Studies Investigating Aggressive Behavior and Alcoholism

酒精中毒经常与攻击性行为、吸烟和饮食变化/缺乏联系在一起。为了探索这些常见共病的各个方面，我们启动了几项临床研究，旨在探索它们与酒精中毒的病理生理学的关系。研究表明，饮酒和暴力行为之间存在很强的关联，然而，酒精引发攻击行为的实际机制(S)却知之甚少。在过去的一年里，我们开发了一项研究计划，在家庭暴力事件频繁发生的特定患者群体中探索暴力和酗酒之间的联系。我们希望确定5-羟色胺再摄取抑制剂的治疗是否能显著改善用于量化这一精选患者群体的攻击性的标准化测量方法。我们研究的另一个方面与最近戒酒的人戒烟有关。据估计，60%-70%的被诊断为酗酒的人也依赖烟草产品。尼古丁依赖和酒精中毒之间的这种明显的联系得到了研究的加强，研究表明酒精摄入量和吸烟增加之间存在正相关，但吸烟在酒精中毒的病理生理学中扮演什么角色尚不清楚。为了探索这种相互作用，我们正在分析先前收集的吸烟者和非吸烟者入院后不久以及戒酒/戒烟过程中的脑脊液代谢物数据。预计这些结果将为酗酒者吸烟和抵制戒烟提供深入的见解。清醒的酗酒者经常报告说，他们暴饮暴食是为了减少饮酒的欲望。这种对甜食的夸大欲望促成了一种假设，即酒精消费受到与碳水化合物摄入量调节相同的机制的调节。为了探索这一假设，我们研究了长期戒酒的人中，葡萄糖代谢对下丘脑功能和碳水化合物摄入量的影响。在这一年中，我们已经证明(酒精临床经验25：781-786,2001)，以前报道的三周清醒酒精患者的下丘脑功能障碍在长期康复的酒精患者中不存在。另外两项研究的结果目前正在准备发表。一篇文章比较了酗酒者和对照组脑脊液单胺类物质与血糖的关系。第二项研究考察了酗酒者在休息和代谢压力后的碳水化合物摄入量。酗酒者经常出现营养摄入障碍，这可能会导致情绪(即抑郁和敌意)和认知的变化。与这两种临床状态相关的一种可能的营养物质是二十二碳六烯酸(DHA)。由于长期饮酒会消耗大脑中的DHA，我们设计了一项研究，使我们能够量化和成像最近戒酒的人和健康对照组的大脑对DHA的摄取。这项研究很重要，因为目前还没有一种方法可以让我们评估DHA在人脑中的代谢。

Alcoholism is frequently associated with aggressive behaviors, smoking and dietary changes/deficiencies. To explore facets of each of these common co-morbidities, we have initiated several clinical research studies designed to explore their association with the pathophysiology of alcoholism. It has been shown that there is a strong association between alcohol consumption and violent behavior, however, the actual mechanism(s) by which alcohol induces aggressive behavior is poorly understood. During the past year, we developed a research initiative to explore the association between violence and alcoholism in a select patient population characterized by frequent episodes of domestic violence. We hope to determine if treatment with a serotonin reuptake inhibitor can produce a significant improvement on standardized measures used to quantify aggression in this select patient population. Another aspect of our research is related to smoking cessation in recently detoxified alcoholics. It is estimated that 60-70% of individuals with the diagnosis of alcoholism are also dependent on tobacco products. This apparent link between nicotine dependence and alcoholism is reinforced by studies showing a positive correlation between alcohol ingestion and increased smoking, yet it is unclear what role smoking plays in the pathophysiology of alcoholism. To explore this interaction, we are analyzing previously collected CSF metabolite data obtained from smoking and non-smoking alcoholics shortly after their admission to the hospital and during the course of their alcohol/smoking withdrawal. It is anticipated that these results will provide insights into why alcoholics smoke and resist smoking cessation. Sober alcoholics frequently report that they binge on sweets to decrease their desire to drink alcohol. This exaggerated desire for sweets has contributed to the postulate that alcohol consumption is regulated by the same mechanisms that regulate the intake of carbohydrates. To explore this postulate we examined the effects of glucoprivation on hypothalamic function and carbohydrate consumption in long-term sober alcoholics. During this year we have shown (Alcohol Clin Exp Res 25:781-786, 2001) that the disturbances in hypothamic function previously reported in three-week sober alcoholics are not present in long-term recovering alcoholics. Findings of two additional studies are currently being prepared for publication. One paper compares the relationship between CSF monoamines and plasma glucose in alcoholics and controls. The second examines carbohydrate consumption in alcoholics at rest and following metabolic stress. Alcoholics frequently have disturbances in nutritional intake that may contribute to changes in mood (i.e., depression and hostility) as well as cognition. One possible nutrient that has been implicated in both of these clinical states is docosahexaenoic acid (DHA). Since chronic alcohol intake depletes DHA from the brain, we designed a study that would allow us to quantify and image the uptake of DHA in the brains of recently detoxified alcoholics and healthy controls. This study is important because there is no methodology currently available that will allow us to assess DHA metabolism in the human brain.