keyboard, the other scratching his pee-stained underwear, the droplets of bacon lard coating his three-day growth glistening in the light from his monitor, absolutely seething with a mix of embarrassment and hatred.

It’s OK Danny, I have a good sense of what you’re going through – I’ve watched this very scenario play out among your low-carb compatriots more times than I care to remember. Right now your brain is lighting up like a switchboard at a Jerry Lewis fundraiser, your mind frantically scrambling for rebuttals to the points I’ve raised and battling to piece together rationalizations for your inherently foolish and utterly pseudoscientific behaviour.

Yup, I might not look like Laurence Fishburne and my name ain’t Morpheus, but I know you jokers better than you know yourselves. You’re so utterly predictable it’s beyond boring.

But I’m not a heartless guy. Truth be told, I love rescuing people from the suffocating carbphobia that arises from blind, unquestioning obedience to the low-carb sham. So I’m happy to let you know you’ve got two options here, Danny:

1. Keep trying to discredit me and keep hating on me, an option that is akin to swimming in quicksand, for the simple reason that the science is firmly on my side. You can’t beat me, buddy: Many have tried over the last decade, and completely failed. They’ve used all sorts of pseudoscientific chicanery, called me all manner of names, even tried threats and outright defamation. Like you, they all just plain fucked up. I’m still here and I ain’t going anywhere, matey, for one simple reason: I’m right, I’m telling the truth, and you can’t beat the truth because…it’s true!

2. Do the smart thing: Sweep aside your years of low-carb brainwashing, listen to what I’m actually saying, and learn something useful that will immediately benefit you greatly when you apply it to your own diet. This second option is the one taken by folks like Richard “Free the Animal” Nikoley and Kelly Mahoney and an increasing number of other former low-carbers, all of whom have benefited immensely from casting aside their low-carb shackles. They’ve noticed improvements in everything from their physical performance to their mental outlook – even the quality of their sleep!

The choice is yours, Danny: You can cognitively man up and impartially face the truth, or you can keep bitching and pissing and moaning about me and end up a bitter, spiteful, flabby, lonely old web troll like your buddy Fred Hahn.

Personally, I don’t think that should be a hard choice LOL

While you mull that over, let’s take a look at the other anecdotal cases you cite in support of your fatally flawed pro-low-carb argument.

The Low-Carb Athlete Who Desperately Needs to Stop Being a Low-Carb Athlete

After citing the low-carb athlete that never was, Tim Olson, Albers further lists a motley assortment of endurance athletes, old -time bodybuilding ‘gurus’, and a couple of powerlifters in support of his argument.

Albers admits he doesn’t even know the actual carb intake of many of these athletes:

“Very Low Carb Athletes…(skirting keto.. hard to say)…They may not be 100% keto but no way total calories from carbs is [SIC] > 20%…The point is this guys [SIC] take advantage of a high level of carb restriction to gain competitive advantage.”

So from this semi-literate ramble, we can see Danny is actually unaware of these athlete’s actual carb intakes, yet he readily embraces the conclusion they are indeed low-carbers and that their reduced carb intake gives them a “competitive advantage”.

Wait a minute! Even if these athletes do indeed follow low-carb diets, how on Earth can Albers claim that their eating habits confer them with a “competitive advantage”? As we saw from the Phinney and Helge studies, zero- and low-carb intakes negatively and significantly reduce both aerobic and anaerobic endurance performance. Which means that if these athletes follow carb-restricted diets and achieve any level of competitive success, they do so in spite of their sub-standard carb intake!

Take the example of Ben Greenfield. Danny, ever the smug sod, belittles me for not mentioning Greenfield:

“Of course Ben has long pushed a low carb diet for triathletes.  I wonder why Anothony [SIC] overlooked Ben?”

“Ben authored this book [A Low-Carb Guide For Triathletes] years ago… I guess he never sent Anthony a copy.”

No Danny, Ben never sent me a copy. Believe it or not, people who are totally unaware of each other’s existence tend not to send each other copies of their books.

No, really!

Which brings us to your accusation that I “overlooked” Ben. Um, again, that would be because I’d never even heard of him until I read your convoluted, typo-ridden post, Danny.

And why hadn’t I heard of him?

Because he’s never won a world class athletic event.

Before I continue, let me make something perfectly clear – what I just wrote is in no way to be construed as a belittlement of Ben. Looking through Ben’s bio page, he indeed has an impressive-sounding list of credentials related to training and coaching. It’s also clear he practices what he preaches, being a triathlon competitor who reportedly competes in 15-20 tris annually, and is a top ranked USAT competitor for his age group.

This is all well and good, but did you ever stop to consider, Danny, that it’s beyond the capability of any single human being to be aware of every last person in the world who has ever completed a sports science degree and competed in triathlons? There would literally be thousands of such individuals on this planet, and to belittle me for not knowing the names and owning the books of every single one of these athletes who also purports to follow a low-carb diet is, I would posit, a most unreasonable display of fucktardedness.

So get over yourself, Danny. I “overlooked” Ben, not through any duplicitous act of evasion or manifestation of incompetence, but because he’s never won the kind of world class athletic event that would reasonably bring him to my attention all the way over the other side of the globe down under in this here sunburnt country known as Osssstrayyyleeeyaaaah [deliberately Americanized pronunciation to help out semi-literate folks like Albers].

But hey, since you brought up Ben Greenfield’s name, let’s take a look at his case to see if it in any way provides evidence that low-carb diets are super sick max awesome wild bro for athletic performance.

You cite Ben as if he constitutes proof athletes can thrive on a low-carb diet. But when we dig a little deeper, a starkly contrasting story quickly begins to emerge.

Here’s a link to a recent and rather telling post by Ben Greenfield:

What Kind Of Damage Happens To Your Body After You Do A Hard Workout, Triathlon or Marathon?

Hmmm, I wonder why Danny “overlooked” it?

If Danny had read it, he would have learned how Ben had some blood work performed before and after he undertook a rather gruelling physical feat: A Half-Ironman, followed by an Olympic distance triathlon less than 24 hours later.

Not surprisingly, Ben’s blood work-up after this gutsy endeavour told a tale of heightened catabolism, muscle damage, inflammation, hormone dysfunction, liver enzyme elevation, and borderline immune suppression. This may all sound rather alarming to the uninitiated, but these kinds of changes are routinely observed immediately after strenuous, long duration endurance events. So long as sufficient rest is taken and the appropriate nutritional protocols are followed, these negative changes will eventually revert back to normal.

So Ben’s post-event blood work is nothing out-of-the-ordinary. His pre-event blood work, however, is an entirely different story. Despite his daily use of adaptogenic Chinese herbs and antioxidant-rich herbal extracts, Ben’s initial rested blood work was, quite frankly, a mess (again, recognizing what a haven the Internet is for sleazy misquoters, I want to reiterate I’m not trying to belittle Ben by pointing this out; he himself admits his pre-event blood work ‘was relatively “messed up”’. The only malice I bear is towards patronizing malevolents who, from out of the blue, see fit to ridicule my alleged selectivity then turn right around reveal how ignorant and evasive they truly are).

Let’s take a look at some of the more alarming results revealed by Ben’s blood work:

–Ben’s pre-race level of the Big T – testosterone – was only 356, right near the bottom of the normal range for adult males (300 -1,000 ng/dL).

–His level of free testosterone – the portion of T that remains unbound and is therefore free to make muscles recover and grow, bones thicken, and a certain critical part of your anatomy promptly stand to attention when you see a smokin’ brunette – was below normal.

–Ben’s IGF-1 levels were also below normal (I’m betting that if Ben had performed the urine test to measure his 24-hour growth hormone level, that would have been low as well). At any rate, his low IGF-1 combined with his low free and total testosterone levels indicates a significantly depressed anabolic response. In plain English, this may impair his ability to recover from hard workouts and increase his susceptibility to injury. If Ben was seeking to add more muscle to his  frame, this unfavourable anabolic profile would seriously impair his efforts.

–His cortisol levels are alarmingly high. Which in turn indicates a struggling HPTA access and a physiology characterized by heightened catabolism. In layman’s terms, this means an increased risk of injury, increased muscle damage, impaired recovery from training, and greater risk of the syndrome popularly referred to as “adrenal fatigue” or “adrenal burnout” (I won’t waste time here arguing about the semantic accuracy of these terms; needless to say, most of us know what they refer to: Heightened, suppressed, or irregular cortisol levels accompanied by such symptoms as fatigue, lethargy, immune dysfunction, lack of training progress, etc, etc…).

–While not in the red zone, his white blood cell count was low at 4.9, right on the borderline of the normal range (4-10.6). This suggests an immune system battling to keep up with his training and lifestyle demands.

–Ben’s TSH (thyroid stimulating hormone) level was high, indicating a struggling thyroid in need of constant prodding to keep churning out sufficient thyroid hormones.

–His liver enzyme levels were elevated, although to be fair this is not uncommon among exercising individuals and may be a lingering after-effect of his regular training regimen.

–His blood urea nitrogen is elevated, most likely from one or both of the following: Lingering muscle breakdown, as per above, or excessive protein intake.

Ben is to be congratulated for his willingness to post his blood work online, and he is to be credited for acknowledging he has some pressing issues that need close attention.

Not so admirable is Ben’s refusal to acknowledge that his low-carb diet is likely a major contributor to his worrying test results. Before I explain just why he urgently needs to cast a far more critical eye on his diet, let’s put Ben’s results in some sort of perspective.

It’s no big secret that levels of key hormones such as testosterone, growth hormone, and IGF-1 tend to peak in a person’s twenties then slowly decline as he/she ages. Nor is it any kind of revelation that booze, drugs, inactivity, poor sleep habits and other displays of intemperance can substantially accelerate this decline. If Ben was a septuagenarian who’d lived a wild and woolly life, his test results would hardly come as a surprise to most doctors. But Ben is not a thrashed-out 70 year old; by all accounts, he is a young, conscientious, health aware, physically active and (I would assume) drug-free individual who avoids weed, excess alcohol and the bizarre assortment of pills and powders that predominates the club scene these days.

Something, therefore, is seriously screwing with Ben’s physiology.

I propose that something is his low-carb diet.

Remember how Ben’s TSH levels were well over the upper limit of normal, indicating suppressed thyroid hormone output?

Ben denies his low-carb diet could possibly have anything to do with this:

“I also realize there are those out there who would propose that my low carbohydrate diet is stripping my body of glucose, which is necessary for the conversion of T4 to T3 in the liver. But because the body can make glucose from both protein and fats, this is unlikely.”

Ben then goes on to instead blame calorie restriction for his thyroid dysfunction.

Like many low-carbers, Ben likes to believe a high dietary protein intake can alleviate all the ills of carbohydrate restriction by substituting the necessary glucose through a process known as gluconeogenesis (the endogenous production of glucose from non-carbohydrate sources).

This belief is wrong.

Rather than recount all the evidence showing low-carbohydrate intakes to consistently suppress levels of key thyroid hormones, and turn this article into a thesis-length production, I strongly suggest all those in denial about this topic read the following article I posted a while back:

Is a Low Carb Diet Bad For Your Thyroid?

The clinical observation that carbohydrate restriction – to both ketogenic and non-ketogenic levels – significantly reduces levels of the grand-daddy thyroid hormone triiodothyronine (T3) is so reliable and consistent you can set your watch by it. It’s been shown time after time, in trial after trial.

Yes, calorie restriction in and of itself can also have this effect: The body can perceive a shortfall of calories as a sign of some kind of stressful situation or starvation threat, and will slow non-essential functions in attempt to tide itself over until the stressful situation dissolves or sufficient calories are once again forthcoming.

But guess what? While the body views calorie restriction as a stressful response, it gets doubly concerned when carbohydrate availability drops. As the above article explains, carbohydrate restriction pounds down T3 levels even when maintenance calories are consumed!

And dietary protein does little to nothing to alleviate the situation, as the studies by Hendler/Bonde and Ullrich (discussed in the article) demonstrate.

Oh, I almost forgot- the Euthyroid Sick Syndrome (ESS) caused by carbohydrate restriction arises from the inhibited conversion of T4 to T3, which is believed to arise from insufficient insulin levels. Not surprisingly, Ben’s insulin levels are at rock bottom. While a lot of low-carb automatons will automatically assume that’s a great thing, it actually sucks big time. The fact is that insulin is an extremely important hormone that serves crucial functions in the body, including glycogen replenishment and anabolic hormone signalling. Sure, too much insulin is no good, but too much of anything is no good. Dietary extremists, such as those who populate the screwball world of Low-Carbia, simply cannot get their heads around this concept. Like most things dietary related, insulin is an either-or proposition for them: “Too much is no good” promptly morphs into “none is best!”

Don’t be a low-carb automaton.

Low-Carb Diets, Immune Function and Cortisol

What about Ben’s worryingly high cortisol levels and immune suppression? Could they have something to do with his sub-optimal carb intake?

You’d better believe it.

Study after study shows that when carbohydrate intake is reduced, cortisol levels are increased, as is the cortisol:testosterone ratio. And this effect is seen even with relatively mild carbohydrate reductions.

University of North Carolina researchers, for example, assigned endurance-trained men to a high-carbohydrate (60% of calories) or low-carbohydrate (30%) group, along with 3 consecutive days of high-intensity training at 70% VO2max. Each training session was performed in a fasted state in the morning and lasted sixty minutes.

Resting cortisol levels increased significantly in the low-carbohydrate group, rising from 24.1 ng/dL at baseline to 27.6 ng/dL at the end of the study. No change in resting cortisol was seen in the high-carbohydrate group[4].

The resting free testosterone:cortisol ratio decreased significantly from pre- to post-study in the low-carbohydrate group (-43%), but no change occurred in the high-carbohydrate group (-3%).

It should be pointed out that, in this study, the “low-carbohydrate” diet provided an average of around 210 grams of carbohydrates per day. While this was more than double the commonly cited cut-off point (100 grams) used to classify low-carb diets, it was still insufficient to prevent the subjects’ physiology from developing a catabolic profile.

So this study involved a moderate carbohydrate intake and only lasted a few days, imagine what would have happened if the carbohydrate restriction was more severe and continued over the longer term. Actually, don’t imagine – refer to Ben’s blood work instead.

Galbo et al examined the effect of four days of zero and 77% carbohydrate diets in healthy men[5]. During exercise at 70% VO2max, levels of the fuel-mobilizing hormones GH, epinephrine, glucagon, and cortisol increased, while physical performance plummeted. This study used isocaloric diets and again did not involve caloric restriction.

When elevated cortisol levels are found in hard-training athletes, indicators of suppressed immune function are usually not far behind.

Gleeson et al examined the effects of a low-carbohydrate diet on plasma glutamine and circulating leukocyte responses to prolonged strenuous exercise[6]. Twelve subjects cycled for 60 minutes at 70% VO2max on two separate occasions, 3 days apart. All performed the first exercise test after a normal diet; they completed the second test after 3 days on either a high-CHO diet (mean 75% CHO) or a low-CHO diet (mean 7% CHO). The low-carb diet was associated with a larger rise in plasma cortisol during exercise, a greater fall in plasma glutamine concentration during recovery, and a post-exercise rise in the neutrophil:lymphocyte ratio (an accepted indicator of exercise stress).

In a similar study, ten men followed a high-carb diet (3,056 calories, 98g protein, 33g fat, 604g carbohydrate) and very low-carb diet (3,080 calories, 214 g protein, 229 g f at, and 34 g carbohydrate) for 2 days each. Prior to commencing each diet, the subjects completed a bout of exercise designed to deplete muscle glycogen. This depletion bout consisted of a 60-minute ride at 70% VO2max, followed by six x 1-minute sprints, with 1 minute of rest between each sprint. After glycogen depletion, the subjects followed the diets for two days while resting, then exercised for 1 hour at 75% VO2max.

Post-workout blood glucose was significantly lower with the low-carbohydrate diet (3.19 vs.4.62 mM) compared to the high-carbohydrate diet, as was post-exercise glutamine (0.410 vs. 0.472 mM).

Cortisol levels were greater with the low-carbohydrate diet (587 vs. 515 nM) throughout the trial. The low-carbohydrate diet also resulted in a greater fall in circulating lymphocyte numbers two hours postexercise[7].

Gleeson also reported that cyclists who performed 60 minutes of exercise at 75% VO2max followed by a 30-minute time trial at 80% VO2max exhibited markedly higher plasma cortisol, IL-1 receptor antagonist and IL-6 responses when given a low-carb diet (< 1 g carbs per/kg of bodyweight per day) compared with a high-carb diet (around 8 g carbs/kg/BW per day) for 3 days prior to the exercise test[8].

In a non-exercise study, Anderson et al compared the effect of ten days adherence by healthy men to a low-carbohydrate (44% protein, 35% carbohydrate, 21% fat) and high-carbohydrate (10% protein, 70% carbohydrate, 20% fat) diet. Again, energy intake was not hypocaloric and was equal on both diets.

Cortisol concentrations were consistently lower during the high-carbohydrate diet than during the high-protein diet (7.74 g/dl vs. 10.6 g/dl, respectively)[9].

Longer-term studies bear out these results. Dr Roland Stimson and his colleagues from the University of Edinburgh[10] took seventeen men and had them complete two phases of a randomised crossover study. Four weeks were spent on a high fat/low carbohydrate (protein 30%, fat 66%, carbohydrate 4%) and a moderate fat-moderate carbohydrate diet (protein 30%, fat 35%, carbohydrate 35%) diet.

In this ad libitum metabolic ward study, energy intakes were 154 calories/day lower on the low-carb diet and weight loss was correspondingly greater (6.3 vs 4.4 kg). The low-carb diet significantly boosted cortisol both by enhancing cortisol regeneration and reducing its inactivation.

In Denmark, Dr Pedersen and colleagues investigated the effects of endurance training for seven weeks on a high-carbohydrate diet (15% protein, 20% f at, 65% carbohydrate) or a high-f at diet (17% protein, 62% fat, 21% carbohydrate). An identical supervised training programme was followed by both dietary groups. During the first four weeks, training was performed 3 times weekly, and during the last 3 weeks, 4 times weekly. Each training session lasted between 60 and 75 minutes and exercise intensity was varied between 50 and 85% of maximal oxygen uptake.

Cortisol levels were not reported, but natural killer cell activity increased in the group on the carbohydrate-rich diet (from 16 to 27%) but decreased in the group on the fat-rich diet from (26 to 20%) in response to training. In other words, “ingestion of a fat-rich diet during training is detrimental to the immune system compared to the effect of a carbohydrate-rich diet.”[11]

At this point in time, we don’t know for sure what’s causing Ben’s disordered hormone, immune and cortisol levels – ‘proof’ that his diet is a contributing factor would come when he acknowledges the whole low-carb thing is a fruitless, counter-productive wank, reverts back to the kind of high-carb intake eaten by world-beating athletes, and observes a reversal of his unfavourable blood results.

Unfortunately, Ben is planning to do the exact opposite: Lower his carb intake even further and go ketogenic!

Sweet Jesus…

BEN. DON’T. DO. IT.

No further comment LOL

Except maybe to again point out that Danny really, really, rooolly should have spent more time doing his homework, because the results seen in Ben Greenfield’s blood work are not something any sane-minded person would even begin to want to emulate.

The Ironic Guru

Danny cites Vince Gironda as an example of a top bodybuilder who followed a ketogenic diet.

Danny, Danny, Danny. Tssk, tssk. You can’t pull that trick on me son, I wasn’t born yesterday!

For those of you who aren’t familiar with Vince Gironda, he was a well-known (for his gruff eccentricity and extremely caustic MuscleMag column replies as much as his actual training advice) bodybuilding figure who died in 1997 at the age of 79.

From all accounts, Gironda did not follow a ketogenic diet on any kind of long-term basis, he simply recommended it as a short-term ‘cutting’ and ‘hormone-boosting’ measure (science has since shown that carbohydrate restriction does bugger all to boost anabolic hormone output, and ward trial after ward has clearly demonstrated calories are the ultimate arbiter of weight loss).

What other diets did he recommend on a short-term basis?

Vegetarian diets.

Yep, Gironda recommended vegetarian diets to “alkalinize” the body and even as “slimming” diets!

Hmmm, I guess Danny kinda “overlooked” that.

Love him or hate him, there’s no denying Vince Gironda was a trailblazer and an important figure in the history of bodybuilding, and some of his advice was spot on. Some of it, however, was patently absurd. For example, he recommended doing flat bench presses by lowering the barbell to your neck, an absolutely fantastic idea for those who wish to annihilate their rotator cuffs. Another well-known and highly questionable assertion by the “Iron Guru” was that you should avoid squats because they allegedly give you a big unsightly ass.

Um, yeah, OK.

Thanks, but I think I’ll keep eating meat, carbs, respecting my shoulders, and doing my squats.

By the way, I know this is somewhat off-topic, but being the versatile, multi-faceted kinda guy I am, I think this is an appropriate moment to share a highly effective chick-pulling secret with all my brothers-in-carbs out there:

Ignore people like Vince Gironda and BUILD THOSE #$%&ING GLUTES!

Seriously, stop with the poncey colognes and dodgey lines already, and build yourself a manly-looking posterior. Because a muscular ass is like chick crack, my friends! Seriously, you’ll know when you’ve done sufficient squats, deadlifts and lunges because you’ll be going about your business at work, in the gym, or in the supermarket, when suddenly you’ll virtually feel all the female eyeballs glued to your ass. The effect is powerful, unmistakable and, I must say, pretty bloody gratifying LOL

Why?

Well, according to evolutionary psychology, males and females have evolved to make quick assessments about a prospective partner’s mating potential by subconsciously assessing certain physical features. Good facial symmetry, for example, is a well-researched feature prized by both sexes because it suggests good health and favourable genetics. Less well known is that females find a well-rounded muscular male butt attractive, so the theory goes, because it indicates, um, good pumping power.

Stop giggling, I’m being serious here, dammit.

This pumping power, it is further theorized, increases the chances of sperm being blasted further up a woman’s, uh, love canal, thereby decreasing the required swimming distance and thus increasing the chances some hardy, heroic, Indiana Jones-like sperm will make it to the fallopian tube, where a nice fertile she-egg will be waiting to make his manly acquaintance: “Hey handsome, I’ve been waiting for you!”

I told you I was a multi-faceted guy hahahaha

Larry, Curly, Mo…uh, I Mean, Larry, Vince and Danny

Awrighty, where was I…oh yeah, old time bodybuilders who supposedly achieved Adonis-like stature on a zero-carb diet of meat, eggs and bacon.

Which brings us to Larry Scott.

Yes indeed, Larry Scott was quoted in IronMan Magazine way back in 1965 saying he ate meat, eggs, cream and bugger all carbs.

To which I would answer…so what?

How does this disprove that low-carb diets suck for glycogen-depleting sports? Larry Scott was a bodybuilder, for crying out loud. ‘Athletic’ competition for him meant standing on a stage in posing briefs, squeezing his muscles while a largely male audience looked on, cheered, and made deep, thoughtful comments about his tibialis anterior development.

Scott recently died of Alzheimers at 79 years of age. Now, if I wanted to resort to the Danny Albers method of debate, I could point out that New York strength phenom Joe Rollino recently died at the age of 104 after a lifetime of vegetarian eating. And the only reason he signed out at 104 was because, sadly, he was hit by a van. By all accounts he was still in great shape for his age and heaven knows how old he would have lived to if it wasn’t for his untimely demise.

Was a vegetarian diet responsible for Rollino’s remarkable strength feats? That’s highly doubtful. More likely, Joe was looked upon favourably when Mother Nature was handing out strength genes – in 2008 he himself said he was just simply born strong.

So what does the case of Larry Scott prove, really? That low-carb diets are perfectly fine for bodybuilders? What would have happened if Scott had chosen to follow a high-carb diet instead? Would he have achieved an even more impressive physique? We’ll never know for sure, but given the superior size, definition and symmetry achieved by the high-carbing bodybuilders who followed him, that’s a definite possibility.

But rather than engage in such retrospective speculation, let’s see what science has to say on the matter.

Why Low-Carb Diets are Not the Best Choice for Bodybuilders

Remember what I said before about insulin being a vitally important hormone that we cannot live without? (If you’re sniggering at this contention, get your ignorant butt back on to Google and discover for yourself what used to happen to type 1 diabetics before the advent of insulin…)

And remember what I said about insulin being extremely important for activation of anabolic hormones and enzymes, a process known as anabolic signalling? The effect of insulin on anabolism is so powerful that many non-diabetic bodybuilders have used injectable insulin in order to boost their muscle growth. A practice, I might add, that is rather stupid. It’s always nice to add a few pounds of extra muscle, but there are better ways to do it than risking hypoglycaemic shock, coma and even death. Like making sure you’re getting enough dietary carbs.

Low-Carb Diets and Muscle Growth Pathways

“Akt” refers to a family of genes involved in cellular survival, muscle growth, and the transport of blood glucose to cells. Akt1 is able to stimulate protein synthesis and is therefore a key signalling protein in the cellular pathways that lead to muscle growth. Akt2 is an important player in the insulin signalling pathway and is required to induce glucose transport.

Researchers from the famed Human Performance Laboratory at Indiana’s Ball State University found that the glycogen depletion resulting from intense training and low-carbohydrate eating blunted the rise in Akt activity otherwise seen after a weight training workout.

Eight experienced male cyclists underwent two trials, a low carbohydrate and a high carbohydrate trial. On Days 1 and 2, they performed exhaustive leg and arm cycling workouts to deplete muscle glycogen. Early in the morning of Day 3, they arrived at the lab following an overnight fast and performed 3 sets of 10 repetitions of leg extensions with 2 minutes’ rest between sets.

During the two day period leading up to the experimental trial, subjects were fed an isocaloric (mean intake of 5200 calories) diet containing 18% protein/80% fat/2% carbohydrate, or 13% protein/7% fat/80% carbohydrate. This equates to a daily carbohydrate intake of 26 grams during the low-carb trial and 1042 grams during the high-carbohydrate trial.

Pre- and post-exercise leg muscle glycogen was far higher in the high-carbohydrate trial than in the low-carbohydrate trial, while intramuscular triglyceride concentration was 40% higher in the low-carb when compared to the high-carb trial prior to exercise.

Akt phosphorylation was similar in both groups prior to exercise and immediately post-exercise. After ten minutes of recovery, Akt activity increased 1.5 fold in the high-carbohydrate trial only. During the low-carbohydrate trial, Akt activity remained unchanged at all time points. The researchers concluded that due to this lack of Akt response, “adaptations to an acute bout of exercise may be blunted”[12].

Insufficient Carb Intake Impairs Strength Recovery After a Workout

Researchers from the University of Rhode Island studied the effect of low- and high-carbohydrate intakes on strength recovery after a strenuous workout. They also examined markers of exercise-induced muscle damage, and whole body protein metabolism.

Eight subjects (4 males, 4 females) were randomly assigned to a low carbohydrate (3.4 g/kg), higher protein (1.5 g/kg) diet, or a high carbohydrate (5.0 g/kg), lower protein (1.2 g/kg) diet. Both diets exceeded the recommended daily allowance (RDA) for protein.

The mean weight of the subjects was 70 kilograms, so the high-carbohydrate diet consisted of 343 grams of carbohydrate, 85 grams of protein, and 62 grams of fat. The low-carbohydrate-higher protein diet was composed of 226 g carbohydrate, 103 g protein, and 67 g fat. The diets supplied enough calories for each subject to maintain weight. The diets were followed for five days, then the subjects performed an eccentric exercise bout to induce muscle damage. For those unfamiliar with weight training terminology, eccentric refers to the portion of a repetition in which the muscle is being lengthened (usually the lowering phase of an exercise, such as the descent in a squat or lowering the bar to the chest during a bench press). Eccentric-only training is known to produce greater muscle damage due to the ability to handle heavier weights than during traditional concentric/eccentric training.

After eccentric exercise, the researchers measured muscle soreness, creatine kinase (a marker for muscle damage), isometric strength, nitrogen retention, and whole-body protein metabolism. The low-carbohydrate diet produced a greater strength loss and lower creatine kinase after exercise when compared with the high-carbohydrate diet. In addition, the high-carbohydrate group experienced a reduced strength loss at 24 hours post-exercise when compared with the low-carbohydrate group (8.1% versus 15.5%). This reduced strength was maintained throughout the study and averaged 28% in the low-carbohydrate group and 8% in the high-carbohydrate group on day four of recovery. The low-carbohydrate group also had a reduced protein turnover, synthesis, and breakdown during recovery. According to the researchers, “these findings indicate that dietary carbohydrate, as opposed to protein, may be a more important nutrient to the novice weight lifter when recovering from eccentric exercise-induced muscle damage”.[13]

Once again, the “low-carbohydrate” diet in this study supplied more than twice the commonly cited 100-gram threshold for low-carb regimens, yet still failed to achieve adequate recovery when compared to a higher-carb diet.

Low-Carb = Low Muscle Glycogen = Increased Muscle Breakdown

When combined with strenuous exercise, low-carbohydrate diets are notorious for causing low muscle glycogen. Previous studies have shown increased urinary excretion of amino acids when exercise is performed in a glycogen depleted state. This is a bad sign, because when you’re trying to maximize your recovery from tough workouts you want amino acids shunted to your muscles for growth and repair, not peed down the toilet. To determine whether this increased excretion was the result of increased protein breakdown or reduced protein synthesis, Canadian researchers examined protein balance in six healthy, active men who followed low- and high-carbohydrate diets. The subjects cycled at 75% VO2peak to exhaustion to reduce glycogen stores, and then consumed either a high carbohydrate (10% protein, 19% fat, 71% carbohydrate) or low carbohydrate (25% protein, 64% fat, 11% carbohydrate) diet for 2 days, in random order. Following each dietary intervention, the subjects performed two hours of two-legged kicking exercise. Biopsy samples confirmed that muscle glycogen was lower on the low-carbohydrate diet at rest, during exercise and one hour afterwards.

Overall muscle protein balance was decreased on the low-carbohydrate diet compared to rest and the high-carbohydrate diet, primarily due to an increase in protein breakdown but also a decrease in protein synthesis late in exercise[14].

Pissing Away Muscle with Ketosis

The effect of ketosis on branched chain amino acid (BCAA) metabolism is another reason why ketogenic diets are best avoided if optimal body composition is your goal. The BCAAs are comprised of three crucial amino acids – leucine, isoleucine and valine – that belong to a group known as the essential amino acids. The BCAAs differ from other essential amino acids in that they are mainly metabolized, not in the liver, but in skeletal muscle. The BCAAs therefore play an important role in the preservation of muscle, and supplementation with BCAAs has been shown to attenuate lean mass losses during caloric restriction[15]. However, when researchers compared ketogenic (25 g/carbs/day) with non-ketogenic (200 g/carbs/day) diets in healthy volunteers eating maintenance calories, they found the keto diet caused blood BCAAs to remain much higher after a beef meal.

This indicates that BCAAs were not being taken up by muscles; an unfavourable development as BCAAs exert their anabolic effects after being absorbed by muscle cells, not by floating aimlessly through the bloodstream. By the way, becoming “fat-adapted” (i.e. following a ketogenic diet for an extended length of time) will not excuse you from this unfavourable scenario. Again, the muscle-sparing agent responsible for muscle preservation on the non-ketogenic diet is most likely insulin. One of insulin’s functions is to promote the uptake of amino acids by muscle cells and stimulate muscle synthesis. Very low insulin levels on the keto diet appear to have impaired the uptake of BCAAs from the bloodstream into the muscle[16].

Another study indicating decreased uptake of ingested protein from ketogenic eating was conducted by Dutch scientist Peter Bisschop and his co-workers[17]. They took six healthy young men and placed them on 3 different diets, each with identical protein levels but varying carbohydrate and fat contents. Each diet was eucaloric (i.e., supplied maintenance level calories), was followed for eleven days, and separated by an 8-10 week “washout” period. The macronutrient breakdown of the 3 different diets was as follows: 1) 2% carbohydrate, 83% fat; 2) 44% carbohydrate, 41% fat, and; 3) 85% carbohydrate, 0% fat.

The researchers observed that twenty-four-hour urinary nitrogen excretion was approximately 28% and 44% higher on the ketogenic (2% carbohydrate) diet than on the moderate- and high-carbohydrate diet, respectively. The researchers concluded that this increase in nitrogen excretion occurred during the several hours after a meal. During digestion, the protein from your steak, chicken or eggs is broken down into amino acids, which are then used to perform various important functions in the body, including the repair and growth of muscle tissue. Eating carbohydrates along with your protein causes an elevation in insulin that increases uptake of these amino acids. The results of Bisschop’s study suggest that, if you are absorbing a decreased amount of protein from your food, then your body may be forced to break down bodily protein to compensate.

This is a major reason why, for optimal muscle preservation or growth, you should always eat some carbohydrates along with your protein. And why, if you seek more muscle and strength, you should give low-carbohydrate diets the cold shoulder.

So how does one explain the numerous bodybuilders displaying impressive muscularity while following low-carb diets?

Simple. Most, if not all, of that muscularity was built while following a high-carb diet. Bodybuilders traditionally used high-carb diets in the off-season, while low-carb diets were used by some (certainly not all) during the weeks leading up to a contest in order to cut weight.

It wasn’t until the late 90s/early 2000s that some bodybuilders started succumbing to the low-carb hyperbole and believing they could just as easily build muscle on a low-carb diet. And some have indeed proceeded to do so. But the weight of the evidence overwhelmingly indicates they would have achieved even better results had they followed a higher-carb diet.

Thankfully, the tide has already started to turn.

At the 2009 Mr. Olympia, considered the Superbowl of bodybuilding, spectators were blown away by what appeared to be a sudden improvement in the quality of physiques when compared to previous years.

Jay Cutler and Branch Warren went on to score first and second place that year, and deservedly so. Their condition was mind-blowing: deep cuts, full muscles, and a healthy glow rather than the all-too-common dehydrated and drawn-out appearance.

Cutler’s transformation was especially impressive. After having lost his title and being criticized for problematic symmetry and muscle imbalances, he did what no dethroned Olympia winner has ever done before – he came back better than ever and blew away the competition to reclaim his title.

Warren, meanwhile, did what few thought a relative newcomer to the Olympia could do and pulled off a surprise second with his excellent combination of cuts, size and symmetry.

As noted earlier, the entire contest was characterized by a higher than usual standard of physiques. The contestants seemed to be doing something different.

Was there a stunning new training regime taking the pro-bodybuilding world by storm? Nope.

Had renegade scientists working in clandestine underground labs formulated some super-powerful new steroid? Nope.

The difference appears to have been carbs. Lots of them.

George Farah, the nutrition consultant who guided Branch to his impressive second place in the Olympia, was perplexed at the widespread use of low-carbohydrate diets in bodybuilding. Many bodybuilders and strength athletes had embraced these diets as eagerly as the general population, but needless to say, the nutritional needs of individuals performing intense daily training differ greatly to someone who spends their day staring at a computer in a seated position.

Farah reported he often had clients on very low-carbohydrate diets coming to see him, exhibiting low morning temperatures of 96ºF that quickly rose when he increased their carbohydrate intake. Farah, not surprisingly, is not a fan of low-carbohydrate diets. He had Warren consume as much as 1,000 grams of carb per day in his preparation for the Olympia[18].

Harry Rambod, the consultant who helped Cutler reclaim his Olympia title in stunning fashion, also shunned the use of low-carb eating and instructed his trainee to eat 750 grams of carbohydrate per day[18]. The rest is history – on the front cover of its January 2010 issue, popular bodybuilding magazine Muscular Development exclaimed “CARBS ARE BACK!” The prodigal son of bodybuilding nutrition had returned, and with a vengeance.

Now, because people, especially low-carbers, are so predictable, I already know what many are thinking right now:

“STEROIDS! Those bodybuilders were on STEROIDS!”

Right. And they were also on steroids when they followed their low-carb diets. Your point?

Yep, that’s right folks; even juicing to the gills doesn’t overcome the catabolic pitfalls of low-carb diets!

Wiping Clean the Rest of the Anecdotal Slate

Bear with me folks, we’re almost done with Danny. I just need to quickly address the remaining anecdotal examples of athletes he cites, then we can get on with the truly important things in life, like arguing whether blondes are better than brunettes, and whether 180mm cranks will help you climb hills faster than 177.5mm cranks. Yessir, these are the truly pressing questions of our times, and every moment we spend addressing Danny’s bollocks is a moment we spend neglecting these monumental issues. That’s just not cricket, so let’s be real quick:

Mark “Doc Ott” – Ultra Endurance Runner. OK, disclaimer time again: The following is meant as absolutely no disrespect whatsoever to Mark. I’m only addressing his case because Danny-Oh brought it up. So here goes: Mark recently placed second in the Rocky Raccoon Trail 100 mile run. My hat goes off to him for his achievement. But it behoves me to point out that the 1st place winner was Michelle Yates, a female runner who follows a high-carb diet…[19]

Darilyn Doddy – Powerlifter and Crossfitter: Extremely impressive lifter! Darilyn holds multiple powerlifting world records and has competed in world championships in Finland, Latvia and the US during the last 3 years – and triumphed at all of them. Darilyn tells me that during the first two years of breaking records, she wasn’t following any particular diet. Last year Darilyn used a ketogenic diet for 20 weeks leading up to November’s world championship. Through the holidays she went back back to a standard diet, then went ketogenic again in early January. So right now she’s into her 19th week of “eating only around 15g of carbs/day coming from either asparagus or broccoli with one of my meals which is what I was doing leading up to that competition as well.”

Darilyn acknowledges she’s not a long-term low-carber, rather it’s something she’s come across in the last year and “I do plan on continuing to see how my body reacts. I keep gaining strength, strongest I’ve ever been actually and have an ample amount of energy, so I really have no reason to add in carbs.”

Darilyn also notes that some of her records were broken in and some out of ketosis.

Out of all the anecdotal cases Albers cites in support of his argument, Darilyn is by far the most impressive. Carbs or no carbs, this is one strong girl! But I should point out the obvious: Powerlifting does not even begin to qualify as a glycogen-depleting sport. Unlike the moderate- to high-rep pump and burn training favoured by many bodybuilders (which also fails to deplete glycogen to anywhere near the same extent as endurance activities like cycling, running, etc), powerlifting training is typically characterized by low-rep sets that literally last a matter of seconds, followed by rest breaks that last minutes.

If you’re going to discuss the role of carbs in athletic activity, it behoves one to make the requisite distinction between activities of a glycogen-dependent and non-glycogen-dependent nature. That’s why I’ve previously discussed the two issues in two separate articles:

Why Low-Carb Diets are Terrible for Athletes: Part 1
Why Low-Carb Diets are Terrible for Athletes: Part 2
and
Why Low-Carb Diets are Inferior For Strength & Muscle Gains

Again, I guess Albers never bothered to read them. I’m not sure whether this is yet another example of Danny-A duplicity, or whether he remains generally ignorant to the vastly different glycogen demands of endurance activities such as cycling versus strength and power-based sports like powerlifting. Not that this info is any big secret; when I was undergoing my fitness trainer certification many moons ago, one of the first things they taught us were the main energy pathways utilized in various physical activities. Doing a max attempt in the squat or cracking hard-shelled nuts between your biceps to impress your mates at the pub relies primarily upon the ATP-creatine phosphate energy pathway, while setting out to climb the Zoncolan on your bike will rely very heavily on your glycogen stores. Nowadays, this info is available to anyone with an Internet connection; perhaps if Danny had spent an hour researching some basic sports science precepts instead of desperately scrounging around for examples of low-carb athletes, he might have saved himself a lot of embarrassment. And emerged a little smarter as a bonus!

So, yes, powerlifters and bodybuilders can indeed gain strength and size on low-carb diets, but all the available science indicates a high-carb diet will do the job even better. Darilyn might disagree on that last point, but I have to go with the controlled science. On that point, it’s probably worth reiterating that Darilyn is not a long-term low-carber but has been cycling in and out of ketosis over the last year. Many of you will no doubt be familiar with Mauro DiPasquale and his “Anabolic Diet” which, rather than intersperse lengthy periods of low- and high-carb intakes, instead cycles carb intake on a weekly basis: 5-6 days low-carb, 1-2 days high-carb (and often very high-carb). Mauro, a former champion lifter, reportedly followed the diet back in his powerlifting days. Some low-carbers might consider the Anabolic Diet an endorsement of low-carb eating, but I have to go with the assessment of my friend Will who surmises that opting for cyclic ketogenic diets instead of the straight ketogenic variety is an implicit acknowledgement that carbohydrates impart important benefits.

Jamie Caporosso – Powerlifter. Again, impressive transformation. Danny asks how would I explain it? Um, is this a trick question, Danny?

1. Jamie is a powerlifter: Read what I just wrote in regards to Darilyn.

2. At no point have I ever said people can’t lose fat and gain muscle on a low-carb diet (for the record, I’ve done it myself), only that they will do the latter more easily on a high-carb diet. Again, that’s not my wishful thinking, it’s what the controlled science shows.

Like I said, I myself have gained muscle and strength on a low-carb diet. But my best ever body composition and strength results, not to mention overall fitness, have unquestionably occurred while following high-carb diets. How do you explain THAT, Danny?

Oh, and I must point out that Jamie has also been in ketosis for a mere matter of weeks.

Mike Morton – Ultra Endurance Runner. Credits The Art and Science of Low Carbohydrate Living by Stephen Phinney for his ‘success’ in adopting a low-carb diet. Lawdy lawdy: Refer back to my discussion on Phinney…

Has also been following a ketogenic diet for a mere 3 months.

Folks, notice a pattern with the last 3 examples?

All have been following a ketogenic diet for a few months at the most! How will they feel about their wonderful new diet in a year, 2 years, or even 5 years?

Let me give you an idea, from a guy who was once a very passionate low-carb devotee and who earnestly believed low-carb diets conferred no performance disadvantage whatsoever. This gentleman spent far, far longer on a low-carb diet than Mark “Doc Ott”, Darilyn Doddy, Jamie Caporosso or Mike Morton. This guy followed every variation of a low-carb diet you could think of: Non-ketogenic, cyclic ketogenic, targeted ketogenic, intermittently fasted ketogenic, intermittently fasted targeted ketogenic, and on and on and bloody on.

I have no qualms about citing this guy, because I’m intimately familiar with his situation.

That guy is me.

Yep, I followed a low-carb diet for some 7-8 years, and convinced myself for most of that time that I was doing just fine. My main form of physical activity during this time was lifting weights, along with grappling and MMA classes. I made some good strength gains over the years, even during the ketogenic phase, and for years my body fat percentage hovered around the 6% mark. Like Darilyn, Mike and Joel, I appeared to be living, breathing testimony that low-carb diets were just fine for active individuals.

That is, until the day in 2006 that I bought myself a shiny new road bicycle.

I started riding that baby in the hills, and at first everything seemed fine. But then reality started biting me on the ass, as it always does when you’ve been living under a delusion for way too long. It was only a matter of weeks before my legs started to feel like concrete blocks and my ride times started going to hell in a handbasket. The day I got dropped up Monbulk-Olinda Road by some guy with pipestem legs was the last straw. I went home, said goodbye and good riddance to my ketogenic ways, and was delighted to see my performance on the bike improve immediately.

Fast forward another 2 years, and I gave not just ketogenic but low-carbing in general the big middle finger. And it was truly one of the best and most liberating things I’d ever done (yep, dietary divorce can be just as invigorating as the real thing hahaha). Along with further dramatic improvements in my cycling fitness, I noticed improvements in mood and something else that was quite memorable: My shockingly low tolerance for cold weather had disappeared. No longer did my nose and fingers feel ice cold to the touch in winter, and no longer did I have to use 3 doona covers on my bed. Hell, it sounds absurd looking back, but that’s where I was. Yep, thanks to my low-carb diet, I’d endured years of Euthyroid Sick Syndrome and had no idea why until after I dumped this sorry way of eating.

So when the two Mikes, Darilyn and Joel eventually abandon low-carb eating (and going by statistical odds alone, there is a very strong chance at least some of them will), will Danny make a big song and dance about that? Or will he just stick his head in the sand and ignore their departure from low-carbing like it never happened? What about all the other folks who’ve dropped low-carbing and experienced immediate and marked improvements in their energy levels? Why doesn’t Danny mention them?

He insinuates I suffer confirmation bias and that I engage in cherry-picking, and he says “I do not think Mr. Colpo searched all that hard” for low-carb athletes, but what about Danny’s own wilful evasion?

Why do you blatantly ignore folks who unsuccessfully tried every which way for years on end to make a low-carb diet work for their training, and instead loudly wank on about folks who have not yet reached that point, folks who’ve only been low-carbing for a few months at most?

And you allude that I’m the one suffering bias?

What a crock.

The Bottom Line

Danny Albers should stick to downing Buds and cracking bad jokes with Fred Hahn.

Because as a sports nutrition commentator, he fails miserably. He cites papers he hasn’t even read as clinical proof low-carb diets are just fine for athletes, when in fact those papers show no such thing.

He blatantly ignores the clinical trials that show both ketogenic and non-ketogenic diets to impair cycling performance. Nope, doesn’t so much as even mention them.

He cites Tim Olson as an example of a low-carb athlete, but Tim Olson by his own admission is not a low-carber.

He cites Ben Greenfields as an example of a successful low-carb triathlete, but Ben is plagued by a dysfunctional hormonal and immune profile, and there is excellent evidence to indicate his low-carb diet is at least partly to blame.

He cites Vince Gironda as an example of a ketogenic bodybuilder, making no mention that Gironda only recommended keto diets for a short time, and that he also recommended short-term vegetarian diets!

He cites four other athletes/exercisers whose names he pulled from the Internet, and while their achievements and efforts certainly command respect and admiration, only one of them (Darilyn) has competed in and won world class events. And most of them have only been following their diets for a very short time, so we don’t know how they’re going to fare when the obligatory honeymoon period of novelty, excitement and overlooking flaws wears off (yep, as Mike Stone once hilariously pointed out, new diets are often a whole lot like new girlfriends).

All this tomfoolery on the part of Danny Albers completely fails to refute my point that LOW-CARB DIETS ARE INFERIOR TO HIGH-CARB DIETS FOR ATHLETIC PERFORMANCE and that TOP ATHLETES DO NOT FOLLOW LOW-CARB DIETS.

Granted we have the sole exception of Darilyn Doddy (low-carbers also keep citing the name of Bjorn Ferry, a Swedish athlete who won gold in the 2010 Winter Olympic biathlon and reportedly follows a low-carb diet. However, no-one has been able to supply me with a detailed English-language breakdown of the nutritional plan he was following leading up to and at the time of his victory. According to Google’s English translation of his website, Bjorn’s diet is “Swedish, organic and high in fat”, which sure leaves a lot of wiggle room regarding his carbohydrate intake…)

Like it or not Danny, in the world of endurance sports, the best of the best unquestionably eat high-carbohydrate diets. Go ahead mate, go off and spend another three weeks scouring Google for examples of athletes who once won the Gunkston South Annual Cow Patty Tossing Trophy while following a low-carb diet, but you cannot change this simple fact. You can jump up and down, accuse me of cherry-picking and confirmation bias all you want, but that’s the plain truth, Ruth!

Ladies and gentlemen of the jury, I rest my case.

Specially for Danny: A group photo of all the world-class, gold medal-winning athletes who we know for sure to follow a low-carb diet.

Some Parting Advice for Danny Albers

Danny, let’s face it: You acted like a complete Wally. You loudly called me out, patronized me, and claimed I was wrong based on research papers you hadn’t even read, then to top it off you cited anecdotal evidence that was sloppier than a baby’s regurgitated breakfast.

Not very smart, huh?

You know, I could give you a final middle finger cyber-salute at this point then proceed to completely purge your obnoxious, fight-picking memory from my consciousness. But like I said before, I’m not a total bastard. If you’re prepared to have a good think about what you did and why you did it, and can admit you prematurely ejaculated over this whole low-carb thing, I’m happy to extend the olive branch. Maybe you can even join folks like Kelly Mahoney as one of the former low-carbers who once furiously hated my guts but then changed their tune when they realized I was actually right.

Again, I’ll let you mull over that while I discuss something else:

Why is it that low-carbers, when confronted with articles by yours truly discussing pitfalls or false claims pertaining to their beloved religion diet, automatically go into HDA (Hateful Defamatory Asshole) mode?

Heaven forbid these people stop to thoughtfully consider my arguments and impartially examine the evidence I cite. Heaven forbid they consider I might actually be… correct!

Hell no, they can’t do that, because that would involve admitting they might be wrong, something they simply don’t have the character to do. It’s much easier for them to reflexively go into defensive mode, and tell themselves I’m just some loopy, dishonest bastard who’s part of some evil, hidden pro-carb agenda. They then have no qualms about going off half-cocked, piously accusing me of dishonesty, duplicity, and incompetence. When I ask them to provide some actual coherent, tightly controlled scientific evidence involving real live human beings to support their accusations, they fail to deliver every single time.

This ad hominem tactic has since been enthusiastically embraced by the vegan crowd. What I find eternally bemusing is that vegans never accuse me of dishonesty/duplicity/incompetence when I’m discrediting low-carb dogma, and low-carbers never accuse me of dishonesty when discrediting vegan hyperbole. It’s only when I turn my critical eye to their own cherished dogmas that I suddenly become dishonest/duplicitous/incompetent!

What a bloody joke.

The sad truth is that both the vegan and low-carb camps are full of shit. They might hold polar opposite beliefs about diet and health, but they use the exact same methods to rabidly defend their beliefs. They care for science only when it can be distorted and misrepresented in a manner that supports what they wish to believe. Dietary debate for them is not about an impartial quest for the plain facts, but a lawyer-like endeavour in which outwitting and out-sleazing your opponent at every turn and at all costs are the only things that matter.

That my friends, is just plain friggin’ pathetic.

So, Danny, if you’re not yet ready to reach out to me, here’s another suggestion: Get together with your fellow Colpo-hating low-carb and vegan brethren, and form a group called Dietary Fucktards Anonymous. Or would that be Dietary Fucktards Not-So-Anonymous? Whatever…you jokers could at last begin to make inroads into dealing with the shameless duplicity arising from the cognitive dissonance you find so discomforting:

[Danny]: “Hi, Fred, Michael, Pee Pee, Janet, Martin…my name’s Danny, and like you guys I’m guilty of acting like a complete fucktard towards people whose only crime was to dispassionately state facts I didn’t want to hear. I thought this would make me some kind of Internet big shot, but all it did was make me look like an ignorant, smart-assed little dick!”

[Janet]: “That’s okay Danny, everyone here has been where you are! You’re among friends now, we’re all here to support each other as we overcome our crippling fucktardedness … one day at a time!”

[Fred]: “Yeah, welcome to your new family, Danny!”

[Pee Pee]: “Mmmmm mmmmm, yessssth, welcum daaarling!”

[Martin]: “Greetings Danny! Can I offer you some cheesecake?”

[Michael]: “Has anybody got some Zantac? My GERD is killing me! And has anyone seen my girdle, I’m sure I left it by the cooler…”

Wow, that shit brings tears to my eyes. Well, almost. And probably not for the reasons you’re thinking LOL. But anyway, Danny, I wish you all the best as you grapple with your cognitive issues, hopefully you’ll conduct some ruthlessly objective introspection soon and do some serious mental house-cleaning.

Because you sure as hell need it.

—

PS: I almost forgot! Before I sign off, I want to hand out this month’s Titanic Testa di Cazzo Award. No, not to Danny, but to the sad sack of shameless misrepresentation known as Jeff Consiglio who, in Albers’ comments section, writes:

“I used to be a fan of Colpo’s work, but he really lost me when he started with the whole “eat lots of carbs to be as elite as me” meme.”

Mr Consiglio, you know as well as I do that I have never, ever claimed to be “elite”, and I’d dearly love to see exactly where I posted this alleged meme. I won’t hold my breath for you to send me the link, because we both know full well it doesn’t exist.

So congratulations Jeff, for demonstrating to the world just what a blatant liar you are, and for joining the long line of low-carb sleazeballs who can’t factually refute what I say so instead make up false allegations about my personal character!

For those not yet wise to the ways of low-carb wankery, what Jeff really means when he writes the above slop is:

“I used to be a fan of Colpo’s work, but then he started saying things that conflicted with my low-carb mind conditioning. The subsequent cognitive dissonance was simply too much to bear, so I constructed this tale in my head that Colpo was just a conspiracy-theorizing dipshit who boasts of being elite. My feeble brain was able to cope much better after that!”

In recognition of Jeff’s woefully deficient intellect and distinctly unItalian(-American) behaviour, I’d like to address the following meme and video to him.

Keep believing all that dubious propaganda Jeff, whether it comes from your screwball low-carb cohorts or from the shambolic and increasingly oppressive outfit that constitutes the United States Government! Yessir, you keep swallowing that Kool Aid, buddy!

To read Danny Albers’ reply to this article, click here.

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Note: Article first posted May 24, 2013 (AEST), updated May 25, 2013 (as a result of email correspondence with Darilyn Doddy, and to add mention of Bjorn Ferry).

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Please send all hate mail to: tellsomeonewhocares@carefactorzero.com

—

Anthony Colpo is an independent researcher, physical conditioning specialist, and author of The Fat Loss Bible and The Great Cholesterol Con. For more information, visit TheFatLossBible.net or TheGreatCholesterolCon.com

Copyright © Anthony Colpo.

Disclaimer: All content on this web site is provided for information and education purposes only. Individuals wishing to make changes to their dietary, lifestyle, exercise or medication regimens should do so in conjunction with a competent, knowledgeable and empathetic medical professional. Anyone who chooses to apply the information on this web site does so of their own volition and their own risk. The owner and contributors to this site accept no responsibility or liability whatsoever for any harm, real or imagined, from the use or dissemination of information contained on this site. If these conditions are not agreeable to the reader, he/she is advised to leave this site immediately.

References

1. Phinney SD, et al. Capacity for moderate exercise in obese subjects after adaptation to a hypocaloric, ketogenic diet. Journal of Clinical Investigation, Nov, 1980; 66 (5): 1152-1161.
2. Dr. Coggan’s comment was made in a 1995 post on the USENET newsgroup rec.sport.triathlon, which can be accessed here: http://www.rice.edu/~jenky/sports/coggan.html
3. Helge JW. Adaptation to a fat-rich diet: effects on endurance performance in humans. Sports Medicine, Nov, 2000; 30 (5): 347-357.
4. Lane AR, et al. Influence of dietary carbohydrate intake on the free testosterone: cortisol ratio responses to short-term intensive exercise training. European Journal of Applied Physiology, 2010; 108: 1125–1131.
5. Galbo H, et al. The effect of different diets and of insulin on the hormonal response to prolonged exercise. Acta Physiologica Scandinavica, Sep, 1979; 107 (1): 19-32.
6. Gleeson M, et al. Effect of low and high carbohydrate diets on the plasma glutamine and circulating leukocyte responses to exercise. International Journal of Sports Medicine, 1998; 8: 49–59.
7. Mitchell JB, et al. Influence of carbohydrate status on immune responses bef ore and af ter endurance exercise. Journal of Applied Physiology, 1998; 84: 1917–1925.
8. Gleeson M, Bishop NC. Modification of immune responses to exercise by carbohydrate, glutamine and anti-oxidant supplements. Immunology and Cell Biology, 2000; 78: 554–561.
9. Anderson KE, et al. Diet-hormone interactions: protein/carbohydrate ratio alters reciprocally the plasma levels of testosterone and cortisol and their respective binding globulins in man. Life Sciences, 1987; 40: 1761-1768.
10. Stimson R, et al. Dietary Macronutrient Content Alters Cortisol Metabolism Independently of Body Weight Changes in Obese Men. Journal of Clinical Endocrinology & Metabolism, 2007; 92 (11): 4480-4484.
11. Pedersen BK, et al. Training and natural immunity: Ef f ects of diets rich in f at or carbohydrate. European Journal of Applied Physiology, 2000; 82: 98–102.
12. Creer A, et al. Influence of muscle glycogen availability on ERK1/2 and Akt signaling after resistance exercise in human skeletal muscle. Journal of Applied Physiology, Sep, 2005; 99 (3): 950-956.
13. Benjamin L, et al. Dietary Carbohydrate and Protein Manipulation and Exercise Recovery in Novice Weight-Lifters. Journal of Exercise Physiology Online, Dec, 2009; 12 (6).
14. Howarth KR, et al. Effect of glycogen availability on human skeletal muscle protein turnover during exercise and recovery. Journal of Applied Physiology, Aug, 2010; 109 (2): 431-438.
15. Mourier A, et al. Combined effects of caloric restriction and branched-chain amino acid supplementation on body composition and exercise performance in elite wrestlers. International Journal of Sports Medicine, Jan, 1997; 18 (1): 47-55.
16. Gelfand RA, et al. Dietary carbohydrate and metabolism of ingested protein. Lancet, Jan, 1979; 1 (8107): 65-68.
17. Bisschop PH, et al. Dietary Carbohydrate Deprivation Increases 24-Hour Nitrogen Excretion without Affecting Postabsorptive Hepatic or Whole Body Protein Metabolism in Healthy Men. Journal of Clinical Endocrinology & Metabolism, Aug, 2003; 88: 3801-3805.
18. Gwartney D. Carbs make a comeback. Muscular Development, January 2010: 122-126.
19. Michelle discusses her diet in this interview: http://www.coloradorunnermag.com/2013/01/23/exclusive-athlete-interview-with-michele-yates-suszek/
    “I pretty much eat the same things everyday which consist of fruits, veggies, lean proteins, The Simply bars, and Honey Nut Chex!  I use GU Energy products pre, during, and post workouts…and GU Brew is great after workouts.”—

Danny Albers didn’t waste any time replying to my recent article Sorry Danny Albers, But Low-Carb Diets Still Suck for Athletes! I’ve reprinted his actual Facebook posts and my subsequent responses below.

Danny pretty much admits the whole exercise was a stunt to draw attention to his blog. Well, in that he succeeded, but I’m not sure it’s quite the kind of attention he was hoping for LOL. I think the key words used by Danny when attempting to explain his ill-conceived antics are “shameless” and “amateur”

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Anthony Colpo is an independent researcher, physical conditioning specialist, and author of The Fat Loss Bible and The Great Cholesterol Con. For more information, visit TheFatLossBible.net or TheGreatCholesterolCon.com

Copyright © Anthony Colpo.

Disclaimer: All content on this web site is provided for information and education purposes only. Individuals wishing to make changes to their dietary, lifestyle, exercise or medication regimens should do so in conjunction with a competent, knowledgeable and empathetic medical professional. Anyone who chooses to apply the information on this web site does so of their own volition and their own risk. The owner and contributors to this site accept no responsibility or liability whatsoever for any harm, real or imagined, from the use or dissemination of information contained on this site. If these conditions are not agreeable to the reader, he/she is advised to leave this site immediately.

Just like the shrill “saturated fat and cholesterol will kill you!” theory of heart disease, the establishment war on salt is another poorly conceived charade with no foundation in sound science.

For years, I’ve been advising all my clients and anyone else who’ll listen to go ahead and salt their food. When it comes to athletes, especially those that experience large sweat losses from exercising in the heat, the anti-salt sham is more than just a pseudoscientific wank – it’s potentially dangerous.

When someone complains to me their energy levels tend to wane during hot and especially humid weather, and they can’t work out why, one of the first things I ask about is their salt intake. More often than not they’re on a low-salt diet, not for any justifiable medical reason, but simply because that’s what our supposedly all-knowing health authorities and the ‘experts’ who blindly follow their edicts tell them they should do.

My suggestion to these folks is to start adding salt to their foods, and to start adding a little salt to their drinking water and to the carb drinks they use during long training sessions. When this suggestion is on target – and it usually is – the improvements can be quite dramatic.

I’d dearly love to sit down and write an expose on the whole salt issue but, as my regular readers will know, when I throw myself into something it’s never a half-assed affair. The reality is I just don’t have the time at the moment to do this subject justice.

Thankfully, a report on this very issue has just been released by a panel of US researchers under the auspices of the Institute of Medicine of the National Academies. Titled “Sodium Intake in Populations: Assessment of Evidence”, you can access the PDF for free right here (you’ll need to register first).

If you want the Cliff notes version, Gina Kolata over at the New York Times has put together a worthy piece about the new report. She notes:

“In a report that undercuts years of public health warnings, a prestigious group convened by the government says there is no good reason based on health outcomes for many Americans to drive their sodium consumption down to the very low levels recommended in national dietary guidelines.”

She goes on to note that some studies not only show these guidelines to be of little efficacy, but to in fact increase mortality in certain patient groups.

The New York Times story can be read in full here:

No Benefit Seen in Sharp Limits on Salt in Diet

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Anthony Colpo is an independent researcher, physical conditioning specialist, and author of The Fat Loss Bible and The Great Cholesterol Con. For more information, visit TheFatLossBible.net or TheGreatCholesterolCon.com

Copyright © Anthony Colpo.

Disclaimer: All content on this web site is provided for information and education purposes only. Individuals wishing to make changes to their dietary, lifestyle, exercise or medication regimens should do so in conjunction with a competent, knowledgeable and empathetic medical professional. Anyone who chooses to apply the information on this web site does so of their own volition and their own risk. The owner and contributors to this site accept no responsibility or liability whatsoever for any harm, real or imagined, from the use or dissemination of information contained on this site. If these conditions are not agreeable to the reader, he/she is advised to leave this site immediately.

Yours truly recently had the pleasure of being interviewed by Janah, Stephanie and Brett from That Paleo Show. We talked about my own personal health journey, the cholesterol sham, and how controlling your bodily iron levels might just be the most effective strategy in existence for preventing heart disease. The podcast is now online, you can listen to it by clicking the link below:

http://thewellnesscouch.com/tps/tps-19-an-interview-with-anthony-colpo

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Anthony Colpo is an independent researcher, physical conditioning specialist, and author of The Fat Loss Bible and The Great Cholesterol Con. For more information, visit TheFatLossBible.net or TheGreatCholesterolCon.com

Copyright © Anthony Colpo.

Disclaimer: All content on this web site is provided for information and education purposes only. Individuals wishing to make changes to their dietary, lifestyle, exercise or medication regimens should do so in conjunction with a competent, knowledgeable and empathetic medical professional. Anyone who chooses to apply the information on this web site does so of their own volition and their own risk. The owner and contributors to this site accept no responsibility or liability whatsoever for any harm, real or imagined, from the use or dissemination of information contained on this site. If these conditions are not agreeable to the reader, he/she is advised to leave this site immediately.

Regular readers will know I’m no fan of nutritional epidemiology. This is where researchers gather up a bunch of people, give them a diet questionnaire every few years and pretend this is an accurate representation of their daily diet, then record who suffers or dies from whatever disease they are supposedly studying.

One routinely reads headlines and articles claiming “New study shows red meat causes cancer!” or “whole-grain cereals lower heart disease risk”, but when you source the study this allegedly life-saving revelation came from, invariably it was an epidemiological project. This is despite the fact that epidemiological studies can’t even begin to “show” that red meat/eggs/full cream milk/yellow Smarties/pickled gherkins cause heart disease, cancer, diabetes or any other ailment.

Nutritional epidemiological studies can’t prove diddly, because they are manifestly inadequate to detect anything other than statistical associations. They cannot, I repeat cannot, establish causality. The first rule of good science is association does not equal causation. Unfortunately, this rule is routinely ignored in this day and age where health authorities prefer to dredge supportive data from epidemiological studies, having well learned over the years that randomized clinical trials have the annoying tendency to thoroughly demolish their most cherished beliefs.

And so we have the prevailing trend nowadays in which researchers, health authorities and other so-called ‘experts’ discuss the findings of epidemiological studies as if they were physiological fact.

Epidemiology’s Biggest Wank of All

The cholesterol theory of heart disease – the same contradiction-riddled theory that dominates modern CVD prevention attempts, that gave us cholesterol-free but cancer-causing omega-6-rich vegetable oils, utterly ineffective low-fat diets and toxic cholesterol-lowering drugs that wreak havoc upon muscles, tendons, nerves and even sexual organs – was built upon epidemiology.

More specifically, it was built upon the back of one of the most pathetic and selective epidemiological exercises conducted in the very spotted history of humankind. I’m talking, of course, about the Six Countries study by Ancel Keys. This was the ‘study’, published in 1953, in which Keys took the data for six countries, plotted them on a graph, and was able to show a wonderfully linear and positive association between national fat consumption and CHD mortality[1]. Other researchers tried to point out that data was actually available for 22 countries at the time and that Keys had simply handpicked the ones supporting his preconceived thesis[2]. At a 1954 conference in Geneva, the Minnesota cherry-picker – by now used to getting his own way – was stunned to find his ideas were met with much skepticism. British professor George Pickering interrupted Key’s presentation to ask in calm, understated James Bond-like fashion:

“Professor Keys, would you be kind enough to cite for us the principle piece of evidence that you think supports this diet-heart theory of yours?”

At this crucial moment, Keys, not usually at a loss for words, was caught off guard. His long-time friend and collaborator Henry Blackburn recalled: “…Ancel fell into a trap, he made a mistake; he cited a piece of evidence and they were able to destroy it. Instead of citing ‘well, this theory’s based on a body of evidence that we’ve seen here and here from the clinic, from the laboratory, and from comparing populations’, he didn’t make his case. He cited a piece–destroyed.”[3]

So when Keys presented his cherry-picked hogwash to a panel of top heart surgeons and researchers from around the world, he was almost laughed out of the room. But it didn’t matter; back home in the USA, Keys’ connections, his domineering manner, and his burning desire to avenge his humiliation in Geneva allowed him to worm his way onto the American Heart Association’s nutrition advisory panel, and his diet-heart hypothesis eventually became official policy.

The world has never been the same since.

Before I talk a little more about Keys and his absurd ‘research’, I want to share with you, my dear readers, a conversation I recently had with one of the studliest creatures the world has ever known. A man whose square jaw, rippling muscles, inhuman chest-to-waist ratio, thick bull-like neck and glowing golden coat sends bitches into instant heat, causing owners of female dogs to sense something is terribly amiss and tremble with fear from as far as 100 metres away.

I’m talking, of course, about my dog Ramone. A few days ago, I was sitting at my computer and looked over at him, only to see him looking right back at me with an unmistakable expression on his face. Drawing upon the finely tuned mental intuition that develops between a dog and his master, I could tell instantly he was wondering why I was tapping away and staring at this stupid screen instead of goofing around with him outside. And so I called him over for a little father-son chat:

Life According to Anthony, as Told to Ramone the Studliest Dog in the World

“Come here buddy and let me explain something…

[Sound of paws traversing tiled floor]

Humans, Ramone, are freakin’ insane. Well, not all of them. I mean, the Ramones were pretty damn cool, which is why I named you after them. And you know I’ve got your back, along with the rest of the family. But the bulk of humanity, my canine sofa-hogging friend, is just one big crapshoot. Humans long for leadership, tend to flock to authority figures, and will believe the most unlikely bullshit so long as it comes from an ‘official’ and ‘respected’ source. Here, let me give you a hypothetical example so you’ll understand where I’m coming from:

Imagine if that grumpy pitbull called Lex from up the street one day came up with this idiotic idea that bones caused canine heart disease (CHD). To support his theory, he plots six countries on a graph that shows as national bone consumption rises, so too does CHD. He ignores the other sixteen countries whose data refute his theory, but despite his fraudulent methods he still gets his screwball theory published in The International Journal of Dogshit, and while you and Kermit and Indy and the rest of your doggy buddies conclude this is one pitbull that’s completely lost his marbles, a bunch of toffy poodles in white coats eventually get together with Lex and form a ‘consensus’ that dog bones do indeed cause CHD. Never mind that dogs have been happily chewing away on bones ever since there were dogs, and therefore have thoroughly developed the necessary genetic machinery to enable you guys to efficiently process whatever nutrients you extract from bones.

Heck, researchers even do a bunch of clinical trials clearly showing no increase in canine heart disease nor overall mortality among dogs randomized to chew bones every day. In fact, some of these trials show a lower mortality rate among the bone-chewing dogs! But by this point the CHA (Canine Heart Association) has been formed and they’re making a fortune selling “Heart Licks” to manufacturers of 100% animal-free vegan-friendly dog bones.

When proponents of Lex’s theory complain that many dogs simply will not or cannot give up chewing on real bones, a company called Pfurzer promptly brings a new bone-blocking ‘wonder’ drug to market called Poochastatin. Not to be outdone, Bristol Meyer Rover promptly releases Woofastatin, followed by FidoSmithKline who gain FDA approval for a slow release version called Droolastatin. Before you know it, there are more statins on the market than fleas on Lex.

But investigative journalists do a little digging and find out that statins are toxic drugs whose official side effect rates have been dramatically under-reported. They also discover that the CHA is really run by high-flying cats who receive hundreds of millions of dollars each year from drug companies and vegan-friendly dog bone manufacturers, but no-one seems to be listening. Your fellow dogs, in what appears to be a collective state of trance-like stupidity, start believing the sham. You, Indy and Kermit try and make them see sense, but you’re promptly written off, most ironically, as a bunch of “quacks” and “cherry-pickers”.

Now, Ramone, I know by the way you’re looking at me that there’s no need for me to go on. Yep, you dogs would never fall for such crap. You dogs are pretty straightforward, no-bullshit creatures. You can tell if someone is full of shit simply by sniffing them. You don’t form governments to oppress and spy on your fellow dogs, you don’t sell drugs to each other’s kids, you don’t commit genocide and wipe out thousands of your own kind on a daily basis, you don’t spend thousands on brand name bollocks and useless gadgets in order to impress each other…so why on Earth would you be dumb enough to believe a perfectly natural food you’ve been eating for thousands of years with much success has suddenly become unhealthy?

But that’s exactly what humans do, buddy.

No, I’m not kidding.

Sigh.”

 Coming soon: Ramone’s Guide to Pulling More Chicks Than a Rock Star: Why Being Buff and Just Plain Friggin’ Awesome Beats Corny Lines, Expensive Cars & Neck Tattoos Every Single Time!

Yep, us humans could learn a lot from dogs. But sadly, after some 15,000 or so years of hanging out with man’s best friend, pretty much all we’ve picked up from them is how to mount our partners from behind.

Crikey.

Look, nothing against the doggy position, it’s a time-honoured favourite that has undeniably bought much joy to mankind. And womankind, too. But maybe if we started emulating dogs in other ways, such as doing a little more sniffing around before embracing every oddball theory our industry-sponsored health authorities try to impose upon us, we might be in a much better place. A place where we can largely avoid heart disease by natural, safe methods instead of relying upon low-fat pseudo-foods, dubious vegetable oils, and toxic drugs with side effects that include muscle and tendon damage, sexual dysfunction, mood disturbances and more.

Which brings us back to the late Ancel Keys.

People often say you shouldn’t speak ill of the dead. But there does exist a sub-clause allowing exceptions to this rule if the dead person in question was an egotistical, megalomaniacal asshole whose actions caused massive and irrevocable harm to humankind.

Which is why, for example, no-one except the most devoted Neo-Nazis get upset when you talk about what an asshole Adolf Hitler was, and why no-one except the most devoted low-carbers get upset when you post irreverent and rather hilarious film clips depicting the fanatical Fuhrer as a tubby ketotic diet failure. You know, like this one (nice work Señor Green hahaha):

Ancel’s Ego versus Public Health: Ancel Won

Ancel Keys is a man whose fraudulent and ego-driven behaviour brought irrevocable harm to mankind. Granted, his shenanigans have helped make oceans of money for drug companies, heart associations and vegetable oil manufacturers, but I think you’ll agree public health should take precedence over profiteering any day.

Remember the Geneva conference where Keys was flabbergasted to find that, unlike back home, the participants did not hold him and his absurd theories in gushing awe? According to Blackburn, Keys was “so stung by this event that he left the Geneva meeting intent on gathering the definitive evidence needed to establish or refute this Diet-Heart theory”[4].

“He got up from being knocked to the ground and went out saying, ‘I’ll show those guys,’ and designed the Seven Countries Study”[3].

The Seven Countries study was to be Ancel “Screw You George Pickering!” Keys’ revenge on all those who doubted him. Sadly, millions of innocent people would suffer in the process, falling victim to the useless preoccupation with animal fats and cholesterol that would proceed to distract the world from the real causes of CVD.

The Minnesotan bully immediately went about organizing a ‘real life’ version of his Six Countries study, this time adding an extra country. Unlike 6C which was purely a paper exercise, 7C was a prospective study that involved recruiting groups of men in various countries, surveying them about their diet and checking their cholesterol levels, then recording coronary and all-cause mortality over the subsequent ten years.

As with the garbage Six Countries study, 7C also featured nations hand-picked by Ancel Keys (Finland, Greece, Italy, Japan, Yugoslavia, Netherlands, U.S.A.) that just happened to show a correlation between saturated fat intake, cholesterol levels, and CHD mortality.

Well, at least that’s how the study was reported. And continues to be reported by people who should damn well know better, but whose reliance on the cholesterol sham for a salary thoroughly blinds them to the bleedingly obvious.

Those who aren’t hopelessly blinkered by the cholesterol bollocks and who’ve bothered to look at the 7C data for themselves will come across some rather interesting findings.

In 7C, the lowest cholesterol levels were found amongst the Japanese, who experienced a far lower incidence of coronary deaths than the U.S. and Finland, the two countries with the highest mean serum cholesterol readings. Which, of course, would tend to support the cholesterol thesis. However, the lowest rates of heart disease in the entire study occurred amongst the residents of Crete, in Greece, whose average cholesterol levels were positioned right between the middle of the two extremes. The Cretans, in fact, were the healthiest participants in the entire study, experiencing the lowest death rates not just from heart disease, but all causes.

The Cretans had an average serum cholesterol of 202; across Greece, on the island of Corfu, cholesterol levels were 198, yet coronary deaths were five times higher than those seen in Crete.

Correlation shmorrelation!

In Crevalcore and Montegiorgio, two different districts in Italy, mean serum cholesterol levels were identical, yet death rates from heart disease were 2.5 times higher in the former than the latter.

In Rome, Croatia and the Netherlands, serum cholesterol also showed no relationship with CHD mortality. As with saturated fat, cholesterol levels within nations were not a reliable indicator of heart disease risk[5].

It was the same with diet. Inside countries, cardiovascular mortality varied widely between regions, despite similar dietary habits and risk factors. In Finland, CHD deaths were four times higher in Karelia than in Turku, even though similar diets were consumed in both regions. In Greece, Cretans experienced a far lower incidence of CHD than residents of Corfu, despite similar saturated fat intakes. ECG readings also showed no correlation between diet and heart disease risk. Importantly, unlike the clinical diagnosis, which was conducted by local doctors with varying degrees of competence, all electrocardiograms were analyzed in the American study center.

Despite these findings, Ancel Keys – ever the shameless bullshitter – claimed his study showed that low cholesterol levels and a low fat intake, especially from saturates, reduced heart disease risk.

It showed no such thing, but that didn’t even begin to stop his hopelessly biased findings being embraced by an orthodoxy that was both desperate for some kind of theory that explained the puzzling prevalence of CHD and also increasingly aware of the massive commercial potential conferred by the diet-heart hypothesis (manufacturers of n-6 polyunsaturate-rich cereal and nut oils were the first industry benefactors of this hypothesis, a role the drug companies subsequently and gleefully took over when it became evident saturated fat restriction was an outright failure in preventing CHD).

Keys got his revenge, but the rest of us still don’t have a cure for heart disease. Despite some six decades of what essentially constitutes a collective and highly irrational phobia of cholesterol and animal fats, and despite the best efforts of drug companies to manipulate ‘therapeutic’ cholesterol targets so that as much of the public as possible can be pushed onto statin drugs, CVD is still as prevalent as ever and still remains the  number one killer in the Western world.

Heck, the shifty bastard even moved to Italy, a country where monounsaturate-rich olive oil rather than polyunsaturate-rich sunflower and corn oils reigned supreme, and where surgically trimming the fat from your meat was such a foreign behaviour it was likely to raise questions about your sexual orientation. While the rest of us separated our egg whites from the yolks, drank watery skim milk, forced down mouthfuls of fartaceous whole-grains, and laced our salads with tumour-inducing amounts of linoleic acid, Ancel Keys privately ate like an Italian and lived to be 100 years old.

Moral of the Story: If you’re an anti-cholesterol shill who wants to live to a ripe old age, practice not what you preach.

It worked for Ancel.

MONICA, Oh MONICA, Where Art Thou?

Unlike 6C, 7C cost a lot of money, involved ‘real’ people and a huge assembly of researchers, giving it the veneer of a worthwhile research project. And by ignoring the intra-country results, de-emphasizing Crete and instead wanking on about the low rates of CHD in Japan and the high rates in USA and Finland, the cross-country results could be made to look supportive of the cholesterol hypothesis of CHD.

But there is a more recent study that also compared ten year mortality rates both among and within various countries, and cannot even begun to be twisted in such a manner.

Which, I might add, is why most of you have never even heard of it.

The MONItor trends in CArdiovascular diseases (MONICA) project is without question the largest study into the relationship between ‘risk factors’ and cardiovascular disease ever conducted on this here planet. Born in the early 1980s, MONICA was a collaborative effort involving thirty-two centers in twenty-one countries around the globe, monitoring a whopping ten million men and women aged between 25-64 years for a period of ten years.

Read that again folks: 10,000,000 people, followed for ten years, in 21 countries around the world. That is a humungous study.

But I’m betting almost all of you who’ve not read The Great Cholesterol Con or The Cholesterol Myths have never heard of it. For some strange reason, MONICA doesn’t even begin to get the same kind of attention awarded to famous but much smaller projects like Seven Countries or Framingham.

Why is that, do you think?

I couldn’t find any pictures of “The MONICA Project”, but I did come across this picture of “MONICA BELLUCCI” so I posted that instead. I hope you don’t mind. If you do, you probably eat too much soy.

After all, you’d think such an important and massive study would deserve pride of place in any discussion examining the epidemiological relationship between animal fats, cholesterol and heart disease. With over ten million participants, MONICA is a big girl who absolutely dwarfs over anything that came before her. Even when a bunch of researchers whose writing committee was made up of people who made their living working for an outfit that receives funding from drug companies and the British Heart Association (who in turn receives generous ‘donations’ from drug companies) conducted a meta-analysis involving data for some sixty-two non-MONICA prospective epidemiological studies, the total number of pooled subjects still amounted to only 1.24 million.

Needless to say, if I was putting together a paper on the epidemiological relationship between cholesterol and heart disease in prospective epidemiological studies, MONICA would be first on the list.

However, let’s pretend for a moment I made my living promulgating the cholesterol hypothesis and worked for an outfit that received money from cholesterol drug manufacturers. Let’s pretend I was quite fond of the cholesterol theory because, hey, it put a roof over my head, clothes on my back, and a nice, highly-tuned Lotus in my garage. In this circumstance, it would be a real bummer for me to have to include MONICA in the meta-analysis. And so I might just conveniently modify my exclusion criteria on rather inane grounds so that, lo and behold, MONICA no longer meets the eligibility requirements. Or I might just flat out ignore her and hope no-one notices.

Why would I do this?

Because MONICA, the most MASSIF cardiovascular epidemiological study in the history of humankind, completely failed to support the cholesterol hypothesis. The highest cardiovascular mortality was observed in Central and Eastern Europe, despite the fact that these regions exhibited blood cholesterol levels and dietary saturated fat intakes similar to those seen in Western Europe and the U.S.A.[6]. Central and Eastern Europe did differ from the West in other important ways; the intake of dietary antioxidants from domestic and imported fruits, vegetables, nuts was substantially lower, while struggling economical and political systems gave rise to greater psychological stress. Alcohol abuse was also widespread in the Eastern bloc countries[7].

And so while MONICA was a huge disappointment for lipid hypothesists, it does throw out a few important clues for the non-dogmatic as to what some of the true contributors to CHD might be.

Cross Country, Intra-Country

When you compare the relationship between cholesterol and CHD among different countries, as MONICA did above, you are performing what is known as an ecological comparison. Ancel Keys’ initial bad joke, the Six Countries study, was an ecological comparison. His Seven Countries study, as we saw above, examined not just international (ecological) but intra-national cholesterol levels and CHD mortality.

So too did MONICA.

Sorry folks, still can’t find any pictures of “The MONICA Project”, damnit.

And like the 7C study, MONICA also found a disconnect between cholesterol not just at the ecological level but also at the intra-national level.

In Italy, for example, mean serum cholesterol levels among those aged 35-64 declined in Friuli (FRI) residents but rose among the folk in Brianza (see Figure G46 on page 205 of this MONICA paper). According to the cholesterol thesis, CHD should have dropped in Friuli but risen in Brianza (BRI).

But the cholesterol thesis is utter bullshit. Which goes a long way to explaining why CHD mortality declined to similar degrees in both populations during the same period these cholesterol changes were recorded. Lung cancer, total cancer, stroke, total CVD, and overall mortality similarly declined in the two locations (see Table 1 here).

Now, if I was a lipid hypothesist, I might call this the “Italian Paradox”, which is another way of saying “I have no clue how to explain this glaring contradiction to my cherished beliefs”.

If I was a lipid hypothesist and was tempted to do this, I would also need to create a “Swiss Paradox”. In the Vaud/Fribourg (VAF) region of Switzerland, cholesterol levels slightly declined while Ticino (TIC) saw the greatest rise in mean serum cholesterol levels in the entire population. Again, this should have resulted in a sharp disparity in CHD mortality, but coronary mortality declined to a similar degree in both populations (see Figure G22 on p. 181 of this paper).

Thankfully, researchers have already dreamed up a “French Paradox” to describe the ‘puzzling’ observation that the French eat a diet rich in animal fats yet have much lower rates of CHD than most other countries. Again, this observation is not at all puzzling to those aware of what complete garbage the cholesterol hypothesis is, but those who aren’t may well like to again apply the paradox tag to the fact that in France, cholesterol levels rose significantly in Strasbourg (STR) but slightly declined in Toulouse (TOU). Once more, despite this allegedly ‘atherogenic’ change in the former, it experienced a similar decline in CHD mortality to the latter.

And then there was the “Swedish Paradox”. Mean blood cholesterol hardly changed in Northern Sweden (NSW), but dropped by 0.5 mmol/l in Gothenburg (GOT). Despite this, coronary mortality declined to a greater degree among men in Northern Sweden compared to Gothenburg, and to a similar degree among women.

I could go on and on, but I have a rather energetic pooch here yearning to be taken outside for a lengthy stroll. If you want to find more “paradoxes” of your own, feel free to keep searching through Fig G46 here and Fig G22 here.

But I think most of you will have gotten the point by now. Not only is epidemiology highly flawed, but it must be cherry-picked selectively by those who would have us believe the nonsensical fairy tale that is the cholesterol hypothesis of heart disease. MONICA, the most massive epidemiological CVD study of all time, does not afford the anti-cholesterol crowd such an opportunity, so despite its massive stature it is simply ignored.

Epidemiology’s One Redeeming Feature

I will reiterate once more: Epidemiology is terribly inferior to tightly controlled clinical research, and the modern-day habit of awarding findings from the former similar status as the latter is an absolute disgrace.

But epidemiology isn’t totally useless. While 99% of the nutritional epidemiology polluting our journals is time- and tax money-wasting pap designed to support a preconceived agenda, every now and then epidemiology does detect statistically robust relationships that are worthy of further investigation in the clinical setting.

And lo and behold, the MONICA finding that cholesterol levels were unrelated to CVD mortality, while dietary intake of antioxidant-rich fruits and vegetables was, has indeed been strongly supported by a number of randomized clinical trials.

We’ll talk about those trials the next time we meet. Until then, au revoir.

—

References

1. Keys A. Atherosclerosis: a problem in new public health. Journal of Mount Sinai Hospital, 1953; 20:  118-139.
2. Yerushalmey J, Hilleboe HE. Fat in the diet and mortality from heart disease. A methodological note. New York State Journal of Medicine, 1957; 57: 2343-2354.
3. No author listed. Health Revolutionary: The Life and Work of Ancel Keys. Available online: http://www.asph.org/movies/keys.pdf
4. Dunn Gifford, K. Introduction to the 2003 Conference on the Mediterranean Diet, Jan 12-14, 2003, Boston, Massachusetts.
5. Keys, A. Coronary heart disease in seven countries. Circulation, 1970; 41 (Suppl 1): 1-211.
6. No authors listed. Ecological analysis of the association between mortality and major risk factors of cardiovascular disease. The World Health Organization MONICA Project. International Journal of Epidemiology, Jun, 1994; 23 (3): 505-516.
7. Ginter E. Cardiovascular disease prevention in eastern Europe. Nutrition, May, 1998; 14 (5): 452-457.

—

Anthony Colpo is an independent researcher, physical conditioning specialist, and author of The Fat Loss Bible and The Great Cholesterol Con. For more information, visit TheFatLossBible.net or TheGreatCholesterolCon.com

Copyright © Anthony Colpo.

Disclaimer: All content on this web site is provided for information and education purposes only. Individuals wishing to make changes to their dietary, lifestyle, exercise or medication regimens should do so in conjunction with a competent, knowledgeable and empathetic medical professional. Anyone who chooses to apply the information on this web site does so of their own volition and their own risk. The owner and contributors to this site accept no responsibility or liability whatsoever for any harm, real or imagined, from the use or dissemination of information contained on this site. If these conditions are not agreeable to the reader, he/she is advised to leave this site immediately.

“In earlier times, they had no statistics, and so they had to fall back on lies.”
-Original author unknown

—

Hey everyone,

Last time we spoke, I promised my next article would discuss the type of diet that’s been shown in clinical trials to reduce cardiovascular mortality. However, something else has crossed my desk that I need to comment on pronto.

As a result, this article is going to be about a type of eating pattern that, despite all the lavish claims made for it, has never been shown to reduce CVD mortality in clinical trials. In fact this style of eating, despite the reigning propaganda, has never been shown to reduce death from any cause.

I’m talking, dear readers, about vegetarianism.

An EPIC Wank

Late last year a big ballyhoo was made about an analysis of the large EPIC-Oxford epidemiological study in England that compared cardiovascular outcomes in those who called themselves vegetarians with those who did not. As I explained in this article, an earlier analysis of the EPIC-Oxford cohort found no reduction in cardiovascular mortality among vegetarians. It did, however, find that overall mortality was slightly albeit non-statistically significantly higher among this group. For some strange reason, this study attracted very little attention from the media.

Not content with these uninspiring results, the EPIC researchers – two of whom belong to organizations whose express purpose is to promote vegetarianism – decided to conduct another analysis, this time combining both fatal and non-fatal cardiovascular outcomes. Analysing each of these outcomes alone had failed to produce any kind of statistically significant risk reduction, but using the old trick of combining endpoints finally produced a result that could be used to further the vegetarian cause. The researchers promptly drafted another paper completely ignoring the previous unfavourable all-cause mortality results, instead gushing on about the “reduced risk” of combined fatal and non-fatal heart disease. Media outlets all around the world quickly proceeded to insult our intelligence with headlines such as “Vegetarian diets reduce heart disease risk by a third.”

Hmmm, I guess they never received any glowing press releases for the previous EPIC paper showing no reduction in CVD mortality, a higher rate of colorectal cancer, and a slightly higher rate of overall mortality among vegetarians. And I guess no-one ever explained to them that the only reason vegetarians enjoyed any reduction in CVD was their significantly younger mean age, their lower rate of smoking, and higher rates of exercise.

Funny that.

I debunked that study here, and explained why vegetarian diets are more likely to promote rather than prevent cardiovascular disease. Today, I’m going to dismantle another audaciously misleading pro-vegetarian paper.

When Religion Combines with Diet Dogma – Literally

So let’s leave the UK, and travel over to the US where there resides another group of researchers conducting a large-scale epidemiological comparison of vegetarians and omnivores.

The population being studied is comprised of Seventh Day Adventists, a religious denomination that advises its members to follow a vegetarian diet. From all accounts, this admonition is not administered with quite the same vigour as, say, the Jewish and Muslin proscriptions against pork. And so not all Adventists follow a truly vegetarian diet, allowing researchers to follow what would appear to be a relatively homogenous population consuming various levels of animal products.

This page contains “The Seventh-day Adventist Position Statement on Vegetarian Diets”, and states:

“The vegetarian diet recommended by Seventh-day Adventists includes the generous use of whole grain breads, cereals and pastas, a liberal use of fresh vegetables and fruits, a moderate use of legumes, nuts, seeds. It can also include low fat dairy products such as milk, yogurt and cheeses and eggs.   It is best to avoid high saturated fat and cholesterol foods such as: beef, lamb, pork, chicken, fish and seafood.  Coffee, tea and alcoholic beverages provide few nutrients and may interfere with the absorption of essential nutrients.”

It goes on to claim:

“Vegetarians have reduced risks of certain diseases because of their increased consumption of whole grains, dried beans, nuts, fresh and dried fruits, and vegetables.  Vegetarians are exposed to fewer carcinogens and mutagens because they do not eat meat.”

Here’s the truth: There exists no reliable evidence whatsoever that avoidance of meat reduces the incidence of cancer nor any other disease. As for the 7DA proscription against tea and coffee, both are antioxidant-rich beverages that show little evidence of harm when consumed in sensible amounts. Heck, even epidemiologists struggle to find harmful associations between tea, coffee and health and mortality outcomes; quite the opposite, in fact[1].

It’s also most ironic that whoever drafted this position statement criticizes tea and coffee for their alleged nutrient-inhibiting effects when whole-grains contain a plethora of what researchers refer to as anti-nutrients, which have been well documented to inhibit the absorption or production of such critical nutrients as zinc, magnesium, calcium, selenium, and vitamins B6 and D. Unlike tea, which clinical trials indicate is a most health-enhancing beverage, controlled trials have repeatedly shown increased whole-grain consumption to produce negative health outcomes.

Hmmm. A religious organization making claims with no foundation in sound science. Gee, who would’ve thought?

As to why the 7DA religion settled on this eating style in the first instance:

“For more than 130 years Seventh-day Adventists (SDAs) have practiced a vegetarian dietary lifestyle because of their belief in the holistic nature of humankind. Whatever is done in eating or drinking should honor and glorify God and preserve the health of the body, mind and spirit.”

I’ll leave aside the fact that after thousands of years, none of the worshippers of the various “Gods” has been able to provide anything resembling proof for the existence of said Gods. And therefore that eating or drinking with the goal of “honouring” and “glorifying” any of these Gods might not be the most intelligent way to determine one’s eating patterns.

Some people worship Elvis. You might think that’s strange, but at least they can prove he existed LOL

Nope, I won’t bang on about that because, ultimately, people are free to believe whatever they want. If you want to believe in virgin births, resurrections from the dead, or that a bunch of invisible goblins lives under your kitchen table, then good for you. Ditto if you choose to believe avoiding meat somehow affirms the “holistic nature of humankind”, despite the fact that Paleolithic humans – who didn’t just talk the talk but really did live in harmony with nature (like they had a choice) – ate meat on a very regular basis with remarkable evolutionary success for some 2.4 million years.

As anyone who has studied both Paleontology and the history of vegetarianism will know, the latter was quite literally born out of religion. Archaeological evidence, along with observation of surviving hunter-gatherer societies, invariably indicates animal flesh (especially fat-rich animal flesh) was an important and highly valued component of the human diet. It wasn’t until Homo sapiens moved from a nomadic hunter-gatherer existence to a sedentary agrarian lifestyle that they had the time to sit around, gaze at their navel, and dream up concepts such as “non-violent” food acquisition. The first ‘enlightened’ thinkers that came up with this concept were probably written off as a bunch of soft-cocks by their hardy peers, but vegetarian ideologies eventually gained traction, especially when the ruling classes realized the potential advantages to be conferred by forbidding meat consumption in areas where grain cultivation was a much less ecologically expensive method for sustaining rapidly expanding populations.

Those who want to explore this phenomenon further are highly advised to consult the outstanding Cannibals and Kings by Dr Marvin Harris. My goal here is to simply point out that vegetarianism came into being as an ideology among sedentary, agrarian ‘thinkers’. Thousands of years later and little has changed. Vegetarianism is still an ideology with no foundation in anything resembling sound science.

Which would be all fine and dandy if the promoters of vegetarianism stuck to their theoretical ethical musings and made no pretence about the healthfulness of their diet being supported by sound science.

Which in turn brings up a second important point about vegetarianism. It was born from theories about “peaceful” food acquisition and non-violence towards animals which, no matter how admirable their intent, can hardly be considered end-products of the scientific method. Claims for the alleged health benefits of vegetarianism came later. And the science for that came much, much later again.

I’ll repeat: The ideology came first, the science came after.

My long-time readers will be familiar with how this works (think cholesterol hypothesis of heart disease): A theory is constructed based on someone’s interesting but unfounded ideas. The theory holds appeal but the supportive scientific evidence is lacking so researchers go about amassing it after the fact. Instead of testing the hypothesis with ruthless impartiality, the subsequent research is constructed and interpreted in a manner that will support the pre-existing beliefs.

By now you should be starting to see where I’m heading with all this. It’s hardly a secret the Seventh Day Adventist religion has a bias towards vegetarian eating. It makes claims about this style of eating which are of questionable veracity, but when challenged can cite scientific research that supposedly proves its vegetarian exhortations are backed by more than religious commandment.

But guess what?

The same studies examining Adventists and claiming beneficial findings for vegetarian diets are also conducted by Adventists. Specifically, the team of researchers housed in the “Adventist Health Studies” department in the School of Public Health at Loma Linda University.

Loma Linda is home to one of the largest 7DA congregations in the world, and the university is owned by the 7DA church. This university has treated us to a string of papers over the years, many hailing the risk reductions in death and disease that allegedly accompany a vegetarian diet.

Given the longstanding and well documented concerns arising from research conducted by individuals with a vested interest in the results, I’d say a very strong dose of scepticism is warranted when analysing their papers.

Before we take a look at the most recent paper from this team, let’s take a quick look at some of their Greatest Hits from the 70s, 80s, and 90s.

C’mon Baby Lay Your Stats on Me

In 1975, the Loma Linda researchers presented mortality data from over 35,000 Seventh-Day Adventists whom they monitored during the period 1958-1965. Sure enough, this group showed reduced rates of mortality from a number of cancers, but many of these were readily explained by a lower prevalence of smoking and alcohol consumption. Furthermore, the incidence of prostate cancer, which is typically attributed to the consumption of high fat animal foods, was similar between Adventists and non-Adventists.

In addition, recent converts showed a lower risk of breast and colon cancer than life-time Adventists. If animal foods truly contributed to such malignancies then the opposite should have been evident; risk should have declined with increasing length of time as a practicing Adventist.

It has long been recognized that, within populations, individuals from higher socioeconomic backgrounds with higher educational qualifications tend to experience lower rates of various degenerative illnesses than less-educated folks of lower socioeconomic standing. Because Seventh-Day Adventists were generally higher educated than average, the researchers also compared the cancer and all-cause death rates of Adventist and non-Adventist physicians, two groups with very similar educational and career status. They examined the incidence of mortality among over 6,000 medical practitioners who graduated between 1901 and 1971 from Loma Linda University (where over 75% of the graduates were Adventists) and the University of Southern California (where less than 5% of graduates were Adventists).

As expected, the death rate among physicians was lower than the general population, but the “startling” finding was that there was little difference in the rate of cancer or all-cause mortality among the two groups. In fact, the Loma Linda graduates showed a trend towards higher rates of gastro-intestinal and colon cancers, again contradicting prevailing beliefs about the role of animal foods in cancer promotion.

Finally, the researchers examined the relationship between diet and the incidence of colon and breast cancer within the Adventist population itself. Adventists with colon cancer were found to consume more meat, fish and cheese, seemingly supportive of the vegetarian hypothesis. However, colon cancer patients also ate significantly more highly-processed and nutrient-depleted fodder such as ice cream, fried potatoes, fried foods, cakes, and pies. The patients also ingested less green leafy vegetables than cancer-free Adventists. In other words, it was the overall dietary pattern of these patients – one featuring a higher proportion of refined junk – that was associated with colon cancer, not simply the presence of animal foods. Indeed, when the researchers examined the role of each food in isolation, the association between meat, fish and colon cancer disappeared[2].

Consider also a more recent study of over 34,000 Californian Seventh-Day Adventists, published in 1999, which found that vegetarians had lower risks of hypertension, diabetes, arthritis, colon cancer, prostate cancer, fatal CHD in males, and death from all causes. Again, vegetarians displayed a number of healthful dietary habits unrelated to meat intake that were not shared by their omnivorous brethren. Vegetarians consumed more tomatoes, nuts, and fruit, but less donuts than non-vegetarians. Non-vegetarian Seventh-Day Adventists also consumed alcoholic beverages twenty times more frequently than their vegetarian counterparts[3].

As with the earlier study of Adventists published in 1975, these observations clearly showed that those who shunned meat also adopted other dietary measures that protected their health.

Before we discuss more Loma Linda findings, let’s catch another flight, this time over to Norway to check out some research on 7DAs conducted by non-7DA researchers at the University of Tromso.

They studied the mortality pattern of SDAs in the Netherlands during the period 1968-1977. Standardized Mortality Ratios for total mortality, cancer and cardiovascular diseases were significantly lower than for the total Dutch population. Mean age at death as well as life-expectation at baptism were significantly higher in SDAs, both in males and females, compared with Dutch males and females.

To try and find out why, the researchers administered a health survey among a sample of the SDAs population and a group of “friend controls”.

These researchers, who presumably had little incentive to prop up the vegetarian sham, concluded that abstinence from cigarette smoking was likely the main factor explaining the low mortality from ischaemic heart diseases among SDAs, while “presumably an appropriate (prudent) diet confers additional benefit for example on colon cancer mortality”[4].

Notice the emphasis on smoking, and also note how they refer to a “prudent” diet, rather than a vegetarian diet.

In a later study by the same department, little difference in cancer incidence was found between 7DAs and the general population. Total mortality was significantly lower only in 7DA men, especially cardiovascular mortality. They found entering the church at an early age had a large effect on later mortality. They concluded “An early establishment of a healthy lifestyle seems to be of decisive importance in the risk of later disease.”[5]

Notice the emphasis on a “healthy lifestyle”, as opposed to diet.

Ok, now back to California. In their earlier reports, the Loma Linda researchers occasionally dropped their guard and also presented findings supporting the thesis that an overall healthier lifestyle rather than a vegetarian diet was what really explained any lower incidence of disease and mortality.

A 1984 paper, for example, reported lower breast cancer mortality among 7DA women. But, in the researchers own words: “The differences, however, were no longer significant when stage at diagnosis was taken into account. It seems likely that the lower breast cancer death rates reported among Seventh-day Adventist women as compared with the general population result in part from better survival patterns due to earlier diagnosis and treatment.”[6]

Gary E. Fraser, a prominent member of the Loma Linda pro-vegetarian research team, wrote in 1988:

“The lower risk for IHD [ischaemic/coronary heart disease] in Adventist men, at least, is probably related to their dietary habits, nonsmoking status, possibly their better exercise habits, and greater social support.”[7]

That’s a lot closer to the truth than some of his more recent conclusions, but let me re-word the above sentence so that it’s even more in accord with valid science:

“The lower risk for IHD in Adventist men has nothing to do with avoidance of meat, but everything to do with their far lower rates of smoking, greater participation in exercise, maintenance of a lower BMI, and quite possibly the stress-buffering effects of greater social support.”

The following year, Fraser and his colleagues published a paper examining prostate cancer risk among some 14,000 Seventh-day Adventist men who completed a detailed lifestyle questionnaire in 1976 and who were monitored for cancer incidence until the end of 1982. Now, before I relay their findings, remember that meat and animal fats are incessantly blamed for causing prostate cancer.

So what did they find?

–“Increasing educational attainment was associated with significantly decreased risk of prostate cancer in this study.”  Nothing to do with diet, obviously.

–“age at first marriage was also inversely associated with risk, although this was not significant” (and also totally unrelated to diet).

–“A history of prostate “trouble” was associated with a 60% increase in risk which was highly significant.”

–“Although there were suggestive relationships between increasing animal product consumption and increased risk, these results did not persist after accounting for the influence of fruit and vegetable consumption. Nor was exposure to the vegetarian lifestyle during the childhood years associated with alterations in subsequent risk. However, increasing consumption of beans, lentils and peas, tomatoes, raisin, dates, and other dried fruit were all associated with significantly decreased prostate cancer risk.”

That same year they also examined the link between diet and breast cancer. They found:

“Age at first live birth, maternal history of breast cancer, age at menopause, educational attainment, and obesity were all significantly related to risk. However, increasing consumption of high fat animal products was not associated with increased risk of breast cancer in a consistent fashion. Nor were childhood and early teenage dietary habits (vegetarian versus nonvegetarian) related to subsequent, adult risk of developing breast cancer. Also, a derived index of percent of calories from animal fat in the adult years was not significantly related to risk. These results persisted after simultaneously controlling for other, potentially confounding variables, utilizing Cox proportional hazard regression models.”[8]

In other words, in these studies consumption of animal foods and SFA (Saturated Fatty Acids) had SFA to do with the likelihood of getting prostate or breast cancer. It was other health and lifestyle characteristics that explained the difference.

Another paper from 1988 is worth mentioning here. It also found a similar lack of risk from animal foods and breast cancer mortality, but a look at the relative risks is good for a chuckle:

“Odds ratios of 1.00, 1.22, and 1.03 were observed for meat consumption categories of none or occasional, 1-3 days/week, and 4+ days/week, respectively.”[9]

If we’re to take this epidemiological pap seriously, then avoidance of meat, milk, cheese, and eggs confers zero increase in fatal breast cancer risk, rises by 22% in relative terms with consumption 1-3 days/week, but then pretty much returns to zero with consumption 4 or more days/week.

Yeah, that makes sense…

A little later, in 1994, the researchers found no difference in cancer incidence between 7DA and non-7DA, except for endometrial cancer which was significantly higher among 7DA women. Overall cancer mortality was lower in 7DA men, with the exception of prostate cancer, which was significantly higher[10]. If we’re to attribute the lower cancer incidence of 7DA men to diet, then it’s only fair we also ascribe the higher incidence of prostate cancer to their eating habits.

Personally I think all this epidemiology is a load of confounder-prone bollocks, and I’m not prepared to ascribe jack to jack until a little later when we look at the RCT data.

For now, let’s jump forward to the present, and check out the paper the Loma Linda researchers published earlier this year. While it didn’t get quite the same level of coverage as the EPIC paper from last year, this paper was still awarded misleading headlines from unthinking journalists, including these gems:

“Vegetarian diet may reduce risk of early death” – CBS News

“Lower risk of death is associated with vegetarian diets” – Examiner.com

“Are vegetarian diets secret to long life? People who avoid meat have better health due to lower blood pressure” – Daily Mail UK

Holy beefsteak, Batman.

My dear readers, I have a dream…that our children will one day live in a world where the media forbids health and nutrition stories to be written by anyone other than those who have a clue about health and nutrition and also know how to impartially read and pick apart a scientific paper.

Because as it stands, most journalists who write diet and health articles don’t have the first clue about diet and health, nor do they even bother to read the studies they report on. Instead they rely on the hyperbolic press release issued by the research team or the medical journal in question. If they need further information to pad out their article, instead of doing their own research they’ll simply contact the head researcher for a bunch of quotable quotes.

While this journalistic cluelessness makes life a lot easier for purveyors of dietary disinformation, it sucks massively for all those who would like their dietary information to be of the factual, scientifically valid, non-BS variety.

And make no mistake: The claims made for the latest study out of Loma Linda are complete BS.

The Bizzarro World of Statistics: When a Lower Risk of Mortality is a Higher Risk of Mortality.

This most recent 7DA paper, published in the JAMA Internal Medicine on June 3, reported on 73,308 participants from the Adventist Health Study 2 (AHS-2) who, based on their questionnaire responses, were categorized into 5 dietary patterns: nonvegetarian, semi-vegetarian, pescovegetarian, lacto-ovo–vegetarian, and vegan[11].

The researchers claim:

“The adjusted hazard ratio (HR) for all-cause mortality in all vegetarians combined vs nonvegetarians was 0.88…The adjusted HR for all-cause mortality in vegans was 0.85…in lacto-ovo–vegetarians, 0.91…in pesco-vegetarians, 0.81…and in semi-vegetarians, 0.92 compared with nonvegetarians. Significant associations with vegetarian diets were detected for cardiovascular mortality, noncardiovascular noncancer mortality, renal mortality, and endocrine mortality.” (All these findings statistically significant at 95% confidence interval).

You’ll note their repeated use of the word “adjusted”; we’ll explore the significance of this in a moment.

In the meantime, this study has so many flaws it’s hard to know where to start.

I could elaborate on what a joke it is to claim ‘significance’ for a 12% risk reduction from a confounder-prone epidemiological study (in randomized controlled clinical trials, such miniscule RRs are routinely dismissed as too weak to get excited over, and we’re talking studies with far less confounding than the epidemiological slop being served up to us by the Loma Linda team).

I could also elaborate on the sheer stupidity inherent in the term “pescovegetarian”. Let’s get something straight – if you eat fish, you ain’t no vegetarian. If you’re going to stick with this high and mighty moral routine that forbids the killing of living creatures, then plain basic logic dictates you must acknowledge fish are also living creatures that must be killed in order for you to consume them. After all, how can it be in harmony with “the holistic nature of humankind” to avoid killing land-based animals for food, but to go ahead and kill aquatic creatures for the exact same purpose?

I could elaborate on these things and more, but I won’t. Instead I’m going to plunge a cyber-knife right into the guts of this study and expose it outright for the utter fraud it is.

And make no mistake: Any claim this study demonstrates lower mortality among vegans, vegetarians, fish eaters (the so-called “pescovegetarians”) and semi-vegetarians is a patently fraudulent one.

Why?

Because that’s what the researchers’ own data shows. The raw data, that is. The actual, unmolested figures the researchers present before proceeding to “adjust” them in a manner that delivers a result far more palatable to the vegetarian cause.

OK folks, put your thinking caps on, and take a good look at the following:

This is Table 3 from the AHS-2 paper. Without yet reading any of the fine print underneath the table, I want you to take a look at the figures in the column second from the right, the one titled “Death Rate, Deaths/1000 Person-years (95% CI)a“.

You’ll see that the researchers have cited mortality rates ranging from 5.33 to 6.16 deaths/1000 person years for the various vegetarian categories, while the lowly meat eaters return a rate of 6.61 deaths/1000 person years.

Here’s what you need to know about these death rate figures:

They’re complete bullshit.

And you’re now going to prove this to yourself, instead of taking my word for it. Grab your calculators, kids, it’s time for Debunking Epidemiological Hogwash 101.

Everybody got their calcs handy? Good. Let’s get to work.

The first thing we’re going to do is re-calculate the rate of deaths/1000 person years. This is pretty simple: Simply take the number in the “Deaths” column for each dietary category, divide it by the number in the “Time, Person-years” category, then multiply the resultant figure by 1000.

Doing so will give you the following deaths/1000 person years figures:

Non-vegetarian: 5.67
Vegan: 6.00
Pescovegetarian: 6.08
Lacto-ovo vegetarian: 6.53
Semi-vegetarian: 6.74

Now, take a good look at those figures and note who has the lowest death rate.

Yep, the non-vegetarians!

A similar result is returned when you calculate the number of deaths as a percentage of total number of participants in each dietary category (you can eliminate the difference in mean follow-up by multiplying each figure by the percentage 5.72 constitutes of the other longer mean follow-up periods).

No matter which way you work it, the raw data speak for themselves: The lowest death rate in the study is enjoyed by those who eat the most meat.

This, mind you, is despite the fact that the meat eaters clearly lived the unhealthiest lifestyles. They were far more likely to smoke cigarettes than the other categories, exercised less, got less sleep at night, and had higher BMIs. And yet they still exhibited the lowest mortality rate during the mean 5.7 year follow-up period.

That to me sounds like a pretty glowing endorsement of meat consumption, rather than a damning indictment!

The obvious question then, is how on Earth did the researchers arrive at their conclusion that vegetarians had lower mortality, and where on Earth did they derive the death/1000 year figures in Table 3?

Statistics, my friends, statistics.

Be Good to the Numbers and They’ll Be Good to You

Statistics are a lot like people: Rub them the right way, and they’ll often return the favour. Scratch their back, and they’ll scratch yours.

In fact, if you’re a real smooth operator, statistics are kind of like those girls who seem kinda shy at first, but with the right encouragement will proceed to do some shockingly raunchy stuff. Work them the right way, then once they’re sufficiently loosened up you can manipulate them into positions they would never normally go in their non-manipulated state. Darken the room, light some scented candles, play some Crazy P, start rubbing in the exotic oils, and those hot little numbers will promptly shed all their inhibitions, allowing them to freely perform the most unspeakable acts, in the process making all your wildest dreams an ecstatic reality.

Okay, okay, so epidemiologists don’t really use scented candles or essential oils or play Crazy P when they’re trying to bend the data in their preferred direction.

Instead, they use mathematical formulas.

Yep, who needs to waste time arranging velvety smooth sheets or selecting mood-enhancing tunes when you’ve got so many other statistical tools at your fingertips:  Multivariate Analysis, Variance Components Analysis, Linear Mixed Models, Generalized Linear Models, Generalized linear mixed models, Loglinear Analysis, Kaplan-Meier Survival Analysis, Cox Regression Analysis, Time-Dependent Covariates, Regression Analysis, Multiple Regression Analysis, Curve Fitting…the list goes on and on.

And on.

Statisticians: They’d Like to Do it With the Entire Population, But Only Get a Small Sample

Let’s go back to Table 3 of the AHS-2 paper. We saw, before our very eyes, how running the numbers unmistakably returns figures showing lower mortality rates among non-vegetarians. Yet in the same table, the researchers present death rates showing the exact opposite.

So how did the researchers arrive at these numbers? Well, notice that little “a” next to “Death Rate, Deaths/1000 Person-years (95% CI)“? Look at the corresponding footnote underneath the table. It reads: “Adjusted for age, race, and sex by direct standardization.”

Welcome to the wonderful world of statistical manipulation, my friends. The only thing real and indisputable about this study is that the raw data show the lowest rates of mortality among non-vegetarians. Once the researchers take the data and start “adjusting” it, we move from the realm of concrete reality into the land of speculation, assumption, estimation and, all too often, outright bollocks.

So in Table 3, the researchers begin moving us into the latter realm by using a process known as direct standardization.

What, I hear you asking, is direct standardization?

“Direct Standardization (SDR1) calculates a weighted average of the region’s age-specific mortality rates where the weights represent the age-specific sizes of the standard population.”

If that sounds totally foreign to you, that’s the whole point. An essential part of pulling the wool over people’s eyes is using methods they don’t understand. This makes you seem real smart, a process encapsulated by the saying “If you can’t dazzle them with brilliance, baffle them with bullshit!”

Heck, I think I just summed up the entire field of statistics in one single sentence!

Can I go home now?

No? You want me to finish tearing this AHS-2 bollocks apart?

Bugger.

Alright, let’s continue…

To perform direct age standardization, one first has to select a reference population. The death rate in the population you are studying is then compared to the death rate recorded for the reference population. In the 7DA-2 paper, the researchers used the entire 7DA-2 study population itself as the reference.

Next, one computes the age-specific rates within the study group (in this case, each dietary category). Then, one multiplies these rates by the number of people in that age group in the reference population. These expected counts are summed and divided by the total population size of the reference population to yield the directly standardized rate.

Again, that probably sounds a bit foreign to many of you, but here’s the gist of what happened: The mean age of the 7DA-2 non-vegetarian sample was 55.9, in the other groups the mean age was 57.5-58.8. By using age standardization, the non-vegetarian group was penalized for having a mean age 1.6-2.3 years younger than that of the other groups. But would the results really have been much different if every group had, for example, a mean age of 57.58 (the average of the 5 groups)?

As for gender, the non-vegetarian group was middle of the field in terms on percentage of females, and second highest after the ‘pescovegetarians’ in percentage of blacks.

So again, what would the results have been if all groups had not only the same mean age but also the same number of female and black participants?

The only honest answer to that is that we don’t know. However, the researchers go ahead and claim otherwise, ignoring the raw deaths/1000 person-years data, running direct standardization and presenting the results as fact.

If the researchers had presented the raw data, then run the direct standardization calculations, then said something like the following, they would have been on much more honest ground:

“The raw data show that, despite their unhealthier lifestyles, non-vegetarians had the lowest death rates in the study. Adjustment of the data via direct standardization reversed these results, but we must emphasize that direct standardization is purely a paper exercise in speculation. Running a bunch of equations on our computers does not in any way change what actually happened in reality. And the reality is that non-vegetarians had the lowest mortality.

The only way to know if the results of the direct standardization analysis would hold up in real life is if we were able to re-conduct the study with five groups all sporting the same mean age/gender/race characteristics. Or even better, ditching this whole epidemiology wank and conducting a real study – i.e. a randomized controlled clinical trial that takes a large group of people and randomly assigns them to diets similar in every respect except that one contains meat and the other does not.”

But of course, the Loma Linda researchers didn’t say anything like this. Instead, having the direct standardized data they needed, they then proceeded to the next phase of their caper: Cox Regression Analysis.

Stop Fiddling with Cox, it’s Most Unbecoming

So now I hear you all asking: “Anthony, what the hell is Cox Regression Analysis?”

I must say, you’re a wonderful and very engaging audience, asking so many questions like this.

Cox Regression analysis was invented by a bloke called Sir David Cox, believe it or not. Sir Cox “observed that if the proportional hazards assumption holds (or, is assumed to hold) then it is possible to estimate the effect parameter(s) without any consideration of the hazard function.”

Again, that will sound like a load of gobbledegook to many of you, but all you really need to note here are the words “assumption”, “assumed” and “estimate”. Those words pretty much tell us everything we need to know. Or should already know. After all, it’s hardly a secret that humans are in no way omnipotent and cannot predict the future nor wave a wand and magically remove the influence of any and all confounders after the fact.

The best they can do is attempt to estimate the potential effect of confounding variables by using formulas based on assumptions.

In other words, they can guess. The fact that these guesses are based on sophisticated mathematical models still does not change one iota the fact that, ultimately, they are guesses.

Yep, a highly educated guess is still a guess, my friends.

And highly educated people, I might add, often screw up royally (a big hello at this point to every highly decorated researcher who has ever claimed saturated fat and cholesterol cause heart disease).

Anyways, so the Loma Linda researchers got their Cox on…oh wait, that didn’t sound right…um, they got to work with the Cox analyses in order to “adjust” for the effect not just of age/race/gender but also smoking, exercise, income, educational level, marital status, sleep and region.

The Cox analysis, remember, is an estimate of the impact of these various confounders, as is the Multivariate analysis that is also widely used in epidemiological studies.

Quick quiz:

Q: What are the formulas inherent in these analyses based on?

A: The results of other epidemiological studies.

Yep, epidemiology isn’t just your regular run-of-the-mill wank, folks – it’s a Ponzi-style wank!

And this elaborate multi-layered wankology, ladies and gentlemen, is how you take a set of raw actual figures and totally transform them into something they’re not. By the time they’re done, the Loma Linda researchers have managed to return 8-19% reductions from overall mortality in the vegetarian groups. Meanwhile, the hapless meat-eaters suddenly find themselves portrayed as having the highest death rate in the study from just about every listed cause!

Again, this wouldn’t be so outrageous if the researchers took pains to emphasize these reductions were purely speculative estimates arising from mathematical exercises. But they do the exact opposite, concluding:

“…vegetarian dietary patterns were associated with lower mortality. The evidence that vegetarian diets, or similar diets with reduced meat consumption, may be associated with a lower risk of death should be considered carefully by individuals as they make dietary choices and by those offering dietary guidance.”

What the Loma Linda researchers want us to believe is that, despite having the lowest mortality rate in the study, non-vegetarians actually had the highest death rate in the study!

Got that?

And they further believe that people issuing dietary advice to the public should seriously consider basing their recommendations on this fantasy-based nonsense!

Holy cow.

Why Vegetarians Don’t Like Clinical Trials

The Loma Linda team have been publishing papers for almost forty years now, many claiming reductions in mortality, heart disease and cancer to be associated with vegetarianism.

Like most of their epidemiological brethren, these researchers seem utterly unwilling to acknowledge the speculative nature of their work, and totally oblivious to the fact that statistical associations are just that: Statistical associations.

I’ve already said this 1,000 times, and I’ll no doubt say it another 1,000 times, but the first rule of good science is…that…

ASSOCIATION DOES NOT EQUAL CAUSATION!

Breathe Anthony, breathe LOL

So here’s my advice to the folks from Loma Linda University and EPIC-Oxford, along with all those who incessantly cite epidemiological associations as if they constitute solid evidence of the superiority of vegetarian diets:

Quit the statistical chicanery, and take the large amount of tax money you waste on this epidemic of epidemi-hogwash and instead use it to conduct some real studies. That is, randomized controlled clinical trials in which large groups of participants are randomly assigned to one of two diets similar in every respect except that one contains meat and the other doesn’t. Go ahead and throw in a fish-eating diet as well if it makes you feel better, but for crying out loud just don’t call it “pescovegetarian”.

You vegetarian proponents have actually had decades to do this, but with a few small exceptions have shunned the opportunity. Instead, you’re happy to keep supporting your dogma by citing distorted data from confounder-prone epidemiological studies involving health-conscious vegetarians versus health-indifferent omnivores.

Why is that I wonder?

Let’s take a look at those few small exceptions I just mentioned to find out.

Vegetarian Diets on Trial

The EPIC study shows that, despite their healthier lifestyle habits, vegetarians experience a slightly higher mortality rate than their omnivorous peers. And the raw unadulterated data from AHS-2 suggests the exact same thing. Far from providing support for the highly-hyped superiority of vegetarian diets, these results suggest that vegetarian diets are so nutritionally inferior they completely negate the benefits of exercise, non-smoking, good sleep habits and lower BMI and alcohol consumption.

And, lo and behold, the clinical research performed to date supports this very contention.

Despite all the lavish claims made for vegetarianism, there is amazingly little long-term clinical research directly comparing their effects on cardiovascular disease, cancer and overall mortality with omnivorous diets. The randomized clinical trial evidence in this genre pretty much begins and ends with two small studies, one published by Dr Dean Ornish and the other by a group of Oregon researchers.

Ornish’s trial, the Lifestyle Heart Trial, was published back in 1990. This is the same clinical trial that provided the springboard for the well-known low-fat and vegetarian author to launch a lucrative career claiming he could reverse heart disease. This claim is made despite the fact that Ornish’s intervention has completely failed under randomized controlled conditions to save even a single life.

Ornish’s “Lifestyle” program actually involves several interventions aside from the omission of meat. Participants are counselled to exercise, engage in stress reduction activities, and to cut all the refined and heavily processed junk from their diets. All these factors on their own could have a significant and favourable impact on CHD risk, but despite these confounding factors Ornish routinely cites his intervention as proof of the efficacy of meat-free and low-fat diets.

But just how effective is his program, anyway?

After one year of follow-up in the Lifestyle trial the researchers reported 82% of those in the experimental group experienced regression of arterial plaque, compared to only 42% of those in the control group, as determined  by angiography. The experimental group subjects also experienced significantly less chest pain[12]. But these factors could easily be due to exercise and stress reduction.

In 1998, the Journal of the American Medical Association published the five-year follow-up data for the Lifestyle Heart Trial. While the experimental group experienced a significantly reduced overall incidence of cardiac events (a composite classification that included angioplasty, bypass surgery, heart attack, and hospitalization for any cardiac cause), the treatment group actually experienced one more death than the control group (two people in the intervention group died compared to one person in the control group)[13].

Ornish claims that one of the treatment group deaths was in a participant who had stopped following the intervention. Another intervention subject allegedly got a little too enthusiastic whilst exercising, exceeding his prescribed target heart rate with fatal consequences. So it would seem luck just wasn’t on the intervention group’s side during the Lifestyle Heart Trial.

However, a similar scenario unfolded during the trial by Oregon researchers. This trial involved what the authors referred to as the “PrimeTime” program, which incorporated Ornish’s vegetarian “Reversal” diet, exercise, smoking cessation, and daily stress reduction activities (meditation, relaxation, deep breathing, visualization). Twenty eight women with pre-existing CHD were successfully recruited for the study, 16 of whom were randomized to the treatment group. The remaining twelve women in the control group continued to receive usual care from their own doctors.

A 2000 report hails the intervention as a great success, reporting a reduction in hypertensive medication dosage among the PrimeTime participants. The researchers also noted that chest pain frequency decreased in this group throughout the 2-year study, but a look at the data shows chest pain severity increased in both groups, though this did not reach statistical significance in either group. Other peculiarities include not only an increase in severity but also the duration of chest pain in the PrimeTime group at 4 months, despite frequency of chest pain reportedly having been reduced markedly at this point. These discordant results are probably explained by the fact that chest pain frequency, severity and duration were attained via questionnaires administered to the patients, and therefore highly susceptible to the vagaries of subjective recall.

The incidence of actual heart attack and stroke were not reported in the study, but the researchers did report on the most important and objective outcome of all:

Death.

One patient in the intervention group died of a heart attack. Another two PrimeTime subjects had to withdraw from the study due to “discomfort with the program”, but the researchers do not elaborate; whether this referred to adverse health effects or inconvenience arising from the intervention is unknown.

Meanwhile, all the control subjects survived and completed the two-year follow-up[14].

And that, ladies and gentlemen, pretty much constitutes the entire body of randomized controlled clinical evidence comparing cardiovascular and overall mortality outcomes among participants following vegetarian and omnivorous diets. In both trials, the treatment groups had the advantage of being compared to people who were doing little to no exercise and not receiving any specialized dietary advice, not engaging in any structured stress relief strategy, nor participating in regular and dedicated counselling. Despite the highly touted improvements in so-called “risk factors”, both intervention groups experienced higher mortality rates.

Actually, the story doesn’t quite end with these two small trials. There is one more study comparing participants on Ornish’s program, but it wasn’t a randomized trial. The Multicenter Lifestyle Demonstration Project sought to apply the intervention in Ornish’s original trial to a larger group of patients recruited from clinics across the U.S. Practitioners from eight medical centres around the country were trained in all aspects of the Lifestyle program, which they proceeded to administer to patients with coronary artery disease. As noted, the study was not conducted in the manner of a randomized, controlled trial; instead, outcomes in the 194 patients who completed the intervention were compared with 139 patients who did not take part in the Lifestyle program but had recently undergone revascularization procedures.

So did the Lifestyle program finally deliver its claimed lifesaving, heart disease-reversing benefits?

Nope.

After three years, there were no significant differences in cardiac event rates or mortality between patients in the intervention and control groups. The number of cardiac events per patient year of follow-up when comparing the experimental group with the control group was as follows: 0.012 versus 0.012 for myocardial infarction, 0.014 versus 0.006 for stroke, 0.006 versus 0.012 for non-cardiac deaths, and 0.014 versus 0.012 for cardiac deaths (none of the differences were statistically significant)[15].

Again, this is despite the fact that the Lifestyle participants received dedicated counselling, lost weight and improved their exercise tolerance. No corresponding data were given for the control group, but given the absence of the intense counselling afforded to the intervention group, it is unlikely that the former would have experienced such changes – a contention supported by the original Lifestyle trial.

In his 1998 paper reporting on the MCLP results, Ornish writes as if these uninspiring results were a great success. His reasoning is that his program is cheaper than revascularization, yet produced similar coronary event and mortality rates. Because 150 of his 194 patients avoided revascularization (44 still had to be wheeled into the operating theatre during the 3-year study), Ornish’s selling point in the paper is that his program is a cheaper alternative to revascularization.

That all sounds great, but if you’ve read The Great Cholesterol Con you’ll know when revascularization is put to the test in RCTs, it has repeatedly failed to show any mortality advantage and some studies have actually shown a slight disadvantage, when compared to patients receiving standard non-invasive medical care. So, in effect, Ornish’s 1998 paper is boasting that his program is no more effective but at least cheaper than another largely ineffective option.

Remember, Ornish’s program included exercise, and we know that an intelligently prescribed exercise program can do wonders for cardiovascular health, even in those that have already suffered a heart attack. In the March 2004 issue of Circulation, German researchers reported on a study in which 101 male patients with stable coronary artery disease were randomized to either undergo stent angioplasty or to participate in an exercise-training program. For the first two weeks, those in the exercise group trained in the hospital 6 times a day, 10 minutes at a time, on a stationary bicycle at 70% of their symptom-limited heart rate (the symptom-limited heart is the heart rate at which evidence of ischemia becomes apparent during an exercise test; needless to say, this should be ascertained during a professionally supervised session).

After this initial two-week period, the exercising patients took their stationary bikes home with them. They were asked to cycle at the prescribed heart rate for twenty minutes per day, and to participate in one 60-minute group aerobic exercise session each week.

The aim of the study was to see which strategy produced the most favourable effect on clinical outcomes – including heart attack, stroke, hospitalization for worsening angina, surgery or further angioplasty – during a twelve-month follow-up period. Thankfully, none of the patients died, but when the final data was tallied, it was observed that 21 of the 50 patients who underwent PCI had a subsequent coronary event, as compared to only 6 of the 51 exercising patients – a highly significant difference.

The exercisers also experienced far greater improvements in maximal exercise tolerance, and were 32% less likely to experience progression of atherosclerosis. Furthermore, the superior results seen in the exercise group were achieved at half the cost necessitated by the PCI procedure[16].

Vegetarianism: The ‘Healthy’ Way to Die Sooner?

What is apparent from the aforementioned Lifestyle and PrimeTime studies is that, despite their inclusion of proven treatments such as exercise and weight loss and the strong link between stress and coronary disease, Ornish’s vegetarian diet still failed to reduce the incidence of heart attack, stroke or coronary mortality. This would indicate that a meatless diet actually negates the effect of the other positive aspects of his intervention.

To put it another way, vegetarian diets have a number of known nutritional pitfalls and, similar to the epidemiological research, the Ornish and PrimeTime studies indicate these pitfalls are so detrimental they cancel out the benefits that would normally be expected from exercise, weight loss, elimination of junk food, and stress reduction.

Stay tuned for Part 2, where we’ll discuss these pitfalls in all their gory detail.

Disclosure Statement: The author of this article has absolutely no relationship, financial or otherwise, with the meat, dairy, or egg industries. The author, according to the bizarre Loma Linda University system of dietary classification, is a “carno-pesco-lacto-ovo-vegetarian”, which means he enjoys a bloody good steak on a very regular basis.

References

1. Gardener H, et al. Coffee and Tea Consumption Are Inversely Associated with Mortality in a Multiethnic Urban Population. Journal of Nutrition, 2013 jn.112.173807; first published online Jun 19, 2013.
2. Phillips RL. Role of lifestyle and dietary habits in risk of cancer among Seventh-Day Adventists. Cancer Research, Nov, 1975; 35: 3513-3522.
3. Fraser GE. Associations between diet and cancer, ischemic heart disease, and all-cause mortality in non-Hispanic white California Seventh-day Adventists. American Journal of Clinical Nutrition, Sep, 1999; 70 (3): 532S-538S.
4. Berkel J, de Waard F. Mortality pattern and life expectancy of Seventh-Day Adventists in the Netherlands. International Journal of Epidemiology, Dec, 1983; 12 (4): 455-459.
5. Fønnebø V. The healthy Seventh-Day Adventist lifestyle: what is the Norwegian experience? American Journal of Clinical Nutrition, May, 1994; 59 (5 Suppl): 1124S-1129S.
6. Zollinger TW, et al. Breast cancer survival rates among Seventh-day Adventists and non-Seventh-day Adventists. American Journal of Epidemiology, Apr, 1984; 119 (4): 503-509.
7. Fraser GE. Determinants of ischemic heart disease in Seventh-day Adventists: a review. American Journal of Clinical Nutrition, Sep, 1988; 48 (3 Suppl): 833-836.
8. Mills PK, et al. Dietary habits and breast cancer incidence among Seventh-day Adventists. Cancer, Aug 1, 1989; 64 (3): 582-590.
9. Mills PK, et al. Animal product consumption and subsequent fatal breast cancer risk among Seventh-day Adventists. American Journal of Epidemiology, 1988 Mar; 127 (3): 440-453.
10. Mills PK, et al. Cancer incidence among California Seventh-day Adventists, 1976-1982. American Journal of Clinical Nutrition, 1994: 59 (suppl): 1136S-1142S.
11. Orlich MJ, et al. Vegetarian Dietary Patterns and Mortality in Adventist Health Study 2. JAMA Internal Medicine. Published online Jun 3, 2013. doi:10.1001/jamainternmed.2013.6473
12. Ornish D, et al. Can lifestyle changes reverse coronary heart disease? The Lifestyle Heart Trial. Lancet, Jul 21, 1990; 336 (8708): 129-133.
13. Ornish D, et al. Intensive Lifestyle Changes For Reversal of Coronary Heart Disease. Journal of the American Medical Association, Dec 16, 1998; 280 (23): 2001-2007.
14. Toobert DJ, et al. Physiologic and related behavioral outcomes from the women’s lifestyle heart trial. Annals of of Behavioral Medicine, 2000; 22 (1):  1-9.
15. Ornish D, et al. Avoiding Revascularization with Lifestyle Changes: The Multicenter Lifestyle Demonstration Project. American Journal of Cardiology, Nov 26, 1998; 82 (10B): 72T-76T.
16. Hambrecht R, et al. Percutaneous Coronary Angioplasty Compared With Exercise Training in Patients With Stable Coronary Artery Disease: A Randomized Trial. Circulation, Mar, 2004; 109: 1371-1378.

—

Anthony Colpo is an independent researcher, physical conditioning specialist, and author of The Fat Loss Bible and The Great Cholesterol Con. For more information, visit TheFatLossBible.net or TheGreatCholesterolCon.com

Copyright © Anthony Colpo.

Disclaimer: All content on this web site is provided for information and education purposes only. Individuals wishing to make changes to their dietary, lifestyle, exercise or medication regimens should do so in conjunction with a competent, knowledgeable and empathetic medical professional. Anyone who chooses to apply the information on this web site does so of their own volition and their own risk. The owner and contributors to this site accept no responsibility or liability whatsoever for any harm, real or imagined, from the use or dissemination of information contained on this site. If these conditions are not agreeable to the reader, he/she is advised to leave this site immediately.

“I don’t mean to insult you, but most journalists are idiots.”
-AIDS activist Luke Sissyfag to journalist Paul Sheehan, 1996.

—

LUKE Sissyfag was born Luke Montgomery, in 1974. A precocious lad, at 17 he changed his name by deed poll, and it didn’t take long for his new moniker to start making headlines. By the ripe old age of 21 he had heckled Bill Clinton six times, disrupted speeches by the Secretary of Health, appeared on The Phil Donahue Show, conducted hundreds of interviews around the USA, and even run for Mayor of Washington in 1994 on the platform, “AIDS is the issue”.

Sissyfag was the lipstick-wearing heckler who shouted down President Bill “Slick Willie” Clinton on World AIDS Day, 1993, and was subsequently dragged away by secret service agents.

Many of you, at this point, are no doubt wondering why I’m discussing the antics of a militant AIDS activist in an article whose title also mentions a couple of prominent low-carb dogmatists. If that’s you, hang about, because the story of Luke Sissyfag is massively relevant to the point I will be making today.

Journalists, and Why Bullshitters Love ‘Em

Luke Montgomery has undergone quite the transformation since his angry heyday of the early 90s. He subsequently dropped the Sissyfag surname and in, a dramatic turnaround, became a vocal critic of what he saw as the childish self-indulgence and blatant dishonesty displayed by many in the gay activist movement.

That dishonesty included, but was not limited to, the deliberate dissemination of false claims about the susceptibility of heterosexual women to AIDS, and the prevalence of homosexuality among males.

When journalist Paul Sheehan asked Montgomery in 1996, “You admit you were cooking the statistics?”, the latter stated outright:

“Absolutely! … We used to skew statistics on a regular basis. We could make one statistic say the opposite of what it really meant, and it’s very simple to do. For example, claiming that AIDS is growing most rapidly among young heterosexual women … It was just scaremongering. Media manipulation.”

And the unlikely yet oft-repeated claim that 10% of men are gay? As Sheehan noted in his 1996 article, “The latest General Social Survey conducted by the University of Chicago found last year that 2 per cent of the men surveyed had engaged in homosexual sex and 1 per cent considered themselves to be exclusively homosexual. These figures align with other recent studies: in the US in 1992 (2.4 per cent), France in 1992 (1.4 per cent), Britain in 1991 (1.4 per cent) and Canada in 1990 (1 per cent). Even the Kinsey Institute, which started the 10 per cent myth 40 years ago with studies now completely discredited, found in a more recent study that only 1.4 per cent of its interview subjects defined themselves as homosexual.”

So how, exactly, did Montgomery and his former activist colleagues succeed in having patently false statistics reprinted in newspapers all around the world?

“One thing I learned quickly was that if you could write a really good press release, you could write the story,” Montgomery told Sheehan. “I don’t mean to insult you but from my experience most journalists are idiots.”

I can’t say I disagree with him. I never ceased to be amazed at the utter garbage that routinely appears in newspapers and current affairs shows. Whether it’s hunger for ratings, a woeful lack of intelligence and critical thinking skills, or perhaps a combination of these and other factors, journalists are amazingly adept at presenting us with sensationalist bullshit that we are supposed to accept at face value. And the terribly sad reality is that, most of the time, they succeed in this very goal.

The ABCs of Anti-Carb Bollocks

For the edification of readers outside Australia, the ABC (Australian Broadcasting Commission), also known Down Under as “Channel 2”, is a government-owned, taxpayer-funded TV station that first went to air in 1932. Being a “non-commercial” station, it is free of advertisements and has long served as an alternative to the remaining handful of “free-to-air” commercial stations that feature both heavy advertising and a large proportion of American programming.

I used to like the ABC because, in between the lame British comedies, they would often air some great documentaries, the candid and revealing kind you would rarely see on the commercial networks. Unfortunately, the quality of ABC content seems to have taken a noticeable dive in recent times; maybe it’s just me, or maybe it’s a result of increasing pressure for the ABC to become more “business-like”.

The ABC is also well known for its current affairs and investigative reporting-type shows. One of these is Catalyst, which the ABC bills as “Australia’s premier science investigation series … an exciting half hour of Australian and international stories”.

I’m not a regular watcher of Catalyst, but occasionally catch an episode when I go over to my Mum’s place for dinner. And so there I was, sitting on Mum’s comfy Chesterfield, enjoying the ecstatic post-meal bliss that IMC (Italian Mum Cooking) is well known to induce. The TV was tuned to Channel 2 when all of a sudden my ears pricked up – from above the conversation, I heard the words “toxic sugar” emanating from the idiot box. I focused my attention on the screen and was treated to Catalyst’s preliminary blurb for the first of the two stories that appeared on the show that evening.

I knew the segment’s scientific credibility was in trouble when none other than Gary Taubes’ tired, greying mug appeared on the screen; when this was followed by footage of the rabid Robert Lustig, I suspected I was in for, not “an exciting half hour”, but some 15 minutes of excruciating bullshit.

My suspicions were confirmed, and then some.

Yep, last Thursday (8 August, 2013), “Australia’s premier science investigation series” presented its viewers with a segment titled “Toxic Sugar?”  that featured a litany of idiotic claims about exercise, carbohydrates, insulin, and fat loss.

Rather than post an exhaustive, extensively-referenced critique of each and every piece of hogwash spouted on Catalyst that night, I figured it would be much more instructive to share with readers an email I sent a few days after the show to Maryanne Demasi, the journalist responsible for the “Toxic Sugar?” segment. Her subsequent reply is also shown below (those with a high bullshit pain threshold can also view the actual episode here).

This, by the way, is not the first contact I’ve had with Demasi – more on that later.

—

Anthony Colpo to Maryanne Demasi, Aug 11, 2013.

Re: Catalyst ‘Sugar’ segment

Dear Maryanne,

just writing to say how disappointed I was with your “Toxic Sugar?“ segment that aired on Catalyst the other night.

Let me preface by stating I wholeheartedly agree excess sugar consumption can lead to a wide array of adverse health consequences. Your segment had the potential to make a worthwhile statement on the matter, but instead quickly degenerated into an alarmist, pseudoscientific farce.

This was in large part due to the two so-called ‘experts’ who featured most prominently in the segment: Author/journalist Gary Taubes and pediatrician Robert Lustig, both of whom made claims that were utterly false.

The few brief highlights of the segment, such as your mention of the commercially-driven dubiousness of the National Heart Foundation’s “Heart Tick” program, were totally overridden by the shrill and untenable claims made by the aforementioned commentators.

I was especially dismayed to see Taubes repeat his repeatedly disproved claim that exercise does not assist fat loss, and your complete lack of critical scrutiny of this patently absurd statement.

This claim doesn’t even begin to pass the commonsense test, but I do realize commonsense is in very scarce supply these days. So let’s look at what science has to say on the matter:

–As physical activity levels/calories burned from physical activity increase, body mass index decreases in both adults and adolescents (see, for example, Table 1 of Weinstein 2004, also Sulemana 2006).

This finding should readily fall into the category of NSS (No Shit Sherlock!) … that I even need to mention it is a sad, sad reflection on the modern state of journalism.

But let’s continue.

Taubes claims the reason why exercise fails to produce weight loss is because it simply makes you hungrier.

In people who exercise vigorously, this is often true. But what Taubes conveniently neglects to mention is that any increase in hunger brought about by exercise is in response to the increased caloric expenditure of exercise and that any subsequent increase in caloric intake is typically overridden by the increased calorie burn from exercise.

Unlike Taubes, who carefully cherry-picks the studies that support his science-fiction and ignores those that do not, C. Alan Titchenal conducted an extensive review of the research on this very subject (see attached) and found:

“Energy intake in humans is generally increased or unchanged in response to exercise. When energy intake increases in response to exercise it is usually below energy expenditure, resulting in negative energy balance and loss of bodyweight and fat. Thus, if energy intake is expressed relative to energy expenditure, appetite is usually reduced by exercise.

Highly trained athletes and lean individuals usually increase energy intake in response to increased levels of exercise, whereas untrained or obese individuals often do not change energy intake in response to increased physical activity…”[Titchenal 1988]

More recently, Elder and Roberts undertook a similar review of the literature and came to similar conclusions:

“The results show consistent effects of exercise on body fatness in the absence of prescribed dietary change, with a progressive loss of body fat associated with higher exercise energy expenditures in both men and women. In part, these effects appear to be mediated by a spontaneous reduction in hunger associated with participation in exercise.”[Elder & Roberts 2007]

Which I guess is why you don’t see any obese blokes competing in the Tour de France, as pro cyclists have pretty enormous calorie expenditures. Taubes has claimed elsewhere – in all seriousness – that this is because pro athletes like Lance Armstrong were simply born lean. Well, Taubes’ ludicrous theory didn’t hold up when the greatest road cyclist of all time, Eddy Merckx, retired from racing. Renowned for his voracious appetite, Merckx failed to match his caloric intake to the sudden and drastic drop in post-retirement caloric expenditure, and promptly became overweight as a result. I’ve written about this here:

http://anthonycolpo.com/eddy-mercx-dr-michael-eades-and-the-inescapable-reality-of-calories-in-fat-loss/

So epidemiological, empirical and clinical trial evidence shows Taubes’ claim to be nonsense. Which of course doesn’t deter him one bit from repeating it every chance he gets. How sad you provided him with yet another platform for again misinforming people and discouraging them from such a highly beneficial activity.

Now let’s turn our attention to Dr Lustig. Like Taubes, he is hopelessly devoted to the nonsensical belief that carbohydrates, via their effect on insulin, increase body fat gain. Most disappointingly, you repeated this mantra in sing-song fashion, evidently unaware that this too has been repeatedly and decisively debunked.

If insulin makes us fat, could you please explain the following anomalies:

–Why differences in insulin resistance and blood sugar control are not a reliable predictor of weight loss in response to calorie restricted diets in obese women?[McLaughlin 1999][de Luis DA 2006].

–Why, given the astronomical financial rewards awaiting innovators of effective fat loss drugs, Big Pharma – world famous for its relentless and often unethical pursuit of profits – is hardly tripping over itself to bring insulin-lowering obesity drugs to market? Or why it is not promoting/seeking approval for the use of already available insulin-reducing drugs for this purpose?

–Why overweight and obese subjects placed on a calorie-restricted diet and randomly assigned to the insulin-lowering drug diazoxide did indeed develop lower insulin levels than those on placebo, but experienced no difference in weight loss, fat loss, resting energy expenditure or appetite?[Due 2007]. (I guess the answer to that will also give you the answer to the previous question…)

–As for carbohydrates themselves, you claimed “starch” was fattening. If so, then why do the white rice-devouring Japanese enjoy lower rates of obesity than most Western countries – including obesity chart-toppers like Australia and the United States of Supersize Me – despite consuming a higher percentage of their calories as carbohydrate?

–If low-carb diets are so superior for weight loss, why do all the RCTs lasting 12 months (long enough for the short-term satiety and novelty factors to wear off) or more show no difference in weight loss or compliance rates as compared to low-fat, high-carb diets?

–Could you also explain why, if dietary carbohydrate is so inherently fattening, why metabolic ward studies (the only kind in which isocaloric intakes can be assured) have repeatedly failed to show any greater non-fluid weight or fat loss than isocaloric diets high in carbohydrate?

One of these ward studies did find a low-carb diet led to greater visceral fat loss in type II diabetics [Myashita 2004], but overall fat or weight loss was not different from the high-carb group. I could go on about how iron reduction, low-GI nutrition, and exercise are all alternatives (far superior ones, in my opinion) for improving glycemic control in diabetics, but that’s a discussion for another time. The point here is that ward trial after ward trial has shown the claims made on your show about carbs, insulin and fat gain to be totally false. I won’t bother listing the two dozen+ references for these ward studies here because, being the most important evidence of all in any debate about the alleged fattening effects of carbs, you already examined them all prior to airing your segment…right?

These ward studies, by the way, stretch as far back as 1935 and have repeatedly failed to find the so-called “metabolic advantage” espoused by Taubes, Lustig et al. But these individuals, hopelessly wedded to their low-carb dogma, are still stuck in the Atkins Dark Age, which most of humanity discarded circa 2004 AD.

Your Catalyst segment, it seems, would have us go right back to this hyperbolic era, believing that the key to losing body fat is not exercise and/or caloric restriction (both of which have been repeatedly shown in controlled research and real life to actually work), but to instead embrace the already failed approach of ignoring calories and instead focusing on carbohydrates.

In other words, let’s replace pseudoscientific anti-fat idiocy with pseudoscientific anti-carbohydrate idiocy.

No thanks.

What’s really sad about this is that your personal blurb on the ABC site claims that you are a “medical research scientist”, have a PhD, and have “been awarded National Press Club of Australia prizes in 2008 & 2009 for…Excellence in Health Journalism”.

All these sterling credentials, yet when some joker came on your show making the patently stupid and blanket claim that exercise does not assist fat loss, you didn’t even begin to question his statement?

When some pediatrician who would have us all believe fructose is the new thalidomide claimed that carbs, not calories, were the cause of obesity, did you make any attempt at all to consult the vast amount of literature showing this claim to be false?

Why are you journalists so uncritically accepting of such easily-disproved rot?

I’d love to hear your answers to all these questions, but please consider when replying that I may and probably will reprint your reply on my website. Media propagation of dietary and health pseudoscience is not only a perennial source of interest/dismay/bemusement for myself, but also many of my readers.

Kind regards,

Anthony.

PS. The following is also a worthy read re Robert Lustig:

http://www.alanaragonblog.com/2010/01/29/the-bitter-truth-about-fructose-alarmism/

Maryanne Demasi to Anthony Colpo, Aug 11, 2013.                       

Hi Anthony,

Yes, I’ll try and answer this email as soon as I can’t but I it may take a couple of weeks.  I’m working to a tight deadline doing a 1 hour on cholesterol and heart disease….its the story we talked about a couple of years ago after reading your book.  In fact, you may be helpful in assisting with factual accuracy with this story…are you happy for me to run through it with you in a couple of weeks when the script is written?

Maryanne

Anthony Colpo to Maryanne Demasi, Aug 11, 2013.

Hi Maryanne,

unfortunately I won’t be able to assist in the fact-checking of your cholesterol story…but I’d still be interested to learn why you allowed such nonsensical statements by Taubes and Lustig to air on your “Toxic Sugar?” segment.

Kind regards,

Anthony.

Maryanne Demasi to Anthony Colpo, Aug 11, 2013.                       

Ok, I’ll get to it as soon as I have free time.

Cheers

M

—

So there you have it. Whether Demasi follows through on her promise to answer the questions I posed remains to be seen, although I must say I’m rather sceptical. I couldn’t sum up her reply any better than a good friend who, upon viewing Demasi’s email, remarked:

“Wow. So her response is ‘I don’t have time right now to admit that I effed up and did no research.  Can you help me do additional work that I will take credit for?’”

Regarding Demasi’s rather audacious request that I help her with a segment on cholesterol that “we” spoke about while simultaneously deflecting my questions…the last time “we” spoke was 3 years ago, back in September 2010. Demasi had contacted me after learning about me online, and was apparently interested in doing a segment that questioned whether cholesterol really caused heart disease. Given the sad lack of attention awarded to this issue in the mainstream media, I was initially more than happy to help. But in the course of our subsequent communication, both by email and phone, Demasi’s focus seemed to shift from diet, cholesterol and heart disease to the potential relationship between statins and cancer, and then back again. I quickly started to get the impression she really didn’t know what angle to approach the issue from.

At the same time Demasi was communicating with me, she was also emailing a representative of Australia’s National Heart Foundation, who not surprisingly held polar opposite views to mine about cholesterol and CHD. Demasi would email this person’s answers to me and expect me to provide point-by-point rebuttals. The first time this happened, that’s exactly what I did. I cited studies that refuted this person’s claims and explained their results, in addition to sending Demasi a free electronic copy of The Great Cholesterol Con, and a number of other PDFs that included my published paper on LDL cholesterol.

When Demasi sent me another email with a long-winded reply from the National Heart Foundation that she again wanted me to address, I decided enough was enough. While the NHF representative was no doubt drawing a nice salary for his PR duties, I was answering Demasi’s incessant queries on my own time and starting to wonder exactly what the point of the whole exchange was. I ignored her last email; she subsequently phoned and I explained to her that she needed to work out a solid angle before proceeding with her story. I explained that pursuing the statins-cancer angle was not a good idea, because the link was quite weak. I explained that while the early animal toxicology studies and bits and pieces of subsequent human evidence had suggested a link, the drug companies would be able to flood her with a bunch of published papers purporting to show no relationship between statins and cancer incidence.

I explained there were far better angles from which to approach a cholesterol-heart disease story from. I told her she needed to make sure whatever angle she chose was one she could back up with plenty of supportive evidence, because those with a vested interest in the cholesterol paradigm would be sure to throw a hissy fit and unleash their PR monkeys in response (and I wasn’t joking: When Channel 7’s Today Tonight did a story on statins and transient memory loss – a real and documented side effect of statins – a few years earlier, Pfizer promptly responded by placing full page ads in every major Australian newspaper reminding the public what a wonderfully upstanding and humanitarian outfit they were. Pfizer also sent a letter to every doctor in Australia reassuring them that statins were wonderfully safe drugs and solemnly advising them to ignore the concerns raised by the naughty folks at Today Tonight).

And, until last Sunday, that was the last I heard from Demasi.

Needless to say, I feel little incentive to help someone who has already impinged upon my time and whose most recent TV outing demonstrates a sad lack of critical analysis, research skills, and plain commonsense. To be fair to Demasi, she’s hardly alone on this score. Poor research and the uncritical relaying of nonsensical claims made by so-called ‘experts’ are not rarities but par for the course among journalists. With the exception of a single genuine and tenacious reporter from Today Tonight, my dealings with this profession have pretty much led me to the same conclusion as that asserted by Luke Montgomery.

It’s truly regrettable that so many individuals with so little ability and/or desire to separate fact from hogwash are endowed with the ability to influence the perception of thousands, and often millions, of others.

“Oh, they could look lean and healthy if they wanted to, but they just prefer the soft, flabby, tired look!” One question I forgot to ask Demasi was why, if they know so much about fat loss, are Taubes and Lustig in such appalling shape? These individuals openly ridicule both the “calories in/calories out” paradigm of weight loss and those of us who sensibly acknowledge it, so why are they the ones sporting such prodigious waistlines?

What does Italian hottie Cristina Buccino have to do with dodgey reporting and anti-carb propaganda? Nothing really, my eyes simply craved for some visual relief after those photos of Taubes and Lustig! Italian women, by the way, recently checked in as the second slimmest female population in all of Europe. Let’s hear it for pasta, pizza, risotto, and pane bianco (white bread)!

—

Anthony Colpo is an independent researcher, physical conditioning specialist, and author of The Fat Loss Bible and The Great Cholesterol Con. For more information, visit TheFatLossBible.net or TheGreatCholesterolCon.com

Copyright © Anthony Colpo.

Disclaimer: All content on this web site is provided for information and education purposes only. Individuals wishing to make changes to their dietary, lifestyle, exercise or medication regimens should do so in conjunction with a competent, knowledgeable and empathetic medical professional. Anyone who chooses to apply the information on this web site does so of their own volition and their own risk. The owner and contributors to this site accept no responsibility or liability whatsoever for any harm, real or imagined, from the use or dissemination of information contained on this site. If these conditions are not agreeable to the reader, he/she is advised to leave this site immediately.

You’ve heard it time and time again:

“Whole grains are healthier than refined grains because they contain more fibre, more nutrients, and don’t spike your blood sugar like refined grains do!”

This statement, like so many other pieces of mainstream nutritional wisdom, is nonsense. There is nothing “healthy” about whole-grains; in fact, an impartial, side-by-side comparison based on actual scientific evidence clearly shows refined grains to be the superior choice.

You know, there are compelling reasons as to why even pre-industrial populations went to the trouble of milling their grains…

Fully aware of my very low tolerance for dietary hogwash, the folks over at 180 Degrees Health recently called my name, threw me a nice juicy piece of whole-grain propaganda, then stood back just to see what would happen. Rascals.

The result was my most extensive dissection to date of the untenable fairy tale that constitutes the whole-grain myth.

Discover the absurd epidemiological foundation the whole-grain thesis was built on, the researcher with a rather odd fascination for faeces that pioneered this thesis, and how it continues to be promoted despite being repeatedly rebuked in controlled clinical trials.

You can read Part 1 here:

http://180degreehealth.com/2013/08/healthy-grains

—

Anthony Colpo is an independent researcher, physical conditioning specialist, and author of The Fat Loss Bible and The Great Cholesterol Con. For more information, visit TheFatLossBible.net or TheGreatCholesterolCon.com

Copyright © Anthony Colpo.

Disclaimer: All content on this web site is provided for information and education purposes only. Individuals wishing to make changes to their dietary, lifestyle, exercise or medication regimens should do so in conjunction with a competent, knowledgeable and empathetic medical professional. Anyone who chooses to apply the information on this web site does so of their own volition and their own risk. The owner and contributors to this site accept no responsibility or liability whatsoever for any harm, real or imagined, from the use or dissemination of information contained on this site. If these conditions are not agreeable to the reader, he/she is advised to leave this site immediately.

Note: This post features the occasional use of language you wouldn’t normally include in a Mother’s Day card. If you are easily offended, please close this page now.

If scientists ever decided to rename the human species, I’d have several choice recommendations for them. Near the top of the list would be Homo superficialis, a moniker that pays tribute to the long-standing human obsession with superficial bullshit.

Humans, in large part, don’t like thinking. While it doesn’t require any actual muscular exertion, thinking nevertheless does require effort.

Now, before I go on, I’d like to share an email that Richard Nikoley over at FreeTheAnimal.com recently received from one of his readers (Rich, as some of you may be aware, was not exactly a big fan of mine several years ago, but has since changed his opinion):

“KL” writes to Richard:

Hey Richard,

I’m new to your blog, and have been reading with much appreciation, as I got there by researching the now very old Eades vs. Colpo mess.  I’m confused.  At the end of this blog entry:  http://freetheanimal.com/2010/03/isnt-it-time-for-anthony-colpo-to-get-a-life.html, you state “3/3/2012: Things have changed substantially. All explained in this post by Anthony Colpo.”  I read that post, and it seems to me that nothing has changed at all – Colpo seems to keep singing the same old tune.  Maybe it was dripping sarcasm that flew over my head, like your earlier statement: “In case you don’t know, Colpo has run a most ridiculous campaign against Dr. Michael Eades, begun way back in 2008 or before. You can see all the posts at his state-of-the-art website.”  – His website, to me, looks like it was designed by a rank amateur, probably AC himself – so I took that statement to be dark humor.  In Eades’ blog comments, I see readers who noticed that AC’s website was down for awhile and came back redesigned.  If I’m now looking at the “improved” redesign, I cringe when I imagine the horribleness of what existed before.  In any case, if it wasn’t sarcasm, and things on 3/3/12 really have changed substantially, could you please enlighten me as to what you meant?

Thanks,

Kyle

Richard’s reply to “KL”:

Hi [KL],

In a word, honesty. While I’ve met Dr Eades and Marry Dan, been their guests and sat with them and luv ‘em to death, and believe they truly want what’s best for people, I conclude that Anthony Colpo has better info and believe its better for this whole paleo/LC deal people are going through.

Almost nobody really digs into the science. Anthony does, and he finds that not only does it matter how much you eat, it matters a little how much you move, though I personally don’t think exercise outside of an active life matters for general health.

I swallowed my bullshit pride and emailed Anthony a long time back. He even blogged about it. I have not seen anything from him since that would make me regret that.

Richard

My reply to Rich when he forwarded KL’s email:

Hey Richard,

thanks for the kind words in my defense. What’s scary about this guy’s email is that he seems far more concerned with the visual appearance of my website rather than the scientific veracity of what I’m actually saying. Given that my website deals with the science of nutrition/training/health issues, and not the world of graphic design, the site’s appearance is a big fat non-issue.

Having said that, since changing the website graphics I’ve received nothing but compliments, and my daily hit rate rose markedly in the subsequent months, so maybe this poor fellow needs to get his glasses checked lol [Anthony's postscript: Before anyone writes to piss and moan about their difficulties reading sites with dark backgrounds, please click the green print icon at the beginning of this or any other article on my site...problem solved]

You may want to forward to this reader the following video of Russell Brand taking a bunch of air-headed MSNBC hosts to task for their preoccupation with superficial nonsense, and ask him if he can see the parallels between their behaviour and his own email

Cheers,

Anthony.

Russell Brand mocking some vacuous MSNBC show hosts for their preoccupation with banal nonsense. Also note the male anchor’s thinly-veiled and unprovoked condescension towards Brand (insecure men often do this in the presence of other males they subconsciously perceive as a sexual/competitive threat).

KL has a problem. A big problem:

He can’t think for himself to save his life.

When attempting to make sense of what he calls the “Eades vs. Colpo mess”, did he consult the research cited by the the girdle-wearing one and yours truly, and analyze it for himself to see who was most accurately representing scientific reality?

Hell no. That would require, you know, thinking and shit.

Instead, he used my website graphics as his foundation for assessing my worthiness as a diet and health commentator!

Not surprisingly, that didn’t get him very far. But even then, he still didn’t turn to the science. Instead, he did what all clueless sheep do:

He asked someone else for their opinion.

Thankfully, in this instance that someone was Richard, although whether Rich’s answer was what KL was hoping for is doubtful. I get the distinct impression KL was hoping Rich would reply with some kind of Colpo hate-fest.

Good on ya, KL.

You’re Joshing Me, Right!?

As my regular readers know, I don’t post in forums, I don’t have a comments section on my website, and I don’t leave comments on other people’s blogs. The reason is because, well, I have a life.

However, I recently made a rare exception on Evelyn “Carbsane” Kocur’s blog. I like Evelyn and think she’s done a great job of debunking the pseudoscientific drivel of Gary “Exercise is Useless for Fat Loss!” Taubes. And so when Evelyn recently tagged me on Facebook for a post about a certain crusty old low-carb guru and his newfound South African admirer, I moseyed on over to her site to check it out:

http://carbsanity.blogspot.ca/2013/08/calories-starvation-and-bygone-gurus.html

In the course of reading Evelyn’s article, I was surprised to see a reprinted comment, apparently left by one Professor Richard Feinman at Eades’ blog some time ago, in which he claimed he sent yours truly a “challenge” to define a “nutritional calorie”, and that my lack of response suggested to him that I’d undergone “spontaneous combustion”.

The only thing lamer than Dick Feinman’s challenge is the fact he never issued it. At least not to me. Feinman, it would appear, suffers from Harley Johnstone Syndrome, a debilitating mental condition in which the sufferer experiences delusions of grandeur, which in turn leads him to publicly wank on about ‘challenges’ that occurred only within the masturbatory confines of his own mind.

And so, in the interests of historical accuracy, I found myself clicking the comment button and explaining what really happened. Namely, the only email I ever received from the reality-challenged Feinman was a totally unsolicited one circa late 2005, right when the low-carb camp was getting its panties in a right royal twist over my comments about calories being the ultimate arbiter of weight loss. In this email, Feinman boasted about his 30 years of experience in teaching thermodynamics, and that he was willing to “teach” me some of this stunning wisdom. This, mind you, from a cherry-picking low-carb shill who – like Taubes and Eades – carefully selects the small handful of studies that can be distorted to support his argument, while blatantly ignoring the dozens of tightly controlled metabolic ward studies that show his claims to be utter garbage.

As I recounted on Evelyn’s blog, upon receipt of Feinman’s email I did what I usually do when confronted by the self-aggrandizing hogwash of a braggart who thinks he knows so much but in fact knows so little: I shook my head, marveled at his audacious self-conceit, then promptly went back to eBay to score some more Ramones memorabilia.

The Ramones: Innovative, pioneering, talented, energetic, entertaining, uncompromisingly sincere about their art, and just plain friggin’ awesome. Oh, and – despite consuming pizza before every show – slim. Everything that low-carb gurus aren’t.

End of story. Or so I thought.

Some joker called “Josh” then chimed in to the conversation, not to ask me about diet, nor fat loss, nor training…but why I called my website a “website” instead of a “blog”. I couldn’t help but wonder why this would even matter to anyone, but nevertheless I politely replied to Josh that my website functioned as a static site and not a blog, and therefore I referred to it as such. I even quoted from the Wikipedia definition of a blog, which says one of the defining characteristics of a “blog” is its interactivity, which includes social networking and a comments section. Yes, I have the little social networking buttons – as do plenty of other static websites – but I don’t have a comments section. As I stated to Josh, “social networking” is of little concern to me; yes, I’m on Facebook, but to date I’ve never posted a Youtube video, ignore the daily requests to join LinkedIn, and will start “Tweeting” the same day my brain and testicles bid me farewell and head off to a retirement village in Queensland. My website serves as a vehicle for me to relay my thoughts and findings on diet, health and nutrition, not to make new pen pals.

Again, I thought I’d explained myself clearly and figured that was the end of the matter.

What happened next literally stunned me. You can read the comments here, but in short, the almighty “Josh” promptly launched into a tirade, calling me “cowardly” and a “bullshitter” for insisting my website was a static site and not a blog. Josh started wanking on about what technically constitutes a blog, and claimed that both the WordPress platform and the graphics theme I used were conclusive evidence I was a “blogger”.

Geezus…

It’s not Josh’s name-calling that left me bewildered. The Internet is worse than alcohol for turning little pussies into roaring lions, because it allows people to abuse the object of their disaffection without the risk of getting their jaw smashed in return. That lifetime members of the 2-Inch Club like Josh use this safety aspect of the Internet to run at the mouth is hardly breaking news.

What took me back is the reason why Josh felt compelled to call me names. My heinous crime, in Josh’s eyes, was, not to rob someone’s grandmother or to issue audaciously false claims about nutrition and health, but to claim my website was a static site and not a blog.

!

For the record, I use a pre-packaged template called LondonCreative from ThemeForest which comes packaged with both a static component and a blog option. If you look at the live preview of the theme here, you’ll note there is a tab up the top that says “BLOG”. Now, if you look at the exact same spot on this here website, you’ll notice there is no such tab. The reason for that is simple: I did not activate the blog option when installing the theme. This here is a static website, my friends.

However…let’s pretend that a panel of really bored preeminent IT experts from around the world convened one day, and formed a consensus that my website did indeed technically qualify as a blog. The logical response to that would have to be…

WHO GIVES A SHIT.

So here we are: After 2.4 million years of human ‘evolution’ and ‘survival of the fittest’, and this species is still pumping out scores of superficial, utterly clueless numbskulls like Josh and KL.

Why?

For the answer to that question, we need to dig into a little evolutionary psychology.

Why Humans are So Clueless and Superficial

When humans are presented with new information of unknown veracity, they are faced with a number of choices. The ideal choice would be for them to engage their rational faculties, and begin assessing the accuracy of that information by using such qualities and strategies as reason, logic, past experience, empirical evidence and examination of any controlled research on the issue they are assessing.

The problem is, no modern human can reasonably be expected to conduct a rigorous investigation of every single piece of new information they will encounter throughout their lives.

Even primitive Stone Age humans faced this conundrum, so they adopted a number of time-saving shortcuts. One of which was:

Listen to your elders, authority figures, and other people who give the impression they know what they’re talking about.

When a tribal elder told you not to eat the leaves of the Unga Bunga plant, it was because many moons ago some of his forebears had done just that and became violently ill. Some even died. Those witness to this unfortunate turn of events wisely concluded the leaves of the Unga Bunga plant were unfit for human consumption, and they proceeded to share this vital piece of knowledge with the rest of the tribe. As the word spread, Stone Age mums, dads, uncles, aunties, nonnas, nonnos and other authority figures subsequently passed this life-saving knowledge onto their siblings and grandkids, who in turn relayed the information to their own siblings and grandkids:

“[Grunt] No eat Unga Bunga plant or [grunt] you DIE [double grunt]!“

And so those who listened to their elders and avoided contact with the Unga Bunga plant lived to a ripe old age (around 30 years), long enough to bear offspring and ensure their genes would keep on keeping on long after they’d stopped grunting and left this earth for that big cave in the sky.

In contrast, those cheeky mavericks who figured, “Ah, what do those hairy old farts know? How bad can a few chews of an Unga Bunga leaf be? I heard it gives you a kick-ass buzz!”, weren’t so lucky. Their lack of regard for authority and established wisdom often cost them their lives, removing them from the reproductive pool before they had the opportunity to pass on their genes.

In this manner, human evolution routinely weeded out rebellious, independent thinkers and ensured the majority of humans were conformist creatures who placed great emphasis on the edicts of authority figures.

Humans also worked out early on that there was safety in numbers; that their survival and replication prospects were greatly enhanced when they were part of a cohesive tribe that pooled its food acquisition efforts, united against outside attackers, and provided a selection of potential partners with which they could copulate and create offspring. And so not only did humans evolve to revere authority, they also evolved to place great emphasis on peer approval and what others thought about them.

These were actually protective traits back in the Stone Age, when the main threats to survival were well established and life pretty much revolved entirely around finding food and avoiding predation from wild animals and hostile neighbouring tribes. Ignoring well-established tribal wisdom about which plants were okay to eat, about which animals were okay to approach and which to run like buggery from the minute you spotted them, often led to a greatly shortened lifespan. Acting in a manner that alienated other members of the tribe placed you at risk of being ostracized from the tribe, greatly reducing your ability to secure sufficient food, protection and sexual opportunities.

In short, back in the Stone Age, being a conformist sheep actually wasn’t such a bad thing.

However, life has changed a lot since the Paleolithic era.

Agriculture: Why it Brought Much More than Just Gluten Intolerance

The advent of agriculture forever changed humankind as we know it. With the advent of crop cultivation and animal domestication, humans went from being nomadic to sedentary. When I say sedentary, I don’t mean that cavefolk began sitting around on their fat asses all day eating Krispy Kremes, Facebooking and watching Internet porn. That shit came later.

The term sedentary, as used by Paleontologists, archeologists and anthropologists (if there any other relevant gists I neglected to mention, they have my sincere apologies) refers to the phenomenon of groups of human beings permanently settling in one location.

When agriculture first kicked off, those sedentary groups were quite small. But then something interesting occurred. Women, no longer having to simultaneously perform the demanding task of gathering food while carrying their infant children, started having more babies. Yep, this was the original baby boom, and its effects were truly world-changing. Population growth accelerated, leading to communities far larger than those ever seen in hunter-gatherer times. Researchers have observed repeatedly that breaking point for a nomadic tribal group is around 150 members; once a group grows larger than this, intra-group conflicts intensify to the point where the group will splinter into 2 or more smaller outfits.

But with people rooted to a fixed geographic location because of the new realities of food production, populations quickly surged past the 150 mark. This led to the formation of villages and the emergence of what anthropologists refer to as “big men”: Individuals whose social skills, charisma and/or cunning allowed them to hold sway over their fellow citizens, to the extent where they became societal leaders who organized and directed food production activities.

You should know the rest by now…villages became cities, and “big men” became kings with access to armies that they used to seize the land and resources of neighbouring populations. The small and relatively egalitarian societies of hunter-gatherer tribes were eclipsed by state societies ruled by autocratic individuals and families. While the rule of royalty  was eventually succeeded in most modernized countries by ‘democratically elected’ governments, the underlying (and rather remarkable) phenomenon remained: Never before had so few people had such all-encompassing control over the behaviour of so many others.

This stunning degree of obedience simply would not have been possible if not for the inbuilt human tendency to revere authority – an evolutionary hard-wired trait that remains as strong as ever to this day.

The Paleo Diet Mind

Evolutionary psychology is the cognitive equivalent of the “Paleo” school of nutrition – but without the religious cultism, thank goodness. Ask any die-hard “Paleo” adherent about their eating style and they’ll break into a sing-song diatribe about how cavemen ate meat, veggies, and berries, and how humans are not suited to cereal grain consumption because we only started eating grains 10,000 years ago. They may also break into a similar rant about dairy, depending on whether they subscribe to The Original Paleo® or Paleo 2.0 – Now with Butter & Cream!®

The Paleolithic diet concept certainly is a valid one, but the details are a little more complex than what typical “Paleo” dogma would have you believe.

In a nutshell, humans are omnivorous creatures that do best on a mixed diet comprised of animal flesh and plant foods, which is the kind of diet we spent millions of years evolving on. Contrary to the self-serving and dogmatic hogwash emanating from the low-carb and vegan camps, there is plenty of evidence to show diets comprised entirely of either animal or plant foods are nowhere near optimal for human health. As for cereal grains and dairy, which we’ve had 10,000 years or less to genetically adapt to, they do tend to be far more problematic than most other foods in terms of intolerance and allergy. Contrary to Official Paleo Dogma™, this doesn’t mean all humans should avoid all grains and all dairy – it simply means these foods tend to cause problems for a lot more people than other foods humans have been consuming for far longer. The reason being that humans as a species simply haven’t had enough time to fully genetically adapt to these fundamental changes in diet composition.

Now here’s what a lot of people don’t realize: Humans didn’t just eat a certain way for millions of years, but they also lived and behaved in certain ways during that time, and those lifestyles and behaviours resulted in cognitive patterns that were common to humans all around the globe. These included, but were certainly not limited to:

-Submission to authority figures and reverence for those with high social status;

-Great emphasis on conformity and peer approval;

-Heavy reliance on superficial characteristics (e.g. appearance, body language and voice characteristics) when assessing unfamiliar individuals.

Just as humans have not yet had sufficient time to fully and physically adapt to the dietary changes wrought by the Agricultural and Industrial revolutions, humans have not yet had time to fully cognitively adapt to the massive environmental and psychosocial changes wrought by these same revolutions.

Psychologically, we are “Stone Agers living in the fast lane”. We like to think of ourselves as more civilized and enlightened than our Paleolithic forebears, but so much of our daily behaviour is still beyond our control and even our comprehension. We frequently and automatically respond to situations and stimuli using largely subconscious responses that were cognitively hard-wired into us hundreds of thousands and even millions of years ago.

Hi, I’m From the Government, and I’m Here to Bend You Over

These are the very same universal characteristics that allow small groups of politicians and bureaucrats, most of whom are in rather pathetic physical condition and couldn’t fight their way out of a wet paper bag, to easily control millions of their fellow citizens and to dictate to them what they can and can’t do. This remarkable power even extends to the ability to blatantly expropriate  a substantial portion of the population’s yearly earnings. When organized criminals attempt to do this, it’s called extortion; when the government does it, it’s called taxation, even though both issue exorbitant bills for substandard and often unnecessary services and use the same underlying mechanism of enforcement (i.e., physical force).

Perhaps the most frightening marker of the power these individuals wield is that, throughout history and to this day, they have easily convinced millions of younger citizens to join their armed forces and fight wars essentially based on nothing other than personal aggrandizement, seizure of resources, and financial profit for vested interests, such as the military-industrial complex which relies on continued human bloodshed for its obscene profits. George W. Bush was a chimp-like creature who struggled to mouth a coherent sentence, and ex-Australian Prime Minister John Howard struggled to bowl a cricket ball without falling on his ass, but that didn’t stop them from ordering thousands of young men and women off to foreign countries to get bombed and shot at.

Any species that submits to subhuman fucktards like this has serious issues with authority worship.

This klutz led Australia for eleven years, sending our kids off to fight in a fraudulent war and, like his narcissistic predecessors, signing us up for ‘free trade’ agreements in which we got the raw end of the deal. And if you think he was bad, you should see the two losers that came after…

Oh, and lest you think I’m some “lefty” picking on the “right”, rest assured there is little I find so sadly confirming of human sheepishness as the totally undeserved reverence routinely awarded to Barack Obama. Never before in recent history has someone sounded so grandiose and reassuring while uttering nothing but a complete load of meaningless, inane bullshit. Oh Bummer has failed miserably to deliver his incessant promise of “Change!” and has followed up his promise to reverse government intrusion in our lives by overseeing even more government intrusion and attempting to justify it at every turn.

And people love him for it.

@#$%!

The Invisible Hand, and How it Effortlessly Takes Your Money

Politicians are hardly the only ones who exploit the sheep-like nature of Homo sapiens.

You’d better believe that the big advertising firms are fully aware of how human psychology can be manipulated and exploited for profit; heck, they’ve made a virtual science out of it.

Advertisers know damn well they can manipulate our worship of authority and social status, our need for peer approval, and our desire to be popular and wanted. That’s why advertisers creates ads with celebrities pimping products they’ve never used; while there’s nothing to suggest a Hollywood celebrity or famous athlete knows more about beverages or fragrances than the next person, we’ve been evolutionary programmed to place great emphasis on what those with high social status think and do.

Advertisers know full well there is little difference between a $30 pair of jeans and a $300 pair. But they know plenty of people will still fork out the extra $270 if the latter can be built into a trendy brand name, because the human need for peer approval is so strong. People will by the $300 pair because, subconsciously, they believe this will help portray a more favourable impression of themselves to others.

Some people are actually quite proud of their clueless stupidity.

Check Your SQ (Superficial Quotient)

How many US readers are aware that right now, right under their noses, their Government is building what amounts to a domestic military force? If you’re wondering why, it’s worth remembering the adage “You don’t put a rubber on unless you’re planning to fuck somebody.”

That “somebody” looks to be the US citizenry.

How many of my fellow Australians are aware that the standard of their children’s education is on a continual downward slide compared to the rest of the world? And of those who are aware and applauded in robotic fashion Government plans to throw millions of taxpayer dollars at the problem, how many know Australian teachers are already among the best paid in the world? How many know taxpayer funding of schools in Australia increased by 24 per cent between 2008 and 2010 – more than four times the average OECD increase of five per cent? The problem with Australian education isn’t a lack of funding – it’s a lack of quality! Giving more money to a broken, self-serving system isn’t going to change diddly.

How many readers are aware that the US Government is employing drones to conduct a number of “unannounced and undeclared” wars? Yeah, why make a big announcement, send in hordes of troops, and have to deal with such pesky annoyances as public disapproval and congressional debate? That malarkey is for anachronistic freedom-loving types who believe in the Constitution and stuff. Just send in the drones and start shooting for crying out loud, who cares if innocent civilians are still getting killed?

How many people are aware of just how dire the situation in Fukushima really is, and the possible global consequences? Yeah…Fukushima…remember…the big nuclear disaster in Japan? No, it’s not yesterday’s news – the situation is still critical and getting worse.

Now…

…how many of you are aware that Prince William and Kate Middleton recently had a baby?

I rest my case.

This species places way too much emphasis on superficial bollocks, and not enough on the things that really matter.

BREAKING NEWS: BRITISH COUPLE HAVE A CHILD! Shit, like that’s never happened before…

Yes, this Stuff Does Concern You

I know what some of you are thinking: “Who gives a shit about Australian education or an impending US police state? So long as I’ve got the new iPad and an abundant supply of Cheerios, life is good!”

If that’s you, I’ve got two recommendations:

1: Piss off.
2: Get a vasectomy immediately (to prevent replication of your toxic Clueless+Superficial chromosomes).

The handful of you that remain will be basically divided into two groups: Those who are already fully onboard with what I’m saying, and those who have been guilty of what I’m explaining, but can feel the seeds of awareness sprouting within.

For the latter, I strongly urge you to do everything you can to cultivate the qualities of rational, independent thought and critical analysis. Especially on matters pertaining to your physical health and wellbeing. When judging, for example, the worth of a diet/health commentator, realize that things like the colour scheme of their website are utterly irrelevant.

So too is whether or not they are wearing a white coat or suit and tie in their promo pics. The former is a thinly-veiled ploy to implant an air of scientific credibility in your subconscious, the latter an air of professionalism. That these thinly-veiled strategies actually work quite well is attested to by the runaway success of fat loss books written by fat people pictured in suits and white coats.

Um, no comment…

It is beyond the capability of this article to provide you with a complete how-to guide on reversing the evolutionary programmed tendency to be swayed by superficial appearances, peer approval, authority and “social proof”, and instead becoming an independent-thinking dynamo. But there is plenty of easily accessible, reader-friendly material that can help you do just that. Two especially worthy suggestions, both of which would have to rank in my Top Ten of “Must-Have” books, are:

Influence: The Psychology of Persuasion by Dr. Robert Cialdini

Why We Lie: The Evolutionary Roots of Deception and the Unconscious Mind by David Livingstone Smith

Buy them. Read them. Again and again. You’ll learn a lot, not just about human behaviour, but yourself. There’s plenty of published research on evolutionary psychology, but these books are great primers (as is just about anything written by David M. Buss).

Yes, I know, I know…reading takes effort, but crikey, that’s a small price to pay if it helps you avoid becoming a KL or Josh.

Ciao,

Anthony “Don’t Call it a Blog!” Colpo.

—

Anthony Colpo is an independent researcher, physical conditioning specialist, and author of The Fat Loss Bible and The Great Cholesterol Con. For more information, visit TheFatLossBible.net or TheGreatCholesterolCon.com

Copyright © Anthony Colpo.

Disclaimer: All content on this web site is provided for information and education purposes only. Individuals wishing to make changes to their dietary, lifestyle, exercise or medication regimens should do so in conjunction with a competent, knowledgeable and empathetic medical professional. Anyone who chooses to apply the information on this web site does so of their own volition and their own risk. The owner and contributors to this site accept no responsibility or liability whatsoever for any harm, real or imagined, from the use or dissemination of information contained on this site. If these conditions are not agreeable to the reader, he/she is advised to leave this site immediately.

Back in August, I reprinted an email I’d sent to journalist Maryanne Demasi asking why her recent Toxic Sugar segment on the ABC show Catalyst was so replete with nonsensical claims. I listed several of the false statements made on the show by herself, the narrator and the guests (which included book authors Gary Taubes and Robert Lustig). I cited research that readily disproved these claims, and asked Demasi how she could possibly reconcile the results of that research with the statements made on the show.

Demasi’s response was to claim she was busy working on a segment about cholesterol, and that she’d answer my questions as soon as possible. Then, in a rather remarkable display of audaciousness, she asked if I would help her prepare her segment on cholesterol.

Um, no thanks.

As I fully expected, I never heard back from Demasi. But on August 27, I did receive the following email from a Kirstin McLiesh, who identified herself as “Head, Audience and Consumer Affairs” at the ABC:

Dear Mr Colpo,

I refer to your email of 11 August to Maryanne Demasi.

In accordance with ABC Complaint Handling Procedures, your correspondence has been referred to ABC Audience and Consumer Affairs.  Audience and Consumer Affairs is separate to and independent of content making areas in the ABC.  Our role is to investigate complaints alleging that ABC content has breached the ABC’s editorial standards.  These editorial standards are set out in our Editorial Policies and Code of Practice, available here – http://about.abc.net.au/how-the-abc-is-run/what-guides-us/our-editorial-policies/.

The concerns outlined in your email are currently being assessed. The ABC endeavours to respond to all complaints within 30 days of receipt. However, please be aware that due to the large volume of correspondence we receive, and the complex nature of some matters, responses may at times take longer than 30 days.

Yours sincerely,

Kirstin McLiesh

Head, Audience and Consumer Affairs

I’m not sure who passed on my email to the Corporate Affairs crew at the ABC, but at any rate, I didn’t expect much to come of their so-called “independent” investigation (for the record, when an outfit investigates itself, it is not an independent investigation; a bonafide independent investigation would be one conducted by a party totally unrelated to the ABC and with no vested interest in the findings).

And so I pretty much forgot about the whole charade until September 19, when I received another email from the ABC, this time from someone identifying himself as “Mark Maley, Audience & Consumer Affairs”.

Here’s the email, followed by my comments:

Dear Mr Colpo

Thank you for your email of 11 August concerning the Catalyst program, “Toxic Sugar”.

As your correspondence raised concerns of misleading content, your email was referred to Audience and Consumer Affairs for consideration and response. The unit is separate and independent from ABC program areas and is responsible for investigating complaints alleging a broadcast or publication was in contravention of the ABC’s editorial standards. In light of your concerns, we have reviewed the broadcast and assessed it against the ABC’s editorial requirements for accuracy, as outlined in section 2 of the ABC’s Code of Practice: http://about.abc.net.au/wp-content/uploads/2012/12/CodeofPractice2013.pdf . In the interests of procedural fairness, we have also sought and considered material from Catalyst.

This segment was a presentation of theories expounded principally by Robert Lustig and also by Gary Taubes. Some of their conclusions are controversial and some experts do not agree with their concentration on the effects of fructose and insulin as the principal agents of increasing obesity and metabolic disease. However, the program did not endorse their theories or present them as fact. The program, however, stands by its assessment that Robert Lustig and Gary Taubes are credible and responsible and that their theories are worth consideration.

Your email focussed on two of their claims that you assert are misleading. Firstly that the reason why exercise fails to produce weight loss is because it simply makes you hungrier and secondly that carbohydrates, via their effect on insulin, increase body fat gain.

In relation to exercise Gary Taubes said:

“The studies show that exercise has virtually no effect on weight loss. One thing exercise does is it makes people hungry.

The program then summarised his argument:

“Burning calories through vigorous exercise triggers hunger signals in your brain so that you eat to replace those calories. Your body knows it’s losing vital energy stores, so it reacts by slowing down your metabolism to conserve that energy.”

Catalyst advises that Taubes’ statement  was based partly on literature from the American Heart Association and the American College of Sports Medicine who published joint guidelines for physical activity and health.  They did not conclude that physical activity would lead to weight loss, they concluded the following:

“It is reasonable to assume that persons with relatively high daily energy expenditures would be less likely to gain weight over time, compared with those who have low energy expenditures. So far, data to support this hypothesis are not particularly compelling.”

Mr Taubes also cites a 1989 Dutch study in which researchers trained couch potatoes to run a marathon. After 18 months of training and having run a marathon, the men lost 5 pounds of body fat; the women had 0 percent change in body composition.

Catalyst notes that evidence exists both for and against the role of physical activity in weight control. High levels of physical activity and successful maintenance of body weight may be a result of better coupling between energy intake and energy expenditure, potentially mediated by physiological changes in appetite, albeit in the presence of large inter-individual variability. Prospective studies, however, find little evidence of the more physically active members of a population gaining less excess weight than those who are the least physically active.

Dr Demasi prefaced the discussion of the issue by noting that “overeating and being sedentary can make you gain weight” and summarised this section of the segment by saying that “exercise does have other health benefits that extend beyond weight loss”. She was not saying that exercise has no role in weight control, rather that Gary Taubes is saying that the role of overconsumption of sugar and starch is of much greater significance in the rising incidence of obesity and that controlling their intake is the crucial factor in weight loss.

The role of exercise in weight loss among overweight individuals is controversial. However, the focus of this section was not to advise against exercise but rather against the excess consumption of sugar and carbohydrates. On review, we are satisfied that reasonable efforts were made to ensure factual elements were accurate and that the section was not materially misleading.

On Insulin, Professor Robert Lustig said:

Our fat consumption has stayed exactly the same over the last 30 years. And look at the disaster that has befallen us. And that is because our consumption of dietary carbohydrate has gone through the roof. Anything that drives insulin up will drive weight gain.

The idea that carbohydrates stimulate the insulin response and that insulin is one of the main hormones that promotes fat storage is not disputed by most obesity experts. Professor Cowley, for example, said in the program:

“If you constantly provide carbohydrates to the body, you’ll have constantly high insulin levels, and that will lead to increased fat deposition in tissues.”

The program advises that it interviewed one of Australia’s top nutritionists Dr Alan Barclay for the story.  Dr Barclay pointed out that starch is just as much of a problem as sugar when it comes to the insulin response. The segment did not advocate the Atkins Diet and did not say that people cannot lose weight due to calorie restriction.  Taubes and Lustig believe that calorie restriction is difficult for people to maintain for a long period of time, and that lowering insulin by lowering carbohydrates is the option they would take.

The program was clear that there is still ongoing debate surrounding these theories. Dr Demasi emphasised that:

“There is still ongoing debate surrounding Professor Lustig’s theories. Some nutritionists warn against demonising sugar in the same way we demonised fat in the ’70s. They say the focus on sugar will result in unbalanced dietary advice.”

In summary, Audience and Consumer Affairs are satisfied that the segment made it sufficiently clear that the more controversial aspects of Taubes’ and Lustig’s theories were unproven and not factual. We are also satisfied that reasonable efforts were made to ensure the accuracy of factual statements made in program.

Thank you for taking the time to write; your feedback is appreciated.

For your reference, the ABC Code of Practice is available online at http://about.abc.net.au/reports-publications/code-of-practice-2013/

Should you be dissatisfied with this response to your complaint, you may be able to pursue your complaint with the Australian Communications and Media Authority, http://www.acma.gov.au .

Yours sincerely

Mark Maley

Audience & Consumer Affairs

Okay, before I answer Maley’s reply, I have to say that I don’t like having my intelligence insulted, and I strongly object to people taking me for an idiot. I’m not sure if this was Mr Maley’s intention, but nevertheless it’s exactly what he proceeds to do in his email.

As for the results of the ABC’s distinctly non-independent investigation: It’s hardly surprising that the ABC ruled in favour of itself. I wasn’t exactly expecting them to write back with, “You know what Anthony, we double-checked the statements made by our narrator, Demasi, Taubes and Lustig, and guess what? You were right! They have no foundation in sound science and we apologize for ever putting this slop to air!”

The ABC did what I fully expected it to do; it simply avoided the evidence I presented and instead reflexively defended itself with a mix of half-truths and outright lies.

There are so many mistruths contained in Maley’s email it’s hard to know where to start. Well, before we hit the hard science, how about we address the allegedly “credible” and “responsible” nature of the guests on their show.  Maley claims:

“The program, however, stands by its assessment that Robert Lustig and Gary Taubes are credible and responsible and that their theories are worth consideration.”

I suspect Catalyst’s “assessment” of Gary Taubes wasn’t very thorough. If they’d done their homework they would have quickly found out he’s got quite the reputation for cherry-picking evidence that supports his arguments while blatantly ignoring that which doesn’t.

Now, anyone can accuse someone else of being a cherry-picker, and the accusation is thrown around quite freely these days by proponents of opposing dietary viewpoints. But I must say, Taubes seems to go out of his way to confirm the allegations made against him. He evinces a strong and consistent habit of citing only the evidence that supports his own arguments, while blatantly and unashamedly ignoring that which doesn’t.

And according to many of those who’ve been interviewed by Taubes, his one-sided approach to constructing arguments hardly stops at selective research citation. Taubes was widely lambasted for misquotation after his seminal 2002 New York Times article titled “What if it’s all been a big FAT Lie?” This is the article that blasted Taubes into the public consciousness and lined him up for a book deal with Alfred Knopf for which he received a cool $750,000 advance.

According to several of the researchers interviewed by Taubes, it was indeed all “a big FAT Lie” – his article, that is. Reading like a giant infomercial for Atkins, it quoted a number of prominent researchers and academics who – once staunch opponents – suddenly appeared to be supporting the low-carb Atkins Diet with which Taubes had become so enamoured with.

Gerald Reaven, the Stanford University researcher who coined the term “Syndrome X”, was one of many who complained he had been quoted out of context. “The article was incredibly misleading”, he said[1]. In fact, Reaven was so embarrassed and angered by what Taubes had done that when another writer, Michael Fumento from Reason magazine, contacted him for commentary he refused to be interviewed. Eventually he relented and told Fumento:

“I thought [Taubes'] article was outrageous. I saw my name in it and all that was quoted to me was not wrong. But in the context it looked like I was buying the rest of that crap.” He added, “I tried to be helpful and a good citizen, and I ended up being embarrassed as hell. He sort of set me up.”[2]

“He took this weird little idea and blew it up, and people believed him,” says John Farquhar, also a professor emeritus at Stanford University. “I was greatly offended at how Gary Taubes tricked us all into coming across as supporters of the Atkins diet,” says Farquhar.  “I think he’s a dangerous man. I’m sorry I ever talked to him.”[2]

Taube’s article ended with a quote from Farquhar, asking: “Can we get the low-fat proponents to apologize?” But the quote was taken out of context. “What I was referring to wasn’t that low-fat diets would make a person gain weight and become obese,” explains Farquhar. Like Willett and Reaven, he was worried that the low-fat, high-carbohydrate diet incessantly promoted as the epitome of healthy eating could in fact raise the risk of heart disease. “I meant that in susceptible individuals, a very-low-fat diet can raise triglycerides, lower HDL cholesterol, and make harmful, small, dense LDL,” said Farquhar[1].

“We’re overfed, over-advertised, and under-exercised,” says Farquhar. “It’s the enormous portion sizes and sitting in front of the TV and computer all day” that are to blame. “It’s so gol’darn obvious—how can anyone ignore it?”[1]

“It’s silly to say that carbohydrates cause obesity,” said George Blackburn of Harvard Medical School and the Beth Israel Deaconess Medical Center in response to Taubes’ article, which misleadingly portrayed him as an avid supporter of the Atkins Diet. “We’re overweight because we overeat calories.” [1]

On the contentious subject of ketosis, Taubes’ article included reassuring words from National Institutes of Health researcher Richard Veech, who said that “ketosis is a normal physiologic state.” Veech told Fumento the quote was correct, but that Taubes conveniently “omitted to say that I strongly urged people to not use the Atkins diet without the supervision of a physician”, due to Veech’s concerns about potential cardiovascular complications[2].

“He knows how to spin a yarn,” said Barbara Rolls, an obesity researcher at Pennsylvania State University. “What frightens me,” she said of Taubes, “is that he picks and chooses his facts.” Taubes interviewed her for some six hours, and she sent him “a huge bundle of papers,” which he simply brushed aside. “If the facts don’t fit in with his yarn, he ignores them,” she said[1].

Taubes was “very selective in what he chooses to include because he’s trying to sell a specific line,” said Rolls. “He is a good writer; that’s the thing that scares me. This is such a good example of how you can pick and choose your facts to present the story you want. But that’s not how science should be done. You can’t interview everybody and simply ignore the people you don’t want to hear.” [2]

But from all accounts, that’s exactly what Taubes did. The truly remarkable aspect of Taubes’ NYT article was, not the compelling scientific support for its central claims (despite masquerading as a science-based exposé, it did not include a single scientific reference), but the consistency with which the supposedly supportive “experts” he cited rushed to distance themselves from the article. One after the other, they couldn’t emphasize strongly enough that Taubes had left out critical (and non-supportive) statements, and blatantly quoted out of context those he did see fit to include.

Danish researcher Arne Astrup, who had already published two extensive reviews confirming the efficacy of low-fat weight loss diets, was interviewed by Taubes for the article. Astrup’s two papers analysed results from 20 studies involving nearly 2,000 people who followed low-fat diets. In one report published in 2001 in the International Journal of Obesity and Related Metabolic Disorders, Astrup found low-fat diets “prevent weight gain in normal weight subjects and produce weight loss in overweight individuals.” The other report, published in the Proceedings of the Nutrition Society, Astrup and his colleagues concluded low-fat diets “consistently demonstrate a highly significant weight loss” of seven to nine pounds in normal-weight and overweight participants.

But none of this found its way into Taubes’ NYT article. When Washington Post writer Sally Squires asked Taubes why, he replied: “Astrup is problematic”. Taubes said he didn’t like the fact Astrup “chose studies that put people on low-fat, low-calorie diets and compared them to people who ate normally,” a rather pointless criticism given the goal of such studies is often to determine whether alternative approaches work better than those believed to be causing the very problem being studied, in this case obesity.

Simply by enrolling people in a weight loss study, Taubes claimed, “you turn them into healthier people and intervene in their lives,” which he says is why he didn’t mention the findings in his article. Again, this was a most disingenuous excuse given many of the trials reviewed by Astrup did in fact control for this potential confounder. Taubes, apparently, has no understanding of the concept of clinical trial randomization. Or maybe he just doesn’t want to understand it; Astrup says he explained this to Taubes during a half-hour telephone conversation, but again, Taubes did not see fit to include this inconvenient information. “I reviewed all the evidence suggesting that low-fat diets are the best documented diets and was extremely surprised to see that he didn’t use any of that information in his article,” Astrup said[3].

Another researcher Taubes considered ‘problematic’ was F. Xavier Pi-Sunyer, director of the Obesity Research Center, St. Luke’s-Roosevelt Medical Center in New York. Pi-Sunyer was part of a 12-member National Heart, Lung, and Blood Institute panel who authored the 1998 Clinical Guidelines on the Identification, Evaluation and Treatment of Overweight and Obesity in Adults. The panel identified four dozen published, well-designed, randomized controlled clinical trials on low-fat diets. A review of this literature led the panel to conclude that cutting dietary fat can “help promote weight loss by producing a reduced calorie intake” and that “reducing fat as part of a low calorie diet is a practical way to reduce calories.”

So why didn’t Taubes mention this?

“Anything that Pi-Sunyer is involved with, I don’t take seriously,” Taubes said during an interview in which he mistakenly identified Pi-Sunyer as a psychiatrist (Pi-Sunyer is in fact an endocrinologist). “…He just didn’t strike me as a scientist. He struck me as a grand old man… Pi-Sunyer was one of the people who in the course of interviewing I decided was not a good scientist.”

Yep, just like that. With no further explanation of just it was about Pi-Sunyer that made him such a poor scientist and nothing more than “a grand old man”, Taubes conveniently eliminated another two-dozen studies that failed to support his preconceived conclusion.

Similarly ignored was renowned obesity researcher Dr Jules Hirsch, whom Taubes interviewed in his office at Rockefeller University in New York. Hirsch had published ground-breaking research in which volunteers were fed isocaloric diets of greatly varying macronutrient composition. Low-carb, no-carb, high-carb, moderate-carb…it didn’t matter; so long as caloric intake was kept the same, it didn’t make a whit of difference to the subjects’ weight status.

“I just kept telling him, it doesn’t matter what kind of calories you eat,” says Hirsch, but Taubes clearly wasn’t listening[2]. Taube’s’ hearing seems to mysteriously shut off when presented with information that conflicts with his preconceived “insulin and carbs make you fat!” thesis.

Perhaps the most telling comment from Taubes came when he told Squires, “I know…I sound like if somebody finds something I believe in, then I don’t question it.”[3]

Damn straight. The overwhelming consensus among the aforementioned researchers was Taubes had already decided the conclusion of his story long before he interviewed them, and that his article was a terribly one-sided affair that ignored a wealth of contradictory evidence.

Now I know what Mark and some of you die-hard Taubes fans are saying at this point:

“Hey man, that New York Times article was way back in 2002. Maybe Gary’s cleaned up his act since then?”

Yeah, good old 2002. I remember it clearly. People got around by horse and cart, washed their clothes on a scrubbing board, and listened to the football on a scratchy old radio.

Seriously, apart from Facebook and iPads, not a whole lot has changed since 2002. Our politicians are still full of shit and promising change that never comes, the military-industrial complex is still waging ‘freedom’ on Middle Eastern nations, and Gary Taubes is still peddling the same old rot about carbs, insulin, and exercise – and he’s still using the same highly creative and selective methods of evidence acquisition.

Taubes is still unwavering in his claim that insulin and carbohydrates make us fat. Along with Lustig, he’s claiming the effects of insulin and carbohydrate are independent of calories, and that carbohydrates and insulin – not calories – are what determine whether we lose or gain weight.

As Mark Maley’s response clearly shows, both he and the crew from Catalyst think this is a valid claim. In fact, Catalyst’s own narrator stated unequivocally, despite the complete lack of supporting science, that “The higher your insulin, the more likely you are to store fat, because insulin is the main hormone that puts fat into fat cells.”

Maley, by the way, also claims:

“The idea that carbohydrates stimulate the insulin response and that insulin is one of the main hormones that promotes fat storage is not disputed by most obesity experts.”

I don’t want to give too much credence to statements like this, because they rely on the “Appeal to Authority” fallacy. This fallacy occurs when people who cannot construct a sound argument for whatever viewpoint they are supporting instead point out that a lot of people with big credentials and fancy initials after their name believe in said viewpoint, and therefore it must be valid.

I couldn’t give a rat’s rectum whether or not a bunch of purported ‘experts’ support a particular theory; I’m far more interested in the evidence they cite in support of that theory. Nonetheless, it behoves me to point out that Maley’s claim about the carbohydrate-insulin hypothesis not being disputed by most ‘obesity experts’ is absolute nonsense. Most of those whom could reasonably be described as “obesity experts” – i.e. pioneering and prolific researchers who have performed substantial research on the subject, as opposed to hyperbolic book authors – maintain that calories are the overriding determinant of fat gain and loss.

Arne Astrup, George Bray, George Blackburn, Jules Hirsch, Theodore Van Itallie, Barbara Rolls … are you familiar with any of these names, Mr Maley? Probably not, because none of them have written popular format diet books that sold a squillion copies by promising easy weight loss, and none of them shamelessly pimp gimmicky solutions to obesity instead of the plain, unsexy truth about calories.

But the fact remains these are the biggest names in obesity research, and they will all tell you in no uncertain terms that a calorie surplus is what causes obesity, not insulin or carbohydrates.

Dr Arne Astrup was recently ranked among the world’s top five on a list of the world’s 172,000 most productive obesity research authors.

Did Catalyst, which apparently places so much value on “credibility”, bother to seek out Dr Astrup for his views?

Evidently not. Catalyst was happy to simply round up two hyperbolic American book authors making nonsensical claims, along with an Australian nutritionist and an Australian professor who happily parroted these untenable claims. In other words, Catalyst made no effort whatsoever to present a balanced story – it simply rounded up a small handful of commentators already committed to the “Insulin and carbs make you fat” world view, and presented their views unopposed. On top of this, Mr Maley then has the audacity to claim that the disproved pseudoscientific view of this small hand-picked selection is representative of the scientific community at large.

What rubbish.

But even if the majority of ‘experts’ did believe in the insulin-carbs fairy tale, that still doesn’t change the fact it’s a fairy tale. Ultimately, Mark, it doesn’t matter what ‘obesity experts’ claim or think. It only matters what tightly controlled evidence shows. The truth is determined by demonstrable fact, not collective consensus. That you have to keep deferring to other commentators merely confirms my contention that neither you nor the folks at Catalyst have a clue yourselves as to the real science behind obesity. That’s fine, as we can’t all be experts on everything … but why pretend to be worthy disseminators of sound science on a subject you clearly don’t know anything about?

Here’s a quick crash course in obesity research for Mr Maley and the folks at Catalyst.

How to Determine When a Low-Carb Shill is Trying to Hoodwink You, in One Easy Step!

If someone claims that diets low in carbohydrate cause greater fat loss or less weight gain than isocaloric diets high in carbohydrate, then there is only one way they can validate this unlikely claim.

No, it’s not to incessantly spout a bunch of clever-sounding hogwash about the fat-producing effects of insulin.

Because the fat-producing effects of insulin are a very short-term phenomenon that cannot be reproduced over the longer-term. Sure, intravenously infusing insulin into the arms of experimental subjects or exposure of fat and muscle cells to insulin in a petri dish can indeed produce immediate-term reductions in lipolysis and increases in lipogenesis[4-6].

One of the most time-honoured cons in science is to take such isolated pieces of experimental data, then use them to paint a bigger picture that doesn’t exist. The low-carb crowd exemplify this approach with their “insulin makes you fat” sham. They take the results of the aforementioned experiments, and use them to create a world view in which eating carbs causes insulin release, which in turn blocks fat burning and increases fat deposition, which in turn makes people fat.

There’s a wee problem with this worldview: It’s complete rubbish.

The reason it’s rubbish, Mark, is because it ignores critical events that promptly follow on from the immediate changes in lipolysis and lipogenesis. Namely, when you eat more carbs, rather than converting the extra carbohydrate to fat and stockpiling it in adipose cells, the body responds to increases in carbohydrate intake simply by increasing the amount of carbohydrate used as fuel. At the same time, the body decreases the amount of fat used for energy[7]. That’s why, when volunteers are fed high- and low-carbohydrate diets of equal caloric content, the subsequent differences in lipogenesis are so small as to be meaningless in terms of fat gain[7,8].

Lustig and Taubes never mentioned any of that, huh?

Yep, the “insulin blocks fat-burning” theory is simply an exercise in manipulating metabolic minutiae, Mark: The practice of blowing up isolated bits of experimental laboratory data into something they’re not. As a substitute for controlled experimentation of the actual effects of isocaloric diets on weight status in real live human beings, it fails miserably.

So too does selectively quote food consumption data, as Lustig did on your show.

His claim that fat consumption has not increased over the last 30 years can be maintained only by citing data from the CDC. Taubes also uses this tactic in his book Good Calories, Bad Calories, citing a 2004 CDC article reporting that total fat intake increased among women by a mere 6.5 grams but decreased among men by 5.3 grams[9]. The impression this gives is that overall fat intake has remained relatively unchanged.

That’s all well and good, but it flatly ignores the USDA data (see below) that shows fat intake did indeed increase during this time.

So why the two disparate data sets? Well, the fat intake changes reported by the CDC were derived from the four National Health and Nutrition Examination Surveys (NHANES) conducted by the US Government to track food consumption trends. These surveys are not without their problems: They rely on the ability of people to accurately recall their food intake, and they involve only a small portion of the US population.

In NHANES, the sample sizes ranged from 14,167 men and women in NHANES III (1988-1994), to only 3,733 men and women in NHANES 1999-2000[9]. These samples were then assumed to be representative of the entire US population. Each of the men and women from these samples took part in a single dietary recall interview about the foods and beverages they consumed during the preceding 24 hours; this 24-hour recall was then taken to be representative of each subject’s diet for the 1- to 6-year periods covered by each NHANES project.

Stop and think about this for a moment; how many people eat exactly the same thing every day for several years in a row? Obviously, questioning someone about what they ate during a single 24-hour period is a manifestly inadequate way in which to ascertain someone’s intake over a period spanning years. However, because of the random selection of respondents and the consistent method of questioning from one survey to the next, the NHANES data is still helpful in assessing overall trends.

Except, perhaps, for fat intake. There is a wealth of evidence showing food recall surveys are routinely plagued by underreporting. Again, if this held constant among macronutrients and from one survey to the next, we would still get a reasonable picture of overall trends. However, the research on dietary misreporting shows that dietary fat is the most underreported macronutrient of all. Given that the aforementioned NHANES surveys occurred during a period when dietary fat was being roundly vilified as a fattening and artery-blocking toxin, it’s not hard to understand why respondents (especially those participating in a face-to-face interview) would be inclined to significantly underreport their intake of this nutrient.

In contrast to NHANES, the USDA determines the total amount of food available in the US, then calculates what remains available for human use after deducting exports, farm and industrial uses, and end-of-year inventories. This amount is then divided by the population of the US to give a per capita “food disappearance” figure. The obvious flaw of food disappearance data is that it cannot account for food wastage; both food outlets and households discard significant amounts of food due to expiration, spoilage and incompletely consumed meals. As a result, while self-reported data like that from NHANES is likely to under-report true fat and calorie intakes, food disappearance data would tend to overestimate individual caloric and macronutrient intakes.

Obviously, both methods of estimating food intake have serious shortcomings, although you could make a case that the USDA data, which always involves nationwide data as opposed to small random fragments of the US population, is more consistent. You could also point out that the USDA data does not involve food recall surveys, and therefore is not prone to personal under-reporting of fat intake in a culture where fat is roundly vilified as some kind of dietary villain.

At any rate, good science dictates you discuss both data sets when attempting to tie in nationwide dietary trends with concomitant changes in obesity prevalence. Neither Lustig nor Taubes, however, evidently have time for conflicting data sets. They simply cite the NHANES data they think supports their argument and ignore the USDA data that doesn’t. Lustig also ignores the fact that even the NHANES data showed an increase in overall caloric intake in the period 1971-2000.

And again, that’s evidently A-OK with the mob over at Catalyst. But I don’t think it’s OK, so for those who would like both sides of the story as opposed to the very one-sided case presented by Taubes, Lustig, and Catalyst, here’s the USDA data:

 Per capita carbohydrate intake, 1909-2000

Lustig and Taubes are quick to point out that carbohydrate intake increased over the last 30 years, as evinced by NHANES food surveys and also USDA food disappearance data, the latter of which is depicted above.

Per capita calorie intake, 1909-2000

Per capita fat intake, 1909-2000 (total fat intake represented by the upper broken line)

The above two graphs show USDA food disappearance data for the period 1909-2000; starting in the early 80s, per capita disappearance of calories and fat rose significantly. While quick to selectively cite the NHANES data showing an increase in carbohydrate consumption, neither Taubes nor Lusting feel it necessary to discuss the above USDA data. Despite the very selective manner in which they cite research, the ABC maintains Taubes and Lustig are “credible” and “responsible” commentators.

So if wanking on about metabolic minutiae and throwing around food consumption data of questionable accuracy don’t cut it, what does? How, exactly, do you determine whether or not a low-carbohydrate diet causes greater fat-derived weight loss than an isocaloric high-carbohydrate diet?

Simple: You conduct clinical trials. In each of these trials, you take a bunch of people, randomly assign half of them to follow a low-carbohydrate diet, and the remainder to follow an isocaloric high-carbohydrate diet.

Or you can take the same volunteers, and have them follow both diets at different points in time, for similar periods and in random order (this is known as a “crossover” trial).

There’s one very important criteria that must be fulfilled if the results of these trials are to be taken seriously: Namely, they must be conducted under tightly controlled ward conditions, so we can be sure the participants really did eat the same number of total calories on the low- and high-carbohydrate diets.

And guess what? Such studies have indeed been performed – over two dozen of them – since 1935, and they have repeatedly shown that low- and even zero-carb diets offer absolutely no fat-derived weight loss advantage over isocaloric high carb diets.

None whatsoever.

I mentioned these studies in my email to Demasi, and interestingly neither you nor her ever bothered to email back and ask for the citations.

Which indicates one of two things:

–You guys already have the citations, but ignored their results, or;

–You don’t have the citations, and are not interested in them because you fear they are going to refute the claims made on Catalyst.

Neither possibility gives much confidence in the level of scientific rigor employed at Catalyst, does it?

Don’t worry, you’re not alone in ignoring these studies. They completely demolish the entire “metabolic advantage” sham promoted by the low-carb movement, so this movement – including leading lights such as Taubes and Lustig – blatantly ignore them.

There was one other low-carb guru who also attempted to ignore them, but then his sizable ego, pomposity and self-conceit got the better of him. Things didn’t go too well for him after that:

The Great Eades Smackdown Part 1

The Great Eades Smackdown Part 2

I guess Lustig and Taubes have learned from the fate of their buddy Eades; any evidence that doesn’t support your preconceived conclusions is better left ignored.

ABC and Catalyst Trying to Back Away From their False Claims About Exercise?

As for exercise, you claim “Catalyst notes that evidence exists both for and against the role of physical activity in weight control. “

No it didn’t. It clearly quoted Gary Taubes as saying:

“The studies show that exercise has virtually no effect on weight loss. One thing exercise does is it makes people hungry.”

How did Catalyst attempt to balance this wild claim? It didn’t. It actually supported it with the following outlandish statement spoken, not by Taubes or Lustig or Barclay or Cowley, but by your very own narrator:

“Burning calories through vigorous exercise triggers hunger signals in your brain so that you eat to replace those calories. Your body knows it’s losing vital energy stores, so it reacts by slowing down your metabolism to conserve that energy. This is thought to have helped us evolve as a species and to survive in times of famine.”

Whoa, wait a minute! With that statement, Catalyst unequivocally pronounced that exercise causes human metabolism to slow down. Where is your evidence for this astounding statement? All the available evidence shows that exercise either makes no difference to resting energy expenditure or, in the case of vigorous exercise, increases it due to a process known as excess post exercise oxygen consumption (EPOC)!

Where does Catalyst get off making these patently false claims about exercise? Again, where is the evidence showing that exercise slows metabolism?

Please forward the published papers demonstrating this at your earliest convenience. If these papers are not forthcoming, I will take this as proof you have no such evidence.

You claim “the program did not endorse their [Taubes’ and Lustig’s] theories or present them as fact.”

Could’ve fooled me, not to mention all the readers who wrote to me after the segment agreeing what a load of pseudoscientific, one-sided tripe it was. Your own narration, after all, follows up the above with the comment:

“That aside, exercise does have other health benefits that extend beyond weight loss.”

The inference is quite clear: Exercise doesn’t work for weight loss, but it does have other benefits.

Exercise does have many benefits – and weight loss is one of them. Why remove a major motivating factor for participation in exercise when the evidence simply does not warrant it?

I presented some of this evidence in my email to Demasi, and you simply ignored it.

Why can’t you acknowledge the evidence I cited showing as activity levels increase and calories burned from exercise increase, the incidence of overweight goes down?

Why do you ignore the thorough, all-encompassing reviews I cited from Titchenal and Elder and Roberts that show that the calorie burn from exercise consistently outpaces overall caloric intake and hence commonly results in weight loss? Did you bother to read those reviews and the studies cited within?

Nope, you clearly ignored this evidence and instead claim that “Catalyst advises that Taubes’ statement was based partly on literature from the American Heart Association and the American College of Sports Medicine who published joint guidelines for physical activity and health.  They did not conclude that physical activity would lead to weight loss, they concluded the following:

“It is reasonable to assume that persons with relatively high daily energy expenditures would be less likely to gain weight over time, compared with those who have low energy expenditures. So far, data to support this hypothesis are not particularly compelling.”

Do the folks at Catalyst not have any shame?

Mark, I advise that you need to stop with the politician-like carry on, stop insulting my intelligence, and start actually reading the research if you want me to take you seriously.

For your edification, the citation for the joint AHA-ACSM paper in question is:

Haskell WL, et al. Physical Activity and Public Health: Updated Recommendation for Adults from the American College of Sports Medicine and the American Heart Association. Medicine & Science in Sports & Exercise, 2007; 39 (8): 1423–1434.

I don’t have an online link for this one, but I’m sure someone in your office can scoot their butt down to the nearest uni library and retrieve it for you. If you bother to pull up the full text for yourself instead of relying on Taubes or your ass-covering cohorts over at Catalyst, you’ll discover someone somewhere along the chain of information delivery has deliberately cut that last sentence short. Here’s the full quote:

“It is reasonable to assume that persons with relatively high daily energy expenditures would be less likely to gain weight over time, compared with those who have low energy expenditures. So far, data to support this hypothesis are not particularly compelling (57), but some observational data indicate that men who report at least 45–60 min of activity on most days gain less weight than less active men (16).”

The bold section is the section that Catalyst left out (it is possible that they simply relied on Taubes for this quote, and he left out the bold section before forwarding it to them, but this would merely indicate that the Catalyst staff didn’t bother reading the paper for themselves).

I need to point out a few things here. The aforementioned recommendation paper, co-authored by the AHA and ACSM, was in fact an update of a joint statement first published in 1995 by the CDC and ACSM. It appears that after the AHA and ACSM joined forces, they really didn’t put a whole lot of effort into the update.

You’ll notice, for example, that they cite a grand total of one paper in support of their claim that evidence for a correlation between high energy expenditure and reduced overweight is “not particularly compelling”.  One single paper – that evidently is the best they could muster from all the literature on the subject! To make matters worse, that paper (reference #57) is not a study but in fact another statement paper by Saris et al titled “Outcome of the IASO 1st Stock Conference and consensus statement”.

And so we have the absurd spectacle of a statement paper citing another statement paper! Whatever happened to doing your own research and coming to your own conclusions?

Or is that too much like hard work?

That IASO statement paper, by the way, was published in 2003, so it clearly cannot discuss the Weinstein 2004 and Sulemana 2006 studies I cited in my email to Demasi[10,11]. Again, these studies show that “As physical activity levels/calories burned from physical activity increase, body mass index decreases in both adults and adolescents”. Do you and the folks from Catalyst have anything worthwhile to say about these studies, or are you just going to keep pretending they don’t exist?

While we are talking about the AHA-ACSM statement, let’s return for a moment to the “credible” and “responsible” nature of Gary Taubes, which you jokers over at the ABC apparently hold in such high esteem. Let’s also consider at this point the credibility of the AHA.

Along with Gary Taubes, I personally don’t think the AHA is a worthy source of info on anything these days; we’re talking the same mob, after all, that was instrumental in bringing us the pseudoscientific farce that is the cholesterol hypothesis of heart disease. The AHA is also the same mob that introduced the extremely questionable practice of taking monetary payments for the handing out of so-called “Heart Checks”.  Over the years, AHA-endorsed foods displaying these Heart Checks have included sugar-rich junk foods, juices and cereals – the very same foods that Demasi, Taubes and Lustig railed against in the “Toxic Sugar” segment!

And so while Taubes is quick to lambast the AHA and their low-fat theories, he is more than happy to cite them when they make a pathetically under-referenced statement that appears to support his fallacious claim that exercise is useless for fat loss!

I mean, really Mark? This kind of hypocrisy doesn’t bother you and the folks from Catalyst? Not even a little bit?

As for Taubes’ citation of “a 1989 Dutch study in which researchers trained couch potatoes to run a marathon. After 18 months of training and having run a marathon, the men lost 5 pounds of body fat; the women had 0 percent change in body composition.”

Again … did you or any of the Catalyst jokers bother reading the actual study?

Again, I think we both know the answer to that.

So here we go again, full text time:

Janssen G, et al. Food Intake and Body Composition in Novice Athletes During a Training Period to Run a Marathon. International Journal of Sports Medicine, May, 1989; 10 (Suppl 1): S17-S21.

C’mon’ Mark, read the study with me, it will be instructive.  You won’t even need to reach the end of the abstract to realize Taubes is up to his old tricks again.

As we begin reading through the paper, something quickly becomes evident:

This was not a weight loss study.

Again, repeat after me:

This was not a weight loss study.

It was simply an observational study that took a total of 18 men and 9 women and observed the subsequent dietary and physiological changes as they trained over an 18-month period for a 25km race (held at 12 months) and a marathon (at 18 months).

Once again, in case you missed it the first two (2) times:

Weight loss was not a goal of this study.

Nor was it unlikely to have been much of a concern for the folks involved, as the baseline characteristics show they were not overweight. Mean BMI in the men was 23.4 among the men, and even lower again among the women at 21.1.

Nevertheless, at 12 months, the men lost 2.8kg of fat and the women had lost 2.2kg.

At 18 months, 2-weeks prior to the marathon, when self-reported energy intake was highest among the women, the respective fat losses were 2.4 and 0.9kg, respectively. None of these differences reached statistical significance, hardly surprising given the size of the changes and the small number of subjects involved.

If this was a weight loss study, these would indeed be pretty uninspiring results. But, for the umpteenth time, it was a study of normal weight volunteers who were not trying to lose weight. In fact, food intake data showed the men slightly increased their caloric intake, while the women did not. Keep in mind this food intake data was self-reported, and that there is a wealth of research showing that study participants routinely under-report their food intake, and that women are far more prone to under-report their caloric intake than men[12-18]. That their weights remained relatively unchanged despite a marked increase in their weekly activity levels does indeed indicate (to those who are not brainwashed members of the Latter Day Church of Low-Carb) that the true caloric intakes were greatly underreported in this study.

And so out of all the relevant studies examining exercise and weight loss that Taubes could have discussed, he instead cherry-picks one that did not even attempt to induce weight loss in support of his fantasy-based anti-exercise stance!

And again, you jokers, evidently unable or unwilling to analyse the science for yourselves, fall for it hook, line and sinker.

Bloody brilliant.

By the way, in the very same issue of the International Journal of Sports Medicine, there was an article reporting the daily food and macronutrient intakes of Tour de France cyclists. Taubes can’t claim not to have seen it, because it was only 5 pages after the marathon study he so eagerly misrepresents:

http://world.edu/wp-content/uploads/2012/07/file1571.pdf

This study tracked five pro cyclists as they pounded their way through the Tour de France. At a mean bodyweight of only 69kg, they ingested, on average, a massive 849g of carbohydrate and some 5,800 calories daily. Despite these massive intakes, their weights barely changed during the gruelling 3-week event.

Carbohydrates make you fat and exercise is useless for fat loss?

What utter garbage.

But hey, just like the marathon trainees, these pro cyclists didn’t enter the Tour de France to sharpen up their six-packs. So let’s not fall into Gary’s trap and start wanking on about studies that didn’t even involve weight loss. Instead of cherry-picking irrelevant studies, Taubes needs to dramatically lift his game and start examining studies involving exercise in which the stated purpose was weight loss.

And because a little knowledge can be a dangerous thing, especially in the hands of a notorious cherry-picker like Gary, he needs to (be forced to) factor something very important into his analysis of these studies.

The problem with not an insubstantial number of the published clinical trials examining the impact of exercise on weight loss is their poor design. They’ll do things like take a bunch of obese free-living women, tell them to walk a few times a week, compare their body fat and weight losses after a few months, then proclaim the whole thing a failure when meaningful losses are not forthcoming.

But my dog (who, by the way, devours rice and pasta like there’s no tomorrow yet is much leaner than Taubes, Lustig or any of the other commentators on that woeful Catalyst segment) could easily point out the flaws inherent in these studies.

Huh? What’s that Ramone?

There’s no point in conducting an exercise trial for weight loss if you haven’t factored in the overriding importance of a calorie deficit?

G-o-o-d boy! Smart dog!

 They call him Ramone, The Chosen One. Faster over 1km of suburban streets than a speeding police car, able to leap 7-foot fences in a single bound, and infinitely smarter (and leaner) than any anti-carb diet ‘guru’.

Along with Ramone, non-insane humans know full well you can’t lose weight via dietary means without establishing a calorie deficit.

Yeah, I know, you note that “Taubes and Lustig believe that calorie restriction is difficult for people to maintain for a long period of time, and that lowering insulin by lowering carbohydrates is the option they would take.”

Do you understand what they are saying there, Mark? They are saying that by manipulating carbohydrate intake and lowering insulin, people can lose weight without lowering calories.

They say this even though this false claim has already been repeatedly disproved by tightly controlled clinical ward trials.

Again, I’d be happy to forward you the citations for these trials … you know, if you give a damn about them.

The reality is Mark, that if you, Demasi, Taubes, Lustig, Barclay, Cowley or anyone else on Planet Earth want to lose weight and you want that weight primarily derived from fat, you must create a calorie deficit. That’s an unavoidable law of nature, and it doesn’t magically suspend itself because you work for the ABC, nor because you are allegedly “one of Australia’s leading dieticians”, nor because you have an American accent with which you loudly espouse untenable theories on insulin and carbohydrates (as the photos capturing the prodigious bellies of Taubes and Lustig clearly demonstrate).

If you do lose non-fluid weight on a low-carb diet, it wasn’t because of carbohydrate restriction – it was because you lowered calories. Just because that calorie reduction may have been unintentional does not change one iota the fact that it occurred, and that it is the only reason you lost weight.

Even exercise is not immune to this reality. Exercise too must implemented in accordance with the laws of nature in order to produce fat-derived weight loss. You can’t burn a few extra hundred calories a week by mindlessly plodding on a treadmill, then ‘reward’ yourself with a few extra hundred calories of ice cream, then wonder why you haven’t lost weight.

That’s not a serious attempt at weight loss … it’s a complete toss.

Therefore Mark, if you want to see the true weight loss effects of intelligently-applied exercise, what you need to do then is go looking for exercise-weight loss studies that were conducted by researchers who understood the importance of a calorie deficit in both dietary- and exercise-based attempts at weight loss.

One of the reviews I’m betting Taubes never shared with you or the Catalyst crew, Mark, was conducted by Robert Ross, Jennifer A. Freeman, and Ian Janssen, from the School of Physical Health and Education at Queen’s University in Ontario, Canada.

I don’t have a link to a free full text, so you’ll need to add the following citation to your gopher’s library list:

Ross R, et al. Exercise alone is an effective strategy for reducing obesity and related comorbidities. Exercise and Sport Sciences Reviews, Oct, 2000; 28 (4): 165-170.

As the researchers note in the abstract:

“The commonly held view that exercise alone is not a useful strategy for obesity reduction is drawn from studies with limitations that confound interpretation. Recent evidence counters the dogma that daily exercise produces only modest weight loss and suggests that exercise without diet restriction is an effective strategy for reducing obesity and related co-morbidities.”

What kind of “limitations” are these clued-in Canadians referring to?

Exactly what my precocious pooch said before:

Failure to account for the overriding importance of a calorie deficit.

If you start exercising, but fail to exercise sufficiently, or offset your new increased calorie burn with an increased intake of Cheerios, then – not surprisingly – you will lose bugger all weight.

Ross et al begin their review by noting that in 1998, a group of ‘experts’ (I’m starting to develop a very, very deep distrust of that word) from the NHLBI and other NIH branches got together and had a “round table” session on the topic of obesity. In other words, they sat at a big table on swivel chairs, drank water and bad coffee for a few hours, and pretended to engage in ‘scientific’ discussion on a subject many of them clearly knew little of value about. From this collective charade, they then concluded, as did their buddies over at the AHA years later, that exercise alone was largely ineffective for weight loss.

If you think I’m being overly cynical, I’m not – this is exactly how the absurd cholesterol theory of heart disease became ‘official consensus’: via a NHLBI “Consensus Development Conference” in Maryland in 1984 (I detail the whole sordid story in my book The Great Cholesterol Con, of which I sent Demasi a free eBook copy. When she takes her next lunch break, sit down at her computer and read through Chapter 11, then tell me why we should trust any NIH ‘consensus’).

Like yours truly (and my savvy canine), Ross et al weren’t fooled. They knew something was rather fishy about the NIH-NHLBI exercise ‘consensus’, so they donned their bullshit-repelling skinsuits and dove head-first into the literature.

Here’s what they found:

“…in the vast majority of studies, individual energy intake and expenditure was neither rigorously controlled nor accurately measured.”

“Moreover, with few exceptions, the negative energy balance induced by exercise was modest to the degree that one would not expect substantial weight loss.”

“Indeed, no compelling evidence exists to support the observation that exercise alone is not useful for reducing total or abdominal obesity. In addition, evidence published after the consensus statements suggest that exercise without [dietary] caloric restriction is an effective method for reducing obesity and its comorbidities.”

What Ross et al did was scour through the research for randomized trials in which there was sufficient data to calculate the negative energy balance induced by diet and exercise, respectively.

I’ve reprinted Table 1 from their paper below. You’ll notice that in most of the studies, the diet groups had a significantly greater caloric deficit than the exercise groups. Not surprisingly, the diet groups in these studies lost more weight.

Take a close look at the last two studies listed in the table, the ones headed by Sopko and Ross (yes, the same Robert Ross who also headed the review we are discussing right now – he clearly enjoys doing real, properly-conducted research. If only there were more researchers like him). In both of these studies, the calorie deficit in the exercise and diet groups was identical. And so too was the subsequent weight loss.

In the Sopko et al trial, the authors rigorously ensured that the reduction in calories seen in the diet-only group was matched by an increase in expenditure in the exercise-only group. As a result, both groups maintained a deficit of 3500 calories per week, and after 12 weeks both groups lost 6.1kg (13.5lbs)[19].

In the Ross et al trial, the researchers implemented 700 calorie deficits in the diet-only and exercise-only groups. The latter achieved this 700-calorie burn by walking on a treadmill at 70% maximal heart rate (around 60% Vo2max) for 60 minutes daily. The researchers weren’t messing around; they verified 24-hour energy expenditure in all their groups with the doubly labelled water method. Over 12 weeks, both weight loss groups lost 7.5kg.

The total weight loss figures don’t tell the full story; in both trials, the exercise-only groups lost a greater percentage of weight in the form of fat.

Tell me again how exercise is useless for fat loss?

A summary of weight loss RCTs in which energy deficit was or was not matched between diet and exercise groups. When the energy deficit was the same in both groups, identical weight loss occurred. Unless your name is Gary Taubes or you work for the ABC, this should hardly come as a surprise.

Attention Mark, Catalyst, Gary Taubes: Please take careful note of how the thorough, no-bullshit approaches of Ross et al and Sopko et al are a stark contrast to simply taking a half-assed walk around the block, then exclaiming “whew, I’m knackered!” before dropping onto your couch and demolishing an entire box of muesli bars because, you know, you just worked out so hard and you deserve a little reward for your ‘excruciating’ effort.

The former will produce significant fat loss; the latter will simply lead to failure and provide fuel for duplicitous anti-carb gurus to appear on shows like Catalyst making blatantly misleading claims about exercise.

So instead of roundly and wrongly dismissing exercise as “useless” for fat loss, a far more honest thing for Gary Taubes to say would be:

“If you treat it like some kind of joke and institute it in a half-assed manner, then yes, exercise is very likely to be a waste of time for fat loss. Duh! But if you act like a mature, intelligent adult who is prepared to take responsibility for his physical condition, acknowledge the reality of calories in versus calories out, and exercise like you mean it most days of the week, then exercise is actually very effective for weight loss!”

Of course, saying a distinctly non-sensationalist thing like the above probably won’t grab him the same kind of attention as making sweeping and controversial statements like “exercise is useless for fat loss!” But Taubes is now being enlightened as to the truth about exercise, so his stance from this point on will tell us whether he’s more interested in the truth or whether he’s more interested in continuing to grab attention with sensationalist and patently false claims.

Ditto for the ABC.

Before I finish on the topic of exercise, I think it’s worthwhile to discuss some especially well controlled trials. Ward studies involving exercise, unfortunately, are very rare … much rarer than ward diet studies. But they’re out there.

One of these was conducted by James Hill and his colleagues at the Vanderbilt University School of Medicine, in Nashville, Tennessee. They took obese women (140-180% of ideal body weight) and studied them in a metabolic ward during 1 week of maintenance feeding, followed by 5 weeks of an 800 cal/day liquid formula diet. Five subjects participated in a supervised program of daily aerobic exercise and three subjects remained sedentary.

So what happened?

At this extremely low calorie intake, total weight loss was not different between exercising and non-exercising groups, but don’t get too excited, this in no way supports the anti-scientific bollockery of Taubes. The exercising subjects lost 74% of their weight as fat and only 26% in the form of fat-free mass. The non-exercisers, in contrast, lost only 57% of weight as fat but a hefty 43% as fat-free mass. The exercisers, in other words, lost significantly more fat and significantly less fat-free mass than the subjects who did not exercise.

Exercise is useless for fat loss?

I think not.

The most recent ward trial of exercise and weight loss I’m aware of was conducted by Nancy L. Keim and her colleagues from the USDA’s Western Human Nutrition Research Center in San Francisco. They performed a study involving ten overweight women utilizing diet plus exercise or diet only. At the beginning of the study, the women were subjected to a two-week weight stabilization period where they were fed just enough calories to maintain their weight (median intake of approximately 2,450 calories). The researchers then divided the women into two groups. One group kept eating their ‘maintenance’ diet for 12 weeks, and performed treadmill exercise 6-days a week. The second group performed the same exercise routine, but also had their calorie intake slashed in half for the duration of the 12-week period.

At the conclusion of the study, the group that added exercise to their maintenance-calorie diet lost an average 0.5 kilograms per week. The women who utilized exercise and calorie-restriction lost an average 1.1 kilograms per week – over twice as much as the exercise-only group[21]. These results should come as no surprise to anyone; after all, a greater calorie deficit equals greater weight loss[22].

So here’s the bottom line Mark: When the NHLBI, AHA, ACSM, Catalyst, and Gary Taubes proclaim exercise as being “useless” or of “limited efficacy” for fat loss, they are not accurately representing the science. To the contrary, they are merely showing off their scientific ineptitude for all the world to see.

Don’t encourage them, for chrissakes.

Package for Robert Lustig. Contents: The Sweet Truth

Mark, I need to wrap this up. Unlike you lot, I’m not being paid to do this – unfortunately, I have to debunk fallacious nonsense on my own time and at my own expense (one of the very sad realities of our world is that the dissemination of sensationalist bullshit is a highly lucrative endeavour. Telling the truth? Not so much).

So I think I’ll wrap this up with a little present for Robert Lustig. I mean, I’ve focused mainly on Taubes in this reply and I don’t want poor Rob to feel like Gary’s stealing his limelight.

Judging from his appearance on Catalyst, Robert Lustig is an angry man. I mean, listen to him going off at 0:25 in the Catalyst video – his rage at the suggestion that calories were responsible for the obesity epidemic is palpable. Hey, nothing wrong with getting indignant about something that really is bullshit, but for Lustig to be getting so bent out of shape over a contention that is in fact 100% correct is most unbecoming.

So how can we help Dr Lustig get over his terribly misdirected anger?

Well, I find discovery of the truth to be a very clarifying and uplifting experience, so hopefully Robert will find the same. To that end, I present research showing that when consumed in isocaloric amounts, there is sweet FA difference in weight loss or gain between low- and high-fructose diets, and low- and high-sucrose diets.

Why Sugar Doesn’t Do jack to Make You Fat Unless You Consume Enough to Create a Calorie Surplus

Researchers have been studying the effects of increased sugar intake on subsequent bodyweight changes for decades. After reviewing these trials, I can sum their findings up quite simply:

–If an increase in sugar intake results in an increase in caloric intake, weight gain will occur.

–If an increase in sugar intake is compensated for by a decrease in other non-sugar calorie-containing foodstuffs, so that overall caloric intake remains unchanged, weight remains unchanged.

I’m hardly the only one to have arrived at these conclusions. Lisa Te Morenga, Simonette Mallard and Jim Mann from the University of Otago in New Zealand conducted an extensive review of these same trials, and published their results in the British Medical Journal. You can access their paper freely right here:

http://www.bmj.com/content/346/bmj.e7492.pdf%2Bhtml

In their review of clinical feeding trials, they found:

“In trials of adults with ad libitum diets (that is, with no strict control of food intake), reduced intake of dietary sugars was associated with a decrease in body weight (0.80 kg…P<0.001); increased sugars intake was associated with a comparable weight increase (0.75 kg…P=0.001).”

And when overall caloric intake remained unchanged?

“Isoenergetic exchange of dietary sugars with other carbohydrates showed no change in body weight”.

They concluded:

“Among free living people involving ad libitum diets, intake of free sugars or sugar sweetened beverages is a determinant of body weight. The change in body fatness that occurs with modifying intakes seems to be mediated via changes in energy intakes, since isoenergetic exchange of sugars with other carbohydrates was not associated with weight change.”

In other words, the only way sugar can make you fat is by increasing your overall caloric intake.

One more time, for those who are a little slow off the mark:

INSULIN AND CARBOHYDRATES, INCLCUDING SIMPLE SUGARS, DO NOT AND CANNOT MAKE YOU OVERWEIGHT INDEPENDENT OF CALORIES.

Contrary to the rantings of Lustig, there is nothing inherently fattening about sugar aside from the fact that it is a calorie-dense substance that often lends itself to overconsumption. There is nothing in sugar that causes some bizarre metabolic derangement that subverts the laws of nature and causes unexplained weight gain in the absence of a calorie surplus. To claim otherwise is simply another disingenuous exercise in the dissemination of anti-calorie bullshit.

So what people need to be told is something like the following:

Consuming a surplus of calories – whether it be from sugar, starch, fat, protein or alcohol – for a sufficient length in time will cause bodyweight and bodyfat gain. Some foods and beverages lend themselves to overconsumption due to their low volume and high concentration of calories. Highly palatable foods and beverages that are high in sugar, high in fat, or both, or high in alcohol, are more likely to lead to caloric surpluses. Because of this ability to promote caloric overconsumption, consumption of these foods and beverages should therefore either be avoided or compensated for by concomitant decreases in other caloric sources by those wishing to either lose weight or avoid weight gain.

It should be noted that even when consumed in a manner that does not lead to weight gain, high intakes of sugar-rich foodstuffs and beverages can be problematic for other reasons. Regular consumption of sugar-rich beverages and foods has been implicated in accelerated tooth decay, for example. In sedentary individuals, isocaloric diets containing high amounts of simple refined sugars can also increase visceral and liver fat deposition even though overall bodyweight remains unchanged.

Except when consumed during or immediately following vigorous exercise (the former of which has been repeatedly shown to improve performance in endurance activities and the latter of which promotes accelerated glycogen repletion after exercise), there is little reason for healthy human beings with normal digestive function to consume liquids rich in simple sugars. When consumed away from exercise, sugars should be consumed in the manner nature intended – as part of whole, minimally processed foods.

That is a far more truthful, accurate and balanced appraisal of the science than such bombastic Lustig-style hysteria as:

“An excess of calories and lack of exercise caused the obesity epidemic? GET REAL!! It was insulin, assholes! INSULIN release caused by poisonous sugar, I tell you!!”

It’s also far more sensible and, sadly, modern society seems to have little time or regard for common-sense. Telling people they can eat sugar without fear of weight gain so long as they consume it only in small amounts would mean they have to exercise such traits as restraint and moderation.

Yeah, I can hear some of you sniggering. Those are out-dated concepts that only anachronistic old farts stuck in the 1950s would ever dare recommend, I hear you sneering.

Well guess what? There was no obesity epidemic back in the 1950s.

Yeah, think about that.

One cannot have his cake and eat it, my friends.

Stupid is as Stupid Does

I must state clearly – before I am deliberately misquoted by the sleazy anti-carb crowd – that I am not “pro-sugar”. I’m just anti-bullshit. And to be quite honest, while I’m not pro-sugar, I’m not anti-sugar, either. When consumed in judicious amounts, the harm that will be caused to you by sugar would probably rank right between zero and bugger all. I have numerous Italian relatives who lived into their nineties, and they all added zucchero to the percolated coffee they drank on a daily basis. What they didn’t do was gulp, slurp, burp and fart their way through idiotic amounts of soft drink, fruit juice, and confectionery. It’s sad that as a result of the Anglo-Western predilection for dietary excess, the baby always seems to get thrown out with the bath water.

Heaven forbid we start promoting such concepts as self-responsibility and temperance in our habits. Hell no. This is the 21^st century, where people earnestly seem to believe they should be able to do whatever they want, whenever they want, and suffer absolutely no adverse consequences as a result. As a result of this delusional, reality-evading mindset, a lot of people earnestly seem to believe it is their birth right to be able to sit on their fat asses all day, eat whatever they damn well please, do no exercise, yet still sport the low body fat levels they once enjoyed in their teenage years. And anyone who comes along and tells them this is an unreasonable and untenable attitude is met with a barrage of vitriol. Meanwhile, those who are only too happy to fan the flames of bullshit by telling people that calories are inconsequential, that we’re all just victims of some big evil carbohydrate conspiracy, and that “calories in versus calories out is how we got into this mess” are met with much fawning, media attention, and lavish book deals. There’s a lot of money to be made by telling people what they want to hear and convincing them they’re just poor hapless victims.

Guess what? Contrary to the rabid rantings of Dr “Sugar is a Poison!” Lustig, calories in versus calories out is not how we got into this mess.

IGNORING calories in versus calories out is how we got into this mess!

And spouting a load of untenable bullshit about insulin and carbohydrates sure as hell isn’t going to get us out of it.

Both the NHANES and USDA data indicate that per capita caloric intake increased during the very same period that the obesity ‘epidemic’ occurred. At the same time, rapidly increasing automation has ensured that we are now the most sedentary population in the history of Homo sapiens.

And in spite of this, Robert Lustig claims the reason this obesity epidemic occurred is because people were awarding too much respect to the calories in versus calories out paradigm!

How on Earth can increasing caloric intake coupled with unprecedented levels of sedentary living reflect a failure of the calorie deficit approach to weight loss?!

It doesn’t: It reflects a complete and utter disregard by the population at large for the calorie deficit approach!

As the furious Lustig himself would say:

“GET REAL!!”

This, ladies and gentlemen, is what Maley and the crew from Catalyst consider a “credible” and “responsible” commentator.

Geezus.

You may have heard of a little thing called the low-carb craze, Mark? Came, failed, and fizzled out. Why Lustig and Taubes and the rest of their carb-hating cohorts (and now the ABC) keep trying to flog a dead horse is beyond me.

Yep, welcome to Generation Sook, folks. The tech-laden generation that enjoys the most automated existence in the history of mankind, who will never know the need for the backbreaking labour that was an inevitable part of our forebears daily lives, yet pisses and moans when someone has the temerity to suggest that maybe they shovel a little less shit down their throats and spend 6 or 7 of the 168 hours that comprise a calendar week (i.e. less than 5% of their otherwise sedentary, inactive week) doing some exercise.

I can just see all my hardy late long-lived relatives – no strangers to physical and economic hardship – turning in their graves, face-palming and exclaiming in disbelief:

“Che mucchio di cazzi molli!”

(“What a bunch of soft-cocks!”)

In Closing

Mark, when you folks at the ABC launched your non-independent “independent” investigation, you had the opportunity to right a wrong. You guys had the opportunity to man up, admit that the folks at Catalyst slipped up, and put into place procedures and safeguards to make sure it didn’t happen again.

Instead, you simply chose to cover your asses. I don’t know exactly what occurred during your investigation, but it certainly wasn’t anything intelligent and impartial. Your reply to me is a truly intelligence-insulting catalogue of denial and further false claims.

It is also clear that you have not read the research you cite – if you did, you clearly didn’t understand what you were reading.

What’s especially regrettable about all this is that the ABC, and hence its so-called ‘science’ shows, are funded by the taxpayer. It’s bad enough when the commercial networks bullshit us, but when poor Joe Public funds your existence, and you reward his patronage with content that blatantly misleads him, then that is rather galling.

If I was in charge of whatever government agency had the authority to make you jokers lift your game, I’d designate a number of measures to correct the clear lack of scientific process at the ABC. And until I was satisfied all those procedures were in place and having the desired effect, I’d force your ‘science’ shows to prominently display the following disclaimer at the start of every episode:

“The AABC (Australian Anti-Bullshit Commission) advises that the ABC (Australian Broadcasting Corporation) has been reprimanded for airing misleading content. This content consisted of statements about fat loss that were presented as scientific findings, but were in fact purely the unfounded and already disproved opinions of a small number of handpicked guests, some of whom benefit financially from disseminating the aforementioned false claims. The AABC has instructed the ABC to cease and desist in airing all such misleading content. Until such time as the AABC is fully satisfied that the ABC has ceased in airing misleading content, and has fully instituted the preventive measures recommended by the AABC, the AABC advises that viewers should treat any ‘science’ program on the ABC as being purely for entertainment purposes only. Until these requirements have been met, viewers are strongly advised not to make any decisions that could affect their physical or psychological wellbeing based upon information they may have viewed on any ABC ‘science’ show.”

My original appraisal remains unchanged: With few exceptions, journalists as a group consistently display remarkable gullibility when it comes to the acceptance of untenable health claims, and display a woeful inability to read and understand research for themselves. From what I have seen from their televised content and from my subsequent correspondence with ABC representatives, the journalists at Catalyst are certainly no exception.

Adios,

Anthony “Get Real For Real!” Colpo.

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10. Sulemana H, et al. Relationship between Physical Activity and Body Mass Index in Adolescents. Medicine & Science in Sports & Exercise, 2006; 38 (6): 1182–1186.
11. Lichtman SW, et al. Discrepancy between self-reported and actual caloric intake and exercise in obese subjects. New England Journal of Medicine, Dec 31, 1992; 327 (27): 1893-1898.
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21. Stanko RT, et al. Body composition, nitrogen metabolism, and energy utilization with feeding of mildly restricted (4.2 MJ/d) and severely restricted (2.1 MJ/d) isonitrogenous diets. American Journal of Clinical Nutrition, 1992; (56): 636-640.

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Anthony Colpo is an independent researcher, physical conditioning specialist, and author of The Fat Loss Bible and The Great Cholesterol Con. For more information, visit TheFatLossBible.net or TheGreatCholesterolCon.com

Copyright © Anthony Colpo.

Disclaimer: All content on this web site is provided for information and education purposes only. Individuals wishing to make changes to their dietary, lifestyle, exercise or medication regimens should do so in conjunction with a competent, knowledgeable and empathetic medical professional. Anyone who chooses to apply the information on this web site does so of their own volition and their own risk. The owner and contributors to this site accept no responsibility or liability whatsoever for any harm, real or imagined, from the use or dissemination of information contained on this site. If these conditions are not agreeable to the reader, he/she is advised to leave this site immediately.

The whole-grain cereal myth would have you believe all sorts of awesome health benefits await if only you’d swap your white bread for brown and start eating brown rice instead of white.

While politically correct, this claim is scientifically very incorrect. In fact, it’s complete rubbish.

In Part 1, we traced the origins of the fantasy-based whole-grain cereal hypothesis. It began in the early 70s when Denis Burkitt, a UK researcher with a rather odd fascination for human faeces, claimed that a lack of cereal fibre caused diverticulitis. He promptly expanded his theory to include fibre ‘deficiency’ as a cause of other chronic diseases such as colorectal and breast cancers.

As explained in Part 1, Burkitt formed his hypothesis, not by anything resembling thorough scientific scrutiny, but by a mix of creative thinking and evasion of contradictory evidence. Nevertheless, thanks to his prior and admirable achievements as a missionary in Africa and the appalling lack of scientific rigor so regrettably pervasive among our ‘health authorities’, Burkitt’s claims were readily accepted as fact. It’s now over forty years since Burkitt first published his theory, and there is still no controlled evidence to support the cereal fibre thesis. Yet health organizations, researchers, book authors, journalists, dieticians, and scores of others who pretend to know something worthwhile about nutrition stubbornly persist in claiming whole-grains are good for us.

In Part II, you’ll learn just how wrong these folks are. Discover the clinical trial evidence showing whole-grains are more likely to hurt than help your health!

Read more:

http://180degreehealth.com/2013/09/healthy-grains-part-ii

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Anthony Colpo is an independent researcher, physical conditioning specialist, and author of The Fat Loss Bible and The Great Cholesterol Con. For more information, visit TheFatLossBible.net or TheGreatCholesterolCon.com

Copyright © Anthony Colpo.

Disclaimer: All content on this web site is provided for information and education purposes only. Individuals wishing to make changes to their dietary, lifestyle, exercise or medication regimens should do so in conjunction with a competent, knowledgeable and empathetic medical professional. Anyone who chooses to apply the information on this web site does so of their own volition and their own risk. The owner and contributors to this site accept no responsibility or liability whatsoever for any harm, real or imagined, from the use or dissemination of information contained on this site. If these conditions are not agreeable to the reader, he/she is advised to leave this site immediately.

by George Monbiot

This will not be an easy column to write. I am about to put down 1,200 words in support of a book that starts by attacking me and often returns to this sport. But it has persuaded me that I was wrong. More to the point, it has opened my eyes to some fascinating complexities in what seemed to be a black and white case.

In the Guardian in 2002 I discussed the sharp rise in the number of the world’s livestock, and the connection between their consumption of grain and human malnutrition. After reviewing the figures, I concluded that veganism “is the only ethical response to what is arguably the world’s most urgent social justice issue”. I still believe that the diversion of ever wider tracts of arable land from feeding people to feeding livestock is iniquitous and grotesque. So does the book I’m about to discuss. I no longer believe that the only ethical response is to stop eating meat…

Read the full article here:

I was wrong about veganism. Let them eat meat – but farm it properly.

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Anthony Colpo is an independent researcher, physical conditioning specialist, and author of The Fat Loss Bible and The Great Cholesterol Con. For more information, visit TheFatLossBible.net or TheGreatCholesterolCon.com

Copyright © Anthony Colpo.

Disclaimer: All content on this web site is provided for information and education purposes only. Individuals wishing to make changes to their dietary, lifestyle, exercise or medication regimens should do so in conjunction with a competent, knowledgeable and empathetic medical professional. Anyone who chooses to apply the information on this web site does so of their own volition and their own risk. The owner and contributors to this site accept no responsibility or liability whatsoever for any harm, real or imagined, from the use or dissemination of information contained on this site. If these conditions are not agreeable to the reader, he/she is advised to leave this site immediately.

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