美国科罗拉多大学一项新的研究表明，你的遗传决定你能够比别人喝的更多，而且不会增加酒精中毒或酒精依赖的风险。这项研究指出了具体的遗传通路以及酒精消耗水平相关的基因，该基因与人类和老鼠中的酒精依赖无关。
研究小组使用老鼠对影响酒精消耗行为的遗传通路进行识别。他们发现老鼠的饮酒行为与大脑中的快乐和奖赏通路（the pleasure and reward pathways）有关，也与一些控制对食物的满足和欲望的遗传系统有关。接下来研究人员对老鼠和人类中酒精相关通路中的基因进行比对，试着识别出与酒精消耗有关的普遍遗传因子。
结果是很新奇的，所识别的基因与试验人群的饮酒行为有关，但与酒精依赖并不是同一个基因。
Tabakoff介绍说，我们知道，在那些遗传学上更倾向于依赖的人群中，高水平的酒精消耗会增加酒精依赖的风险。事实上，在这项研究中，我们发现人类中高水平的酒精消耗与酒精依赖是绝对正相关的。然而，由于似乎是不同的基因影响酒精消耗的水平，有的会抵抗酒精依赖的趋势，所以在人类中存在很大的变动。
那些含有趋向于消耗适量酒精的遗传学个体可能仍然有一个遗传学趋势会对饮酒行为失去控制，并可能发展成酒精依赖。相反的，能够饮用大量酒精的遗传学个体可能并没有趋向于酒精依赖的基因。
作者强调说，在本文中研究的表型并不依赖于酒精摄入，是基因影响了这些表型。（生物谷Bioon.com）
酒精与健康研究：
PNAS：饥饿激素可能影响酒精依赖
JCBFM：饮酒6分钟后酒精即“上头”
PNAS：酒精易感性的遗传联系
Am.J.Med：中年人适量饮酒可预防心血管疾病
Alcohol：酒精具有免疫调节作用
生物谷推荐原始出处：
BMC Biology 2009, 7:70doi:10.1186/1741-7007-7-70
Genetical genomic determinants of alcohol consumption in rats and humans
Boris Tabakoff , Laura Saba , Morton Printz , Pam Flodman , Colin Hodgkinson , David Goldman , George Koob , Heather N Richardson , Katerina Kechris , Richard L Bell , Norbert Hubner , Matthias Heinig , Michal Pravenec , Jonathan Mangion , Lucie Legault , Maurice Dongier , Katherine M Conigrave , John B Whitfield , John Saunders , Bridget Grant , Paula L Hoffman and WHO/ISBRA Study on State and Trait Markers of Alcoholism
Background
We have used a genetical genomic approach, in conjunction with phenotypic analysis of alcohol consumption, to identify candidate genes that predispose to varying levels of alcohol intake by HXB/BXH recombinant inbred rat strains. In addition, in two populations of humans, we assessed genetic polymorphisms associated with alcohol consumption using a custom genotyping array for 1,350 single nucleotide polymorphisms (SNPs). Our goal was to ascertain whether our approach, which relies on statistical and informatics techniques, and non-human animal models of alcohol drinking behavior, could inform interpretation of genetic association studies with human populations.
Results
In the HXB/BXH recombinant inbred (RI) rats, correlation analysis of brain gene expression levels with alcohol consumption in a two-bottle choice paradigm, and filtering based on behavioral and gene expression quantitative trait locus (QTL) analyses, generated a list of candidate genes. A literature-based, functional analysis of the interactions of the products of these candidate genes defined pathways linked to presynaptic GABA release, activation of dopamine neurons, and postsynaptic GABA receptor trafficking, in brain regions including the hypothalamus, ventral tegmentum and amygdala. The analysis also implicated energy metabolism and caloric intake control as potential influences on alcohol consumption by the recombinant inbred rats. In the human populations, polymorphisms in genes associated with GABA synthesis and GABA receptors, as well as genes related to dopaminergic transmission, were associated with alcohol consumption.
Conclusions
Our results emphasize the importance of the signaling pathways identified using the non-human animal models, rather than single gene products, in identifying factors responsible for complex traits such as alcohol consumption. The results suggest cross-species similarities in pathways that influence predisposition to consume alcohol by rats and humans. The importance of a well-defined phenotype is also illustrated. Our results also suggest that different genetic factors predispose alcohol dependence versus the phenotype of alcohol consumption.
