Association Between Brain Structure and Alcohol Use Behaviors in Adults

Mavromatis, Lucas A.; Rosoff, Daniel B.; Cupertino, Renata B.; Garavan, Hugh; Mackey, Scott; Lohoff, Falk W.

doi:10.1001/jamapsychiatry.2022.2196

Cited by 37 publications

(21 citation statements)

References 78 publications

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“…This analysis found evidence for a causal effect of brain structure on problematic alcohol use, including greater volume of the pars opercularis, greater thickness of the cuneus and lower volume of the basal forebrain, but no evidence for a causal effect of alcohol use on the brain when phenotypes were reversed. Consistent with these findings, a recent study using MR found evidence for a negative effect of global cortical thickness on DPW and binge drinking, with no evidence for regional effects or effect of alcohol use on the brain 72 …”

Section: Alcohol Involvement and Brain Structure: Assessing The Plaus...mentioning

confidence: 68%

Alcohol use and grey matter structure: Disentangling predispositional and causal contributions in human studies

Baranger,

Paul,

Hatoum

et al. 2023

Addiction Biology

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Alcohol use is a growing global health concern and economic burden. Alcohol involvement (i.e., initiation, use, problematic use, alcohol use disorder) has been reliably associated with broad spectrum grey matter differences in cross‐sectional studies. These findings have been largely interpreted as reflecting alcohol‐induced atrophy. However, emerging data suggest that brain structure differences also represent pre‐existing vulnerability factors for alcohol involvement. Here, we review evidence from human studies with designs (i.e., family‐based, genomic, longitudinal) that allow them to assess the plausibility that these correlates reflect predispositional risk factors and/or causal consequences of alcohol involvement. These studies provide convergent evidence that grey matter correlates of alcohol involvement largely reflect predisposing risk factors, with some evidence for potential alcohol‐induced atrophy. These conclusions highlight the importance of study designs that can provide causal clues to cross‐sectional observations. An integrative model may best account for these data, in which predisposition to alcohol use affects brain development, effects which may then be compounded by the neurotoxic consequences of heavy alcohol use.

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Section: Alcohol Involvement and Brain Structure: Assessing The Plaus...mentioning

confidence: 68%

Alcohol use and grey matter structure: Disentangling predispositional and causal contributions in human studies

Baranger,

Paul,

Hatoum

et al. 2023

Addiction Biology

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“…Other recent neuropsychiatric research has demonstrated that global cortical thinning, a common finding in patients who have had strokes, is associated with an increased risk for alcohol use disorder ( 1 ). As was noted on his most recent CT scan ( Figure 1 ), his brain demonstrates diffuse volume loss as well as a large region of chronic encephalomalacia.…”

Section: Discussionmentioning

confidence: 99%

“…An investigation into the predominant neuropsychiatric mechanism is crucial to guide the overarching therapeutic approach. Plausible mechanisms to explain the change in behavior after his stroke include maladaptive coping mechanisms in the setting of new psychosocial stressors (2,3), cerebrovascular tissue injury leading to impaired neurological functioning (1,(6)(7)(8), and decompensation of a previously well-masked psychiatric illness in the setting of his stroke (9).…”

Section: Discussionmentioning

confidence: 99%

“…Following a stroke, patients can develop behavioral changes due to a variety of underlying mechanisms. Lesions in specific anatomic regions of the brain have well-documented stereotypical manifestations that might explain some of these behaviors ( 1 ). Behavioral changes can also develop as coping mechanisms to deal with the wide array of psychosocial stressors that arise after a large stroke ( 2 , 3 ).…”

Section: Introductionmentioning

confidence: 99%

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Case report: Diagnostic challenges in a patient with alcohol use disorder that developed following a stroke

Zeitlin

Kotbi

2023

Front. Psychiatry

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Patients with comorbid neurological and psychiatric diseases often face considerable impairment, causing challenges that pervade many aspects of their lives. Symptoms can be especially taxing when one or more of these conditions is severely disabling, as the resulting disability can make it more challenging to address comorbidities. For clinicians, such patients can be quite difficult to both diagnose and treat given the immense potential for overlap between the underlying psychiatric and neurologic causes of their symptoms—as well as the degree to which they might exacerbate or, conversely, mask one another. These intricate relationships can also obscure the workup of more acute pathologies, such as alcohol withdrawal and delirium. This report details the complex history and clinical challenges in a 54-year-old man who was no longer able to work after developing multiple neurologic deficits from a left MCA stroke a decade earlier. The intellectual and motor disabilities he faced in the aftermath of his stroke were subsequently compounded by a steady increase in alcohol consumption, with his behavior ultimately progressing to severe alcohol use disorder. The coinciding neurologic and psychiatric manifestations obfuscate the workup—and therefore the management—of his major depressive disorder. In pursuit of the optimal approach to address these comorbid conditions and promote recovery, an investigation into possible mechanisms by which they are interconnected revealed several potential neuropsychiatric explanations that suggest targets for future therapeutic strategies.

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“…Because of complexity in specimen collection and prohibitive cost of TWA, gene expression analyses in response to alcohol use/misuse in living humans are often conducted with selective genes based on research hypotheses 11,12 . Apart from the published animal or in vitro studies [13][14][15] , a recent study by Marvomatis et al utilized genetic data from a large population-based GWAS to impute transcriptomic associations with alcohol consumption patterns, leveraging cis-acting genetic variants 16 . A large-scale study such as this has the advantage of mitigating some of the variability in gene expression amongst individuals.…”

Section: Introductionmentioning

confidence: 99%

Peripheral blood transcriptomic profiling indicates molecular mechanisms commonly regulated by binge-drinking and placebo-effects

Shetty

Sivinski

Cornell

et al. 2023

Preprint

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Molecular changes associated with alcohol consumption arise from complex interactions between pharmacological effects of alcohol, psychological/placebo context surrounding drinking, and other environmental and biological factors. The goal of this study was to tease apart molecular mechanisms regulated by pharmacological effects of alcohol - particularly at binge-drinking, from underlying placebo effects. Transcriptome-wide RNA-seq analyses were performed on peripheral blood samples collected from healthy heavy social drinkers (N=16) enrolled in a 12-day randomized, double-blind, cross-over human laboratory trial testing three alcohol doses: Placebo, moderate (0.05g/kg (men), 0.04g/kg (women)), and binge (1g/kg (men), 0.9g/kg (women)), administered in three 4-day experiments, separated by minimum of 7-day washout periods. Effects of beverage doses on the normalized gene expression counts were analyzed within each experiment compared to its own baseline using paired-t-tests. Differential expression of genes (DEGs) across experimental sequences in which each beverage dose was administered, as well as responsiveness to regular alcohol compared to placebo (i.e., pharmacological effects), were analyzed using generalized linear mixed-effects models. The 10% False discovery rate-adjusted DEGs varied across experimental sequences in response to all three beverage doses. We identified and validated 22 protein coding DEGs potentially responsive to pharmacological effects of binge and medium doses, of which 11 were selectively responsive to binge dose. Binge-dose significantly impacted the Cytokine-cytokine receptor interaction pathway (KEGG: hsa04060) across all experimental-sequences that it was administered in, and during dose-extending placebo. Medium dose and placebo impacted pathways hsa05322, hsa04613, and hsa05034, in the first two and last experimental sequences, respectively. In summary, our findings add novel, and confirm previously reported data supporting dose-dependent effects of alcohol on molecular mechanisms and suggest that the placebo effects may induce molecular responses within the same pathways regulated by alcohol. Innovative study designs are required to validate molecular correlates of placebo effects underlying drinking.

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Association Between Brain Structure and Alcohol Use Behaviors in Adults

Cited by 37 publications

References 78 publications

Alcohol use and grey matter structure: Disentangling predispositional and causal contributions in human studies

Alcohol use and grey matter structure: Disentangling predispositional and causal contributions in human studies

Case report: Diagnostic challenges in a patient with alcohol use disorder that developed following a stroke

Peripheral blood transcriptomic profiling indicates molecular mechanisms commonly regulated by binge-drinking and placebo-effects

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