Alcohol consumption indices of genetic risk for alcohol dependence.

Alcohol consumption indices of genetic risk for alcohol dependence.
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DOI:
10.1016/j.biopsych.2009.05.018
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发表时间:
2009-10-15
影响因子:
10.6
通讯作者:
Heath, Andrew C.
Heath, Andrew C.
中科院分区:
医学1区
文献类型:
--
作者:
Grant, Julia D.;Agrawal, Arpana;Bucholz, Kathleen K.;Madden, Pamela A. F.;Pergadia, Michele L.;Nelson, Elliot C.;Lynskey, Michael T.;Todd, Richard D.;Todorov, Alexandre A.;Hansell, Narelle K.;Whitfield, John B.;Martin, Nicholas G.;Heath, Andrew C.

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以前的研究已经报道了酒精消费的沉重程度和酒精依赖(AD)之间的显著遗传相关性,但这种相关性可能是由AD对消费的影响驱动的,而不是相反。我们测试了阿尔茨海默病症状和没有阿尔茨海默病患者的大量消费指标之间的遗传重叠。这些指标之间的高度遗传相关性将表明,连续的消费指标可能在发现导致依赖风险的基因方面发挥有用的作用。5项酒精使用措施的因子分析被用来建立酒精消费的沉重程度的衡量标准。对1989年澳大利亚双胞胎小组(n=6257人;男性=29.9岁)的访谈数据进行的定量遗传分析评估了饮酒沉重、DSM-IV AD症状、DSM-IV AD症状聚集和DSM-IV酒精滥用之间的遗传重叠。在酒精测量中,遗传影响解释了30-51%的方差,所有测量的遗传相关性都在0.90或更高,非依赖个人的消费和依赖症状之间的相关性估计为0.97(95%CI:0.80-1.00)。即使在普通人群中,即使在非依赖的个体中,消费的沉重程度和阿尔茨海默病症状的遗传重叠程度也很高,这意味着在普通人群中,对依赖风险的遗传影响在相当程度上是通过使用的沉重程度来发挥作用的,消费的定量测量可能在识别导致阿尔茨海默病的基因方面发挥有用的作用。
Previous research has reported a significant genetic correlation between heaviness of alcohol consumption and alcohol dependence (AD), but this association might be driven by the influence of AD on consumption rather than the reverse. We test the genetic overlap between AD symptoms and a heaviness of consumption measure among individuals who do not have AD. A high genetic correlation between these measures would suggest that a continuous measure of consumption may have a useful role in the discovery of genes contributing to dependence risk. Factor analysis of 5 alcohol use measures was used to create a measure of heaviness of alcohol consumption. Quantitative genetic analyses of interview data from the 1989 Australian Twin Panel (n=6257 individuals; M=29.9 years) assessed the genetic overlap between heaviness of consumption, DSM-IV AD symptoms, DSM-IV AD symptom clustering, and DSM-IV alcohol abuse. Genetic influences accounted for 30–51% of the variance in the alcohol measures and genetic correlations were 0.90 or higher for all measures, with the correlation between consumption and dependence symptoms among non-dependent individuals estimated at 0.97 (95% CI: 0.80–1.00). Heaviness of consumption and AD symptoms have a high degree of genetic overlap even among non-dependent individuals in the general population, implying that genetic influences on dependence risk in the general population are acting to a considerable degree through heaviness of use, and that quantitative measures of consumption will likely have a useful role in the identification of genes contributing to AD.
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