222. More about the History of the “Cholesterol” Issue.

It is becoming increasingly obvious to anyone who examines the scientific literature with an open mind that the justification for cholesterol-lowering simply does not exist. So I have been digging into the background to try to find out how it all originated. Although the work of Ancel Keys stimuated interest in cholesterol, it was a trial which commenced in 1958, which started the ball rolling with massive programmes. These have continued to the present day.

The Lipid Research Clinics Coronary Primary Prevention Trial (LRC-CPPT)

This LRC-CPT was a major NHLBI study, which cost about $150 million (1). Men with high TC values were recruited. One group was given a cholesterol-lowering drug, cholestyramine, and the other acted as control.

At the end of the trial it was found that 1.6% of those in the treatment group had suffered a fatal heart attack compared with 2.0% of those in the controls. For all-cause mortality (ACM), the results were almost identical: 3.6% in the cholestyramine group and 3.7% in the controls. So in absolute terms this was not exactly a profound difference. Nevertheless this did not prevent Dr. Basil Rifkind, the trials director, from proclaiming that:

“The cholestyramine group had a 19% reduction in risk …. of the primary endpoint of definite CHD, death or definite nonfatal myocardial infarction” (2).

In Time magazine he claimed the study:

“strongly indicates that the more you lower cholesterol and fat in your diet, the more you reduce your risk of heart disease” (3).

Rather conveniently, there was no mention of the ACM data, which would have totally destroyed the credibility of the study.

This information was announced to the media and presented as a great success, which justified the use of cholesterol-lowering as an important strategy in controlling the high incidence of CHD that was such an issue in the USA the time.

These differences were statistically non-significant, which meant that it could have been due to chance and was not necessarily a genuine difference. Anthony Colpo in his book on cholesterol has described how the data was manipulated in order to claim that the results had achieved “statistical significance” (4). In particular:

  • The original protocol specified that because it was essential to be sure that any observed beneficial effect of cholesterol-lowering was beneficial, stringent standards were specified for assessing the differences between the treated and control groups. These were not achieved.
  • The results for fatal heart attacks and non-fatal attacks on their own did not reach statistical significance.
  • When the 2 sets of results were combined, the difference was significant but this was only achieved at the less demanding level.

At a later follow-up, it was reported that after 13 years, the ACM in the drug treated group was 7.5% and in the control group 8.2% (5). It was also noted that the incidences of benign colorectal tumours (50 vs 34), cancer of the buccal cavity and pharynx (eight vs two), gallbladder disease (68 vs 53), and gallbladder surgery (58 vs 40) were increased in the cholestyramine group although these differences were not statistically significant. Another important result was that those in the treated group had a raised incidence of deaths due to violence and suicide. Hence there is a possibility that this could be a specific effect of low cholesterol per se.

The critics

Dr. Mary Enig pointed out that:

“An interesting feature of the study was the fact that a good part of the trial’s one-hundred-and-fifty-million-dollar budget was devoted to group sessions in which trained dieticians taught both groups of study participants how to choose “heart-friendly” foods—margarine, egg replacements, processed cheese, baked goods made with vegetable shortenings, in short the vast array of manufactured foods awaiting consumer acceptance. As both groups received dietary indoctrination, study results could support no claims about the relation of diet to heart disease” (6).

She also revealed that at a workshop to discuss these results there was widespread criticism of the manner in which the information had been tabulated and manipulated.

Another critic, Colin Rose commented in his blog:

Note also that the LRC-CPPT recruited only men with primary hypercholesterolemia, a rare disorder of lipid metabolism that affects at most one in five hundred of the population and a very small fraction of the total number of people dying of heart attacks. The results, insignificant as they were, were then extrapolated to the entire population without primary hypercholesterolemia.”(7).

Even though both groups had the same diet, it was still claimed that the results provided support for the Diet-Heart Theory and were used to promote the dietary guidelines which recommended low fat and low SFA. As Nina Teicholz commented:

“It’s important to understand that this trial did not test diet. Both groups in the study were advised to eat the same low-fat fare. Therefore, diet was not a variable tested in the trial; only the drug cholestyramine was tested in this design. The reason for not testing different diets, the investigators explained to critics, was that the NHBLI could not, in good conscience, deprive any high-risk man of a cholesterol-lowering diet—even though one of the trial’s original goals was to test whether such a diet would protect against heart disease in the first place. It was a Kafkaesque circle of reasoning. Keys’ hypothesis had evidently managed to sail over the normal hurdles of scientific proof such that the mere act of testing the diet was now considered unethical” (8).

Consensus Conference: The Lowering Blood Cholesterol to Prevent Heart Disease

This conference was held in December 1984 and followed on from the publication of the LRCPPT results. The driving force behind it was Dr. Rifkind.

It was concluded that:

“Elevated blood cholesterol level is a major cause of coronary artery disease. It has been established beyond a reasonable doubt that lowering definitely elevated blood cholesterol levels (specifically blood levels of low-density lipoprotein cholesterol) will reduce the risk of heart attacks due to coronary heart disease. This has been demonstrated most conclusively in men with elevated blood cholesterol levels, but much evidence justifies the conclusion that similar protection will be afforded in women with elevated levels. After careful review of genetic, experimental, epidemiologic, and clinical trial evidence, we recommend treatment of individuals with blood cholesterol levels above the 75th percentile (upper 25 percent of values). Further, we are persuaded that the blood cholesterol level of most Americans is undesirably high, in large part because of our high dietary intake of calories, saturated fat, and cholesterol. In countries with diets lower in these constituents, blood cholesterol levels are lower, and coronary heart disease is less common. There is no doubt that appropriate changes in our diet will reduce blood cholesterol levels. Epidemiologic data and over a dozen clinical trials allow us to predict with reasonable assurance that such a measure will afford significant protection against coronary heart disease” (9).

It is absolutely unbelievable how such a conclusion could have been reached in view of the flimsy nature of the results, which in any case were limited to a very narrow sector of the population. The assumption that results data men could extrapolated to include women simply flies in the face of basic biology.

Clearly the objective was to spell out a clear message that blood cholesterol was an important risk factor for heart disease and that there should be a big push to reduce the TC levels, with changes in diet being strongly recommended. As this was a “consensus”, it really is time to get down to business and take steps to overcome what was regarded a major public health issue in the USA the time.

Was there really a consensus?

However, if we dig beneath all the hype, everything in the garden was not quite so rosy. There were a number of individuals who had serious reservations. One of the leading researchers on cholesterol,

Dr. Edward ‘Pete’ Ahrens, a veteran cholesterol researcher at Rockefeller University was highly critical of the LRC-CPPT study that was crucial to the report stated quite bluntly:

“Since this was basically a drug study, we can conclude nothing about diet; such extrapolation is unwarranted, unscientific and wishful thinking” (10).

In an article in The Lancet he spelled out his concerns:

“I would have been content with the consensus statement if it had confined itself to what we do know and what we do not. It promises benefits without giving the evidence to back up that promise. By failing to emphasise what we do not know, the statement sweeps these weaknesses in our evidence under the-rug, as if they were trivial. I have disagreed with that position” (11).

In Science magazine, Gina Kolata noted that Thomas Chalmers of Mount Sinai Medical School and Paul Meier of the University of Chicago both considered that the consensus report was misleading because the impact of the evidence had been exaggerated (12).


There seems little doubt that the entire edifice of cholesterol-lowering has been constructed on a foundation of sand.



  1. https://www.ncbi.nlm.nih.gov/pubmed/6382999
  2. http://content.time.com/time/subscriber/article/0,33009,921647,00.html
  3. A Colpo (2006) “The Great Cholesterol Con: Why everything you have been told about cholesterol, diet and heart disease is wrong” Lulu
  4. http://archinte.jamanetwork.com/article.aspx?articleid=616413
  5. http://www.westonaprice.org/know-your-fats/the-oiling-of-america/
  6. https://medicalmyths.wordpress.com/drugs/the-lipid-research-clinics-coronary-primary-prevention-trial-lrc-cppt/
  7. N Teicholz (2014) “The Big Fat Surprise: Why butter, meat and cheese belong to a healthy diet” Simon & Shuster New York
  8. https://consensus.nih.gov/1984/1984cholesterol047html.htm
  9. http://content.time.com/time/subscriber/article/0,33009,921647,00.html
  10. http://www.sciencedirect.com/science/article/pii/S0140673685923827/part/first-page-pdf
  11. http://science.sciencemag.org/content/227/4682/40.long
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