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A very interesting article in today's NY times that I am copying an
abstract from:
THE idea that cholesterol plays a key role in heart disease is so
tightly woven into modern medical thinking that it is no longer
considered open to question. This is the message that emerged all too
clearly from the recent news that the drug Vytorin had fared no better
in clinical trials than the statin therapy it was meant to supplant
Vytorin is a combination of cholesterol-lowering drugs, one called
Zetia and the other a statin called Zocor. Because the two drugs lower
LDL cholesterol by different mechanisms, the makers of Vytorin (Merck
and Schering-Plough) assumed that their double-barreled therapy would
lower it more than either drug alone, which it did, and so do a better
job of slowing the accumulation of fatty plaques in the arteries —
which it did not.
Heart disease specialists who were asked to comment on this turn of
events insisted that the result implied nothing about their assumption
that LDL cholesterol is dangerous, only about whether it is always
medically effective to lower it.
But this interpretation is based on a longstanding conceptual error
embedded in the very language we use to discuss heart disease. It
confuses the cholesterol carried in the bloodstream with the
particles, known as lipoproteins, that shuttle that cholesterol
around. There is little doubt that certain of these lipoproteins pose
dangers, but whether cholesterol itself is a critical factor is a
question that the Vytorin trial has most definitely raised. It's a
question that needs to be acknowledged and addressed if we're going to
make any more headway in preventing heart disease.
To understand the distinction between cholesterol and lipoproteins it
helps to know something of the history of cholesterol research./////
snip snip
/////So it is reasonable, after the Vytorin trial, to question the
role of LDL cholesterol in heart disease. Not whether statins help
prevent heart disease, but whether they work exclusively, or at all,
by this mechanism.
There are numerous other ways in which statins might be effective.
They reduce inflammation, which is now considered a risk factor for
heart disease. They act to keep artery walls healthy. And statins act
on lipoproteins as much as on the cholesterol inside them. They
decrease the total number of low-density and very low-density
lipoproteins in the blood, including the smallest and densest form of
LDL, which is now widely believed to be particularly noxious.
Because medical authorities have always approached the cholesterol
hypothesis as a public health issue, rather than as a scientific one,
we're repeatedly reminded that it shouldn't be questioned. Heart
attacks kill hundreds of thousands of Americans every year, statin
therapy can save lives, and skepticism might be perceived as a reason
to delay action. So let's just trust our assumptions, get people to
change their diets and put high-risk people on statins and other
cholesterol-lowering drugs.
Science, however, suggests a different approach: test the hypothesis
rigorously and see if it survives. If the evidence continues to
challenge the role of cholesterol, then rethink it, without
preconceptions, and consider what these other pathways in
cardiovascular disease are implying about cause and prevention. A
different hypothesis may turn out to fit the facts better, and one day
help prevent considerably more deaths.
Gary Taubes is the author of "Good Calories, Bad Calories: Challenging
the Conventional Wisdom on Diet, Weight Control and Disease."
Here is the link:
http://www.nytimes.com/2008/01/27/opinion/27taubes.html?th&emc=th
--
With best wishes,
-Dr. Taher Kagalwala
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