Alcohol-related content (ARC) is pervasive across social media. Existing research suggests that posting of and exposure to such content may affect young adults' drinking and alcohol-related problems. However, a scoping review has yet to examine the literature within this field of research. This scoping review delineates and describes the existing peer-reviewed quantitative research examining the associations between ARC posting and exposure and drinking and alcohol-related problems among young adults ages 18 to 30. Specifically, the authors sought to investigate (1) methodological trends in how exposure to and posting of ARC is assessed; (2) potential moderators of the association between exposure to and posting of ARC and drinking outcomes; (3) how exposure to and posting of ARC is associated with alcohol consumption and alcohol-related problems; and (4) potential gaps in the literature. This review includes original, empirical, quantitative studies, published in English from 2006 to 2023, that measured alcohol consumption and/or alcohol-related problems and the use of ARC on social media in 18- to 30-year-olds. The authors systematically searched the PubMed, Cumulative Index to Nursing and Allied Health Literature (CINAHL), PsycInfo, and Scopus databases on May 30, 2023, and reran the searches on November 1, 2023. The authors designed a form to extract data and statistics related to alcohol drinking and ARC measures. Pairs of authors extracted the data for each study independently, and then a third author reviewed their work to resolve differences. In total, 3,112 papers were selected via preliminary search terms. After removing duplicates and other articles deemed ineligible based on screening articles at the title and abstract level as well as assessing full-text articles for eligibility (n = 3,079), the final review included 33 studies. Overall, the results of the scoping review revealed a lack of consistent definitions and standardized assessments related to ARC. Despite these factors, the authors uncovered robust positive relationships between posting ARCand drinking and alcohol-related problems. The literature also mostly found positive, significant linkages between exposure to ARC and drinking and alcohol-related problems. This scoping review highlights the need for consistentoperationalization and empirically validated measures related to ARC. In addition, the authors propose a theoretical model that may serve as a road map for future interventions targeting young adults.

By 2040, 21.6% of Americans will be over age 65, and the population of those older than age 85 is estimated to reach 14.4 million. Although not causative, older age is a risk factor for dementia: every 5 years beyond age 65, the risk doubles; approximately one-third of those older than age 85 are diagnosed with dementia. As current alcohol consumption among older adults is significantly higher compared to previous generations, a pressing question is whether drinking alcohol increases the risk for Alzheimer's disease or other forms of dementia. Databases explored included PubMed, Web of Science, and ScienceDirect. To accomplish this narrative review on the effects of alcohol consumption on dementia risk, the literature covered included clinical diagnoses, epidemiology, neuropsychology, postmortem pathology, neuroimaging and other biomarkers, and translational studies. Searches conducted between January 12 and August 1, 2023, included the following terms and combinations: "aging," "alcoholism," "alcohol use disorder (AUD)," "brain," "CNS," "dementia," "Wernicke," "Korsakoff," "Alzheimer," "vascular," "frontotemporal," "Lewy body," "clinical," "diagnosis," "epidemiology," "pathology," "autopsy," "postmortem," "histology," "cognitive," "motor," "neuropsychological," "magnetic resonance," "imaging," "PET," "ligand," "degeneration," "atrophy," "translational," "rodent," "rat," "mouse," "model," "amyloid," "neurofibrillary tangles," "α-synuclein," or "presenilin." When relevant, "species" (i.e., "humans" or "other animals") was selected as an additional filter. Review articles were avoided when possible. The two terms "alcoholism" and "aging" retrieved about 1,350 papers; adding phrases-for example, "postmortem" or "magnetic resonance"-limited the number to fewer than 100 papers. Using the traditional term, "alcoholism" with "dementia" resulted in 876 citations, but using the currently accepted term "alcohol use disorder (AUD)" with "dementia" produced only 87 papers. Similarly, whereas the terms "Alzheimer's" and "alcoholism" yielded 318 results, "Alzheimer's" and "alcohol use disorder (AUD)" returned only 40 citations. As pertinent postmortem pathology papers were published in the 1950s and recent animal models of Alzheimer's disease were created in the early 2000s, articles referenced span the years 1957 to 2024. In total, more than 5,000 articles were considered; about 400 are herein referenced. Chronic alcohol misuse accelerates brain aging and contributes to cognitive impairments, including those in the mnemonic domain. The consensus among studies from multiple disciplines, however, is that alcohol misuse can increase the risk for dementia, but not necessarily Alzheimer's disease. Key issues to consider include the reversibility of brain damage following abstinence from chronic alcohol misuse compared to the degenerative and progressive course of Alzheimer's disease, and the characteristic presence of protein inclusions in the brains of people with Alzheimer's disease, which are absent in the brains of those with AUD.

This article is part of a Festschrift commemorating the 50th anniversary of the National Institute on Alcohol Abuse and Alcoholism (NIAAA). Established in 1970, first as part of the National Institute of Mental Health and later as an independent institute of the National Institutes of Health, NIAAA today is the world’s largest funding agency for alcohol research. In addition to its own intramural research program, NIAAA supports the entire spectrum of innovative basic, translational, and clinical research to advance the diagnosis, prevention, and treatment of alcohol use disorder and alcohol-related problems. To celebrate the anniversary, NIAAA hosted a 2-day symposium, “Alcohol Across the Lifespan: 50 Years of Evidence-Based Diagnosis, Prevention, and Treatment Research,” devoted to key topics within the field of alcohol research. This article is based on Dr. Mason’s presentation at the event. NIAAA Director George F. Koob, Ph.D., serves as editor of the Festschrift.

PURPOSEThe purpose of this review is to discuss the literature regarding the concurrent use (co-use) of alcohol and cannabis and competing hypotheses as to whether cannabis acts as a substitute for (i.e., replacing the effects of alcohol, resulting in decreased use) or a complement to (i.e., used to enhance the effects of alcohol, resulting in increased use) alcohol. The impact of cannabis use on alcohol-related outcomes has received increased attention in the wake of ongoing legalization of cannabis for both medical and recreational purposes. Evidence for both hypotheses exists in the literature across a broad range of data collection methods and samples and is carefully reviewed here. In addition, various mechanisms by which cannabis may act as an alcohol substitute or complement are explored in depth with the goal of better understanding equivocal findings.SEARCH METHODSThis review includes articles that were identified from a search for studies on alcohol and cannabis co-use, with a specific focus on studies exploring complementary versus substitution aspects of co-use. Search terms were included in Google Scholar, PsycINFO, MEDLINE, and Web of Science. Eligible studies were those that measured alcohol and cannabis co-use in human samples in laboratory, survey, or ecological momentary assessment studies, or that directly referenced substitution or complementary patterns of use.SEARCH RESULTSSearch results returned 650 articles, with 95 meeting inclusion criteria.DISCUSSION AND CONCLUSIONSResults of this review reveal compelling evidence for both substitution and complementary effects, suggesting nuanced yet significant distinctions across different populations examined in these studies. Several mechanisms for the impact of cannabis use on alcohol-related outcomes are identified, including patterns and context of co-use, timing and order of use, cannabinoid formulation, pharmacokinetic interactions, and user characteristics (including diagnostic status), all of which may influence substitution versus complementary effects. This review will inform future research studies examining this topic in both clinical and community samples and aid in the development of treatment and prevention efforts targeting those populations most vulnerable to negative consequences of co-use. Finally, this review highlights the need for additional research in more diverse samples and the use of mixed-methods designs to examine both pharmacological and contextual influences on co-use.

PURPOSEA growing body of evidence has implicated the endocannabinoid (eCB) system in the acute, chronic, and withdrawal effects of alcohol/ethanol on synaptic function. These eCB-mediated synaptic effects may contribute to the development of alcohol use disorder (AUD). Alcohol exposure causes neurobiological alterations similar to those elicited by chronic cannabinoid (CB) exposure. Like alcohol, cannabinoids alter many central processes, such as cognition, locomotion, synaptic transmission, and neurotransmitter release. There is a strong need to elucidate the effects of ethanol on the eCB system in different brain regions to understand the role of eCB signaling in AUD.SEARCH METHODSFor the scope of this review, preclinical studies were identified through queries of the PubMed database.SEARCH RESULTSThis search yielded 459 articles. Clinical studies and papers irrelevant to the topic of this review were excluded.DISCUSSION AND CONCLUSIONSThe endocannabinoid system includes, but is not limited to, cannabinoid receptors 1 (CB1), among the most abundantly expressed neuronal receptors in the brain; cannabinoid receptors 2 (CB2); and endogenously formed CB1 ligands, including arachidonoylethanolamide (AEA; anandamide), and 2-arachidonoylglycerol (2-AG). The development of specific CB1 agonists, such as WIN 55,212-2 (WIN), and antagonists, such as SR 141716A (rimonabant), provide powerful pharmacological tools for eCB research. Alcohol exposure has brain region–specific effects on the eCB system, including altering the synthesis of endocannabinoids (e.g., AEA, 2-AG), the synthesis of their precursors, and the density and coupling efficacy of CB1. These alcohol-induced alterations of the eCB system have subsequent effects on synaptic function including neuronal excitability and postsynaptic conductance. This review will provide a comprehensive evaluation of the current literature on the synaptic interactions of alcohol exposure and eCB signaling systems, with an emphasis on molecular and physiological synaptic effects of alcohol on the eCB system. A limited volume of studies has focused on the underlying interactions of alcohol and the eCB system at the synaptic level in the brain. Thus, the data on synaptic interactions are sparse, and future research addressing these interactions is much needed.

Opioids and alcohol are widely used to relieve pain, with their analgesic efficacy stemming from rapid actions on both spinal and supraspinal nociceptive centers. As an extension of these relationships, both substances can be misused in attempts to manage negative affective symptoms stemming from chronic pain. Moreover, excessive use of opioids or alcohol facilitates the development of substance use disorder (SUD) as well as hyperalgesia, or enhanced pain sensitivity. Shared neurobiological mechanisms that promote hyperalgesia development in the context of SUD represent viable candidates for therapeutic intervention, with the ideal strategy capable of reducing both excessive substance use as well as pain symptoms simultaneously. Neurocognitive symptoms associated with SUD, ranging from poor risk management to the affective dimension of pain, are likely mediated by altered activities of key anatomical elements that modulate executive and interoceptive functions, including contributions from key frontocortical regions. To aid future discoveries, novel and translationally valid animal models of chronic pain and SUD remain under intense development and continued refinement. With these tools, future research strategies targeting severe SUD should focus on the common neurobiology between negative reinforcement and affective elements of pain, possibly by reducing excessive stress hormone and neurotransmitter activity within shared circuitry.

PURPOSEThe endocannabinoid system has emerged as a key regulatory signaling pathway in the pathophysiology of alcohol-associated liver disease (ALD). More than 30 years of research have established different roles of endocannabinoids and their receptors in various aspects of liver diseases, such as steatosis, inflammation, and fibrosis. However, pharmacological applications of the endocannabinoid system for the treatment of ALD have not been successful because of psychoactive side effects, despite some beneficial effects. Thus, a more delicate and detailed elucidation of the mechanism linking the endocannabinoid system and ALD may be of paramount significance in efforts to apply the system to the treatment of ALD.SEARCH METHODSThree electronic databases (PubMed, MEDLINE, and Cochrane Library) were used for literature search from November 1988 to April 2021. Major keywords used for literature searches were “cannabinoid,” “cannabinoid receptor,” “ALD,” “steatosis,” and “fibrosis.”SEARCH RESULTSAccording to the inclusion and exclusion criteria, the authors selected 47 eligible full-text articles out of 2,691 searched initially. Studies in the past 3 decades revealed the opposite effects of cannabinoid receptors CB1R and CB2R on steatosis, inflammation, and fibrosis in ALD.DISCUSSION AND CONCLUSIONSThis review summarizes the endocannabinoid signaling in the general physiology of the liver, the pathogenesis of ALD, and some of the potential therapeutic implications of cannabinoid-based treatments for ALD.

Sex differences may play a critical role in modulating how chronic or heavy alcohol use impacts the brain to cause the development of alcohol use disorder (AUD). AUD is a multifaceted and complex disorder driven by changes in key neurobiological structures that regulate executive function, memory, and stress. A three-stage framework of addiction (binge/intoxication; withdrawal/negative affect; preoccupation/anticipation) has been useful for conceptualizing the complexities of AUD and other addictions. Initially, alcohol drinking causes short-term effects that involve signaling mediated by several neurotransmitter systems such as dopamine, corticotropin releasing factor, and glutamate. With continued intoxication, alcohol leads to dysfunctional behaviors that are thought to be due in part to alterations of these and other neurotransmitter systems, along with alterations in neural pathways connecting prefrontal and limbic structures. Using the three-stage framework, this review highlights examples of research examining sex differences in drinking and differential modulation of neural systems contributing to the development of AUD. New insights addressing the role of sex differences in AUD are advancing the field forward by uncovering the complex interactions that mediate vulnerability.

Sexually dimorphic effects of alcohol exposure throughout life have been documented in clinical and preclinical studies. In the past, rates of alcohol use disorder (AUD) were higher in men than in women, but over the past 10 years, the difference between sexes in prevalence of AUD and binge drinking has narrowed. Recent evidence adds to historical data regarding the influence of sex steroids on alcohol drinking and the interaction with stress-related steroids. This review considers the contribution of the endocrine system to alcohol drinking in females, with a focus on the hypothalamic pituitary gonadal axis and the hypothalamic pituitary adrenal axis and their reciprocal interactions. Emphasis is given to preclinical studies that examined genomic and rapid membrane effects of estrogen, progesterone, glucocorticoids, and GABAergic neurosteroids for their effects on alcohol drinking and models of relapse. Pertinent comparisons to data in males highlight divergent effects of sex and stress steroids on alcohol drinking and emphasize the importance of considering sex in the development of novel pharmacotherapeutic targets for the treatment of AUD. For instance, pharmacological strategies targeting the corticotropin releasing factor and glucocorticoid receptor systems may be differentially effective in males and females, whereas strategies to enhance GABAergic neurosteroids may represent a biomarker of treatment efficacy in both sexes.

Almost one-third of the U.S. population meets alcohol use disorder (AUD) criteria on a lifetime basis. This review provides an overview of recent research on the prevalence and patterns of alcohol-related improvement and selectively reviews nationally representative surveys and studies that followed risk groups longitudinally with a goal of informing patients with AUD and AUD researchers, clinicians, and policy-makers about patterns of improvement in the population. Based on the research, alcohol use increases during adolescence and early adulthood and then decreases beginning in the mid-20s across the adult life span. Approximately 70% of persons with AUD and alcohol problems improve without interventions (natural recovery), and fewer than 25% utilize alcohol-focused services. Low-risk drinking is a more common outcome in untreated samples, in part because seeking treatment is associated with higher problem severity. Sex differences are more apparent in help-seeking than recovery patterns, and women have lower help-seeking rates than men. Whites are proportionately more likely to utilize services than are Blacks and Hispanics. Improving recovery rates will likely require offering interventions outside of the health care sector to affected communities and utilizing social networks and public health tools to close the longstanding gap between need and utilization of AUD-focused services.