Syed Javid Hasan Syed Aaquil Hasan, Pawirotaroeno Raisa Arifanie O'Zelian, Syed Javid Hasan Syed Abrar Hasan, Abzianidze Elene
Department of Acute Medicine, United Lincolnshire Hospitals NHS Trust, Lincoln, Lincolnshire, United Kingdom.
Department of Emergency, Mungra Medical Center, Nickerie, Suriname.
Glob Med Genet. 2020 Oct;7(3):80-86. doi: 10.1055/s-0040-1721814. Epub 2020 Dec 29.
One of the significant consequences of alcohol consumption is cancer formation via several contributing factors such as action of alcohol metabolites, vitamin deficiencies, and oxidative stress. All these factors have been shown to cause epigenetic modifications via DNA hypomethylation, thus forming a basis for cancer development. Several published reviews and studies were systematically reviewed. Omnivores and vegetarians differ in terms of nutritional intake and deficiencies. As folate deficiency was found to be common among the omnivores, chronic alcoholism could possibly cause damage and eventually cancer in an omnivorous individual via DNA hypomethylation due to folate deficiency. Furthermore, as niacin was found to be deficient among vegetarians, damage in vegetarian chronic alcoholics could be due to increased NADH/NAD ratio, thus slowing alcohol metabolism in liver leading to increased alcohol and acetaldehyde which inhibit methyltransferase enzymes, eventually leading to DNA hypomethylation. Hence correcting the concerned deficiency and supplementation with S-adenosyl methionine could prove to be protective in chronic alcohol use.
饮酒的一个重要后果是通过多种促成因素引发癌症,这些因素包括酒精代谢产物的作用、维生素缺乏和氧化应激。所有这些因素都已被证明可通过DNA低甲基化导致表观遗传修饰,从而为癌症发展奠定基础。对几篇已发表的综述和研究进行了系统回顾。杂食者和素食者在营养摄入和营养缺乏方面存在差异。由于发现杂食者中叶酸缺乏很常见,慢性酒精中毒可能会通过叶酸缺乏导致的DNA低甲基化,对杂食个体造成损害并最终引发癌症。此外,由于发现素食者中烟酸缺乏,素食慢性酗酒者的损害可能是由于NADH/NAD比值增加,从而减缓肝脏中的酒精代谢,导致酒精和乙醛增加,抑制甲基转移酶,最终导致DNA低甲基化。因此,纠正相关缺乏并补充S-腺苷甲硫氨酸可能对慢性饮酒具有保护作用。