More Saturated Fat = Less Coronary Artery Disease!

Anthony Colpo,
November 9, 2004.

The latest issue of the American Journal of Clinical Nutrition has just published a study that gives saturated fat-defending heretics like yours truly something to smile about.

Researchers took 235 postmenopausal women with established coronary heart disease and performed coronary angiographies at the start of the study and after a mean follow-up of 3.1 years. A total of 2243 coronary segments were analyzed.

The women were also divided into four categories according to their level of saturated fat intake.

Saturated fats found to be protective

After adjusting for multiple confounders, a higher saturated fat intake was associated with less narrowing of the arteries and less progression of coronary atherosclerosis during follow-up. Compared with a 0.22-mm narrowing in the lowest quartile of intake, there was a 0.10-mm narrowing in the second quartile, a 0.07-mm narrowing in the third quartile, and no narrowing in the fourth and highest quartile of saturated fat intake.

Carbohydrates found to be harmful

The protective association of saturated fat was more pronounced among women with lower monounsaturated fat and higher carbohydrate intakes. Carbohydrate intake was positively associated with atherosclerotic progression, particularly when the glycemic index was high.

Polyunsaturates found to be harmful

Polyunsaturated fat intake was positively associated with progression of atherosclerosis when replacing other fats, but monounsaturated and total fat intakes were not associated with progression.

The bottom line

The authors concluded: "In postmenopausal women with relatively low total fat intake, a greater saturated fat intake is associated with less progression of coronary atherosclerosis, whereas carbohydrate intake is associated with a greater progression".

"Our findings are not consistent with the hypothesis…that saturated fat intake increases atherosclerotic progression in postmenopausal women but instead suggest that saturated fat intake may reduce such progression, especially when monounsaturated fat intake is low or carbohydrate intake is high. Our findings also suggest that carbohydrate intake may increase atherosclerotic progression, especially when refined carbohydrates replace saturated or monounsaturated fats".

Mere association or direct causation?

After examining the baseline data for the study subjects, it becomes apparent that the results can not be explained away by otherwise healthier lifestyles among those eating the most saturated fat; the high saturated fat group, in fact, had the greatest number of current smokers.

Studies like this do not prove causation, but we do know that saturated fatty acids, because of their lack of vulnerable double bonds, are the least susceptible to free radical damage; polyunsaturates are the most vulnerable. We also know that increased carbohydrate consumption, especially of the refined variety, does a sterling job of raising blood sugar and insulin levels, which accelerates glycation, free radical activity, blood clot formation, and arterial smooth muscle cell proliferation.

Furthermore, the contention that increased polyunsaturated fat and carbohydrate consumption can worsen cardiovascular disease is supported by evidence from clinical trials and by the observation that increasing heart disease incidence throughout the twentieth century has been accompanied by increasing polyunsaturate and refined carbohydrate consumption. Animal fat consumption, in contrast, has remained stable over the last 100 years.

Anti-saturate stupidity

You know, I could take this opportunity to really dump on those who have been incessantly slandering saturated fat all these years, but I won't, because some of my more sensitive readers might write me and accuse me of unfairly impugning the personal and professional integrity of these upstanding citizens. I could point out how many of these anti-saturated fat commentators have built their status and careers on a completely erroneous bunch of nonsense, but again, I won't, because, hey, that wouldn't be nice. I could also point out how their unbridled vitriol against these naturally-occurring fats has probably cost hundreds of thousands, even millions, of lives, but, gee, that wouldn't be a politically correct thing to do.

Nope, I won't mention any of these things (or did I do just that...oops!)…all I will say is that next time you hear some misguided fanatic wailing on about the evils of saturated fat, run--straight to the nearest tub of butter!

Source: The Omnivore

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

Anthony Colpo,
October 2, 2004.

Hi Anthony,

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

The Benefits of High Cholesterol

By Uffe Ravnskov MD, PhD

People with high cholesterol live the longest. This statement seems so incredible that it takes a long time to clear one´s brainwashed mind to fully understand its importance. Yet the fact that people with high cholesterol live the longest emerges clearly from many scientific papers. Consider the finding of Dr. Harlan Krumholz of the Department of Cardiovascular Medicine at Yale University, who reported in 1994 that old people with low cholesterol died twice as often from a heart attack as did old people with a high cholesterol.1 Supporters of the cholesterol campaign consistently ignore his observation, or consider it as a rare exception, produced by chance among a huge number of studies finding the opposite.

But it is not an exception; there are now a large number of findings that contradict the lipid hypothesis. To be more specific, most studies of old people have shown that high cholesterol is not a risk factor for coronary heart disease. This was the result of my search in the Medline database for studies addressing that question.2Eleven studies of old people came up with that result, and a further seven studies found that high cholesterol did not predict all-cause mortality either.

Now consider that more than 90 % of all cardiovascular disease is seen in people above age 60 also and that almost all studies have found that high cholesterol is not a risk factor for women.2 This means that high cholesterol is only a risk factor for less than 5 % of those who die from a heart attack.

But there is more comfort for those who have high cholesterol; six of the studies found that total mortality was inversely associated with either total or LDL-cholesterol, or both. This means that it is actually much better to have high than to have low cholesterol if you want to live to be very old.

Read full article at: Weston A. Price

Reducing the serum cholesterol level with a diet high in animal fat

South Med J. 1988 Jan;81(1):61-3.

Newbold HL.

Multiple food allergies required a group of seven patients with elevated serum cholesterol levels to follow a diet in which most of the calories came from beef fat. Their diets contained no sucrose, milk, or grains. They were given nutritional supplements. This is the only group of people in recent times to follow such a diet. During the study, the patients' triglyceride levels decreased from an average of 113 mg/dl to an average of 74 mg/dl; at the same time, their serum cholesterol levels fell from an average of 263 mg/dl to an average of 189 mg/dl. At the beginning of the study, six of the patients had an average high-density lipoprotein percentage of 21%. At the end of the study, the average had risen to 32%. These findings raise an interesting question: are elevated serum cholesterol levels caused in part not by eating animal fat (an extremely "old food"), but by some factor in grains, sucrose, or milk ("new foods") that interferes with cholesterol metabolism?

PMID: 3336803 [PubMed - indexed for MEDLINE]

Statin Alert

StatinAlert.org
Warning: Your cholesterol-lowering drug may be destroying your health!

Discover the Uncensored Truth about Cholesterol-Lowering Drugs!

StatinAlert.org is a non-profit website.

If you take cholesterol-lowering drugs, or are being urged by your doctor to start taking them, you should be aware that:

*statins can cause severe muscle weakness and pain, even at low doses;
*statins can cause cognitive impairment and memory loss;
*cholesterol-lowering drugs routinely cause cancer in laboratory animals, and there is valid concern that they may do the same in humans;
*statins have been linked to increased risk of heart failure;
*a large percentage of doctors remain astonishingly ignorant of the adverse effects of statins!

Visit the site: statinalert.org

Cholesterol and the Pharmaceutical Industry's Biggest Secret

By Shane Ellison M.Sc.

A commonly held myth is that high cholesterol, especially LDL cholesterol, is a major risk factor for heart disease (known as atherosclerosis). Thus, in a panicked attempt to prevent this pandemic killer millions of people are using cholesterol-lowering drugs. However, when we consider the scientific evidence it appears that the aforementioned myth is the antithesis...

1. With respect to women, researchers at the University San Diego School of Medicine show that no study has shown that cholesterol-lowering drugs lower overall mortality in women.

2. Researchers at the University San Diego School of Medicine UCSD also point out that high cholesterol in those over 75 years of age is protective, rather than harmful and that low cholesterol is a risk factor for heart arrhythmias (leading cause of death if heart attack occurs).

3. The European Heart Journal has published the results of a 3-year study involving 11,500 patients. Researcher Behar and associates found that in the low cholesterol group (total cholesterol below 160mg/dl) the relative risk of death was 2.27 times higher relative to those with high cholesterol. The most common cause of death in the low cholesterol group was cancer while the risk of cardiac death was the same in both groups.

In support of their findings these researchers point out that previous studies found a higher increase in lung cancer when total cholesterol levels were maintained below 170 mg/dl.

This has not stopped Pfizer from implicating that total cholesterol levels should be at 150 mg/dl (see http://www.lipitor.com/)

4. The most widely respected medical journal, The Journal of the American Medical Association, published a study entitled: Cholesterol and Mortality. 30 Years of Follow-up from the Framingham study. Shocking to most, this in-depth study showed that after the age of 50 there is no increased overall death associated with high cholesterol! There was however a direct association between low levels (or dropping levels) of cholesterol and increased death. Specifically, medical researchers reported that CVD death rates increased by 14% for every 1mg/dl drop in total cholesterol levels per year.

5. The Journal of Cardiac Failure published the findings of Tamara and colleagues in a paper entitled Low Serum Total Cholesterol is Associated with Marked Increase in Mortality in Advanced Heart Failure. In their analysis of 1,134 patients with heart disease they found that low cholesterol was associated with worse outcomes in heart failure patients and impaired survival while high cholesterol improved survival rates. Additionally, their findings showed that elevated cholesterol among patients was not associated with hypertension, diabetes, or coronary heart disease.

6. And finally, despite the successful attempts to lower cholesterol with pharmaceutical drugs, the death rate from heart disease has not changed over the last 75 years and mortality from heart failure is more than double what it was in 1996. Hence, those who think they are safe from heart disease due to lowering total cholesterol levels may want to seriously rethink their preventative efforts.

Sadly though, some of the most well-respected health practitioners, medical doctors, and herbalists in the world have fallen victim to pharmaceutical propaganda. This can be seen by their often regurgitated, ill-thought out hypothesis that lowering cholesterol prevents heart disease.

Meanwhile, people continue to die (2700 people die every day from heart disease) while pharmaceutical companies enrich themselves with the sales of cholesterol-lowering drugs. The CEO of Pfizer, makers of the popular cholesterol-lowering drug Lipitor, was compensated 33.9 million dollars last year (does not include the ten’s of millions in stock options). This equates to 2.8 million per month, which is about $94,000 per day.

So, how does one successfully convince the entire U.S that each and every person should have the same cholesterol levels? Easy, pharmaceutical companies work tirelessly to promulgate the cholesterol-lowering myth by conveniently citing supportive studies while burying the unsupportive. As reported in the British Medical Journal, Uffe Ravnskov MD, PhD shows his results of a meta-analysis of 22 published controlled cholesterol-lowering trials. He found that studies which showed to be supportive of low cholesterol were cited six times more often than those that were unsupportive and that unsupportive trials had not been reported since 1970! Further, his research showed that those studies that were supportive of low cholesterol were due to bias on part of the researchers.

With 12 billion dollars worth of cholesterol-lowering drugs sold annually, the average American has become a cholesterol-lowering drug addict without giving any thought to the potential negative side effects. For instance, evidence from the cholesterol-lowering trial known as PROSPER showed that while Pravachol may have prevented 22 deaths from cardiovascular disease the benefit was negated by 24 deaths caused by cancer among those taking Pravachol. Numerous medical journals have shown that cholesterol-lowering drugs significantly increase ones risk of suffering from not only cancer but also CoQ10 deficiency (paradoxically leads to heart disease), rhabdomyolysis, erectile dysfunction and loss of memory and mental focus.

Combined, these facts render America’s best selling drug useless and in some cases deadly (make you wonder about the other less popular drugs). As such, they are among the pharmaceutical industries biggest secrets. You won’t hear about them from your doctor, the media, or a pharmaceutical sales rep.

To circumvent blind addiction to cholesterol-lowering drugs, their deadly side-effects, wasted money, and finally, heart disease itself, Americans must understand the importance of cholesterol in the human body. Moreover, they must learn about natural medicine which rivals synthetic drugs and lifestyle habits that have been proven to prevent and treat heart disease.

References

Patrick, Lyn. Et al. Cardiovascular Disease: C-Reactive Protein and the Inflammatory Disease Paradigm: HMG-CoA Reductase Inhibitors, alpha-Tocopherol, Red Yeast Rice, and Olive Oil Polyphenols. A review of the Literature. Alternative Medicine Review. Volume 6, Number 3. 2001.

Uri Goldbourt. Et al. Choleserol and Coronary Heart Disease in Mortality. A 23 year follow-up Study of 9902 Men in Israel. Arteriosclerosis. Vol 10, No. 4, July/August 1990

Behar, S. Et al. Low total cholesterol is associated with high total mortality in patients with coronary heart disease. European Heart Journal (1997) 18, 52-59.

Horwich TB. Et al. Low Serum Total Cholesterol is Associated with Marked Increase in Mortality in Advanced Heart Failure. J Card Fail. 2002 Aug;8(4):216-214.

Ravnskov. U. Cholesterol-Lowering Trials in Coronary Heart Disease: “Frequency and Citation of Outcome”. BMJ. 305;6852. July 4, 1992. PP 15-9

Anderson KM. Cholesterol and Mortality. 30 Years of Follow-up from the Framingham Study. JAMA 1987 Apr 24;257(16):2176-80

Uffe Ravnskov, et al. Letter to Archives of Internal Medicine, submitted on July 20,2002

STATINS: Saviours of Mankind, or Expensive Scam?

Introduction

Although there is not, and never has been, any convincing evidence that levels of serum cholesterol have any causal relationship with coronary heart disease, that hasn't stopped the cholesterol hypothesis being used as a basis for the sale of drugs to lower cholesterol.

Over the last half of the twentieth century a whole range of drugs were tried. All, without exception, were less than successful. And no evidence was produced that cholesterol-lowering, whether by diet or various older drugs such as clofibrate, gemfibrozil, cholestyramine, colestipol, or nicotinic acid, extends life or reduces overall mortality.

But the new type of cholesterol-lowering drugs called statins do appear to be successful. There is no doubt that in trials there has been a reduction in the numbers of deaths among those taking statins compared to control groups. For the first time cholesterol-lowering has shown significant improvement in mortality rates, from coronary mortality, stroke mortality and total mortality.

Statins are now the drugs of choice and aggressively marketed. As these cost around £400 per person per year, and they have to be taken for life, the drug companies can look forward to several years of very healthy profits until the patents run out.

So statins increase the health of drug companies' bank balances, but do they really increase the health of those who take them? And do they represent good value for money as far as a cash-strapped National Health Service is concerned?

Full article available here: Second Opinions - Barry Groves PhD

Let them eat cake, butter, cream...

For decades the advice has been to cut cholesterol and protect your heart. Now some doctors think it makes no difference

Jerome Burne
Tuesday April 6, 2004
The Guardian

There is almost no connection between the amount of cholesterol in your blood and your risk of a heart attack. Not only that, if you don't already have heart disease, you probably won't live any longer if you bring your cholesterol level down. Finally, statins, the cholesterol-reducing drugs we are all being urged to take, are of little use to women.

These are just a few of the highly controversial claims being made by a loose network of researchers, known collectively as the Cholesterol Skeptics, who are mounting a direct challenge to one of the cornerstones of public health policy - the notion that reducing cholesterol saves lives at risk from heart disease. Any doctor will tell you that if your cholesterol level is higher than five (millimoles per litre) that you should bring it down, probably through taking one of the statins family.

According to the Cholesterol Skeptics, however, this will not only involve the NHS in a massively increased drug bill when many cheaper options are available, but will only benefit men who already have a heart condition. Can such views, which fly so directly in the face of the entire medical establishment, have any basis in fact?

The proponents certainly make some challenging points. For instance, they say that there is precious little evidence that a longer life results for those millions of people who for years have dutifully taken their drugs and endured cholesterol-reducing diets. In fact, a number of trials have found that, even though the number of deaths from heart disease does fall when cholesterol is reduced by a range of means among patients in primary care - that is, at GP level - there is often an increase in the overall death rate from other causes.

Writing in the British Medical Journal (BMJ) at the end of last year, for instance, Rebecca Warburton, a professor at the University of Victoria in Canada, reviewed studies of statins and concluded: "Statins in primary prevention have not consistently reduced the incidence of myocardial infarction [heart attack] or stroke. Other studies have even found that over the age of 50, reducing cholesterol increases the death rate.

The notion that cholesterol is linked to heart disease goes back to the middle of last century, along with the idea of bringing cholesterol levels down with a low-fat diet to protect the heart. But both of these ideas have been strongly challenged. For example, plenty of studies show that only 50% of people who develop heart problems have high cholesterol, while a study in the BMJ in 2001 found no link between changing fat in the diet and heart disease.

"At a global level the link with cholesterol and heart disease is far more tenuous than is generally supposed," says Malcolm Kendrick, a GP from Cheshire who is the most active Skeptic in Britain. "For instance, in Russia at the moment, heart attack rates are rising dramatically but their cholesterol levels are the reverse of what we see in the US and the UK. They often have high levels of the so-called "good" HDL cholesterol and low levels of the "bad" LDL, but they still keel over from heart disease."

Even in the west the link is pretty thin according to Joel Kauffman, a professor at University of the Sciences in Philadelphia. A review he did of statin use last year pointed out that what does correlate with high cholesterol is age, a majorfactor in heart disease. "When you correct for age," he concluded "there is almost no correlation between high cholesterol and heart disease."

This challenge comes at a time when the government, the medical profession and the pharmaceutical industry are united in their approval of cholesterol-reducing drugs. Government figures out last week, for instance, show that heart attack deaths are declining and part of the credit for this is given to statins.

This month the New England Journal of Medicine is due to publish the results of a large trial reporting that the heart patients who reduced their cholesterol down as far as two, had a 16% drop in their risk of experiencing such "vascular events" as heart attacks and strokes. One of the cholesterol-reducing drugs, Lipitor, is among the best-selling prescription drugs in the world with sales worth $16bn (£8.75bn). The message from this trial is likely to be that when it comes to cholesterol "you can't go too low".

So what are the Skeptics basing their apparently highly idiosyncratic challenge on? At this point it is worth making clear the difference between primary care - your GP prescribing statins because he considers you have a raised risk of heart disease - and secondary care, which you get after a heart attack in hopes of preventing another one. Even the Skeptics generally agree that the studies show that taking statins after you have obviously got heart disease can reduce your chances of a further attack.

"But the fact that bringing down cholesterol can help some male heart patients," says Kendrick "doesn't mean it's going to protect otherwise healthy people whose cholesterol is over five. Since the average level in the UK is 5.7, that is an awful lot of people."

But what about trials showing that statins reduce the risk of heart attacks and strokes by a quarter among healthy volunteers? That sounds impressive. But how impressive, say the Skeptics, depends on how you work out the percentages. Heart attacks among healthy people are quite rare, so the actual percentage of people having a heart attack while on statins is just 3% compared to 4% on a placebo. That is indeed a drop of 25% but it is also a mere 1% fewer heart attacks over five years, which is not quite so wonderful. In Sweden official advice is to reserve statins largely for secondary care.

If pushed, experts in favour of aggressive cholesterol reduction may well admit that the value to women is less clear. That is because, although women tend to have higher levels through life, they develop heart disease 15 to 20 years later. An increasing number of doctors are putting post-menopausal women on statins to protect their hearts now that HRT has been discredited. Is this wise?

A resounding "no" was the answer from an analysis of five statin trials conducted by a team of researchers at the University of British Columbia (UBC) in Canada and published last year. Stressing that only 28% of the participants were women, the team concluded: "The results do not support the use of statins by women without heart disease."

The UBC group also raised new queries about side effects. Statins are generally described as safe and well tolerated. But the same report concluded that although patients on statins had a 1.4% lower rate of heart attacks, this was cancelled out by a 1.8% rate of "serious adverse events associated with the drug", including cancer. That, they say, is almost certainly an underestimate since only two of the trials provided details of any serious side effects. The researchers said they had asked the drug producers for the missing data but received no reply.

To an outsider what is curious about this debate is that both sides are using the same data; much of the disagreement is based on how you interpret it. But that is not all that is going on. Two recent developments have given a big impetus to the Skeptics. The first is the huge surge in the popularity of the Atkins diet. So far the results seem to show that eating a diet high in fat doesn't automatically result in a rise in cholesterol. This strikes at the roots of the cholesterol hypothesis," says Kendrick - though the jury is still out on the long-term effects of an Atkins-style diet and bigger trials are ongoing. Another aspect of the Atkins argument is that a diet high in carbohydrates, especially refined carbohydrates such as sugar, damages arteries in the long run.

Akey factor in developing heart disease, say the Skeptics, is inflammation. This is the defensive reaction produced by the body when it feels under attack, the redness that flares up round a cut or bruise. An inflamed point on an artery makes it more likely that plaque will form.

In the past two years, two major studies have found that the amount of inflammation in your body is a better indicator of your heart-attack risk than your cholesterol level. Inflammation is measured by something called C-reactive protein (CRP). Some claim such findings make the cholesterol hypothesis redundant. This could supply an answer to the question raised by the Skeptics' challenge: If cholesterol reduction isn't that beneficial, why do the drugs reduce the number of heart attacks? Probably, say the Skeptics, by reducing inflammation.

The body produces inflammation via a number of complicated pathways many of which involve a molecular switch known as NF kappaB and recent studies show that statins are pretty effective at dimming NF kappaB. However this is what a number of other effective heart treatments also seem to do, such as aspirin and omega three fatty acids found in fish oils, not to mention garlic and vitamin E.

If this turns out to be what is going on, and trials are under way to test the idea, this seems likely to shunt cholesterol reduction into a small corner of the overall picture of heart disease and allow statins to be marketed as "inflammation fighters". Other ways of reducing your C-reactive protein level include stopping smoking, losing weight and exercising.

The cholesterol hypothesis is unlikely to be abandoned in a hurry, given the weight of financial and political muscle behind it. But the Skeptics have raised questions that could ultimately have an impact on the way we think about heart disease.

Source: The Guardian

Ed: Further reading at Thincs - The International Network of Cholesterol Skeptics

Statin Drugs

The Ultimate Manifestation of Anti-Cholesterol Stupidity?

By Anthony Colpo, March 14, 2004.

The last decade has seen a rapid rise in the use of cholesterol-lowering statin drugs. Last week, media reports hailed the results of a new study as "proof" that doctors should more aggressively pursue cholesterol-lowering in CHD patients by using even higher dosages of statin drugs. While they might be hailed as "miracle drugs" by the establishment, statins have been shown to cause muscle damage, liver dysfunction, fatigue, impaired mental function, and may even contribute to heart failure and cancer. In this article we will learn why statins are anything but "miraculous". Before we do that though, let's take a quick journey back in time to learn about the plight of "Acirema"…

Once upon a time, (the late fifties, actually) there existed a prosperous kingdom known as Acirema. Although blessed in many ways, Acirema was unfortunately troubled by very high rates of coronary heart disease (CHD). In response to growing concern throughout the kingdom, the King of Acirema promised the people that he would find a cure for this terrible ailment.

The King of Acirema proceeded to establish the massive National Institutes of Health (NIH), who, along with the Acireman Heart Association (AHA), vowed to engage all their bureaucratic might in order to free the population from the dreaded scourge of CHD.

One day, the fine minds from the NIH and AHA sat down and wondered where they should start in their fight against CHD.

"What if", proffered one of them, "we convince the people of the kingdom to cut all the saturated fat from their diet, and replace it with polyunsaturated vegetable oils. That will lower their cholesterol levels, and we all know that cholesterol causes heart disease in animal studies, right?"

"What a splendid idea!", chirped his fellow bureaucrats in delighted unison.

The people of Acirema did as they were told and cut all the saturated fat from their diet, and began consuming ungodly amounts of vegetable oils. While the polyunsaturated vegetable oil manufacturers became very, very rich, the people of Acerima did not experience any respite from CHD. In fact, a steady rise in cancer became apparent after the kingdom's switch to vegetable oils.

"Oops", said the people from the NIH and AHA.

"What do we do now?" they wondered.

"What if", proffered one of them, "instead of replacing one type of fat with another, we told the villagers to simply cut out fat altogether, and eat carbohydrates instead? We all know that fat is a gooey, sticky substance that clogs up arteries, right?"

"What a splendid idea!", chirped his fellow bureaucrats in delighted unison.

So they convinced the people of Acirema to cut the fat from their diets. The Aciremans reluctantly gave up their steak and eggs, and instead began eating a bizarre array of non-fat, low-fat, and reduced-fat foods. While the manufacturers of these strange new foods became very, very rich, the people of Acirema did not experience any relief from CHD. In fact, the kingdom's switch to low-fat, high-carbohydrate foods was followed by a dramatic jump in obesity and diabetes.

"Oops", said the people from the NIH and AHA.

"What do we do now?" they wondered.

"Drugs!", shouted one of them, "Damn it, if we can't beat CHD with diet, we'll beat it with drugs!"

"What a splendid idea!", chirped his fellow bureaucrats in delighted unison.

So the bureaucrats started experimenting with all sorts of drugs. Noting that the premenopasual womenfolk of Acirema had very low rates of heart disease, they first tried giving female hormones to the menfolk. Unfortunately, the results were not quite what they expected. When the menfolk subsequently grew breasts, became impotent, and started reading Better Homes and Gardens, the bureaucrats realized they had made a big mistake.

Not to be deterred, however, the inquisitive staff from the NIH and AHA then began studying some new cholesterol-lowering drugs called fibrates. When testing the fibrates on the kingdom's guinea pigs, they found that any reduction in coronary heart disease mortality was usually countered by a corresponding increase in non-CHD mortality, usually from violent death and cancer. Mesmerized by the cholesterol-lowering capabilities of the fibrates, they nonetheless ignored the results of the guinea pig tests, and gave the people of the kingdom the drugs anyway. There was a subsequent small reduction in coronary heart disease mortality, but it was countered by a corresponding increase in non-CHD mortality, mainly from violent death and cancer.

The folks from the NIH and AHA became very disparaged. The King was angry because he had promised the kingdom a cure for CHD, and now the people of the kingdom were upset at him because, over thirty years after he had made his promise, there was still no cure for CHD. The King told the heads of the NIH and AHA that if they didn't come up with a cure for CHD soon, there would be royal hell to pay!

Things were looking very bleak indeed for the bureaucrats. They had convinced themselves, the King, and the kingdom that the key to conquering CHD was to lower cholesterol levels, but every cholesterol-lowering strategy they tried drew a blank. With the dismal results seen in their dietary fat interventions, and the poor results seen with the various drugs they had tried, some of the staff from the NIH and AHA began to realize that their cholesterol theory did not have a scientific leg to stand on. So they did what any good vested interest would do when advancing an agenda not backed by facts; they relied on propaganda. Lots of it.

For awhile, the people of the kingdom were placated by the copious daily stream of anti-cholesterol propaganda. This in turn, helped to keep the King off the bureaucrats' backs. Every now and then, though, some brave, independent-thinking practitioner would dare to ask why, if cholesterol-lowering was so beneficial, was the kingdom still experiencing such high rates of heart disease? When this happened, the bureaucrats would call the officers from the Non-Compliance Eradication Program (NCEP) who would capture the dissident, strip him of his qualifications, and banish him to an isolated section of the woods. After ridding the kingdom of the dissident, the NCEP would then institute a special Propaganda-Intensification Program (PIP) as a means of damage control. However, despite the NCEP's best efforts, and the implementation of many, many PIPs, the voices of dissent began to grow ever louder. Tension again started to mount at the NIH and AHA.

Then one day, just as things were beginning to look very shaky for the bureaucrats, along came their savior, their knight in shining armor: a miraculous new class of drugs which they promptly called the "statins"!

Unlike their earlier experiments with cholesterol-lowering pharmaceuticals, randomized trials with these new statin drugs showed decreases in total as well as CHD mortality. They did not appear to cause any increase in cancer or violent death, and they did not cause the menfolk to grow breasts. The bureaucrats were beside themselves: at last, definitive proof that cholesterol-lowering indeed saved lives, and that the massive propaganda machine they had created was good for more than just yanking people's chains! The bureaucrats excitedly reported their research findings to the King, who subsequently decreed that everyone in the Kingdom over the age of two must immediately begin taking the marvelous new statin drugs.

A huge wave of relief swept over Acirema; people were delighted that an effective treatment for CHD had finally been found. News of the magnificent statins rapidly spread to other kingdoms, and they quickly became one of the best-selling drug categories in the world. The King of Acirema was very proud and called the NIH and AHA staff to the royal palace, where they were honored in a huge celebratory feast. The drug companies of Acirema were delighted too - they had grown very, very, very rich, and showered the NIH and AHA staff with tokens of their appreciation. Some of the NIH and AHA staff were even offered prestigious, highly-paid positions within the drug companies.

All was well in the kingdom!

That is, until some of the naughty villagers began pointing out that maybe, just maybe, statin drugs were not quite as wonderful as they had been made out to be.

Uh, oh…

Waking Up From The Statin Fantasy

For those who haven't caught on yet, the above story is no fairy tale. With some name changes to protect the not-so-innocent and a few other slight twists (I made up the bit about Better Homes and Gardens), the above tale pretty well describes the course of what may well be the biggest and most successful scam of the Twentieth Century - the widely accepted theory that elevated cholesterol levels cause heart disease.

After decades of failed drug and dietary intervention trials,(1) the cholesterol hypothesis that the health orthodoxy had invested so heavily in was beginning to look like a total bust. So when the positive results from statin trials started rolling in during the mid-nineties, the powers-that-be could barely contain themselves. Finally, proof that cholesterol-lowering worked! Statins were quickly dubbed "miracle drugs", became a physician favorite, and were transformed into the second-best selling class of drugs in the world. In fact, the current number one selling pharmaceutical in the world, which amassed a staggering 6.4 billion dollars of sales in 2001, is atorvastatin, made by Pfizer and marketed under the name Lipitor.(2)

The monumental success of statin drugs is a powerful, and sad, testament to the madness inherent in the cholesterol phenomenon. While many health authorities, researchers, and physicians just about trip over themselves in their rush to praise statins, a number of safety issues raise serious concerns about their suitability for long term use. Before we address these worrying issues, let's first examine whether cholesterol reductions are in fact responsible for any reduction in CHD mortality produced by statin administration.

Just How Do Statins Work?

While heavily promoted, the claim that the CHD reductions seen in clinical trials with statins are due to their potent cholesterol-lowering action is scientifically baseless. A close look at the data from all of the major controlled, randomized clinical trials with statin drugs reveals that there was no association between the degree of total cholesterol lowering and the CHD survival rate. In other words, the risk of a fatal heart attack was similarly reduced whether cholesterol levels were lowered by a small or large amount. The same applies to LDL, which we have been brainwashed into believing is the "bad" cholesterol; death rates in those with the highest and lowest LDL levels are virtually identical.(3-9) There is one exception - the recent PROSPER trial, which recorded the highest survival rates in both the treatment and control groups among those with the highest LDL levels.(10)

If statins exert a favorable effect on coronary health, it sure as hell isn't through cholesterol reduction!

Beyond Cholesterol.

Statin drugs exert their lipid-lowering effect by blocking an enzyme in the liver that is involved in the early stages of cholesterol synthesis. Statins inhibit the synthesis of mevalonate, a precursor not only to cholesterol, but also to a substance known as geranyl-geraniol. Inhibition of geranyl-geraniol may produce beneficial effects on levels of Nitric Oxide (NO), a substance with anti-inflammatory and artery-dilating properties.(11-13) The consequences of this dual action are widespread:

• In research with mice, statins markedly reduced measures of both inflammation and atherosclerosis, even though there was little change in serum cholesterol levels.(14)
  * Fluvastatin has reversed the progression of atherosclerosis in rabbits, without any accompanying change in serum cholesterol.(15)
  * In an Italian study, researchers placed a collar around one of the carotid arteries in rabbits to stimulate narrowing of the arterial wall. After 14 days, the collared arteries of rabbits treated with fluvastatin, lovastatin and simvastatin narrowed significantly less than those in untreated animals. Cholesterol levels in the rabbits were unchanged.(16)
  * In human volunteers with slightly elevated cholesterol, researchers found that 4 weeks of simvastatin therapy significantly enhanced forearm blood flow, a measure of arterial function. The amount of improvement was unrelated to the degree of cholesterol reduction.(17)
  * In elderly diabetic patients, cerivastatin increased dilation of the brachial artery after only 3 days, before any change in cholesterol levels had occurred.(18)
  * Statins have been shown to reduce blood platelet production of thromboxane, an eicosanoid that encourages blood-clotting. This effect was not seen with the older drugs that lowered total or LDL cholesterol such as cholestyramine, cholestipol, and fibrates.(19)
  * Statins have also been observed to inhibit the migration of smooth muscle cells seen in atherosclerotic plaque formation.(20,21)
  * In the PRISM study, the effect of statin therapy on coronary event rates was evaluated in 1616 patients with proven coronary artery disease and a history of chest pain during the 24 hours prior to hospital admission. At 30 days, statin therapy significantly reduced mortality and the incidence of nonfatal myocardial infarction compared with patients who did not receive statins. The need for revascularization, and the length of hospitalization was also decreased by statin therapy. The benefits were independent of cholesterol-reduction - total cholesterol levels were similar between treatment groups throughout the study.(22)
  * Statins may prevent advanced atherosclerotic plaques, or atheromas, from rupturing. Plaque rupture is believed to be the instigating factor in a significant portion of coronary events.(23)
  * Statins lower C-reactive protein, an inflammatory protein that is a far better predictor of future heart attack risk than the establishment's favorite whipping boy, cholesterol.(24,25)
  * Statins have been shown to reduce the preponderance of small, dense LDL particles; individuals whose LDL profile is characterized by these oxidation-prone small LDL particles have a significantly increased risk of CHD compared to those whose LDL profiles are characterized by large LDL particles.(26, 27)

So much for the theory that statins owe their efficacy to cholesterol-lowering…now, what about their safety record?

All Is Not Well In The Kingdom

A visit to any of the numerous health-oriented forums on the internet will quickly reveal hundreds of posts from dissatisfied statin users, describing an alarming array of side-effects: the most common being extreme fatigue, nausea, gastrointestinal problems, and muscle weakness and pain. Complaints about doctors' inability to link their recent health problems with statin use are frequent. In many instances, users report that they put two-and-two together themselves, stopped taking the drugs, and experienced significant or even complete remission of their symptoms.

Frequent side effects are no doubt a major reason why up to 75% of people taking statins discontinue their use.(29-30)

Of course, defenders of statins are quick to point out the low incidence of adverse effects in controlled, randomized clinical trials as proof of their alleged safety, but as we say here in Australia, "big bloody deal!" When recruiting for statin clinical trials, researchers carefully screen for, and exclude, a wide range of individuals including women of childbearing age, those with a history of drug or alcohol abuse, poor mental function, heart failure, arrhythmia, and other cardiac conditions, liver and kidney disorders, cancer, "other serious diseases", and "hypersensitivity" to statins. Thus, the disparity between the widespread "real-world" prevalence of side effects from statin use and the low prevalence of side effects in clinical trials is hardly surprising. These trials exclude groups that comprise a significant proportion of the real world population, and can hardly be taken as a realistic barometer for the expected incidence of side effects in the general population.

And even with these strict exclusion criteria, there is evidence to show that the clinical experience with statins has been far from trouble-free. Data for the largest statin trial, the Heart Protection Study (HPS), suggest that the daily 40mg dose of simvastatin used was nowhere near as well tolerated as the authors would have us believe. A substantial number of patients did not enter the trial after a six week run-in before randomization; of the 63,603 potential trial participants who entered the original screening, only 32,145 proceeded to the run-in phase. Of these, 11,609 patients - over one third - dropped out before the official start of the trial.(31)

Regardless of what orthodoxy would have us believe, the dangers from statin use are very real, as illustrated by the tragic death of Mrs. Elnoisa Calabio. Mrs. Calabio's story was presented at an FDA public hearing in May 2000:

"On October 7, 1999, at the age of 48, registered nurse, wife and mother,
Elnoisa Calabio, succumbed to the end stages of irreversible dermatomyositis
and interstitial pulmonary fibrosis directly caused by her use of a
prescribed cholesterol-lowering medication, simvastatin (Zocor). Mrs.
Calabio had no substantial risk factors for heart disease. Her blood pressure
was controlled. Her cholesterol was slightly high, but not considered
dangerous. Tragically, in her last days she knew that the cholesterol
lowering drug her doctor had recommended to extend her life was in fact the
cause of her fatal illness."(32)

Contrary to decades of anti-cholesterol propaganda, the mere presence of elevated cholesterol does not constitute a "disease". In any sane world, prescribing potentially deadly drugs to individuals free of heart disease, simply because they failed to meet some arbitrary level of serum cholesterol, would amount to flat-out medical malpractice.

Sadly, Mrs Calabio's family is hardly alone in grieving the needless, statin-induced loss of a loved one. In August 2001, pharmaceutical giant Bayer was forced to withdraw Baycol (cerivastatin) from the market, after at least fifty-two deaths had been linked to the drug. Baycol was causing rhabdomyolysis, a condition characterized by severe muscle damage. This rare disorder occurs when a large number of skeletal muscle cells die, subsequently releasing massive amounts of muscle protein into the bloodstream. This muscle protein saturates the kidneys, effectively overwhelming their filtration capacities. Indeed, kidney failure was reportedly a major cause of death amongst the Baycol victims. Baycol is not unique in its ability to damage muscle - all the statins have been shown to produce muscle disorders in susceptible patients, and muscle pain is one of the most common reasons for patients being taken off statin drugs.(33) Researchers recently reported that some patients may suffer muscle deterioration caused by statins while still maintaining normal levels of creatine kinase, the most commonly used indicator of muscle damage.(34)

Statins have also been shown to deplete the body of Coenzyme Q10 (CoQ10). (35) CoQ10 is a crucial component of mitochondria, the intracellular "engines" responsible for producing almost all of a cell's energy requirements. In addition to this fundamental role in energy production, CoQ10 acts as a potent antioxidant. Not surprisingly, CoQ10 is extremely important for cardiovascular health, with high levels being found in healthy heart tissue.

An indication of C0Q10's vital importance for cardiovascular health can be gleaned from a recent randomized, double-blind, controlled trial, which compared the effects of oral CoQ10 (120 mg/day) with a vitamin-B placebo in 144 patients after acute myocardial infarction. Approximately half of the patients in each group were receiving lovastatin (10 mg/day). After 1 year, both fatal and non-fatal cardiac events were significantly lower in the CoQ10 group. Twenty-five percent CoQ10 patients experienced a cardiac event during the study, compared to 45% of the control subjects. When the researchers examined the incidence of adverse effects, they found that 41% of the control subjects had experienced fatigue, compared to only 7% in the CoQ10 group.(36)

Ironically, while statins reduce the risk of atherosclerotic heart disease, their CoQ10-robbing effects have been linked to an increased risk of congestive heart failure. Figures from the National Center for Health Stastistics show that since the early nineties - when statin drugs began hitting pharmacy shelves - the incidence of congestive heart failure has risen sharply.(37) CHF, in fact, is the fastest growing cardiovascular disorder in the United States. Sadly, there is no cure for CHF short of a heart transplant. Peter H. Langsjoen, MD, a foremost authority on the use of coenzyme Q10 in the treatment of heart disease, has little doubt as to the culprit behind this sharp rise in CHF:

"In my practice of 17 years in Tyler, Texas, I have seen a frightening increase in heart failure secondary to statin usage, "statin cardiomyopathy". Over the past five years, statins have become more potent, are being prescribed in higher doses, and are being used with reckless abandon in the elderly and in patients with "normal" cholesterol levels. We are in the midst of a CHF epidemic in the US with a dramatic increase over the past decade. Are we causing this epidemic through our zealous use of statins? In large part I think the answer is yes." (38)

While CoQ10 is not only critically important for healthy cardiovascular function; the brain is also highly vulnerable to CoQ10 deficiencies. When healthy young men were given either statin drugs or a placebo, those taking lovastatin displayed significant deterioration in cognitive function after only three weeks of treatment.(37) Brian Vonk, M.D., of The Optimal Wellness Center, reported recently that, in his own experience and that of his colleagues, "… statins cause depression or loss of motivation in the majority of patients, probably due to alteration of cholesterol metabolism in the brain. As a result, many of these patients are also on [antidepressant] drugs (e.g. Zoloft, Paxil, Prozac)."(40)

The deleterious effects of statins on CoQ10 levels are hardly news to drug company manufacturers. In 1989, Merck & Co., Inc. filed two patents for the use of CoQ10 with statins in order to prevent CoQ10 depletion and attendant side effects. The patent applications, which can be viewed online at the United States Patent and Trademark Office website,(41) clearly show that the statin manufacturer was aware of the link between CoQ10 depletion and heart failure. One of the Merck patent applications states that: "Since Coenzyme Q10…is of benefit in congestive heart failure patients, the combination with HMG-CoA reductase inhibitors (statin drugs) should be of value in such patients who also have the added risk of high cholesterol."

Research has shown that statin-induced CoQ10 deficiency can be prevented with supplemental CoQ10, without adverse impact on the drugs' cholesterol-lowering or anti-inflammatory properties.(42). Amazingly, even though both of the Merck patents were granted in 1990, the company has neither exercised the patents nor educated physicians or patients about the necessity of taking coenzyme Q10 along with statin drugs. The end result is that most doctors and their patients remain completely ignorant that failure to supplement statin drugs with coenzyme Q10 may have potentially life-threatening consequences.

Statins and Cancer

In 1996 the Journal of the American Medical Association published an extensive review of the research studying the link between cholesterol-lowering drugs and cancer. The authors, Dr Thomas Newman and Dr. Stephen Hulley, stated: "All members of the two most popular classes of lipid-lowering drugs (the fibrates and the statins) cause cancer in rodents, in some cases at levels of animal exposure close to those prescribed to humans." In light of their findings, the authors recommended that: "lipid-lowering drug treatment, especially with the fibrates and statins, should be avoided except in patients at high short-term risk of coronary heart disease."(43)

Newman and Hulley's recommendation has been all but ignored. Statins are being recommended and prescribed, not just to people at high short-term risk, but to perfectly healthy people who show no clinical manifestations of CHD whatsoever, except for the non-disease of hypercholesterolemia. Even children with "elevated" cholesterol levels are being urged to commence statin therapy, marking a new dismally low point in the history of cholesterol paranoia.

Drug companies and health authorities repeatedly assure us that statins are wonderful low-risk drugs that are well tolerated in most people. They claim that clinical trials have shown no increase in cancer incidence with statin use, but the longest of these studies ran for only 6 years (excepting the EXCEL trial, which showed an increase in total mortality after 1 year of lovastatin use, and for which no subsequent mortality data has ever been released(44)). Cancer is a chronic disease that may take decades to manifest itself as a life-threatening illness - can we really conclude from trials lasting five to six years that statins are safe for lifetime use? Even heavy smokers are highly unlikely to develop cancer within six years of taking their first puff; most continue for decades before they come to realize the true value of those little warnings adorning cigarette packets.

Because rodent studies routinely use far higher dosages of drugs than those prescribed to humans, some have questioned the relevance of Newman and Hulley's findings. In many studies, rodents have been shown to eliminate drugs much faster than humans, necessitating higher dosages to maintain constant blood levels of the drug. The authors noted, however, that when the drug exposure was considered in terms of blood levels, carcinogenicity occurred at levels close to those seen in humans. In the same journal in which this review appeared, a commentary critical of Hulley and Newman claimed that higher dosages used in rodents placed inordinate stress on their gastrointestinal tracts, and that most of the cancers seen in rodent studies were malignancies of the gastrointestinal tract and liver.(45) Given that gastrointestinal distress and liver toxicity are among the most frequently reported side effects in patients prescribed statins, this proffered explanation provides little reassurance.

Cancer Incidence In Human Statin Trials: A Closer Look.

The claim that statin trials have not shown any increase in cancer is disputed by the recent PROSPER trial, which found a 25% increase in newly diagnosed cancers among elderly individuals treated with pravastatin. While there were 20 less deaths from CHD and stroke in the treatment group, 24 more deaths from cancer were observed, and, in an ominous confirmation of animal findings, one of the highest increases was observed for gastrointestinal cancers.(46) The PROSPER authors dismissed these findings by referring to a pooled analysis they performed of eight statin trials that lasted three or more years, which showed no statistically significant difference in cancer incidence between the placebo and statin groups (6.9% versus 7.1%, respectively). However, most of these trials involved younger subjects. Because cancer risk increases with age, such a comparison bears little relevance to the PROSPER results. Due to their heightened risk, elderly subjects may act as a far more sensitive barometer to any cancer-promoting capacity possessed by statins.

Furthermore, as researcher Uffe Ravnskov, M.D., PhD., recently pointed out, the PROSPER researchers' analysis did not include skin cancer.(47) Considering the relatively short-term nature of statin trials, it is the incidence of such an easily detectable, superficial cancer that would provide the strongest clue as to the future cancer-causing potential of statins. Only two of the statin trials have reported skin cancer incidence; the 4S and HPS simvastatin trials. Increases in skin cancer were noted in both.(48,49)

In the CARE trial, breast cancer, another readily detectable malignancy, developed in 12 women from the treatment group but in only one of the control individuals - a highly significant difference.(50) Breast cancer was also the malignancy for which the greatest increase was noted in the PROSPER trial. The possibility that statins will lead to future increases in cancer incidence cannot be flippantly dismissed.

To maintain their lipid-lowering effects, statins must be administered on a life-long basis. The reports of carcinogenicity from rodent studies and increases in superficial cancers noted in human trials warrant extreme caution. Given the complete lack of data on the effects of decades of statin administration, users can consider themselves part of a mass experiment in progress, the outcome of which is largely unknown.

Warnings for statin use to be limited to high-risk patients - where dramatically shortened life expectancies may override any concerns about long-term side-effects -have been completely overshadowed by the relentless promotional efforts of drug companies and enthusiastic endorsements from health authorities who are besides themselves at finally having clinical data that, on the surface, appears to support the lipid hypothesis.

Are we witnessing the unfolding of another officially-endorsed health disaster? Only time will tell. For those who do not want to find out the hard way, there are numerous non-drug measures that can help alleviate the risk of CHD. Randomized trials involving increases in fish/fish oil and/or fruit and vegetable consumption have produced risk reductions in mortality similar, and in some instances superior, to those seen in statin trials;(51-57) these safe, natural food items, as well as exercise, stress reduction, sound sleep, and a low glycemic load diet (i.e.., a low-to-moderate carbohydrate diet comprised of unrefined low glycemic foods), would be a far more judicious preventive alternative for those with no clinical signs of CHD.

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23. Brown BG, et al. Lipid-lowering and plaque regression. New insights into prevention of plaque disruption and clinical events in coronary disease. Circulation, Jun 1993; 87: 1781-1791.

24. Jialal I, et al. Effect of Hydroxymethyl Glutaryl Coenzyme A Reductase Inhibitor Therapy on High Sensitive C-Reactive Protein Levels. Circulation, Apr 2001; 103: 1933 - 1935.

25. Ridker PM, et al. C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. New England Journal of Medicine, March 23, 2000; 342 (12): 836-843.

26. Sone H, et al. HMG-CoA reductase inhibitor decreases small dense low-density lipoprotein and remnant-like particle cholesterol in patients with type-2 diabetes. Life Sci. 2002 Oct 4; 71 (20): 2403-2412.

27. Lariviere M, et al. Effects of atorvastatin on electrophoretic characteristics of LDL particles among subjects with heterozygous familial hypercholesterolemia. Atherosclerosis, Mar, 2003; 167 (1): 97-104.

28. Jackevicius CA, et al. Adherence with statin therapy in elderly patients with and without acute coronary syndromes. Journal of the American Medical Association, Jul. 24-31, 2002; 288 (4): 462-467.

29. Avorn J, et al. Persistence of use of lipid-lowering medications: a cross-national study. Journal of the American Medical Association, May 13, 1998; Vol. 279, No. 18: 1458-1462.

30. Cohen JS. Over Dose: The Case Against the Drug Companies: Prescription Drugs, Side Effects, and Your Health. Penguin USA. 2001.

31. MRC/BHF Heart Protection Study Collaborative Group. Heart protection study of cholesterol lowering therapy and antioxidant vitamin supplementation in a wide range of patients at increased risk of coronary heart disease death: early safety and efficacy experience. European Heart Journal, 1999; 20: 7254.

32. Barnett, BP. RE: Notice of request for participation by consumer and interested persons in public hearing June 28, June 29, 2000 [Docket No. 00N-1256]. Available online: http://www.fda.gov/ohrms/dockets/dailys/00/jun00/060200/ape0042.rtf. (accessed 19th Feb. 2003)

33. Omar MA, Wilson JP. FDA adverse event reports on statin-associated rhabdomyolysis. Annals of Pharmacotherapy, Feb, 2002; 36 (2): 288-295

34. Philips, PS et al. Statin-associated myopathy with normal creatine kinase levels. Annals of Internal Medicine, Oct. 1, 2002; 137: 581-585.

35. Jula A, et al. Effects of Diet and Simvastatin on Serum Lipids, Insulin, and Antioxidants in Hypercholesterolemic Men. Journal of the American Medical Association, 2002; 287: 598-605.

36. Singh RB, et al. Effect of coenzyme Q10 on risk of atherosclerosis in patients with recent myocardial infarction. Molecular and Cellular Biochemistry, Apr, 2003; 246 (1-2): 75-82.

37. See figure 1. Deaths from congestive heart failure, 1968-1993. Vital Statistics of the United States, National Center for Health Stastistics, cited in Congestive Heart Failure in the United States: A New Epidemic. Data Fact Sheet. National Heart, Lung, and Blood Institute, National Institutes of Health. Available online at: http://www.nhlbi.nih.gov/health/public/heart/other/CHF.htm (accessed Feb 11, 2004)

38. Langsjoen PH. Statin-induced cardiomyopathy. Introduction to the citizens petition on statins. Available online: http://www.canadiancoalitionforhealthfreedom.ca/article.php?sid=1039 (accessed Feb 11, 2004)

39. Roth T, et al. Comparative effects of pravastatin and lovastatin on nighttime sleep and daytime performance. Clinical Cardiology, 1992; 15: 426-432.

40. Vonk B. How to Determine Your Cardiovascular Health. Optimal Wellness Newsletter, Issue 391, January 4, 2003. www.mercola.com (accessed 15 January 2003).

41. Patent applications 4,933,165 (filed January 18, 1989) and 4,929,437 (filed February 2, 1989) can be viewed by visiting http://patft.uspto.gov/netahtml/srchnum.htm and entering the patent numbers in the 'query' box, then clicking on the 'search' tab (accessed Feb 11, 2004).

42. Langsjoen PH, Langsjoen AM. The clinical use of HMG CoA-reductase inhibitors and the associated depletion of coenzyme Q10. A review of animal and human publications. Biofactors, 2003; 18 (1-4): 101-111.

43. Newman TB, Hulley SB. Carcinogenicity of lipid-lowering drugs. Journal of the American Medical Association, Jan 3, 1996; 275: 55-60.

44. Bradford RH et al. Expanded Clinical Evaluation of Lovastatin (EXCEL) study results. I. Efficacy in modifying plasma lipoproteins and adverse event profile in 8245 patients with moderate hypercholesterolemia. Archives of Internal Medicine, Jan, 1991; 151 (1): 43-49.

45. Dalen J, Dalton W. Does Lowering Cholesterol Cause Cancer?. Journal of the American Medical Association, Jan 3, 1996; 275: 67-69.

46. Shepherd J, et al. Pravastatin in elderly individuals at risk of vascular disease (PROSPER): a randomised controlled trial. Lancet, 2002; 360: 1623-1630.

47. Ravnskov U. Evidence that statin treatment causes cancer, and Ravnskov U, et al. Evidence from the simvastatin trials that cancer is a probable long-term side effect. Unpublished letter to the editor of Lancet, available online: http://www.thincs.org/unpublic.htm (accessed March 27, 2003).

48. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet, 1994; 344:1383-1389.

49. Heart Protection Study Collaborative Group. MRC/BHF heart protection study of cholesterol lowering in 20 536 high-risk individuals: a randomised placebo-controlled trial. Lancet, 2002; 360: 7-22.

50. Sacks FM, et al. The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels. New England Journal of Medicine, 1996; 335: 1001-1009.

51. Burr ML, et al. Effects of changes in fat, fish, and fibre intakes on death and myocardial reinfarction: diet and reinfarction trial (DART). Lancet, 1989; 2: 757-761.

52. Singh RB, et al. Randomized, double-blind, placebo-controlled trial of fish oil and mustard oil in patients with suspected acute myocardial infarction: the Indian experiment of infarct survival-4. Cardiovascular Drugs And Therapy, 1997; 11: 485-491.

53. Marchioli R, et al. Early protection against sudden death by n-3 polyunsaturated fatty acids after myocardial infarction: time-course analysis of the results of the Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico (GISSI)-Prevenzione. Circulation, 2002; 105: 1897-1903.

54. Singh RB. Effect of dietary magnesium supplementation in the prevention of coronary heart disease and sudden cardiac death. Magnesium and Trace Elements, 1990; 9 (3): 143-151.

55. Singh RB, et al. Randomised controlled trial of cardioprotective diet in patients with recent acute myocardial infarction: results of one year follow-up. British Medical Journal, 1992; 304:1015-1019.

56. De Lorgeril M, et al. Mediterranean alpha-linolenic acid-rich diet in secondary prevention of coronary heart disease. Lancet, 1994; 343: 1454-1459.

57. Singh RB, et al. Effect of an Indo-Mediterranean diet on progression of coronary artery disease in high risk patients (Indo-Mediterranean Diet Heart Study): a randomized single-blind trial. Lancet, 2002; 360: 1455-1461.

Re-printed with permission
© Anthony Colpo 2004 - The Omnivore

Statins: Did Your Doctor Tell You . . . ?

Excerpt:
"“Do Statins Have a Role in Primary Prevention” is a review of 10 major statin trials conducted by the Therapeutics Initiative of the Department of Pharmacology & Therapeutics of the University of British Columbia. Here are their conclusions:
• “If cardiovascular serious adverse events are viewed in isolation, 71 primary prevention patients with cardiovascular risk factors have to be treated with a statin for 3 to 5 years to prevent one myocardial infarction or stroke.”
• “This cardiovascular benefit is not reflected in 2 measures of overall health impact, total mortality and total serious adverse events. Therefore, statins have not been shown to provide an overall health benefit in primary prevention trials.”
In plain English, the study says that if you are taking statins to prevent myocardial infarction (“heart attack”) or stroke:
• Only 1 of 71 people (1.4%) will have a heart attack or stroke prevented every 3-5 years. [So, yes, statins do provide some protection against heart attacks.]
• Despite protecting 1 person in 71, the death rate of those taking statins was just as high as those not taking statins: as a group, there was no increase in longevity.
By taking statins you are betting that you will be that 1 person in 71 who benefits, that the statins won’t cause you to die by some other means and that any adverse effects caused by the drug (see below) will be not be too severe."

Download full .pdf file [186KB] here

Article copyright © 2003 by Michael Babcock. All rights reserved.
Permission to reproduce with acknowledgment. (03-09-03)

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

References

1. For examples, see:
http://www.foxnews.com/story/0,2933,51494,00.html
http://www.miami.com/mld/miamiheral...cal/6033947.htm
http://news.bbc.co.uk/1/hi/health/1542293.stm
http://www.foxnews.com/story/0,2933,51813,00.html
http://onenews.nzoom.com/onenews_de...145-1-7,00.html

2. Sanders TAB, Reddy S. The influence of a vegetarian diet on the fatty acid composition of human milk and the essential fatty acid status of the infant. Journal of Pediatrics, 1992; 120: S71-S77.

3. Sanders TAB, et al. Studies of vegans: the fatty acid composition of plasma choline phosphoglycerides, erythrocytes, adipose tissue and breast milk, and some indicators of susceptibility to ischemic heart disease in vegans and omnivore controls. American Journal of Clinical Nutrition, 1978; 31: 805-813.

4. Li D, et al. The association of diet and thrombotic risk factors in healthy male vegetarians and meat-eaters. European Journal of Clinical Nutrition, 1999; 53: 612-619.

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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:

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'Healthy' Diet May Increase Bad Cholesterol

Source: Yahoo

NEW YORK (Reuters Health) - There is a plethora of evidence suggesting that low-fat diets, particularly those rich in fruits and vegetables are "healthy." However, in a small study of women, a diet low in fat and high in fruits and vegetables caused an increase in the plasma levels of oxidized LDL cholesterol, the "bad" cholesterol.

This finding was unexpected, Dr. Marja-Leena Silaste from the University of Oulu in Finland and colleagues write in Arteriosclerosis, Thrombosis. and Vascular Biology: Journal of the American Heart Association (news - web sites).

To explore how alterations in diet affect LDL levels, researchers put 37 healthy women on two different diets. Both diets were low in total and saturated fat. One was low in vegetables and the other high in vegetables and fruits.

They discovered that blood levels of LDL increased by 27 percent in response to the low-fat, low-vegetable diet and 19 percent in response to the low-fat, high-vegetable diet. Both diets also produced small but significant decreases in HDL "good" cholesterol.

Silaste and colleagues think the "most likely reason" for the increase in LDL levels in response to the diets is the increase in a carrier protein called lipoprotein a.

This is certainly possible, Dr. Mohamad Navab and colleagues from the University of California, Los Angeles, write in an editorial, but there are other possibilities as well.

"Whatever the explanation, the findings by Silaste et al are sure to provide the basis for further exciting and potentially important studies," they write.

SOURCE: Arteriosclerosis, Thrombosis, and Vascular Biology, March 2004.

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

The Diet-Heart Hypothesis: A Critique

Published in the American Journal of Cardiology:

Sylvan Lee Weinberg, MD, MACC
Dayton, Ohio

The low-fat "diet heart hypothesis" has been controversial for nearly 100 years. The low-fat, high-carbohydrate diet, promulgated vigorously by the National Cholesterol Education Program, National Institutes of Health, and American Heart Association since the Lipid Research Clinics-Primary Prevention Program in 1984, and earlier by the U.S. Department of Agriculture food pyramid, may well have played an unintended role in the current epidemics of obesity, lipid abnormalities, type II diabetes, and metabolic syndromes. This diet can no longer be defended by appeal to the authority of prestigious medical organizations or by rejecting clinical experience and a growing medical literature suggesting that the much-maligned low-carbohydrate, high-protein diet may have a salutary effect on the epidemics in question.
(J Am Coll Cardiol 2004;43:731-3) © 2004 by the American College of Cardiology Foundation

Download the full article (published with author's permission): The Diet-Heart Hypothesis - A Critique [.pdf file]

High cholesterol may protect against infections and atherosclerosis

U. Ravnskov

Introduction

Many researchers have suggested that the blood lipids play a key role in the immune defence system.1–21 There is also a growing understanding that an inflammatory response of the arterial intima to injury is a crucial step in the genesis of atherosclerosis. and that infections may be one type of such injury.22 These two concepts are difficult to harmonize with the low-density-lipoprotein (LDL) receptor hypothesis, according to which high LDL cholesterol is the most important cause of atherosclerosis. However, the many observations that conflict with the LDL receptor hypothesis, may be explained by the idea that high serum cholesterol and/or high LDL is protective against infection and atherosclerosis.

Read full article: QJM

Benefits of fewer carbs

Eating less of them may lower levels of bad cholesterol.

By Jane E. Allen, LA Times Staff Writer

Overweight people are constantly being advised to take off the pounds. Failing that (and they often do), they might improve their health by limiting carbohydrates. That simple dietary change can lower levels of a particularly bad form of cholesterol linked to heart disease.

A study of moderately overweight men found that even without cutting calories, the fewer carbohydrates they ate, the lower the blood levels of what's called "small, dense low-density lipoprotein."

Low-density lipoprotein cholesterol is known as bad cholesterol. Among many subtypes of LDL, however, small, dense LDL is considered especially damaging to arteries (it's more likely to get into the artery wall and trigger plaque buildup).

Having lots of small, dense LDL, low levels of high-density lipoprotein (HDL or good cholesterol) and elevated triglycerides (another fat in the blood), is strongly linked to obesity, insulin resistance and diabetes and heart disease.

Dr. Ronald M. Krauss, director of atherosclerosis research at Children's Hospital Oakland Research Institute, studied 178 men who were on the path to becoming obese and diabetic. One group followed a 55% carbohydrate diet, approximating what most Americans eat. A second group ate 40% carbohydrates. A third group slashed carb intake to 25%; half of this group ate a diet heavy in the saturated fats found in meats and dairy foods, while the other half was encouraged to eat more monounsaturated fats, such as olive oil.

The 40%-carb group experienced a significant benefit in reduced small, dense LDL, Krauss told colleagues two weeks ago at the American Heart Assn. Scientific Sessions in Orlando, Fla. Restricting carbs to 25% brought further improvement, regardless of whether patients ate saturated or monounsaturated fats.

Unlike the Atkins diet, which virtually eliminates carbs, the test subjects were given more realistic carb reductions. For three weeks, they were told to maintain their weight while limiting carbs. Then for five weeks, everyone cut 1,000 calories a day. All the men lost weight and reduced bad cholesterol, but those on the 25% carb diet already had gotten big reductions in the bad cholesterol before cutting calories. The others' cholesterol dropped once they cut calories.

Carolyn Berdanier, a University of Georgia nutritionist, said that carb reductions might not have the same effect on everyone because of genetic differences.

Source: latimes.com

Why the Atkins diet is healthy

By RFD Columnist Malcolm Kendrick MbChB, MRCGP
(email - malcolm@llp.org.uk )

I was idly watching a programme on the Atkins diet last night which, to my surprise, was reasonably balanced. Yes folks, the Atkins diet has crossed the pond to reach the United Kingdom. Although, in reality, all it is doing is returning. After all we invented it nearly one hundred and fifty years ago.

A man called Banting promoted a diet pretty much indistinguishable from that of Atkins in 1863. In fact, the verb to ‘bant’ is used in Sweden as a term for going on a diet

To find out more about the Banting diet (now known as the Atkins diet) go here.

Anyway, reasonably balanced or not, on this programme there was still an unquestioned view that, even if the Atkins diet did help with weight loss, it was still damaging to health. It would cause kidney disease, and osteoporosis and heart disease. Various professors of nutrition were wheeled out to condemn the Atkins diet as dangerous nonsense.

Ignoring the kidney disease and the osteoporosis for now, the nutritional professors made the usual statements. For example, ‘It is known that saturated fat increases the level of blood cholesterol and causes CHD.’ They didn’t quote any evidence for this. As far as they were concerned it is just a known fact.

Read full article:redflagsdaily.com

Effect of a High Saturated Fat and No-Starch Diet

Effect of a High Saturated Fat and No-Starch Diet on Serum Lipid Subfractions in Patients With Documented Atherosclerotic Cardiovascular Disease

JAMES H. HAYS, MD; ANGELA DISABATINO, RN, MS; ROBERT T. GORMAN, PHD;
SIMI VINCENT, PHD, MD; AND MICHAEL E. STILLABOWER, MD

Full article: Mayo Clinic [PDF file]

Living to 100

Could the Key to Long Life Lie in Bigger Cholesterol?

By John McKenzie

Oct. 29— The older people get, the more they tend to be asked the same question over and over again: What's the secret to a long life?

"Being optimistic, cheering other people up and taking a very understanding view of adversity" is how Irving Kahn sees it. Kahn is 98 years old and still puts in a full day's work as an investment adviser in New York.

"You call here at 6 o'clock, you'll find me here, Monday to Friday, unless I'm out at a meeting," said Kahn.

Being active and optimistic may be part of Kahn's secret to longevity. But studies suggest it might also be what's circulating in his blood. Kahn and many people his age have cholesterol "particles" that are larger than average.

Cholesterol comes not only in the good (or HDL) and the bad (LDL), but also in large and small particles.

"Large cholesterol particle size … seems to protect them from a variety of age-related diseases such as heart diseases, hypertension and diabetes," said Dr. Nir Barzalai of the Albert Einstein College of Medicine in New York, author of a recent study on particle size published in the Journal of the American Medical Association.

Researchers suspect that inside blood vessels, the larger, so-called fluffier cholesterol particles are able to pass more easily. Smaller, denser particles tend to cling to artery walls, which leads to the buildup of plaque and an increased risk of a heart attack or stroke.

An Increasingly Important Distinction

Normally, people focus on their total cholesterol level. But studies show that even among people with the same cholesterol level, those who have lots of large cholesterol particles have only about a third the risk of having a heart attack as those who have mostly small particles.

A handful of labs in the United States now measure blood for particle size. And some doctors are now recommending the test to patients who have a strong family history of heart disease and other risk factors but have only borderline cholesterol levels.

"It's extremely helpful to show them these abnormalities in particle size so they understand why they are at higher risk and why they should be treated," said Dr. Ronald Krauss of the University of California-Berkeley and a researcher in cholesterol particle size.

Doctors say you can make your cholesterol particles larger through a low-carbohydrate diet, exercise and medications, including niacin. Researchers are already working on a drug that would both lower cholesterol levels and reduce particle size.

It's yet another way to improve the odds of living a longer life.

Source: abcnews.com

The Retreat of the Diet-Heart Hypothesis

"The original diet-heart hypothesis was overly optimistic. That's the word from Frank B. Hu and Walter C. Willett, well-known epidemiologists from Harvard University."

by Uffe Ravnskov, MD, PhD

The Association of American Physicians and Surgeons [PDF File]

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

So, what causes heart disease?

By Malcolm Kendrick MbChB, MRCGP (email - malcolm@llp.org.uk )

When you have spent twenty years of your life studying something, you can become somewhat of a bore on the subject. But please bear with me, because I am going to reveal to you the true cause of Coronary Heart Disease (CHD). A bold claim indeed, but I think I can sustain it.

Full article: redflagsweekly

Diet and Disease: Not What You Think

by Sally Fallon and Mary G. Enig, Ph.D.

Heart disease is America's major killer; it's prevention is our most urgent public health priority. Americans must change their diet, say the experts. Steer clear of traditional foods like butter, cream, cheese, eggs, and meat, they tell us. Rich foods contain cholesterol and saturated fats — "artery clogging substances."

The accumulation of hardened plaque in the arteries, or atherosclerosis, is indeed a major cause of heart disease in Western nations.

The accepted explanation for its prevalence in civilized countries is the lipid hypothesis, namely that dietary saturated fat and cholesterol lead to elevated levels of cholesterol in the blood, and that these elevated levels of cholesterol cause the pathogenic atheromas that block blood vessels.

This theory has been promoted by the American Heart Association since the mid-1960s. It forms the basis of governmental nutritional recommendations, which in turn have spurred consumer acceptance of a vast array of low-fat, cholesterol free food products, most of which contain ingredients that are new to the American diet.

Numerous studies, both national and international, have explored the lipid hypothesis — and consumed the lion's share of research dollars in this area — including three major projects funded by the National Heart Lung and Blood Institute, a division of the National Institutes of Health (NIH).

The first and best known of these studies was the Framingham Heart Study, carried out in the town of Framingham, Massachusetts.

Although Framingham is often associated with proof of the lipid hypothesis, the results of this 40-year study have been a disappointment to its promoters.

Investigators claimed that there was a 240% increase in "risk" of coronary heart disease, or CHD, between cholesterol levels of 182 and 244. But the actual rate of increase was only .13%.

Between cholesterol levels of 244 and 294, the rate of CHD actually declined.

Thus Framingham investigators found virtually

no difference in heart disease for serum cholesterol levels between 182 and 284

the vast majority of the U.S. population.

Nor did they find that diets high in fat and cholesterol predisposed an individual to heart disease.

As Dr. William Castelli, the current director of the Framingham project, admitted as recently as 1992: "In Framingham, Massachusetts, the more saturated fat one ate, the more cholesterol one ate, the more lories one ate, the lower people's serum cholesterol...we found that the people who ate the most cholesterol, ate the most saturated fat, ate the most calories weighed the least and were the most physically active."

The second government-funded study was the Multiple Risk Factor Intervention Trial (MRFIT) for 362,000 men.

Researchers found that annual heart disease deaths increased from about 1 per 1,000 for cholesterol levels of 180 to slightly less than 2 per 1,000 for cholesterol levels of 300 — a 100% increase in "risk" but a trivial increase in rate of less that .1%.

A more significant finding was an increase in total deaths for cholesterol levels below 160.

The final major NIH study was the Lipid Research Clinics Coronary Primary Prevention Trial (LRC), a project that cost $150 million and received intense media attention.

All subjects in the trial were put on a low-cholesterol, low-saturated fat diet. One group received a cholesterol lowering drug, the other a placebo. Average cholesterol reduction for the drug group was 8.6% which had, according to researchers, a 17% reduction in rate of heart disease.

This led to the oft repeated statement: "For each 1% reduction in cholesterol, we can expect a 2% reduction in CHD events." But when independent researchers tallied the LRC data, they found no difference in CHD between the two groups. An unequivocal but rarely published finding of the LRC was an increase in deaths from cancer, intestinal disease, stroke, violence, and suicide in the group taking the cholesterol-lowering drug.

Both the popular press and medical journals portrayed the LRC as the long-sought proof that animal fats and dietary cholesterol are the cause of heart disease. The 1984 government-sponsored Cholesterol Consensus Conference called for mass cholesterol screening and defined all Americans with cholesterol levels over 200 as "at risk."

Participating scientists recommended the prudent diet for "at risk" Americans, one low in saturated fat and cholesterol. A specific recommendation was the replacement of butter with margarine. The ensuing National Cholesterol Education Program instructed American physicians in techniques for lowering serum cholesterol through diet ant drugs.

The estimated current cost for cholesterol screening and treatment in the United States now exceeds $60 billion annually.

The application of a modicum of common sense could have prevented the massive expenditures lavished on the lipid hypothesis during the past 30 years.

The lipid hypothesis implies that animal fat consumption must have increased significantly since 1920 to correlate with the rise in heart disease, but in fact the consumption of saturated animal fats in America declined steadily during that period, while use of vegetable fats increased dramatically.

Autopsy studies of vegetarians reveal that although they have lower serum cholesterol values than non-vegetarians, they have as much atherosclerosis as non-vegetarians.

In fact, the International Atherosclerosis Project, which analyzed 31,000 autopsies from l5 countries, found no correlation between animal fat intake and degree of atherosclerosis or serum cholesterol level.

Michael DeBakey, the famous heart surgeon, surveyed 1,700 patients with atherosclerosis and found no relation between levels of serum cholesterol and degree of hardening of the arteries. Other U.S. studies — the Veterans Clinical Trial, the Minnesota State Hospital Trial, the Honolulu Heart Program, and the Puerto Rico Heart Health Study — found no significant relation between a diet high in cholesterol and saturated fats with CHD.

Unfortunately, these studies do not receive front page coverage in American newspapers, and dissenting voices must content themselves with publication in obscure medical journals. One of these voices is the eminent researcher Dr. George Mann, who states categorically:

"The diet-heart hypothesis has been repeatedly shown to be wrong, ant yet, for complicated reasons of pride, profit, and prejudice, the hypothesis continues to be exploited by scientists, fund-raising enterprises, food companies, and even governmental agencies. The public is being deceived by the greatest health scam of the century."

Michael Gurr, Ph.D., renowned expert on lipids and author of the authoritative textbook on lipid biochemistry, recently stated that "whatever causes coronary heart disease, it is not primarily a high intake of saturated fat." He criticized "...the degree of self delusion in research workers wedded to a particular hypothesis despite the contrary evidence!"

So if it ain't saturated fats ant cholesterol, what causes heart disease? There are, in fact, a number of dissenting theories, most of which dovetail into a compelling list of dietary and lifestyle factors that are unique to civilized societies. Consider the following:

• In the 1940s and 1950s, researchers Yudkin and Lopez discovered a link between consumption of refined sugar and heart disease. Sugar consumption lowers the body's resistance to bacteria, viruses, and yeasts that may cause inflammation in both the heart and the arteries. Excess sugar leads to deficiencies in the entire B-vitamin complex, needed for healthy arteries. Ongoing research at the U.S. Department of Agriculture indicates that fructose may be even more dangerous than sugar. Fructose, mainly in the form of high-fructose corn syrup (HFCS), has become the sweetener of choice for soft drinks, condiments and many so-called health foods.

• Also in the 1960s, a researcher named Annand discovered a correlation between the consumption of heated milk protein and a tendency to thrombosis — the formation of blood clots — and noted that the rise in coronary heart disease began in the 1920s with laws requiring milk pasteurization.

• Researcher Kilmer McCulley has found a positive relationship between deficiencies in folic acid, B 6 and B l2 , and severity of hardening or stiffness of the arteries, as well as the buildup of pathogenic plaque. B 6 and B 12 are found almost exclusively in animal products — the very foods that proponents of the lipid hypothesis advise us to avoid. B 6 deficiency is also associated with hardening of the tendons leading to carpel tunnel syndrome. Deficiencies of this heat-sensitive vitamin are widespread in America, partly because B 1 and B 2 added to white flour interfere with its proper use, and partly because it is destroyed during milk pasteurization. (Although pasteurization may help prevent foodborne illness, the process destroys nutrients.) Although McCulley's research has gained widespread, albeit grudging, recognition in the scientific community, it continues to lack appropriate funding and public recognition.

• Vitamin C deficiency makes arterial walls more subject to inflammation and tearing. A diet rich in natural vitamin C complex helps maintain the integrity of both blood vessels and heart muscle. Vitamin C also plays a role in collagen synthesis, along with copper, through the enzyme lysyl oxidase. Deficiencies occur in diets that lack fresh fruits and vegetables.

• Heart disease has been correlated with mineral deficiencies. Coronary heart disease rates are lower in regions where drinking water is naturally rich in trace minerals, particularly magnesium, which acts as a natural anti-coagulant and aids potassium absorption, thereby preventing heartbeat irregularities. Mineral-rich water and soil also supply iodine, needed for a healthy thyroid gland. People with poor thyroid function are very prone to heart disease. Calcium also plays a role in protecting the heart and arteries. Potassium helps maintain proper blood pressure. Traditional meat broths are rich in magnesium, potassium, calcium, and iodine. In America, these have largely been replaced by imitation broth products containing MSG and hydrolyzed protein.

• The most important change in the American diet during the years of CHD increase has been the gradual substitution of vegetable fats for those of animal origin. Hydrogenated fats — in the form of margarine and shortening — have replaced butter and lard, while the consumption of vegetable oils has increased more than 10-fold. Since as early as 1956, a number of researchers have found that consumption of trans-fatty acids in hydrogenated oils contributes to heart disease, including most recently Mensink and Katan in the Netherlands, and Walter Willett at Harvard University.

• An excess of vegetable oils, even when not hydrogenated, seems to play a role in causing heart disease because they cause an imbalance in the production of prostaglandins, localized tissue hormones that play a role in all of the body's complex chemical processes; and because industrially processed vegetable oils contain bee radicals that damage the arteries, thereby initiating plaque deposits.

• Arterial plaque contains cholesterol because the body actually uses cholesterol to repair injuries, tears, and irritations to artery walls. However, like rancid vegetable oils, cholesterol that has been oxidized by high temperatures and exposure to air can itself irritate the arterial walls and initiate pathological buildup. High temperature spray production of powdered milk and eggs, used as additives in many processed foods, began in the early part of the century. Consumption of both hydrogenated fats and products containing oxidized cholesterol increased greatly after the war.

• A recent study found that excess consumption of omega-6 fatty acids, the kind found in commercial vegetable oils made from corn, soy, safflower, and canola, increases the amount of oxidized cholesterol in the arterial plaque. Like sugar and white flour, these vegetable oils, produced by high temperature industrial processing, are new to the human diet. It is the polyunsaturated omega-6 fatty acids — not saturated fat — that form the major fat component of arterial plaque, yet for many years the American Heart Association and many establishment nutrition writers advocated consumption of polyunsaturated oils for the heart.

• The role of vitamin D in protecting against heart disease has been neglected. Vitamin D is essential for the intestinal absorption of many minerals, but particularly calcium and magnesium. Vitamin D deficiency is associated with defective calcification of the bones and pathogenic calcification of the arteries. Synthetic vitamin D added to milk has the same effect as vitamin D deficiency — it causes abnormal calcification of the soft tissues, particularly the blood vessels. Our bodies can manufacture vitamin D from cholesterol by the action of sunlight on the skin, but natural dietary sources give added protection. Vitamin D is found only in animal fats.

• Short- and medium-chain saturated fatty acids have anti-microbial effects and protect against the kind of viruses and bacteria that contribute to heart disease. Best sources of these helpful fats are the tropical oils, especially coconut oil, which have largely disappeared from the American food supply due to unfounded assertions that these healthy fats contribute to heart disease.

• Caffeine in coffee causes the body to excrete calcium and stresses the adrenal glands, leading in some cases to general exhaustion, including exhaustion of the heart muscle. This theory has been subject to intense criticism. Detractors note that heavy coffee drinkers tent to indulge in a number of habits considered unhealthy by orthodox researchers — such as smoking and lack of exercise — as well as consumption of sugar and processed foods, leading to deficiencies not yet accepted by the medical establishment as being contributors to CHD.

• Anti-oxidants such as beta-carotene, selenium, and vitamin E may protect us against damage from highly processed vegetable oils and oxidized cholesterol. Orthodox medicine has ignored or ridiculed vitamin E therapy for heart disease, pioneered by the Shute brothers, physicians in Canada, who found that 100 mg of natural vitamin E from wheat germ oil gave excellent long-term protection from coronary heart disease. Fresh fruits and vegetables supply beta-carotene and hundreds of other carotenoids; butter is a particularly rich source of selenium.

• Other theories related to heart disease include lack of exercise, overweight, high blood pressure, smoking, and exposure to carbon monoxide gas.

Heart Disease Has Many Forms

What emerges is a clear association of heart disease with the increased consumption of devitalized, processed, fabricated food items, including sugar and fructose, pasteurized milk, soft drinks, fortified white flour, miller and egg powders, caffeine, imitation broth products, synthetic vitamins, vegetable oils, and hydrogenated fats.

The lipid hypothesis not only clouds this picture, but inhibits necessary research that could illuminate these connections more clearly. Instead of adding to medical and nutritional understanding, it may be undermining public health — promoting the substitution of newfangled, altered, imitation products for nourishing traditional whole foods, including butter, cream, cheese, eggs, and meat.

Although not unknown, heart disease was relatively rare at the turn of the century, accounting for approximately 8% of all deaths in the United States.

Today coronary heart disease, or CHD, accounts for about 45% of all deaths.

Incidence of heart disease rose precipitously between 1920 and 1960. Since that time, mortality rates from CHD have declined somewhat. This means that victims of heart disease are living longer, due most likely to improved surgical techniques and the advent of angioplasty; but morbidity rates — the incidence of heart disease — continue to rise, although at a lower rate than before.

Of greatest concern is the high rate of heart disease in American men between the ages of 45 to 65.

Heart disease is not a single malady, but a complex of disease coming under a single rubric.

Damage to the heart muscle or myocardium may be due to a congenital defect, or result from inflammation and damage associated with any number of viral, bacterial, fungal, rickettsial or parasitic diseases; from rheumatic fever or syphilis; from toxic chemicals such as carbon monoxide or drugs; from auto-immune reactions or genetic disorders in which important cellular proteins in the heart muscle are deranged; or from disruption of enzymes affecting cardiac function.

The heart may also be damaged by an imbalance between the blood supply and the demands of the heart muscle leading to ischemia, a local deficiency of blood supply, and infarction, the death of an area of heart tissue.

Such deficiency may be caused by physical exertion or emotional trauma, increasing the heart's need for blood; or from a drop in blood supply due to excess bleeding, a spasm in an artery, a blood clot (thrombus) or by coronary artery disease, a condition in which the arteries become gradually blocked by the buildup of abnormal plaque (atheromas) and hardened through calcification. Blockage often occurs in the large arteries feeding the heart (the coronary arteries), or in those supplying the brain, increasing the risk of stroke.

In cases of moderate blockage of the coronary arteries, the patient may suffer from angina pectoris, bouts of brief chest pain; moderate blockage combined with increased demands on the heart, due to exertion or trauma; or severe blockage due to arterial plaque, a clot, a spasm, or any combination of these, may lead to a myocardial infarction, the dreaded heart attack, resulting in cardiac dysfunction and often rapid death. Sudden death is often triggered by an acute arrhythmia — disruption in the rhythms of the heart beat — during a heart attack.

While coronary artery disease is a common cause of heart attack, myocardial infarction may also occur in the absence of arterial blockage, due to a spasm, clot or organic failure of the heart muscle.

Heart disease due to syphilis and infectious disease has been around a long time and probably accounts for a good portion of CHD deaths before 1920. Fatty streaks, lesions, and plaque in the arteries are found in many primitive people, but coronary artery disease, the pathological buildup of hardened plaque leading to partial or total occlusion of major arteries, seems to be a disease of civilization, and probably accounts for a great deal — though not all — of the increase in heart disease between 1920 and 1960, and its continued menace to the present day.

Sally Fallon is the author of Nourishing Traditions: The Cookbook that Challenges Politically Correct Nutrition and the Diet Dictocrats and Mary G. Enig, PhD is the author of Know Your Fats: The Complete Primer for Understanding the Chemistry of Fats, Oils and Cholesterol .

The Health Myths

Myth: "It's that evil cholesterol and saturated fats that cause heart disease"

Book excerpt here

Cholesterol Skeptics and the bad news about statin drugs

By Maryann Napoli
(June 2003)

The cholesterol skeptics were there. So were the physicians who challenge the safety and necessity of cholesterol-lowering drugs. And then there were the lipid researchers whose findings totally contradict the prevailing dietary advice to the public: Avoid saturated fats, limit cholesterol, and use more polyunsaturated oils. Their presentations were met with enthusiastic approval at a conference held last spring in Arlington, Virginia. But then again, the attendees were not the usual people who show up at a conference billed as "Heart Disease in the 21st Century: Beyond the Lipid Hypothesis." They were practicing physicians, biochemists, farmers, greenmarket activists, researchers, cooks, parents of young children, and people who have been told their cholesterol is too high. The general message was: Fats are extremely important to good health...the right kinds of fat, that is.

Cholesterol was the dominant topic of the two-day event, as well as the subject of the opening lecture provocatively entitled, "High Cholesterol Protects Against Disease." Uffe Ravnskov, MD, PhD, a Danish physician who has published many critical papers about the purported association between cholesterol and cardiovascular disease, led off with a slide showing the results of all the major clinical trials that attempted to prove that lowering cholesterol in healthy but high-risk people would reduce their death rate from heart disease. "The reduced rates of cardiovascular mortality were small for men and non-existent for women," said Dr. Ravnskov, who is the author of The Cholesterol Myths, a paperback that refutes the theory that cholesterol in our food and in our blood causes heart disease.

Full article: http://www.medicalconsumers.org

bantransfats.com

"BanTransFats.com, Inc. is a non-profit corporation based in California. Our goal is the reduction and elimination of trans fats from all food products. Our founder is Stephen Joseph, a lawyer based in San Francisco, who is originally from Britain. Our principal consultant is Mary Enig, Ph.D. She is widely regarded as one of the world's foremost authorities on trans fats.

There are four kinds of fats: saturated fat, trans fat, monounsaturated fat, and polyunsaturated fat. Trans fat is the most dangerous.

Many British food products contain trans fat, including Digestive biscuits. It's not just in biscuits. It's in all kinds of foods, even some "health" foods. If you see the words "hydrogenated" or "partially hydrogenated" in the ingredients, the product contains trans fat.

Recent medical research has shown that trans fat causes significant and serious lowering of HDL (good) cholesterol and a significant and serious increase in LDL (bad) cholesterol; major clogging of arteries; type 2 diabetes; and other serious health problems."

Full article, further information and links on the subject: bantransfats.com

New cholesterol guidelines for converting healthy people into patients

Uffe Ravnskov, MD, PhD

In the May 16 issue of the Journal of the American Medical Association an expert panel from the National Cholesterol Education Program has published new guidelines for "the detection, evaluation, and treatment of high blood cholesterol" (read the paper). Their writing seems to be an attempt to put most of mankind on cholesterol-lowering diets and drugs. To do that, they have increased the number of risk factors that demands preventive measures, and expanded the limits for the previous ones.

Full article: Ravnskov

The Cholesterol Myth

"Diet has hardly any effect on your cholesterol level; the drugs that can lower it often have serious or fatal side effects; and there is no evidence at all that lowering your cholesterol level will lengthen your life."

An article drawn from Thomas J. Moore's book, Heart Failure, published by Random House, Inc.

Full article: THE CHOLESTEROL MYTH by T.J. Moore [PDF File]

THINCS

The International Network of Cholesterol Skeptics

For decades, enormous human and financial resources have been wasted on the cholesterol campaign, more promising research areas have been neglected, producers and manufacturers of animal food all over the world have suffered economically, and millions of healthy people have been frightened and badgered into eating a tedious and flavorless diet or into taking potentially dangerous drugs for the rest of their lives. As the scientific evidence in support of the cholesterol campaign is non-existent, we consider it important to stop it as soon as possible.
The International Network of Cholesterol Skeptics (THINCS) is a steadily growing group of scientists, physicians, other academicians and science writers from various countries. Members of this group represent different views about the causation of atherosclerosis and cardiovascular disease, some of them are in conflict with others, but this is a normal part of Science. What we all oppose is that animal fat and high cholesterol play a role. The aim with this website is to inform our colleagues and the public that this idea is not supported by scientific evidence; in fact, for many years a huge number of scientific studies have directly contradicted it.

Site link (highly recommended): Thincs

Atkins diet 'is beneficial and twice as effective as rivals'

The controversial Atkins diet, which severely restricts carbohydrates in favour of unlimited amounts of fat and protein, is twice as effective as conventional diets at shedding excess pounds, new research has shown.

In a six-month trial, volunteers following the regime lost twice as much weight as those on more traditional low-calorie, high-carbohydrate diets.

And despite fears that the bestselling diet could be harmful in the long term, researchers found that the diet protected against heart disease by increasing levels of "good" cholesterol.

Full article: telegraph.co.uk

Why is 5.2 (200) a 'healthy' cholesterol level?

The enclosed three paragraphs, which I wrote last week for the Weston A Price Foundation website to add to the "Oiling of America" article tells how the 200 mg/dl cutoff for serum cholesterol was decided back in 1984.
Mary Enig, PhD

Full article: Second Opinions - Barry Groves, PhD

The Cholesterol Myth

If the hypothesis that a fatty diet causes heart disease is true, why has over fifty years of trials and studies has failed to confirm it? It's certainly not for want of trying.

Part 1: Introduction
Part 2: Dietary Fats and Heart Disease
Part 3: The Bran Wagon
Part 4: The Dangers of Low Blood Cholesterol
Part 5: Cholesterol Lowering Drugs
Part 6: Has Anyone Gained?
Part 7: So Where Does That Leave Heart Disease?
Part 8: A Question of Ethics
Part 9: The Dangers of a "Healthy" Diet

Read all of the above here (highly recommended): Second Opinions - Barry Groves, PhD

Cholesterol Myths (Ravnskov)

The idea that too much animal fat and high cholesterol are dangerous to your heart and vessels is nothing but a myth. Here are some astonishing and frightening facts:

From the contents:

1 Cholesterol is not a deadly poison, but a substance vital to the cells of all mammals. There are no such things as good or bad cholesterol, but mental stress, physical activity and change of body weight may influence the level of blood cholesterol. A high cholesterol is not dangerous by itself, but may reflect an unhealthy condition, or it may be totally innocent.

2 A high blood cholesterol is said to promote atherosclerosis and thus also coronary heart disease. But many studies have shown that people whose blood cholesterol is low become just as atherosclerotic as people whose cholesterol is high.

3 Your body produces three to four times more cholesterol than you eat. The production of cholesterol increases when you eat little cholesterol and decreases when you eat much. This explains why the ”prudent” diet cannot lower cholesterol more than on average a few per cent.

4 There is no evidence that too much animal fat and cholesterol in the diet promotes atherosclerosis or heart attacks. For instance, more than twenty studies have shown that people who have had a heart attack haven't eaten more fat of any kind than other people, and degree of atherosclerosis at autopsy is unrelated with the diet.

5 The only effective way to lower cholesterol is with drugs, but neither heart mortality or total mortality have been improved with drugs the effect of which is cholesterol-lowering only. On the contrary, these drugs are dangerous to your health and may shorten your life.

6 The new cholesterol-lowering drugs, the statins, do prevent cardio-vascular disease, but this is due to other mechanisms than cholesterol-lowering. Unfortunately, they also stimulate cancer in rodents.

7 Many of these facts have been presented in scientific journals and books for decades but are rarely told to the public by the proponents of the diet-heart idea.

8 The reason why laymen, doctors and most scientists have been misled is because opposing and disagreeing results are systematically ignored or misquoted in the scientific press.

MORE (highly recommended): http://www.ravnskov.nu/cholesterol.htm

Why the cholesterol-heart disease theory is wrong (Kendrick)

"Cholesterol is a much maligned substance, the ‘cause’ of heart disease. If it is, it must have killed billions of people. Far more than the plague, every war ever fought, and all plane, train and car crashes ever - all added together, then multiplied by three.

But if it does cause heart disease, how does it do it? The simple ‘answer’ is that, if you eat too much cholesterol, the level in your blood rises, the cholesterol then travels through the artery wall causing cholesterol-laden plaques to develop which then rupture and kill you. That’s the initial cholesterol hypothesis. Dead simple, couldn’t be more simple.

First little problem - dietary intake of cholesterol has no impact on the level of cholesterol in your blood. If we look at two major long-term studies, Framingham and Tecumseh, it is clear that those who ate the most cholesterol had exactly the same level of cholesterol in their blood as those who ate the least cholesterol."

Full article: redflagsweekly.com