The Effect of Cocaine and Cholecystokinin on one’s Appetite.
This reviews the effect of Cocaine and Cholecystokinin in certain areas of the brain that can curve one’s appetite.
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Without having contemplated the long-term affects it may have on the body, there are many who find the use of the narcotic, Cocaine, as an effective weight loss method. Cholecystokinin, also known as CCK, is the hormone secreted in the presence of lipids in the stomach to increase satiety in one’s brain decreasing appetite (3) . By proving they both have the ability to stimulate the brain, CCK has the potential to keep one from experimenting with Cocaine, in hopes for a healthier way to lose weight. Review
One of the United States’ greatest social epidemics is the manner in which our country deals with weight loss and the epidemic of obesity. People all over the world try any and every way possible to loose their excess weight, even if their weight loss is achieved through dangerous measures. What many people do not understand is that if a person listened to the daily, naturally occurring signals their body was sending itself, the use of narcotics or self-starvation would not be necessary to achieve their goals. Unfortunately, there are too many who do not listen to the signals being sent by their bodies, and sadly result in the use and abuse of Cocaine. Cocaine is a drug of various wonders, and has the capability of affecting the brain and body in numerous ways. This includes everything from suppressing one’s hunger drastically, increasing mental awareness severely, to even creating feelings of euphoria and well being (2). With that, it is extremely easy to comprehend why Cocaine becomes such a highly addictive and habit-forming drug of choice for a countless number of people. On the other hand, the naturally-occurring hormone Cholecystokinin, secreted by the gastrointestinal tract, may positively share some resemblance with this dangerous narcotic. If this hormone was correctly manufactured synthetically and had the opportunity to be studied more closely, it has the ability become a dieters dream-drug. This is due to Cholecystokinin’s biological influence over one’s appetite (3). CCK and Cocaine both correlate with neuronal responses that are dependent upon the communication and structure of the neurons throughout an individual’s brain and body. With this type of demanding dependency upon the configuration of neurons, plasticity plays an additional role, particularly when dealing with the brain; cellular mechanisms can also alter these processes, especially if influenced correspondingly with the abuse of drugs (4). Plasticity in these circumstances deals with whether or not the brain’s stem cells can become different type of cells (11). Also, one of the most commonly known side affects associated with Cocaine is how this drug is directly related to rapid weight loss either before or after addiction (2). Cholecystokinin is the natural hormone produced by the cells of the small intestine when the presence of hydrochloric acid or fatty acids reach the duodenum or the stomach and respond by controlling the standard healthy person’s appetite (3). Yet with the use of Cocaine and its affects it has on the brain, it demonstrates a great deal of its addictive properties—creating it into a highly dangerous narcotic (4). Through the background information needed to understand the two better and the neuronal and bodily connections these chemicals are tampering with, both of them share a distinct characteristic; the ability to suppress one’s appetite by stimulating an area of the brain or body to create this reaction. By discovering that this reaction is possible, it has the opportunity to lead to a healthier and safer way for people to manage their weight loss without having to experiment with the...
Citations: 1. Beuming, T., et al. "The binding sites for Cocaine and Dopamine in the Dopamine transporter overlap." Nature Neuroscience 11.7, 2008: Academic OneFile.
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10. Sabatier, N., Leng, G. “Responses to Cholecystokinin in the ventromedial nucleus of the rat hypothalamus in vivo.” European Journal of Neuroscience 31.6. March, 2010. pp. 1127-1135
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