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,

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

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

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

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

Hi,

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

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

Fat facts versus fantasy

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

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

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

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

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

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

Cholesterol and MRFIT

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

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

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

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

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

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

Cholesterol contradictions

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

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

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

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

For sale: one freshly-painted cholesterol myth

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

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

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

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

Independent thinking associated with lower risk of believing establishment hogwash!

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

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

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

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

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

References

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

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

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

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

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

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

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

Source: The Omnivore

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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20. Statins have been shown to inhibit the migration of smooth muscle cells Yasunari K, et al. HMG-CoA reductase inhibitors prevent migration of human coronary smooth muscle cells through suppression of increase in oxidative stress. Arteriosclerosis, Thrombosis, and Vascular Biology, Jun, 2001; 21 (6):937-942.

21. Hidaka Y, et al. Inhibition of cultured vascular smooth muscle cell migration by simvastatin (MK-733). Atherosclerosis, Jul, 1992; 95 (1): 87-94.

22. Heeschen C, et al, on behalf of the Platelet Receptor Inhibition in Ischemic Syndrome Management (PRISM) Investigators. Circulation, Mar. 26, 2002; Vol. 105; No. 12: 1446-1452.

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)

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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.

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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.

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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.

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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