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Ann Intern Med. 1951;35(4):938-943. doi:10.7326/0003-4819-35-4-938
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Although some 40 years have elapsed since Windaus1 reported the predominance of cholesterol and its esters in human atherosclerotic lesions and Anitschkow2 produced experimental atherosclerosis in the rabbit by the feeding of cholesterol, an etiological hypothesis, capable of verification at every step, is still a matter of the future. Experimental investigation at present is quite active and is no longer hampered by the dictum that human atherosclerosis is an inevitable concomitant of the process of aging. The volume of investigations dealing with the relationship of lipid metabolism to atherosclerosis has reached staggering proportions, but the results are still controversial. Recently


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