Alcoholic patients require close attention to drug interactions—for example, they may require higher than average doses of tricyclic antidepressants to reach therapeutic levels. Adverse effects, adherence, history of drug trials, presence of suicidal tendencies, and organization status, that is, ability to comply with disulfiram-related dietary guidelines, should also be considered in drug selection. Disulfiram, naltrexone, and acamprosate are pharmacotherapies approved by the FDA for treating alcohol use disorder (AUD) (Kranzler & Soyka, 2018). There are many FDA-approved antidepressants for treating a depressive disorder, with selective serotonin reuptake inhibitors (SSRIs) considered the first-line pharmacological agent. Similar to the evaluation issues described above, the evidence base is limited regarding the use of pharmacotherapy in patients with comorbid depression and AUD.
Drugs such as clomipramine or amitriptyline are highly toxic. Alcohol causes intoxication of the body, so they mutually exacerbate each other as well. Tricyclic medicines have many side effects, the likelihood and severity of which are increased by alcohol (Kranzler & Soyka, 2018). Both antidepressants and alcohol affect the central nervous system, so the consequences of simultaneous users can be dangerous, up to falling into a coma.
According to the recommendations, antidepressants should be continued for at least six months after people start to feel better. However, it should be remembered that each case is individual, and there is no general time frame for the disappearance of symptoms of depression.
Anxiety disorders are caused by a combination of genetic and environmental factors. Risk factors include a history of child abuse, a family history of mental disorders, and poverty. Anxiety disorders often co-occur with other psychiatric syndromes, preeminent personality and depressive disorders or substance use disorders (Ferreira-Garcia et al., 2017). Predictors are associated with specific risk factors, including environmental factors, internal and external factors, especially age-related chronic diseases (respiratory infections, arrhythmias, and heart failure), lipid levels, obesity, and cognitive impairment.
- One of the foremost common links in the pathogenesis of depression is considered to be hyperactivation of the hypothalamic-pituitary-adrenal axis (HPA axis), which is manifested by an increased level of corticotropin-releasing hormone (CRH) and hypercortisolemia;
- For psychotic depression, an increase in the content of C-reactive protein (CRP) and interleukin-6 (IL-6) in the blood plasma is more characteristic;
- The activity of dopamine-beta-hydroxylase decreases with age; namely, in older patients, the risk of developing psychotic depression increases;
- Lack of cortical regulation of the limbic system in the face of psychosocial adversity can lead to psychotic depression (Yarar, 2020).
While the exact causes are not yet fully understood, the following factors can increase a person’s chance of having a depressive episode:
- Changes in brain function, such as the insufficient activity of dopamine beta-hydroxylase
- Sleep problems
- Heart disease, cancer, and other chronic diseases
- Chronic pain
- Stressful life events such as job loss, loss of a loved one (bereavement), or psychological trauma
- Lack of personal support
Selective serotonin reuptake inhibitors (antidepressants such as Prozac and Zoloft). Usually, SSRIs are taken in reverse to improve sleep quality, but some drugs can cause insomnia, which is often a side effect.
The use of amphetamines, such as Methylin or Adderall, not only increases wakefulness but also reduces total sleep time and the time spent in REM sleep during the night.
Long-acting beta-agonists include albuterol (Ventolin, Proventil), metaproterenol (Alupent), and more. Beta-2-adrenergic agonists alone do not affect sleep unless they are associated with inhaled corticosteroids, which can cause hyperactivity and insomnia.
References
Ferreira-Garcia, R., Mochcovitch, M., Costa do Cabo, M., Nardi, A. E., & Christophe Freire, R. (2017). Predictors of pharmacotherapy response in generalized anxiety disorder: A systematic review. Harvard Review of Psychiatry, 25(2), 65–79. Web.
Kranzler, H. R., & Soyka, M. (2018). Diagnosis and pharmacotherapy of alcohol use disorder. JAMA, 320(8), 815. Web.
Yarar, E. (2020). Role and function of endocannabinoid system in major depressive disease. Medical Cannabis and Cannabinoids, 4(1), 1–12. Web.