Self-medication of anxiety disorders with alcohol and drugs: Results from a nationally representative sample
Department of Psychology, University of Manitoba, Winnipeg, Manitoba, Canada. Journal of Anxiety Disorders
(Impact Factor: 2.96).
04/2008; 23(1):38-45. DOI: 10.1016/j.janxdis.2008.03.013
Self-medication--the use of alcohol or drugs in an attempt to reduce anxiety--has often been invoked as an explanatory mechanism for the high co-occurrence of anxiety and substance use disorders (for reviews, see Allan, C. A. (1995). Alcohol problems and anxiety disorders-A critical review. Alcohol & Alcoholism, 30(2), 145-151; Kushner, M. G., Abrams, K., & Borchardt. (2000). The relationship between anxiety disorders and alcohol use disorders: A review of major perspectives and findings. Clinical Psychology Review, 20(2), 149-171). The current study expands upon previous self-medication research by: (1) examining prevalence and comorbidity of self-medication for anxiety disorders (panic disorder, social phobia, specific phobia, and generalized anxiety disorder); (2) using a nationally representative sample (National Epidemiologic Survey on Alcohol and Related Conditions; N=43,093) to do so; and (3) by differentiating self-medication with alcohol from self-medication with drugs. Prevalence rates ranged from 18.3% (self-medication with alcohol for generalized anxiety disorder) to 3.3% (self-medication with both alcohol and drugs for specific phobia and panic disorder without agoraphobia). Multiple logistic regression analyses determined that self-medication with alcohol was associated with increased likelihood of any mood or personality disorder diagnosis, while self-medication with both alcohol and drugs further increased these associations over and above self-medication with alcohol alone. Findings remained significant after adjusting for sociodemographic and substance use disorder variables, which suggests that independently of substance use disorders, self-medication can be viewed as a marker of severity.
Available from: Munir Gunes Kutlu
- "Therefore, it is possible that nicotine-based self-medication may be effective only for some individuals with specific types of anxiety and/or specific genotypes. In support there is evidence showing that the prevalence of self-medication with alcohol and other drugs among different subtypes of anxiety disorders vary from 3.3% in specific phobias and panic disorder to 18.3% in generalized anxiety disorder . Specific nAChRs seem to have different roles in the effects of nicotine on anxiety (Table 2). "
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ABSTRACT: Anxiety disorders are a group of crippling mental diseases affecting millions of Americans with a 30% lifetime prevalence and costs associated with healthcare of $42.3 billion. While anxiety disorders show high levels of co-morbidity with smoking (45.3% vs. 22.5% in healthy individuals), anxiety disorders are also more common among the smoking population (22% vs. 11.1% in the non-smoking population). Moreover, there is clear evidence that smoking modulates symptom severity in patients with anxiety disorders. In order to better understand this relationship, several animal paradigms are used to model several key symptoms of anxiety disorders; these include fear conditioning and measures of anxiety. Studies clearly demonstrate that nicotine mediates acquisition and extinction of fear as well as anxiety through the modulation of specific subtypes of nicotinic acetylcholine receptors (nAChRs) in brain regions involved in emotion processing such as the hippocampus. However, the direction of nicotine's effects on these behaviors is determined by several factors that include the length of administration, hippocampus-dependency of the fear learning task, and source of anxiety (novelty-driven vs. social anxiety). Overall, the studies reviewed here suggest that nicotine alters behaviors related to fear and anxiety and that nicotine contributes to the development, maintenance, and reoccurrence of anxiety disorders.
Copyright © 2015. Published by Elsevier Inc.
Biochemical pharmacology 07/2015; 97(4). DOI:10.1016/j.bcp.2015.07.029 · 5.01 Impact Factor
Available from: Jennifer Dahne
- "Therapeutic strategies such as psychoeducation, relaxation, and exposurebased strategies could be provided to decrease SP symptoms and the odds of alcohol use. Moving toward intervention, to the extent that alcohol use may develop in order to manage preexisting symptoms of SP (Robinson et al., 2009), intervention programs for alcohol use among adolescents could also directly target symptoms of SP. Although the present sample was a nonclinical sample with relatively low rates of alcohol use, existing theories suggest that one of the functions of alcohol use is to manage SP symptoms and that youth with elevated SP symptoms may be at risk for the development of more problematic levels of SP over time as well as for problematic alcohol use. "
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The current study examined whether social phobia (SP) symptoms in early adolescence prospectively predicted alcohol use through middle adolescence in a community sample of youth.
Data from an ongoing longitudinal study (N = 277) of mechanisms of HIV-related risk behaviors in youth were used to assess the extent to which SP symptoms in early adolescence (mean [SD] age = 11.00 years [0.81]) would predict alcohol use across five annual assessment waves. Adolescents completed measures of SP symptoms, depressive symptoms, and alcohol use at each wave.
Higher SP symptoms at baseline predicted higher average odds of alcohol consumption during subsequent waves but did not significantly predict an increase in the odds of alcohol use as a function of time. Within a lagged model, SP symptoms measured at a prior assessment point (1 year earlier) predicted greater odds of drinking alcohol at the following assessment point. Importantly, alcohol use did not significantly predict SP symptoms over time. These results suggest that early SP symptoms are an important risk factor for increased odds of subsequent alcohol use.
The present findings highlight that elevated SP symptoms place adolescents at risk for early alcohol use. Early interventions targeting SP symptoms may be crucial for the prevention of problematic alcohol use in early to mid-adolescence. Implications for prevention and treatment approaches are discussed.
Journal of studies on alcohol and drugs 11/2014; 75(6):929. DOI:10.15288/jsad.2014.75.929 · 2.76 Impact Factor
Available from: Subhash Pandey
- "Both genetic and environmental factors play important roles in the development of alcoholism (Cloninger, 1987; Heath et al., 1997; Enoch and Goldman, 2001). Anxiety disorders have been found to be potential risk factors for the development of alcohol-use disorders, often co-morbid together (Schuckit and Hesselbrock, 1994; Kushner et al., 2000; Robinson et al., 2009). Acute alcohol exposure produces anxiolytic effects, whereas withdrawal after protracted exposure leads to the development of anxiety-like behaviours (Koob, 2003; Pandey, 2003; Moberg and Curtin, 2009). "
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ABSTRACT: Recent studies have demonstrated the involvement of epigenetic mechanisms in psychiatric disorders, including alcoholism. Here, we investigated the effects of histone deacetylase (HDAC) inhibitor, trichostatin A (TSA) on amygdaloid HDAC-induced histone deacetylation and neuropeptide Y (NPY) expression and on anxiety-like and alcohol-drinking behaviours in alcohol-preferring (P) and -non-preferring (NP) rats. It was found that P rats displayed higher anxiety-like and alcohol-drinking behaviours, higher amygdaloid nuclear, but not cytosolic, HDAC activity, which was associated with increased HDAC2 protein levels and deficits in histone acetylation and NPY expression in the central (CeA) and medial nucleus of amygdala (MeA), as compared to NP rats. TSA treatment attenuated the anxiety-like and alcohol-drinking behaviours, with concomitant reductions in amygdaloid nuclear, but not cytosolic HDAC activity, and HDAC2, but not HDAC4, protein levels in the CeA and MeA of P rats, without effect in NP rats. TSA treatment also increased global histone acetylation (H3-K9 and H4-K8) and NPY expression in the CeA and MeA of P, but not in NP rats. Histone H3 acetylation within the NPY promoter was also innately lower in the amygdala of P rats compared with NP rats; which was normalized by TSA treatment. Voluntary ethanol intake in P, but not NP rats, produced anxiolytic effects and decreased the HDAC2 levels and increased histone acetylation in the CeA and MeA. These results suggest that higher HDAC2 expression-related deficits in histone acetylation may be involved in lower NPY expression in the amygdala of P rats, and operative in controlling anxiety-like and alcohol-drinking behaviours.
The International Journal of Neuropsychopharmacology 02/2014; 17(08):1-14. DOI:10.1017/S1461145714000054 · 4.01 Impact Factor
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