The idea that high levels of cholesterol in the bloodstream puts us in mortal danger is perhaps one of the most firmly entrenched medical ‘facts’ of our time. Repeatedly, consistently and frequently we are warned that the cholesterol in our blood will bung up are arteries and increase our risk of heart disease. Another reminder came this week on the publication of review in the Journal of the American Association [1]. The review was really a revisiting of a previous study which found that in a group of more than 360,000 men, the higher the level of cholesterol, the greater the risk of heart disease was found to be [2]. This original study is known as the MR FIT study (an acronym that comes from the title ‘Multiple Risk Factor Intervention Trial’). The paper puts the original study in the context of other evidence which supports the concept that cholesterol is killing people and is a beast that needs taming.
While studies do indeed show that raised cholesterol levels are associated with an increased risk of heart disease, it does make sense to take a wider view if at all possible. Recently I have reported on a couple of studies which link lower cholesterol levels with an increased risk of cancer. One of these studies found lower cholesterol levels were associated with an increased risk of death too. You can read about there studies here and here. The bottom line is that focusing only on heart disease can give us a somewhat skewed impression of the association between cholesterol and health.
The thing is, though, we don’t need to look beyond the MR FIT study itself to find similar data. In a study published in 1992, the participants of the MR FIT study were assessed for the relationship between a number of conditions [3]. The positive association between cholesterol levels and heart disease was once again noted. However, lower cholesterol levels were found to be associated with an increased risk of bleeding into the brain (intracranial haemhorrage). Here are some other findings from this study: A serum cholesterol level less than 4.14 mmol/L (less than 160 mg/dL) was also associated with a significantly increased risk of death from cancer of the liver and pancreas; digestive diseases, particularly hepatic cirrhosis; suicide; and alcohol dependence syndrome. In addition, significant inverse graded associations were found between serum cholesterol level and cancers of the lung, lymphatic, and hematopoietic systems, and chronic obstructive pulmonary disease.
So, according to this data, the low cholesterol levels are associated with increased risk of, among other things, several forms of cancer. The authors of this week’s JAMA article were also authors of this study revealing the apparent hazards of low cholesterol. But this week’s JAMA article makes no mention of these findings.
However, let us not led also this epidemiological data (which is good only for showing us associations between things) blind us to what the MR FIT study was really about. The clue is in the title: The study took thousands of men and randomised them to undergo multiple interventions in an effort to reduce their risk of heart disease. One of the interventions was intensive counselling on the reduction of fat and cholesterol in their diets. The participants in the active group were also given blood-pressure lowering medication and encouraged to stop smoking. The results over time were compared to individuals who had not undergone these interventions [4].
The result? The interventions did not bring a statistically significant reduction in risk of death from heart disease nor overall risk of death either. This dismal result was not mentioned in this week’s JAMA paper either. We can’t judge from this study whether taking dietary steps to reduce cholesterol is worthwhile or not, because of multifactorial nature of this trial. However, one thing is for certain: the results of the original MR FIT study in no way support the notion that reducing fat and cholesterol is beneficial to health.
What about other evidence? Well, in one meta-analysis taking dietary steps to reduce cholesterol was not found to bring statistically significant benefits in terms of overall risk of death [5]. It’s this sort of data that the JAMA and other medical journals should be drawing our attention to, I reckon.
References:
1. Stamler J, et al. The Multiple Risk Factor Intervention Trial (MRFIT)”Importance Then and Now. JAMA 2008;300(11):1343-1345.
2. Stamler J, et al. Is relationship between serum cholesterol and risk of premature death from coronary heart disease continuous and graded? JAMA. 1986;256(20):2823-2828.
3. Neaton JD, et al. Serum cholesterol level and mortality findings for men screened in the Multiple Risk Factor Intervention Trial. Multiple Risk Factor Intervention Trial Research Group. Arch Intern Med 1992;152(7):1490-500
4. [No authors listed] Multiple risk factor intervention trial. Risk factor changes and mortality results. Multiple Risk Factor Intervention Trial Research Group. JAMA. 1982;248(12):1465-77.
5. Studer M, et al. Effect of different antilipidemic agents and diets on mortality. Archives of Internal Medicine. 2005;165:725-730
Researchers:
Boo hoo, we can’t just let the cholesterol theory meme go. Where would we get our research grants? Who would pay for our luxury junkets? Where would we obtain our prestige and smug ideas that we are saving lives? How would we pay off the Mercedes? How would our self esteem handle not being wanted?
Repeat over and over: The Cholesterol Theory Lives, The Cholesterol Theory Lives…
DIEticians:
Boo hoo. How are we gonna seem like brainy bonces if we can’t bandy around big words like hydroxymethylglutaryl coenzyme A reductase inhibitors? Are we going to be expected to apologise for making generations of people eat rabbit food and replacing any gustatory enjoyment with fear that any minute now that mouthful of cheese is going to despatch you to the grim reaper? The Cholesterol Theory Lives, The Cholesterol Theory Lives…
I still find no publication of the many basic jobs of cholesterol in the human body, nor of the fact that our bodies produce cholesterol if the necessary amounts are not consumed… Don´t we need to know things like what percentage of the human brain is made of cholesterol, and how cholesterol is built up by the body on purpose, when the blood is so acidic that it´s eating away at the arteries, causing a high risk of rupture…? That cholesterol swoops in to seal any break in the blood-stream to keep the person from hemorraging to death… ? Surely there are people finding these things out… but their findings are so hidden away. Surely the Enemy´s greatest weapon is the hiding of the truth…
http://evidenceofhealing.blogspot.com/2006/07/dangers-of-low-cholesterol-so-why-all.html
Having high cholesterol may be associated with heart disease but may not cause it. The arteries get damaged from all sorts of things including viruses and free radicals and the cholesterolis apparently there to help repair the damage. It is oxidised cholesterol which is the problem so more antioxidants needed.
Did you see the webcast debate that Dr B participated in recently at http://media.smartcom.no/ satfatnav/liveplayer.html
It just says it all. Dr B explains that the ‘science’ blaming sat fat doesn’t hold up. Then the Food Standards Agency person unbelievably virtually ignores this point, saying ‘We go with the science. And the bulk of the science says sat fat is the baddie’. Later, Dr B says ‘I thought this debate was supposed to be about whether sat fat causes heart disease or not and I’m shocked that we seem to have taken that as read’ and he’s simply told ‘the science has been around for years and is quite clear’. All credit to Dr B for not banging his head against the nearest wall at this point – I certainly was!
Jackie
I would like to point out that these statistical (mathematical) correlations are not proof of causality. For example, over 50 years ago I showed that there was a very Highly significant correlation between the output of the Tororo Uganda cement factory and the the increase in population in the tsetse population in Busoga 30 miles away. Causal? Don’t be daft.
Also I have looked at the data of fat intake and Coronary Heart Disease (CHD) was based on data taken from the European Cardiovascular Statistics for1998-1999 (http://www.ehnheart.org/files/statistics 2005). When ranked by % Fat Intake (saturated and total) for each country the CHD rate is INVERSELY (significantly) related fat intake. Quite the reverse of Ancel keys selected findings.
For misinformation the HPS study is an important contribution to the use of these drugs. However, there are some interesting questions to be answered.
I have searched the much vaunted HPS report for details of the those 781 dying under therapy (five times more than “saved”). Unlike the 156 that were ESTIMATED to have been “saved” (but which are totally unidentifiable being lost in the other 9488 (93.4%) who survived the trial) those dying can be individually identified. This supports Prof. Boyle’s (National Heart Director for England) comment that “99% will NOT benefit from therapy” but they will be exposed to their adverse reactions. Furthermore, the chairman of the British Heart Foundation, Professor Peter Weissberg, admits: “It (The HPS Study) tried everyone on the drug and only the ones who didn’t have side-effects were continued”. This means that those individuals likely to have side effects were EXCLUDED!!. Wow – Brilliant science when the issue of adverse reactions is so important! See also the summary of simvastatin adverse reactions below. Their FINAL CONCLUSION WAS THAT STATIN THERAPY CAUSED MINIMAL ADVERSE REACTIONS! You can prove anything if you exclude it!
These 781 individuals surely would provide extremely useful information on why the “wonder” drug failed so disastrously in their case. Unfortunately, I have not been able to find such information in the HPS report. Of course, if it succeeded in reducing LDL-C etc. as would be expected, then LOWERING TC CONTRIBUTED NOTHING for these “unsaved” but very dead individuals; thus reducing cholesterol did nothing! Since the deaths represent 83% of the expected number of CHD cases, the role of cholesterol in CHD must be seriously questioned!
Why, Oh why were the cholesterol levels of this group not reported. After all the study was designed about lowering cholesterol and reducing CHD and this is essential data. If the dead individuals had responded badly to cholesterol lowering, the fact would have been reported as supporting the theory that cholesterol was causal to CHD. One suspects that this data was examined but if had it been mentioned, it would have helped kill off the cholesterol myth but once and for all; but once again, ONE WOULD NOT WANT TO SPOIL A GOOD STORY WITH HORRID FACTS. (MC, and Government, the funding organizations, big PHARMA and the JBS would not have been pleased!).
The following authors have commented scholastically in great depth on this subject.
All the other points are more than adequately covered by Dr Uffe Ravnskov in his book The Cholesterol Myths (very erudite examination of the available published research data): and Duane Graveline; Lipitor – Thief of Time (an example of adverse reactions caused by statins); both from http://www.Amazon.co.uk; Colpo, A. The Great Cholesterol Con; ISBN 978-1-4303-0933-8 from http://www.lulu.com (This study examined hundreds of papers by reading – not just the conclusions) ; Kendrick, M. The Great Cholesterol Con, ISBN 978-1-84454-360-1 from John Blake (publishers) (should be compulsory reading for all doctors) ; McCully, K.S. (1999), The Homocysteine Revolution, Keats Publishing, ISBN:0-87983-975-9.
and Research Reports by Prof. RL Smith;. Diet, blood cholesterol and coronary heart disease: a critical review of the literature. Vector Enterprises. Vol. 1, 1989; Vol. 2, 1991.,
– Smith RL. The Cholesterol conspiracy. Warren H. Green. St. Louis, 1991.
– Smith RL. Dietary lipids and heart disease. The contriving of a relationship. American Clinical Laboratory 1989;Nov:26-33.
One call also visit the UK MHRA site and down load the adverse reactions reported for every drug. For example simvastatin is frightening:SIMVASTATIN MHRA Adverse Reaction Reports 2006
Single Const Multi Const
Total Fatal Total Fatal
TOTAL REACTIONS FOR DRUG: 6890 46 16 1
TOTAL REPORTS: 3,939 TOTAL FATAL OUTCOME: 47
Single Const
TOTAL IN COMMUNITY Total Fatal
Assuming a 100% report rate 6890 46
Assuming a 10% report rate 68900 460
Assuming a 1% report rate
(The most likely Medical RR) 689000 4600 ?????
In short, Google pubmed for info.
Much of the Gospel according to MC is debatable, Overweight (Fleagal, et al JAMA. 2005 Apr 20;293(15):1861-7)
Blood pressure and salt – In a 1998 study Alderman and his colleagues followed up the 11,348 Americans whose diet had been checked in the National Health and Nutrition Survey in 1971”5. They found that those with the lowest salt intakes showed the HIGHEST death rates from cardiovascular disease
Obesity: Well studies have shown that that the obese survival surgery and hospitalisation for CHD better than normal weight.
Dieting: a major NIH study found that controlled dieting in women did absolutely NOTHING. This was a study designed to prove the the “Guidelines (US)” were correct; it involved 48000+ women, ran for 8+ years and cost $415 million.
These days when the media come out with some great new therapy or medical view, I immediately disbelieve unless I can get the raw data – difficult
Thank you, Dr. Biffa for publicly standing up to those nonsense anti- saturated fat commentator propagandists.
How did it feel and what was going through your mind when you told them the facts? Did you expect a negative reaction?
Take Care,
Razwell