Don’t smoke pot or you’ll get lung cancer! Right? Wrong!
Just take a look at these studies by major universities.
Smoke pot and get cancer, or just the opposite?
Preet et al. 2008. Delta9-Tetrahydrocannabinol inhibits epithelial growth factor-induced lung cancer cell migration in vitro as well as its growth and metastasis in vivo. Oncogene 10: 339-346.
- Antineoplastic activity of cannabinoid
- Munson AE, Harris LS, Friedman MA, Dewey WL, Carchman RA. Lewis lung adenocarcinoma growth was retarded by the oral administration of delta9-tetrahydrocannabinol (delta9-THC), delta8-tetrahydrocannabinol (delta8-THC), and cannabinol (CBN), but not cannabidiol (CBD). Animals treated for 10 consecutive days with delta9-THC, beginning the day after tumor implantation, demonstrated a dose-dependent action of retarded tumor growth. Mice treated for 20 consecutive days with delta8-THC and CBN had reduced primary tumor size. CBD showed no inhibitory effect on tumor growth at 14, 21, or 28 days. Delta9-THC, delta8-THC, and CBN increased the mean survival time (36% at 100 mg/kg, 25% at 200 mg/kg, and 27% at 50 mg/kg, respectively), whereas CBD did not. Delta9-THC administered orally daily until death in doses of 50, 100, or 200 mg/kg did not increase the life-spans of (C57BL/6 times DBA/2)F1 (BDF1) mice hosting the L1210 murine leukemia. However, delta9-THC administered daily for 10 days significantly inhibited Friend leukemia virus-induced splenomegaly by 71% at 200 mg/kg as compared to 90.2% for actinomycin D. Experiments with bone marrow and isolated Lewis lung cells incubated in vitro with delta9-THC and delta8-THC showed a dose-dependent (10(-4)-10(-7)) inhibition (80-20%, respectively) of tritiated thymidine and 14C-uridine uptake into these cells.
- The inhibition of DNA synthesis by cannabinoids.
- Carchman RA, Harris LS, Munson AE. Several of the cannabinoids found in marihuana have been shown to inhibit tumor growth and increase the life-span of mice bearing the Lewis lung adenocarcinoma. When trypsin-dispersed isolated Lewis lung cells are incubated in vitro, they maintain their capacity to carry out macromolecular synthesis (RNA, DNA, protein). This process can be inhibited by cytosine arabinoside, actinomycin D, or methyl-1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea, whereas cyclophosphamide, an agent that must be bioactivated, was inactive. Inhibition of DNA synthesis as measured by [3H]thymidine uptake into acid-insoluble material was used as an index of cannabinoid activity against isolated Lewis lung cells, L1210 leukemia cells, and bone marrow cells incubated in vitro delta9-, delta8-, 1-hydroxy-3-n pentyl-, and 1-delta8-tetrahydrocannabinol, and cannabinol demonstrated a dose-dependent inhibition of DNA synthesis whereas cannabidiol and 1-hydroxy-3-n-pentylcannabidiol were markedly less inhibitory in our in vitro cell systems. Furthermore, our in vitro observations with these cannabinoids are supported by in vivo tumor inhibition studies. Ring modifications as in cannabichromene or cannabicyclol abolish in vitro activity as does dihydroxylation at the 8beta and 11 positions of 1-delta9-trans-tetrahydrocannabinol. Delta9-trans-tetrahydrocannabinol demonstrated the least toxicity of all inhibitory cannabinoids in vivo; this is supported by its lesser effect on bone marrow DNA synthesis in vitro.
- Endocannabinoids in the immune system and cancer.
- Parolaro D, Massi P, Rubino T, Monti E.
Department of Structural and Functional Biology, Pharmacology Unit, University of Insubria, Via A. Da Giussano 10, Busto Arsizio (Varese), 21052, Italy The present review focuses on the role of the endogenous cannabinoid system in the modulation of immune response and control of cancer cell proliferation. The involvement of cannabinoid receptors, endogenous ligands and enzymes for their biosynthesis and degradation, as well as of cannabinoid receptor-independent events is discussed. The picture arising from the recent literature appears very complex, indicating that the effects elicited by the stimulation of the endocannabinoid system are strictly dependent on the specific compounds and cell types considered. Both the endocannabinoid anandamide and its congener palmitoylethanolamide, exert a negative action in the onset of a variety of parameters of the immune response. However, 2-arachidonoylglycerol appears to be the true endogenous ligand for peripheral cannabinoid receptors, although its action as an immunomodulatory molecule requires further characterization. Modulation of the endocannabinoid system interferes with cancer cell proliferation either by inhibiting mitogenic autocrine/paracrine loops or by directly inducing apoptosis; however, the proapoptotic effect of anandamide is not shared by other endocannabinoids and suggests the involvement of non-cannabinoid receptors, namely the VR1 class of vanilloid receptors. In conclusion, further investigations are needed to elucidate the function of endocannabinoids as immunosuppressant and antiproliferative/cytotoxic agents. The experimental evidence reviewed in this article argues in favor of the therapeutic potential of these compounds in immune disorders and cancer. Copyright 2002 Published by Elsevier Science Ltd.
All of these studies show that lungs cancers are
all susceptible to the assault of cannibinoids.
Amazing. Smoking pot can prevent lung cancer and
cannabis is also a powerful weapon against cancer.
So, how many drugs are in the testing “pipeline”
that take advantage of these wonder drugs,
found in the humble pot plant? None.
How many patients can expect to be benefitted
by everything we’ve are learning about cannibinoids?
Only those that can benefit from smoking pot,
because more effective drugs that concentrate
specific cannibinoids, for specific diseases, will
never happen in your local medical marijuana dispensary,
if you’re lucky enough to have that.
There are so many ways to medicate with cannabis
other than to smoke pot.
Until the mainstream pharmaceutical industry, with
all of it’s research and testing capacity, is let loose
on the pot plant, such highly effective medicines
will never be developed.
Of course, none of it will never happen until sweet reefer
is legal.
Or has it happened already? I’ve heard rumors that all the
Big Pharma companies have a slew of cannabis medications
all ready to test and release, as soon as they can legally do so.
Wouldn’t that be stunning. Believable, but stunning.
Fight for your right to the best medicine,
and to decide how you want to treat your illness.
Do it now, you may be the suffering patient someday!



[...] you should smoke pot even to prevent lung cancer. [...]
Bless you for trying to describe the terminlogy for the noobs!
Yes, yes keep up the good work, information is power so they say. If this is all true, someone needs to hold the damn Government accountable. How many lives could and would be saved.I think we all need to make copies of all these reports along with a copy of the US Governments patent on cannabinoids and other compounds in marijuana and demand they explain why this information has been withheld and why do we still have all the incorrect propaganda they are spewing like our drug czar calling marijuana “poison” when it’s not. I am very tired of being lied to and having beneficial information withheld. Our Government has known this information since 1975, it’s BS.
Here, here, thanks for the support Kevin and Mara