Comorbidity: Grounds for Investigation
Alcohol use and anxiety disorders are commonly comorbid, with alcoholics prone to experiencing symptoms of anxiety compared to the general population.[1] Schuckit & Hesselbrock (1994) report that 2 out of every 3 alcoholics possess the criteria to be diagnosed for another psychiatric disorder, such as anxiety.[2] There are explanations for both directions of the relationship, as people with anxiety may be using alcohol to feel better but alcohol could also lead to anxiety. In other words, anxiety disorders can cause alcohol abuse, and symptoms of anxiety are key aspects of alcohol dependence, particularly during withdrawal.[3] Although the etiology of the relationship between alcohol and anxiety is not clear, there is a link. Understanding the mechanisms behind the link between alcohol and the onset of anxiety can allow for the development of new solutions for stress and alcohol-related disorders.
ADOLESCENTS AT RISK
Alcohol is the most commonly used drug among adolescents and this cohort is also more likely to experience alcohol abuse and dependence.[4] This is significant as adolescence is an important period in brain development during which critical regions of the brain (such as the prefrontal cortex (PFC), responsible for cognition and executive functioning) are still developing.[5] This process of brain development leaves adolescents vulnerable to psychological disorders such as anxiety, and drinking alcohol could exacerbate symptoms of anxiety and/or negatively affect brain development.
UNDERSTANDING THE LINK
Several regions of the brain are implicated in the relationship between alcoholism and anxiety, particularly the PFC and the amygdala. The PFC relays information to the amygdala, which has important implications in pathologic behavior states.[6] The functional connectivity between the PFC and amygdala is crucial for several major psychological processes such as the regulation of emotions and stress. Hyperactivity and hyperreactivity of the amygdala are important measures of anxiety disorders. In particular, the central amygdala (CeA) is a primary component in the regulation of stress and anxiety. The CeA is the major output region in the amygdala and is part of the larger extended amygdala, a network of limbic forebrain structures, which is involved in the transition to alcohol dependence.[7] The CeA transforms emotional and sensory information into physiological and behavioral responses. Specifically, the signaling of the hormone corticotropin releasing factor (CRF) in the amygdala plays a significant role in anxiety as it is a prostress peptide, meaning it promotes anxiety-like behavior.[8,9] Injections of CRF into the amygdala lead to anxiety-like behaviors; therefore reducing levels of this hormone may alleviate anxiety.[10] Similarly, the CeA is a critical region involved in alcohol addiction and the negative reinforcement of alcohol abstinence.[11] Dysregulation of CRF signaling can therefore influence the development of alcoholism.
Dysfunction in the amygdala is associated with both anxiety and substance abuse disorders. Acute and chronic exposure to alcohol have significant effects on synaptic transmission (signaling between neurons) in the amygdala, a key region of stress and anxiety circuitry.[12] This commonality of the involvement of the amygdala in both anxiety and alcoholism suggests a connection between the two disorders. Alcohol has been found to increase stress sensitivity from neurological changes in the amygdala.[13] For instance, CRF is a neuropeptide involved in the stress circuits that regulate anxiety associated with drug dependence. This hormone contributes to the regulation of anxiety and alcohol-related behaviors and thus plays an important role between anxiety and the neurological effects of alcohol consumption. A study by Silberman (2009) found that the release of CRF in the CeA increases in animals that are alcohol-dependent and contributes to anxiety resulting from alcohol-withdrawal.[14] This demonstrates that CRF is the mediating factor between dependence on alcohol and anxiety produced, as drinking alcohol increases the production of CRF in the amygdala, which consequently increases stress and anxiety. CRF plays a critical role in regulating negative affect and excessive alcohol drinking via the CeA.[15] Gilpen et al. (2012) found that binge drinking in dependent and non-dependent adolescent rats produces lasting neural and behavioral changes implicated in anxiety and alcohol use disorders.[16]
IMPLICATIONS FOR SOLUTIONS
It would be beneficial for scientists to further examine the role of the amygdala in anxiety and alcohol consumption, especially in terms of seeking novel treatment options. Since anxiety is a key factor resulting from alcohol withdrawal that often leads to relapse, targeting this anxiety could prevent relapse. Pharmacologic approaches (e.g., developing drugs or medications that target CRF production) could alleviate the anxiety associated with alcohol consumption, which could help alcoholics recover rather than drinking more to alleviate anxiety; it could also prevent people from developing alcoholism by avoiding excessive drinking. Additionally, it could also prevent people from self-medicating their anxiety by consuming more alcohol. Targeting the prevention and reduction of withdrawal symptoms of alcohol consumption could be effective in treating alcoholism.
Further, since adolescents are more vulnerable to developmental neurodegeneration (both in general but also from alcohol consumption) understanding the effects of alcohol on the brain in relation to anxiety could prevent impairments in functional brain activity and cognitive dysregulation.[17] This could benefit adolescents for the rest of their lives, as neurological changes from alcohol consumption that occur during adolescence have the potential to permanently impair their psychological abilities, thus hindering the ability to achieve their goals.
If you or a friend/family member suspect you may have alcohol addiction, please reach out to a licensed mental health provider to discuss treatment options.
Contributed by: Preeti Kota
Editor: Jennifer (Ghahari) Smith, Ph.D.
REFERENCES
1 Schuckit, M. & Hesselbrock, V. (1994). Alcohol dependence and Anxiety Disorders: What is the Relationship? The American Journal of Psychiatry, 151(12), 1723-1734.
2 Ibid.
3 Gilpin, N., Herman, M., & Roberto, M. (2015). The Central Amygdala as an Integrative Hub for Anxiety and Alcohol Use Disorders. Biological Psychiatry, 77(10): 859-869. https://doi.org/10.1016/j.biopsych.2014.09.008
4 Witt, E. (2010). Research on alcohol and adolescent brain development: opportunities and future directions. Alcohol, 44(1): 119-124. https://doi.org/10.1016/j.alcohol.2009.08.011
5 Ibid.
6 Gilpin et al. (2015)
7 Ibid.
8 Ibid.
9 Silberman, Y. (2009). Neurobiological mechanisms contributing to alcohol-stress-anxiety interactions. Alcohol, 43, 509-519. doi: 10.1016/j.alcohol.2009.01.002
10 Gray, T., & Bingaman, E. (1996). The amygdala: corticotropin-releasing factor, steroids, and stress. Critical Reviews in Neurobiology, 10(2):155-68. DOI: 10.1615/critrevneurobiol.v10.i2.10
11 Silberman (2009)
12 Ibid.
13 Gilpin et al. (2015)
14 Silberman (2009)
15 Gilpin et al. (2015)
16 Gilpin, N., Karanikas, C., & Richardson, H. (2012). Adolescent Binge Drinking Leads to Changes in Alcohol Drinking, Anxiety, and Amygdalar Corticotropin Releasing Factor Cells in Adulthood in Male Rats. PLoS ONE, 7(2): e31466. doi:10.1371/journal.pone.0031466
17 Zeigler, D., Wang, C., Yoast, R., Dickinson, B., McCaffree, M., Robinowitz, C., & Sterling, M. (2005). The neurocognitive effects of alcohol on adolescents and college students. Preventive Medicine, 40(1), 23-32. https://doi.org/10.1016/j.ypmed.2004.04.044