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Objectives: Previous research has found an association between alcohol use and hippocampal volume (Wilson et al., 2017). Research from our group (Wilson et al., 2018) using a cotwin-control design in a sample of twins provided evidence consistent with a direct effect of drinking on hippocampal volume that was independent of genetic and environmental factors that might confound associations between drinking and volume. However, the sample was small and consisted entirely of females. Thus, the extent to which smaller hippocampal volume is a consequence of drinking or instead reflects premorbid risk for problematic use remains unknown. Additionally, although a large proportion of adolescents and young adults drink a high volume of alcohol, people generally moderate their drinking as they get older, and though much is known about the plasticity of the hippocampus to other experiences, not much research has been done on the possible reversal of alcohol-exposure effects on the hippocampus after moderation. We are investigating the relationship between levels of drinking and subsequent changes in drinking on hippocampal volume in another large sample of adult twins. We hypothesize that hippocampal volume will be inversely related to drinking level, and that it will also be inversely related to recent changes in drinking level.
Methods: Our sample is a cohort of adult twins who have been assessed multiple times from ages 11 to 34. Alcohol use will be assessed using various indicators of quantity, intensity, and frequency of drinking to create an index measure of both recent and cumulative alcohol use. Anatomical MRI data was collected at age 34 and will be assessed using output from FreeSurfer. We will investigate the relationship between left and right hippocampal volume at age 34 and cumulative drinking up to ages 24, 29, and 34 using linear mixed-effects models. Additionally, we will investigate the changes in drinking from age 24 to age 34 and how these changes relate to left and right hippocampal volume at age 34. In addition to looking at the individual-level information, we plan to use the co-twin control analyses for these investigations to help distinguish between pre-existing liabilities to drinking and effects of drinking independent of genetic and environmental confounds.
Implications: Using a large sample of twins will provide further evidence about the relationship between alcohol use and hippocampal volume helping us to assess whether there is an exposure-related effect or simply another pre-existing liability. Additionally, information about the changes in alcohol consumption and possible subsequent changes in hippocampal volume will help inform our understanding of the hippocampus' and the brain's ability to recover from unhealthy experiences like problematic alcohol use.
Feasibility: All of the data for this planned analysis has been collected. Additionally, the MRI data, raw alcohol use data, and the data for other covariates of interest have been reviewed and processed. Our drink index data has been compiled from all assessments. We are therefore well-positioned to construct the measures to be used in this investigation: a measure of cumulative use to age 34 as well as changes in use between 24 and 34.