The Effect of Cocaine and Cholecystokinin on One’s Appetite Essay

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.

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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 xtremely 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 dangerous affects and consequences that Cocaine has on a their body.

Cocaine, as mentioned previously, is an addictive narcotic that controls behaviors and bodily communications. It is a drug containing a countless number of defining characteristics, that make it truly unique. Before being crushed into a powder that one is able to snort or inject, Cocaine is know by its white color that is achieved from a crystalline alkaloid obtained from the coca plant’s leaves (2). This narcotic, with the chemical formula of C17 H21 NO4, goes by many names, including: crack, coke, blow, devil’s dandruff, and white dragon-with the list continuing on.

Countless names that refer to the drug that contains a countless number of effects on a human body (6). Even though there have been hundreds of names this narcotic has been given over the years, there are only a few ways of consumption that for it to be abused. This includes how it is most generally consumed, snorting, as well as when people mix the Cocaine powder with water and inject it into oneself. By doing this, the narcotic is inserted into the blood stream directly and quickly.

Yet another way to achieve the same high, only more quickly, is by “free-basing”; a form of smoking the drug in hopes for it to reach the brain instantaneously (2). In spite of the abusive uses that people do illegally, there are various uses for the drug that are done for legitimate medical treatments. These treatments include topical anesthetics from anywhere on the body, beginning with the eyes and ear drums to the mucous membranes of the respiratory system and the nose and the mouth.

Longing for the immediate high that this drug inhibits, the euphoria that is sent off quickly diminishes, resulting in the addiction that drives the need to achieve the high once again (6). The drug portrays addictive behaviors in the abusers from the enhanced levels of dopamine neurotransmitters that are sent out to certain areas of the brain (11). With that, Cocaine’s affect on the brain is much greater then just a simple release of dopamine. Dopamine is the cause for delightful feelings of pleasure, and it is with this increased “pleasure release”.

That pleasure release soon becomes a behavioral habit for many people, in turn resulting in the strong addiction countless users are unable to overcome (4). Neurons that contain dopamine receptors are located in the substantia nigra of the midbrain, and dopamine is a chemical that is secreted on a day-to-day basis which acts similarly to another chemical messenger, adrenalin. It acts in this way by allowing different sensations to be experienced throughout the body including traits like fast heart rate and feelings of well-being (1).

Not only does dopamine generate elated highs, but it is significantly important in controlling the effects of one’s physical movements, emotional responses, and unfortunately, the feeling of pain (6). Cocaine deals with psychostimulant effects that are directly linked to the inhibition of dopamine transporters, also known as DATs. The intake of dopamine from the synaptic cleft is under the control of the DATs, this means that the dopamine transporters are responsible for mediation of signaling of the release or discontinuation of the neurotransmitter, Dopamine.

It has been established that when Cocaine reaches the brain, it competitively attaches to the Dopamine transporter’s binding sites and lies on top of the areas that are normally bound to by the Dopamine substrates. What causes the reinforcement of Cocaine abuse is due to the high affinity—or attraction—Cocaine has for the Dopamine transporters. This results in an increase of extra-cellular Dopamine along with increased levels of catecholamine, which is then maintained inside the brain’s midbrain for longer then normal, allowing the sensations of euphoria to last for around thirty minutes or less—depending on the method of use (1).

Due to the constant need for the euphoric sensations that only last for, in most opinions, an unsubstantial period of time, addiction is seen to be effortlessly developed incredibly quickly. Additionally, those people who are understood to have little to no self-control, easily become excellent candidates to fall into the downward spiral that Cocaine has for a user’s future. Just this one chemical is accountable for having the ability to alter someone’s entire outlook on life, change their personality completely and lastly, modify their mental and physical health immensely (2).

The effects that addiction has on someone’s life is exactly what alters the way they live their lives, while also having a huge impact on every aspect of their life—especially their appetite. Addiction begins inside the region of the brain named the substantia nigra; a part of the midbrain that is in charge of the clusters of neurons that create the neurotransmitter discussed earlier, Dopamine (7). As the use of Cocaine is started through any of the available methods, the narcotic is instantaneously circulated throughout the blood where it then travels towards the brain.

The process of Cocaine particles attaching themselves to the Dopamine transporter binding sites occurs until the abuser reaches his desired high or until the feelings are diminished where this process is begun once again (1). Sadly, one will thrive for this elated feeling he or she just experienced; that feeling is the exact driving force behind the need for reusing this narcotic over and over again. Not to mention that there are reasons otherwise then just the high that they can acquire, yet the consequences it comes with allows an outsider to recognize a user easily.

Appetite suppression is known to be one of the biggest signs of Cocaine usage in addicts, and the weight loss that is quickly attained after using the drug daily is considerably noticeable for many(2). Unfortunately, this rapid weight loss is a popular starting point to why people even experiment with the drug in the first place. On the safer side, Cholecystokinin is the hormone that is released in the human gastrointestinal tract that controls a person’s feelings of fullness before, after and during a meal (8).

It is largely known for its affect on an individual’s appetite. Knowing more about this hormone, will allow for the discovery of whether or not both of these substances—Cholecystokinin and Cocaine—stimulate the same area of the brain or body, which in return, directly or indirectly control the intake of food and suppression of hunger. Cholecystokinin has much simpler features, compared to Cocaine, that attribute to its unique abilities of controlling ones hunger through the secretion of this hormone produced by the gastrointestinal tract.

However, this hormone is generated in both the neurons of the brain where it performs as a neuromodulator and as a neurotransmitter and in gastrointestinal tract, otherwise known as the GI, where it behaves as an intestinal hormone in hopes of slowing down gastric motility. In the GI tract, Cholecystokinin focuses on its primary target organs and functions; this includes the activation of the digesting enzymes and hormones secreted by the pancreas, contractions of the gallbladder and lastly the secretions of the parietal cells of the stomach (11).

Enzymes secreted by the pancreas include the two most popular glucagon and insulin, both are hormones that increase and decrease blood glucose levels and glycogen transport and break down during or after a meal has taken place (7). Interestingly, Cholecystokinin is among the few hormones that has the ability to function as both a neurohormone and as a neurotransmitter, at the same time (11). Even though scientists do not know for sure if CCK’s affect on one’s satiety s due to its additional existence as a neurotransmitter in the brain but they do know that the stimulus for the release of Cholecystokinin is because of the arrival of fatty acids and several amino acids into the stomach (3) . Satiety is, in general, the feelings of fullness that is directed by the hypothalamus (11). The attachment of CCKB receptors (a type of receptor of Cholecystokinin) onto the parietal cells located in the stomach are the result of the hormone’s direct relationship to the gastrin family of hormones located inside the gastrointestinal tract (9).

This means that the hormones Gastrin and Cholecystokinin share structural similarities, which in return allows Cholecystokinin to perform actions that are equivalent to what the Gastrin family executes in the GI. Some of these actions include the secretion of gastric acid—HCL, which kills the digested bacteria throughout the stomach and denatures protein structures making the enzymes released by the pancreas accessible to them (11). Throughout these characteristics, Cholecystokinin has the ability to control one’s appetite through a couple different processes that occur in the gastrointestinal tract.

The way the hormone Cholecystokinin physiologically suppresses an appetite is in reality quite simple. It begins with the intake of a “fatty” meal that will activate the gastrointestinal tract to release Cholecystokinin that soon notify one’s self to stop eating (9). The afferent vagus nerve plays a role in this process to as it controls CCK’s inhibitory actions by the innervations of vagal fibers located in the stomach and intestine (11). With that, when the Cholecystokinin receptors in the intestine are activated, they send messages about the meal’s nutritional information to the brain (9).

Being a component of the cranial nerves, the vagus is in charge of sensory and parasympathetic motor functions of most of the abdominal organs (7), as well as carrying different efferent signals specifically to the gastrointestinal tract and to the heart, as well as dealing with homeostatic responses (11). When in the presence of lipids or amino acids, enteroendocrine cells secrete the hormone Cholecystokinin. In return, it works by activating a response in its another one of its receptors—CCK1—otherwise known as CCKA located on the vagal nerve that innervates the intestinal mucosa (8).

Preceding the activation of Cholecystokinin’s receptors, signals are relayed throughout the afferent vagus nerve directly to the brainstem first. After the brainstem is reached, the message is the carried to the ventromedial nucleus of the hypothalamus in the brain. This is the area of the brain that is vastly important in satiety regulation, while the hypothalamus as a whole can control the regulation of one’s appetite (10). If the ventromedial nucleus of the hypothalamus is damaged and cannot work properly, it would consequently lead to overeating during meals and result in obesity (5).

It is thought that the hormone’s control over the suppression of one’s appetite is due to the presence of the Cholecystokinin-receptors that reside in both the brain and the gastrointestinal tract of the body. By that, it shows that without the stimulation of the hypothalamus in the brain because of the release of Cholecystokinin that is discovered in the small intestine, along with the activation of the CCK-1 receptors, messages in return would not have the ability to be sent out or maintain one’s satiety during the consumption of a meal (8).

Not only does Cholecystokinin affect a person’s control over their appetite by sending neuronal messages from the intestine to the ventromedial nucleus of the brain, but it has the capability of monitoring satiety through a different method also (10). The way it can manage satiety is by reducing the actual rate by which food is passed through a person’s stomach and entire gastrointestinal tract (5).

By the slowing of gastric movements and emptying, with the assistance of the stomach, it allows for a steady pace to be established and maintained that can then permit each reaction throughout the stomach to reach a full completion before the bolus or chyme, depending on the area of digestion, has the ability to be moved to the next section of the GI tract (3). A bolus is simply a mass of food that has not been fully digested. The bolus then turns into chyme, which is a substance with a soupy consistence produced after digestion has occurred (11).

This occurs by the same way explained earlier. When lipids or proteins have reached the small intestine, a release of the hormone Cholecystokinin is secreted by cells in the gastrointestinal tract. The release of CCK causes the gallbladder to contract, allowing for the expulsion of bile to be released into the small intestine. By the end of the contraction, additional room is created and can be opened up in the gallbladder for the addition of newly created bile, which was just manufactured by the liver, and now has the need to be stored (5).

Gallbladder contractions, or gastric peristalsis, will occur directly behind the bolus, pushing it down the gastrointestinal tract as the contractions keep the movements of the smooth muscle in the gastrointestinal tract slow and controlled. The contractions of the gallbladder play an important role because the stomach can only allow a minor amount of fat into the intestine so it is critical that Cholecystokinin can slow down the gastric motility, especially since the digestion of fats occurs much slower then the digestion of consumed carbohydrates or proteins (11).

Without the release of this specific hormone, Cholecystokinin, the world could only imagine how much more obese the people living in it would be. Yet clinically, if this could be synthetically or naturally produced into a pill one has the ability to ingest, it could help solve one of the United States’ growing problem—obesity, while it could also keep metabolic dysfunctions people experience under control. By knowing about each chemical—Cholecystokinin and Cocaine—both in the end have a slight more in common to one another then just starting with the same letter, “C”.

Both the narcotic and hormone play a part in suppressing or controlling a person’s hunger, with the exception that Cholecystokinin manages one’s appetite through direct mechanisms and Cocaine has the ability to administer this process indirectly. Through studies that were performed and the information provided, appetite suppression is in fact an outcome that is related to the usage of Cocaine, yet it is not the specific region in the brain—substantia nigra—that is to blame for the drastic weight loss of those who are addicted to the drug.

This, remember, is the area in the brain in which Dopamine receptors are bound to by the Cocaine, stimulating the affect Cocaine has on the users state of mind and body (7). It is through an indirect way that Cocaine can restrain one from feeling the need to eat a cheese burger or even fill their stomachs with a hearty meal . There were no studies that showed that with the direct usage of the narcotic, Cocaine, there would be a stimulus that would melt away fat or keep you from eating; however, it is the power of the addiction that keeps one only thinking about using Cocaine rather than considering indulging into a meal.

The addiction of the users is capable of having control over their wants and desires, and unfortunately, eating is not one of the desires that the addicted user has on his mind at any given time. Cocaine becomes their only necessity and is an indirect way of controlling their need for food and for that, anything besides the usage of this narcotic (6). With daily and constant use of the drug, addiction begins to grow more and more, becoming the uncontrollable monster within one’s mind that disregards everything besides finding a new method that allows them to reach their next better and bigger high.

Sadly, this takes over their entire lives by altering their mind, personality, and even can lead to a depressing death if it is not regulated or stopped in a timely matter. This results in risky nutritional problems including low body weight, respiratory problems and even chance of heart attack or stroke that millions who utilize this narcotic deal with everyday. So many people begin using this drug without the correct knowledge about what truly is the cause for the drastic weight loss that Cocaine provides and the long-term consequences that come with using (4).

With the direct way that Cholecystokinin provides within the areas of hunger suppression and appetite control, this could be a synthetic way that more people can exercise instead of believing that the only effective way for losing the excess weight is through the use of Cocaine. By ingesting a synthetically-made pill that has the effective hormone, Cholecystokinin, manufactured inside, it would trigger the receptors that are located in the gastrointestinal tract directly.

Through the activation of the receptors, signals would be sent through the vagus nerve and up to the hypothalamus stimulating that there is a presence of lipids or carbohydrates situated in the small intestine or stomach of a person (8). This means that if there is a presence of the hormone, the person’s brain would believe that there is food introduced into the body, relaying the message of satiety to them and keeping one from eating more then he or she should (11).

Theoretically, this may not be the healthiest way for someone to lose weight if they only took the pill and did not eat anything at all, but scientifically it is one of the most natural ways to produce the thoughts of satiety. If consumed correctly, one would also be able to consume a healthy and correct amount of food on a daily basis. Also, this is method is significantly much safer and healthier than allowing one’s body to suffer though experimenting with the dangerous affects that Cocaine posses on a user’s body. Discussion

In all, the goal of this was to discover whether or not the usage of the narcotic Cocaine and the production of the hormone Cholecystokinin in the gastrointestinal tract can both stimulate the same area in the brain or body in order to suppress one’s hunger. However it was determined through research that Cocaine, in a broader aspect, stimulates the substantia nigra in the brain for the product of a high that this narcotic releases, but it does not stimulate specifically a certain area that tells one’s brain to stop eating (7).

Nonetheless the hormone CCK that is created, activates receptors that send signals up the vagus nerve to the midbrain where then the message is relayed to the ventromedial nucleus of the hypothalamus of the brain (10). In general, this is the area of the brain that regulates a person’s appetite control in their body (7). As the creation of Cholecystokinin is manufactured, it would be able to partner with the knowledge we have already gained.

Those who have been seriously risking not only their health, but their lives as well, simply in the vain hopes of weight loss, would be able to change the strategy they were trying to envelop. This development could very well keep a countless amount of people’s lives out of the dangerous affects that Cocaine can have on their body, while instead being able to lose weight using a hormone that the body itself produces. We could consider it a form a birth control for weight; a natural hormone that is synthetically developed for the use and better control of our bodily needs.

The development of synthetically produced, and humanly regulated CCK may not end the use of Cocaine, but it may very well be a step in curbing the use of it for the triumphs of weight loss alone.

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. 2. “Cocaine” Encyclopedia Britannica. Encyclopedia Britannica Online. Encyclopedia Britannica, 2011. . ?3. “Cholecystokinin” Encyclopedia Britannica. Encyclopedia Britannica Online.

Encyclopedia Britannica, 2011. 4. Chandler, L. J. , Kalivas, P. “Brain’s defense against Cocaine: long-term exposure to Cocaine changes the organization of synaptic connections within the addiction circuitry of the brain. This process might protect against the development and persistence of addiction. ” Nature 455. 7214. 2008. Gale, Science In Context. 5. Blass, E. M. “Hunger,” in AccessScience. McGraw-Hill Companies, 2008. 6. Gregutt, P. , et al. “Cocaine. ” Gale Science In Context. Gale, 2009. AcademicOneFile. 7. Mckinley, M. P. , O’Loughlin, Valerie D.

Human Anatomy. McGraw-Hill Higher Education. 2009. 8. Montmayeur, J. P. , et al. “Fat Detection: Taste, Texture, and Post Ingestive Effects. ” Boca Raton: CRC Press; 2010. 9. Moran, T. H. “Gut peptides in the control of food intake”. Int J Obes. 2009; 33: S7-S10. 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 11. Silverthorn, D. U. , et al. Human Physiology: An Integrated Response. Pearson Education, 2010.

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