This blog was stimulated by the recent surge to have government endorse/require lower salt in the diet. There is, of course, no direct evidence that a low salt diet prolongs life. In the recommendations, lowering salt in the diet is taken as a surrogate for lowering blood pressure. It is assumed that lowering the amount of salt in the diet by 3 grams/day will lower systolic blood pressure between 3.5 and 5.5 mm; no estimate is given for the effect on diastolic blood pressure (is there any?). It is claimed that this will reduce death by heart attacks and other problems.
High blood pressure is a demonstrated risk (i.e. there a correlation, but an 0.80 correlation is a 0.8x0.8 or 64% estimate) for strokes, hypertensive heart disease, and abdominal aortic aneurysms (the latter in male smokers). However, every study of lowering blood pressure (usually by diuretics) only shows a reduction in the risk of strokes; there is NO demonstrated reduction in mortality or hypertensive heart disease. I should also mention that reduction of blood pressure by beta-blockers alone has shown no reduction in any risk of stroke or heart attack. In addition, there has been no prospective study to see if lowering the amount of salt in the diet has any injurious effect, and a lot of medicine is counter-intuitive. I recall a study that lowering the salt in the diet INcreases the risk for heart failure, but who really knows?
A related dietary question deals with lowering the amount of sugar in the diet (?by taxing sodas). I pause here to remind my lay readers that just because diabetes is evidenced by elevated blood sugar, this does NOT mean that increasing the amount of sugar in your diet causes diabetes, assuming you gain no weight. And we will also ignore the white lab rat study that shows that if we keep lab rats 30% below their IBW (and who determines the Ideal Body Weight for a lab rat?) they live longer. The flip side is the recent studies that demonstrate that overweight adult humans (BMI 26-29) have an increased chance of surviving a heart attack.
Now let us assume that we wish to lose weight. What is the most efficient and surest way to do this? (Remember that when you lose weight as an adult, your fat cells shrink, and get smaller and have a smaller net surface area for metabolism.) Of course, the obvious method is to eat less. No one was overweight in a concentration camp. The lap-band surgery shrinks the functioning volume of your stomach, so you can't ingest many calories, and again you lose weight, and usually cure your diabetes as well. Anorectics have absolutely no problem in losing weight. In another vein,liposuction sucks the fat cells away from your body,and these cells can never increase in size again.
But the brain demands homeostasis, and strives to keep your body parameters as constant as possible. Most people's weight varies very little from year to year. All nutritionists agree that 3500 calories = 1 pound. If you divide 3500 by 350 days, you find that you have to micromanage your food intake to plus or minus 10 calories a day to keep your weight constant for the year. Not even the most dedicated fanatic can do this. Obviously, the brain has a mechanism to raise or lower your metabolism to keep your weight constant, sort of a feedback mechanism, which has nothing to do with leptin. This metabolic/mass inertia is what makes it equally difficult to gain or lose a lot of weight. In fact studies have shown that when you gain weight, your metabolism increases, and when you lose weight, your metabolism decreases, in a true negative feedback manner, which is why most dieters hit intermittent weight plateaus.
In order to lose weight, you must feel good about yourself, and be relatively happy and free from anger. Food was the first pleasure, given to you by your mother. It is very difficult to deny yourself this pleasure if you are not "in a good place". If you are mentally at peace, then you can walk around hungry without feeling (emotionally) deprived. You can be satisfied by the flavor of half a chocolate chip cookie rather than a whole box of Mallomars. So losing weight is not a matter of pure will-power, but rather a matter of not being too out of rhythm with the world and ego-dystonic. This is not to say that all overweight people are neurotic. Many are very happy with themselves, and see no need to change their body habitus. Your self-image is everything to you, and this is what we all rely on and judge ourselves by. This is why I don't think special diets are the answer. We all eat the way we like, and no one does Weight Watchers forever. The answer is always portion control. Why torture yourself by eating foods you don't like , instead of simply eating less of the foods you do like?
Let me close by saying eating "healthy" food is less important than eating less and losing weight. We know very little about nutrition. When I went to school as a child, the food pyramid was the exact inversion of what it is now. We don't even know (i.e. have good evidence) if the biggest meal of the day should be breakfast, lunch, or dinner. Should we have one large meal a day or six small ones. For every study, there is a counter-study. Do lefties live longer than righties? Do short people live longer than tall people? Why does overall health correlate so strongly with economic position in life? Maybe we all would be healthier if everyone were a millionaire? Any time any person or authority tries to tell you that something is "good" for you, or "good for your health" always ask the same question we asked reflexively in physics and on hospital rounds: "Do you have a published article to support that opinion?".
Showing posts with label Salt. Show all posts
Showing posts with label Salt. Show all posts
Tuesday, February 16, 2010
Friday, January 22, 2010
Cholesterol, Statins, Zetia,Niacin, ASCVD, and MI's
This blog was stimulated by several recent articles and studies about statins, zetia, Niacin, ASCVD, and MI's. We must not lose sight of the fact that virtually all researchers have concluded that an MI is triggered by the rupture of an atheromatous plaque in a coronary artery, although the actual rupture has not, I think, ever been seen dynamically. Nevertheless, when a coronary artery is found clotted off at autopsy, and the clot is adjacent to and newer than the plaque, and the surrounding tissue is necrosed, then the conclusion is probably correct.
The first fact to notice at such an autopsy is that the atheromatous-clotted artery, as a rule, has a larger diameter anatomically before and after the clot than does another coronary artery. In other words, the probability of a rupture-to-clot process does not seem to depend vitally on the pre-clot diameter, although there is, of course, some influence. Just recall how many times an artery with 97%-99% stenosis is not occluded, but is stented instead.
So we then come to the question: what causes (or prevents) the plaque in a coronary artery from rupturing, clotting off the artery, and causing an MI? Clearly there must be some degree of inflammation which sets the plaque up to be susceptible to the shearing force of coronary blood flow. So we can have some equation that the probability of clot formation varies as (C)x(probability of plaque)x(?thickness of plaque)x(probability of rupture), where C is a factor to indicate that an MI has occurred before; if C=1 we are dealing with primary prevention, and if C is greater than one, we are dealing with secondary prevention.
Since we have plenty of data on secondary prevention, I am going to concentrate on primary prevention. Now CRP, a measure of inflammation, has been variously correlated with the risk of MI as has 81 mg/day of ASA, with no clear-cut primary prevention shown by either lowering CRP or by daily ASA. But in experimental physics we have a saying: If you are arguing about the significance of data, then the data is not significant, similar to the last data point in a particle physics experiment.
We do know that diabetes, cigarette smoking and hypertension are synergistic with cholesterol levels in causing a plaque as well as a clot. This shows at least two mechanisms at work, since it is difficult to imagine that hypertension increases local plaque inflammation. Similarly Zetia, which lowers cholesterol, does not seem to increase coronary artery diameter, but these studies did not look at MI or CVA as an endpoint, so we don't know if Zetia affects plaque inflammation and rupture. A curious observation is that if your "native" cholesterol is 200, your risk of an MI is greater than if Crestor was used to lower your native cholesterol from 240 to 200. This clearly indicates to me that statins have an additional preventive effect, probably lowering inflammation of the plaque, over and above lowering cholesterol and/or reducing the size of the plaque. Similarly Niacin, which raises HDL, has a beneficial effect beyond its size effect, and probably lowers inflammation as well. And patients (usually female) with cholesterols over 300 and 85+ years old without and ASCVD are outside our explanations and models.
But to me, the most amazing drug is C2H5OH, or ethanol. In matched pairs, people who drink "moderately" (= 1 drink/day for men, and one every other day for women) have a lower heart attack rate and LARGER DIAMETER CORONARY ARTERIES AT AUTOPSY than do non-drinkers. This result holds for numerous studies with whiskey, beer, slivovitz (plum brandy), scotch, etc,in homogeneous populations (e.g.native-born Japanese males in Hawaii) and seems to be a pure alcohol effect. We have known this since 1974 (see article in JAMA). No one knows the mechanism by which this occurs, but I assume constant research is going on. Since young people already have atheromatous plaques, then if we want to reduce heart disease in our older population, it seems to me we should encourage a glass of wine with dinner starting with high school seniors. There is no argument in the literature about this effect, as there is about lowering CRP, adding ASA, or lowering salt in the diet.
With regard to lowering salt in the diet, there were two long articles (one pro and one con) about this subject published years ago in Lancet. The con argument was that just as eating sugar will not make you a diabetic, so will eating salt (with normal kidney function) not give you hypertension. I have a more fundamental ethical objection to imposing salt reduction. In hospitals and research clinics, when an experiment is performed on human subjects, it must be passed by the Institutional Review Board, and each subject must be warned of possible negative side effects and given a chance to withdraw. No such board will review the law if low salt diets are mandated, and I am concerned that 10 years down the road we may learn that we have done irreversible harm to the subjects, our fellow citizens, or to the children in school cafeterias.
The first fact to notice at such an autopsy is that the atheromatous-clotted artery, as a rule, has a larger diameter anatomically before and after the clot than does another coronary artery. In other words, the probability of a rupture-to-clot process does not seem to depend vitally on the pre-clot diameter, although there is, of course, some influence. Just recall how many times an artery with 97%-99% stenosis is not occluded, but is stented instead.
So we then come to the question: what causes (or prevents) the plaque in a coronary artery from rupturing, clotting off the artery, and causing an MI? Clearly there must be some degree of inflammation which sets the plaque up to be susceptible to the shearing force of coronary blood flow. So we can have some equation that the probability of clot formation varies as (C)x(probability of plaque)x(?thickness of plaque)x(probability of rupture), where C is a factor to indicate that an MI has occurred before; if C=1 we are dealing with primary prevention, and if C is greater than one, we are dealing with secondary prevention.
Since we have plenty of data on secondary prevention, I am going to concentrate on primary prevention. Now CRP, a measure of inflammation, has been variously correlated with the risk of MI as has 81 mg/day of ASA, with no clear-cut primary prevention shown by either lowering CRP or by daily ASA. But in experimental physics we have a saying: If you are arguing about the significance of data, then the data is not significant, similar to the last data point in a particle physics experiment.
We do know that diabetes, cigarette smoking and hypertension are synergistic with cholesterol levels in causing a plaque as well as a clot. This shows at least two mechanisms at work, since it is difficult to imagine that hypertension increases local plaque inflammation. Similarly Zetia, which lowers cholesterol, does not seem to increase coronary artery diameter, but these studies did not look at MI or CVA as an endpoint, so we don't know if Zetia affects plaque inflammation and rupture. A curious observation is that if your "native" cholesterol is 200, your risk of an MI is greater than if Crestor was used to lower your native cholesterol from 240 to 200. This clearly indicates to me that statins have an additional preventive effect, probably lowering inflammation of the plaque, over and above lowering cholesterol and/or reducing the size of the plaque. Similarly Niacin, which raises HDL, has a beneficial effect beyond its size effect, and probably lowers inflammation as well. And patients (usually female) with cholesterols over 300 and 85+ years old without and ASCVD are outside our explanations and models.
But to me, the most amazing drug is C2H5OH, or ethanol. In matched pairs, people who drink "moderately" (= 1 drink/day for men, and one every other day for women) have a lower heart attack rate and LARGER DIAMETER CORONARY ARTERIES AT AUTOPSY than do non-drinkers. This result holds for numerous studies with whiskey, beer, slivovitz (plum brandy), scotch, etc,in homogeneous populations (e.g.native-born Japanese males in Hawaii) and seems to be a pure alcohol effect. We have known this since 1974 (see article in JAMA). No one knows the mechanism by which this occurs, but I assume constant research is going on. Since young people already have atheromatous plaques, then if we want to reduce heart disease in our older population, it seems to me we should encourage a glass of wine with dinner starting with high school seniors. There is no argument in the literature about this effect, as there is about lowering CRP, adding ASA, or lowering salt in the diet.
With regard to lowering salt in the diet, there were two long articles (one pro and one con) about this subject published years ago in Lancet. The con argument was that just as eating sugar will not make you a diabetic, so will eating salt (with normal kidney function) not give you hypertension. I have a more fundamental ethical objection to imposing salt reduction. In hospitals and research clinics, when an experiment is performed on human subjects, it must be passed by the Institutional Review Board, and each subject must be warned of possible negative side effects and given a chance to withdraw. No such board will review the law if low salt diets are mandated, and I am concerned that 10 years down the road we may learn that we have done irreversible harm to the subjects, our fellow citizens, or to the children in school cafeterias.
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