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Evidence for an alcohol‐related “harm paradox” in individuals with internalizing disorders: Test and replication in two independent community samples
Background Internalizing (anxiety and mood) disorders (INTD) commonly co‐occur (are “comorbid”) with alcohol use disorder (AUD). The literature suggests that excessive alcohol use aimed at coping with INTD symptoms is, at best, a partial explanation for the high comorbidity rates observed. We hypoth...
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Published in: | Alcohol, clinical & experimental research clinical & experimental research, 2023-04, Vol.47 (4), p.713-723 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Background
Internalizing (anxiety and mood) disorders (INTD) commonly co‐occur (are “comorbid”) with alcohol use disorder (AUD). The literature suggests that excessive alcohol use aimed at coping with INTD symptoms is, at best, a partial explanation for the high comorbidity rates observed. We hypothesized that individuals with INTD experience greater susceptibility to developing AUD symptoms due to the partially shared neurobiological dysfunctions underlying both conditions. We probe this hypothesis by testing the prediction that, after accounting for the volume of alcohol intake, individuals with INTD experience higher levels of alcohol‐related symptoms.
Methods
Data from the National Epidemiological Survey on Alcohol‐Related Conditions (NESARC) Wave 3 were used for the primary analyses, and NESARC Wave 1 data were used for independent replication analyses. Individuals who reported any alcohol use in the prior year were categorized as: (1) never having had an INTD diagnosis (“INTD‐Never”); (2) having a remitted INTD diagnosis only (“INTD‐Remitted”); or (3) having current INTD diagnosis (“INTD‐Current”). Between‐group contrasts of alcohol‐related symptoms controlled for total alcohol intake (past year), drinking pattern (e.g., binging) and variables previously shown to mark exaggerated AUD symptoms relative to drinking amount (e.g., SES, gender, and family history).
Results
With all covariates in the model, individuals in the INTD‐Current group and the INTD‐Remitted group reported significantly greater alcohol‐related symptoms than those in the INTD‐Never group but did not themselves differ in level of alcohol‐related symptoms. These results were replicated in the NESARC 1 dataset.
Conclusions
Individuals with INTD experience more alcohol‐related symptoms than those who drink at the same level. While considering other explanations, we argue that this “harm paradox” is best explained by the view that INTD confers a neurobiologically mediated susceptibility to the development of AUD symptoms.
Some neurobiological dysregulations underlying anxiety/depression (“internalizing”) disorders are also associated with addiction. We hypothesized that this causes a neurobiologically‐mediated susceptibility to develop addiction symptoms among those with internalizing disorders. We predicted and found that drinkers with internalizing disorders do manifest more alcohol‐related symptoms than others even after controlling daily use level and other known confounders (e.g., f |
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ISSN: | 0145-6008 2993-7175 1530-0277 2993-7175 |
DOI: | 10.1111/acer.15036 |