Studies Investigating Aggressive Behavior and Alcoholism

酗酒通常与攻击性行为、吸烟和饮食改变/不足有关。为了探索这些常见合并症的各个方面，我们开展了几项临床研究，旨在探索它们与酒精中毒病理生理的关系。研究表明，饮酒与暴力行为之间存在着密切的联系，然而，人们对酒精诱发攻击行为的实际机制知之甚少。在过去的一年中，我们开展了一项研究倡议，以探索暴力与酗酒之间的关系，选择了一些以频繁发生家庭暴力为特征的患者群体。我们希望确定5 -羟色胺再摄取抑制剂治疗是否能显著改善用于量化这一特定患者群体攻击性的标准化措施。我们研究的另一个方面与最近解毒的酗酒者的戒烟有关。据估计，60-70%被诊断为酒精中毒的人也依赖烟草制品。这种尼古丁依赖和酒精中毒之间的明显联系被酒精摄入和吸烟增加之间的正相关研究所证实，然而吸烟在酒精中毒的病理生理中所起的作用尚不清楚。为了探索这种相互作用，我们分析了先前收集的脑脊液代谢物数据，这些数据来自吸烟和不吸烟的酗酒者在入院后不久以及戒酒/戒烟过程中。预计这些结果将为酗酒者吸烟和拒绝戒烟的原因提供见解。清醒的酗酒者经常报告说，他们狂吃甜食是为了减少喝酒的欲望。这种对甜食的过度渴望促成了一种假设，即酒精的消耗受到与调节碳水化合物摄入相同的机制的调节。为了探索这一假设，我们研究了长期清醒的酗酒者葡萄糖剥夺对下丘脑功能和碳水化合物消耗的影响。在这一年中，我们已经表明（酒精临床实验，2001年，25:781-786），以前在三周清醒的酗酒者中报道的下丘脑功能紊乱在长期恢复的酗酒者中并不存在。目前正在编写另外两项研究的结果以供出版。一篇论文比较了酗酒者和对照组脑脊液单胺与血浆葡萄糖的关系。第二项研究调查了酒精中毒患者在休息和代谢应激后的碳水化合物消耗情况。酗酒者经常在营养摄入方面有障碍，这可能会导致情绪（即抑郁和敌意）和认知方面的变化。一种可能与这两种临床状态有关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解毒的酗酒者和健康对照者大脑中DHA的摄取。这项研究很重要，因为目前还没有方法可以让我们评估人脑中的DHA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.