Biomedical subjects
Publications and source records attributed to P Boldrini.
Lanosterol, a precursor of cholesterol, is ingested with human diet and occurs in the body in concentrations exceeding solubility. Flesh of immature animals is a common source of dietary lanosterol, which may form with cholestanol and water an insoluble adjunct, CL-2W. As the latter may contribute to various disorders, exogenous lanosterol should be avoided by diet adjustment.
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The water-insoluble cholesterol-cholestanol-water adduct C-C-2W, chemical and physical cause of atherosclerosis and gallstones, has now been found in tendinous xanthoma as well; C-C-2W, and not cholestanol, is the initial compound deposited in hereditary CTX (cerebrotendinous xanthomatosis). From these and other findings it is theorized that what have been termed cholesterol or cholestanol lipidoses should instead be characterized as C-C-2W lipidoses. More than 1 mg of cholestanol . H2O present in the body causes crystallizaion of C-C-2W . This happens when the steroid meets cholesterol . H2O in sufficient concentration to reach a solubility product of 10(-7) mg/ml. In this light the literature can be interpreted to indicate that C-C-2W exerts negative effects on liver, intima tissue, eyes, lungs, and other parts of the body. Those effects include inflammation, cell necrosis, destruction of cell membranes, abnormal growth and, perhaps, neoplastic activity. Up to 200 g of C-C-2W in the body may be tolerated if evenly spread but not if localized in one or two areas only; e.g., the brain or the cardiovascular system. It is estimated that about 1000 g of C-C-2W, even if spread, are beyond the limit of human tolerance.
Cholesterol gallstones are made up of cholesterol.H20, traces of body temperature cholesterol, and a cholesterol-cholestanol-water adduct (C-C-2W). For the first time C-C-2W has been chemically and optically located in such gallstones, specifically in the nucleus, in the groove, and on the surface. These findings suggest a novel yet rational theory of cholesterol-stone quantitatively related to prevention and dissolution: (1) Bile is chemically abnormal if cholestanolH2O is present as a foreign unwanted substance. (2) When cholestanol.H2O in portal blood approaches 10(-4) mg/ml, precipitation of C-C-2W occurs in the hepatocytes because it finds sufficient cholesterol.H2O to reach the solubility product of the adduct. The resulting C-C-2W microcrystallites flow with bile down the biliary tree and then seed the supersaturated cholesterol solution in the gallbladder. (3) On the other hand, for concentrations of cholestanol.H2O around 10(-5) mg/ml, C-C-2W precipitation occurs exclusively in the gallbladder. (4) The adduct is the physical cause of cholesterol gallstones since however it arrives in the gallbladder, it produces swift crystallization of cholesterol.H20.
The atheromas of adult aortas have been found to be composed mostly of tabular crystals of a highly insoluble cholesterol-cholestanol-water adduct designated C-C-2W. Early feeding of cholestanol risks precipitation of C-C-2W on the incomplete membranes of infants. Resultant impairment of cell permeability and reactivity can give rise to incipient atherosclerosis. The pathological condition becomes patent only with adulthood, when the aorta intima-media will be stacked with the adduct and fatty streaks will occur. Cholesterol, as provided by the usual dietary sources, contains from 3 to 10% of cholestanol, quantities more than sufficient to reach the solubility product of C-C-2W: 10(-7) mg/ml. It follows that much atherosclerosis could be avoided if cholestanol-containing foods, specifically dietary cholesterol, were not fed to infants or children. Cholestanolosis and hypercholestanolemia are new concepts to be considered in dietary approaches to control of atherosclerosis.
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