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    Old 12-19-2004, 12:45 AM   #1
    Ultrouvaille's Avatar
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    Marijuana & Cancer

    The hypothesis that marijuana causes cancer at any level of exposure has not been disproved, but the evidence to date does not support the claim that marijuana is "more potent than tobacco at causing cancer."

    Marijuana smoke & cannabinoids are potent inducers of cytochrome enzymes and have profound receptor-mediated effects on hydrocarbon metabolism. There is much scientific evidence favoring the induction of cytochrome enzymes for the prevention rather than the cause of PAH-related cancers. Ostensible carcinogens (viz., hydrocarbons) that induce certain cytochrome enzymes are often anti-carcinogenic against PAH-induced cancers when administered concomitantly (Conney 2003).

    If the primary concern is that the tissues exposed directly to marijuana smoke are vulnerable to malignant transformation, then relevant effects would be most evident from repeated localized application of cannabinoids directly to cancers pre-existing in tissues that receive the highest exposure from smoke (since there has never, to my knowledge, been an in vivo study to demonstrate cannabinoids or marijuana smoke induces cancer). In animal experiments in vivo, marijuana smoke devoid of cannabinoids produced dose-related antineoplastic effects, whereas tobacco smoke devoid of known carcinogens induced cancers without dimished potency.

    Cannabinoids themselves have demonstrated modest to robust anti-neoplastic effects, especially on highly aggressive malignancies (viz., lung adenocarcinoma, squamous cell carcinoma, and leukemia). Independently replicated research supports the anti-neoplastic role of cannabinoids in vivo (whether through vanilloid, CB1, or CB2 receptors, etc.).

    Cannabinoids -- esp. in vitro -- can be immunosuppressive or induce proliferation. Two uncorroborated in vivo studies (Zhu et al. 2000 & Gardner et al. 2003) demonstrated that cannabinoids promote tumor growth via immunosuppressive cannabinoid receptor ligation and COX2 elevation, respectively. These 2 studies administered cannabinoids systemically at inordinately high doses -- a route and dosage irrelevant to most marijuana smokers. Furthermore, these in vivo results are directly contradicted by those from comparable independent in vivo studies, conducted both in the US and abroad, which demonstrated that, rather than promoting, i.p. cannabinoids inhibit malignancies via CB1 & CB2 receptor ligation, respectively (Portella et al. 2003 & McKallip et al. 2002). If a substance induces tobacco-related cancers with less exposure and frequency compared with tobacco, would its primary constituents (which smokers are exposed to more so [30% of smoke] than to PAHs or nitrosamines) consistently reduce tumor volume, increase survival, or 'cure' animals bearing tumors across doses ranging from as low as 0.5 mg/kg (Portella et al. 2003) or 3 mg/kg (McKallip et al. 2002) to more than 200 mg/kg (Chan et al. 1996 & Munson et al. 1975) in vivo?

    Beyond lurid case-reports and in vitro studies, evidence of an association between marijuana smoking and aerodigestive cancer derives from small case-control studies using matched controls (Zhang et al. 1999; Sasco et al. 2002). Most (6/8) epidemiologic studies do not support the hypothesis that marijuana smoking increases the risk of developing aerodigestive cancer (Zhu et al 2002; Rosenblatt et al. 2004; Ford et al. 2001; Lewelleyn et al. 2004a; Lewelleyn et al. 2004b; Sidney et al. 1997; Zhang et al. 1999; Sasco et al. 2002). Furthermore, evidence both from larger case-control studies using random selection (Zhu et al 2002; Rosenblatt et al. 2004; Ford et al. 2001) and from the only prospective study (Sidney et al. 1997) would suggest, if anything, that marijuana smoking is associated with a reduced risk for tobacco-related cancers.

    About the Ford et al. 2001 study: Though mentioned in the foreword as one of the largest NIH-funded studies, and a negative one at that, the case-control study Ford et al. presented at the 2001 NIDA conference was the only presentation omitted from publication in the 2002 special issue of The Journal of Clinical Pharmacology on the latest marijuana research. Instead, Zhang et al.'s 1999 study was rehashed with Ford's name added to it, as if Ford et al.'s findings support a link between marijuana and cancer. In an interview with *****, Ford presented his findings just as they are posted on NIDA's web page: in sharp contrast with Zhang et al.'s. Upon my calling the study by Ford et al. to his attention, Wayne Hall, one of the leading authorities on marijuana and health, assured me it would be published soon, probably in a more specialized oncology journal (the only explanation for the conspicuous omission of Ford's own data from the very article he co-authored on the matter). In fact I have seen references to the Ford et al study as being suggestive of a link. In each case, the mislead author(s) were grateful for my calling attention to the misnomer.

    Excerpted from the Rosenblatt et al. 2004 study: Blood donors comprise a highly self-selected population likely to be depleted of individuals with high-risk lifestyle behaviors; thus, the prevalence of marijuana use by blood donor controls in Zhang et al. may have been spuriously low in comparison with what would have been observed in a group of controls that more closely reflected the source population for their cases. Alternatively, as Zhang et al. hypothesized, controls may in general underreport marijuana use to a greater extent than cases. Zhang et al. used published NHSDA estimates to show that the observed prevalence of ever marijuana use among their controls was similar to the prevalence expected in the general population. The published data from which Zhang et al. calculated expected numbers, however, excluded persons who had initiated marijuana use after 20 years of age whereas the observed number of users among their controls included individuals who had used marijuana regardless of the age at initiation. We recalculated the sex- and birth cohort-adjusted expected prevalence of ever marijuana use among controls in Zhang et al. without the exclusion based on age at initiation (using publicly available NHSDA data for individuals who were 18 years old in 19921994). The expected number of ever marijuana users was 40.6, whereas only 17 users were observed. If a similar deficit was not present among the HNSCC cases in Zhang et al., some or all of the 2.6-fold association with marijuana use they observed would be due to a spuriously low exposure prevalence among their controls. The results of similar calculations performed for our control group showed no difference in the observed and expected number of ever marijuana users.

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