Does Body Fatness Modify the Association Between Dietary Cholesterol and Risk of Coronary Death ? Results from the Chicago Western Electric Study

The hypothesis that body fatness modifies the relation between dietary cholesterol and 25-year coronary mortality was examined in a cohort of 1,792 middle-aged men employed by the Western Electric Company in Chicago. Relative risks of coronary death (and 95% confidence intervals) associated with a 225 mg/day greater intake of dietary cholesterol for men with a subscapular skinfold thickness less than or equal to 14, 15-20, and greater than or equal to 21 mm were 1.44 (1.10-1.90), 1.07 (0.84-1.36), and 0.95 (0.76-1.20), respectively, after adjustment for age; serum total cholesterol level; systolic blood pressure; cigarette smoking; family history of cardiovascular disease; evidence of major organ system disease at baseline; and intake of saturated fatty acids, polyunsaturated fatty acids, energy, and ethanol. Adjusted relative risks associated with a 15-mm greater subscapular skinfold thickness for men with a dietary cholesterol intake less than or equal to 649, 650-799, and greater than or equal to 800 mg/day were 1.76 (1.04-2.98), 1.64 (1.04-2.57), and 1.00 (0.69-1.55), respectively. Fatter men apparently did not benefit from a diet lower in cholesterol, while men who ate a diet high in cholesterol apparently did not benefit from leanness. These results support the hypothesis that body fatness modifies the relation between dietary cholesterol and coronary mortality, perhaps because leaner men are more responsive than fatter men to the effects of dietary cholesterol on the concentration of low density lipoprotein cholesterol.</jats:p

Does body fatness modify the effect of dietary cholesterol on serum cholesterol? Results from the Chicago Western Electric Study.

The hypothesis that lean persons are more responsive than fat persons to the effects of dietary cholesterol was investigated in 1,903 middle-aged employed men who were examined in 1958 and 1959 as participants in the Chicago Western Electric Study. Change in intake of dietary cholesterol was positively associated with change in serum cholesterol for men in the lowest tertile of body mass index (defined as weight (kg)/height (m)2) (26.6) after adjustment for change in body mass index and change in intakes of energy and saturated and polyunsaturated fatty acids. A decrease of 150 mg/1,000 kcal in dietary cholesterol was associated with mean changes of -0.46, -0.18, and 0.13 mmol/liter in serum cholesterol for men with body mass indices of 26.6, respectively. Body mass index was strongly correlated with subscapular skinfold thickness; thus, these differences in body mass index reflect true differences in adiposity. These results may help to explain inconsistencies that have occurred in feeding experiments with dietary cholesterol, and they suggest that a reduction in dietary cholesterol should have a more favorable effect on the serum cholesterol levels of fat persons after they have lost weight

Monocyte-to-HDL-cholesterol ratio as a prognostic marker in cardiovascular diseases

Inflammation and lipid accumulation are two basic hallmarks of atherosclerosis as a chronic disease. Inflammation not only is a local response but can also be considered as a systemic process followed by an elevation of inflammatory mediators. Monocytes are a major source of proinflammatory species during atherogenesis. In atherosclerosis, modified low-density lipoproteins (LDLs) are removed by macrophages; these are recruited in the vessel wall, inducing the release of inflammatory cytokines in inflamed tissue. Hence, inflammatory cholesterol ester-loaded plaque is generated. High-density lipoprotein-cholesterol (HDL-C) exhibits antiatherosclerotic effects by neutralizing the proinflammatory and pro-oxidant effects of monocytes via inhibiting the migration of macrophages and LDL oxidation in addition to the efflux of cholesterol from these cells. Furthermore, HDL plays a role in suppressing the activation of monocytes and proliferation-differentiation of monocyte progenitor cells. Thus, accumulation of monocytes and reduction of HDL-C may participate in atherosclerosis and cardiovascular diseases (CVD). Given that the relationship between the high number of monocytes and low HDL-C levels has been reported in inflammatory disorders, this review focused on understanding whether the monocyte-to-HDL ratio could be a convenient marker to predict atherosclerosis development and progression, hallmarks of CV events, instead of the individual monocyte count or HDL-C level