Cholesterol Does Not Cause Heart Disease

Those who have heart disease have on average slightly higher cholesterol readings than those who do not. Here=s a graph from the Framingham study data:

First of all, the graph implies that risk increases steadily from 20% at 200mg% to 90% at 300mg%, but this must be squared with the findings of Dr Carl Seltzer who showed there were virtually identical death rates for the range of values between 205mg% and 264mg% at the study=s 30^th year. Perhaps the risk rises steeply beyond 264mg% but since only 3% of the Framingham population were over 300mg%, it=s not of great import (unless, of course, it’s your cholesterol that’s around 300mg%!).

Where the curves cross, at about 240, the cholesterol levels of those with CAD is the same as the cholesterol level of those who are CAD-free, so in this region cholesterol level has no predictive value whatsoever! But let=s say our cholesterol is between 212 (the average for the disease-free group) and 225 (the average for those with Coronary Artery Disease), where most of us are. The question is: which curve are we on? The answer is: We don=t know!

Until we bite the big one, if we bite the big one, we simply cannot tell. So far as this data goes, it=s magical thinking to expect a change in our chances by manipulating our cholesterol level, and this is implicit in the statistic that half of all heart attacks occur in people with normal cholesterol levels. In other words, it may be worth messing with your cholesterol level if it=s around 300, but even if you get it down, you still have a 40% chance of death from coronary artery disease!

Cholesterol risk factors don’t even predict heart disease very well!

Analysis of the Framingham results published in 1980 showed that the 10% of the population with the highest risk according to the cholesterol measures experienced less than 25% of the CHD. In other words, the cholesterol risk factors are a very poor predictor of heart disease. (Orchard J, Epidemiology in the 1980s: Need for a change? The Lancet, 1980; ii:845-6)

But let=s say you buy the hype, and you want to work with your doctor to lower your cholesterol. He puts you on the National Cholesterol Education Program “prudent diet.” But the Framingham data is unequivocal: neither your intake of cholesterol nor your intake of saturated fat affects your cholesterol or your LDL cholesterol one bit! Here are the blood cholesterol figures for the low and high dietary cholesterol intakes from the Framingham population:

	Cholesterol Intake	Blood Cholesterol Low Intake	Blood Cholesterol High Intake
Men	483 to 925 mg	231 mg/dl	231 mg/dl
Women	322 to 662 mg	251 mg/dl	235 mg/dl

It is crystal clear that cholesterol in the diet has no effect on blood cholesterol!

Lowering cholesterol has never been shown to reduce the incidence of heart disease. In an interesting meta-analysis of all the 26 cholesterol-lowering trials prior to the advent of statin drugs, about 60,000 people had their cholesterol lowered by various means, and the incidence of heart disease among them was compared with the rate in about 54,000 people who made no attempt to change their cholesterol level:

	Treatment groups	Control groups
Nonfatal heart attacks	2.8%	3.1%
Fatal heart attacks	2.9%	2.9%
Total deaths	6.1%	5.8%

(Ravnskov U, BMJ 1992, 305:15-9)

There were only 0.3% fewer nonfatal heart attacks, the same number of fatal heart attacks, and 0.3% more deaths from all causes in the treatment groups! Even the 0.3% reduction in nonfatal heart is probably due to chance because there were more such heart attacks in the treatment groups in the longer trials than there were in the shorter trial, and you would expect fewer heart attacks in the longer trials because of the lesser exposure to high cholesterol levels. The analysis concludes:

Lowering serum cholesterol concentrations does not reduce mortality and is unlikely to prevent coronary heart disease. Claims of the opposite are based on preferential citation of supportive trials.

Notwithstanding, the first prescription for those at risk of CHD is the Therapeutic Lifestyle Change diet which is designed to lower cholesterol levels by avoiding saturated fat and replacing it with vegetable oils, and avoiding cholesterol-containing foods. Never mind that in the Tecumseh Study, which evaluated the effect of cholesterol, fat and saturated fat on the blood level of cholesterol, saturated fat was found to have no effect whatsoever on cholesterol levels:

Intake of:	Blood Cholesterol Lowest third:	Blood Cholesterol Middle third:	Blood Cholesterol Highest third:
Cholesterol	554 mg	566 mg	533 mg
Saturated fat	52 mg	52 mg	54 mg
Total fat	128 mg	134 mg	133 mg

The Table shows that the average intake of saturated fat was virtually identical in the groups with low, medium and high cholesterol! Further, the average intake of cholesterol-containing foods was also virtually identical in the groups with low, medium and high cholesterol. This means that cholesterol in the diet has not effect on cholesterol in the bloodstream! The study concluded that “Serum cholesterol and triglyceride values were not positively correlated with selection of dietary constituents.” In other words, there is absolutely no relationship here between saturated fat, total fat or cholesterol consumption and blood cholesterol!

But this shouldn’t really come as a surprise. Here=s what Ancel Keys, author of The Seven Countries Study which kicked off the whole lunatic cholesterol fiasco, had to say:

In the adult man the serum cholesterol level is essentially independent of the cholesterol intake over the whole range of human diets. (1956)

There=s no connection whatsoever between cholesterol in food and cholesterol in blood. And we=ve known that all along. Cholesterol in the diet doesn=t matter at all unless you happen to be a chicken or a rabbit. (1997)

Key=s thrust was that fat consumption caused high cholesterol in the blood, which caused heart disease. However, this hypothesis is as defective as the cholesterol-in-the-diet idea. Keys cherry-picked data from six countries which seemed to show this relationship, but when Uffe Ravnskov plotted the data for all the countries for which data was available, you can see that the relationship is actually weak:

Needless to say, cherry-picking your data to show relationships you believe to exist, but which your data does not support, is deeply bogus.

So the prescribed diet, which has those at risk of CHD avoiding saturated fat and cholesterol-containing foods in order to lower blood cholesterol level, cannot succeed in lowering the blood cholesterol level! The guidelines say that the diet should be tried for three months, and if it is without effect, then medications should be employed. But it is a lead-pipe cinch that the diet will fail! It seems to me that the purpose of the whole exercise is to avoid the criticism that lifestyle changes were not tried before a drug program was instituted.

The 2002 National Heart, Lung and Blood Institute report on Detection, Evaluation and Treatment of High Blood Cholesterol in Adults actually acknowledges this, and abandon cholesterol for LDL-cholesterol:

Dietary cholesterol causes marked hypercholesterolemia in many laboratory animals, including non-human primates. High intakes of cholesterol in humans, however, do not cause such a marked increase in serum cholesterol. Nonetheless, controlled metabolic studies in humans indicate that high cholesterol intakes raise LDL cholesterol. The degree of rise varies from person to person as is true for all nutrients. Meta-analysis of studies done in controlled settings confirm the LDL-raising action of dietary cholesterol.(652,653). (page V-9 of the 3^rd Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation and Treatment of High Blood Cholesterol in Adults)

Uh-oh. The studies cited are meta-analyses, statistical manipulations of pooled studies which are only used when weak associations need to be teased out of data with mathematical techniques!

Meta‑analysis, by promising a precise and definite answer when the magnitude of the underlying risks are small or when the results from individual studies disagree, seems an attractive proposition both in aetiological studies and in observational effectiveness research. (Spurious precision? Meta‑analysis of observational studies, Egger M et al, BMJ 1998; 7124(316))

The two studies are: Dietary lipids and blood cholesterol: Quantitative meta-analysis of metabolic ward studies (Clarke R et al, BMJ 1987; 314:112-7), and Effects of dietary cholesterol on serum cholesterol: a meta-analysis and review (Hopkins PN, Am J Clin Nutr 1992; 55:1060-70). The conclusion of Clarke=s meta-analysis was that, in typical British diets, replacing 60% of saturated fats by other fats, and avoiding 60% of dietary cholesterol, would reduce LDL-cholesterol by 8-12%. Such a drastic dietary change for such a small reduction in LDL-cholesterol levels seems hard to justify, especially when you consider that there is only an association between LDL-cholesterol and heart disease, and there is still a big question whether LDL-cholesterol really is a threat to the heart. Dr Uffe Ravnskov reviewed the studies cited by the NHLBI in support of the LDL-cholesterol – heart disease link, and pointed out that:

In conclusion, the @large body of evidence@ [of the harmful nature of LDL-cholesterol] was cooked down to one single study, which showed a predictive value for LDL‑cholesterol but for a few age groups only. LDL‑cholesterol is neither centrally nor causally important, it has not the strongest and most consistent relationship to risk of CHD, it has not a direct relationship to the rate of CHD, and it has not been studied in more than a dozen randomized trials. (Read the complete Uffe Ravnskov excerpt from The Cholesterol Myths)

The “one single study” showed LDL-cholesterol was “predictive for heart disease, but only for men between 35 and 49 and for women between 40 and 44.” In other words, the National Research Council=s massive review of the evidence in support of the LDL-heart disease link cited many studies which either did not support any such link, or didn’t discuss the issue at all! Dr Ravsnkov is saying, in effect, that the LDL-cholesterol-causes-heart-disease notion is supported by very little beyond breathtaking, outright scientific fraud.

In his book The Cholesterol Myths (New Trends, Washington DC, 2000), Dr Uffe Ravnskov, wrote:

Our ancestors did not know better because they had only the naked eye and lacked the technology needed to discover the truth. But the proponents of the diet-heart idea ought to know. Instead, their cocksure writings demonstrate that for them the idea has become a fact, the cholesterol Earth is flat. Or is it only a game? Those of you who read this book will realize that scientists who support the diet-heart idea and who are honest must be ignorant, either because they have failed to understand what they have read or else, by blindly following the authorities, they have failed to check the accuracy of the studies written by those authorities. But some scientists must surely have realized that the diet-heart idea is impossible and yet, for various reasons, have chosen to keep the idea alive.

LDL-cholesterol: "Bad" Cholesterol or Bad Science?

Anthony Colpo

It is almost unprecedented for an article to be published in The Journal of American Physicians and Surgeons by anyone who is not an MD, yet Anthony Colpo, a fitness consultant, wrote this article. In it, he reviews the evidence, or rather the lack of evidence, that LDL-cholesterol is a risk factor for heart disease. Incredibly, like cholesterol, LDL-cholesterol has gained its reputation from studies which quote studies which do not actually support the contention that LDL-cholesterol is dangerous to the heart!

In other words it’s of marginal value, yet has LDL-cholesterol become the exclusive focus of the heart disease prevention and even of its treatment! No wonder that the incidence of heart disease continues to rise (although deaths have remained at the 1970 level, probably because of improved surgical treatments). As we shall see, oxidized LDL-cholesterol is atherogenic – but the presence of oxidized LDL-cholesterol is a marker for deficiencies of antioxidant vitamins and minerals. So cholesterol and saturated fat in the diet have little effect on blood cholesterol.

This might just be an entertaining walk on the wild side where the loonies rant, but he is not alone. Dr Edward Pinkney sounded such a warning in The Cholesterol Controversy in 1978, Dr Russell Smith wrote The Cholesterol Conspiracy in 1991, pioneer Framingham Study researcher Dr George V Mann published Coronary Heart Disease: The Dietary Sense and Nonsense in 1993, which was followed by Dr Uffe Ravsnkov’s The Cholesterol Myths in 2000, just to hit the nigh notes. Most recently, LDL Cholesterol: "Bad" Cholesterol or Bad Science? (J Am Physicians & Surgeons 2005; 10(3)) is an admirably clear summary of the evidence to date which exonerates LDL-cholesterol. Apparently, the loonies doing the ranting here are members of the American medical establishment. So how did cholesterol become the villain? Apparently, this came to be through the political process!

There is no nonsense too arrant to become policy with sufficient interference by the government

Bertrand Russel

In (Science 3/30/2001; 291:2536-45), Journalist Gary Taubes wrote The Soft Science of Dietary Fat, which was published in the journal Science. It is almost unprecedented for an article to be published in Science by anyone who is not an accredited scientist, yet Gary Taubes, a journalist, wrote this article. There’s a pattern emerging here. Journals that lose faith in the cholesterol paradigm are publishing critical articles by non-professionals who cannot be hurt by the cholesterol mafia. Taubes reveals how the orphan cholesterol theory became the darling of a government committee:

Science by committee

Like the flourishing American affinity for alternative medicine, an antifat movement evolved independently of science in the 1960s. It was fed by distrust of the establishment--in this case, both the medical establishment and the food industry--and by

counterculture attacks on excessive consumption, whether manifested in gas-guzzling cars or the classic American cuisine of bacon and eggs and marbled steaks. And while the data on fat and health remained ambiguous and the scientific community polarized, the deadlock was broken not by any new science, but by politicians. It was Senator George McGovern's bipartisan, non-legislative Select Committee on Nutrition and Human Needs - and, to be precise, a handful of McGovern's staff members--that almost single-handedly changed nutritional policy in this country and initiated the process of turning the dietary fat hypothesis into dogma. … McGovern and his fellow senators--all middle-aged men worried about their girth and their health--signed on; McGovern and his wife had both gone through diet-guru Nathan Pritikin's very low fat diet and exercise program. McGovern quit the program early, but Pritikin remained a major influence on his thinking.

McGovern's committee listened to 2 days of testimony on diet and disease in July 1976. Then resident wordsmith Nick Mottern, a former labor reporter for The Providence Journal, was assigned the task of researching and writing the first "Dietary Goals for the United States." Mottern, who had no scientific background and no experience writing about science, nutrition, or health, believed his Dietary Goals would launch a "revolution in diet and agriculture in this country." He avoided the scientific and medical controversy by relying almost exclusively on Harvard School of Public Health nutritionist Mark Hegsted for input on dietary fat. Hegsted had studied fat and cholesterol metabolism in the early 1960s, and he believed unconditionally in the benefits of restricting fat intake, although he says he was aware that his was an extreme opinion. With Hegsted as his muse, Mottern saw dietary fat as the nutritional equivalent of cigarettes, and the food

industry as akin to the tobacco industry in its willingness to suppress scientific truth in the interests of profits. …

Creating "consensus"

Once politicians, the press, and the public had decided dietary fat policy, the science was left to catch up. In the early 1970s, when NIH opted to forgo a $1 billion trial that might be definitive and instead fund a half-dozen studies at one-third the cost, everyone hoped these smaller trials would be sufficiently persuasive to conclude that low-fat diets prolong

lives. The results were published between 1980 and 1984. Four of these trials, comparing heart disease rates and diet within Honolulu, Puerto Rico, Chicago, and Framingham, showed no evidence that men who ate less fat lived longer or had fewer heart attacks. A fifth trial, the Multiple Risk Factor Intervention Trial (MRFIT), cost $115 million and tried to amplify the subtle influences of diet on health by persuading subjects to avoid fat while simultaneously quitting smoking and taking medication for high blood pressure. That trial suggested, if anything, that eating less fat might shorten life. In each study, however, the investigators concluded that methodological flaws had led to the negative results. They did not, at least publicly, consider their results reason to lessen their belief in the evils of fat.

The sixth study was the $140 million Lipid Research Clinics (LRC) Coronary Primary Prevention Trial, led by NHLBI administrator Basil Rifkind and biochemist Daniel Steinberg of the University of California, San Diego. The LRC trial was a drug trial, not a diet trial, but the NHLBI heralded its outcome as the end of the dietary fat debate. In January 1984, LRC investigators reported that a medication called cholestyramine reduced cholesterol levels in men with abnormally high cholesterol levels and modestly reduced heart disease rates in the process. (The probability of suffering a heart attack

during the seven-plus years of the study was reduced from 8.6% in the placebo group to 7.0%; the probability of dying from a heart attack dropped from 2.0% to 1.6%.)

So this enormous dietary experiment lessened heart risk by less than a quarter of one percent for each year of the study, yet, incredibly, study director Basil Rifkind suggests that the results "strongly indicate that the more you lower cholesterol and fat in your diet, the more you reduce your risk of heart disease." Dr Scott Grundy, a Professor at Southwestern Medical Center, wrote to Science in criticism of Taubes that “the article obscures the potential for public health benefits of substituting unsaturated for saturated fatty acids in the American diet.” However, Dr Uffe Ravsnkov addressed Dr Grundy’s letter:

Grundy also writes in his letter that lowering serum LDL cholesterol by dietary means reduces CHD risk. But the study he cites did not specifically address this question (15), and more to the point, meta-analyses of all controlled and randomized trials that have used modification of dietary fat as the only type of intervention have shown that neither the incidence of nonfatal CHD, nor coronary or total mortality, was lowered significantly (16, 17).

Grundy's way of presenting scientific data is not unique. An analysis of three influential reviews in this field showed that insignificant findings in favor of the diet-heart connection were systematically inflated, and unsupportive studies were either not included or they were quoted as if they were supportive (18).

This is incredible. Tactics like these are used by Creationists trying to refute the Theory of Evolution! I see that the cholesterol-heart disease idea is a belief system, an article of faith. There is no science behind it, just the strong conviction of some that fats are harmful. You can see how funding only the research proposals of these “true believers” has got us to the national cholesterol delusional state we are in today.

For what a man had rather were true he more readily believes

Francis Bacon

America’s low-fat diet is a gigantic experiment, not the scientifically-validated strategy it pretends to be. And it is apparent that not only has the experiment failed to reduce heart disease, it has untoward consequences such as increasing the incidence of cancer and obesity. In his New York Times article What If It’s All Been A Big Fat Lie?, Gary Taubes marshals the evidence that the current epidemic of obesity, type II diabetes, diabetes in children, and syndrome X (meaning abdominal obesity, high triglycerides, insulin resistance and high blood pressure) are direct consequences of replacing calories from fat and cholesterol-containing foods with calories from sugar, corn syrup and refined flour products. Paradoxically, all these conditions actually elevate the risk of heart disease and diabetes, and perhaps depression and violence besides!

And other than that, Mrs. Lincoln, how did you enjoy the play?

Violent death and suicide increase in the treatment groups of the cholesterol-lowering trials. This effect is so reliable that s meta-analysis of 6 cholesterol-lowering trials found that:

Mortality from coronary heart disease tended to be lower in men receiving interventions to reduce cholesterol concentrations compared with mortality in control subjects (p = 0.06), although total mortality was not affected by treatment. No consistent relation was found between reduction of cholesterol concentrations and mortality from cancer, but there was a significant increase in deaths not related to illness (deaths from accidents, suicide, or violence) in groups receiving treatment to lower cholesterol concentrations relative to controls (p = 0.004). (Muldoon MF et al, Lowering cholesterol concentrations and mortality. BMJ 1990; 301:309-14)

The author of this study points out that low blood cholesterol levels are most often seen in criminals, people with diagnoses of violent or aggressive-conduct disorders, homicidal offenders with histories of violence and suicide attempts related to alcohol; and people with poorly internalized social norm and low self-control.

A prospective study in Sweden kept track of more than 50,000 people for twenty years, and found 20 suicides among those with cholesterol under 207, but only five in people with cholesterol over 296:

A strong negative relation between cholesterol concentration and mortality from injuries was found in men during the first seven years of follow up. The relative risk in the lowest 25% of the cholesterol distribution was 2.8 (95% confidence interval 1.52 to 4.96) compared with the top 25%. Most of the excess risk was caused by suicide with a corresponding relative risk of 4.2 (p for trend = 0.001). (Lindberg G et al, Low serum cholesterol concentration and short term mortality from injuries in men and women. BMJ 8/1/1992; 305:277-9)

A 1998 review of all the cholesterol lowering trials between 1965 and 1995 found the effect so strong as to conclude that low cholesterol causes violent behavior:

A significant association between low or lowered cholesterol levels and violence is found across many types of studies. Data on this association conform to Hill's criteria for a causal association. (Golomb G, Cholesterol and violence: is there a connection? Ann Int Med 3/15/1998; 128(6):478-87)

I’m afraid we’re seeing the tip on an iceberg here. Many who lower their cholesterol with statins and the AHA low-fat diet feel dreadful, but rationalize it as due to aging, life circumstances or whatever. And many I have talked to are too frightened to make the experiment of letting their cholesterol find its own level. This is a dreadful human tragedy which I fear will only be appreciated in retrospect.

The gang who can=t shoot straight

Ancel Keys, Robert Levy, William Castelli, Antonio Gotto, Jeremiah Stamler, Mark Hegsted, Basil Rifkind, Scott Grundy, William Kannel – names from the small group of cholesterol zealots who simply disregard each failed trial, declaring them successes, and embark on yet larger studies, each of which fail in their turn. MRFIT ($115m), LRC ($140m), ALLHAT ($125m) and the other cholesterol trials all produced trivial risk improvements which were spun into public-relations triumphs. In any other field of scientific endeavor, their derisory results would spell doom for the approach, but somehow they emerge with the funding for the next, larger, more expensive, even more lunatic trial. It beggars the imagination.

The luck of the nine blind bastards

Australian slang meaning >very lucky indeed=

Then, lo, by a miracle, the statin drugs appeared, which both lower cholesterol and reduce heart deaths by the unrelated mechanism of decreasing inflammation, albeit only slightly (as in the 0.16% per year risk reduction in the Scandinavian Simvastatin study). If they can spin cholesterol thin air into the appearance of success, what will they do with statins? The answer is that they suggest that statin drugs be used for ‘prevention’ in previously healthy persons, such as myself!

The true unimportance of cholesterol levels

Remember also that in 1900, heart attacks were so rare that they weren=t recognized as a cause of death, and cholesterol levels have not much changed since then. Furthermore, people with very high cholesterol levels caused by a genetic condition called familial hypercholesterolemia did not die prematurely of heart disease in 1900, although they do now:

Mortality was not increased in carriers of the mutation during the 19th and early 20th century; it rose after 1915, reached its maximum between 1935 and 1964 (standardized mortality ratio 1.78, 95% confidence interval 1.13 to 2.76; P=0.003), and fell thereafter. (Sijbrands EJG et al, Mortality over two centuries in large pedigree with familial hypercholesterolemia: family tree mortality study. BMJ 2001; 322:1019‑23)

This suggests environmental factors absent in 1900 and in place by 1915 increased heart attack deaths. The vitamin and mineral content of the American diet fell precipitously during this period as the use of sugar and bleached white flour became widespread, and trans-fats were introduced with Crisco in 1911.

I=m reminded of another conclusion of the Framingham study:

From 1951 to 1955 serum cholesterol levels were measured in 1959 men and 2415 women aged between 31 and 65 years who were free of cardiovascular disease (CVD) and cancer. Under age 50 years, cholesterol levels are directly related with 30‑year overall and CVD mortality; overall death increases 5% and CVD death 9% for each 10 mg/dL. After age 50 years there is no increased overall mortality with either high or low serum cholesterol levels. There is a direct association between falling cholesterol levels over the first 14 years and mortality over the following 18 years (11% overall and 14% CVD death rate increase per 1 mg/dL per year drop in cholesterol levels). Under age 50 years these data suggest that having a very low cholesterol level improves longevity. After age 50 years the association of mortality with cholesterol values is confounded by people whose cholesterol levels are falling‑‑perhaps due to diseases predisposing to death. (Cholesterol and mortality. 30 years of follow‑up from the Framingham study. (Castelli WP et al, JAMA 1987;257(16):2176‑80.)

This study is usually quoted in support of the oft-repeated statement that each “1% reduction in an individual's total serum cholesterol level translates into an approximate 2% reduction in CHD risk.” However, I can’t find anything in this study which even remotely supports this, but maybe, just maybe it’s true for those under 47 years of age. However, I=m 59, so my cholesterol has bugger all to do with my risk of CVD. In fact, I’m at 99% greater risk of mortality over the next 18 years because my cholesterol level fell from 275 to 165 between 1983 and 2003 (a fall of 110), and further reduction would seem to increase this risk! Yet the guidelines suggest a statin and a diet to lower my already low cholesterol even though the study on which the recommendations are supposedly based found that falling cholesterol predicts death!

That low cholesterol predicts death is not an orphan finding. For example, the Honolulu Heart Study concluded:

AA generally held belief is that cholesterol concentrations should be kept low to lessen the risk of cardiovascular disease. However, studies of the relation between serum cholesterol and all-cause mortality in elderly people have shown contrasting results. Y Methods Lipid and serum cholesterol concentrations were measured in 3572 Japanese/American men (aged 71-93 years) as part of the Honolulu Heart Program. We compared changes in these concentrations over 20 years with all-cause mortality using three different Cox proportional hazards models. Findings Mean cholesterol fell significantly with increasing age. Age-adjusted mortality rates were 68.3, 48.9, 41.1, and 43.3 for the first to fourth quartiles of cholesterol concentrations, respectively. Relative risks for mortality were 0.72 (95% Cl 0-60-0-87), 0.60 (0-49-0-74), and 0.65 (0-53-0-80), in the second, third, and fourth quartiles, respectively, with quartile 1 as reference. A Cox proportional hazard model assessed changes in cholesterol concentrations between examinations three and four. Only the group with low cholesterol concentration at both examinations had a significant association with mortality (risk ratio 1.64, 95% Cl 1.13-2.36). Interpretation We have been unable to explain our results. These data cast doubt on the scientific justification for lowering cholesterol to very low concentrations (<4.65 mmol/L) in elderly people. (Schatz I et al, Cholesterol and all-cause mortality in elderly people from the Honolulu Heart Program: a cohort study. Lancet 2001; 358: 351-55)

Translation: People over 72 with low cholesterol were at considerably greater risk of death than those with high cholesterol, and falling cholesterol apparently heralds approaching death. I=m left with this thought from Dr William Castelli, Director of the Framingham Heart Study at the time, that:

In Framingham, Massachusetts, the more saturated fat one ate, the more cholesterol one ate, the more calories 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. ... In view of this, this study fails to describe a relationship of those traditional dietary constituents, saturated fat and cholesterol, known to have an adverse effect on blood lipids, and thereby, on the subsequent development of coronary disease end points. (Castelli WP, Concerning the possibility of a nut ... Arch Intern Med 1992; 152:1371‑2)