Why are we arguing?
Marshall E. Deutsch, a member of the International Network of Cholesterol Skeptics, wrote an article in Skeptic magazine and spoke at TAM4 on this topic. I wrote a rebuttal in the following issue of Skeptic. I am skeptical about cholesterol too, and I agree with some of Deutsch's points, but I think he has gotten some of his facts wrong and has misinterpreted others. I think he throws out the baby with the bath water.
I have engaged him in an e-mail discussion and have received his permission to copy our exchange to the forum.
Here's my initial e-mail to him:
Here's where I agree with you:
(1) Cholesterol has been demonized and is no where near as important as the general public thinks.
(2) Cholesterol by itself is not "the" cause of atherosclerosis in the sense
that the TB bacillus is the cause of tuberculosis.
(3) The data do not support testing the cholesterol levels of all young
children.
(4) The data do not support recommending a low fat, low cholesterol diet for
all young children.
(5) Dieting doesn't make much of an impact on cholesterol levels.
(6) Statins are overprescribed; they can cause harm, and they don't
accomplish as much good as doctors and patients would like to think they do.
Here are some areas where I think our apparent disagreement is more of a
miscommunication:
(1) There is a big difference between primary prevention (preventing heart
attacks in the first place) and secondary prevention (preventing heart
attacks in patients who already have heart disease. In every statement, we
need to make clear which group we are talking about.
(2) There is a big difference between making a statement about risk factor
statistics and making lifestyle change recommendations based on those
statistics. There is plenty of room for legitimate disagreement in this
area.
(3) Advice that may be good for an individual may be bad advice when applied to a whole society.
This is the original letter which HH sent me to initiate a dialog concerning my article in SKEPTIC magazine. As I compare it with the original article, I see no way in which my article contradicts anything in this letter. As for her letter in SKEPTIC rebutting my article, not only does it not do so, but it is full of errors which are rebutted, with literature references, in the following letter by Dr. Joel M. Kauffman, which I expect to see in the next issue of SKEPTIC.Harriet Hall, MD, takes Marshall Deutsch, PhD, to task for using mixed data from developed countries and undeveloped countries to show that low serum total cholesterol (TC) levels mean higher mortality [1]. In fact, within the 4 developed countries alone, lower TC was associated with higher death rate; and also was in the 2 undeveloped countries alone. Cholesterol is highly protective against cancer, infection and atherosclerosis [2].
Hall also made the argument that, for adults, the medical propaganda recommending screening for cholesterol levels proves its value. There was never any scientific basis for such recommendations [3]. Among the elderly the lethal effects of low TC and low LDL were found to be pronounced. In a prospective study on residents of northern Manhattan, NY, in which the 2,277 subjects were followed for 10 years. Subjects were 2/3 female and also about 1/3 each Hispanic, Afro-American and white. Subjects were 65-98 years old at baseline, mean 76. The chance of dying was twice as great in the lowest quartile of TC or LDL levels, while HDL and triglyceride levels were not related to all-cause mortality in this age group. Women had higher baseline TC and LDL levels (206 and 124) than men (191 and 117), yet the women lived longer. Men with the same TC and LDL levels as women lived as long. Of the subjects, 1/5 were taking statin drugs to lower TC and LDL [4]. This is an excellent confirmation that high TC and LDL levels are beneficial, certainly in the elderly who are most likely to be prescribed a statin drug.
LDL levels both pre- and post-treatment with statin drugs in 176 patients with moderate atherosclerosis were equally as useless as TC as predictors of atherosclerotic plaque progression. Patients with baseline LDL levels of 84, 117 and 158 mg/dL were given large doses of statin drugs to lower LDL levels to 76, 74 and 85 mg/dL. After about 1.2 years electron beam tomography showed no difference between the groups in the amount of plaque progression. [5]
In the huge INTERHEART study on 30,000 subjects in 52 countries, the effect of many modifiable risk factors on heart attacks (MIs) was studied. Smoking led the list, but total cholesterol (TC) and (LDL) were not even listed, perhaps because the outcomes were not the ones desired by some of the sponsors of the study, which included AstraZeneca, Novartis, Aventis, Abbott Labs, Bristol-Myers Squibb, King Pharma and Sanofi-Synthelabo. [6]
The Japan Lipid Interevention Trial (J-LIT), a primary prevention trial utilizing simvastatin was carried out on 47,300 Japanese patients. Since they are more sensitive to statin drugs than occidentals, the dose was 5 mg/day for 90% and 10 mg/day for 10%. All were followed for 6 years including those who stopped the drug, which was open-labeled. There was no placebo group. Those whose TC was most reduced had the highest all-cause death rate. The statin makers often stress that the main “benefit” of statins is to reduce LDL rather than TC. Those with lowest achieved levels of LDL also had the highest all-cause death rate. Obviously, there is no reason to reduce TC below 250, or LDL below 130 mg/dL. Here is the best evidence yet that the tiny gains in lifespan shown in other trials on statin drugs with placebo groups are not due to TC or LDL lowering. [7]
Dr. Hall neglected to mention, in touting statin drugs, that in 3 older trials reporting gender-specific mortality, there was a 1% decrease, a 12% increase, and a 57% increase in women, so the omission of gender-specific data in most trials can have serious consequences for women. [8] If women are included in an RCT on a statin drug, the percentage of them is low, so that the known bad effects in women will not make the overall trial result negative for the statin.
Researchers at the University of Sheffield took a hard look at the earlier RCTs: AFCAPS, 4S, LIPID, WOSCOPS and CARE. They reported that statin use could be associated with an increase in mortality of 1% in 10 years. “This would be sufficiently large to negate statins’ beneficial effect on CVD mortality in patients with a [fatal] CVD event risk of less than 13% over a 10 year period.” [9]
This could go on, but overwhelming evidence shows that high TC and LDL levels are beneficial at all ages. Some serious medical scientists do not think that screening for them is worthwhile. [10]
1. Hall H, Hormone Replacement Myths and the Real Truth about Cholesterol, Skeptic 2005;11(6):27-29.
2. Ravnskov, U. (2003). High cholesterol may protect against infections and atherosclerosis. Quarterly Journal of Medicine, 96:927-934.
3. Ravnskov, U. (2002a). Is atherosclerosis caused by high cholesterol? Quarterly Journal of Medicine, 95:397-403.
4. Schupf N, Costa R, Luchsinger J, et al. (2005). Relationship Between Plasma Lipids and All- Cause Mortality in Nondemented Elderly. Journal of the American Geriatrics Society 53:219-226.
5. Hecht HS, Harman SM (2003). Relation of Response of Subclinical Atherosclerosis Detected by Electron Beam Tomography to Baseline Low-Density Lipoprotein Cholesterol Levels. American Journal of Cardiology, 93:101-103.
6. Yusuf S, Hawken S, Ôunpuu S, et al. (2004). Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. Lancet 364:937-952.
7. Matsuzaki M, Kita T, Mabuchi H, et al. (2002). Large Scale Cohort Study of the Relationship Between Serum Cholesterol Concentration and Coronary Events with Low-Dose Simvastatin Therapy in Japanese Patients with Hypercholesterolemia. Circulation Journal, 66:1087-1095.
8. Criqui MH, Golomb BA (2004). Editorial Comment. Low and lowered cholesterol and total mortality. J Am Coll Cardiol 44:1009-1010.
9. Jackson, P. R., Wallis, E. J., Haq, I. U., Ramsay, L. E. (2001). Statins for primary prevention: at what coronary risk is safety assured? Br J Pharmacology 2001;52:439-446.
10. Kmietowicz, Z. (1998). Cholesterol screening is not worthwhile. British Medical Journal, 316:725.
Can somebody offer a quotation from my original article and explain how it is a misinterpretation? Can someone describe the baby which I've thrown out with the bathwater? Incidentally, Kauffman has recently published a book entitled "Malignant Medical Myths" in which he casts doubt on the benefit of low-dose aspirin, pointing out, among other things, that the original study which suggested this benefit was carried out with Bufferin which contains other ingredients in addition to aspirin, and that one or more of these other ingredients (e.g., potassium) may be responsible for the observed effect.
