Suppr超能文献

对当前饮食脂质建议中悖论的批判。

A critique of paradoxes in current advice on dietary lipids.

作者信息

Lands Bill

机构信息

6100 Westchester Park Drive, #1219, College Park, MD 20740 USA.

出版信息

Prog Lipid Res. 2008 Mar;47(2):77-106. doi: 10.1016/j.plipres.2007.12.001. Epub 2007 Dec 15.

Abstract

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.

摘要

关于饮食导致疾病的可信假说,仍需要明确的介质来进行逻辑证明或证伪。我们知道食物能量会引发短暂的餐后氧化损伤,且这种损伤可能无法完全逆转。此外,食用食物中维生素样的18碳多不饱和脂肪酸(PUFA)可维持组织中20碳和22碳的高度不饱和脂肪酸(HUFA)。组织中的HUFA形成类似激素的介质,在心血管疾病(主要的可预防死因)中,这些介质会将短暂的餐后损伤放大为致命的炎症、血栓形成和心律失常事件。类似的基于饮食的放大事件也可能发生在其他炎症增殖性疾病中,包括癌症、痴呆、关节炎和哮喘。这种情况的碎片化观点产生了令人困惑的悖论,这些观点在过于简化的信息中传达了不完整的知识。现在有工具可以通过可信的饮食预防干预措施成功预防两种致命的食物失衡,但帮助收集证据的组织者和资助者仍然未知。关于饮食、疾病和死亡积累的总体证据可能正接近一种范式转变,即先前观察到的事实依然存在,但对其公认解释的信念发生了变化。

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