Crack-cocaine, the most commonly used illicit drug worldwide due to the similar feelings of extreme euphoria caused by stimulating key pleasure centers within the brain and known for its continuous problems affecting the body and mind. In this paper, the reaction of crack cocaine in the human body and brain is explored along with how treatments can be used to solve lasting effects of usage. Crack-cocaine causes many mental and physical problems such as cardiovascular complications including myocardial inflammation and even sudden cardiac death.
Long-term effects of cocaine cause dilated cardiomyopathy, which is a condition where the heart cannot pump blood effectively and systolic dysfunction occurs, this is supported by research Cher, Shiow, Chia, Hua and Shin (2014).
To better understand crack-cocaine, it is important to know the way it effects the human body. Research done by Dinis Oliveira and Ricardo Jorge (2015) shows that symptoms of COC in the central nervous system which include euphoria, increased self-confidence and alertness at lower doses.
With higher doses aggressiveness, disorientation, and hallucinations start to show. These symptoms can persist and result in long term effects especially with repetitive use. Long term use result in the depletion of the dopamine storage that may lead to intense craving. There are also Changes not only in the brain but in physical appearances as well changes in the oral mucosa of crack cocaine users which was proven and studied by Webber et. al., 2016). The Exposure to clastogens increases abnormal germ cells and contributes to developmental effects in the fetus upon fertilization due to crack cocaine users showed higher amounts of MN (micronuclei) (Webber et al.
, 2016). The presence of MN indicates that DNA breaks and is clastogenic due to the disturbances in the mitotic spindle caused by exposure to genotoxic agents specifically crack-cocaine.
In a study done by Garcia, Torres, Balestien, Andrioli, Florio, and De Oliveria (2017A study conducted in 2017, examined the relation of if AMCE (Anhydroecgonine methyl ester) to the cocaine pyrolysis contributing to cocaine behavioral sensitization.(Garcia et al., 2017). Through this experiment, AMCE was found to not have a connection to behavioral sensitization, but is a biomarker by contributing to cocaine-induced behavioral changes and dopamine increases in brain regions involved in addiction (Garcia et al., 2017). Repetitive administration of addictive drugs shows change in the mesocorticolimbic circuitry (Garcia et al., 2017). In relation, this neural circuitry becomes hypersensitized to drug effects or drug-associated stimuli, triggering an excessive motivation for drugs, leading to the pathological dilemma of drug seeking (Garcia et al., 2017). In another research project relating to AMCE, done by Gomes, Lipaus, Martins, Araujo and Mendonca (2018), AMCE was connected, not only to behavioral sensitization, but also to impairing spatial working memory and oxidative stress (Gomes et al., 2018). Both studies utilized rats as users to analyze what happens in the brain and relate that with what happens to humans. It was found that AEME disrupted spatial long-term working memory, increased the level of AOPPs (related proteins that are damaged by oxidative stress) which is also found in diseases like Alzheimer’s. It also had an increase in GPx enzyme activity (an antioxidant enzyme) observed in the striatum after AEME exposure, involving effects at muscarinic receptors, which could be connected with the spatial working memory deficits produced by this compound(Gomes et al., 2018). As shown by both sides of the research, AMCE found that relation to cocaine use can have an effect on the brain, causing memory loss, oxidative stress and long-term changes to behavior (Gomes et al., 2018).
Crack-cocaine use has dangerous side effects. Some people are prone to addictive tendencies, they can put others at risk including young child, especially one’s inside the belly. (Harvey et al., 2001), used rabbits to show that cocaine exposed neonates displayed a permanent impairment in signal transduction of the D1 dopamine receptor which is used to regulate neuronal growth, development and mediate some behavioral responses(Harvey et al., 2001). The impairments found were located in the caudate nucleus (this is important to the development and use of language and communication skills), the frontal cortex and the cingulate cortex (Harvey et al. 2001). The issue with the D1 dopamine receptor in the caudate nucleus was shown to have behavioral consequences in that young or adult rabbits, exposed to Crack-cocaine in utero, failed to show motor responses normally seen after activation of D1 receptors in the caudate (Harvey et al., 2001). The findings of the experiment suggest that the disconnect of the D1 receptor from its G protein may be the reason of the anatomic, cognitive and motor disturbances seen in rabbits exposed to cocaine in utero (Harvey et al. 2001). The cognitive and motor deficits observed in the rabbit model are in relation with the reports indicating that persistent attentional and behavioral deficits and may be in connection to cocaine exposed children as they grow older and are more challenged to master complex cognitive tasks.
Shown briefly in the previous research study, the frontal lobe of cocaine exposed neonates were seen to have some effects on development (Harvey et al., 2001). While grown adults are not as sensitive to the effects of cocaine, but they can still be affected and cause damage to their frontal lobes which was supported by Ke, Streeter, Lowen, Nassar, Parow, Hennen and Renshaw (2003). The study did not go into the issues cocaine can have on the frontal lobe, but how to fix it within cocaine-dependent users. In heavy cocaine users it was supported by various researchers that abnormal structures were located in the frontal lobe of the brains of those who used cocaine repetitively, finding that huge chunks of grey matter are lost (Ke et al., 2003). Across the study sample a treatment for cocaine dependence appears to increase frontal lobe phosphocreatine levels by 14% and non-responding cocaine users (Ke et al., 2003) had lower baseline PCr (Phosphocreatine) levels than those of responding cocaine users. PCr is important because it helps produce a chemical in muscles known as ATP which regular cocaine users have a depletion in (Ke et al., 2003).
Another study to help cocaine users by Malvaez, McQuown, Rogge, Astarabadi, Jacques, Carreiro and Wood (2013) described that (HDAC) inhibition was shown to facilitate the extinction of drug-seeking behavior. What the experiment is conducted around is what nonspecific histone deacetylase (HDAC) is at work to aid the extinction of drug-seeking behavior. These scientists using the HDAC3 in RGFP966 (a selective inhibitor), they investigated the role of HDAC3 in extinction and found that systemic treatment with RGFP966 facilitates extinction in a manner resistant to reinstatement using mice in relation to the human mind (Malvaez et al., 2013). The results shown in the experiment was demonstrated that HDA3C inhibition facilitates extinction by enhancing the memory process and with the treatment of HDA3C inhibition resulted that a rapid and persistent extinction of cocaine use (Malvaez et al., 2013).
There are only so many treatments, that avid cocaine addicts can use. There are multiple paths to take to help the effects left from cocaine, but there are some doubts of any of them working . An example of this is a study done by Valarie prince (2018) where she linked topiramate as a treatment of cocaine use disorder. Topiramate is a medication to prevent and control seizures, also used in aid to prevent migraine headaches (Wikipedia contributors Topiramate). While this experiment did not have conclusive results due to different patients used in the study having different effects, is was shown that topiramate, when used in combination with CBT (Cognitive behavioral therapy) it may be effective in reducing short-term cocaine use (Valarie Prince, 2018). Topiramate is now considered a possible treatment option (Valarie Prince, 2018). Another research done by Xiabin, Liu, Hou, Jin, Zhang, Zheng and Zhan (2016) involves treatment by using Long-acting cocaine hydrolase for addiction therapy. The results found that highly efficient cocaine hydrolases (CocHs) can efficiently detoxify and inactivate cocaine without affecting normal functions of the CNS (Xiablin et al., 2016). A single dose of CocHs was able to accelerate cocaine metabolism in rats that were used in the experiment, even after 20 days and thus blocked cocaine-induced hyperactivity and toxicity for a long period of time (Xiablin et al., 2016). Since the general observation of that the biological split life of a protein drug is significantly longer and stronger in humans than in rodents, the CocHs reported in this study maybe start allowing dosage once every 2-4 weeks, or longer, for treatment of cocaine addiction in humans (Xiablin et al., 2016).
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