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Journal Article

Citation

Skogen JC, Harvey SB, Henderson M, Stordal E, Mykletun A. Addiction 2009; 104(9): 1519-1529.

Copyright

(Copyright © 2009, John Wiley and Sons)

DOI

10.1111/j.1360-0443.2009.02659.x

PMID

unavailable

Abstract

Aims The aim of this study was to examine the levels of anxiety and depression among individuals consuming low levels of alcohol.


Design Prospective and cross‐sectional population‐based study.


Setting and participants This study employed data from the Nord‐Trøndelag Health Survey (HUNT‐2, n = 38 930).


Measurements Alcohol consumption was measured by self‐report of usual alcohol consumption during a 2‐week period. Low‐level alcohol consumption was defined as self‐reported abstainers and non‐abstainers currently consuming no alcohol. Anxiety and depression were measured using the Hospital Anxiety and Depression Rating Scale. Potential explanatory variables included somatic illness and symptoms, health‐related behaviour, socio‐economic status and social activity. In a subsample (n = 20 337), we also looked at the impact of previous heavy drinking among abstainers ('sick‐quitting').


Findings A U‐shaped association between alcohol consumption and the risk of anxiety and depression was found. Abstention was related to increased odds for both case‐level anxiety [1.34, 95% confidence interval (CI) 1.19–1.52] and depression (1.52, 95% CI 1.30–1.77). This association was accounted for partly by adjustments for socio‐economic status, social network, somatic illness, age (depression only), gender (anxiety only) and ‘sick‐quitting’. We also identified significant differences between participants who label themselves as abstainers compared to those who report no usual alcohol consumption, but who do not label themselves as abstainers.


Conclusions The risk of case‐level anxiety and depression is elevated in individuals with low alcohol consumption compared to those with moderate consumption. Individuals who label themselves as abstainers are at particularly increased risk. This increased risk cannot fully be explained by somatic illness, social activity or ‘sick‐quitting’.

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