09 Jul response to peer- psychopathopharmacology

Post 1-

Compare and contrast obesity as an impulsive-compulsive disorder and impulsive-compulsive disorders of behavior.

Obesity is a major global health burden associated with many different comorbidities. There are many factors associated with obesity. Psychological and behavioral factors play a major role in its development. Impulsivity is a personality trait defined as a “predisposition toward rapid, unplanned reactions to internal or external stimuli without regard to the negative consequences of these reactions to the impulsive individuals or to others” (Benard et al., 2017). The most common scale to assess impulsivity is the Barratt Impulsiveness Scale. It is a self-reporting questionnaire. Impulsive individuals tend to have rapid and unplanned reactions toward food which could be the cause to their obesity. A study has shown a significant higher impulsivity level among overweight people compared to people of normal weight (Benard et al., 2017).

Psychiatric disorders are known to be associated with clients with obesity. Obsessive-compulsive disorder (OCD) is a mental health disorder presenting as obsessive unwanted, intrusive thoughts or urges that trigger intense feelings (IOCDF, 2021). OCD may be an exception and it has been found to not be associated with obesity. OCD was found to be associated with a significantly lower rate of obesity then other conditions (Abramovitch et al., 2019). 

Neurocognitive tests have shown a correlation with weight gain and obesity. Self-reported impulsivity traits have shown a positive correlation with caloric consumption. Neurocognitive measures for impulse control, decision-making, and reward valuation are associated with eating behavior and BMI (Abromovitvh et al., 2019). Specific behaviors may contribute to weight gain through overeating or reduced physical activity. Studies have shown that overweight clients had higher scores for food-related obsessions and food-seeking compulsive behaviors than those with a normal BMI. It was found that obsessive-compulsive behaviors resulted in the intake of unhealthy food intake (MNB, 2021).

Post-2

Compare and contrast nicotine and alcohol addictions. For this discussion, emphasized the mechanism of action, receptors and any pathways involved.

Nicotine and alcohol use disorders (AUD) are both leading causes of preventable death in developed countries, causing nine million deaths worldwide. “World Health Organization (2011, 2018) state an economic burden estimated over 4% of the European GDP (EC report) and a cost of over $300 billion in the United States for tobacco addiction and $250 billion for AUD” (Morel et al., 2019). Tobacco usage and alcohol use are two behaviors that are intimately linked. As a result, persons who consume alcohol are more inclined to smoke, and vice versa. Nicotine accelerates histamine production in the gastric mucosa but not in the lungs or the skin (Stahl, 2013). Furthermore, alcohol modulates histamine synthesis, release, and turnover in the brain, affecting histamine levels. Histamine receptor antagonists can influence the compassion of nature to the hypnotic paraphernalia of alcohol and modify ethanol metabolism (Stahl, 2013). 

While drinking might be harmful to your health, smoking is far more dangerous. Tobacco usage has no benefits at any level, unlike alcohol at low or moderate amounts (Palmer et al., 2019). When you smoke, you inhale a variety of substances that can harm cells and cause cancer as well as artery damage. Some studies have found that ethanol increases the activity of nicotine-responsive brain receptors. In contrast, others have found that ethanol dampens the sensitivity of specific subtypes of the so-called nicotinic receptors (Stahl, 2013).

Nicotine directly causes dopamine release in the nucleus accumbens by binding to a4B2 nicotinic presynaptic receptors of glutamate neurons in the VTA which in turn leads to dopamine release in the nucleus accumbens. There are two types of major subtypes of nicotine receptors a4b2 subtype and the a7 subtype (Stahl, 2013). Nicotine’s action is in the ventricle. Nicotine also seems to desensitize a4b2 postsynaptic receptors on GABA interneurons in the VTA; the reduction of GABA neurotransmission disinhibits mesolimbic dopamine neurons and thus is a third mechanism for enhancing dopamine release in the nucleus accumbens, PFC, prefrontal cortex: PPT/LDT, pedunculopontine tegmental and laterodorsally tegmental nuclei (Stahl, 2013). The a4b2 nicotinic receptors adapt to a chronic intermittent pulsatile delivery of nicotine in a way that leads to addiction. Nicotine actions in the ventral tegmental area are those linked to addiction. Treating nicotine dependence is not easy (Stahl, 2013). There is evidence that nicotine addiction begins with the first cigarette, with the first dose showing signs of lasting one month. Cravings begin within a month of repeated administration (Morel et al., 2019).