Alcohol, clinical & experimental research · 2025
Correlational and causal modeling of alcohol-related symptoms and internalizing disorder status: Further elucidation of a harm paradox.
СтатьяПоддержка NIH: внешняя программаНазвание и аннотация: Перевод в очереди
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Anker Justin, Andrews Bryan, Kummerfeld Erich, Thuras Paul, Kushner Matt G
Аннотация
BACKGROUND: Individuals with internalizing (anxiety and depressive) disorder (INTD) suffer from an alcohol-related "harm paradox"; that is, they experience more alcohol-related symptoms in aggregate than do others who drink at the same level. Here, we extend this earlier finding by examining the association of INTD with a wide range of individual alcohol-related symptoms.
METHODS: The study sample included respondents in the NESARC Wave 3 who reported having consumed alcohol in the past year (N = 24,485). We used logistic regression analysis to identify the association between INTD and risk for 37 individual alcohol symptoms. We used the BOSS causal discovery algorithm to identify the best-fitting causal model for the full dataset and for 100 resampled datasets, each composed of a randomly selected 50% of the full dataset. Causal edges that appeared in at least 80% of the resampled datasets were deemed "highly stable."
RESULTS: After controlling for the level of daily alcohol volume and demographic variables, INTD significantly increased the relative odds of having all 37 alcohol-related symptoms measured (ORs ranged from 1.5 to 4.6). Interactions between INTD and the level of alcohol use were largely nonsignificant. Highly stable direct (unmediated) causal edges emanated primarily from INTD to the symptoms of alcohol withdrawal and dependence.
CONCLUSIONS: Those with INTD are at greater risk for a wide range of alcohol symptoms than others who drink at the same level, even at relatively low levels of alcohol use. We consider that INTD could exert a direct causal influence specifically on withdrawal and dependence symptoms due to overlapping experiential and/or neurobiological aspects of these alcohol use symptoms and INTD. We conclude that the harm paradox likely contributes to the elevated risk of developing alcohol use disorder comorbidity among those with INTD.
METHODS: The study sample included respondents in the NESARC Wave 3 who reported having consumed alcohol in the past year (N = 24,485). We used logistic regression analysis to identify the association between INTD and risk for 37 individual alcohol symptoms. We used the BOSS causal discovery algorithm to identify the best-fitting causal model for the full dataset and for 100 resampled datasets, each composed of a randomly selected 50% of the full dataset. Causal edges that appeared in at least 80% of the resampled datasets were deemed "highly stable."
RESULTS: After controlling for the level of daily alcohol volume and demographic variables, INTD significantly increased the relative odds of having all 37 alcohol-related symptoms measured (ORs ranged from 1.5 to 4.6). Interactions between INTD and the level of alcohol use were largely nonsignificant. Highly stable direct (unmediated) causal edges emanated primarily from INTD to the symptoms of alcohol withdrawal and dependence.
CONCLUSIONS: Those with INTD are at greater risk for a wide range of alcohol symptoms than others who drink at the same level, even at relatively low levels of alcohol use. We consider that INTD could exert a direct causal influence specifically on withdrawal and dependence symptoms due to overlapping experiential and/or neurobiological aspects of these alcohol use symptoms and INTD. We conclude that the harm paradox likely contributes to the elevated risk of developing alcohol use disorder comorbidity among those with INTD.