“…Future research using causally informative study designs is needed to determine the causal relationship between problematic alcohol use and reduced hippocampal volume in humans. There is increasing evidence, from longitudinal studies that prospectively assess alcohol use and brain morphometry over time, high-risk family studies that compare substance-naïve offspring at high and low familial risk for problematic alcohol use, and co-twin control studies that compare twins who vary in their alcohol use, that at least some of the brain deviations observed among individuals with problematic alcohol use reflect premorbid abnormalities (see Jacobus & Tapert, 2013; Wilson et al 2015 a , b ). However, this body of research is as yet relatively small, and the few studies on the hippocampus have yielded inconsistent findings.…”
Background
A number of studies reports reduced hippocampal volume in individuals who engage in problematic alcohol use. However, the magnitude of the difference in hippocampal volume between individuals with v. without problematic alcohol use has varied widely, and there have been null findings. Moreover, the studies comprise diverse alcohol use constructs and samples, including clinically significant alcohol use disorders and subclinical but problematic alcohol use (e.g. binge drinking), adults and adolescents, and males and females.
Methods
We conducted the first quantitative synthesis of the published empirical research on associations between problematic alcohol use and hippocampal volume. In total, 23 studies were identified and selected for inclusion in the meta-analysis; effects sizes were aggregated using a random-effects model.
Results
Problematic alcohol use was associated with significantly smaller hippocampal volume (d = −0.53). Moderator analyses indicated that effects were stronger for clinically significant v. subclinical alcohol use and among adults relative to adolescents; effects did not differ among males and females.
Conclusions
Problematic alcohol use is associated with reduced hippocampal volume. The moderate overall effect size suggests the need for larger samples than are typically included in studies of alcohol use and hippocampal volume. Because the existing literature is almost entirely cross-sectional, future research using causally informative study designs is needed to determine whether this association reflects premorbid risk for the development of problematic alcohol use and/or whether alcohol has a neurotoxic effect on the hippocampus.
“…Future research using causally informative study designs is needed to determine the causal relationship between problematic alcohol use and reduced hippocampal volume in humans. There is increasing evidence, from longitudinal studies that prospectively assess alcohol use and brain morphometry over time, high-risk family studies that compare substance-naïve offspring at high and low familial risk for problematic alcohol use, and co-twin control studies that compare twins who vary in their alcohol use, that at least some of the brain deviations observed among individuals with problematic alcohol use reflect premorbid abnormalities (see Jacobus & Tapert, 2013; Wilson et al 2015 a , b ). However, this body of research is as yet relatively small, and the few studies on the hippocampus have yielded inconsistent findings.…”
Background
A number of studies reports reduced hippocampal volume in individuals who engage in problematic alcohol use. However, the magnitude of the difference in hippocampal volume between individuals with v. without problematic alcohol use has varied widely, and there have been null findings. Moreover, the studies comprise diverse alcohol use constructs and samples, including clinically significant alcohol use disorders and subclinical but problematic alcohol use (e.g. binge drinking), adults and adolescents, and males and females.
Methods
We conducted the first quantitative synthesis of the published empirical research on associations between problematic alcohol use and hippocampal volume. In total, 23 studies were identified and selected for inclusion in the meta-analysis; effects sizes were aggregated using a random-effects model.
Results
Problematic alcohol use was associated with significantly smaller hippocampal volume (d = −0.53). Moderator analyses indicated that effects were stronger for clinically significant v. subclinical alcohol use and among adults relative to adolescents; effects did not differ among males and females.
Conclusions
Problematic alcohol use is associated with reduced hippocampal volume. The moderate overall effect size suggests the need for larger samples than are typically included in studies of alcohol use and hippocampal volume. Because the existing literature is almost entirely cross-sectional, future research using causally informative study designs is needed to determine whether this association reflects premorbid risk for the development of problematic alcohol use and/or whether alcohol has a neurotoxic effect on the hippocampus.
“…A growing number of studies has examined whether brain deviations associated with alcohol addiction are evident prior to its onset. Evidence from longitudinal and high-risk family studies indicate that many of the brain deviations associated with problematic alcohol use considered to reflect a neurotoxic effect on the brain are actually evident prior to initiation of alcohol use and instead reflect pre-existing liability toward problematic alcohol use (see Jacobus & Tapert, 2013; Malone et al 2014; Wilson et al 2015a, b).…”
Section: Discussionmentioning
confidence: 99%
“…Growing evidence from research using causally informative study designs, including longitudinal studies that prospectively assess alcohol use and neural indicators over time, high-risk family studies that compare substance-naïve offspring at high and low familial risk for problematic alcohol use, and co-twin control studies that compare twins who vary in their alcohol use, indicates that at least some of the brain deviations observed among individuals with problematic alcohol use reflect pre-existing liabilities (see Jacobus & Tapert, 2013; Malone et al 2014; Wilson et al 2015 a , b ). However, the few causally informative studies that have considered the hippocampus have yielded inconsistent findings.…”
The association between problematic alcohol use and smaller hippocampal volume likely reflects an alcohol exposure-related effect. Differentiating pre-existing brain deviations that confer risk for problematic alcohol use from those that reflect effects of alcohol on the brain will inform etiological models of addiction and further prevention and intervention efforts.
“…A handful of studies has examined gray matter development as a function of subclinical alcohol use in community samples of adolescents (see Ewing et al, 2014 , Wilson et al, 2015 ; see Table 1 for an overview). A series of reports from one research team has examined cross-sectional associations between adolescent alcohol use and brain morphometry.…”
Developmental changes in structure and functioning are thought to make the adolescent brain particularly sensitive to the negative effects of alcohol. Although alcohol use disorders are relatively rare in adolescence, the initiation of alcohol use, including problematic use, becomes increasingly prevalent during this period. The present study examined associations between normative drinking (alcohol initiation, binge drinking, intoxication) and brain morphometry in a sample of 96 adolescent monozygotic twins. A priori regions of interest included 11 subcortical and 20 cortical structures implicated in the existing empirical literature as associated with normative alcohol use in adolescence. In addition, co-twin control analyses were used to disentangle risk for alcohol use from consequences of alcohol exposure on the developing brain. Results indicated significant associations reflecting preexisting vulnerability toward problematic alcohol use, including reduced volume of the amygdala, increased volume of the cerebellum, and reduced cortical volume and thickness in several frontal and temporal regions, including the superior and middle frontal gyri, pars triangularis, and middle and inferior temporal gyri. Results also indicated some associations consistent with a neurotoxic effect of alcohol exposure, including reduced volume of the ventral diencephalon and the middle temporal gyrus.
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