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假说:节日性心源性猝死:食物和酒精对 SULT1A 酶的抑制作用作为促发因素。

Hypothesis: holiday sudden cardiac death: food and alcohol inhibition of SULT1A enzymes as a precipitant.

出版信息

J Appl Toxicol. 2012 Oct;32(10):751-5. doi: 10.1002/jat.2764. Epub 2012 Jun 8.

DOI:10.1002/jat.2764
PMID:22678655
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3504075/
Abstract

Sudden cardiac death is a significant health issue, causing millions of deaths worldwide annually. Studies have found that the likelihood of such death is higher in winter. Further studies identified that the highest likelihood occurs on Christmas Day and New Years Day, but not the interim period. Thanksgiving, Independence Day and the Islamic holiday Eid Al-Fitr also show significant increases in the rate of cardiac events or death. A number of mechanisms have been proposed, but none have satisfactorily explained the evidence. This article reviews the data supporting the existence of a holiday cardiac death phenomenon, the involvement of catecholamines and the normal modes of human catecholamine deactivation. Further evidence is reviewed that supports a hypothesized mechanism whereby critical SULT1A catecholamine deactivation enzymes can in some patients be inhibited by naturally-occurring phenols and polyphenols in foods and alcohols. If deactivation is inhibited by holiday consumption excesses, holiday stress or excitement could lead to a buildup of catecholamines that can cause fatal arrhythmias. Awareness of this mechanism could reduce deaths, both through doctor/patient education leading to a moderation in consumption and through the potential identification of patients with a predisposition to SULT1A inhibition. This hypothesis also raises parallels between sudden cardiac death in adults and Sudden Infant Death Syndrome (SIDS). The possible involvement of SULT1A inhibition in SIDS is discussed.

摘要

心脏性猝死是一个重大的健康问题,每年在全球范围内导致数百万人死亡。研究发现,这种死亡的可能性在冬季更高。进一步的研究表明,这种情况在圣诞节和元旦最高发,但在中间期并非如此。感恩节、独立日和伊斯兰教开斋节也显示出心脏事件或死亡的发生率显著增加。提出了许多机制,但没有一个令人满意地解释了证据。本文回顾了支持节假日心脏性猝死现象存在的相关数据,涉及儿茶酚胺和人类儿茶酚胺失活的正常模式。进一步的证据支持一个假设的机制,即某些患者中,关键的 SULT1A 儿茶酚胺失活酶可能会被食物和酒精中的天然酚类和多酚类物质抑制。如果失活被节假日过量摄入、节假日压力或兴奋所抑制,儿茶酚胺可能会积聚,导致致命的心律失常。这种机制的认识可以通过医生/患者教育来减少饮酒量、并通过潜在识别易受 SULT1A 抑制影响的患者,从而降低死亡率。这一假设还提出了成年人心脏性猝死和婴儿猝死综合征 (SIDS) 之间的相似之处。本文还讨论了 SULT1A 抑制在 SIDS 中的可能作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b972/3504075/08d92bce9ae2/jat0032-0751-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b972/3504075/08d92bce9ae2/jat0032-0751-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b972/3504075/08d92bce9ae2/jat0032-0751-f1.jpg

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