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Contents
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Effects of NCEP step
2 diet and/or exercise on lipids
The National Cholesterol Education Program (NCEP) provides two diets,
Steps 1 & 2, to treat abnormal lipoprotein levels. Step 2 (< 7% SFA) is
lower in SFAs than step 1 (~ <10% SFA, 10% MUFA, 10% PUFA). Both allocate
fat as ~30% of total calories, rather than as g/kg ideal body weight (as
proposed by Dr. Siguel). A study asked ~ 400 M&W to follow, for 1 year, one
of four approaches: their usual diet +usual habits, NCEP step 2 diet + usual
habits, usual diet + exercise, or NCEP step 2 diet + exercise. The study showed
that "…the NCEP Step 2 diet failed to lower LDL cholesterol levels in M or
W with high-risk lipoprotein levels who did not engage in aerobic
exercise." People on diet + exercise lost weight, much more than the other
groups (as expected). Diet + exercise produced < 10% decreases in TC after 1
year. Levels of TC/HDLC and TG were not affected in any group. (Stefanick ML, Mackey S, Sheehan M, Ellsworth N et al.
Effects of diet and exercise in men and postmenopausal women with low levels of
HDL cholesterol and high levels of LDL cholesterol. N Eng J Med 1998;
339:12-20.)
Discussion. As with most lipid lowering studies, there were huge individual differences that obscured the findings. It would have been much better if the authors published individual results (i.e., plots of before and after for each subject). We suspect that a few subjects are mostly responsible for the mean values and, while many subjects improved, many got worse (particularly those who did not lose weight). The decrease in TC is clinically quite small, but consistent with values reported in trials of similar diets. This decline is most likely due to weight loss.
When Dr. Siguel was responsible for lipid testing at two teaching hospitals in Boston (as part of his clinical lab residency), he observed that many patients admitted to the ICU, even those with severe CAD, had excellent lipid levels. Fasting or reduced caloric intake caused by the admission process was the primary cause. Almost any diet that causes weight loss will decrease TC. Decreasing TC/HDLC or high TG is more difficult.
Patients with abnormal lipids are unlikely to benefit from current nutritional therapies recommended in most medical books and patient education brochures. In a paper presented to the American Heart Assoc. several years ago, Dr. Siguel suggested drastic changes to the NCEP diets. He stated that the key modifying variables are total calories, grams/day of PUFAs, and distribution of PUFAs. Incidentally, the usual diet + exercise group ate more calories than the other 3 groups & lost barely 1 lb (people may feel hungry after exercise, and eat more, a danger of exercising and socializing). Perhaps these subjects gained muscle but lost fat.
Diabetes
& Heart disease
Ref:
Haffner, SM, Lehto, S, Ronnemaa, T, et al. Mortality from Coronary Heart
Disease in Subjects with Type 2 Diabetes and in Nondiabetic Subjects with and without
Prior Myocardial Infarction. NEJM, July 23 1998; 339(4): 229-234.
Non-Insulin Dependent Diabetes Mellitus (NIDDM, Type 2 Diabetes) is associated with increased risk of CAD (coronary artery (heart) disease). This study found that patients with NIDDM but no previous MI (Myocardial Infarction = heart attack) are as likely to have MIs as are nondiabetics with prior MIs (high risk). It follows that patients with NIDDM should be treated for CAD risk factors the same way as subjects with a previous MI are treated (quite actively, to prevent death).
Researchers studied 45-64 y.o. subjects in Finland. Seven year rates of MI + stroke were about 5% (no prior MI), 26% (prior MI), 30% (no prior MI, NIDDM), and 65% (prior MI, NIDDM). Based on evaluation of internal carotid arteries, CAD in NIDDM appears to be caused by accelerated atherosclerosis. Drugs used to treat abnormal lipids (such as "statins") may therefore be effective in NIDDM.
Discussion. The biochemical basis for accelerated atherosclerosis among NIDDM patients is not established. However, research by Horrobin, Brenner, Holman, Siguel and many others suggests a strong connection between abnormalities of metabolism of EFAs, accelerated atherosclerosis, and CAD. The authors in the above study did not report EFA abnormalities, and therefore may have missed the most significant biochemical variable. If they evaluated EFAs, I believe they would have found many individual abnormalities and deficiencies of EFAs which, if corrected, could have prevented many MIs.
The authors found that people with diabetes are at high risk of MI, as was already known. I attribute the high probability of MI and premature death to bad lifestyles. I believe people in Finland are not eating foods appropriate for their genes and environment.
Although the MI rate in Finland is higher than that in the US, similar principles apply here. Treating diabetics and other patients with drugs such as statins and niacin may prevent deaths from MI within 10 years, but the survivors may face undesirable consequences, such as neurological disorders and brain damage. If the underlying problem is an EFA abnormality, drugs may postpone death without correcting the problem (like anti-hypertension medications, which do not correct the cause of hypertension, but lower blood pressure and may reduce blood flow to outlying body areas, leading to premature cell death).
Society is encouraging humans to become dependent on drugs for pleasure, depression, sex, performance, and disease. No wonder drug addiction is big money. To prevent complex diseases such as accelerated atherosclerosis, we need radically different strategies. Current nutrition therapies fail.
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© 1998 Edward
Siguel. All rights reserved |
modified 1/15/00 |