Study disentangles genetic and environmental influences on progression of alcohol use disorder to related medical conditions

Newswise – A new study has shown that alcohol-related illnesses are caused by environmental and genetic factors, a proportion of which is not shared with the underlying alcohol use disorder (AUD). Medical conditions resulting from alcohol abuse include alcoholic liver disease, pancreatitis, cardiomyopathy, and neuropathy, but not all people with AUD suffer from medical problems related to their alcohol use. The factors that influence the responsibility for alcohol-related medical conditions (AMC) in people with AUD are not fully understood. In a large study published in Alcoholism: clinical and experimental research, researchers from Sweden and the United States quantified the extent to which genetic and environmental factors shared with, versus, AUD contribute to progression to AMC.

The researchers used Swedish medical and criminal records to identify pairs of identical and non-identical twins, siblings and half-siblings, where at least one of the two had documented AUD. Then, they identified which of these individuals had also been diagnosed with one (or more) of the ten AMCs. By studying the correlation of AUD and AMC between pairs of siblings of different genetic kinship and fitting statistical models to the data, the researchers were able to identify the sources of genetic and environmental variance that contribute to the blame. AUC and AMC.

Overall, 3% of women and 9% of men in the birth cohort analyzed had AUD (totaling approximately 86,000 people), and among these, 14% of women and 15% of men had AMC ( around 13,000 people). The proportion of sibling pairs in which both siblings had AUD, or in which both siblings had AMC, generally declined as genetic relatedness declined; this suggests a role of genetic factors in AUD and AMC. Overall, about one-third of the risk of AMC has been found to be genetic, while two-thirds of the risk could be attributed to environmental factors. Of note, most (77%) of the environmental influence on AMC was unique to AMC (rather than shared with that of AUD), as was about 40% of genetic influence.

The results confirm the relevance of genetic factors specific to AMC, highlighting the need for further studies to identify the genes involved and determine how they contribute to the etiology of AMC – potentially through metabolic pathways or physiological responses to them. toxins or damage. The results also highlight the considerable influence of environmental factors specific to CMA, providing an important opportunity for follow-up studies to identify the exposures that distinguish people with AUD who develop versus those who do not. no AMC. Relevant environmental factors, some of which may be modifiable and therefore viable targets for prevention, may include other medical conditions, lack of preventive care, and diet. Additionally, the finding that some genetic and environmental responsibility for AMC is shared with AUD underscores that ongoing efforts to prevent AUD will have an overall positive impact, reducing AMC’s personal and economic toll. as well as the AUD.

The researchers note some limitations. First, the analyzes grouped a wide range of different AMCs into a single AMC result, potentially obscuring important etiologic differences between different body organs affected by heavy alcohol consumption. Second, the risk of AMC is likely to depend at least in part on the level of alcohol consumption, for which data was not available. These factors should be explored in future studies. It is also unclear whether the findings can be generalized to countries without socialized medicine, such as the United States. For example, reduced access to AUD treatment among certain patient groups, such as the socio-economically disadvantaged, could have an impact on AUD / AMC combinations.

Genetic and environmental influences on the progression of alcohol use disorders to alcohol-related medical conditions. Alexis C. Edwards, K. Sundquist, J. Sundquist, KS Kendler, S. Larsson Lönn (pages xxx).


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