Alcohol (Hanover, York County, Pa.)最新文献

Following the Fukushima Daiichi nuclear power plant disaster in 2011, a large longitudinal study was conducted to examine the interplay between disaster exposure and problem alcohol use among a unique cohort of workers from the Daiichi and Daini plants. The study (Tajima et al., 2024), which followed participants over a three-year period following the disaster, provides insights into long-term impacts of disaster-related experiences and stressors on individuals' drinking behaviors. Tajima et al. (2024) found that there was an increase in the prevalence of problem drinking in the first 3 years after the disaster. Furthermore, disaster exposure and related experiences were associated with the pattern and longitudinal course of problem drinking, with some differences across different disaster-related experiences. Overall, these findings parallel previous literature that disaster-related experiences are associated with heightened risk for alcohol and substance use and related problems and mental health challenges (Fergusson et al., 2014; Flory et al., 2009; North et al., 2011; North & Pfefferbaum, 2013).

One of the most important contributions of Tajima et al. (2024) is its examination of disaster-related experiences and problem drinking through the analysis of longitudinal data. With few exceptions (e.g., Pietrzak et al., 2012), much of what is known about disaster and behavioral and psychiatric health outcomes relies on postdisaster cross-sectional data, often limited to single-timepoint assessment. By using a longitudinal approach, Tajima et al. (2024) report a temporally sustained increase in problem drinking as assessed by the CAGE questionnaire (Bush et al., 1987) over the years of follow-up. This study represents an important step in understanding the dynamic processes underlying the effects of disaster experiences on individuals' problem drinking behaviors over time. Despite the study's strengths of using a longitudinal design, one notable limitation is the lack of data on participants' predisaster alcohol use and disorder status. This absence precluded the identification of, for example, onset of problem drinking or postdisaster relapse. Furthermore, this limitation is especially critical in view of the evidence that only a small number of individuals develop a new alcohol use disorder postdisaster (North et al., 2011). Thus, this emphasizes the necessity of conducting studies with longer intervals. More generally, while disasters offer a unique, natural opportunity to study how individuals respond to stressors, analyses relying only on postdisaster data are not meant to be interpreted causally.

One approach to strengthen inferences in observational epidemiological data is to integrate comprehensive pre- and postdisaster information. This allows for delineation of temporal trajector

The neurodegenerative effects alcohol use disorder (AUD) have been well characterized and are likely due to the long-term effects of alcohol on the brain. The molecular events that underlie regional neuronal loss are a focus of current research. Chronic inflammation in the central nervous system, termed neuroinflammation, contributes to the progressive loss of neurons in the brain. Using data from genome-wide association studies and genetic and gene expression data, α-synuclein was identified as a gene of interest for AUD almost 10 years ago. Despite this and the well-recognized role of α-synuclein in mediating neuroinflammation in other neurodegenerative diseases, its role in alcohol-induced brain damage and AUD is yet to be elucidated. This systematic literature review quantifies and analyzes relationships between AUD, α-synuclein, and neuroinflammation. The review identified fewer studies focused on the role in AUD of α-synuclein (30) than on neuroinflammation (177), with published studies heavily centered on the myeloid differentiation primary response 88 (MyD88)-dependent toll-like receptor 4 (TLR4) pathway. The systematic review revealed that no original literature investigates the roles of α-synuclein and neuroinflammation in AUD and that there are significantly fewer published articles on the role of α-synuclein in AUD than in other neuroinflammatory conditions. Studies of the role of neuroinflammation in AUD are largely centered on the TLR4 signaling cascade, followed by TLR2 and TLR3, and soluble cytokines such as IL-10, IL-1β, and TNF-α. Key research themes identified in other neurodegenerative disorders provide new insights for further investigation in AUD.

Evidence suggests that a relationship exists between the gut microbiome and the pathogenesis of alcohol use disorder (AUD) and alcohol-associated liver disease (AALD). This systematic review identified studies that investigated the gut microbiome in individuals with an AUD or an AALD. A search was conducted on October 27, 2022, in PubMed, Web of Science, and Embase databases. Fifty studies satisfied eligibility criteria. Most studies found evidence for gut dysbiosis in individuals with AUD and AALD. Microbiome intervention studies have mostly been conducted in AALD patients; fecal microbial transplant interventions show the most promise. Because most studies were conducted cross-sectionally, the causal relationship between the gut microbiome and alcohol use is unknown. Furthermore, almost all studies have been conducted in predominantly male populations, leaving critical questions regarding sex differences and generalizability of the findings. The study summaries and recommendations provided in this review seek to identify areas for further research and to highlight potential gut microbial interventions for treating AUD and AALD.