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Alcohol Abuse Disorder and Its Consequences

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Epidemic: Alcohol Abuse Disorder

Around two billion people worldwide consume alcohol with some degree of regularity. In the United States alone, the number of people suffering from Alcohol Abuse Disorder (AUD) is estimated to be around three million. It is an exceptionally damaging epidemic that leads to a variety of other health risks such as malnutrition, diabetes, and cirrhosis of the liver, to name a few (Comer, 2015). Both overdose and withdrawal can result in death; 44 percent of suicides and around 30 percent of all violent crimes committed involve alcohol use (Comer, 2015). The danger of this disorder cannot be underestimated. This article will discuss the physical, physiological, and psychological consequences of AUD and briefly identify and discuss potentially helpful treatments for sufferers.

Signs of Consequences of Alcoholism

Alcoholism can come in several shades. Individual use patterns may vary but all are prone to similar consequences. According to the DSM-5, it is a problematic pattern of alcohol use leading to clinically significant impairment or distress and there are several patterns – consistent daily use, binge drinking periods, and a combination.

It is generally signified by: consuming large amounts while having a persistent desire or unsuccessful attempts to cut down or control use, organizing lifestyle choices and activities to maximize drinking opportunities, having cravings or urges to consume alcohol, failing to meet obligations in daily life, important social or personal activities are given up in favor of maximizing drinking habits, physically hazardous use and marked tolerance resulting in increased use and withdrawal symptoms that are potentially fatal such as seizures (DSM-5, 2013).

Consequences are physical, psychological and sociological. Physical issues that are attributed to chronic use include a compromised immune system, memory disorders, malnutrition, delirium tremens (DTs) due to neurological damage, cirrhosis of the liver, coronary heart disease, insomnia and sexual dysfunction. Psychological issues include major depressive disorder, anxiety, irritability, loss of focus, will and motivation and occasionally hallucinations associated with DTs. Sociologically, alcoholism affects millions of families and friendships – not just the individuals themselves. Inability to keep promises, engagements, memories and careers causes a great deal of turbulence. Additionally, lack of impulse control, aggression and criminal history increase can tax relationships, cause car accidents and destroy self-esteem (Comer, 2015). Availability, addictability and consequences are what make alcohol the most used substance of abuse (Comer, 2015).

How Alcohol Affects the Body

Ethyl alcohol is the primary ingredient in alcoholic beverages that affects the central nervous system and various parts of the brain, specifically the neurotransmitters that mitigate depressant states and the organs of the brain that manage motor function and memory (Advokat, Comaty and Julien, 2014). Alcohol is quickly spread throughout the blood stream and evenly distributed by rapidly being absorbed through the stomach and upper intestines. Within fifteen to sixty minutes depending on the person’s size, one ounce is at its peak. Distribution through the blood-brain barrier and placenta also occurs freely and rapidly; in essence, alcohol goes everywhere. Eighty-five percent is metabolized in the liver, and fifteen percent is carried out by gastric enzymes known alcohol dehydrogenase (ADH) catalyzed by coenzymes known as nicotinamide adenine dinucleotide (NAD). These enzymes break ninety-five percent of alcohol down into acetic acid. Acetic acid is then further broken down into carbon dioxide and water burning calories and excreting the remaining five percent through respiration (Advokat, Comaty, and Julien, 2014).

Neurotransmitter pathways that are affected in the brain include GABA, dopamine (DA), serotonin (5-HT), opioid and glutamate paths. Primarily affected are depressant pathways and reward pathways and are both excitatory and inhibitory; it is these changes over chronic use periods that cause AUD to become prevalent in a person (Banerjee, 2014). GABA is affected both pre-synaptically and post-synaptically in alcoholism by antagonizing components that interfere with the GABAA receptor and stimulating or agonizing compounds on the GABAB receptors in the amygdala, ventral pallidum, and stria terminalis – areas known to aid in emotional functionality. In chronic use, these GABA receptors become permanently affected as neuroactive steroids that regulate them are agitated and increased with alcohol use (Banerjee, 2014). Depression by ethanol of NMDA receptors that release glutamate restrict areas of the amygdala, hippocampus and striatum, as well, affecting motor coordination and memory. Chronic suppression seen in AUD creates a rise in NMDA receptors that can cause substantial neurologic side effects like seizures and delirium tremens during withdrawal periods (Advokat, Comaty and Julien, 2014). These affects to the hippocampus can also cause memory loss symptoms such as delirium, Korsakoff’s Syndrome and eventual permanent dementia (Comer, 2015). Opioid pathways related to DA are targeted by ethanol and the release triggers a pleasure reward. DA pathways involve the mesolimbic system affecting motivation regulated by the nucleus accumbens (Serecigni, 2015) and affect cognitive dysfunction in the prefrontal cortex (Trantham-Davidson and Chandler, 2015). Being heavily agonized during alcohol use, dopamine then drops off exceptionally in withdrawal periods inducing craving. This rollercoaster effect can lead to major depression, general anxiety and even suicidal ideation (Banerjee, 2014; Advokat, Comaty and Julien, 2014). Finally, 5-HT receptors are also during chronic use by being depleted leading to impulsivity during drinking and a drive to relapse during withdrawal (Banerjee, 2014).

Demographic Patterns in Alcoholism

Sufferers of AUD include both sexes, all ages and all races so its consequences do as well. There are a growing number of youth, adolescent and young adult issues with drinking but AUD is difficult to diagnose as a majority of people grow out of it (Korchmaros and Stevens, 2014). That being said, 83% of college campus arrests are alcohol related and over 700,000 college students are traumatized by an alcohol related incident annually in the U.S. (Comer, 2015). Females are more likely to experience the symptoms of drunkenness more quickly due to a reduced amount of NAD coenzymes to break ethanol down, compared to men, leaving them more vulnerable in situations where alcohol abuse is prevalent (Advokat, Comety, and Julien, 2014). Caucasians and Native Americans are more affected by AUD than other races according to population to use ratios. The elderly are more prone to AUD particularly when depressed due to lack of control, feelings of burdensomeness and depression (Comer, 2015). Psychological effects of all users tend to consist of major depressive disorder, suicidal ideation, aggression, memory issues, general anxiety issues – particularly about where next drink will come from, and increased criminal history due to lack of impulse control.

Treatment Options

Treatment options for alcohol abuse disorder are limited and generally ineffective (Advokat, Comety, and Julien, 2014), but that has not stopped their research and development. A majority of existing pharmacological treatments tend to focus on managing cravings, withdrawal symptoms and side effects of AUD more than ceasing it. Some success has been seen with cessation attempts using aversion and pleasure-removing therapies such as Antebuse, naltrexone, baclofen and acomprosate but personal efficacy to quit is directly linked to success (Chithiramohan and George, 2015). However, various psychological treatments have targeted cessation such as cognitive behavioral therapies, relapse prevention training, group therapy such as Alcoholics Anonymous (AA) and treatment centers and have met with the most success when used in combination with benzodiazepines, SSRI antidepressants or cessation drugs (Korchmaros and Stevens, 2014). Finally, the use of Vitamin B3 or niacin treatments have met with some success in severe cases of chronic abuse due to the substantial malnutrition comorbidity with AUD (Prousky, 2014). Stress reduction and maintenance is seen as a proactive method of defeating AUD and was a focus of the Third International Congress in 2014 (NIH, 2014).

Limitations to treatment abound. Lack of efficacy seems to be the primary factor in failures regardless of treatment style; to quit, one must simply want to do so – everything else is an aide. The problem with Antebuse is that vomiting is not a desirable alternative to drunkenness, so the user may elect the pill unnecessary. The issues with acomprosate, baclofen and nalproxen are that they are temporary and poorly absorbed so require high-doses and, often, big price tags. SSRIs and barbiturates affect sex drive and weight gain along with other unfortunate side effects. Psychological therapies are elective and also require consistency which is not a strong suit of sufferers of AUD and Vitamin B3 is limited to helping with malnutrition and does little to subside craving (Huebner and Wolfgang Kantor, 2011). Lastly, stress is an unavoidable truth of all human beings. Stress management is not only a personal coping experience jaded by genetics, upbringing and environment but it is, in itself, difficult - drinking is not (Russell, 2002).

Final Thoughts

The consequences of Alcohol Use Disorder are far-reaching, and reprieves from the disorder are short-lived and require a great deal of willpower. The brain and body are vastly affected by alcohol and in turn, so is the human psyche. Managing symptoms and cravings is a difficult road with unfavorable likelihood of positive outcomes, but it is entirely possible with the efficacy to quit. Regardless of the current methods and lack of success, further research must be done in order to find effective methods of treating and defeating alcoholism.

References

Advokat, C.; Comaty, J.; Julien, R. (2014) Julien’s Primer of Drug Action. Worth Publishing. Pg 125-158.

APA. (2013) Diagnostic and Statistical Manual of Mental Health. 5th edition. Washington, D.C., American Psychiatric Publishing.

Beaurepaire, R. (2014) The use of very high-doses of baclofen for the treatment of alcohol dependence: a case series. Frontiers In Psychiatry, Vol. 5, Art. 143 pg. 1-5.

Banerjee, N. (2014) Neurotransmitters in alcoholism: A review of neurobiological and genetic studies. Indian Journal of Human Genetics. Jan-Mar Vol. 20, Issue 1 Pg. 20-31

Chithiramohan, A.; George, S. (2015) Pharmacological interventions for alcohol relapse prevention. International Journal of Medical Update. Vol. 10, No. 2. Pg. 41-45.

Comer, R. (2015) Substance Abuse Disorders. Abnormal Psychology. 9th Ed. pg. 385-389.

Huebner, R. and Wolfgang Kantor, L. (2011) Advances in Alcoholism Treatment. Alcohol Research and Health, Vol. 33, No. 4, pg. 295-299.

Korchmaros, J. and Stevens, S. (2014) Examination of the Role of Therapeutic Alliance, Treatment Dose and Treatment Completion in the Effectiveness of The Seven Challenges. Child Adolescent Social Work, Vol. 31, pg. 1-24.

Naqvi, N., Morgenstern, J. (2010) Cognitive Neuroscience Approaches to Understanding Behavior Change in Alcohol Use Disorder Treatment. Alcohol Research: Current Reviews, Vol. 37, no. 1 pg. 29-38.

NIH. (2014) Commentary on the Third International Congress on “Alcoholism and Stress: A Framework for Future Treatment Strategies”. Science Direct, Alcohol. Vol. 49 e1-e2.

Prousky, J. (2014) The Treatment of Alcoholism with Vitamin B3. Journal of Medicine. Vol. 29, No. 3. Pg. 123-131.

Russell, M. (2002) Heredity and The Human Condition: A Study of 20th-Century Genetic Accounts of Alcoholism. Virginia Polytech Institute and State University, Blacksburg, VA. 22 Nov 2002.

Serecigni, J. (2015) Opioid Receptor Antagonists in the Treatment of Alcoholism. Addicciones. Vol. 27, No. 3. Pg. 214-230.

Talani, G.; Lovinger, D. (2015) Interactions between ethanol and the endocannabinoid system at GABAergic synapses on basolateral amygdala principal neurons. Science Direct: Alcohol. Vol. 49, Pg. 781-794.

Trantham-Davidson, H.; Chandler, J. (2015) Alcohol-induced alterations in dopamine modulation of prefrontal activity. Science Direct: Alcohol. Vol 49. Pg. 773-779.

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