Alcoholism is both a health and social issue that needs to be regulated or treated when necessary. Although the Alcoholic Anonymous support group was founded in 1935, the issue of alcohol abuse did not capture the attention of the US government until the second half of the 20th century when they started providing funds for rigorous scientific research on the physiological and psychological mechanisms responsible for the development of the disorder (Longabaugh & Magill, 2011). Today, pharmacological research is directed towards understanding the pathophysiology of alcoholism to develop suitable treatments while psychological research aims to understand the role of external factors and their interaction with personality traits in the development of alcohol abuse.
Negative Impact of Alcohol Abuse
The World Health Organization (WHO) ranks alcohol as one of the main factors contributing to social issues and disorders in developed countries (Spangel, 2009). Besides alcoholism, irresponsible consumption can result in internal damage and disorders associated with the malfunctions of the brain, pancreas, and liver. Alcohol is also a major issue when taken during pregnancy because it results in fetal alcohol syndrome (Spangel, 2009). All age groups, ethnic groups, and social groups are at risk when it comes to alcohol abuse and its consequences (Spangel, 2009).
Physiological Effects of Alcohol
Historical research and alcoholism treatment mainly relied on studying the symptoms, withdrawal effects, physiological changes, and application of drugs for treating the condition (Heilig, Egli, Crabbe, & Becker, 2010). While drugs were often used to treat the withdrawal symptoms, it became evident that more than 70 percent of the successfully treated patients would relapse one year after treatment (Heilig et al., 2010).
With various brain mapping technologies, such as functional magnetic resonance imaging or positron emission tomography (PET), studies can also explain the neurophysiological changes that occur when people frequently consume alcohol. During the 1980s researchers found that alcohol consumption reduced the blood flow to the brain and caused morphological abnormalities in the frontal region of the brain (as cited in Moselhy, Georgiou, & Kahn, 2001).
Today, because of refined animal models and other advances in laboratory procedures and functional imaging, various studies were able to improve the understanding of alcoholism. New studies take in account the limitations of previous research and focus on long-term neural plasticity that is responsible for regulation motivational systems, which can be correlated with alcoholism development (Heilig et al., 2010).
Alcohol Consumption Motivation
There are several perspectives that attempt to explain the behavior of people who suffer from substance addiction. While alcohol is generally used as a social ritual and a substance suitable for recreational use, the main interest for alcoholic behavior explanation in research is its development. Heredity, exposure to trauma, and other psychological disorders are the most common motivators that cause the development of alcohol abuse.
Heredity. Narayanan, Stevens, Jiantonio, Krystal, and Pearlson (2013) suggest that the N-methyl-D-aspartate (NMDA) receptor’s increased function can be associated with family history of alcohol abuse, and the activity of the receptor can suggest a heritable risk to alcoholism. While the importance of genes and heredity in alcoholism risk is noteworthy, it is important to remember that like most psychological disorders, alcoholism occurs when genetic factors interact with external factors that act as triggers to stimulate addictive behavior (Spangel, 2009). Heredity also defines the individual’s resilience to external factors, so it can be correlated with alcohol abuse development.
Peer-pressure. Because peer-pressure is often the main determinant of alcohol experimentation during adolescence, people who try alcohol during adolescence will be susceptible to alcoholism during adulthood (Johnson, 2010).
Exposure to trauma. Exposure to both physical and psychological traumatic events is a trigger for the development of post-traumatic stress disorder (PTSD). PTSD is diagnosed when the patient exhibits lack of emotions and constant states of psychological arousal for at least one month. Several types of trauma exposure, including childhood victimization, sexual abuse, witnessing accidents, combat, and physical assault, were associated with the development of alcoholism (Stewart, 1996). However, those situations can only be considered triggers because resilience to external factors also partially determines the integrity and future development of the individual who experiences traumatic events.
Comorbidity. Alcohol is rarely the only disorder, but it is often present alongside of different psychological disorders. For example, the comorbidity of alcoholism and depression is well-documented, and 22.6 percent of patients who reported alcoholism suffered from life-long major depression disorder (Brown, Evans, Miller, Burgess, & Mueller, 1997). It is possible to conclude that alcoholism is often the secondary disorder when another psychological issue is present.
Diagnosis and Treatment
Alcohol abuse is defined as a heterogenous disorder, and researchers agree that alcoholism can be divided into many different subtypes (American Psychiatric Association [APA], 2000). However, the two main subtypes, which are type-A and type-B, are the most common ones used to assess the patients and create treatments (Johnson, 2010). Type-B occurs before the age of 25 and is mainly caused by peer-pressure and impulsive behavioral traits while type-A has a late onset, and is often related to psychosocial issues (Johnson, 2010).
Alcohol has a high level of comorbidity with other disorders, so treatment methods are often personalized to meet the client’s needs (Spangel, 2009). Alcoholism is treated only when it is identified as the primary disorder. For example, some patients may suffer from life-long major depression disorder, so the treatment could primarily target depression and consequently cure alcoholism.
Both pharmacological and behavioral treatments can be used together in alcoholism interventions. Various behavioral models were recently developed to improve the model of simple mediation in change, but research shows inconsistent results (Longabaugh & Magill, 2011). Further investigations are necessary to optimize the mechanisms of change in cognitive-behavioral therapy.
Conclusion
In terms of theoretical knowledge, the pathological mechanisms are well-understood. It is known that alcohol mainly alters the brain functions by reducing blood flow, and it primarily impacts the γ-aminobutyric acid A, neuronal nicotinic acetylcholine, and glycine 5-hydroxytryptamine-3 receptors (Spangel, 2009). However, further research needs to understand the patterns of alcohol effects on neurotransmitters beyond its primary targets. Long-term alcohol abuse needs further research to understand how it affects behavior by altering neurotransmitters and how long-term effects cause changes in gene expressions.
The growing body of research in the field of alcohol abuse suggests that the issue is not yet resolved, and clinical implications of theoretical findings need to be investigated. For example, researching personalized medicine is required to optimize drug treatments because different drugs and comorbid disorders can impact the effectiveness of the treatment (Johnson, 2010).
It is evident that the use of drugs to overcome withdrawal symptoms is not an effective long-term strategy (Heilig et al., 2010), so the knowledge of pathophysiological mechanisms can be used only to administer acute interventions. For long-term planning and developing lasting strategies that will correct alcoholism-related behavioral problems, researchers need to focus on studying how psychosocial support and psychological development influence the recovery in addition to behavioral or cognitive-behavioral therapy.
References
American Psychiatric Association. (2000) Diagnostic and statistical manual of mental disorders (4th ed.). Washington, D.C.: American Psychiatric Association.
Brown, R. A., Evans, D. M., Miller, I. W., Burgess, E. S., & Mueller, T. I. (1997). Cognitive-behavioral treatment for depression in alcoholism. Journal of Consulting and Clinical Psychology, 65(5), 715-726.
Heilig, M., Egli, M., Crabbe, J. C., & Becker, H. C. (2010). Acute withdrawal, protracted abstinence and negative effect in alcoholism: Are they linked? Addiction Biology, 15(2), 169-184.
Johnson, B. A. (2010). Medication treatment of different types of alcoholism. The American Journal of Psychiatry, 167(6), 630-639.
Longabaugh, R., & Magill, M. (2011). Recent advances in behavioral addiction treatments: Focusing on mechanisms of change. Current Psychiatry Reports, 13(5), 382-389.
Moselhy, H. F., Georgiou, G., & Kahn, A. (2001). Frontal lobe changes in alcoholism: A review of the literature. Alcohol and Alcoholism, 36(5), 357-368.
Narayanan, B., Stevens, M. C., Jiantonio, R. E., Krystal, J. H., & Pearlson, G. D. (2013). Effects of memantine on event-related potential, oscillations, and complexity in individuals with and without family histories of alcoholism. Journal of Studies on Alcohol and Drugs, 74(2), 245-257.
Spanagel, R. (2009). Alcoholism: a systems approach from molecular physiology to addictive behavior. Physiological Reviews, 89(2), 649-705.
Stewart, S. H. (1996). Alcohol abuse in individuals exposed to trauma: A critical review. Psychological Bulletin, 120(1), 83-112.
