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+ | ====== Smoking tobacco ====== | ||
+ | Smoking has been called "the single most preventable risk of disease" | ||
+ | * Pathogens have been detected in cigarettes.(({{pubmed> | ||
+ | * Smoking has been shown to decrease production of antimicrobial peptides. Some evidence has emerged that smoking offers sick people symptomatic relief – through immunosuppression, | ||
+ | * Sick people are less likely to quit smoking, which may artificially inflate estimate of the harmful effect of tobacco. For example, schizophrenic patients, have reported that they smoked " | ||
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+ | ===== "The single most preventable risk of disease" | ||
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+ | The World Health Organization estimates that tobacco caused 5.4 million deaths in 2004(([[http:// | ||
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+ | ===== Bacteria have been detected in cigarettes ===== | ||
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+ | {{ : | ||
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+ | Compounds in cigarettes have been said to be carcinogenic. As discussed in [[home: | ||
+ | ===== Smoking and prolonged stress decrease production of antimicrobial peptides ===== | ||
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+ | Smoking and prolonged stress have been linked to increased susceptibility to bacterial infection. A 2010 study appearing in //Cell Host and Microbe// shows that this may be caused by a decrease in antimicrobial peptide (AmP) activity as a result of increased stimulation of a neuroendocrine signalling pathway.(({{pubmed> | ||
+ | ===== Sick people are less likely to quit smoking ===== | ||
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+ | Though tobacco undoubtedly has some role in death and disease, the validity of these conclusions may not be as strong as some researchers have argued. Because conducting randomized controlled trials of tobacco users will likely never be conducted for ethical reasons, conclusions about tobacco must rely on certain statistical assumptions. Epidemiological studies of tobacco use multivariate analysis to control for any number of factors associated with likelihood of disease: education, age, ethnicity, income, gender, etc. | ||
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+ | These types of studies assume that after controlling for all these key factors, people who smoke are statistically identical to people who don't smoke. But, epidemiological models may not fully account for the fact that people who are ill (or, especially people who are more likely to become ill) are more inclined to begin smoking, and more disinclined to discontinue smoking. Some evidence has emerged that smoking offers sick people symptomatic relief – through immunosuppression, | ||
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+ | Schizophrenic patients, for example, have reported that they smoked " | ||
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+ | If people smoke for symptomatic relief, there is a possible epidemiological paradox. As the health risks associated with smoking become more well-known, the less likely any given person is to smoke because of any reason but symptomatic relief. Under these circumstances, | ||
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+ | This hypothesis deserves further exploration. | ||
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+ | ===== Smoking and Chlamydia pneumoniae ===== | ||
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+ | Smoking, an independent risk factor for cardiovascular disease, has also been shown to be an independent risk factor for //C. pneumoniae// | ||
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+ | ===== Notes and comments ===== | ||
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+ | Also should list under high 1,25-D section? | ||
+ | < | ||
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+ | Similarly, we can increase CYP3A4, another enzyme which inactivates 1,25-D. This enzyme is increased by activating the PXR receptor, for example, with minocycline or rifampin. | ||
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+ | trevor | ||
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+ | Toxicol Sci. 2009 May; | ||
+ | The aryl hydrocarbon receptor activator benzo[a]pyrene enhances vitamin D3 catabolism in macrophages.(({{pubmed> | ||
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+ | Matsunawa M, Amano Y, Endo K, Uno S, Sakaki T, Yamada S, Makishima M. | ||
+ | Division of Biochemistry, | ||
+ | Abstract | ||
+ | Benzo[a]pyrene (BaP), a polycyclic aromatic hydrocarbon produced by cigarette combustion, is implicated as a causative agent in smoking-related cancer and atherosclerosis. 1, | ||
+ | PMID: 19244278 | ||
+ | </ | ||
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+ | ===== References ===== |