Risks Associated With the Use of Substances - Essay Example

The Neuropharmacological Basis for the Risks Associated with the Use of Cocaine, Ecstasy, Heroin, Cannabis Teacher               The Neuropharmacological Basis for the Risks Associated with the Use of Substances Cocaine, Ecstasy, Heroin and Cannabis naturally cause deadly risks and side effects once taken continuously and in large amounts. A knowledge of the detailed function of these drugs from the neuropharmacological point of view is therefore necessary in order to emphasize their lethal effects. Risks associated with the use of Cocaine include heart attacks and strokes. These two things may lead to death. Deaths due to cocaine may also result from cardiac arrest and arrest of breathing (DrugFacts: Cocaine, 2013). The intake of cocaine in the body produces excessive neurotransmitters in the central and peripheral nervous system. This usually leads to tachycardia and vasoconstriction. Moreover, if vasoconstriction combines with platelet aggregation, there will be all sorts of cardiac complications which may occur even in the absence of a preexisting heart disease. Such cardiac-related complications also does not depend on taking massive doses of cocaine (Chakko & Myerburg, 1995). Cocaine intake can also cause risky sexual behavior (DrugFacts: Cocaine, 2013). The reasons for the increased sexual risk associated with cocaine use is usually not due to anything pharmacological but due to poverty and sexual power dynamics as well as the frequent sharing of infected needles and syringes. There is also an increased number of partners with cocaine use, the frequency of unprotected intercourse, as well as an exchange of sex for drugs or money (Ciccarone, 2011). Thus, there is increased sexual risk with the use of cocaine. Nevertheless, perhaps, as sex is often equated as a reward system, then this may actually be internally triggered by the fact that cocaine intake increases the concentrations of extracellular dopamine in the reward circuit. The human reward circuit of the CNS includes these dopamine pathways (Ciccarone, 2011). Thus, when this reward circuit is excessively and repeatedly activated through cocaine, then the frequency of desire for sex is also activated. Cocaine can also cause severe paranoia or full-blown paranoid psychosis characterized by auditory hallucinations (Cocaine Use and Its Effects, 2014). This is a result of the toxic and dysphoric effects of cocaine as brought about by escalating effective doses of the drug, or the greater amount and more efficient route of the drug. This is because as the amount of cocaine intake escalates, there are changes in brain structure such as a decrease in the volume of the frontal cortex and an enlargement of the basal ganglia, as well as consequent cognitive impairment due to these changes (Ciccarone, 2011). Cocaine can also cause kidney failure (Cocaine Use and Its Effects, 2014). This is usually due to the excessive intake of cocaine resulting in hemodynamic actions of the drug, glomerular inflammation, and glomerulosclerosis leading to renal injury. There is also an occurrence of acid-base and/or electrolyte disorders leading to the progression of kidney problems until it becomes chronic renal failure (Nzerue et al., 2000). There is also the development of atherosclerosis in renal vessels as brought about by excessive cocaine intake (Gorelick et al., 2013). Risks associated with the use of Ecstasy include high blood pressure (Problems using ecstasy, 2014). Ecstasy produces high blood pressure because of the “amphetamine-induced catecholamine and 5-HT surge” that brings about hypertension, tachycardia and hyperthermia (Hahn, 2013). Specifically, Ecstasy reduced diastolic pressure but did not have any adverse effect on systolic pressure (Bexis & Docherty, 2006). Another risk concerned with the use of Ecstasy is severe depression (Problems using ecstasy, 2014). Severe depression among Ecstasy users is usually caused by the corresponding decrease in serotonin reuptake transporter, or SERT, both in terms of function and numbers. In fact, the recovery of SERT may take up to months and there is a possibility with permanent serotonergic damage with chronic use of Ecstasy. This will then produce more or less permanent depression, panic attacks, anxiety and insomnia (Hahn, 2013). A third risk is decreased emotional control (Problems using ecstasy, 2014). Still, SERT may play a very active role in the individual’s ability to control his emotions. Lack of control may also manifest in terms of short-term memory impairment as well as difficulty in concentrating. These are all brought about by a decrease in SERT function and numbers (Hahn, 2013). One more risk is “possible nerve cell damage” (Problems using ecstasy, 2014). Nerve cell damage is also dependent on the inability of the SERT to recover from chronic use of the drug. Continual decrease of SERT function and number usually leads to permanent serotonergic damage of the terminals and axons of the nerve cell. Moreover, another effect of chronic Ecstasy use – the serotonin syndrome – may also bring about central 5-HT receptor hyperstimulation. This then results in autonomic instability and massive serotonin release (Hahn, 2013). Continual increase of these things eventually leads to damage of nerve cells. Another risk associated with Ecstasy is tachycardia, or increase in heartbeat greater than 100 beats per minute (Problems using ecstasy, 2014). Tachycardia, just like hypertension and hyperthermia, is also brought about by the “amphetamine-induced catecholamine and 5-HT surge” that brings about all three deadly conditions together (Hahn, 2013). There is also the possibility of a coma (Problems using ecstasy, 2014). The possibility of a comatose state in an Ecstasy user may actually be brought about by hyponatremia, or an abnormally low sodium count in the plasma. Water intake, physical exertion, vasopressin release will lead to the syndrome of inappropriate antidiuretic hormone secretion, or SIADH. However, this may lead to complications such as cerebral edema and seizures (Hall & Henry, 2006). Furthermore, this may lead to other complications like mental status changes and coma (Campbell & Rosner, 2008). Risks associated with the use of Heroin include negative and permanent changes in one’s cognitive function and losing the ability to make good decisions and controlling one’s impulses (Dangers of Heroin, 2014). Cognition is impaired when there is excessive intake of heroin because of the gradual organic damage of the area of the brain which governs short-term verbal memory. This usually happens when heroin intake has been for more than a year already (Mitrovic et al., 2011). Pneumonia, tuberculosis and sexually-transmitted diseases may also be immediate risks for heroin users (Dangers of Heroin, 2014). Pneumonia is seen in many users of heroin because the drug impairs airway reflexes, thus causing the body to acquire community-acquired pneumonia, aspiration pneumonia, HIV-associated pneumonia and septic pulmonary emboli (Bhaskar & Andelkovic, 2012). As for tuberculosis, the chances of acquiring this disease are all about the interplay of risk factors, the environment and the drug user. Heroin actually poses deleterious effects on the immune system, thus the cell-mediated response of the immune system is more or less impaired by the drug. Other epidemiologic factors that would bring about tuberculosis to the users of heroin include tobacco and alcohol (Deiss et al., 2009). Heroin also causes severe constipation (Dangers of Heroin, 2014). The reason for this is that excessive intake of the drug affects the autonomic nervous system and naturally affects one of its parts – the small intestine. The consequence is that the small intestines have a reduced efficiency and function, thus resulting in constipation (Heroin Addicts & Constipation, 2004). Cannabis is just as deadly as the other aforementioned three drugs. One risk associated with the use of Cannabis includes paranoia and other forms of mental or psychotic illness (The dangers of cannabis, 2014). According to a 2011 study at the University of West Ontario, cannabis intake usually acts on pathways located in the amygdala, or the part of the brain connected with the fight-or-flight response or fear. The cannabinoid pathways of the amygdala therefore activate to produce fear. However, continuous intake of marijuana may simply shut down the endocannabinoids naturally produced by the brain to reduce fear and stress. However, with claims that marijuana is becoming the popular drug of choice for post-traumatic stress disorder, or PTSD, further research on the matter is needed (Study Explains Why Marijuana Makes You Paranoid, 2014). Cannabis may also make it difficult for someone to learn and concentrate (The dangers of cannabis, 2014). Cannabis increased cerebral blood flow but long-term exposure causes the reverse – an overall reduction of blood flow in the cerebrum. What then follows is the enhanced dopaminergic neurotransmission in certain brain regions, thus affecting cognitive performance or normal behavior. Moreover, these brain regions include the cannabinoid receptors in the brain, which are mainly responsible for the modulation of learning and the maintenance of working memory and short-term memory (Shrivastava et al., 2011). Cannabis can also reduce sperm count, sperm motility and ovulation (The dangers of cannabis, 2014). Cannabis, especially delta-9-tetrahydrocannabinol, the primary cannabinoid contained in the drug, causes a disruption in the mitochondrial function of the sperm cell by altering the membrane potential of the mitochondria. This will then uncouple the electron transport and thus inhibit the synthesis of ATP leading to a reduction in sperm motility. This will therefore adversely affect male fertility (Whan et al., 2005). Cannabis may also bring about head, neck and lung cancers, as well as other forms of cancers (Armentano, 2014). Regular smoking of marijuana produces chronic cough and sputum as well as inflammation of the airways, leading to the dysregulated growth of respiratory epithelial cells that could then serve as precursors to lung cancer (Kothadia et al., 2012). The delta-tetrahydrocannabinol in marijuana binds and deactivates the human cannabinoid receptors CB1 and CB2. These receptors are actually associated with the N-arachidonoylethanolamide, or AEA. AEA binds and stimulates the production of the transient potential vanilloid receptor type 1, or TRPV1, which is actually responsible for conferring heat resistance to maturing sperm cells. Therefore, an abnormal process will result if CB1 and CB2 receptors are not functioning well (Lacson et al., 2012). Thus, in this series of pathways, one can see how cannabis can actually produce cancers associated with the reproductive system. One more risk associated with the use of cannabis is reduction in IQs (Drug Facts: Marijuana, 2014). This is, however, somehow strongly linked to the socioeconomic status of the drug user. Thus, those who are found to have lowered IQs among the cannabis users are those who already have a low socioeconomic status, poor self-control, and previous conduct problems (Rogeberg, 2013). So far, Cocaine, Ecstasy, Heroin and Cannabis cause significantly adverse effects on the body’s cells at the biomolecular level. This is evidenced by numerous researches and studies. This fact somehow makes scientists and medical experts conclude one thing about these four drugs – that they cause diseases and risk factors by attacking the cell and even the smallest biomolecular pathways that determine health at the cellular level. References Armentano, P. (2014). Cannabis Smoke and Cancer: Assessing the Risk. Retrieved from NORML: http://norml.org/component/zoo/category/cannabis-smoke-and-cancer-assessing-the-risk Bexis, S. & Docherty, J. R. (2006). 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L., McClure, N. & Lewis, S. E. M. (2005). Effects of delta-9-tetrahydrocannabinol, the primary psychoactive cannabinoid in marijuana, on human sperm in vitro. Fertility and Sterility, 85(3), 653-660. Read More