Recently the International Atherosclerosis Society published their new guidelines for the management of “atherogenic” blood lipids. The number of misleading statements is almost endless. Let me comment some of the most serious ones. Here they come.
“Some elevation of LDL seemingly is required for atherogenesis”.
What the authors mean is that high LDL is the cause of atherosclerosis. The word “seemingly” apparently indicates that the authors are not totally sure. They should know that no study of unselected individuals has ever found an association between any of the blood lipid values and degree of atherosclerosis. People with low total or LDL-cholesterol become just as atherosclerotic as people with high values. Neither has any trial found an association between the degree of cholesterol lowering and the outcome; read my paper about that issue
“The role of LDL is best exemplified by familial hypercholesterolemia”
It is true that many people with familial hypercholesterolemia are more atherosclerotic than normal people, but there are exceptions. How do these experts explain that the arteries of the brain in people with familial hypercholesterolemia are not more atherosclerotic than normal people´s and their risk of suffering a stroke is also the same? This fact has been documented by many authors, for instance by Rodriguez and coworkers in 1994 and by Hutter and coworkers in 2004. Even brain arteries of people with homozygous familial hypercholesterolemia, a condition with extremely high cholesterol values, are normal. This was documented by Postiglione and coworkers in 1991.
“Diets rich in saturated fatty acids…raise LDL-C levels, as does a high cholesterol intake”
Nothing could be further from the truth; read my review about that issue published fifteen years ago. . And even if it were true, it doesn´t matter because high cholesterol does not cause atherosclerosis.
“A few RCTs (Randomised Controlled Trials) have evaluated the effects of saturated fats and unsaturated fats on incidence of CHD; those on a diet high in unsaturated fats had fewer CHD events”
Here the authors refer to a dietary experiment by Dayton and coworkers. No effect on heart mortality or total mortality was achieved in that experiment, however. There was a small benefit as regards non-fatal heart attacks, but the result was not corrected for the higher number of octogenarians and smokers in the control group. Furthermore, no differences were found as regards degree of atherosclerosis among those who died; if anything, there were more complicated atherosclerotic lesions in the diet group.
The authors also refer to the Finnish Mental Hospital trial as support, a trial that did not satisfy the most basal criteria for a correctly performed experiment. The fact is that in my meta-analysis of all the dietary trials, no effect was found. In some of the trials mortality was lowered a little; in other trials mortality increased.
Statin treatment is of course recommended, because, as they state:
“such treatment have reduced the risk of cardiovascular events by 25-45 %”.
As usual, the benefit is expressed in percentage, not in percentage points. The truth is that no trial has succeeded in lowering the risk by more than a few percentage points, and only in young and middle-aged high-risk men. No trial has for instance succeeded in prolonging the life for women.
“Statins have proven to be safe for most patients…The most common side effect of statins is myalgia. Up to 10% of patients taking statins complain of muscle aches, weakness or other symptoms…
No, at least 25 % of physical active patients suffer from muscular problems; read this paper by the independent researchers Sinzinger and coworkers
”Rare patients experience muscle damage.”
They are rare because in the industry-sponsored trials muscle damage is only recorded if CK, the substance in the blood that reflects muscle damage, is more than ten times higher than the upper normal level, and at two subsequent occations. However, Paul Phillips and his coworkers have shown that muscular damage, documented by microscopy of the muscle tissue, may be present with normal CK levels. A relevant question is, what happensafter many years of statin treatment with those whose CK is “only” nine times higher?
”Recently statins have been linked to new onset diabetes. The risk seems small, is of questionable clinical relevance, and is far outweighed by benefit of risk reduction for cardiovascular disease.”
In the largest dietay trial, Women´s Halth Initiative about twelve percent of those who were on statin treatment had type 2 diabetes at follow-up, but only about eight per cent among the untreated women. This four per cent difference is not ”far outweighed” by the statins´ benefit; it is larger than the difference in heart events obtained in most statin experiments. Besides, as mentioned, no statin trial has succeeded in prolonging the life for women
Not a word about the risk of cancer! As we have documented recently there is much evidence that the statins, or rather low cholesterol, promotes cancer and it has been confirmed in a recent study by McDougall and coworkers
”Epidemiological studies in several populations show that risk for CHD falls progressively down to a total cholesterol of approximately 150 mg/dL (3.9 mmol/L)”
Data from WHO are not in support. The figures for women rather tell the opposite as shown by the following diagrams, where each dot represents the values in a specific country. As you see, in countries where the mean cholesterol is low, cardiovascular (CVD) mortality for women is the highest. For men there is no association.
Let us also have a look at total mortality:
As you see, low cholesterol isn´t beneficial. In countries where blood cholesterol is low, life expectancy is lower than in countries where cholesterol is high. The reason is that low cholesterol is a risk factor for infectious diseases and cancer.
Now, let us have a look at their recommendations
”The majority of the IAS panel favored setting an optimal LDL-C for primary prevention to be a level of < 100 mg/dL (2.6 mmol/L).”
Have they forgotten the results from the study by Sachdeva and his coworkers. They measured LDL in 137,000 patients from 541 hospitals in the US admitted because of an acute heart attack. To their surprise, they found that their LDL was lower than normal, and a similar but smaller study found the same. To be precise it was 105 mg/dl (2.7 mmol/l). Indeed a little higher than the experts´ optimal LDL, and therefore the authors lowered the patients´ cholesterol even more.
But three years later there were twice as many who had died among those whose LDL had been lowered even more.
Reduce intake of saturated fatty acids to < 7% of total calories, and at least to < 10%.
As readers of my books, papers and newsletters know there is no evidence whatsoever that saturated fat is dangerous to health. You can read more about that in my most recent paper about saturated fat
Consider using plant sterols/stanols (2 g/day) as a dietary adjunct
As you know from my September 2012 newsletter the intake and the level of plant sterols in the blood are associated with an increased risk of heart disease, not the opposite.
”Ezetimibe is currently being testing as add-on to high dose statin in IMPROVE-IT; however, the results of this trial have not been reported.”
But other ezetimibe trials have been reported and the results were scary. In the SEAS trial ezetimibe (Vytorin) was added to simvastatin. The combined effect of these two drugs was indeed effective because cholesterol was lowered by more than 60%. But four years later 11.1 percent in the treatment group had cancer against only 7.5 percent in the untreated control group, a difference that could not be explained by chance.
In another ezetimibe experiments called ENHANCE an additional reduction in LDL-cholesterol in people with familial hypercholesterolemia was achieved by adding 10 mg of ezetimibe to 80 mg simvastatin. This treatment was compared with 80 mg simvastatin alone in just as many participants. An x-ray analysis of the carotid arteries two years later showed that although cholesterol was lowered much more in the first group, no difference was seen; or rather, progress was more pronounced in the two-drug group. Although these results were known shortly after the termination of the trial, their publication were delayed by nearly two years. During that time sales of Vytorin generated billions of dollars in annual sales.
I assume that the purpose with the new guidelines is of the same kind.