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首页> 外文期刊>Alcohol >Workshop on alcohol use and health disparities 2002: a call to arms.
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Workshop on alcohol use and health disparities 2002: a call to arms.

机译：2002年饮酒与健康差异讲习班：呼吁武装。

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The National Institute on Alcohol Abuse and Alcoholism (NIAAA) of the National Institutes of Health (NIH) sponsored a "Workshop on Alcohol Use and Health Disparities 2002: A Call to Arms," on December 5, 2002, in Bethesda, Maryland, USA. This workshop was part of the NIAAA/NIH comprehensive strategic plan to reduce, and ultimately eliminate, health disparities. Eleven topics were addressed: (1) biomedical risk factors that may contribute to disparities in the toxic effects of alcohol; (2) alcohol and gene-environment interactions that affect the health of diverse groups; (3) alcohol pharmacogenetics in Mexican-Americans; (4) determinants of risk for alcoholism in minority populations; (5) consideration of population groups in linkage-disequilibrium studies to identify genes associated with alcohol dependence; (6) interaction between alcohol dependence and African-American ethnicity in disordered sleep, nocturnal cytokines, and immunity; (7) disparities of brain functional reserve capacity affecting brain morbidity related to substance abuse; (8) alcohol and pregnancy disparities; (9) role of alcohol in cancer risk disparities; (10) ethnic diversity in alcoholic cardiomyopathy; and (11) postmenopausal health disparities. On the basis of these presentations, seven conclusions emerged: (1) Genetic variations in alcohol-metabolizing enzymes exist in various populations. (2) These enzymes play a role in the variation in health effect outcomes seen in different populations, owing to alcohol consumption. (3) Differences between and among population groups can be critically important for the design and interpretation of studies in genetics. These include differences in expression of phenotype, in locus heterogeneity, in risk alleles, and in population structure. (4) Incidence rates for fetal alcohol syndrome and fetal alcohol spectrum disorders are greater in African-Americans and Native-Americans than in Caucasians. Genetic polymorphisms, nutrition, and other factors may account for these differences. (5) The highest mortality rate for cirrhosis has been found in white Hispanic men. (6) Mexican-Americans have a low frequency of the protective alleles ADH1B(*)2 and ALDH2(*)2 and a relatively high frequency of CYP2E1 c2, which is associated with early onset alcoholism. (7) The incidence rate for cancer is greater for African-Americans than for Caucasians, and part of the higher risk may be attributed to heavier drinking.
机译：美国国立卫生研究院（NIH）的国家酒精滥用和酒精中毒研究所（NIAAA）于2002年12月5日在美国马里兰州贝塞斯达市发起了“ 2002年酒精使用与健康差异研讨会：呼吁武装”。 。该研讨会是NIAAA / NIH减少并最终消除健康差异的全面战略计划的一部分。讨论了以下11个主题：（1）可能导致酒精毒性作用差异的生物医学危险因素; （2）影响不同群体健康的酒精和基因-环境相互作用; （3）墨西哥裔美国人的酒精药物遗传学; （4）少数群体中酗酒风险的决定因素; （5）在连锁不平衡研究中考虑人群，以鉴定与酒精依赖相关的基因; （6）酒精依赖与非裔美国人在睡眠紊乱，夜间细胞因子和免疫力之间的相互作用; （7）影响与药物滥用有关的脑病的脑功能储备能力的差异; （8）饮酒与怀孕差距; （9）酒精在癌症风险差异中的作用; （10）酒精性心肌病的种族多样性; （11）绝经后的健康差异。根据这些表述，得出了七个结论：（1）酒精代谢酶的遗传变异存在于各种人群中。 （2）由于饮酒，这些酶在不同人群对健康影响的结果变化中起作用。 （3）人口群体之间的差异对于遗传学研究的设计和解释至关重要。这些包括表型表达，基因座异质性，风险等位基因和种群结构的差异。 （4）非裔美国人和美洲原住民的胎儿酒精综合症和胎儿酒精谱系疾病的发生率高于白种人。遗传多态性，营养和其他因素可能解释了这些差异。 （5）白人西班牙裔男性的肝硬化死亡率最高。 （6）墨西哥裔美国人的保护性等位基因ADH1B（*）2和ALDH2（*）2的频率较低，而CYP2E1 c2的频率较高，这与早期发作的酒精中毒有关。 （7）非裔美国人的癌症发病率比高加索人高，部分较高的风险可能归因于饮酒量增加。

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