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早年开始饮酒并非成年期酒精使用障碍的原因,而是遗传风险的主要指标。一项基于人群的双胞胎研究。

Early age of alcohol initiation is not the cause of alcohol use disorders in adulthood, but is a major indicator of genetic risk. A population-based twin study.

作者信息

Ystrom Eivind, Kendler Kenneth S, Reichborn-Kjennerud Ted

机构信息

Department of Genetics, Environment and Mental Health, Norwegian Institute of Public Health, Oslo, Norway.

出版信息

Addiction. 2014 Nov;109(11):1824-32. doi: 10.1111/add.12620. Epub 2014 Aug 19.

Abstract

BACKGROUND AND AIMS

An early age of alcohol initiation (AAI) is associated with and has been hypothesized to be a cause of alcohol use disorders (AUD) in adulthood. Results from twin studies, however, indicate that AAI is an indicator of risk for AUD. We aimed to test a causal hypothesis versus a risk indicator hypothesis for the relationship between early AAI and AUD.

DESIGN

A population-based twin study using biometric twin modelling.

SETTING

Norway.

PARTICIPANTS

A population-based sample of 1336 Norwegian twins.

MEASUREMENTS

Life-time DSM-IV AUDs were assessed by structured clinical interview and AAI by questionnaire.

FINDINGS

The risk indicator model in which the association between AAI and AUD was explained by common vulnerability was the best fitted to the data. The heritability was 37% [95% confidence interval (CI) = 21%, 53%] for AAI and 62% (95% CI = 51%, 73%) for AUD. Genetic risk for AAI accounted for 44% (95% CI = 17%, 71%) of the total genetic risk for AUD and the correlation between genetic factors for AAI and AUD was -0.66 (95%CI -0.87, -0.46). Individual-specific environmental risk for AAI explained only 1% (95% CI = 0%, 3%) of the risk for AUD. Shared environmental factors did not influence AUD, but accounted for 25% (95% CI = 7%, 35%) of the variance in AAI.

CONCLUSIONS

The association between early age of alcohol initiation and alcohol use disorders in later life does not reflect a causal relationship, but is due almost entirely to common genetic risk factors.

摘要

背景与目的

饮酒起始年龄(AAI)较早与成年期酒精使用障碍(AUD)相关,并且被假设为成年期酒精使用障碍的一个病因。然而,双生子研究结果表明,AAI是AUD风险的一个指标。我们旨在检验关于早期AAI与AUD之间关系的因果假设和风险指标假设。

设计

一项基于人群的双生子研究,采用生物统计学双生子模型。

地点

挪威。

参与者

一个基于人群的1336名挪威双生子样本。

测量

通过结构化临床访谈评估终生DSM-IV酒精使用障碍,通过问卷评估AAI。

结果

由共同易感性解释AAI与AUD之间关联的风险指标模型最符合数据。AAI的遗传度为37%[95%置信区间(CI)=21%,53%],AUD的遗传度为62%(95%CI =51%,73%)。AAI的遗传风险占AUD总遗传风险的44%(95%CI =17%,71%),AAI与AUD遗传因素之间的相关性为-0.66(95%CI -0.87,-0.46)。AAI的个体特异性环境风险仅解释了AUD风险的1%(95%CI =0%,3%)。共享环境因素不影响AUD,但占AAI方差的25%(95%CI =7%,35%)。

结论

早期饮酒起始年龄与晚年酒精使用障碍之间的关联并不反映因果关系,而几乎完全是由于共同的遗传风险因素。

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