IN the period from 1955-1957, the experimental elevation of either the plasma phosphatide or triglyceride of the laboratory animal was observed 1-5 to induce a hypercholesteremic state. Previous to these findings, we, like most investigators in this field, considered the plasma excess of phosphatide, triglyceride, or both in various hypercholesteremic states as secondary to or compensator for an initial derangement in cholesterol metabolism. However after such observations had been made, we began to reexamine various common clinical hypercholesteremic states with the possibility in mind that perhaps the plasma excess of phosphatide and/or triglyceride was not a sequent of the hypercholesteremia but the latter's causant. Such reexaminations now have convinced us that in various hypercholesteremic states, the initial cause of the disorder is indeed a lipogenic one in that it has been caused or set in motion by a primary error in phosphatide or triglyceride metabolism. Some of the reasons leading
FRIEDMAN M, BYERS SO, ROSENMAN RH. Lipogenic Hypercholesteremia: A Guide for Reorientation in the Consideration of Lipid-Cholesterol Relationships. Arch Intern Med. 1965;116(6):807–809. doi:10.1001/archinte.1965.03870060005001
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