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Alcohol Consumption and its Effects on Neurotransmitter Adaptations, Psychological and Physiological Symptoms, Relapse and Treatment

   

Added on  2023-04-23

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ALCOHOL CONSUMPTION
Alcohol Consumption
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ALCOHOL CONSUMPTION
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).
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
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ALCOHOL CONSUMPTION
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).
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, &
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