Alcohol Research : Current Reviews最新文献

Post-traumatic stress disorder (PTSD) and alcohol use disorder (AUD) are highly comorbid. Although recent clinical studies provide some understanding of biological and subsequent behavioral changes that define each of these disorders, the neurobiological basis of interactions between PTSD and AUD has not been well-understood. In this review, we summarize the relevant animal models that parallel the human conditions, as well as the clinical findings in these disorders, to delineate key gaps in our knowledge and to provide potential clinical strategies for alleviating the comorbid conditions.

This article reviews literature aiming to explain the widespread reductions in binge and problem drinking that begin around the transition to young adulthood (i.e., "maturing out"). Whereas most existing literature on maturing out emphasizes contextual effects of transitions into adult roles and responsibilities, this article also reviews recent work demonstrating further effects of young adult personality maturation. As possible mechanisms of naturally occurring desistance, these processes could inform both public health and clinical interventions aimed at spurring similar types of drinking-related behavior change. This article also draws attention to evidence that the normative trend of age-related reductions in problem drinking extends well beyond young adulthood. Specific factors that may be particularly relevant to problem drinking desistance in these later periods are considered within a broader life span developmental framework.

Binge drinking thresholds have long been set at four or more drinks for women and five or more drinks for men over the course of a few hours. However, a significant number of people regularly consume much higher amounts of alcohol: double or even triple the standard binge drinking threshold. Researchers have begun to distinguish between typical binge drinking and this kind of "high-intensity drinking," which is common among certain types of binge drinkers and is often associated with special occasions, including holidays, sporting events, and, notably, 21st birthdays. To understand the social and physical influences of alcohol consumption, it is important for researchers to set standard definitions for high-intensity drinking and distinguish it from other types of alcohol use.

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.