The triacylglycerol hypothesis
Dietary effects on serum cholesterol or LDLs alone provide an inadequate basis on which to explain the relationship between diet and CHD within populations. The ability of humans to protect themselves against an overaccumulation of cholesterol in their vascular system through nutritional changes depends to a much greater extent on increasing the efficiency of the HDL pathway and utilization of TAG-rich lipoproteins. The latter represent the precursors of potentially harmful cholesterol-rich remnants and LDLs that contribute to coronary atherosclerosis. The effects of diet, and in particular dietary fats, in modu-lating the clearance of TAG-rich lipoproteins in the postprandial period is of paramount importance in preventing the accumulation of atherogenic remnants and development of proatherogenic abnormalities in LDL and HDL. The actions of insulin coordinate the metabolism of TAG-rich lipoproteins but can become defective through energy imbalance, weight gain, and ultimately obesity. As a consequence, the most common abnormalities in lipoproteins to increase risk in populations arise from a primary defect in the metabolism of TAG, induced through insulin resis-tance and not cholesterol per se. Equally important is the fact that these metabolic defects originate, in part, through nutrient–gene interactions and are thus highly amenable to dietary modification.
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