If Everybody Believes the Same Thing, It Must Be True, Right? Wrong!

Anthony Colpo,
October 2, 2004.

Hi Anthony,

Thanks for your site, perhaps the very best. I have been re-reading Loren Cordain's writings [note: Cordain is the author of The Paleo Diet and a contributor to BeyondVeg.com] and have some problems. Loren seems to have accepted the diet heart myth; he states that polyunsaturated fats lower blood cholesterol while saturated fats raise it and that this seems to matter. He says that more than 200 to 300 grams of protein will make you ill, but later says it is palatable if taken with fat or carbohydrate.

He is keen on low GI fruit but likes oranges and bananas. He is anti-saturated fat and says avoid lamb, cut fat off meat and avoid eggs and poultry skin.

I have slowly lost six stone over the last two years, starting with Dr Atkins and moving towards Wolfgang Lutz; in fact I am recommending the low-carb (around 70 grams carbs per day) to my patients, I am a psychiatrist… it wasn't until I discovered Dr Atkins that I started to lose any significant amount of weight.

I am not going to change my diet now, but why is Loren Cordain so stuck on saturated fat and cholesterol?

Hi,

thank you so much for the kind words about the site, and sincere congratulations on the health improvements you have made. I also find it highly encouraging that you are recommending non-ketogenic reduced carb eating to your patients--avoiding both high and extremely low carbohydrate intakes will help stabilize blood sugar and avoid those hypoglycemic lows that can produce depression-like symptoms and irritability.

As for why Loren Cordain is so "stuck on saturated fat and cholesterol", I really can't tell you with any certainty--he would have to answer that question for himself. All I can say is that his angst against saturated fat completely lacks any scientific backing.

Fat facts versus fantasy

Cordain claims in his writings that the wild game available to our ancestors was leaner than the domesticated animals we eat today, and on the allegedly rare occasion when our ancestors did get naughty and eat high fat animals, the saturated fatty acid content of these wild animals was proportionately lower than it is today.

Cordain obviously knows little of rhinos, hippos, mammoths, etc, all hunted enthusiastically by many Paleo populations and all carrying a hefty load of body fat (an adult hippo, for eg, carries 90kg of adipose tissue). Cordain must also be unfamiliar with east African nomad populations such as the Masai and Samburu tribespeople, that have been observed to eat very large amounts of animal fat year round and yet exhibit outstanding cardiovascular health.

As for the claim that the fat from wild game is proportionately lower in saturated fat than domesticated meats, a quick check on the USDA database shows otherwise. The fat from wild bison, for example, has a similar percentage of saturated fatty acid content to beef fat. Animals like antelope, buffalo, caribou, wild boar, elk, and so on contain 30-38% saturated fat--the fat from domesticated pork, by comparison, contains 37% saturated fat.

Cordain also harps on about how the individual saturated fatty acid profile differs in modern-day meat, which I think is really getting pedantic. If it bothers you, just eat grass-fed meat for crying out loud, which will have the fatty acid profile nature intended!

I think that instead of endlessly pontificating over the finer points of myristic/palmitic/stearic acid ratios, it would be far more productive to avoid the hell out of omega-6-rich polyunsaturated vegetable oils and to consume or supplement with long-chain omega-3 fats on a regular basis (fish oil/cod liver oil is the easiest way to do this). By the way, please don't follow Cordain's bizarre suggestion, featured in many of the recipes in his Paleo Diet book, to marinate meats in flax oil before cooking them. As numerous concerned commentators have pointed out, flax oil is extremely prone to oxidative damage when subjected to high temperatures. Ingestion of heat-damaged polyunsaturated oils increases free radical activity inside the body, and free radical damage is a major player in the pathogenesis of such killers as heart disease and cancer.

I find it highly ironic that a Paleolithic researcher would denigrate saturated fat, a natural component of foods that humans have been eating for millions of years, yet enthusiastically recommend the consumption of heat-damaged flax oil, a food item that did not even exist in the Paleolithic era!

Cholesterol and MRFIT

On the BeyondVeg.com site--which truly is a great resource if you can disregard all the anti-saturated fat nonsense--Cordain claims that the massive MRFIT study, involving over 360,000 men, offers conclusive proof that elevated cholesterol and saturated fat cause heart disease. While increasing cholesterol levels were indeed associated with increasing incidence of CHD mortality in the MRFIT screenees, Cordain does not point out that overall mortality was highest at both the high and low ends of the cholesterol spectrum. The lowest overall mortality was actually seen across the 160-219 mg/dl range of cholesterol.(1)

Cordain also does not mention the results of the actual MRFIT clinical trial itself, which was the primary reason the enormous MRFIT project was instigated in the first place. In the official MRFIT trial, half of the almost 13,000 participants were randomized to receive anti-hypertensive medication, encouragement to quit smoking, and intensive counseling on reducing their fat and cholesterol intake. Despite these extensive interventions, this group did not experience any reduction in cardiovascular or all-cause mortality.

The MRFIT trial is hardly the only clinical trial to fall on its butt when trying to prove that saturated fat is harmful--no properly-controlled clinical trial has ever shown saturated fat restriction to lower mortality.(2)

Repetition--the key to turning myths into 'truths'

Personally, I find the anti-saturated fat sentiment of folks like Cordain--who judging by his published research on Paleolithic diet and health, appears to be an otherwise highly intelligent and perceptive individual--to be a symptom of a much larger problem. The widespread misguided sentiment towards saturated fat and cholesterol is a glowing testimony to the power of repetitive indoctrination. We have all heard, over and over again, that saturated fat is so harmful, so toxic to our arteries, that many of us simply take it for granted that it must be bad for us. If everybody believes and says something, it must be true, right? As Vladimir Lenin, one of history's most heinous masters of propaganda, stated: "A lie told often enough becomes the truth."

Methinks most people need to spend a hell of a lot less time worrying about saturated fat and cholesterol and a hell of a lot more time working on their critical and independent thinking skills...

Cholesterol contradictions

Those who still subscribe to the cholesterol theory have never been able to coherently explain why cholesterol is only associated with heart disease in younger individuals, but not in those over 55--the group in which most CHD fatalities occur. To claim that cholesterol is harmful in younger folks, but benign in older folks is a physiological absurdity.

Even if we close our minds to this disparity, just as so many supporters of the cholesterol theory have done, any association between elevated cholesterol and increased heart disease does not mean the former causes the latter. And it certainly does not 'prove' that saturated fat causes heart disease. In Framingham, for example, researchers noted that increasing cholesterol levels were indeed associated with higher CHD rates but also observed that those who ate the most saturated fat had the lowest rates of CHD and overall mortality!(3)

The fact is, there are numerous factors that promote CHD and also raise cholesterol levels--eg stress, inactivity, high blood sugar, low intakes of various vitamins and minerals, etc. Like an innocent bystander apprehended at the scene of a crime after the real crooks have made their getaway, cholesterol--a substance absolutely critical to our continued well-being--gets blamed for a crime it did not commit.

Cholesterol does not cause heart disease, and I never cease to be amazed by the massive numbers of so-called health 'professionals' who subscribe to the idiotic notion that it does!

For sale: one freshly-painted cholesterol myth

To help readers appreciate how utterly stupid the whole 'lower your cholesterol and you can lower your risk of heart disease' charade is, I will use the example of an article I read several years ago, about how red cars were involved in a disproportionately higher number of road accidents and therefore attracted higher insurance premiums.

If we used the mentality of the anti-cholesterol crowd, the solution to this problem would be to sneak into red car owners' driveways at night and repaint their vehicles another color. This of course, wouldn't achieve a damn thing, because red paint has never been demonstrated to cause car accidents, just as cholesterol has never been demonstrated to cause heart disease.

Any relationship between red cars and increased vehicular accidents is likely due to the type of people that typically drive them. If we were to examine a large subset of individuals who drive red cars, we may find that they are more likely to be younger and less experienced drivers, to posses more impulsive personalities, to drive faster, to own cars whose performance capabilities far exceed their own driving skills, and so on. To lower the rate of accidents among this population, we would need to successfully change their attitude towards motor vehicle use and on-road behavior. In contrast, instituting a nationwide car-repainting campaign would simply be an unproductive and self-delusional wank.

For the last fifty years, mainstream medicine has approached the heart disease problem like a bunch of spray painters who believe the road toll can be lowered by repainting red cars. This moronic approach is no doubt why the incidence of heart disease has not declined one iota,(4-6) and why CHD is still our number one killer.

Independent thinking associated with lower risk of believing establishment hogwash!

I'm not sure what the hell they teach in medical and dietetic courses these days--my experience with universities is limited to the area of their faculties that actually contain factual, solid data--that is, their libraries. It is in the libraries where one finds journals replete with research showing the cholesterol theory to be a complete bunch of crap. Obviously, most graduates never see these articles, because their indoctrination, uh, I mean education curriculum evidently does not allow for facts that contradict the reigning anti-cholesterol dogma.

I make the following appeal to all those young student minds that still have some semblance of independent cognitive function remaining inside them--as you embark on your tertiary education, be aware that it is highly geared towards making you a faithful and obedient servant of the reigning health and medical monopoly. Oh, sure when you establish your own practice and plunk down the first down payment on your new Lexus, you may well feel that you are truly the master of your domain. Don't kid yourself. As long as you fail to verify the claims of the medical hierarchy for yourself; as long as you merely glance over the abstracts in journals instead of reading the full text; as long as drug companies remain your primary source of drug information; as long as food and drug companies control the flow of information emanating from the health associations, institutes, and organizations that you look to for professional guidance, then you remain simply a puppet of our disgustingly corrupt orthodoxy.

If you think I am I exaggerating and being a wee bit hyperbolic, if you think that the present system isn't as bad as I make it out to be, then explain to me why the current health system is America's third leading cause of death,(7) and why the anti-saturated fat, pro-carbohydrate campaign has endowed us with unprecedented levels of obesity and diabetes?

The sooner more of us wake up to the inescapable reality that most of our health authorities are, quite frankly, full of shit; the sooner we start thinking for ourselves; the sooner we start taking more responsibility for our own health; and the sooner we start demanding that health officials start paying attention to the facts instead of vested corporate interests; then the sooner we can bring about meaningful improvements in public health.

Until then, expect more of the same old same old…

References

1. Iso H, et al. Serum cholesterol levels and six-year mortality from stroke in 350,977 men screened for the Multiple Risk Factor Intervention Trial. New England Journal of Medicine, April, 1989. Vol. 320, No. 14: 904-910.

2. Corr LA, Oliver MF. The low fat/low cholesterol diet is ineffective. European Heart Journal, 1997; 18: 18-22.

3. Castelli WP, Concerning the Possibility of a Nut… Archives of Internal Medicine, Jul, 1992; 152: 1371-1372.

4. Rosamond WD, et al. Trends in the Incidence of Myocardial Infarction and in Mortality Due to Coronary Heart Disease, 1987 to 1994. New England Journal of Medicine, Sep 24, 1998; 339 (13): 861-867.

5. Center for Disease Control. Hospitalization Rates for Ischemic Heart Disease - United States, 1970-1986. MMWR Weekly, Apr 28, 1989; 38 (16); 275-276, 281-284.

6. Sytkowski PA, et al. Changes in risk factors and the decline in mortality from cardiovascular disease. The Framingham Study. New England Journal of Medicine, Jun 7, 1990; 322 (23): 1635-1641.

7. Starfield B. Is US health really the best in the world? Journal of the American Medical Association, Jul 26, 2000; 284 (4): 483-485.

Source: The Omnivore

Disputed: "The 10 best reasons a Low Carb Diet is Wrong!"

From the Low Carb UK mailing list:

There is a nutritional booklet currently circulating in the USA called "The 10 best reasons a Low Carb Diet is Wrong!"
One of my list members was really worried about it, but "Elaine in Cumbria" took time out to refute all of its claims.

Read the full article here: Low Carb UK

An Open Letter to Victorian Health Minister Bronwyn Pike

Ms Pike, get off the anti-low-carb bandwagon!

By Anthony Colpo, March 29, 2004.

Dear Ms Pike,

Recently, you announced a new campaign, to be conducted by your government at taxpayer expense, that would endeavor to alert Victorian residents to the alleged "dangers" of low-carbohydrate diets. To the best of my knowledge, this action is unprecedented in Australian political history, for no state government has ever taken it up on themselves to issue warnings against a specific diet, despite the fact that certain dietary regimens have indeed been directly linked to ill-health and death. Such potentially dangerous nutritional regimes include vegan diets, which have claimed the lives of numerous infants around the world, and resulted in legal proceedings against the misguided parents of these youngsters.(1) Along with their potentially fatal effects on infants, vegan diets have also demonstrated the ability to harm children, adolescents, and even adults. So far, while you have had much to say about low-carb nutrition, you have not uttered a word about vegan diets. Before I discuss just why you are so wrong on low-carb diets, lets take a closer look at vegan regimens.

Vegan Diets - Fast Track To Ill-Health

Among their many nutritional shortcomings, vegetarian diets supply sub-optimal amounts of vitamin B12 and essential long-chain omega-3 fatty acids such as DHA and EPA. B12 is essential for optimal cognitive function, while DHA is a major component of brain tissue. Not surprisingly, analyses of blood samples from vegetarians consistently show lower dietary and lower blood levels of long-chain omega-3 fatty acids. (2-7) These fatty acids can be formed in the body from plant-based omega-3 fats, but numerous studies show that the conversion rate is very low.(8,9) Because of their complete abstinence from animal foods, deficiencies of these and other nutrients are much more pronounced in vegans than in lacto-ovo vegetarians. Below are observations, published in peer-reviewed journals, of the harm that can befall those following these truly unbalanced diets:

• In 1986, Dutch researchers observed that vegan infants had markedly lower B12 levels and impaired psychomotor functioning when compared to control infants.(10,11) On the basis of these findings, the researchers made dietary recommendations to the families of the infants, who subsequently began switching their youngsters to lacto-vegetarian, lacto-ovovegetarian, or even omnivorous diets. On average, the children were six years old when the dietary change took place. In 2000, researchers reported on follow-up examinations of these same subjects, who were now aged between 10 to 16. Two-thirds of the formerly vegan adolescents still suffered from B12 deficiency, whereas all of the subjects in a similarly aged omnivorous control group had normal B12 levels. When given a series of cognitive tests, the ex-vegan group achieved poorer results than the lifetime-omnivore group. A significant association was found between low B12 status and poorer performance on tests measuring fluid intelligence, spatial ability, and short-term memory. Because fluid intelligence involves reasoning, the capacity to solve complex problems, abstract thinking ability, and the ability to learn, the authors pointed out that: "Any defect in this area may have far-reaching consequences for individual functioning." (12).
  
  * British researchers found that, compared to omnivores and lacto-ovovegetarians, vegans suffered a higher frequency of abnormal electroencephalogram (EEG) readings, a test designed to detect abnormalities in the electrical activity of the brain (13). In one of their studies, B12 supplementation improved EEG scores in most of those registering abnormalities, but three of the vegans failed to respond to heavy supplementation with either oral or injected B12.
  
  * In 2000, French researchers reported the case of a 33-year-old patient who lost most of his eyesight after following a strict vegan diet since the age of 20. Ironically, the man had adopted the diet for "improved health", and did not use any supplements. Blood samples showed that his levels of vitamin B1, B12, A, C, D, E, zinc, and selenium were all measurably below normal. Vitamin B12, in particular, is vitally important for maintaining the health of the optic nerve that transmits signals from the eye to the brain. Administration of intramuscular and oral multivitamins normalized blood levels of the aforementioned nutrients, but his eyesight did not recover. They concluded that the nutritional deficiencies in the patient's vegan diet - particularly the insufficient amount of vitamin B12 he had been absorbing - were the most likely cause for the optic nerve deterioration that had resulted in irreversible blindness. (14)

In a recent newspaper article, you stated that: "When we know something is bad for people, like smoking, then we let people know what the health risks are". I eagerly await to see if your department issues any warnings against vegan diets, for unlike low-carb diets, these posess a demonstrated poor safety record.

And what about low-carb diets?

In response to criticisms of your sadly misguided campaign against low-carbohydrate diets, you also stated in the aforementioned article: "Some people might come out and say, 'This is a nanny state - now they are telling us what to eat' ... But while I don't think it is the role of the politician to dictate individual preference and behaviour, it is my role to point out when something can actually harm you."

Seeing as you are taking it upon yourself to become a taxpayer-funded dietary commentator, it behooves you to learn as much as possible about the dietary regimens you intend to comment on. The statements you have made so far in regards to low-carbohydrate diets clearly show that you have not done this.

You claim that low-carbohydrate diets raise the risk of cancer, heart disease, osteoporosis, and even depression. From what peer-reviewed literature did you obtain such information?

Heart Disease

The claim that low-carbohydrate diets raise the risk of heart disease strains all boundaries of logic. Low-carbohydrate diets, via a reduction in cereal grain intake and an increase in meat and fruit and vegetable intake, increase the ingestion of many key heart-healthy nutrients. These include vitamin C, bioflavonoids, magnesium, carnitine, long-chain omega-3 fatty acids, vitamins B6, B12, and folic acid.

Bioflavonoids and vitamin C are important for the formation and maintenance of the collagen inside our arteries. Vitamins B6, B12 and folic acid lower blood levels of homocysteine and C-reactive protein (the former is believed to be directly atherogenic, the latter is an accurate measure of inflammatory activity in the body and a far superior predictor of future CHD risk than LDL cholesterol).(15-17) Long-chain omega-3 fatty acids, meanwhile, have demonstrated an ability to reduce CHD and overall mortality in randomized clinical trials, not just in the wishful-thinking minds of health bureaucrats. Magnesium and carnitine are essential for muscular contraction and energy production; both have been shown to lower mortality from CHD and heart failure in overseas trials.(18-20) When researchers compared a low-carbohydrate diet with a high-carb diet, they found that the former increased carnitine absorption, despite the equal carnitine contents of the two diets.(21)

Allegedly "healthy" cereal grains (whole or otherwise) contain no vitamin C, no B12, contain only omega-6 fatty acids but no omega-3 fats, contain phytates that impair the absorption of magnesium, and contain a substance known as pyridoxine glucoside, which has been shown to reduce the availability of vitamin B6 by 75-80%.(22) The only dietary intervention trial to compare the effects of increased whole-grain intake on CHD outcomes was the DART trial; in this study, men assigned to eat more brown bread and wheat fiber actually suffered a slight increase in CHD mortality (in the same study, men who were instructed to eat a low-saturated fat diet experienced no change, while men instructed to consume fish/fish oil reduced their CHD risk by almost a third).(23)

Sorry, but I don't see any reason why cereal grains should even be included in anyone's diet, let alone form the foundation of said diet. No-one "needs" cereal grains; in fact, those with gluten sensitivity and celiac disease should quite literally avoid them like the plague! Maybe you would care to include these facts in your future public awareness efforts...

Meat is by far the richest source of carnitine, vitamin B6, B12 and (in the case of organ meats), folic acid. Animal foods are also the only non-supplemental source of long-chain omega-3 fatty acids (brain tissue is the richest source, followed by fatty fish).

Non-cereal plant foods (fruits, vegetables, and nuts) - the kind encouraged by virtually all of the current crop of low-carb authors - contain magnesium, folic acid, bioflavonoids, and are the richest dietary sources of vitamin C.

Those who are still obsessed with "risk factors" (e.g, much of the medical establishment) should know that low-carb diets typically raise HDL cholesterol, improve the HDL:LDL ratio, and lower elevated triglyceride levels, while low-fat, high-carbohydrate diets often have the opposite effect. In clinical studies, low-carbohydrate diets have repeatedly been shown to produce significant fat loss; overweight and obesity is well-known to be associated with an increased risk of heart disease (and cancer).

Depending on one's food choices, adopting a low-carb diet will result in an increase of saturated fat intake. Despite the hysterical anti-saturated fat rantings of mainstream low-fat proponents, there exists no sound scientific evidence whatsoever to support any causative role for these fats in the pathogenesis of CHD. Consider carefully the following facts, available in the scientific literature for anyone who cares to look:

1) Four decades worth of dietary intervention trials have completely failed to produce any reduction in CHD that can be attributed to cholesterol-lowering or saturated fat restriction.(24)

2) Ironically, the only cholesterol-lowering strategy that has shown any noteworthy benefit in the reduction of CHD - the use of statin drugs - does not even work by cholesterol-lowering. These drugs operate via anti-inflammatory, artery-dilating, and antioxidant mechanisms.(25-41)

Cancer

The confident proclamations of many that meat and animal fats cause cancer are rather remarkable considering the complete lack of reliable clinical evidence to support such a notion. Even the allegedly "strong" epidemiological evidence is highly suspect. For example, if meat and saturated fat caused cancer, then vegetarians should by all rights experience lower rates of cancer. As a pooled analysis of the largest vegetarian studies shows, they don't.(42)

One of the few randomized clinical trials to examine the above topic was the Polyp Prevention Trial. In this study, over two-thousand patients who had one or more confirmed adenomatous colorectal polyps (adenomatous polyps are considered forerunners to colorectal cancer and are used as markers for colorectal cancer risk) removed within the previous 6 months were randomly assigned to follow either their usual diet, or a low fat, high fiber diet. Compared to the controls, subjects assigned to the high-fiber diet significantly increased their intake of whole-grains and legumes, and ate an average of 2.25 more servings of fruits and vegetables each day. The intervention group was also advised to reduce their consumption of red meat, which they did.

Total fat consumption in the control group averaged 34%, while those following the treatment diet reduced their fat intake to only 24%. After 4 years, colorectal cancer was diagnosed in 10 subjects from the high fiber group, and only 4 from the usual diet group eating more red meat. Even after excluding those diagnosed within the first year of the study, the results were similarly unfavorable; 4 cases in the intervention group as compared to 2 in the control group. Polyp recurrence was virtually identical between the two groups.(43)

In animal studies, the one fat that shows consistent tumor-promoting effects is the omega-6 fatty acid linoleic acid (found in so-called "heart-healthy" polyunsaturated vegetable oils).(44) While animal fat consumption in America has remained stable over the last 100 years (in terms of grams consumed per person per day), the consumption of vegetable oils and margarines has risen dramatically.(45,46) During this time, age-adjusted cancer rates have also risen in both males and females. To hold stable animal fat consumption responsible for rising cancer rates requires a complete abandonment of one's rational faculties.

Osteoporosis

Ms. Pike, the well-worn claim that high-protein diets can cause osteoporosis really is a bad joke, considering that it is a well-established fact that protein is an essential component of bones, and that epidemiological studies repeatedly show that it is low-protein intakes, not high protein intakes, that are associated with reduced bone density.(47)

It is typically claimed that high protein intakes will cause an increase in calcium excretion. Researchers recently examined this premise by performing a series of experiments in which intestinal calcium absorption was measured (using dual stable calcium isotopes) in pre- and postmenopausal women who were fed diets of varying protein content. Unlike a number of similar previous experiments, the diets of the women were tightly controlled, and the wide variations between individuals in calcium absorption were countered by using each women as her own control. Under these well-controlled conditions, the researchers found that calcium absorption was significantly lower during periods of low protein consumption (0.8g/kg and below) than during periods of high protein consumption. The researchers concluded, in a rather understated manner, that these studies "call the traditional high protein hypothesis to question". No kidding!(47)

Depression

The claim that low-carb diets cause depression has been doing the media rounds recently after Massachussetts Institute of Technology researcher Judith Wurtman and her team allegedly found an increase in depressive mood symptoms on people eating high protein diets compared to those following low-protein diets. This study has not yet been published, so there is no information on the exact diet the control and intervention groups followed, the methods used to determine mood changes, etc, etc. I contacted the MIT media department shortly after news of the study broke in the media requesting more information, and never received a reply. One should refrain from using this study as evidence until its results are peer-reviewed and published. It should be noted that Judith Wurtman has published several books promoting low-carbohydrate diets. While that in itself is no guarantee of impropriety or bias, she can hardly be considered a totally impartial voice on the subject.

And that's not all...

Ms. Pike, if you intend to be a credible and objective source of information to the Victorian public on low-carb diets, then it is incumbent upon you to point out, in addition to their alleged flaws, any health benefits they may possess. Researchers have indeed uncovered several characteristics of carbohydrate-reduced diets that could prove extremely valuable in the quest for improved public health.

• 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 diets. None of these has shown superior weight loss on the latter, apart from a highly suspect study (click here for details) conducted by Richard Fleming, the Nebraska cardiologist who obtained the late Dr. Atkins death report under highly dubious circumstances. In every study except Fleming's, low carbohydrate diets produced either markedly superior weight loss or statistically non-significant differences in weight loss.(48-65) Despite the oft-repeated claim that low-carb diets are hard to stick to, most studies reporting drop out rates have found higher rates of attrition in the low fat, high-carbohydrate diet groups.
  
  * 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. Numerous studies have compared the effects of lower- versus higher-carbohydrate diets on blood glucose control and, in virtually every instance, the carbohydrate-restricted regimens produced superior results.(66-84) 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.(85) 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 tends to be a very poorly-received piece of advice. 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."(86)

Do Your Homework.

Ms. Pike, it is unfortunate that you did not sit down and review the evidence before embarking on your misguided crusade to save Victorians from the supposed harm that awaits them if they adopt low-carbohydrate nutrition. Scandalous media reports arising from misleading press releases by vested interests do not constitute reasonable grounds for commencing a campaign that has the potential to affect public health, for better or worse.

Much of the recent media commotion over low-carbohydrate diets can be traced back to an American vegan organization known as the Physicians Committee for Responsible Medicine. If you are not familiar with this group, whose behavior so far has been anything but responsible, then I suggest you click here. This "Committee" in fact serves as a front-group for the People for Ethical Treatment of Animals (PETA), a radical animal rights and vegan activist group that has given documented financial aid to green terrorist groups.

Perhaps your heroic streak was triggered into action after Australia's most popular current affairs show featured footage of a Melbourne nutritionist claiming that "medically-supervised low-carbohydrate diets" had caused sixty deaths. You should know that this individual was referring to deaths that occurrred over twenty years ago among individuals following liquid protein diets, a crucial fact that was conveniently ommitted (click here to see for yourself). These deaths did not occur among people following the current crop of popular low-carbohydrate diets, people eating real food - you know, meats, eggs, dairy, fruits, nuts, and vegetables! Needless to say, several hundred calories per day derived solely from protein-based powder and water does not constitute a healthy diet, regardless of whether it accompanies a low or high carbohydrate intake.

It should also be mentioned that the individual who appeared on A Current Affair issuing these misleading claims also has authored a number of low-fat diet books. You may like to read a detailed critique of this author's work, and his subsequent reply to this critique, at the following links:

Just How Low Will the Anti-Low-Carb Crowd Go?

A Reply to Bilsborough

Ms. Pike, Your Actions Have Consequences - Bad Ones!

Several days ago, I received an e-mail from a business owner in NSW who, a little while back, started an innovative low-carb meal delivery service in response to the growing popularity of low-carb diets. The ready-made meals delivered by her business include lean meats and vegetables, and, to avert the stigma associated with saturated fats (no matter how misguided this sentiment may be), derive their fat content mainly from monounsaturated sources. Until recently, this individual was doing a roaring trade, having established a franchise chain of 15 outlets delivering delicious low-carb meals around the country. This entrepreneurial mother-of-three saw a niche and filled it, via honest and productive effort (something that more of our politicans should try to emulate), and started reaping the rewards that were rightly hers.

That is, until some misguided politician appeared on national TV and in the nation's newspapers announcing her latest novel waste of money - an anti-low-carbohydrate crusade!

"Since the negative PR has appeared in the recent news, my company is really suffering", said our understandably disheartened low-carb entrepreneur. "Here in Sydney it was as if someone has 'turned off the tap', that's how quiet our phones have been. It is a devastating blow to our businesses from which we hope to recover, but there are no guarantees."

Did customers stop ringing because they had subsequently died from heart disease and cancer, or because they were hospitalized with broken osteoporotic bones and/or depression, or because they had fallen prey to some other alleged adverse effect of low-carb diets?

Nope.

Customers stopped ringing because, not being familiar with the scientific literature, they relied on the media to deliver their diet and health information. So when a bunch of radical vegan activists from North America tried to infer that the death of the late Dr. Atkins was a result of his own dietary prescriptions, and the media lapped it up, they became worried. When some axe-grinding nutritionist from Melbourne appeared on A Current Affair and told the nation that low-carb diets had killed sixty people, they got scared. And when a Victorian politician announced that low-carbohydrate diets were such a threat to public health that her government was going to actively warn people away from them, people ran for the doors. Not being familiar with the scientific literature, which actually indicates that low-carb diets possess an array of favorable qualities and are definitely worthy of increasing research attention, these folks evidently believed what they were hearing on TV and in the newspapers.

Despite the volumes I read and hear about how people supposedly distrust politicians and how they distrust what they read in the papers and see on TV, a significant portion of the population in this country appears to have been suckered beautifully by yet another fallacious government and media beat-up!

Forgive me if I'm wrong, but I thought the notion of someone getting off their butt and "having a go" was supposed to be admired here in Australia. I don't know about others, but I think it is extremely unfair for someone who was making an honest, productive living to now be faced with the prospect of going out of business simply because of misleading, sensationalist bullshit.

I also think it is extremely unfair for some politician to take my tax money, and use it to tell me how I should abandon the very diet that has personally brought me nothing but benefits! Puhleez!

Perhaps most unfair of all is that thousands of people are being scared away from diets that have clearly been shown to benefit a number of common conditions - diabetes and obesity, for example - and hold great promise for treating many other ailments.

Conclusion

Ms. Pike, I know you have already travelled a fair way down your proposed path, and it might make you look rather silly if you abandon your sadly-misguided anti-low-carb campaign after creating such a commotion in the media. Nonetheless, I urge you to study the scientific evidence thoroughly, and then carefully reconsider your current stance. There are far better ways to spend taxpayer funds than on discouraging people from trying diets that may just benefit their health, and from sending flourishing businesses down the tube. I know such a change in stance will not impress the flour and baking industry, who are lobbying hard to try and avoid the same fate that is currently befalling their counterparts in the US, where low-carb diets have undergone phenomenal growth, but I think your primary concern should be public health, not the financial well-being of vested industries.

Sincerely,

Anthony Colpo.

To tell Bronwyn Pike that taxpayer funds should be used in a more responsible manner, e-mail: bronwyn.pike@parliament.vic.gov.au

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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. Copyright information:

Any articles on this website authored by Anthony Colpo may be reproduced for non-commercial purposes only, providing full credit is given to the author, and that the website name www.theomnivore.com is cited. A hyperlink would also be greatly appreciated. Those wishing to reproduce articles for commercial purposes should e-mail: contact@theomnivore.com

Book Review: The Cholesterol Myths

The Cholesterol Myths: Exposing the Fallacy that Saturated Fat and Cholesterol Cause Heart Disease

by Uffe Ravnskov, M. D., Ph. D.
Published by the New Trends Publishing Co., Washington, D. C., 2000, xiv + 297 pp, ISBN 0-9670897-0-0 $20.00 To order, call New Trends Publishing at 877-707-1776, or on the web at http://www.newtrendspublishing.com.

With courage and care Dr. Ravnskov exposes the lack of experimental evidence for the diet-heart theory, which claims that eating less fat and cholesterol will prevent atheroslcerosis (hardening of the arteries) and myocardial infarctions (heart attacks). By examining original peer-reviewed literature, the author finds no support for the diet-heart theory. He gives examples of scientific fraud among efforts to support the theory, including the deliberate selective omission of data points, and the deliberate assignment of subjects in a clinical trial to treatment or to control groups by physicians with the subject's medical records in hand. He shows how the abstract or conclusions of a number of papers are at odds with the actual data in the papers. He demonstrates how the use of one statistical method in preference to another can give a false impression that there is an effect, where there is, in fact, none. He shows how the reporting of differences in fatality rates by per cent reduction (say, a 50% reduction in relative risk) is actually misleading when the actual death rates are quite small in both the treatment and control groups of subjects in diet or drug studies. For example, a treatment that changes the absolute survival rate over a multi-year period from 99.0% to 99.5% represents a 50% reduction in relative risk, from 1% to 0.5% absolute. This is often described in papers as a 50% reduction in death rate. However, when the difference is barely significant statistically, as was often the case, Ravnskov points out that there is no real reason to recommend adoption of the treatment, especially if there are serious side-effects.

I have provided an abnormal number of quotations in order to show how meticulous this author is, and how skeptically we should regard some of the peer-reviewed literature, or recommendations from the medical establishment, or claims of effectiveness of anti-cholesterol drugs. Surprisingly, this author has included about 2 dozen cartoons to make this very wrenching exposé more palatable. The chapters are called Myths. Here are the chapter titles along with some quotations from and discussion of each:

"Myth 1: High-fat foods cause heart disease." In a striking graph from one of the papers of John Yudkin, M. D., Dr. Ravnskov shows that the number of deaths from coronary heart disease (CHD) in England and Wales between 1910 and 1956 is closely correlated with the number of new radio and television sets purchased each year. This is a perfect example of a correlation without a cause. Another line on the same graph shows that the number of grams of animal fat consumed per day changed by only ± 10% during this period. There is no correlation whatever between fat consumption and death rates from CHD, which increased 6-fold during this time period. "In the US, coronary mortality increased about ten times between 1930 and 1960, leveled off during the '60s and has since decreased slowly. During the decline of heart mortality the consumption of animal fat declined also, but during the thirty years of sharply rising coronary mortality the consumption of animal fat decreased [also]."

"While the death rate from coronary disease increased in most countries after World War II, it decreased in Switzerland. If this decrease had been preceded by a decline in the intake of animal fat, Switzerland would have been a model for health care in other countries. But the diet-heart proponents never mention Switzerland because during the decline in heart mortality, the Swiss intake of animal fat increased by 20%."

"The Masai [of Kenya] drink 'only' half a gallon of [whole] milk each day...Their parties are sheer orgies of meat; on such occasions four to ten pounds of meat [eaten] per person is not unusual, according to Professor [George] Mann [of Vanderbilt University in Nashville, TN, USA]. If the diet-heart idea were correct, coronary heart disease would be epidemic in Kenya. But Professor Mann found that the Masai do not die from heart disease - although they might die from laughter if they heard about the campaign against foods containing cholesterol and saturated fat. But this was not the only surprise. The cholesterol of the Masai tribesmen was not sky-high as Mann had expected; it was the lowest ever measured in the world, about 50% lower than the value of most Americans."

"In Puerto Rico and in Honolulu, heart attack victims had consumed more polyunsaturated oils than those who had not had a heart attack [in a study conducted by Dr. Tavia Gordon]. Although this observation is contrary to what was expected and thus most discouraging for those who advise people to consume more vegetable oils, the study authors did not mention this fact in the summary of their research."

"By 1998, a total of 27 studies had been published including 34 groups (cohorts) of patients and control individuals...[totaling more than 150,000]. In 3 of these 34 cohorts, patients with coronary disease had eaten more animal fat than the control individuals, and in 1 cohort they had eaten less. In the rest of the groups - 30 in all - investigators found no difference in animal fat consumption between those who had heart disease and those who did not. In 3 cohorts the patients had eaten more polyunsaturated vegetable oils than the control individuals, and in only 1 had they eaten less..."

"If you go to the library and look into the tables of these papers [all are fully cited in the book] you will see that the differences found were not statistically significant, which means that the results were simply due to chance."

"...[T]here is a weak association between the coronary mortality in various countries and the amount of fat available [in each] for [the citizens] to eat, but no difference between the amount of fat [actually] eaten by coronary patients and by healthy individuals."

"Myth 2: High cholesterol causes heart disease." "Most supporters of the diet-heart idea think that the increased risk of CHD is present at all cholesterol levels. Those who have a cholesterol level of 200 mg/dL, for example, are worse off than those with a cholesterol level of 150 mg/dL; and those who have a cholesterol level of 250 mg/dL are at even greater risk. The pharmaceutical companies love this concept for it implies that almost everyone should be treated, even those with normal cholesterol levels."

"The truth, were it known, would send pharmaceutical stocks plunging. In most studies, the increased risk is present only above a level of cholesterol that includes just a small percentage of the total population. [These are the approximately 1% of people with a genetic defect called familial hypercholesteremia.] And women can stop worrying immediately because high cholesterol is not a risk factor for the female sex. Few comments have been made on this peculiar fact in all the vast literature on cholesterol. When it is mentioned at all, it is said that female sex hormones protect against heart attacks."

"In fact, it seems more dangerous for women to have low cholesterol than high. Dr. Bernard Forette and a team of French researchers from Paris found that old women with very high cholesterol live the longest. The death rate was more than 5 times higher for women who had very low cholesterol. In their report, the French doctors warned against cholesterol lowering in elderly women. But they could as well have warned against cholesterol lowering in any woman, or, to be more precise, in anyone at all."

Dr. Ravnskov showed how the results of many studies, including those of Dr. Ancel Keys, as well as MRFIT and others, have conclusions that are at odds with the authors' own data, albeit sometimes this problem was confined to the abstract of a paper, as though no further funding would be obtained if honest and complete interpretations had been made.

Your reviewer checked one of the citations on MRFIT [O. Paul et al., J. Amer. Medical Assoc. 248 (12), 1465-1477 (1982)], to find that the summary noted honestly that the treatment group had less mortality from CHD and more overall than the controls did. That the former was not statistically significant was in the abstract; that the latter was not statistically significant was not in the abstract, but in the body of the paper. The problem with both this and some other studies is that the interventions included diet, anti-hypertensive drugs and smoking cessation all at once. The authors thought that less smoking was beneficial and that anti-hypertensive drug therapy was harmful. But the diet for the treatment group called for lower saturated fat and cholesterol intake and higher polyunsaturated fat intake. The authors did not admit the possibility that this intervention could have been harmful. In an end-note Ravnskov simplified a table in this paper and showed that the entire difference in death rates of sub-groups was due to quitting smoking, which cut the death rate in half for those who quit.

"Thus, high cholesterol is said to be dangerous for Americans but not for Canadians, Stockholmers, Russians or Maoris. High cholesterol is said to be dangerous for men, but not for women; it is said to be dangerous for healthy men, but not for coronary patients; and it is said to be dangerous for men of 30, but not for those of 48 [or older]. And high cholesterol may even be beneficial for older people. Such discrepancies indicate that the association between high cholesterol and CHD is not due to simple cause and effect. The most likely interpretation is that high cholesterol is not dangerous in itself but [that it is] a marker for something else."

Dr. Ravnskov went on to show that higher levels of high-density-lipoprotein (HDL, "good" cholesterol) are not protective against CHD, and that lower levels of low-density-lipoprotein (LDL, "bad" cholesterol) are not beneficial, although the expected associations of each with CHD are present. Here again, conclusions at odds with the researchers' own data were presented. Intimations that there are "many" or "definitive" studies in reports and papers were shown to be false by showing that citations often led to other reviews, each trusting the last, and ending at very few original studies.

Studies in test animals that artificially raised their LDL-cholesterol levels, thereby supposedly creating atherosclerosis, were shown to be misinterpretations. While the topic should have been in Myth 1, not in Myth 2, triglycerides were said to be even less correlated with CHD than cholesterol is; that the assay for triglycerides is worthless unless the patient has been fasting 12 hours; and that the assay is only accurate to ± 50%.

"Myth 3: High-fat foods raise blood cholesterol." Dr. Ancel Keys was one of the main proponents of this myth. In a paper published in 1958, Keys showed a graph of the per cent calories from fat in the food of various countries vs. the mean serum cholesterol levels. The data points fell on a straight line, showing an excellent correlation. Dr. Ravnskov added data points from a number of countries deliberately ignored by Dr. Keys. These fall nowhere near the line. Furthermore, CHD death rates among subjects in Finland, Greece and Yugoslavia with similar serum cholesterol levels varied 5-fold depending on which area of the country they lived in!

Four studies in the US, one in the UK, one in Israel and one in Finland failed to show any correlation between diet and serum cholesterol levels.

"Numerous studies have shown that in people who eat a normal Western diet, the effect on blood cholesterol of eating 2 or 3 extra eggs per day over a long period of time can hardly be measured..."

"To find out how egg consumption influenced my own blood cholesterol, I once used myself as a human guinea pig without asking the ethics committee at my university. Before and during the experiment I analyzed my [total serum] cholesterol. My usual egg consumption is one or two eggs per day, and my cholesterol value at the start of the experiment was 278 mg/dL, very close to a determination of blood cholesterol made 10 years earlier." On day 0, Dr. Ravnskov ate 1 egg; on day 1, 4 eggs; on day 3, 6 eggs; and on days 3-8, 8 eggs per day! "The data from my daring experiment showed that instead of going up, my cholesterol went down a little [to 246 mg/dL]."

"Myth 4: Cholesterol blocks arteries." "As early as 1953 Ancel Keys wrote: 'It is a fact that a major characteristic of the sclerotic artery is the presence of abnormal amounts of cholesterol in that artery.' And he added: 'This cholesterol is derived from the blood.' No proofs and no arguments - not from Keys and not from his followers. The cholesterol comes from the blood, and that's the end to it."

Dr. Ravnskov explains that older people have higher concentrations of cholesterol in their blood than younger people. If the serum cholesterol is graphed against the degree of atherosclerosis with all age groups lumped together, there seems to be a direct relationship. But if only people of about the same age and sex are considered, there is only a weak relationship with a correlation coefficient of 0.29. (A perfect correlation would have a correlation coefficient of 1.00.) When the subjects with familial hypercholesteremia are left out, even the weak correlation vanishes.

"The first study designed to demonstrate a possible correlation between blood cholesterol and degree of atherosclerosis was published by the pathologist Kurt Landé and the biochemist Warren Sperry of the Department of Forensic Medicine at New York University. The year was 1936. They studied large groups of individuals who had died violent deaths. To their surprise, they found absolutely no correlation between the amount of cholesterol in the blood and the degree of atherosclerosis..."

"Because Landé and Sperry were cautious and methodical, their study should have nipped the diet-heart idea in the bud. Or, more accurately, if those who promoted the diet-heart idea later on had read Landé and Sperry's paper before beginning their research, they would probably have dropped the idea at once... But the few who remember Landé and Sperry misquote them and claim that they found a connection, or they ignore their results by arguing that cholesterol values in the dead are not identical with those in the living..."

"In the city of Agra in India, Dr. K. S. Mathur and his co-workers performed a similar study [in 1961]. Their first step was to measure blood cholesterol in 20 patients shortly before death and then a varying number of hours afterwards. They found that the cholesterol values were nearly the same if samples [were taken] before death and within 16 hours afterwards. Thus, blood samples taken very shortly after death are reliable - an important confirmation of the study done by Drs. Landé and Sperry. Dr. Paterson's group in Canada did a similar test and obtained a similar result.

"Next Dr. Mathur and his colleagues studied 200 people who had died in an accident, without any preceding disease. Like Drs. Landé and Sperry, and like Dr. Paterson, the Indian researchers could find no connection between cholesterol values and the degree of atherosclerosis. Those with low cholesterol had just as much atherosclerosis as those whose cholesterol was high.

"Similar studies have also been performed in Poland, in Guatemala, and in the US, all with the same result: No correlation between the level of cholesterol in the blood stream and the amount of atherosclerosis in the vessels."

A report from the Framingham Study found a weak correlation coefficient, 0.36. Dr. Ravnskov found what distinguished this report from all the others he studied: only 14% of the Framingham dead were chosen for autopsy, not close to 100% as in the other studies. The risk of preferentially selecting subjects who probably had familial hypercholesteremia was said by Ravnskov to be great. To prove that high cholesterol is the villain - and not just an innocent bystander - demands that a change in the cholesterol concentration in each individual is followed by a change in degree of atherosclerosis in the same direction. Examination of all studies on this relationship showed no correlation.

"Myth 5: Animal studies prove the diet-heart idea." "When it comes to cholesterol, none of the other mammals is like us. They have other amounts of it in their blood, different dietary habits, and most of them do not become atherosclerotic.

"Many mammals never eat food containing cholesterol . If they are force-fed a cholesterol-rich diet, the cholesterol level of their blood rises to values many times higher than ever seen in normal human beings. And since such animals cannot dispose of the cholesterol they have eaten, every organ soaks up the cholesterol like a sponge soaks up water...

"Using cholesterol-rich fodder, it is possible to induce arterial changes that vaguely resemble human atherosclerosis in rhesus monkeys, but it was not possible in baboons. How do we know whether man reacts like a rhesus monkey or like a baboon or in some other way?...

"It is true that cholesterol is also deposited in the arteries of the [force-fed] rabbit, but these deposits do not even remotely resemble those found in human atherosclerosis. Cholesterol appears in different places in a rabbit's vessels than in man's, the microscopic changes are different, no hemorrhages or clefts appear as they do in man, and no thrombus or aneurysm formation in the arterial wall is seen. The most striking fact is that it is impossible to induce a heart attack in a rabbit by dietary means alone."

"Myth 6: Lowering your cholesterol will lengthen your life." Dr. Ravnskov reviewed the evidence presented earlier - that cholesterol levels in blood, or HDL or LDL levels, or the ratio of the latter are not correlated with either atherosclerosis or heart attack rates. It follows that forcible reductions of cholesterol levels by drugs (since diet alone does not change the levels much) would not be expected to change the rate of CHD. However, two things are possible with allopathic drugs. First, some unknown mechanism unrelated to cholesterol could lengthen lifespan. Second, some side-effect unrelated to cholesterol could shorten lifespan. The pervasive misconceptions about cholesterol has made it nearly impossible to carry out a placebo-controlled trial of new drugs because it is mistakenly considered unethical not to treat people with high cholesterol levels!

"In the 1960s, Professor Jeremy Morris of London, England, led a team of physicians and scientists in an investigation to see whether the replacement of animal fat with soybean oil could have some preventive effect on CHD. This oil is rich in polyunsaturated fatty acids, those that are considered [erroneously to be] protective against atherosclerosis and CHD. Enrolled in the trial were about 400 middle-aged men who had previously been admitted to 4 London hospitals because of a heart attack; half of these received a diet containing large amounts of soybean oil. (This is one of the few trials sponsored solely by a government, and not by a drug company or any other vested interest.)"

"When the researchers analyzed the results 4 years later, they could find no beneficial effects from using soybean oil. Although, in this particular trial, blood cholesterol had decreased considerably in the treatment group, 15 had died of a heart attack. In the control group, 14 had died; and the number of non-fatal heart attacks was the same in both groups." Other trials gave the same result.

These trials on patients who already had symptoms of CHD are called "secondary prevention" trials. Now Ravnskov describes some of the "primary prevention" work, that is, trials with healthy or, at least, symptomless patients. Much larger numbers of subjects are needed to obtain good statistical results, and compliance is always suspect because of the severe side-effects of many of the treatments or drugs used in subjects who are basically healthy, and thus may not be compliant because of lack of fear of poor health. When you recall the conclusions in Myth 2, that high cholesterol does not cause CHD, you will not be surprised at the negative findings now to be described.

In 1967 the Coronary Drug Project tested nicotinic acid, clofibrate, thyroid hormone, and estrogen to lower cholesterol levels in middle-aged men who had already had at least one heart attack. After 7 years the death rates were the same as that of the controls. Worse, all 4 drugs had severe side-effects. The researchers fell victim to the "surrogate endpoint". This is the use of an easily measured factor, such as total cholesterol level or blood pressure, as a surrogate or substitute for what is really important - increasing lifespan or the quality of life. In a later chapter Ravnskov calls this a "surrogate outcome".

In 1970 the Upjohn Co., Kalamazoo, MI, US, sponsored a trial with controls on 2000 men and women with high cholesterol of its then new drug colestipol. Two years later no effect was seen in the women. The number of heart attacks in the men in the treatment group was cut in half, a remarkable result never seen before or since. But Ravnskov found the snag: The selection of the patients to be in either the treatment or control groups was done by Upjohn's scientists with the results of the participants' blood assays in hand; it was anything but random. Ravnskov noticed that there were too many control patients with familial hypercholesteremia. Your reviewer notes that, in the 1996 Physicians Desk Reference entry for this drug, there is not a shred of evidence for longer lifespan; moreover, there were no restrictions on prescribing this drug for women.

For the World Health Organization trial, researchers assayed blood cholesterol in 30,000 healthy, middle-aged men in Edinburgh, Prague and Budapest. The 10,000 men with the highest blood cholesterol levels were selected for the trial, half to receive clofibrate, half placebo. After 5 years there were more fatal heart attacks in the clofibrate group. There were 128 total deaths in the clofibrate group and 87 in the placebo group. "Yet clofibrate is still recommended in many countries as a useful drug."!!

The Oslo, Norway, trial was shown to be typical of several such trials in that dietary advice to lower cholesterol intake, cessation of smoking and loss of weight were all varied at once. The barely significant difference in death rate - those in treatment did better than the control subjects - could not be assigned to any one factor.

The Multiple Risk Factor Intervention Trial (MRFIT) sponsored by the National Heart, Lung and Blood Institute (of the NIH, US) selected the 12,000 men considered most at risk for heart attack from 360,000 middle-aged men from 18 American cities. Those in treatment smoked less, took drugs for blood pressure, and ate less cholesterol. After 7 years the number of deaths from all causes was 265 in the treatment group and 260 in the control group! When a scientific experiment does not produce results supporting a hypothesis, the scientists are supposed to admit it immediately; such honorable actions have engendered respect for scientists. Not in this case, however. The researchers arbitrarily excluded the results from certain groups of subjects, changed the type of statistics used, and reported that MRFIT was a success in some media, according to Ravnskov, although not in the paper by O. Paul cited above.

The National Heart, Lung and Blood Institute embarked on a new jumbo trial called The Lipid Research Clinics Coronary Primary Prevention Trial (LRC) to test the effectiveness of cholestyramine (Bristol-Myers Squibb). To find about 4,000 test subjects, the 0.8% of 500,000 middle-aged men with the highest cholesterol levels were selected. All were given a few weeks of dietary indoctrination to solve the supposed ethical dilemma of not otherwise treating the controls. Half received cholestyramine and half placebo for 7-8 years. Of those treated, 190 (10%) had nonfatal heart attacks against 212 (11.1%) of the controls. For fatal heart attacks the figures were 1.7% and 2.3%, a difference of 0.6% absolute or 12 individuals. In the summary of the paper on this trial these unimpressive results were presented as a 19% lowering (relative risk) of nonfatal heart attacks and a 30% lowering of fatal heart attacks.

"And this was not the only way in which the LRC figures were manipulated. In order to reach their 30% figure, the LRC directors included the uncertain cases, those who may or may not have died from a heart attack, and to reach their 19% figure, they excluded the uncertain cases. If it had been the other way around the results would have been 24% rather than 30, and 15% rather than 19. In other words, they selected data that gave them the results they were seeking." Even worse, the directors abandoned the 99% confidence level with a 2-tailed t-test and settled for a 95% confidence level with a 1-tailed t-test. [In an end-note Ravnskov points out that scientists have agreed that a 1-tailed t-test should be used only when it is certain that the result will go in just one direction. It is not supposed to be used when the drug (or other intervention) may do harm rather than good.] Very revealing is the absence of the number of deaths from all causes. More men in the treatment groups died by violence or suicide (11 vs. 4). In the misleading manner used by the LRC to present results, they could have said that violent death was 175% more likely in the treatment group. In order to achieve essentially nothing, the treatment group suffered gas, heartburn, belching, bloating, abdominal pain, nausea and vomiting. The study's report assured readers that the side-effects were not serious. Some promoters then claimed that now that it had been proven that it is worthwhile to lower cholesterol no more trials were necessary!"

Ravnskov goes on to show that trials with a seemingly positive result are cited much more frequently than trials with a negative result. This gives a positive feedback effect, reinforcing the dogma than reducing cholesterol level is beneficial, but this sort of misdirected effort actually does not produce better health.

A study showed that patients treated with lovastatin and colestipol had their coronary arteries narrowed as shown by X-rays. The title of the paper on this study indicated the opposite: "Regression of coronary artery disease as a result of lipid lowering therapy..."

Ravnskov then presents the results of a meta-analysis of 26 cholesterol-lowering trials that met his standards. Result - no benefit.

Ravnskov presents the results of a number of trials of statin drugs in which total death rates are slightly lower than those of the controls. In an early trial of lovastatin (EXCEL) on 8,000 subjects the absolute death rate from all causes after just 1 year was 0.5% vs. 0.2% in the placebo group.

Your reviewer checked the report on the results of another study, this one lasting 5.2 years [Downs et al., J. Amer. Medical Assoc.279 (20), 1615-1622 (1998)]. There were no results given for death from all causes in this study, which was called AFCAPS/TexCAPS. So, even though lovastatin reduced the incidence of first coronary events by 37% in this trial, there is still not enough evidence to warrant using this drug. Nevertheless, Downs et al. suggest that 6 million Americans may benefit from LDL-cholesterol reduction by lovastatin!

Regarding studies carried out on lovastatin lasting 10 years, Ravnskov found no reports on total death rates. Ravnskov queried Merck & Co. directly and was told that the trial was not designed to measure the total clinical outcome!

Deaths from heart attacks were significantly lower in some trials of other statin drugs, but total deaths were 3% absolute lower at best. In the CARE trial Ravnskov showed that a 12% reduction in heart attacks (-1% absolute) was overbalanced by a 1500% increase in cases of breast cancer (+4% absolute). Total deaths were not given. Once again this shows that women should not be treated with statin drugs (or at all), and the benefit for men is quite limited at best with simvastatin and pravastatin.

The incidence of breast cancer was said to be a fluke, and was not observed in the LIPID trial lasting 6 years, in which overall mortality was said to be reduced by 22%; but this was relative risk, an overall drop in mortality of 3% absolute was achieved in subjects with a broad range of initial cholesterol levels [Tonkin et al., New England J. Medicine 339 (19), 1349-1357 (1998)].

In middle-aged men with hypercholesteremia treated with pravastatin for 5 years, death from all causes was reduced by 22%; but this was relative risk; an overall drop in mortality of 1% absolute was achieved [Tonkin et al., New England J. Medicine 333 (120), 1301-1307 (1995)].

"Myth 7: Polyunsaturated oils are good for you." Ravnskov tries to explain what the polyunsaturates are chemically. His effort is one of the few weak points in this book. The degree of saturation actually refers to whether hydrogen can be added to the oil. If so, some of the carbon-carbon bonds in the fatty acid portion of the oil molecule must have been double bonds in which 4 electrons are shared, rather than 2 electrons in the much more common single bonds. Olive and canola oils are the best examples of monounsaturated oils (a sole double bond in each fatty acid portion), and safflower, cottonseed and soybean are examples of polyunsaturates (two or more double bonds in each fatty acid portion). If hydrogen cannot be added in the presence of a catalyst, the oil (or more likely the fat) is said to be saturated, meaning that it cannot take up any more hydrogen. Palm and coconut oils are the best examples. Tallow, lard and chicken fat have some saturated and some monounsaturated fatty acids in their molecules.

Ravnskov cites a survey that showed that high consumption of polyunsaturates leads to premature aging. Also, researchers at a San Francisco, CA hospital thought that babies admitted with edema, anemia and blood cell disturbances were victims of commercial baby milk formulas containing skim milk and polyunsaturates.

Chickens fed polyunsaturates develop brain damage very quickly, but perhaps this should not be expected to apply to humans. A study cited in Myth 1 found that heart attack victims in Puerto Rico and in Honolulu consumed more polyunsaturated oils than those who had not had a heart attack.

The risk of eating transfats is presented at some length. (The reader may avoid transfats by not eating or drinking anything for which the words "partially hydrogenated" appear in the ingredients list.)

"Myth 8: The cholesterol campaign is based on good science." Ravnskov gives examples of reports of interventions with little or no statistical significance being denied time for presentation at meetings, and that offers to write minority dissenting reports on certain trials were being denied on the grounds that the conference was supposed to produce a consensus. Statements of diet-heart proponents and their recommendations are quoted followed by a Ravnskov's refutation of the claimed evidence. He reiterates that even drastic lowering of cholesterol levels with drugs (diet being ineffective) is of no benefit to women and of marginal benefit to men. Ravnskov presents arguments against trying to lower cholesterol levels in children.

"Myth 9: All scientists support the diet-heart idea." If Ravnskov were a lone voice among the Philistines his credibility would be lowered. In this chapter he gives the names of several of the scientists who support his position. This includes Mary Enig, President of the Maryland Nutritionists Association, whose research concerned the hazards of transfats, and who has written a book on the composition and effects of fats in the diet.

Michael Gurr, Professor of Biochemistry, School of Biological and Molecular Sciences, Oxford University, pointed out the insufficient correspondence in vascular pathology between animal models and man, the selection bias in epidemiologcal evidence, the lack of correlation between CHD and fat consumption, and the lack of improvement in coronary mortality after dietary and drug intervention.

George Mann, Professor of Medicine and Biochemistry at Vanderbilt University, TN, realized, from his studies of the Masai in Kenya, that animal fat could not possibly be the cause of high cholesterol and CHD, and he has been open and fearless in his criticism of the LRC directors, and has called the diet-heart theory "the greatest scientific deception of this century, perhaps of any century".

Michael F. Oliver, former Professor and Director of the Wynn Institute for Metabolic Research, London, UK, has warned against campaigns for cholesterol lowering in the general population; criticized those who think that the increased mortality from non-medical causes in trials, such as suicide, is due to chance; and is uneasy about the link between low cholesterol and cancer.

Edward R. Pinckney, editor of a number of medical journals, published a book in 1973 called The Cholesterol Controversy which summarized all the inconsistencies in the cholesterol literature, describes the dangers of lowering one's cholesterol , and devotes an entire chapter to the political drama preceding an early anti-cholesterol campaign.

Raymond Reiser is a former Professor of Biochemistry at Texas A & M University. He decried the practice of referring to other reviews, each taking the last on faith, which has led to the acceptance of a phenomenon (diet-heart) that may not exist. He reviewed work on fatty acids in the diet, found flaws in most of the studies, and concluded that the type of fat in the diet does not make much difference. He analyzed the references used by the American Heart Association in its rationale for dietary recommendations, and found no supportive studies, but instead, some that contradicted the recommendations.

Ray Rosenman is the retired Director of Cardiovascular Research in the Health Sciences Program at SRI International in Menlo Park, CA, and Associate Chief of Medicine, Mount Zion Hospital and Medical Center in San Francisco, CA. He has been a cardiologist and researcher since 1950. In a recent review he wrote that neither diet nor the identity of serum lipids (fats or oils) can explain wide national or regional differences in rates of CHD, or the 20th century variations in rates of CHD. Also that the CHD-preventive effects of diets and drugs have been exaggerated by a tendency in trial reports, reviews, and other papers to cite and inflate supportive results, while suppressing discordant data.

The late Russell Smith was an American experimental psychologist with a strong background in physiology, mathematics and engineering. In his 1989-91 review of the diet-heart theory he wrote: "...studies are often poorly designed and data are often inappropriately analyzed and interpreted... Much of the literature, therefore, is nothing less than an affront to the discipline of science..." He considered much of the work of the National Heart, Lung and Blood Institute and of the American Heart Association to be "incompetent" and "sloppy", and that their political and financial power is enormous and without equal, producing a juggernaut willing and able to suppress evidence and logic. "Equally culpable are the editors of the many journals who publish articles without regard to their quality or scientific import. It is depressing to know that billions of dollars and a highly sophisticated medical research system are being wasted chasing windmills."

William E. Stehbens, Professor at the Department of Pathology, Wellington School of Medicine, New Zealand, exposed the cholesterol myths in reviews: "...Scientific evidence for the role of dietary fat and [also] hypercholesterolemia in the causation of atheroscleosis is seriously lacking..."

Now retired, Lars Werkö, previously Professor of Medicine at Sahlgren's Hospital, Gothenburg, Sweden, Scientific Director at the Astra Co. (now Astra-Zeneca), and head of the Swedish Council on Technology Assessment in Health Care, criticized the design of the Framingham Study, and pointed out inaccuracies and sloppy data gathering in the MRFIT trial.

In the Introduction and Epilogue of this book, Dr. Ravnskov invites the reader to study original papers and follow the arguments. Without the detail he has provided, his voice might be considered "just another opinion". As it happens, a number of other physicians and scientists in addition to the ones in Myth 9 agree with his positions.

Linus Pauling, in his 1986 book: How to Live Longer and Feel Better, quotes John Yudkin, M. D., who found that the correlation between CHD and fat intake is not as good as the correlation with sugar intake. He noted that the Framingham Study showed no correlation between CHD and fat intake, or with cholesterol intake. However, Pauling was fooled by the study on cholestyramine, and failed to note total death rates.

Thomas J. Moore, a medical reporter based in Washington, DC, wrote an article in the September, 1989 issue of The Atlantic Monthly actually called The Cholesterol Myth in which he examined the literature much as Ravnskov did. Moore's conclusions: "Lowering your cholesterol is next to impossible with diet, and often dangerous with drugs - and it won't make you live any longer." This review was also used in Moore's 1990 book Heart Attack.

William Campbell Douglass, Jr., M. D., in 1993 wrote a brochure called Eat Your Cholesterol: How to Live off the Fat of the Land and Feel Great! This might still be available from Second Opinion Publishing, P. O. Box 467939, Atlanta, GA, 30346-9989. Many of the dietary studies and trials are the same ones evaluated by Ravnskov, but are treated in a very popular tone.

John B. Allred came to nearly all the same conclusions as Dr. Ravnskov in his article Lowering Serum Cholesterol: Who Benefits? in the Journal of Nutrition 123: 1453-1459 (1993).

Kilmer S. McCully, Ph. D., M. D., in technical papers and a book: The Heart Revolution: the Extraordinary Discovery that Finally Laid the Cholesterol Myth to Rest, Harper Perennial, 2000, wrote: "But no study anywhere has ever proven that lowering the amount of cholesterol in the diet reduces the risk of heart disease. And lowering cholesterol through drugs won't prevent arteries from hardening if homocysteine is high." McCully is the discoverer of the fact that the undesirable amino acid called homocysteine is an actual cause of atherosclerosis and CHD.

Based on Ravnskov's meticulous analyses as well as the considerable support for his stance shown by others who have also studied the cholesterol data, this book is recommended without reservation. Physicians and other health professionals as well as anyone threatened with cholesterol-lowering treatments would be enlightened, and better able to resist worthless treatments. Health insurers might reconsider compensation for frequent (or any) clinical assays for cholesterol or triglycerides, let alone expensive treatments to lower cholesterol levels that reduce quality of life without prolonging it significantly.

Disclaimer: Any recommendations herein are based on studies published in peer-reviewed scientific journals. I am not an M. D. and cannot engage in the practice of medicine. (My degrees are: B. S. in Chemistry from the Philadelphia College of Pharmacy and Science, and a Ph. D. in Organic Chemistry from the Massachusetts Institute of Technology. My experience includes about 10 years of exploratory drug development at the former and 4 years at the Massachusetts College of Pharmacy.)

Joel M. Kauffman
Research Professor Chemistry
University of the Sciences in Philadelphia
600 South 43rd St.
Philadelphia, PA 19104

Source: health911.com

The book is available at Amazon

On The First Law of Thermodynamics

From the British Medical Journal

Author: Barry Groves, Independent Researcher OX7 6LP

Weight loss on a low-carb diet has two components:

1. Reducing carb (and protein if necessary) intake so that the body no longer has a ready supply of glucose.

2. Increasing fat intake to supply an alternative energy supply.

The aim is to get the body to burn fats -- and crucially for weight loss, this includes body fats. The body will only do this in two circumstances:

1. Starvation (including low-calorie dieting)

2. When glucose is restricted by other means and fats are the only fuel supply available (low-carb, high-fat diets).

But what about the Laws of Thermodynamics?

The laws of thermodynamics, so often quoted by 'experts' (I have another word for them: 'ignorants') in support of the 'calories in = calories out' hypothesis, is a complete red herring as it takes no account of the way the body deals with different nutrients.

One major flaw in their argument is that the body does not use all the food we eat to provide energy. The primary function of dietary proteins, for example, is body cell manufacture and repair: making skin, blood, hair, and finger- and toe-nails, enzymes, etc. The amount of protein needed for this purpose is generally accepted to be about one gram per kilogram of lean body weight. As meats contain approximately 23 grams of protein per 100 grams, a person weighing, say, 70 kg (154 lbs) needs to eat about 300 g (11 oz) of meat, or its equivalent, every day just to supply his basic protein needs. Even eating this volume of lean chicken would provide some 465 kcals. These calories are not used to supply energy, they contribute nothing to the body's calorie needs and so must be deducted if you are counting calories.

Much of the fat we eat is also used to provide materials used by the body in processes other than the production of energy: the manufacture of body cell membranes, bile acids, hormones, the essential fatty acids for the brain and nervous system, and so on. All these must be deducted as well. Thus trying to determine, from food intake and energy expenditure alone, how much excess energy your body will store as fat will give a completely wrong answer. However, these other factors cannot be measured. Calorie counting, which is the foundation of practically every modern slimming diet, is both totally misleading and a complete waste of time.

There are also other anomolies: A figure often used is that one kilogram of body fat represents about 3500 calories. But according to the United States Department Of Health, Education and Welfare:

'On a high-fat diet, 4703 to 8471 excess calories were required for each kilogram of added weight. On a low carbohydrate VLCD [very low calorie diet], replacing fat calories with 8g/day of equivalent carbohydrate calories reduced weight loss by 1.68kg, corresponding to 3300 calories of carbohydrate/kilogram, possibly 2500 calories per kilogram for carbohydrate alone.'(Department of HEW Publication: NIH 75-708, Government Printing Office, 165-86.)

Are they are saying that it takes 4,703 to 8,471 excess calories of fat to add a kilogram of weight, yet it takes only 2,500 to 3,300 calories of carbohydrate to add the same amount? If so 'a calorie is a calorie is a calorie' is not so meaningful after all: a carbohydrate calorie is obviously much more fattening than a fat calorie. So do calories count? Well, perhaps -- but some don't count half as much as others.

Actually, excess fats aren't stored in the body. Any unused fat calories are excreted in urine and faeces. (Endocrinology 1962; 70: 579. Experientia 1963; 19: 319. Metabolism 1964; 13: 87-97. Proc Soc Exp Biol Med 1964; 115:424. Nature 1964; 201: 924)

There is an emerging scientific consensus that weight control is a highly complex topic and the old ideas that overweight people are lazy gluttons are now realised to be as absurd and insulting as the overweight have always thought they were.

By the way, ketones are derived from fats in food which has been bought and paid for. They are a valuable source of energy for cells that usually use glucose. It makes no sense to create in the body a situation where they are flushed down the lavatory.

Source: British Medical Journal

Ketosis: Is it safe?

Why do some people say it's dangerous?

On July 7, 2002, the New York Times published "What if It's All Been a Big Fat Lie?" written by Gary Taubes.

I quote the article: " 'Doctors are scared of ketosis,' says Richard Veech, an N.I.H. [National Institutes of Health] researcher who studied medicine at Harvard and then got his doctorate at Oxford University with the Nobel Laureate Hans Krebs. ''They're always worried about diabetic ketoacidosis. But ketosis is a normal physiologic state."

"Simply put, ketosis is evolution's answer to the thrifty gene. We may have evolved to efficiently store fat for times of famine, says Veech, but we also evolved ketosis to efficiently live off that fat when necessary. Rather than being poison, which is how the press often refers to ketones, they make the body run more efficiently and provide a backup fuel source for the brain. Veech calls ketones ''magic'' and has shown that both the heart and brain run 25 percent more efficiently on ketones than on blood sugar." You can read the full article here.

Being in ketosis means your body has burned a large amount of fat in response to the fact that it didn't have sufficient glucose available for energy needs. Under everyday conditions, the carbohydrates you eat are converted to glucose, which is the body's primary source of energy. Whenever your intake of carbohydrates is limited to a certain range, for a long enough period of time, you'll reach a point where your body draws on its alternate energy system, fat stores, for fuel.

This condition called dietary ketosis, means your body burns fat and turns it into a source of fuel called ketones. Ketones are produced whenever body fat is burned. When you burn a larger amount of fat than is immediately needed for energy, the excess ketones are discarded in the urine.

Dietary ketosis is among the most maligned and misunderstood concepts in nutrition because it is often confused with ketoacidosis, which is a life-threatening condition most often associated with uncontrolled insulin-deficient Type 1 diabetes. In the Type 1 diabetic, the absence of insulin leads to a toxic build-up of blood glucose and an extreme break-down of fat and muscle tissue. This condition doesn't occur in individuals who have even a small amount of insulin, whether from natural production or artificially administered.

Dietary ketosis, however, is a natural adjustment to the body's reduced intake of carbohydrates as the body shifts its primary source of energy from carbohydrates to stored fat. The presence of insulin keeps ketone production in check so that a mild, beneficial ketosis is achieved. Blood glucose levels are stabilized within a normal range and there is no break-down of healthy muscle tissue.

The most sensitive tests of ketosis ("NMR" and "blood ketone level") show that everyone is in some degree of ketosis every day, particularly after not eating overnight and after exercising. Ketosis is the body's survival system. It is not an abnormality nor does it present any medical danger, except to a Type I insulin-dependent diabetic. The body functions naturally and effectively while in a state of dietary ketosis.

Some of the benefits many people experience while in a state of dietary ketosis for intentional weight loss may include rapid weight loss, decreased hunger and cravings, improved mood, increased energy and, as long as protein intake is adequate, protection of lean muscle mass.

Source: http://www.ketosis-ketoacidosis-difference.com/

The Mediterranean Paradoxes

The 'French Paradox' has been well documented over the years. This paradox describes the low levels of heart disease enjoyed by the French, despite the fact that they eat an 'unhealthy' high-fat diet. This is, of course, seen as a 'paradox' because conventional wisdom has it that such a diet should increase heart disease rates...

Read full article: Second Opinions - Barry Groves, PhD

The Myths and Realities of Ketosis

Critics of low-carb eating often cite the metabolic state of ketosis as reason enough to forget about restricting carbohydrates in your diet. They offer an assortment of reasons that ketosis is dangerous and to be avoided - without acknowledging that almost everyone enters a state of ketosis at some point within a 24 hour period of time...when they sleep!

I'd like to use this edition of the Low-Carb Guru to sort the fact from fiction and provide you with information you can use to make your own decision whether to follow a low-carb plan low enough to trigger ketosis, or low enough to lose while remaining in primary glucose metabolism!

Let's start with what ketosis is. It is a metabolic state where your body "switches" from primarily using glucose for energy to primarily using fat for energy. The fat used for energy will come from both dietary fat sources and body fat. Ketosis is the natural result of limiting carbohydrates in your diet to a low enough level - you're NOT eliminating them - that your body can't meet its energy needs primarily from glucose. This is because all carbohydrates are converted to glucose for energy and if you limit your intake, the body will still need energy (calories) and will find another way to get them - ketosis - fat burning is its source of its primary energy.

But wait, you say, the body needs glucose!

Read full article: countcarbs.com

Common Myths About Low Carb Diets

According to the defenders of low-fat/high-carb diets, following a low carbohydrate diet will clog your arteries, blow out your kidneys, cause rampant bone loss, and give you the physical proportions of a blimp! Read the newly-updated version of this popular article, which explains why you should readily dismiss such nonsense for the self-serving propaganda it truly is...

Full article at theomnivore.com: Common Myths About Low Carb Diets