|
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
Related articles
Common
myths about low carbohydrate diets
Just how low will the anti-low carb crowd go?
|
