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Source:
http://thecannaculturist.blogspot.ca/2011/10/marijuana-or-tobacco-smoke-which-is.html
Snip: "Researchers at the Jonsson Comprehensive Cancer Center, part of the UCLA School of Medicine, have pitted tobacco and cannabis against each other in how much they encourage cancerous growth through the activity of the enzyme
CYP1A1 in the liver. Activity of this enzyme on
*polycyclic aromatic hydrocarbons* (PAHs) has been linked to the formation of carcinogens in the body, leading to cancer. What are PAHs, you ask? Stay with me here. When we cook a steak on the grill, PAHs are formed. When we burn a campfire, we have produced PAHs. PAHs are a by-product of combustion. Unfortunately, our bodies do not take too kindly to them. Our liver metabolizes them into nastier chemicals that cause genetic mutations, even to the point of altering or halting a cell's normal apoptosis.This would ultimately lead to the development of cancer. Anyway, the researchers discovered that cannabis does exhibit far greater tar build-up (meaning more PAHs) in the lungs (because it is generally packed looser than cigarettes when smoked, cannabis smoke is typically held in the lungs longer, AND cigarettes generally have filters). The crazy thing is that the researchers found that THC found in cannabis tar reduced the effects of the PAHs in tar by inhibiting the actions of CYP1A1 ."
Study Findings Source:
http://ajrcmb.atsjournals.org/content/24/3/339.full
Snip: "In summary, we found that tar from marijuana cigarettes was more potent than tobacco tar at inducing expression of CYP1A1 in Hepa-1 cells. This enhanced effect was due to Δ9-THC, which, like conventional PAHs, acted through the aryl hydrocarbon receptor complex to increase CYP1A1 mRNA. The presence of CYP1A1 and the aryl hydrocarbon receptor complex, as well as the capacity of PAHs to induce CYP1A1, are well documented in lung epithelium and in lung cancer cells (
11,
12,
35,
36). Our studies therefore raise important questions about the role of marijuana smoking as a lung cancer risk factor. Induction of CYP1A1 by Δ9-THC could result in greater activation of smoke-related procarcinogens and contribute to the high rate of DNA damage and mucosal abnormalities observed in marijuana smokers (
2-5). However, the capacity of Δ9-THC to competitively inhibit the CYP1A1 enzyme could moderate these consequences, decreasing the production of carcinogens. The
in vivo balance between enzyme induction and competitive antagonism likely depends on many factors that were not addressed in this study. In addition, results with Hepa-1 cells may not exactly predict the regulatory effects of Δ9-THC on lung tissue. Our results support a role for Δ9-THC in promoting carcinogenesis but suggest that further testing is required in order to determine its clinical impact on lung tissue
in vivo."
*** This is way too in-depth for my brain injury to absorb, but it is apparent that a final 'conclusion' is not completed without further studies. Either way, all the above makes for an interesting read to draw your 'own' conclusions for the available data.
