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LONDON, ONTARIO, CANADA. It is a common belief that elevated cholesterol is
a risk factor for stroke. On the webpage of the US NIH National Institute
of Neurological Disorders and Stroke (updated October, 2014) one finds
"Excess LDL can cause cholesterol to build up in blood vessels, leading
to atherosclerosis. Atherosclerosis is the major cause of blood vessel
narrowing, leading to both heart attack and stroke". This NIH webpage
gives a way of calculating stroke risk. Eight risk factors are given:
age, systolic blood pressure untreated, systolic blood pressure, diabetes,
smoking cigarettes, having a history of cardiovascular disease, atrial
fibrillation or left ventricular hypertrophy. Numerical points are given
to each risk factor. Add up the points and look up the 10-year probability
of a stroke. Incidentally, this approach presented in 2014 is taken
directly from a 1994 report based on the Framingham study.
What happened to LDL cholesterol mentioned in the NIH introduction?
Certainly cholesterol was on the minds of the Framingham investigators.
In fact it was a very big deal and launched almost universal cholesterol
testing, dietary avoidance and the demonizing of this chemical vital
in human biochemistry and present in cell walls. Ultimately the result
was a significant fraction of the older members of the populations
in the developed world were on statins and other cholesterol lowering
drugs. It appears that the Framingham study could not find a significant
association that would motivate them to include the LDL level in their
point system calculator. Furthermore, as your editor has pointed out
many times in this newsletter, the notion that circulating cholesterol
drives atherosclerosis is falsified by a large number of studies based
on autopsy results and more importantly, imaging of coronary artery
plaque. There is no correlation. Consistent with this, cholesterol
lowering has no impact on coronary artery calcium scores or coronary
plaque progression.
However, it is part of the conventional wisdom that statins reduce
the risk of stroke. Dr. David Newman, MD has examined the literature
to obtain the absolute risk reduction. For individuals without known
heart disease, the number needed to treat to prevent one event was
154 over 5 years whereas if there was a history of heart disease, it was
125. Converging these into percentages of those treated who do not
benefit, we get 99.5% and 99.2%, respectively (see NNT.com). Individuals
at risk need something a lot better than this.
Ware WR. The mainstream hypothesis that LDL cholesterol drives
atherosclerosis may have been falsified by non-invasive imaging
of coronary artery plaque burden and progression. Medical Hypotheses 2009;
In press
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