Alcohol Research : Current Reviews最新文献

Binge drinking is a pattern of alcohol drinking that raises a person's blood alcohol concentration to at least .08%, which amounts to consuming five alcoholic drinks for men and four alcoholic drinks for women in about 2 hours. It is the most common form of alcohol misuse in adolescents and young adults. Heavy drinking includes the same criterion as binge drinking, but with higher frequency (i.e., 5 or more days in the past 30 days). Although binge drinking or heavy drinking alone is insufficient to meet the criteria for an alcohol use disorder (AUD) diagnosis, there are neurobiological changes, as well as an increased risk of developing an AUD later in life, associated with this form of alcohol misuse. This review describes the recent neuroimaging findings in binge drinking and heavy-drinking adolescents and young adults, a developmental period during which significant neuromaturation occurs.

Studies have focused on the effects of chronic alcohol consumption and the mechanisms of tissue injury underlying alcoholic hepatitis and cirrhosis, with less focus on the pathophysiological consequences of binge alcohol consumption. Alcohol binge drinking prevalence continues to rise, particularly among individuals ages 18 to 24. However, it is also frequent in individuals ages 65 and older. High blood alcohol levels achieved with this pattern of alcohol consumption are of particular concern, as alcohol can permeate to virtually all tissues in the body, resulting in significant alterations in organ function, which leads to multisystemic pathophysiological consequences. In addition to the pattern, amount, and frequency of alcohol consumption, additional factors, including the type of alcoholic beverage, may contribute differentially to the risk for alcohol-induced tissue injury. Preclinical and translational research strategies are needed to enhance our understanding of the effects of binge alcohol drinking, particularly for individuals with a history of chronic alcohol consumption. Identification of underlying pathophysiological processes responsible for tissue and organ injury can lead to development of preventive or therapeutic interventions to reduce the health care burden associated with binge alcohol drinking.

During the critical developmental periods of childhood when neural plasticity is high, exposure to early life stress (ELS) or trauma may lead to enduring changes in physiological stress systems and enhanced vulnerability for psychopathological conditions such as post-traumatic stress disorder (PTSD) and alcohol use disorder (AUD) in adulthood. Clinical and preclinical studies have sought to understand the possible mechanisms linking ELS, PTSD, and AUD. Preclinical studies have employed animal models of stress to recapitulate PTSD-like behavioral deficits and alcohol dependence, providing a basic framework for identifying common physiological mechanisms that may underlie these disorders. Clinical studies have documented ELS-related endocrine dysregulation and genetic variations associated with PTSD and AUD, as well as disruption in crucial neural circuitry throughout the corticomesolimbic region. Despite limitations and challenges, both types of studies have implicated three interrelated mechanisms: hypothalamic pituitary adrenal (HPA) axis and glucocorticoid signaling dysregulation, genetics, and epigenetics. ELS exposure leads to disruption of HPA axis function and glucocorticoid signaling, both of which affect homeostatic cortisol levels. However, individual response to ELS depends on genetic variations at specific genes that moderate HPA axis and brain function, thus influencing susceptibility or resilience to psychopathologies. Epigenetic-influenced pathways also are emerging as a powerful force in helping to create the PTSD and AUD phenotypes. Dysregulation of the HPA axis has an epigenetic effect on genes that regulate the HPA axis itself, as well as on brain-specific processes such as neurodevelopment and neurotransmitter regulation. These studies are only beginning to elucidate the underpinnings of ELS, PTSD, and AUD. Larger human cohorts, identification of additional genetic determinants, and better animal models capable of recapitulating the symptoms of PTSD and AUD are needed.

Alcohol use and traumatic brain injury (TBI) are inextricably and bidirectionally linked. Alcohol intoxication is one of the strongest predictors of TBI, and a substantial proportion of TBIs occur in intoxicated individuals. An inverse relationship is also emerging, such that TBI can serve as a risk factor for, or modulate the course of, alcohol use disorder (AUD). Critically, alcohol use after TBI is a key predictor of rehabilitation outcomes, prognosis, and additional head injuries. This review provides a general overview of the bidirectional relationship between TBI and AUD and a discussion of potential neuropsychological and neurobiological mechanisms that might underlie the relationship.

Co-occurring post-traumatic stress disorder (PTSD) and alcohol use disorder (AUD) are costly and consequential public health problems that negatively affect the health and well-being of U.S. military service members and veterans. The disproportionate burden of comorbid PTSD and AUD among U.S. military service members and veterans may be due to unique factors associated with military service, such as aspects of military culture, deployment, and trauma exposure. This review addresses the prevalence of co-occurring PTSD and AUD in military and veteran populations, population-specific factors that contribute to development of the comorbid conditions, and evidence-based treatments that have promise for addressing these conditions in military and veteran populations. Future directions for research and practice relevant to military and veteran populations are discussed.

The College Alcohol Intervention Matrix (CollegeAIM) is a user-friendly, interactive decision tool based on a synthesis of the substantial and growing literature on campus alcohol use prevention. It includes strategies targeted at both the individual and environmental levels. Commissioned by the National Institute on Alcohol Abuse and Alcoholism (NIAAA), CollegeAIM reflects the collective knowledge of 16 separate experts in the field, which makes it unique relative to other summaries of the science. CollegeAIM is designed to help college stakeholders compare and contrast different evidence-based prevention strategies to select a mix of individual and environmental strategies that will work best on and around their campuses. CollegeAIM is a living document, which will be updated to keep pace with the science. Colleges are therefore encouraged to ensure that evaluations of individual- or environmental-focused strategies on their campuses or in their communities make it into the published literature.

Rates of alcohol consumption continue to be a concern, particularly for individuals who are college age. Drinking patterns have changed over time, with the frequency of binge drinking (consuming four/five or more drinks for women/men) remaining high (30% to 40%). Young adults in the college age range are developmentally and socially at higher risk for drinking at binge levels. Changes in autonomy, parental control, norms, and attitudes affect binge drinking behaviors. This article reviews those changes, as well as the individual and environmental factors that increase or decrease the risk of participating in binge drinking behaviors. Risk factors include risky drinking events (e.g., 21st birthdays), other substance use, and drinking to cope, while protective factors include religious beliefs, low normative perceptions of drinking, and use of protective behavioral strategies. Additionally, this article discusses the physical, social, emotional, and cognitive consequences of consuming alcohol at binge levels. Alcohol policies and prevention and intervention techniques need to incorporate these factors to reduce experiences of alcohol-related problems. Targeting policy changes and prevention and intervention efforts toward young adults may increase effectiveness and prevent both short- and long-term consequences of binge drinking.

Alcohol use disorder (AUD) and post-traumatic stress disorder (PTSD) are highly comorbid, and treatment outcomes are worse in individuals with both disorders. Several neurobiological systems have been implicated in the development and maintenance of AUD and PTSD, and pharmacologic interventions targeting these systems for singular diagnoses of AUD or PTSD have proven effective. However, there are no established treatments for co-occurring AUD and PTSD, and relatively few studies have examined potential pharmacotherapy for treating symptoms of both AUD and PTSD in comorbid populations. This review provides a brief overview of the studies to date on pharmacotherapeutic treatment interventions for comorbid AUD and PTSD and highlights future directions for promising targets that have potential in the treatment of individuals with this dual diagnosis. Clinical implications of these findings are also discussed. While current medications targeting the opioidergic, noradrenergic, serotonergic, and GABAergic/glutamatergic brain systems are only modestly efficacious in improving symptoms in individuals with comorbid AUD and PTSD, novel targets within these neurobiological systems may be clinically useful for treating alcohol use outcomes and PTSD symptom severity. More work is needed to optimize pharmacologic treatment strategies that target both alcohol-motivated behavior and PTSD-related symptoms in individuals with co-occurring AUD and PTSD.

Post-traumatic stress disorder (PTSD) and alcohol use disorder (AUD) are common comorbid conditions that affect large segments of the population. Individuals with comorbid PTSD/AUD face greater clinical and functional stressors than those with diagnoses of either PTSD or AUD alone. The purpose of this article is to review the phenomenology and functional associations of PTSD/AUD and address the common social, occupational, and psychological concerns associated with both disorders. Given the increased problems associated with comorbid PTSD/AUD, clinical and research efforts should focus on targeting functional and psychosocial problems in conjunction with psychiatric symptoms.