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Minggu, 27 Januari 2008

[Supertraining] Re: HDL and Training

First up, here is the latest meta-analysis of HDL and exercise.

Kodama S, et al. Effect of aerobic exercise training on serum levels
of high-density lipoprotein cholesterol: a meta-analysis. Arch Intern
Med. 2007 May 28;167(10):999-1008.

Summary: "Regular aerobic exercise modestly increases HDL-C level.
There appears to exist a minimum exercise volume for a significant
increase in HDL-C level."

Here is what the Harvard Men's Health Letter says:

HDL cholesterol, Part II.(high-density lipoprotein)
"Exercise is an important way to boost HDL levels. On average,
sedentary people who start to exercise regularly can expect their HDL
levels to rise by 3% to 20%. <snip> In general, the duration of
exercise is more important than the intensity; that means any type of
moderate exercise is likely to help, as long as you do enough and do
it regularly."

The general medical opinion seems to be that aerobic exercise is best
and there is data that show a dose response relationship between
number of miles run each week and HDL increases. However, I do agree
wtih Ralph that weightlifters, powerlifters, bodybuilders have not
been studied as well. Earlier studies were compounded by steroid use
which can halve HDL numbers. Testosterone supplementation should also
cause HDL to reduce.

Earlier studies were also confounded by weight loss. Reducing belly
fat in men tends to increase HDL and reduce triglycerides but an
exercise effect should be considered separately. Again, as Ralph
points out, genetic variation can make it impossible to predict who
will respond and who will not.

As for the mechanism, the process seems to be tied up with glucose,
insulin, and the arcane manipulations of the liver. Low-carb diets
tend to raise HDL and lower triglycerides and so do low-GI, high-
fibre diets. There is also a suggestion that if you want to
manipulate your next cholesterol test for HDL, eat a stir fry with
olive oil and mainly non-starchy vegetables the night before and do
an exercise session in the morning before the test. I can't verify
this and no, I have not tried it, but glycolytic pressure, ie, high
blood glucose, definitely seems to lower HDL.

As for Gary Taubes article in the NYT, Taubes, a medical journalist,
has been an campaigner against the cholesterol hypothesis for many
years. In my opinion, he's mostly wrong. The fact that people with
cholesterol below 150 mg/dl (4mmol/L) total cholesterol have very low
cardiovascular risk is *absolutely* undeniable. What he's banging on
about is that between 150-200 TC, heart attacks/CVD start to rise. In
this range and above, it becomes difficult to predict CVD risk by
total cholesterol because it is multifactorial, yet cholesterol,
mainly high LDL and low HDL are still substantial risk factors for a
large proportion of the population.

This latest trial failure does not change that. Artificially lowering
cholesterol with two drugs in people with very high initial risk is
hardly a premise for determining what works if achieved naturally
with diet and exercise.

Paul Rogers
Gympie, Australia

--- In, "carruthersjam"
<Carruthersjam@...> wrote:
> The below article seems relevant to recent discussions:
> _r=1&oref=slogin
> 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
> 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
> (Merck and Schering-Plough) assumed that their double-barreled
> therapy would lower it more than either drug alone, which it did,
> 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
> 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
> helps to know something of the history of cholesterol research.
> In the 1950s, two hypotheses competed for attention among heart
> disease researchers. It had been known for decades that cholesterol
> was a component of atherosclerotic plaques, and people who have a
> genetic disorder that causes extremely high cholesterol levels
> typically have clogged arteries and heart attacks. As new
> enabled them to look more closely at lipoproteins, however,
> researchers began to suspect that these carrier molecules might
> a greater role in cardiovascular disease than the cholesterol
> them. The cholesterol hypothesis dominated, however, because
> analyzing lipoproteins was still expensive and difficult, while
> cholesterol tests were easily ordered up by any doctor.
> In the late 1960s, biochemists created a simple technique for
> measuring, more specifically, the cholesterol inside the different
> kinds of lipoproteins — high-density, low-density and very low-
> density. The National Institutes of Health financed a handful of
> studies to determine whether these "cholesterol fractions" could
> predict the risk of cardiovascular disease. In 1977, the
> reported their results: total cholesterol turned out to be
> surprisingly useless as a predictor. Researchers involved with the
> Framingham Heart Study found that in men and women 50 and
> older, "total cholesterol per se is not a risk factor for coronary
> heart disease at all."
> The cholesterol in low-density lipoproteins was deemed a "marginal
> risk factor" for heart disease. Cholesterol in high-density
> lipoproteins was easily the best determinant of risk, but with the
> correlation reversed: the higher the amount, the lower the risk of
> heart disease.
> These findings led directly to the notion that low-density
> lipoproteins carry "bad" cholesterol and high-density lipoproteins
> carry "good" cholesterol. And then the precise terminology was
> jettisoned in favor of the common shorthand. The lipoproteins LDL
> HDL became "good cholesterol" and "bad cholesterol," and the
> lipoprotein transport vehicle was now conflated with its
> cargo. Lost in translation was the evidence that the causal agent
> heart disease might be abnormalities in the lipoproteins
> The truth is, we've always had reason to question the idea that
> cholesterol is an agent of disease. Indeed, what the Framingham
> researchers meant in 1977 when they described LDL cholesterol as
> a "marginal risk factor" is that a large proportion of people who
> suffer heart attacks have relatively low LDL cholesterol.
> So how did we come to believe strongly that LDL cholesterol is so
> for us? It was partly due to the observation that eating saturated
> fat raises LDL cholesterol, and we've assumed that saturated fat is
> bad for us. This logic is circular, though: saturated fat is bad
> because it raises LDL cholesterol, and LDL cholesterol is bad
> it is the thing that saturated fat raises. In clinical trials,
> researchers have been unable to generate compelling evidence that
> saturated fat in the diet causes heart disease.
> The other important piece of evidence for the cholesterol
> is that statin drugs like Zocor and Lipitor lower LDL cholesterol
> also prevent heart attacks. The higher the potency of statins, the
> greater the cholesterol lowering and the fewer the heart attacks.
> This is perceived as implying cause and effect: statins reduce LDL
> cholesterol and prevent heart disease, so reducing LDL cholesterol
> prevents heart disease. This belief is held with such conviction
> the Food and Drug Administration now approves drugs to prevent
> disease, as it did with Zetia, solely on the evidence that they
> LDL cholesterol.
> But the logic is specious because most drugs have multiple actions.
> It's like insisting that aspirin prevents heart disease by getting
> rid of headaches.
> One obvious way to test the LDL cholesterol hypothesis is to find
> therapies that lower it by different means and see if they, too,
> prevent heart attacks. This is essentially what the Vytorin trial
> and why its results argue against the hypothesis.
> Other such tests have likewise failed to confirm it. A recent trial
> of torcetrapib, a drug that both raises HDL and lowers LDL
> cholesterol, was halted midstream because the drug seemed to cause
> heart attacks and strokes rather than prevent them. Estrogen
> replacement therapy also lowers LDL cholesterol, but it too has
> failed to prevent heart disease in clinical trials. The same goes
> eating less saturated fat.
> So it is reasonable, after the Vytorin trial, to question the role
> LDL cholesterol in heart disease. Not whether statins help prevent
> heart disease, but whether they work exclusively, or at all, by
> 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
> 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
> 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
> 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
> 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
> 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.
> ===========================
> Jamie Carruthers
> Wakefield, UK

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