Beliefs about credible hypotheses of dietary causes of disease still need well-defined mediators to test for logical proof or disproof. We know that food energy causes transient postprandial oxidative insults that may not be fully reversible. Also, eating vitamin-like 18-carbon polyunsaturated fatty acids (PUFA) in foods maintains the 20- and 22-carbon highly unsaturated fatty acids (HUFA) in tissues. Tissue HUFA form hormone-like mediators that each amplify transient postprandial insults into fatal inflammatory, thrombotic and arrhythmic events in cardiovascular disease, a major preventable cause of death. Similar diet-based amplified events may also occur in other inflammatory proliferative disorders including cancer, dementia, arthritis and asthma. Puzzling paradoxes come from fragmented views of this situation which convey incomplete knowledge in oversimplified messages. Tools now exist to demonstrate successful prevention of two fatal food imbalances with credible dietary preventive interventions, but organizers and financers to help gather the evidence remain unknown. The overall evidence accumulated about diet, disease and death may be nearing a paradigm shift in which prior observed facts remain while beliefs about their accepted interpretation change.
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| http://dx.doi.org/10.1016/j.plipres.2007.12.001 | DOI Listing |
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