At the request of my sister, Kathryn Mackel, also a blogger and a published author- she's the one responsible for getting me started blogging- I am reading Good Calories, Bad Calories by Gary Taubes. It will eventually promote a specific type of diet for weight loss and maintenance, but I haven't gotten that far yet. Some of what Taubes says is accurate, some raises good questions, but some is blatantly untrue, and like anything in print, including this blog, it needs to be looked at carefully. On page five, he says "It took the AHA ten years to give public support to Keys hypothesis that heart disease was caused by dietary fat, and closer to thirty years for the rest of the world to follow." The AHA has never, and does not now, claim that heart disease (often labeled CAD for Coronary Artery Disease) is caused by dietary fat. It does, however, name (high) cholesterol as a RISK FACTOR for developing CAD. The other known risk factors it cites are increasing age, a family history of heart disease, hypertension, smoking, obesity, diabetes and a sedentary lifestyle. High HDL is even recognized as a "negative" risk factor. The AHA goes on to cite other "contributing" risk factors, but never singles one out as a sole cause, nor does any medical institution make that claim. Go to their website for more information (google AHA, you'll find it and many others).
His description of heart disease and what happens in a heart attack is fuzzy, and reflects old thinking that was once widely prevalent even in the medical community.
CAD is really a disease of the lining of the blood vessels - the enothelium - of the arteries of the heart. As we get older (and sometimes even in young people), we develop some arterial plaques. The placques are pockets of lipids on the endothelial walls, covered with solid cells that form a cap, so that the lipid core is completely enclosed under the cap. Very rarely does a plaque get so large that it completely occludes an artery. In fact, many of the larger plaques are more stable and less dangerous than smaller plaques, probably because the cap on them is thick. Most MIs occur when an unstable plaque ruptures, releasing the internal lipid into the bloodstream and setting off a cascade that forms a clot. The clot then occludes the artery completely, cutting off blood supply to part of the heart. This is a myocardial infarction. The same thing can happen in the brain, causing a stroke. The first line of treatment is usually the administration of a clot-dissolving drug in the ER, after a blood test for cardiac enzymes confirms that an MI has occurred. By the way, this is the reason why, should you ever suspect you are having a heart attack, you need to get to the ER - NOT your doctor's office -right away.
An interesting development concerning the statins, a class of drugs consistently proven to reduce the risk of MI and stroke, is the recognition that their effect is likely due to more than their effect on lowering cholesterol. A newly recognized risk factor for CAD is arterial inflammation, and the statins reduce arterial inflammation. Arterial inflammation and how to measure it was totally unknown when the statin studies were initiated. They may have even more, as yet undiscovered, effects on endothelium stabilization.
The cause of arterial plaques is still not completely understood, but most adults have some. The plaques do contain cholesterol. Anything that can cause damage to the endothelium contributes to the formation of plaques, and you do not have to have "high" blood cholesterol to form plaques, although epidemiological studies suggest that the after a certain level, people with higher cholesterol are at higher risk for MIs. High blood pressure causes damage because of excessive shear force on the arteries. High insulin levels associated with pre diabetes and Type 2 diabetes injure the endothelium. Cigarette smoke contains many chemicals that get into the blood stream and damage the endothelium. The fact that family history predisposes you to heart disease suggests an as yet undiscovered genetic link. Heart disease is multi factorial, it certainly does not have a single cause.
It is true that the effect of limiting cholesterol in your diet has a varying effect on what happens to blood cholesterol. Some people can have a substantial reduction, some people have none, and more recent thinking (but limited solid research in humans) suggests that blood cholesterol levels may be effected by lowering intake of trans and saturated fat, and also refined carbohydrates, especially sugar and sugar or high fructose corn syrup laden food products. It is a very complicated issue, and the answers wills not be known for a long time. Another important issue is that each person is individual. If you look at the effect of exercise on raising HDL, the studies show an overall modest but positive effect. If you could look at the individual results for people in the study, however, what you would see is almost no effect for some and dramatic increases for others. So, the effect of exercise on HDL for you really depends on your heredity. I exercise moderately, except when I'm training for an event. When I started exercising many years ago, my HDL went from 40 to 70, lucky for me, and thanks to my parents. But I have friends with low HDL who exercise vigorously, even to being marathoners, with no effect on their HDL. And eating monounsaturated fat can also raise HDL.
Many physicians are now taking a point of view with which I disagree (they have no evidence and neither do I). They are taking the position that when it comes to LDL, lower is better, not considering the possibility that there may be an optimal "low" value. What leads me to believe that this thinking may be flawed comes from considering other physiological systems. We know there is such a thing as blood pressure that is too low, because it becomes symptomatic. And there is such a thing as blood sugar that is too low, because it is also symptomatic. We don't know if there is such a thing as LDL that is too low, since we don't know what the symptoms are, if any. It is possible that they will appear over time.
Further complicating the issue is the fact that cardiologists have now recognized that LDL is not a single entity, but that there are different kinds, and some kinds of LDL seem to be more atherogenic than others.
Coronary Artery Disease is multi factorial. We don't know all the factors involved in its cause. But, the American Heart Association has not named dietary fat as THE cause. They do still recommend cutting dietary cholesterol and saturated fat, but they also recommend smoking cessation, achieving a healthy weight, controlling diabetes and exercise. Readers, beware.
Wednesday, January 9, 2008
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