Originally posted by MORALLY SUPERIOR BEING III: The Quest for 911 Truth
In fairness, despite millions being spent trying to find a positive correlation (but not vice versa), no material increase in lung cancer has been observed in weed smokers, despite the fact that smoke is certainly slightly carcinogenic. Therefore it is logical to assume that weed does somehow help prevent lung cancer.
Lol "slightly carcinogenic"
https://www.le.ac.uk/ebulletin-archive/ebulletin/news/press-releases/2000-2009/2009/06/nparticle.2009-06-17.html“There have been many studies on the toxicity of tobacco smoke. It is known that tobacco smoke contains 4000 chemicals of which 60 are classed as carcinogens. Cannabis in contrast has not been so well studied. It is less combustible than tobacco and is often mixed with tobacco in use. Cannabis smoke contains 400 compounds including 60 cannabinoids. However, because of its lower combustibility it contains 50% more carcinogenic polycyclic aromatic hydrocarbons including naphthalene, benzanthracene, and benzopyrene, than tobacco smoke.”
The researchers add that the ability of cannabis smoke to damage DNA has significant human health implications especially as users tend to inhale more deeply than cigarette smokers, which increases respiratory burden. "The smoking of 3-4 cannabis cigarettes a day is associated with the same degree of damage to bronchial mucus membranes as 20 or more tobacco cigarettes a day," the team adds.
The argument you're talking about comes from this
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1277837/Smoke from tobacco and cannabis contains many of the same carcinogens and tumor promoters [20,21]. However, cannabis and tobacco have additional pharmacological activities, both receptor-dependent and independent, that result in different biological endpoints. Polycyclic aromatic hydrocarbons found in smoke are pro-carcinogens that are converted to carcinogens by the enzymatic activity of the cytochrome P4501A1 oxidase protein (CYP1A1 gene product). Benzo [a] pyrene is converted to its carcinogenic metabolite diol epoxide, which binds to specific hyper-mutable nucleotide sequences in the K-ras oncogene and p53 tumor suppressor [22]. Recent work by Roth et al. demonstrates that THC treatment of murine hepatoma cells caused a dose dependent increase in CYP1A1 gene transcription, while at the same time directly inhibiting the enzymatic activity of the gene product [23]. Thus, despite potentially higher levels of polycyclic aromatic hydrocarbons found in cannabis smoke compared to tobacco smoke (dependent on what part of the plant is smoked), the THC present in cannabis smoke should exert a protective effect against pro-carcinogens that require activation. In contrast, nicotine activates some CYP1A1 activities, thus potentially increasing the carcinogenic effects of tobacco smoke [24].
Also this is an interesting tidbit:
Nicotine receptors are widely distributed and are found in the epithelial cells lining respiratory passages. Cannabinoid receptors are also widely distributed, but have not been reported in respiratory epithelial cells. The differential expression of receptors may account for the apparent difference in carcinogenic activity that results from smoking tobacco compared to cannabis.
So you can see there's a clear link between marijuana and cancer even if some casual studies say otherwise. Results are pretty inconclusive. It's theorized the difference may be due to genetics.
The big idea behind weed causing cancer is that it stunts growth/kills cells by preventing the development of blood vessels needed to form a tumor. It does not stop cancers from forming in the first place. At least in theory. It's kind of hard to test in vivo.
If you're having trouble with some of the terminology above, this puts the whole thing pretty succinctly
The signal transduction pathway described above represents one means by which the carcinogenic affects of tobacco are amplified in a contrasting manner to what occurs with cannabis. The immunological effects resulting from smoking tobacco or cannabis are also distinctive and result in opposite end-points. Again, the carcinogenic potential of smoke is increased by tobacco, whereas it is uniquely reduced by the specific immune regulatory activity of cannabinoids in cannabis smoke. The introduction of hot gaseous material containing both carcinogens and particulate material into the respiratory passages produces pro-inflammatory immune responses [41]. The inflammatory state is a double-edged sword that can serve to protect or kill an organism. A functional characteristic of the pro-inflammatory state is the production of free radicals [42]. These reactive chemical species are essential armaments in the body's defense against various pathogens, in particular against intracellular parasites and bacteria. Free radicals are thought to be contributing etiological agents behind a number of pathological states [43] including cardiovascular and neuro-degenerative diseases [44], cancers, and aging in general [45]. Endocannabinoids are specific immunological homeostatic modulators when acting on "peripheral" CB2 receptors [30]. Both endo- and exo-cannabinoids push the immune system towards the relatively anti-inflammatory Th2 cytokine profile [46]. Thus, cannabinoids inhaled in cannabis smoke physiologically reduce the potential amplification of carcinogens in smoke that results from biologically produced free radicals. This response is not induced by tobacco smoke.
In conclusion, while both tobacco and cannabis smoke have similar properties chemically, their pharmacological activities differ greatly. Components of cannabis smoke minimize some carcinogenic pathways whereas tobacco smoke enhances some. Both types of smoke contain carcinogens and particulate matter that promotes inflammatory immune responses that may enhance the carcinogenic effects of the smoke. However, cannabis typically down-regulates immunologically-generated free radical production by promoting a Th2 immune cytokine profile. Furthermore, THC inhibits the enzyme necessary to activate some of the carcinogens found in smoke. In contrast, tobacco smoke increases the likelihood of carcinogenesis by overcoming normal cellular checkpoint protective mechanisms through the activity of respiratory epithelial cell nicotine receptors. Cannabinoids receptors have not been reported in respiratory epithelial cells (in skin they prevent cancer), and hence the DNA damage checkpoint mechanism should remain intact after prolonged cannabis exposure. Furthermore, nicotine promotes tumor angiogenesis whereas cannabis inhibits it. It is possible that as the cannabis-consuming population ages, the long-term consequences of smoking cannabis may become more similar to what is observed with tobacco. However, current knowledge does not suggest that cannabis smoke will have a carcinogenic potential comparable to that resulting from exposure to tobacco smoke.
It will probably be another couple decades before we can definitively tell. Note that some tobacco cancer studies were inconclusive as well. We aren't really sure exactly how the genotoxic attributes of cannabis interact with it's carcinogenic properties. I mean we know that enzyme inhibition on some cytochrome proteins may help diminish it's carcinogenic nature, but we aren't sure if it actually DOES and honestly there's no reason to believe it will protect you in full. Nobody ever said that people who consume marijuana NEVER get cancer. It would be pretty stupid to think that.
