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Marijuana Smokers are at a Significantly Lower Risk of Carcinogenicity - Research Proposal Example

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This paper "Marijuana Smokers are at a Significantly Lower Risk of Carcinogenicity" discusses whether marijuana should be made legal or not is widespread. In some regions of the West marijuana is distributed freely because it is thought to be harmless, even more so than tobacco…
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Marijuana Smokers are at a Significantly Lower Risk of Carcinogenicity
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Hypothesizing that Marijuana Smokers are at a Significantly Lower Risk of Carcinogeni Relative to Tobacco-Non-Marijuana Smokers Introduction The debate concerning whether marijuana should be made legal or not is widespread. In some regions of the West marijuana is distributed freely because it is thought to be harmless, even more so than tobacco. On the other hand, some states in the United States have banned marijuana, even growers with the rationale that marijuana is harmful for health. These controversies have their roots in controversial research studies on smoking marijuana and its effects. Every now and then research findings present new properties of marijuana that raise up concerns among the public for medical, social and legal reasons. There has been no conclusive results of these findings, and the effects of marijuana smoking on cancer remain hypothetical according to Chen et al (2008, p.263). For this purpose Chen et al have undertaken a study of marijuana to evaluate its carcinogenicity (the agent that causes cancer) of marijuana smoke. Their purpose is to enumerate on the effects of marijuanas usage and how its properties could be used to further medicinal development for treatment of cancer patients. The following critical evaluation of their study, shall try to assess the factors that lead to the conclusion that marijuana is not cancerous. Thesis Statement Based on Chen et als study, the following discussion shall argue that marijuana smoking does not lead to cancer. If anything it actually lowers the risk of cancer among non-tobacco smokers. Discussion Past researchers have established a link between marijuana smoking and cancer but have not been able to positively establish its effects on cancer. There are four major areas of marijuana research, which are related to cancer implications but a cohort study by Chen et al indicates that marijuana actually lowers the risk of cancer among non-tobacco smokers rather than increase it. Their understanding is based on the study results based on the following assumptions. - Marijuana contain carcinogenic PAH activation Marijuana is considered to be cancerous because of its carcinogenic property. Researches have established that carcinogenic hydrocarbons, an agent which accelerate cancer, are emitted by marijuana smoke. Carcinogenic PAHs (Polycyclic Aromatic Hydrocarbons) are active in marijuana as compared to tobacco smoke. This characteristic is considered to be the cause for influencing the levels of cannabinoids which increase the level of cancer risk. However, literature review by Chen et al (p.264) indicate that the cancer susceptibility by marijuana is non-conclusive as statistics indicate that the probability of developing cancer by marijuana smoking is less than if they smoke marijuana and not tobacco, as compared to if they smoked tobacco and not marijuana. Despite this fact Chen et al does not negate the fact that marijuana smoking does not elicit cancer as opposed to smoking tobacco which has been proven cancerous. These leads the author to the second factor related to marijuana carcinogenicity to evaluate cannabinoid resistance property of marijuana. - Cannabinoids administration Cannabinoids are a group of compounds which is present in marijuana, considered to have pharmacological effects when interact with cannabinoids receptors. This property is actually beneficial for the human bodies. When cannabinoids interact with cell membranes, they stop the growth of cancer. Whether administered locally or systematically literature indicates, with varying dosage and depending on different species, cancer cells can be stopped from progressing if they interact with cannabinoids. Cannabinoids are distributed within the body to eradicate malignant enzymes if marijuana is administered into the body. Indeed research indicates that cannabinoids can actually help control the growth of human cancers but this diagnosis is highly dependent on cell type, species, timing, dosage, serum, proteins and so on. Statistics in the cohort study (Chen et al, 2008) indicate that females smoking marijuana have less probability of developing breast cancer as compared to those who do not smoke marijuana, and those who smoke tobacco. This is perhaps why cannabinoids are popular in breast cancer treatment. It is often used by doctors of breast cancer who administer cannabinoids in patients to control the growth of cancer. Yet, these vague results do not really establish whether marijuana actually stops the growth of cancer. They merely indicate that cannabinoids do have some effects on cancerous cells, and may be further researched upon. Perhaps this is the reason why researchers are concerned about the precancerous lesions developed by marijuana. - Marijuana smokers develop precancerous lesions Literature and studies indicate that smoking marijuana leads to precancerous lesions, similar to those caused by tobacco smoke. Marijuana smoke exposes the respiratory systems to squamous metaplasia (SM) which is a precancerous epithelium lesions developed among tobacco smokers. This conclusion has been developed by tests conducted in laboratory on mice and it is considered to be valid on humans as well. This evaluation however has little implications on the conclusion that marijuana smoking is cancerous because SM and its effects are considered to be reversible and have little predictive value. Lesions are not actually cancerous at all instances. Therefore it is inconclusive to assume so when they can be developed by factors that are non-smoking related. In fact Chen et al establish that precancerous lesions are present in both tobacco and marijuana smokers. Furthermore, marijuana smoke in its natural concentrate cannot reach the lungs bronchial epithelium that easily. This leads to the conclusion that epidemiological findings are inclusive as regard to marijuana administration whether through smoke or concentrate. - Marijuana Tar Effects There is another concern which has led researchers to conclude that marijuana is cancerous. Research on mice indicates that marijuana tar from its smoke when come into contact with skin of animals produces tumors. This development is similar to those of tobacco smoke which tend to produce benign tumors when tobacco tar comes into contact with monkey skins for a prolonged period of time. On the other hand, other research indicates that marijuana smoke when in contact with skins actually slows down the growth of sarcoma among rats. This fact merely adds to the conclusion that marijuana actually retards cancer rather than increases its chances. The fact that marijuana smoke regress carcinoma of the skin is related to the tendency of cannabinoids to inhibit cancer cells from growing. Nevertheless, researchers admit that marijuana does causes lesions on the skin which indicates that marijuana tar from its smoke develop benign tumors. Conclusion What do these researches signify to the general reader? As Proctor (2004) write, "In evaluating the carcinogenicity of any type of smoke, it might help to remember that it was epidemiology, rather than animal research, that first incriminated tobacco smoke as a carcinogen" (quoted Chen et al, 2008, p. 265). Clearly none of the studies evaluated by Chen et al have any conclusive results because most of the experiments have been conducted on animals rather than humans. Animals have different health constituents, epidemiology, and are susceptible to chemicals in different ways than humans. For this reason, so far the argument that marijuana smoking results in cancer is inconclusive. The researcher agrees with Proctor that carcinogenicity experiments and evaluation should be more direct rather than indirect. There should be a direct link of the hypothesis that marijuana smoking or cannabinoids leads to carcinogenicity rather than assume its repercussions in absence of, say, tobacco or other chemicals which produces similar properties. Furthermore, the cohort study as evaluated by Chen et al indicates that the majority of marijuana studies have been based on hypothesis and generalization of cancer risk factors and its effects on humans. This is because marijuana is illegal, and any long-term study of its effects on users requires researchers to delve into the ethics of the research such as breaching privacy, illegal administration or so on. This limits the scope of studying the effects of marijuana on cancer prevention, development or inhibition. As mentioned earlier, it is epidemiology which really has value to research on marijuana and its implications on health rather than the social recreational behavior of the users. Yet, the study conducted by Chen et al (2008) merely demonstrates the statistical results of marijuana smoking and its effects on recreational users. It does not really address the cannabinoids element of marijuana, and how it could be used in epidemiological situations. These aspects lead the researcher to conclude that marijuana is not as harmful as it is thought generally. None of the research has proved anything conclusive as to marijuanas carcinogenicity or its cannabinoids consistency. The lack of epidemiologic evidence indicates that further research need to be carried out in order to fully explore the implications of marijuana, its smoke and administration in humans. Aspects that need to be addressed include human study of epidemiologic drugs, cannabinoids, marijuana tar exposure, and lesions properties among tobacco/other types of smoke and marijuana smoke. Reference Chen et al, (2008). Hypothesizing that Marijuana Smokers are at a Significantly Lower Risk of Carcinogenicity Relative to Tobacco-Non-Marijuana Smokers: Evidenced Based on Statistical Reevaluation of Current Literature. Journal of Psychoactive Drugs. Vol. 40 (3), September, pp. 263. Read More

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