Did the Atkins Diet Really Kill Dr. Atkins?

Science, not scare-mongering, should be dominating
the low-carbohydrate versus low-fat diet debate.


By Anthony Colpo.

February 17, 2004.

Dr. Robert Atkins was never a stranger to controversy. His high-fat, low-carbohydrate dietary guidelines contradicted virtually every closely-held tenet of mainstream nutrition, bringing him under constant attack from defenders of the low-fat diet doctrine. Atkins died in April last year from a head injury he sustained after falling on an icy New York footpath, but his demise has done little to stem the controversy surrounding his dietary recommendations. As the recent commotion surrounding the New York diet guru's death report clearly illustrates, his nutritional legacy is still a subject of heated debate.

The current uproar began after a Nebraska-based cardiologist by the name of Richard Fleming wrote to the New York medical examiner's office requesting a copy of Atkins' death report. Despite the confidential nature of such reports, someone at the office readily obliged Fleming, who, after receiving the report, passed a copy along to his acquaintances at the Physicians Committee for Responsible Medicine (PCRM). The PCRM in turn contacted the Wall Street Journal, who broke the story and ignited a world-wide debate in the process.

The ease with which the PCRM has been able to cause such an uproar is a sad indictment of the woefully inadequate investigative methods employed by many journalists reporting on health and nutrition issues. As an independent researcher, one of the first things I do when studying new information is to verify its source. Foremost among my concerns is whether or not the information has come from someone with a vested interest, and whether the information is being issued in order to advance some sort of concealed agenda.

If certain journalists had bothered to investigate the PCRM's background, for instance, they would have had little difficulty in discovering that this group of so-called "physicians" is little more than a band of radical vegan activists with a long history of distorting facts in order to advance their agenda. PCRM president Neal Barnard, for instance, has been quoted as saying that: "Meat consumption is just as dangerous to public health as tobacco use", and: "To give a child animal products is a form of child abuse."

It was only in December last year that the Center for Consumer Freedom recently revealed that the PCRM has long-standing ties with People for the Ethical Treatment of Animals (PETA), an extreme animal rights organization that has funneled over $850,000 to its "physician" front group. The Center reported that Barnard, a non-practicing psychiatrist, co-chairs the PETA Foundation with PETA co-founder Ingrid Newkirk.

In addition to banishing every last trace of animal products - meat, poultry, seafood, dairy, eggs - from our diet, PETA have repeatedly stated their goal is "total animal liberation." This means no pets, no zoos, no circuses, no fishing, no leather, no animal testing for lifesaving medicines - heck, even guide dogs for the blind would go the way of the dodo if the folks from PETA had their way. PETA has repeatedly attacked groups like the March of Dimes, the Pediatric AIDS Foundation, and the American Cancer Society, for conducting animal testing to find cures for birth defects and life-threatening diseases.

In order to help achieve their goal of animal liberation, PETA has given thousands of dollars to convicted arsonists and other violent criminals. PETA has links to a violent animal-rights group called Stop Huntingdon Animal Cruelty (SHAC). In August 2002, nine SHAC extremists were arrested near San Antonio for harassing a Marsh insurance executive at his home. During the same month, a British SHAC member was sentenced to 54 months in prison for threatening to kill several of Huntingdon Life Sciences' investment and banking managers.

PETA has also used their contributors' tax-exempt donations to fund the Earth Liberation Front, a criminal organization that the FBI has labeled a "domestic terrorist group".

So much for the PCRM.

What about Richard Fleming, the Omaha, Nebraska cardiologist who obtained Atkins' death report under such highly dubious circumstances? Fleming is an outspoken critic of high-protein, low-carbohydrate diets, and just happens to be the author of the only published study to have ever found greater weight loss in individuals randomized to follow a high-carbohydrate, low-fat diet than individuals following a low carbohydrate diet.

If legitimate, Fleming's study is indeed a landmark, for every other published randomized clinical trial has found either greater weight loss among those assigned to follow low carbohydrate diets, or statistically insignificant differences (the non-significant difference, by the way, invariably favoring the low carbohydrate dieters). In addition to being the only trial in which high-carbohydrate dieters reportedly lost more weight than low carbohydrate dieters, Fleming's paper reported some truly unique blood-test findings. While Fleming's high-carbohydrate dieters recorded marked triglyceride reductions, the low-carbohydrate dieters experienced an initial modest decrease, which then reversed itself and ended up slightly higher than baseline levels by the end of the study. If these results are genuine, then Fleming's study is again a milestone in nutrition research history, as every other relevant study has found low-carbohydrate diets to produce either similar or greater reductions in blood triglycerides than calorie-restricted high-carbohydrate diets.

A close look at Fleming's paper, which was published in a lesser-known journal called Preventive Cardiology, suggests that it may be more than mere co-incidence that the only non-supportive low carbohydrate weight-loss study comes from someone who just happens to be an avid critic of high-protein, low-carbohydrate diets.

Fleming claims that one hundred men and women were placed on one of four diets (a low carbohydrate diet, one of two low-fat, high-carbohydrate diets, or a "high-fat" diet) then followed for one year. This would make Fleming's trial one of the largest and longest-running - and hence, most expensive - high- versus low-carbohydrate diet trials ever conducted. As any clinical investigator will tell you, conducting randomized intervention trials is a costly, difficult, and time-consuming task. Even small trials can easily cost hundreds of thousand dollars; as a recent example, recruitment for the Diabetes Prevention Program, a randomized, controlled trial designed to test whether diet and exercise or medication can prevent or delay the onset of type 2 diabetes in susceptible individuals, was estimated to cost $1,075 for each participant. This figure was purely for recruitment, and did not include staff costs! In addition to enlistment, clinical trials employing dietary interventions and regular blood testing require substantial manpower in the form of investigators, nurses, dietitians, and technicians.

Despite the significant number of participants and the extended duration of Fleming's trial, his paper does not list a single source of funding, even though funding acknowledgement is standard procedure in any respected, peer-reviewed journal article. The Preventive Cardiology paper also lists no co-authors, nurses, dietitians, or technicians who may have assisted in the trial which, again, is par for the course in published papers. Fleming identifies himself as the "Medical Director of Preventive Cardiology, The Camelot Foundation at The Fleming Heart & Health Institute", but a visit to his web site indicates that this Institute has one lone member - Fleming! How did Fleming fund such an expensive undertaking? And how did he manage to conduct such a time-consuming project with so little, if any, assistance? Your guess is as good as mine...

Science reporter Gary Taubes has little doubt as to the validity of the Omaha cardiologist's findings; "Frankly, I think Fleming made it [the data] up," he told a Washington Post reporter (an accusation hotly denied, of course, by Fleming). In addition to the aforementioned anomalies, Fleming wrote that the participants "were randomly assigned to one of the four dietary regimens based upon dietary preferences." Such a description is a contradiction in terms if ever there was one. As Taubes pointed out; "If patients were assigned to diets based on their dietary preferences, then they weren't randomly assigned. If they were randomly assigned, then their preferences must be irrelevant. The two methods are incompatible. If this paper was peer-reviewed, it was done poorly. If this constitutes high-quality research in this field, then I suggest even more skepticism is necessary."

Call me a hopeless skeptic, but any information originating from the likes of the PCRM or Richard Fleming should be met with extreme caution.

Which, of course, brings us to the actual contents of Atkins' death report. Does it really implicate low carbohydrate nutrition as the cause of the late diet guru's untimely demise?

According to the Wall Street Journal, the medical report stated that Atkins weighed 255 lbs (116kg) at the time of his death. An Atkins company statement released in response to the WSJ article vehemently refuted the obesity charge, claiming that Atkins weighed 196lbs (89kg) at the time of his accident, and gained weight while in a coma. "As he deteriorated and his major organs failed, fluid retention and bloating dramatically distorted his body," the statement said.

Indeed, swelling (edema) from fluid retention is not at all uncommon in heart failure, a condition from which Atkins suffered. As blood flow out of the heart slows down, blood returning to the heart backs up, causing congestion in the tissues. Heart failure also affects the kidneys' ability to shed sodium and water, thereby aggravating the water retention.

Because no autopsy was performed on Atkins' corpse, any speculation as to whether his excess weight was from fluid retention or excess body fat is just that - speculation. So too is any conjecture over the true nature of Atkins' heart condition. While it was well known that Atkins suffered from viral-induced cardiomyopathy in his final years - the late guru openly discussed his condition on national television - his critics are now claiming that atherosclerotic heart disease played a major role in his death. In contrast to cardiomyopathy, which is often instigated by genetic pre-disposition, birth defects, or viral infections, atherosclerotic heart disease is believed to be influenced most heavily by dietary and lifestyle factors.

According to a statement released by Atkins' wife Veronica, his coronary arteries showed only minimal and clinically insignificant signs of atherosclerosis when he was diagnosed with cardiomyopathy four years ago, "consistent with what would be expected in a 69-year old man". There's nothing earth-shattering there - arterial hardening is an inevitable part of aging, and even the healthiest and fittest amongst us will have at least some evidence of atherosclerosis by the time we reach our seventies. According to Veronica, "Robert did have some progression of his coronary artery disease in the last three years of his life including some new blockage of a secondary artery ... He did not have a heart attack."

Veronica Atkins then goes onto identify what is without question the most regrettable aspect of this whole messy affair: "I now find myself in the uncomfortable position of having to relive my late husband's horrific accident and defend him from people who would convince you that stolen and irrelevant bits and pieces of his medical history carry more validity than published scientifically controlled and peer-reviewed research out of Harvard, Duke University, the American Heart Association and the National Institutes of Health."

The fact that Atkins' accidentally-leaked death report, the contents of which were not based on autopsy and are the subject of considerable speculative conjecture, has been allowed to hi-jack the entire low-carbohydrate versus low-fat diet debate - even if only temporarily - is appalling. The outcome of this debate has the potential to affect the lives and well-being of millions of people around the globe, and should at all times be based on nothing other than scientific facts. That this critical debate has been derailed by muck-raking vegan activists is a very sad testimony to the ability of scare-mongering hype to triumph over both science and plain commonsense.

Those who place more weight on scientific reality than vegan propaganda may wish to avail themselves of the following findings, all of which have been published in peer-reviewed journals:

  • Apart from Flemings' suspect trial, there have been over a dozen randomized dietary intervention trials published since the mid-eighties, ranging in duration from four weeks to one year, that directly compared the weight-loss efficacy of low- and high-carbohydrate, low-fat diets. None of these - not one - has shown superior weight loss on the latter. In every study, low carbohydrate diets produced either markedly superior weight loss or statistically non-significant differences in weight loss.
     
  • In addition to spiraling obesity rates, we are currently experiencing an epidemic of type 2 diabetes, the prevalence of which began accelerating skywards soon after orthodoxy embraced the low-fat, high-carbohydrate paradigm. Dozens of studies have compared the effects of low- versus higher-carbohydrate diets on blood glucose control and, in virtually every instance, the carbohydrate-restricted regimens produced superior results. Given that the United Nations has forecast over 300 million diabetics worldwide by 2025, the potentially beneficial public health implications of carbohydrate-restriction are enormous.
     
  • Low carbohydrate diets are proving themselves to be invaluable in the most surprising of circumstances. High-protein diets have been traditionally regarded as a no-go zone for individuals with kidney impairment, but in a recent issue of Diabetes, Italian researchers reported that a special low-carbohydrate, unrestricted protein diet, based on low-iron foods, produced dramatic benefits in patients with advanced kidney disease. Compared to patients following a traditional low fat, low-protein, high-carbohydrate diet, those on the low-iron, low-carbohydrate diet were 50% less likely to progress to the point where they either died or required kidney replacement. Very low carbohydrate, or ketogenic, diets are also a well-established and effective treatment for childhood epilepsy.
     
  • Low-carbohydrate diets may eventually prove themselves to have life-extending properties. In animal research, the only consistent intervention that produces increases in life span is calorie-restriction. Whether the same applies to humans has not yet been established, but we do know that cutting calorie intake often produces marked improvements in important health parameters, such as blood glucose control. Unfortunately, telling people to voluntarily limit their calorie intake on a long-term basis is usually about as well-received as Janet Jackson's recent Super Bowl performance. Low carbohydrate diets, however, may render such unpopular admonitions redundant. Dietary intervention studies have revealed a rather unique phenomenon; subjects following low carbohydrate diets, despite being told to limit only carbohydrate intake and to eat unrestricted amounts of protein and fat, often inadvertently reduce their total calorie intake to levels similar to those seen in subjects who have been explicitly instructed to lower their total calorie intake.
     
  • The possible life-extending effects of low carbohydrate diets have not escaped the attention of longevity researchers at Baltimore's National Institute of Aging. In a recent journal article they stated: "The Atkins Diet is ketogenic resulting in reduced appetite and therefore a reduced calorie intake; individuals who can comply with the diet may therefore exhibit some physiological changes observed in rodents and monkeys subjected to caloric restriction including reduced body weight, and decreased insulin and glucose levels." The researchers, however, expressed reservations about the alleged cardiovascular harm arising from low-carbohydrate diets that are high in saturated fat. Why such concerns are completely unfounded is the next point of discussion.
     
  • Despite widespread acceptance of the notion that saturated fat-induced cholesterol elevations lead to heart disease, controlled dietary intervention trials have shown dietary cholesterol-lowering to be a complete and utter failure in fighting heart disease. Three double-blind studies have examined the impact of saturated fat-restriction on heart disease mortality; two of these, the National Diet-Heart Study and the Minnesota Survey, showed no benefit. The third, the Los Angeles Veterans Administration Study, did show a noteworthy decrease in CHD fatalities among the treatment group, but the results were biased by a significantly higher proportion of heavy smokers in the control group. Despite this advantage, the treatment group still suffered a significantly higher frequency of cancer deaths which neutralized the mortality reduction from CHD. The total death count in each of the two groups after eight years was virtually identical. One can't help but wonder what the result would have been had there been a similar proportion of heavy smokers in both treatment and control groups.

    The only cholesterol-lowering intervention that has produced any noteworthy decrease in CHD mortality in double-blind trials is the use of statin drugs. However, a rapidly-growing body of research clearly shows that statins work by means other than cholesterol-lowering. Statins possess potent anti-inflammatory, artery-dilating actions not shared by their largely-ineffective predecessors, a group of drugs known as fibrates. A close look at the data from all of the major controlled, randomized clinical trials with statin drugs reveals that there is no association between the degree of total cholesterol lowering and coronary mortality. In other words, the risk of a fatal heart attack is similarly reduced whether cholesterol levels were lowered by a small or large amount. The same applies to LDL, which we have been brainwashed into believing is the "bad" cholesterol; death rates in those with the highest and lowest LDL levels are virtually identical. The sole exception is the recent PROSPER trial, which recorded the highest survival rates in both the treatment and control groups among those with the highest LDL levels.

All the existing and emerging evidence points to the same conclusion: low carbohydrate diets hold the potential to improve the health of millions worldwide. In order to find out how these diets can impact upon various health conditions, and how they can be best constructed to meet the widely-varying needs of individual users, continued research into these diets should be an absolute priority. However, it appears that after years of vilifying high-fat diets and promoting high-carbohydrate nutrition as the key to weight loss and well-being, many health commentators are more concerned with saving face than saving millions of people from the misery and suffering that goes hand-in-hand with degenerative illnesses such as obesity, diabetes, and heart disease.

Anthony Colpo is an independent researcher and certified fitness consultant with 20 years' experience in the physical conditioning arena. To contact: contact@theomnivore.com

Disclaimer: This article is presented for information purposes only and is not intended as medical advice. Persons with medical conditions should institute dietary changes whilst being monitored by a competent medical practitioner.

Anthony Colpo 2004.  http://www.theomnivore.com



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