Did you know that cholesterol research is seriously flawed?
There are serious flaws in the cholesterol - blocked arteries - heart attack
source data.
What does this mean? The data shows only a weak and indirect link (correlation) between the health conditions above.
Our national narrative mis-represents this relationship as strong and direct.
The Cholesterol Myths is an intriguing and insightful review of cholesterol study data from 1950 to present. This book is exceptionally well referenced - including over 20 pages of medical journal references (many included at the end of this article).
Ravnskov presents an impressive survey of cholesterol studies including Keys' Seven Countries Study, Framingham, MRFIT, the Coronary Drug Project, the Dubbo study, the Bronx study, the Upjohn trial, the WHO trial, Valio, the Oslo trial, and the Lipid Research Clinics trial. The survey results contradict the 'cholesterol is bad' message trumpeted by our national media - which monopolizes the conversation - preventing any intelligent discussion of the actual research data.
We need cholesterol. Cholesterol is vital for healthy cell function. Cholesterol is a peculiar molecule...impossible to dissolve
in water. All living creatures use this indissolubility cleverly,
incorporating cholesterol into their cell walls to make cells waterproof, a mechanism vital for proper function...
The fact that cells are waterproof is especially critical for normal functioning of nerves and nerve cells. Thus,
the highest concentration of cholesterol in the body is found in the brain and other parts of the nervous system.
[2]
US television advertising has women worried about their cholesterol intake. What does the source data
actually show regarding cholesterol and gender? Would it surprise you to know that
...high cholesterol is not a risk
factor for the female sex.
[3. Forette B, Tortrat D, Wolmark Y., Cholesterol as risk factor for
mortality in elderly women. The Lancet 1, 868-870, 1989.]
Ravnskov further details this research effort by Dr.Forette. The quotes below are only the beginning of the research data analyzed.
...it seems more dangerous for women to have low cholesterol than high.
Dr. Bernard Forette and a team of French
researchers from Paris found that old women with very high cholesterol live the longest. The death rate was more than
five times higher for women who had very low cholesterol. In their report, the French doctors warned against
cholesterol lowering in elderly women, but they could as well have warned against cholesterol lowering in any women,
or, to be more precise, in anyone at all.
[3. Forette B, Tortrat D, Wolmark Y., Cholesterol as risk factor for
mortality in elderly women. The Lancet 1, 868-870, 1989.]
At a workshop held at the National Heart, Lung and Blood Institute, researchers looked at every study that had been
published about the risk of having high or low cholesterol and came to the same conclusion: Mortality was higher for women
with low cholesterol than for women with high cholesterol...
[4. Jacobs D., et al., Report of the conference on
low blood cholesterol: Circulation 86, 1046-60, 1992.]
Because of its size, length and funding by NIH, Framingham data is often quoted in research reviews and viewed as foundational research data in the medical community.In 1948, Framingham Massachusetts was chosen as the site for a longitudinal cholesterol-heart study lead by researchers from the National Heart, Lung, and Blood Institute (NHLBI) and Boston University School of Medicine. Approximately 5,000 healthy residents of Framingham between 30-60 years of age (both male and female) participated in the initial study group and associated 10 year follow-up. In 1971 approximately 5,000 children and spouses of the original participants were added in order to track two generations within the study. The Framingham data also includes a 30-year follow up study. [6] Ravnskov analyzes and details some of the 30-year Framingham study results:
...the researchers [Drs. Anderson, Castelli and Levy in the 30 year follow-up study results] asked themselves what had happened.
This time, a few more of those with high cholesterol
levels had died. I use the word few for a reason. On average one percent of all men with high
cholesterol died each year during the 30 follow-up years. During the first ten years, about a quarter of one percent
of the total died each year. As time passed, the percentage that died each year natually grew larger and larger.
Among those with the lowest cholesterol values, only half as many died: and, as in almost all earlier investigations,
women with low cholesterol died equally often as did women with high cholesterol. But these figures concerned all causes of death. The researchers said nothing about death from heart disease!
And heart mortality was the main issue of the whole project. We are entitled to ask just why the Framingham investigators
forgot to tell us about it.
Now to the most interesting point, illustrated in Figure 2B.
For men above age 47, cholesterol levels made no difference. Those who had low cholesterol at the age of 48 died just
as often as those with high cholesterol!
...With these facts in mind, how do you explain the findings that high cholesterol seems to be dangerous at the
age of 30, but not after 47? If high cholesterol produces raised lesions because its level in the blood is a little
higher than usual, why is high cholesterol a risk factor at the age of 30, when cholesterol is rarely found in the
atherosclerotic lesions and raised lesion are rare, but not after 47, the period of life when
cholesterol is likely to build up in the blood vessels?
[7. Anderson KM, Castelli WP, Levy D., Cholesterol and mortality. 30 years of follow-up from
the Framingham Study. Journal of the American Medical Association 257, 2176-2180, 1987.]
One might expect researchers to adjust course when the data fails to validate the study premise. Yet
the high cholesterol - blocked arteries - heart attack
idea is not open to discussion in many research centers -
contradictory data is explained away and established medical doctrine is perpetuated.
...Perhaps you think that the cholesterol campaign was cancelled after the results of the Framingham study came in.
Not at all. The reason low cholesterol levels were associated with greater mortality, said the investigators, was
that people with low cholesterol levels were dying of other diseases. But their results contradicted that explanation.
Wrote the authors:
Those whose cholesterol had decreased by itself during those 30 years ran a greater risk
of dying than those whose cholesterol had increased.
To cite the report: For each 1% mg/dl drop of cholesterol
there was an 11 percent increase in coronary and total mortality.
Thus, not only total mortality but also coronary mortality had increased. Now, stop for a moment!
For many years we have been told how important it is to lower our cholesterol to prevent coronary heart disease.
But the Framingham study demonstrated that if blood cholesterol decreases by itself, the risk of dying increases.
[8]
...The Framingham findings are not a rare exception. High cholesterol has no importance in
Australian men above age 74 either, according to a study by Dr. L. A. Simons and his co-workers at
St. Vincent's Hospital in Sydney, Australia (Dubbo Study). Similar finding findings were uncovered in a study by Dr.
Peter Zimetbaum and his co-workers at the Albert Einstein College of Medicine in the Bronx, NY (Bronx study). They
found that neither total nor LDL-cholesterol predicted the risk of having a heart attack or any other
cardiovascular disease in very old men.
[9. Simons LA and others. Risk factors for coronary heart disease in the prospective Dubbo
study of Australian elderly. Atherosclerosis 117, 107-118, 1995.]
[10. Zimetbaum P and others. Plasma lipics and lipoproteins and the incidence of cardiovascular disease in the very
elderly. The Bronx aging study. Arteriosclerosis 12, 416-423, 1992.]
What about the elderly? If the 'cholesterol - blocked arteries - heart attack' idea is true should we not expect the elderly with high cholesterol to die from heart attacks more often than those with low cholesterol?
In the elderly, high cholesterol even seems to be protective. This was the surprising finding of Dr. Harlan
Krumholz and his co-workers at the Department of Cardiovascular Medicine at Yale University. They followed 997
elderly men and women living in the Bronx, NY. During a four-year period, about twice as many of the individuals
with low cholesterol had a heart attack or died from one compared to those with the highest cholesterol levels."
[11. Krumholz HM and others. Lack of association between cholesterol and coronary heart disease
mortality and morbidity and all-cause mortality in persons older than 70 years. Journal of the American Medical
Association 272, 1335-1340, 1994.]
Most Americans, deluged by the 'cholesterol is bad' message, assume that research data shows
a strong correlation between cholesterol and blocked arteries. Is this true? Does cholesterol
block arteries? The data correlation in the Framingham study is weak, yet the media presents it as conclusive.
...The correlation in Framingham was minimal, however. In statistical terms, the correlation coefficient was only 0.36. Such a
low coefficient indicates a desperately weak relationship between variables, in this case, of course, between
cholesterol and atherosclerosis. Usually, scientists demand a much higher correlation coefficient before they
conclude that there is a biologically important relationship between two variables. Usually... but Framingham
was not quite the usual case. It involved huge amounts of government funding.
[12]
..Similar studies have
also been performed in Poland, in Guatemala and in the US, all with the same result: no correlation between the
level of cholesteol in the blood stream and the amount of atherosclerosis in the vessels.
[13a-c]
The 1936 study of Kurt Lande and Warren Sperry from the Department of Forensic Medicine at New York University
showed an intriguing relationship between blood cholesterol and levels of atherosclerosis - none.
... To their
surprise, they found absolutely no correlation between the amount of cholesterol in the blood and the degree of
atherosclerosis. In age group after age group, their diagrams looked like the starry sky.
[14. Lande KE.,
Sperry WM., Human atherosclerosis in relation to the cholesterol content of the blood serum. Archives of Pathology 22,
301-312. 1936.]
...if those who promoted the diet-heart idea later on had read Lande and Sperry's paper before beginning their
research, they would probably have dropped the idea at once... But the few who remember Lande and Sperry misquote
them and claim that they found a connection, or they ignore their results by arguing that cholesterol values in the dead
are not identical with those in the living (Epstein & OStrander).
[15]
In the city of Agra in India, Dr. K.S. Mathur and his co-workers performed a similar study. Their first step was
to measure blood cholesterol in 20 patients shortly before death and then a varying number of hours afterwards. They
found that the cholesterol values were nearly the same if sampled before death and within 16 hours afterwards. Thus,
blood samples taken very shortly after death are reliable - an important confirmation of the study done by Drs. Lande
and Sperry...
[16. Mathur Z. and others. Serum cholesterol and atherosclerosis
in man. Circulation 23, 847-852. 1961.]
...Next, Dr. Mathur and his colleagues studies 200 people who had died in accidents, without any
preceding disease. Like Drs. Lande and Sperry, and like Dr. Paterson, the Indian researchers could find no
correlation betwen cholesterol values and the degree of atherosclerosis. Those with low cholesterol had just as much
atherosclerosis as those whose cholesterol was high.
[17. Mathur Z., Jaegermann K., CIba T. Atherosclerosis and levels of serum cholesterol in postmortem investigation.
American Heart Journal 63, 768-774, 1962.]
Weak relationships mis-represented as strong are a serious flaw in Framingham Study data. Other studies continue this pattern.
Two studies with a design similar to that of the Framingham study were conducted in Japan. One, led by Dr. Noriya
Okumiya, took place at Kyushu University; the other, directed by Drs. Shuichi Hatano and Toshihisa Matsuzaki, took
place at the geriatric Hospital in Tokyo. In both studies the researchers said that the level of blood cholesterol
correlated with the degree of atherosclerosis. But in the first of these autopsy studies, the correlation appeared
only in people with a low or normal cholesteol level; in the second, it appeared only in elderly people. The reports
of the studies presented no individual figures, merely correlation coefficients, and these were as small as those in
the Framingham study (0.36). Moreover, the researchers did not explain the fact that the small correlation
coefficient between cholesterol and atherosclerosis was present only in some groups but not in others.
Even more remarkable, among the dead people with high cholesterol, the degree of atherosclerosis was the same,
whether these people were young or old. Logically, since atherosclerosis develops over time as people grow
older, it should develop faster in poeple whose cholesterol is high, at least is should if the diet-heart idea
were true.
Perhaps you're thinking that the degree of atherosclerosis was the same in all age groups because death had
consistently weeded out only the most atherosclerotic. But all degrees of atherosclerosisi were present among those
who had died.
[18. Okumiya N. and others. Coronary and antecedent risk factors: Pathologic and epidemiologic study in Hisayama, Japan.
American Journal of Cardiology 56, 62-66, 1985.]
and [19. Hatano S., Matsuzaki T., Atherosclerosis in relation to personal attributes of a Japanese population in homes
for the aged. International Symposium of Atherosclerosis IV. Edit.: Schettler G., Goto Y., Hata Y., Klose G.,
Springer-Verlag, New York, 1977, p. 116-120.]
Similar peculiar results turned up in a study done in Oslo, Norway, where scientists have investigated atherosclerotic
diseases for many years in studies involving a great number of the city's inhabitants....in their final report, these
authors claimed that in Oslo, too, the degree of atherosclerosis correlated with the level of blood cholesterol.
But, as in the previous studies, the correlation was weak. And the correlation may have stemmed from the fact that
the researchers did not consider the 20-year age difference between the youngest and the oldest of the people
they studied.
[20. Solberg LA., and others. Stenoses in the coronary arteries. The Oslo study. Laboratory Investigation
53, 648-655, 1985. Unsystematic relationships, selected autopsy studies and low correlation coefficients were also found in the
following papers: Rhoads GG and others. Coronary risk factors and autopsy findings in Japanese-American man.
Laboratory Investigations 38, 304-311, 1978 and Reed DM and others. Serum lipids and lipoproteins as predictors of
atherosclerosis. An autopsy study. Atherosclerosis 9, 560-564, 1989.]
How did the 'cholesterol is bad' message become doctrine in the US medical community and the general population? Why is there hardly any discussion of valid research data contradicting the 'cholesterol is bad' message in the US? One name is Dr. Ancel Keys. In 1953 Keys and his research team presented data from six nations correlating dietary cholesterol levels to heart attack frequency. However, data from 22 nations was available at the time - but not used - it did not show the strong correlation Dr. Keys wanted. Keys purposefully presented only a sub-set of data - giving the false impression that his premise was correct.
...But why did Dr. Keys limit his data to a mere six countries? At
that time information was available from 22 countries. The reason is that if all of the countries were included, the
association became rather weak. The death rate from coronary heart disease in Finland, for instance, was seven
times that of Mexico, although fat consumption in the two nations was almost the same.
[21. Keys A. Atherosclerosis:
A problem in newer public health. Journal of Mount Sinai Hospital 20, 118-139, 1953.]
The most famous one is the Seven Countries study by Dr. Ancel Keys ...in which Keys pointed to an association between
blood cholesterol and heart mortality in seven countries. 'The correlation is obvious,' wrote Dr. Keys. He illustrated
his words with a graph...It is not apparent from Dr. Keys' paper how he constructed his graph, but it is possible to
draw a graph oneself by using the numbers from his tables....If the diet-heart idea is correct, heart attacks should,
of course, be consistently rare in areas where cholesterol levels are low and common where they are high. But as seen
from my graph, in several countries some provinces had widely differing rates of heart disease, even though average
blood cholesterol values were the same. Oddly, this important chart is not included in Dr. Keys' paper, although his
paper is loaded with more or less relevant graphs....Although the Seven Countries study flatly contradics the
diet-heart idea, proponents continually refer to it as proof. Their mantra: 'Look at Finland and Japan.
[22]
The MFRIT (Multiple Risk Factor Invervention Trial) study, funded by NIH and lead by Dr. Jeremiah Stamler out of Chicago, surveyed the blood cholesterol of over 300,000 middle aged, American men from over 18 American cities over a seven year time period. MFRIT tracked three major risk factors: high cholesterol, smoking and high blood pressure. The group of 300,000 participants was divided into 10 equally sized groups (deciles) by cholesterol value, from lowest to highest, i.e. the tenth decile had the highest blood cholesterol values. The results presented by the study authors showed that four times as many men in the high cholesterol tenth decile had died than in the first decile with low cholesterol. However, a correlation between high cholesterol and high dietary fat was not clear. [23] MFRIT study results were presented for maximum diet-heart marketing impact. Ravnskov analyses the data:
The researchers' analysis showed that in the tenth decile, four times more men had died
of a heart attack than in the first decile. Professor Stamler's team put it another way: The risk of
dying from a heart attack with cholesterol above 265 was 413 percent greater than with cholesterol below 170.
Four Hundred and thirteen percent! How frightening! But let us look at the real figures, not just the percentages.
With statistics you can change black to white, or vice versa, as any politician will tell you.
[24]
Ravnskov continues to dig through the numbers:
How many men in the MFRFIT study had, in fact, died of a heart attack? The total number was 2258, or 0.6 percent
of the more than 300,000 men investigated. You could also say that 99.4 percent did not die from a heart attack.
Four hundred ninety four of those with the
highest cholesterol value (the tenth decile), or 1.3 percent, died from a heart attack. We could also describe these
results by saying that 98.7 percent of those with the very hightest cholesterol values were alive after six years.
Among those with the lowest values, the first decile, 95 men, or 0.3 percent, died from a heart attack,
while the rest, 99.7 percent, survived. Thus, the difference in numbers of deaths between the first and the tenth decile was only
one percentage point(99.7 percent minus 98.7 percent). One percentage point doesn't have the same alarming effect
as Dr. Stamler's 413 percent, but both figures are correct because 1.3 is 413 percent of 0.3.
[25. Stamler J., Wentworth D., Neaton JD. Is relationship between serum
cholesterol and risk of premature death from coronary heart disease continuous and graded? Journal of the American
Medical Association 256, 2823-2828, 1986.]
In addition to the problems described above, there were complications regarding the methods used in the MRFIT study:
The figures from the MRFIT study included both the 12,000 participating men, but also the more than 300,000 men
who were excluded for various reasons. A large number of studies concerning the follow-up of these screenees has been
published in well-known international medical journals, and these studies are cited again and again as the strongest
proof that there is a linear association between blood cholesterol concentrations and the risk of future heart disease...
Unfortunately, the data presented in the MRFIT reports have been carelessly produced. In a systematic search of the
literature on the MRFIT study, Professor Lars Werko, then director of the Swedish Council on Technology Assessment
in Health Care, a independent governmental agency known for its integrity, found 34 papers reporting the relationship
between serum cholesterol and mortality.....
Worse than being repetitive, the data was inconsistent and highly
questionable. For instance, the number of screenees varied greatly between the studies, from 316,099 to 361, 266.
In particular, Professor Werko was critical of the studies reporting how many had died and why, because it is highly
unlikely that all of 361, 266 individuals could have been tracked after 6-12 years....How the cause of death had
been established was not reported but we can be rather confident that most of the reported causes were based on
death certificates written by general practitioners. Not only is the information from death certificates highly
unreliable (see pages 17-21), but, in many cases (between 6 and 20 percent, depending on the report), death
certificates were actually missing. Yet some of the reports gave a detailed list of diagnoses for almost all deaths.
Furthermore, during the initial screening it came to light that one of the participating centers had falsified its data
to increase the number of participants in the trial, possibly in order to obtain more financial support from the
National Institutes of Health. This embarrassing matter received little mention in the follow-up reports, nor did the
study authors mention the possibility that data falsification could have occurred in other centers as well...
[26.
Werko L., Analysis of the MRFIT screenees: a methodological study, Journal
of Internal Medicine 237, 507-518, 1995.]
Since research data only indicates a weak relationship between high cholesterol and blocked arteries (atherosclerosis)
what does high cholesterol mean? Ravnskov comments that according to the research data, the most accurate statement
that can currently be made regarding cholesterol is: ...Such discrepancies indicate that the association between high cholesterol and coronary heart disease is not
due to simple cause and effect. The most likely interpretation is that high cholesterol is not dangerous
in itself but is a marker for something else...
[27]
Additional reading on this topic.
High cholesterol may protect against infections and atherosclerosis, Oxford Journals 2003; Vol 96: 927-934.
The presence of cholesterol is both necessary in every human cell and is a vital component of liver function and especially liver bile. One main function of liver cells is to produce bile, which drains through the biliary channels within the liver and can also be stored in the gall bladder. One complex, interdependent system in human biology involves cholesterol, healthy bile flow, healthy bilirubin maintenance and healthy blood. Jaundice (hyperbilirubinemia) can be one symptom of a malfunction in this complex system.