LAUSR

Dietary cholesterol is absorbed in proportion to the amount ingested, blocking its hepatic synthesis, increasing its biliary excretion, only slightly increasing production of bile acids while potentially raising the serum concentration of the atherogenic low-density lipoprotein. Humans lie midway between rats and rabbits that respond to dietary cholesterol, respectively, with high and low capacity to produce bile acids, and low or high capacity to raise blood cholesterol. There are regular studies exonerating as well as blaming dietary cholesterol as a cardiovascular risk factor, particularly in genetic hypercholesterolemic individuals. We then resorted at reviewing all meta-analyses on the subject but failed to reach at a clear conclusion useful in medical practice. Nevertheless, ingestion of the same amount of cholesterol results in wide variation in the amounts absorbed and in plasma lipoprotein profiles depending on poorly understood genetic factors. Several genetic conditions are capable of interfering with the absorption and synthesis of cholesterol. Hyperabsorption of dietary cholesterol elicits the accumulation of cholesterol in the liver and in plasma. In this regard, most cases of familial hypercholesterolemia that have a case of intestinal hyperabsorption of cholesterol also demonstrate the same defect. A practical useful suggestion is to measure for a few weeks the total serum cholesterol and its fractions at least three times before and during the intake of eggs that the candidate wishes to maintain in his usual dietary practice as an efficient procedure to identify those who respond with undesirable increases in serum cholesterol.