______________________________________________________________ Alcohol and Alcohol Use Disorder
less serious adverse effects than tricyclics, but some, like fluoxetine, work slowly and cause sexual performance side effects. SSRIs, such as fluoxetine, sertraline, and paroxetine, and herbal remedies such as St. John’s wort have been tried in a variety of studies and are generally able to help alleviate depression, but do not appear to help with drinking outcomes. Results of a systematic review found only low-quality evidence to support the use of antidepressants for the treatment of co-occurring depression and alcohol use disorder [231]. A Japanese study observed lower response to antidepressant treatment in patients with comorbid depression and alcohol use disorder [232]. Venlafaxine and bupropion appear to be especially effective in treating patients with depression and alcohol use disorder. Venlafaxine is well suited to treat alcohol use disorder with depression and even depression with anxiety [233]. Venlafaxine is effective in mild and severe depression with anhedonia. Bupropion is effective as well, but it has seizure risks in this population [234]. One study that evaluated treatment outcomes in patients with comorbid alcohol use disorder and depression found venlafaxine and bupropion to be less effective than antidepressants [235]. Men with depression who are using alcohol appear very sensitive to the sexual side effects of the SSRIs and may discontinue their use and drop out of treatment. Both pharmacologic and behavioral treatments have demonstrated efficacy for patients with comorbid depression and alcohol use disorder; however, treatment response is modest, particularly for drinking outcomes [236]. Transcranial magnetic stimulation is now available for refractory depression, and studies are in progress for its use in treating substance use disorder [237]. BIPOLAR DISORDER A 2000 study analyzed the substance/alcohol abuse patterns of 89 patients with a confirmed diagnosis of bipolar disorder (71 with bipolar I and 18 with bipolar II) [238]. The diagnosis was confirmed by a structured clinical interview for DSM-IV Axis I, an attending psychiatrist, a medical records review, and family members. The age of the patients ranged from 18 to 65 years. Among those with bipolar disorder I, 41 patients (57.8%) abused or were dependent on one or more substances (including alcohol), 28.2% abused or were dependent on two substances, and 11.3% abused or were dependent on three or more substances. Among those with bipolar disorder II, 39% of patients abused or were dependent on one or more substances, 17% were dependent on two or more substances, and 11% were dependent on three or more substances. The risk for substance or alcohol abuse was higher among patients with bipolar I disorder than with bipolar disorder II. Patients with both bipolar disorders I and II abused alcohol more often than any other substances [238]. One study sought to identify the demographic and clinical differences between patients with bipolar disorder both with and without alcohol use disorder [239]. Data from 238 patients with bipolar disorder included alcohol use, social demographics, longitudinal course of bipolar disorder, clinical features of depressive episodes, comorbid physical diseases, anxiety disorder, and other substance use disorder. Of the 238 patients with bipolar disorder, 74 had
alcohol use disorder, with the best predictors of alcohol use disorder being male sex, younger age, and comorbidity with other unclassified substance dependence [239]. ANXIETY Alcohol withdrawal causes many of the signs and symptoms of anxiety and can even mimic panic attacks. Alcohol works much like a benzodiazepine; many people who abuse and are dependent on alcohol have learned to drink to temporarily relieve anxious feelings. Special problems exist for people who drink to self-medicate the symptoms of a true generalized anxiety disorder, social phobia, or panic disorder. Alcohol may provide temporary relief, but it is not a good treatment for shyness or an anxiety disorder. The price a person may pay for self-medication are two diseases: anxiety and alcohol use disorder. Social anxiety can be a major impediment to active participation and even attendance to group therapy and 12-step meetings. PAIN Pain is a subjective experience, and the perception of being in pain is an important factor of the alcohol use disorder. It is hypothesized, as well as established in some research, that individuals in pain will drink as a means to decrease their perception of pain or as a reaction to painful stimuli [240]. According to the National Institute on Alcohol Abuse and Alcoholism, an estimated one in four adults in chronic pain reports self-medicating with alcohol and 43% to 73% of people with alcohol use disorder report experiencing chronic pain [241]. ABUSE/DEPENDENCE ON OTHER DRUGS All drugs of abuse, including alcohol, cause dopamine release in the mesolimbic system in the brain. This dopamine system, sometimes referred to as the neuroanatomy of pleasure or reinforcement, starts in the ventral tegmental area and projects to the nucleus accumbens. Alcohol- or drug-taking results in a dopamine reward that stimulates its taking. Pavlovian conditioning to environmental cues (e.g., sights, smells, and sounds of a bar) that precede use become associated with use of the drug. Notably, this sense of “reward,” which confers evolutionary fitness, is more likely to be perceived as crucial than even that produced by natural, survival-oriented stimuli (e.g., food, sex). This conditioning is reflective of synaptic strengthening mediated by the glutamatergic system, with neuroplasticity changes in brain areas thought to mediate drug- taking behavior, including the amygdala (stress and anxiety), hippocampus (memory), and dorsal striatum (routine motor movements). Natural stimuli (e.g., food, sex, other previously pleasurable activities) become less enjoyable, resulting in a profound state of anhedonia. With time, alcohol use disorders become ingrained. Ultimately, this preference for alcohol compared to natural rewards is mediated through a process of “bad learning,” or neuroplasticity changes in the extended amygdala, also referred to as the antireward system. The anti- reward system involves stress-response hormones, including
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