dinoiii
December 11th, 2005, 09:37 AM
The Cholesterol Controversy Part I
INTRODUCTION
In any piece of writing that takes on the subject of fat and related issues, it is necessary to say some words about cholesterol-the longtime, nearly mythological nemesis of any dieter.
It is sometimes remarked that medical "truths" often are reversed every 30-40 years. In mid-2002, this observation was borne out with a vengeance in the case of hormone replacement therapy (HRT). Long promoted as being heart protective and having a track record going back to roughly 1975, HRT was discovered to actually increase the rate of heart attack - and several other causes of death - in women (1). Even the benefits against fracture risks appear to have been greatly overstated (2). Interestingly, some epidemiologists never bought into the promises of HRT (3). More curious still is the fact that the increased rates of heart disease in women on HRT resulted despite the fact that several cardiovascular disease "markers" or "risk factors," such as cholesterol levels, were significantly decreased.
A similar reversal is slowly taking shape in the area of research concerned with cradiovascular disease, markers of blood lipids, and cholesterol-lowering drugs. The theory that dietary cholesterol intake is the primary contributor to cardiovascular disease has not been well supported by dietary intervention trials. Similarly, prior to the advent of the statin drugs, which work by NON-cholesterol mechanisms (SEE LATER), decades of use of pharmaceuticals that strikingly lower serum lipids has not resulted in reductions from the death rate from heart disease.
Serum Studies
Many studies performed over the last decade demonstrate that the sizes of the various subclasses of HDL and LDL cholesterol are more predictive of heart disease risk than are levels of HDL, LDL, and total cholesterol. Larger particles of LDL are less atherogenic (damaging to the walls of the arteries) than are smaller particles. Larger particles of HDL are more effective at carrying LDL back to the liver for disposal than are smaller HDL particles. Also, there are other blood lipids and markers that have shown to be risk indicators of heart attack and heart disease: lipoprotein(a), homocysteine, intermediate-density lipoproteins (IDLs), apolipoportein B, apolipoprotein E4, and so forth. However, the standard lipid panel does not provide this information, and moreover, the entire cholesterol theory was put forward and defined by way of its original evidence and argument, is clearly unsubstantiated, and the new data, in turn, may end up fitting other explanatory paradigms much better than they do the cholesterol theory.
Likewise, the recommendations based upon the cholesterol theory, such as radically reduced-fat diets, either have failed when put to the test or yielded such trivial results taht significance has been achieved only by studying massive numbers of individuals. A recent review of low-fat diets found that a reduction in dietary fat was associated with reduced cardiovascular morbidity, but not reduced total mortality. The finding that cardiovascular deaths were reduced by 9%, and cardiovascular events by 16% - the positive finding - fell when the Oslo Diet-Heart Trial, which examined the effects of fish oil, was excluded. With this exclusion, cardiovascular deaths were reduced by 6%, cardiovascular events by 14%, but overall actual death rates actually INCREASED 2%. Fish oil, of course, contains omega-3 fatty acids.
The best that can be said after 40 years regarding the simple reduction of fat in the diet is, as the authors of the Cochrane review, a major medical review. recently concluded, "findings are suggestive of a small, but potentially important reduction in cardiovascular risk in trials longer than 2 years (4)." This on diets which the intervention obviously would have led to changes in more than just fat consumption, hence it is likely that the positive outcomes , such as they were, reflected factors other than just reductions in fat intake. (For those reading this that wonder how an assessment of low-fat diets could be positive even though life exectancy was not improved, I HAVE NO ANSWER!) The critical assessments of the smae decades of dietary intervention by a research group associated with Walter Willet at Harvard points out that, "metabolic studies have long established that the type of fat, but not total amount of fat, predicts serum cholesterol levels (5)."
Victory!?!
Public health authorities loudly trumpet the reduction in coronary heart disease over the last 30 years as evidence of the success in steadily reducing the level of fat in the American diet over the same period. Such claims pale a bit when placed against a backdrop of steadily rising rates of obesity, diabetes, and hypertension data from 1987-1994 showing stable or increasing rates of heart attack, and so on. What is really going on? it is actually quite simple: medical intervention after the attack and not prevention, is at work in these claims to success. When scientists at the School of Public Heath at the University of North Carolina, Chapel Hill, looked at the relationship between the new cases of heart attack and the rate of death from heart diseasde, they found the former was actually decreasing during the period of their study, whereas the latter was going down.
From 1987-1994, we observed a stableor slightly increasing incidence of hospitalization for myocardial infarction. nevertheless, there were significant annual decreases in mortality from CHD (coronary heart disease). The decline in mortality in the four communities we studied may be largely to improvements in the treatment and secondary prevention of myocardial infarction (6)."
Statistical analyses based on data running through the ned of the 1990s indicate that declines in in-hospital CHD mortality during that decade were nearly three times greater than declines in out-of-hospital mortality (7). Such statistics indicate that at least three quarters of the modern reduction in deaths from coronary heart disease has come from hospital interventions. All other factors combined, such as the much-touted changes in dietary-fat intake and the widespread prescription of cholesterol-reducing medications and a host of other drugs, likely accounts for no more than 25% of the improvement!
STATIN DRUGS
Many critics argue these days that statin drugs do NOT work by influencing cholesterol levels (originally though to influence HMG-CoA reductase), but rather by reducing inflammation in the artery wall and by idrectly inhibiting the proliferation of smooth muscle of the arterial endothelium. Indeed, the impact of these drugs upon the synthesis of cholesterol likely is undesirable because drugs thatinhibit the synthesis in the manner of the statins also inhibit the production of coenzyme Q10, hence leading to increases in deaths from cardiomyopathy, and so on, and to declines in health in other areas, such as cognitive functioning.
SUMMING UP PART I
In light of the emerging research linking cardiovascular diseases ever more closely to inflammatory processes and ever more distantly to cholesterol as such, we can begin to structure how dietary changes (i.e. - caloric restriction, macronutrient variation, and the like) ultimately will influence cardiovascular risk factors. In Part II, we will begin to see some of these blood lipid influences and how lifestyle modification truly can influence the path of health outcome - namely, cardiovascular - AND IT IS NOT GOING TO BE WHAT YOU THINK EITHER.
A Full set of references will be listed at the conclusion of this series!
INTRODUCTION
In any piece of writing that takes on the subject of fat and related issues, it is necessary to say some words about cholesterol-the longtime, nearly mythological nemesis of any dieter.
It is sometimes remarked that medical "truths" often are reversed every 30-40 years. In mid-2002, this observation was borne out with a vengeance in the case of hormone replacement therapy (HRT). Long promoted as being heart protective and having a track record going back to roughly 1975, HRT was discovered to actually increase the rate of heart attack - and several other causes of death - in women (1). Even the benefits against fracture risks appear to have been greatly overstated (2). Interestingly, some epidemiologists never bought into the promises of HRT (3). More curious still is the fact that the increased rates of heart disease in women on HRT resulted despite the fact that several cardiovascular disease "markers" or "risk factors," such as cholesterol levels, were significantly decreased.
A similar reversal is slowly taking shape in the area of research concerned with cradiovascular disease, markers of blood lipids, and cholesterol-lowering drugs. The theory that dietary cholesterol intake is the primary contributor to cardiovascular disease has not been well supported by dietary intervention trials. Similarly, prior to the advent of the statin drugs, which work by NON-cholesterol mechanisms (SEE LATER), decades of use of pharmaceuticals that strikingly lower serum lipids has not resulted in reductions from the death rate from heart disease.
Serum Studies
Many studies performed over the last decade demonstrate that the sizes of the various subclasses of HDL and LDL cholesterol are more predictive of heart disease risk than are levels of HDL, LDL, and total cholesterol. Larger particles of LDL are less atherogenic (damaging to the walls of the arteries) than are smaller particles. Larger particles of HDL are more effective at carrying LDL back to the liver for disposal than are smaller HDL particles. Also, there are other blood lipids and markers that have shown to be risk indicators of heart attack and heart disease: lipoprotein(a), homocysteine, intermediate-density lipoproteins (IDLs), apolipoportein B, apolipoprotein E4, and so forth. However, the standard lipid panel does not provide this information, and moreover, the entire cholesterol theory was put forward and defined by way of its original evidence and argument, is clearly unsubstantiated, and the new data, in turn, may end up fitting other explanatory paradigms much better than they do the cholesterol theory.
Likewise, the recommendations based upon the cholesterol theory, such as radically reduced-fat diets, either have failed when put to the test or yielded such trivial results taht significance has been achieved only by studying massive numbers of individuals. A recent review of low-fat diets found that a reduction in dietary fat was associated with reduced cardiovascular morbidity, but not reduced total mortality. The finding that cardiovascular deaths were reduced by 9%, and cardiovascular events by 16% - the positive finding - fell when the Oslo Diet-Heart Trial, which examined the effects of fish oil, was excluded. With this exclusion, cardiovascular deaths were reduced by 6%, cardiovascular events by 14%, but overall actual death rates actually INCREASED 2%. Fish oil, of course, contains omega-3 fatty acids.
The best that can be said after 40 years regarding the simple reduction of fat in the diet is, as the authors of the Cochrane review, a major medical review. recently concluded, "findings are suggestive of a small, but potentially important reduction in cardiovascular risk in trials longer than 2 years (4)." This on diets which the intervention obviously would have led to changes in more than just fat consumption, hence it is likely that the positive outcomes , such as they were, reflected factors other than just reductions in fat intake. (For those reading this that wonder how an assessment of low-fat diets could be positive even though life exectancy was not improved, I HAVE NO ANSWER!) The critical assessments of the smae decades of dietary intervention by a research group associated with Walter Willet at Harvard points out that, "metabolic studies have long established that the type of fat, but not total amount of fat, predicts serum cholesterol levels (5)."
Victory!?!
Public health authorities loudly trumpet the reduction in coronary heart disease over the last 30 years as evidence of the success in steadily reducing the level of fat in the American diet over the same period. Such claims pale a bit when placed against a backdrop of steadily rising rates of obesity, diabetes, and hypertension data from 1987-1994 showing stable or increasing rates of heart attack, and so on. What is really going on? it is actually quite simple: medical intervention after the attack and not prevention, is at work in these claims to success. When scientists at the School of Public Heath at the University of North Carolina, Chapel Hill, looked at the relationship between the new cases of heart attack and the rate of death from heart diseasde, they found the former was actually decreasing during the period of their study, whereas the latter was going down.
From 1987-1994, we observed a stableor slightly increasing incidence of hospitalization for myocardial infarction. nevertheless, there were significant annual decreases in mortality from CHD (coronary heart disease). The decline in mortality in the four communities we studied may be largely to improvements in the treatment and secondary prevention of myocardial infarction (6)."
Statistical analyses based on data running through the ned of the 1990s indicate that declines in in-hospital CHD mortality during that decade were nearly three times greater than declines in out-of-hospital mortality (7). Such statistics indicate that at least three quarters of the modern reduction in deaths from coronary heart disease has come from hospital interventions. All other factors combined, such as the much-touted changes in dietary-fat intake and the widespread prescription of cholesterol-reducing medications and a host of other drugs, likely accounts for no more than 25% of the improvement!
STATIN DRUGS
Many critics argue these days that statin drugs do NOT work by influencing cholesterol levels (originally though to influence HMG-CoA reductase), but rather by reducing inflammation in the artery wall and by idrectly inhibiting the proliferation of smooth muscle of the arterial endothelium. Indeed, the impact of these drugs upon the synthesis of cholesterol likely is undesirable because drugs thatinhibit the synthesis in the manner of the statins also inhibit the production of coenzyme Q10, hence leading to increases in deaths from cardiomyopathy, and so on, and to declines in health in other areas, such as cognitive functioning.
SUMMING UP PART I
In light of the emerging research linking cardiovascular diseases ever more closely to inflammatory processes and ever more distantly to cholesterol as such, we can begin to structure how dietary changes (i.e. - caloric restriction, macronutrient variation, and the like) ultimately will influence cardiovascular risk factors. In Part II, we will begin to see some of these blood lipid influences and how lifestyle modification truly can influence the path of health outcome - namely, cardiovascular - AND IT IS NOT GOING TO BE WHAT YOU THINK EITHER.
A Full set of references will be listed at the conclusion of this series!