Understanding The Neurobiological Basis Of Alcohol Use Disorder: Implications For Diagnosis And Treatment

Neurotransmitters in Alcoholism

Alcohol use disorder in the DSM-5 criteria is referred to the large amount of alcohol consumption and not able to stop the alcohol intake (American Psychiatric Association, 2013). It causes strong desire of craving and impulsivity to consume alcohol. Heavy alcohol consumption can disturb the school and work activities. With the same, it can also lead to social and interpersonal problems (APA, 2013). It is also to note that the Alcohol use disorder is related to psychological symptoms such as anxiety and other depressive symptoms (Banerjee, 2014). After abstaining from consuming alcohol, James experiences anxiety, embarrassment and depression. He faces lack of enjoyment and cognitive problems such as poor concentration. Moreover, anxiety is associated with muscular tension, psychological and physiological problems. It leads to fight and flight behaviours. Thus, avoidance of unpleasurable feeling such as being anxious, having headaches, uneasiness and some really strong craving can lead a person to drink more alcohol to alleviate (Gilpin & Koob, 2008).

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Alcohol consumption can cause neurotransmitter, physiological and psychological changes. Initially, neurotransmitter also play an important role during positive reinforcement because of the fact that dopamine activates in the limbic system and interact through the glutamate receptors (Gimeno et al., 2017). Therefore, the release of dopamine contributes pleasurable feeling. In the mesolimbic system, dopamine is neurotransmitter which projects from the ventral tegmental area to the nucleus accumbency in the brain. The excitatory neurotransmitter increases the response activation of the nerve cells and the inhibitory neurotransmitter decrease (Banerjee, 2014). However, the alcohol gives depressant effects in nervous system which can change the several neural pathways such as the reduction of excitatory neurotransmitters and the increasing of inhibitory neurotransmitter in the brain function. Alcohol has direct effect on several neurotransmitter receptors such as GABA, glutamate, endocannabinoids. With the same, it can enhance the GABA action and antagonise glutamate action; thus, these neurotransmitters are related to many types of anxiety disorders. Also, the dopamine systems can inhibit after alcohol abstain. Hence, reducing the level of dopamine is related to mood changes, depression and other psychological disorders. Therefore, alcohol dependent person can continue to seek more alcohol to attain the certain level of dopamine to get pleasure (Banerjee, 2014).

Heavy alcohol consumption is the cycle of both positive and negative reinforcement which include arousal, reward and stress (Gilpin & Koob, 2008). Passive exposure of alcohol consumption can be positively reinforced through repetitive behaviour by getting pleasure or rewards. It leads to persistent alcohol seeking behaviour even after abstinent because of the physiological and neuroadaptation in the brain function (Banerjee, 2014). Consequently, it follows negative reinforcement which is the behaviour that try to avoid un comfortable feeling such as strong craving, headaches and unease. Thus, it leads people to consume more alcohol to alleviate those symptoms. Therefore, motivational process of positive and negative reinforcement of physiological arousal, pleasurable rewards and stress can become transition to relapse and alcohol dependence. These positive and negative reinforcement behavioural process can be strengthened, based on their previous experiences (Gilpin & Koob, 2008).

Effects of Heavy Alcohol Consumption

People with alcohol dependent can elicit their automatic physiological responses to the alcohol related cue even after abstaining. This consist with classical conditioning model because its stimuli was repeatedly paired with the alcohol incentives (Drummond, Cooper & Glautier,1990).  The study conducted by Papachristou et al. (2011) show that people with heavy alcohol dependent consumer have stronger reaction to alcohol related cues than light consumers. The environmental stimuli are neutral known as unconditional stimulus (US) before pairing with alcohol (Drummond et al., 1990). However, it become conditioned stimulus (CS) even when the absence of the alcohol because it was repeatedly paired with the alcohol. Therefore, the environmental cue can elicit to the conditioned response (CR) of alcohol withdrawal. The association between CR withdrawal and relapse for the drug and alcohol use which is the behaviour that motivated by the avoidance of aversive or unpleasant feeling. Therefore, craving can lead to alcohol seeking behaviour and relapse because people tend to consume more alcohol to reduce their craving, anxiety and other unpleasurable feelings that they experience during abstaining (Drummond et al., 1990).

James no longer enjoys consuming alcohol to alleviate the symptoms of craving, headache and unease because heavy alcohol consumption is associated with stress, anxiety and depression. Consuming alcohol to alleviate fosters negative reinforcement of avoidance behaviour, because it is more than the positive reinforcement to get pleasure from the early stages of alcohol consumption (Drummond et al., 1990). Moreover, the neurotransmitter adaption involves in negative reinforcement because dopamine D2 receptors reduce in during withdrawal and abstain (George, 2013).  The study by (Uhart & Wand, 2009), the transitions of occasional drug uses to drug dependence, stress and glucocorticoids which produce to dysfunction of brain rewards systems.  Therefore, Chronic hypothalamic pituitary adrenal HPA axis dysregulation is related to anxiety disorder and depression. During alcohol or drug addiction, the high levels of stress and glucocorticoids can produce internal form of stress like anxieties behaviour. For people with alcohol abstinent and drug dependent, when they expose to stress can increase drug craving. In the stress stage, the hypothalamus, amygdala and limbic system are involved in the stress response. The hypothalamic pituitary adrenal (HPA) axis is started the corticotrophin to release from the paraventricular neurons inside the hypothalamus. Hance, the stress can activate the sympathetic adrenomedullary system to release norepinephrine and epinephrine. Therefore, these neurotransmitter and physiological functions can produce the anxiety and other stress behaviours (Uhart & Wand, 2009). Furthermore, the study by (Ruusa, Bergman, & Sundell, 2000), depression is associated with heavy alcohol consumption, patient with alcohol detoxification or abstain, they have physiological or psychological effects of abstinence even after day 1 of alcohol abstaining. Therefore, alcohol use disorder is related to stress, anxiety and other depressive symptoms which make people hate drinking because this stage of alcohol consuming is more about avoiding aversive stimuli (Drummond et al., 1990).

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Positive and Negative Reinforcement Challenges

Emotional, mental and physical relapse prevent people from quitting alcohol consumption (Melemis, 2015). People are not thinking about drinking alcohol during emotional relapse. However, they have lack of self-care which include isolating, loneliness, focusing on other problems, not having healthy diet and sleep. Emotional, psychological and physical care are needed in selfcare. People have contradictory in their mind during mental relapse stage which includes want to use alcohol or not using it. In this stage it shows craving for alcohol, thinking about alcohol related environmental cues and thinking about better control using alcohol, seeking for relapse opportunities and even planning for relapse.  Physical relapse is a person start using alcohol again (Melemis, 2015). These relapse stages are difficult to resist and lead people to consume more alcohol.

Furthermore, alcohol withdrawal can produce dopamine deficiency which can lead to depression and other psychological symptoms, therefore they are seeking more alcohol to retain the pleasurable feeling (Ruusa, Bergman, & Sundell, 2000). The relation to alcohol relapse alcohol related environmental cue can provoke intense craving even after abstaining, however, the impulsivity is also moderately interrelated for the heavy alcohol consumption (Papachristou, Nederkoorn, Havermans, Horst, & Jansen, 2011). Therefore, heavy alcohol consumers have experience of immediate positive reinforcement for the pleasure from drinking alcohol without consideration of the negative consequences. For the reason that people with heavy drinking have deficient in response inhibition such as difficulty resisting to alcohol related stimuli or the situation when the alcohol is available (Papachristou et al., 2011).  Impulsivity and alcohol related environmental cues can prevent people from quitting alcohol (Papachristou et al., 2011).

 The process of neurotransmitter adaptions, psychological and physiological terms for the symptoms people experiences after abstaining from alcohol consuming and relapse are important for the understanding of addiction and substance use disorders. This process can be researched through associated learning models that people learnt from the previous experiences, automatic response and the reinforcing behaviour. Therefore, we can further apply these principles to the implication for proper diagnosis and treatment.

References

American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Washington, D.C.  American Psychiatric Association. .

Banerjee, N. (2014). Neurotransmitters in alcoholism: A review of neurobiological and genetic studies. Indian Journal of Human Genetics, 20(1). doi: 10.4103/0971-6866.132750.

Drummond, D. C., Cooper, T., & Glautier, S. (1990). Conditioned learning in alcohol dependence: implications for cue exposure treatment. British Journal of Addiction, 85(6). doi: 10.1111/j.1360-0443.1990.tb01685.x.

George, K. (2013). Negative reinforcement in drug addiction: the darkness within. Current opinion in neurobiology, 23(4), 559-63. doi:10.1016/j.conb.2013.03.011.

Gilpin, N. W. & Koob, G. F. (2008). The Neurobiology of alcohol dependence: focus on motivational mechanisms. Alcohol research & health: the journal of the National Institute on Alcohol Abuse and Alcoholism, 31(3), 185-95.

Gimeno, C., Dorado, M. L., Roncero, C., Szerman, N., Vega, P., Martomez, V.B., & Alvarez, F. J. (2017). Treatment of Comorbid Alcohol Dependence and Anxiety Disorder: Review of the Scientific Evidence and Recommendations for Treatment. Frontiers In Psychiatry, 8(137). doi:10.3389/fpsyt.2017.00173.

Koob, G. F. (2008). A Role for Brain Stress Systems in Addiction. Neuron, 59(1), 11-34. doi:10.1016/j.neuron.2008.06.012.

Melemis, S. M. (2015). Relapse prevention and the five rules of recovery. Yale Journal of Biology and Medicine. 88(3), 325-332.

Papachristou, H., Nederkoorn, C., Havermans, R., Horst, M. V., & Jansen, A. (2011). Can’t stop the craving: The effect of impulsivity on cue-elicited craving for alcohol in heavy and light social drinkers. Psychopharmacology, 219(2), 511-518. doi:10.1007/s00213-011-2240-5.

Ruusa, J., Bergman, B., & Sundell, M. L. (2000). Alcohol Withdrawal, Psychological Symptoms, and Treatment Success. Substance Abuse, 21(3), 129-135. doi 10.1023/A:1007884316677.

Uhart, M., & Wand, G. S. (2009). Stress, alcohol and drug interaction: an update of human research. Addiction Biology, 14(1): 43–64. doi:10.1111/j.1369-1600.2008.00131.x.