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Cell-free Biochemical Fluorometric Enzymatic Assay for High-throughput Measurement of Lipid Peroxidation in High Density Lipoprotein
Published on: October 12, 2017
Coronary heart disease, hypercholesterolemia, and atherosclerosis. II. Misrepresented data
1Department of Pathology and Molecular Medicine, Wellington School of Medicine, Wellington, New Zealand.
Abstract:
Early development of the hypercholesterolemic/lipid hypothesis of atherosclerosis was based on false premises including fallacious national mortality rates and misrepresentation of the vascular lesions in cholesterol-overfed animals and monogenic hypercholesterolemias (MH). Nonspecific coronary heart disease (CHD) was inappropriately used as a surrogate of atherosclerosis, unmeasured and unseen. Causality was assumed and implied by classifying statistical correlates of CHD as atherogenic risk factors. These faults were compounded by methodological errors, pooling of all causes of CHD, a large clinical diagnostic error, biased age selection of cohorts leading to confounding by age and MH, and emphasis on population and cohort mean values which conceal heterogeneity within cohorts and are inapplicable to individuals. Overzealous investigators neglected to review the premises and relevant pathology on which the hypothesis was based or to reconcile valid criticisms, inconsistencies, and invalidation of CHD epidemiology by pathological, experimental, and iatrogenic evidence. Statistical data, pertaining to CHD but with no scientific applicability to atherosclerosis, progressively imparted to readers a misleading perception of the relationship of serum cholesterol to CHD. Concurrently the statistical serum cholesterol range was unjustifiably abandoned. The evidence establishes that the lipid hypothesis of atherosclerosis lacks scientific basis.
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