Impact of depressive symptoms on future alcohol use in patients with co-occurring bipolar disorder and alcohol dependence: a prospective analysis in an 8-week randomized controlled trial of acamprosate.

Clinical Neuroscience Division, Department of Psychiatry and Behavioral Sciences, Medical University of South Carolina, Charleston, South Carolina 29425, USA.
Alcoholism Clinical and Experimental Research (Impact Factor: 3.42). 09/2011; 36(3):490-6. DOI: 10.1111/j.1530-0277.2011.01645.x
Source: PubMed

ABSTRACT Bipolar disorders and alcohol use disorders commonly co-occur, yet little is known about the proximal impact of bipolar symptoms on alcohol use in patients with this comorbidity. The present study examined the impact of depressive symptoms and alcohol craving on proximal alcohol use in patients with co-occurring bipolar disorder and alcohol dependence.
Data were collected during an 8-week randomized controlled trial of acamprosate for individuals with co-occurring bipolar disorder and alcohol dependence (n = 30). Depressive symptoms and alcohol craving were assessed biweekly using the Montgomery Asberg Depression Rating Scale (MADRS) and the Obsessive Compulsive Drinking Scale (OCDS), respectively. Daily alcohol use data were available via administration of the Time-line Follow-back interview at baseline and at subsequent weekly study visits. Correlational analyses and hidden Markov modeling were used to examine the prospective relationships between depressive symptoms, alcohol craving, and alcohol use.
Depressive symptoms and alcohol craving were significantly correlated with proximal (i.e., 1 week later) alcohol use across a variety of alcohol consumption summary measures. In hidden Markov models, depressive symptoms (OR = 1.3, 95% credible interval = [1.1, 1.5]) and alcohol craving (OR = 1.6, 95% credible interval = [1.4, 1.9]) significantly predicted transitioning from a light to a heavy drinking state, or remaining in a heavy drinking state.
The results from the present study suggest that depressive symptoms and alcohol craving increase proximal risk for alcohol use in individuals with co-occurring bipolar and alcohol use disorders.

  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Alcohol abuse can result in significant alterations to the structure of the brain and ultimately to behavioral dysfunctions. Epidemiological studies have shown that alcoholism is closely associated with impaired memory and judgment. However, the degree of deficit (brain injury) depends on factors such as the age of onset, duration of heavy drinking, continuous versus periodic (binge) drinking and the typical amount consumed per session. In recent years, neuroinflammation has been proposed as one of the alcoholism-induced neuropathological mechanisms, since increased levels of microglial markers are observed in the brains of both post-mortem human alcoholics and various alcohol-treated animals, from new-born or adolescent rodents to adult rodents. Many studies have investigated how microglia modulate alcohol-induced behavioral changes such as cognitive deficits, abnormal locomotor activity, motor impairment and mood disturbance. Importantly, we try to characterize and compare the distinct features in different ethanol (EtOH)-induced neurodegenerative disease (NDD) models. Moreover, mounting evidence indicates that in response to certain environmental toxins, microglia can become over-activated under oxidative stress, releasing pro-inflammatory mediators that cause central nervous system (CNS) disease. The molecular mechanisms involve free radical formation and the release of pro-inflammatory cytokines that are detrimental to neighboring neurons and interfere with the molecules regulating cell-cell interactions. The identification and understanding of the cellular and molecular mechanisms of microglial activation are described, as well as multiple downstream targets, in different alcohol-treated animal models. This review might contribute to the development of treatments and/or therapeutic agents that can reduce or eliminate the deleterious effects of alcohol-induced NDD.
    Pharmacology & therapeutics. 07/2014;
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Relatively little is known about the temporal relationship between alcohol use and subsequent mood changes in patients with bipolar disorder, and the available findings are inconsistent. The present study was a fine-grained analysis of the temporal relationship between alcohol use and short-term mood-switching probabilities. The study included 137 patients with bipolar disorder who performed daily self-ratings of their mood symptoms and the number of alcohol units consumed for a period of up to 52 weeks by using the National Institute of Mental Health self-rated prospective Life Chart Method. At baseline, the Structured Clinical Interview for DSM-IV was administered and demographic, social, and clinical characteristics were obtained. Multi-state models were used to assess the impact of the number of alcoholic drinks on patients' transition through different states of mood (depression, euthymia, and mania). The effect of alcohol use on the change in mood states was limited. For women in a depressive state, higher alcohol use was associated with a shorter time before entering the euthymic state [hazard ratio (HR) = 1.18, 95% confidence interval (CI): 1.03-1.36, p < 0.05], whereas, for men in an euthymic state, higher alcohol use was associated with a longer time before entering a manic state (HR = 0.81, 95% CI: 0.71-0.92, p < 0.05). The correlation between the consumed number of drinks per week and the average mood severity score of the following week was -0.01 (p < 0.001), indicating that only 0.01% of the variance in mood severity in this population is explained by alcohol use. Possible explanations for these findings are discussed. The current study, using a fine-grained analysis, suggests that alcohol use does not have a direct effect on the course of bipolar disorder in patients using mood stabilizers.
    Bipolar Disorders 03/2014; · 4.62 Impact Factor
  • Source
    Angelo Giovanni Icro Maremmani, Silvia Bacciardi, Luca Rovai, Fabio Rugani, Enrico Massimetti, Denise Gazzarrini, Liliana Dell'Osso, Icro Maremmani
    [Show abstract] [Hide abstract]
    ABSTRACT: Background: Glutamate system is modified by ethanol and contributes both to the euphoric and the dysphoric consequences of intoxication, but there is now growing evidence that the glutamatergic system also plays a central role in the neurobiology and treatment of mood disorders, including major depressive disorders and bipolar disorders. We speculate that, using acamprosate, patients with bipolar depression (BIP-A) can take advantage of the anti-glutamate effect of acamprosate to "survive" in treatment longer than peers suffering from non-bipolar depression (NBIP-A) after detoxification. Method: We retrospectively evaluated the efficacy of a long-term (six-month) acamprosate treatment, after alcohol detoxification, in 41 patients (19 males and 22 females), who could be classified as depressed alcoholics, while taking into account the presence/absence of bipolarity. Results: During the period of observation most NBIP-A patients relapsed, whereas a majority of BIP-A patients were still in treatment at the end of their period of observation. The cumulative proportion of 'surviving' patients was significantly higher in BIP-A patients, but this finding was not related to gender or to other demographic or clinically investigated characteristics. The treatment time effect was significant in both subgroups. The treatment time-group effect was significant (and significantly better) for bipolar patients on account of changes in the severity of their illness. Limitations: Retrospective methodology and the lack of DSM criteria in diagnosing bipolarity. Conclusions: Bipolarity seems to be correlated with the efficacy of acamprosate treatment in inducing patients to refrain from alcohol use after detoxification (while avoiding relapses) in depressed alcoholics. Placebo-controlled clinical trials are now warranted to check the validity of this hypothesis.
    Int J Environ Res Public Health. 01/2014; 11.

Full-text (2 Sources)

Available from
May 28, 2014