Thc Cures Cancer

sup all,

so recently ive been hearing about THC curing cancer, and i'll admit, at 1st, i was like 'YEAH RIGHT..whatever'. however, i have never been one to deny a persons right to freedom of opinion, thus i heard about this video 'Run form the cure-the rick simpson strory' and thought its would be wrong of me to just instantly assume it to be garbage.

Having watched the video last Sunday, i was very intrigued, to say the least, and simply had to find out more. Having spent numerous hours explaining to 9/11 nuts why you tube videos are NOT credible, nor reliable, sources of information, i was determined to find out if what Rick simpon said is even remotely possible. i mean even if there was just a slight inclination that THC is an effective treatment for cancer cells, thats a HUGE step for the community. Little did i know that after a few days research i have come to discover that the use of THC as an effective drug to combat cancer, is not just slightly possible, but , infact, VERY PROBABLE, indeed.

Im gonna begin by explaining some things 1st, given this is a stoner web page. Any one from either the academic or scientific community will be familar with the term 'peer review'. what this essentially means is that your work, what ever it may be, has been checked by a fellow peer, i.e any other person of equal or greater qualifications. If you think you have made an important find with in a study, you put your research paper up for peer review. which essentially gives your report an official stamp of approval.

This was my mission, to not only find clinical studies correlating THC with a cure for cancer, but that these studies are peer reviewed, and thus, are taken to be FACT, albeit with exceptions of any errors that can occur. so far i have found studies from a variety of institutions such as Journal of the National Cancer Institute, The british Journel of Cancer, The American asscosciation for cancer research,National Institute of Environmental Health Sciences and a variety of universities from all over the world including Complutense University, Spain, University of Massachusetts Medical School, Virginia Commonwealth University, Wonkwang University, Korea, University of Milan, Italy, Umea University, Sweden etc. etc

so lets get started shall we

BioMed Central | Abstract | Delta-9 tetrahydrocannabinol (THC) inhibits lytic replication of gamma oncogenic herpesviruses in vitro
THC specifically targets viral and/or cellular mechanisms required for replication and possibly shared by these gamma herpesviruses, and the endocannabinoid system is possibly involved in regulating gamma herpesvirus latency and lytic replication. The immediate early gene ORF 50 promoter activity was specifically inhibited by THC. These studies may also provide the foundation for the development of antiviral strategies utilizing non-psychoactive derivatives of THC
Peer Reviewed Results of New York State-sponsored Cancer/Marijuana Studies

A prospective pilot study of the use, of Inhalation marijuana as an antiemetic for cancer chemotherapy was conducted. Fifty-six patients who had no Improvement with standard antiemetic agents were treated and 78% demonstrated a positive response to marijuana. Younger age and prior marijuana exposure were factors that predicted response to treatment. Toxicity was mild and consisted primarily of sedation and xerostomia. This preliminary trial suggests the usefulness of Inhalation marijuana as an antiemetic agent. Because of the lack of a randomized placebo control group, the precise role of this agent is unclear. Further studies should include derivatives of this substance in combination with standard effective drugs to control chemotherapy-induced nausea and vomiting.
Oncogene - Abstract of article: [Delta]9-Tetrahydrocannabinol inhibits epithelial growth factor-induced lung cancer cell migration in vitro as well as its growth and metastasis in vivo

Tetrahydrocannabinol (THC) is the primary cannabinoid of marijuana and has been shown to either potentiate or inhibit tumor growth, depending on the type of cancer and its pathogenesis. Little is known about the activity of cannabinoids like THC on epidermal growth factor receptor-overexpressing lung cancers, which are often highly aggressive and resistant to chemotherapy. In this study, we characterized the effects of THC on the EGF-induced growth and metastasis of human non-small cell lung cancer using the cell lines A549 and SW-1573 as in vitro models. We found that these cells express the cannabinoid receptors CB1 and CB2, known targets for THC action, and that THC inhibited EGF-induced growth, chemotaxis and chemoinvasion. Moreover, signaling studies indicated that THC may act by inhibiting the EGF-induced phosphorylation of ERK1/2, JNK1/2 and AKT. THC also induced the phosphorylation of focal adhesion kinase at tyrosine 397. Additionally, in in vivo studies in severe combined immunodeficient mice, there was significant inhibition of the subcutaneous tumor growth and lung metastasis of A549 cells in THC-treated animals as compared to vehicle-treated controls. Tumor samples from THC-treated animals revealed antiproliferative and antiangiogenic effects of THC. Our study suggests that cannabinoids like THC should be explored as novel therapeutic molecules in controlling the growth and metastasis of certain lung cancers.
Control of the cell survival/death decision by can...[J Mol Med. 2001] - PubMed Result
Cannabinoids, the active components of Cannabis sativa (marijuana), and their derivatives produce a wide spectrum of central and peripheral effects, some of which may have clinical application. The discovery of specific cannabinoid receptors and a family of endogenous ligands of those receptors has attracted much attention to cannabinoids in recent years. One of the most exciting and promising areas of current cannabinoid research is the ability of these compounds to control the cell survival/death decision. Thus cannabinoids may induce proliferation, growth arrest, or apoptosis in a number of cells, including neurons, lymphocytes, and various transformed neural and nonneural cells. The variation in drug effects may depend on experimental factors such as drug concentration, timing of drug delivery, and type of cell examined. Regarding the central nervous system, most of the experimental evidence indicates that cannabinoids may protect neurons from toxic insults such as glutamaergic overstimulation, ischemia and oxidative damage. In contrast, cannabinoids induce apoptosis of glioma cells in culture and regression of malignant gliomas in vivo. Breast and prostate cancer cells are also sensitive to cannabinoid-induced antiproliferation. Regarding the immune system, low doses of cannabinoids may enhance cell proliferation, whereas high doses of cannabinoids usually induce growth arrest or apoptosis. The neuroprotective effect of cannabinoids may have potential clinical relevance for the treatment of neurodegenerative disorders such as multiple sclerosis, Parkinson's disease, and ischemia/stroke, whereas their growth-inhibiting action on transformed cells might be useful for the management of malignant brain tumors. Ongoing investigation is in search for cannabinoid-based therapeutic strategies devoid of nondesired psychotropic effects.
Biosynthesis and degradation of bioactive fatty ac...[Eur J Biochem. 1998] - PubMed Result

The endogenous cannabinoid, anandamide (arachidonoylethanolamide), and the sleep-inducing factor, oleamide (cis-9-octadecenoamide), represent two classes of long-chain fatty acid amides with several neuronal actions and metabolic pathways in common. Here we report that these two compounds are present in human breast carcinoma EFM-19 cells and rat adrenal pheochromocytoma PC-12 cells, together with the enzyme responsible for their degradation, fatty acid amide hydrolase, and the proposed biosynthetic precursors for arachidonoylethanolamide and related acylethanolamides, the N-acyl-phosphatidylethanolamines. Lipids extracted from cells labelled with [14C]ethanolamine contained radioactive compounds with the same chromatographic behaviour as arachidonoylethanolamide and acyl-PtdEtns. The levels of these compounds were not influenced by either stimulation with ionomycin in EFM-19 cells or two-week treatment with the nerve growth factor in PC-12 cells. The chemical nature of arachidonoylethanolamide, related acylethanolamides and the corresponding acyl-PtdEtns was confirmed by gas chromatographic/mass spectrometric analyses of the purified compounds, which also showed the presence of higher levels of oleamide. The latter compound, which does not activate the central CB1 cannabinoid receptor, exhibited an anti-proliferative action on EFM-19 cells at higher concentrations than arachidonoylethanolamide (IC50 = 11.3 microM for oleamide and 2.1 microM for arachidonoylethanolamide), while at a low, inactive dose it potentiated an arachidonoylethanolamide cytostatic effect. The CB1 receptor selective antagonist SR 141716A (0.5 microM) reversed the effect of both arachidonoylethanolamide and oleamide. EFM-19 cells and PC-12 cells were found to contain a membrane-bound [14C]arachidonoylethanolamide-hydrolysing activity with pH dependency and sensitivity to inhibitors similar to those previously reported for fatty acid amide hydrolase. This enzyme was inhibited by oleamide in both intact cells and cell-free preparations. The presence of transcripts of fatty acid amide hydrolase in these cells was shown by northern blot analyses of their total RNA. The rate of [14C]arachidonoylethanolamide hydrolysis by intact cells, the kinetic parameters of arachidonoylethanolamide enzymatic hydrolysis and the amounts of the fatty acid amide hydrolase transcript, were not significantly influenced by a two-week treatment with nerve growth factor and subsequent transformation of PC-12 cells into neuron-like cells. These data show for the first time that: (a) induction by nerve growth factor of a sympathetic neuronal phenotype in PC-12 cells has no effect on arachidonoylethanolamide/oleamide metabolism, (b) arachidonoylethanolamide and oleamide are autacoid suppressors of human breast cancer cell proliferation. Moreover these data lend conclusive support to the previous hypothesis that oleamide may act as an enhancer of arachidonoylethanolamide actions through competitive inhibition of its degradation.
Suppression of nerve growth factor Trk receptors a...[Endocrinology. 2000] - PubMed Result

Anandamide and 2-arachidonoylglycerol (2-AG), two endogenous ligands of the CB1 and CB2 cannabinoid receptor subtypes, inhibit the proliferation of PRL-responsive human breast cancer cells (HBCCs) through down-regulation of the long form of the PRL receptor (PRLr). Here we report that 1) anandamide and 2-AG inhibit the nerve growth factor (NGF)-induced proliferation of HBCCs through suppression of the levels of NGF Trk receptors; 2) inhibition of PRLr levels results in inhibition of the proliferation of other PRL-responsive cells, the prostate cancer DU-145 cell line; and 3) CB1-like cannabinoid receptors are expressed in HBCCs and DU-145 cells and mediate the inhibition of cell proliferation and Trk/PRLr expression. Beta-NGF-induced HBCC proliferation was potently inhibited (IC50 = 50-600 nM) by the synthetic cannabinoid HU-210, 2-AG, anandamide, and its metabolically stable analogs, but not by the anandamide congener, palmitoylethanolamide, or the selective agonist of CB2 cannabinoid receptors, BML-190. The effect of anandamide was blocked by the CB1 receptor antagonist, SR141716A, but not by the CB2 receptor antagonist, SR144528. Anandamide and HU-210 exerted a strong inhibition of the levels of NGF Trk receptors as detected by Western immunoblotting; this effect was reversed by SR141716A. When induced by exogenous PRL, the proliferation of prostate DU-145 cells was potently inhibited (IC50 = 100-300 nM) by anandamide, 2-AG, and HU-210. Anandamide also down-regulated the levels of PRLr in DU-145 cells. SR141716A attenuated these two effects of anandamide. HBCCs and DU-145 cells were shown to contain 1) transcripts for CB1 and, to a lesser extent, CB2 cannabinoid receptors, 2) specific binding sites for [3H]SR141716A that could be displaced by anandamide, and 3) a CB1 receptor-immunoreactive protein. These findings suggest that endogenous cannabinoids and CB1 receptor agonists are potential negative effectors of PRL- and NGF-induced biological responses, at least in some cancer cells.
Inhibition of rat C6 glioma cell proliferation by ...[J Pharmacol Exp Ther. 2001] - PubMed Result

The effects of the endocannabinoids anandamide (AEA) and 2-arachidonoylglycerol (2-AG) upon rat C6 glioma cell proliferation were examined and compared with a series of synthetic cannabinoids and related compounds. Cells were treated with the compounds each day and cell proliferation was monitored for up to 5 days of exposure. AEA time- and concentration-dependently inhibited C6 cell proliferation. After 4 days of treatment, AEA and 2-AG inhibited C6 cell proliferation with similar potencies (IC(50) values of 1.6 and 1.8 microM, respectively), whereas palmitoylethanolamide showed no significant antiproliferative effects at concentrations up to 10 microM. The antiproliferative effects of both AEA and 2-AG were blocked completely by a combination of antagonists at cannabinoid receptors (SR141716A and SR144528 or AM251 and AM630) and vanilloid receptors (capsazepine) as well as by alpha-tocopherol (0.1 and 10 microM), and reduced by calpeptin (10 microM) and fumonisin B(1) (10 microM), but not by L-cycloserine (1 and 100 microM). CP 55,940, JW015, olvanil, and arachidonoyl-serotonin were all found to affect C6 glioma cell proliferation (IC(50) values of 5.6, 3.2, 5.5, and 1.6 microM, respectively), but the inhibition could not be blocked by cannabinoid + vanilloid receptor antagonists. It is concluded that the antiproliferative effects of the endocannabinoids upon C6 cells are brought about by a mechanism involving combined activation of both vanilloid receptors and to a lesser extent cannabinoid receptors, and leading to oxidative stress and calpain activation. However, there is at present no obvious universal mechanism whereby plant-derived, synthetic, and endogenous cannabinoids affect cell viability and proliferation.
In vivo effects of cannabinoids on macromolecular ...[Cancer Biochem Biophys. 1977] - PubMed Result

Cannabinoids represent a novel class of drugs active in increasing the life span mice carrying Lewis lung tumors and decreasing primary tumor size. In the present studies, the effects of delta9-THC, delta8-THC, and cannabidiol on tumor macromolecular biosynthesis were studied. These drugs inhibit thymidine-3H incorporation into DNA acutely, but did not inhibit leucine uptake into tumor protein. At 24 h after treatment, cannabinoids did not inhibit thymidine-3H incorporation into DNA, leucine-3H uptake into protein or cytidine-3H into RNA.
Effects of cannabinoids on L1210 murine leukemia. ...[Res Commun Chem Pathol Pharmacol. 1977] - PubMed Result
The effect of cannabinoid derivatives on thymidine-3H uptake in L1210 murine leukemia was determined. In experiments at 200 mg/kg 3 hrs after treatment, the order of activity was delta9-tetrahydrocannabinol less than cannabinol less than cannabidiol less than abnormal cannabidiol less than 11-hydroxy-delta9-tetrahydrocannabinol less than delta8-tetrahydrocannabinol. The inhibitory effect of delta8-tetrahydrocannabinol was 99%. When animals were dosed on consecutive days with delta9-tetrahydrocannabinol and killed on the third day, thymidine-3H incorporation was increased while delta8-tetrahydrocannabinol retained its inhibitory activity under the same conditions. Delta-9-tetrahydrocannabinol and delta8-tetrahydrocannabinol inhibited RNA and protein synthesis in a fashion analagous to the inhibition of DNA synthesis

Antineoplastic activity of cannabinoids. [J Natl Cancer Inst. 1975] - PubMed Result

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 [size=20pt]71%[/size] 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. CBD was active only in high concentrations (10(-4)).
Low dose oral cannabinoid therapy reduces progress...[Nature. 2005] - PubMed Result

Atherosclerosis is a chronic inflammatory disease, and is the primary cause of heart disease and stroke in Western countries. Derivatives of cannabinoids such as delta-9-tetrahydrocannabinol (THC) modulate immune functions and therefore have potential for the treatment of inflammatory diseases. We investigated the effects of THC in a murine model of established atherosclerosis. Oral administration of THC (1 mg kg(-1) per day) resulted in significant inhibition of disease progression. This effective dose is lower than the dose usually associated with psychotropic effects of THC. Furthermore, we detected the CB2 receptor (the main cannabinoid receptor expressed on immune cells) in both human and mouse atherosclerotic plaques. Lymphoid cells isolated from THC-treated mice showed diminished proliferation capacity and decreased interferon-gamma secretion. Macrophage chemotaxis, which is a crucial step for the development of atherosclerosis, was also inhibited in vitro by THC. All these effects were completely blocked by a specific CB2 receptor antagonist. Our data demonstrate that oral treatment with a low dose of THC inhibits atherosclerosis progression in the apolipoprotein E knockout mouse model, through pleiotropic immunomodulatory effects on lymphoid and myeloid cells. Thus, THC or cannabinoids with activity at the CB2 receptor may be valuable targets for treating atherosclerosis.
Boron trifluoride etherate on silica-A modified Le...[Arch Pharm Res. 1998] - PubMed Result

Geraniol (1), olivetol (2), cannabinoids (3 and 4) and 5-fluorouracil (5) were tested for their growth inhibitory effects against human oral epitheloid carcinoma cell lines (KB) and NIH 3T3 fibroblasts using two different 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay and sulforhodamine B protein (SRB) assay. Cannabigerol (3) exhibited the highest growth-inhibitory activity against the cancer cell lines.
Antitumor effects of ajulemic acid (CT3), a synthe...[Biochem Pharmacol. 2001] - PubMed Result

One of the endogenous transformation products of tetrahydrocannabinol (THC) is THC-11-oic acid, and ajulemic acid (AJA; dimethylheptyl-THC-11-oic acid) is a side-chain synthetic analog of THC-11-oic acid. In preclinical studies, AJA has been found to be a potent anti-inflammatory agent without psychoactive properties. Based on recent reports suggesting antitumor effects of cannabinoids (CBs), we assessed the potential of AJA as an antitumor agent. AJA proved to be approximately one-half as potent as THC in inhibiting tumor growth in vitro against a variety of neoplastic cell lines. However, its in vitro effects lasted longer. The antitumor effect was stereospecific, suggesting receptor mediation. Unlike THC, however, whose effect was blocked by both CB(1) and CB(2) receptor antagonists, the effect of AJA was inhibited by only the CB(2) antagonist. Additionally, incubation of C6 glioma cells with AJA resulted in the formation of lipid droplets, the number of which increased over time; this effect was noted to a much greater extent after AJA than after THC and was not seen in WI-38 cells, a human normal fibroblast cell line. Analysis of incorporation of radiolabeled fatty acids revealed a marked accumulation of triglycerides in AJA-treated cells at concentrations that produced tumor growth inhibition. Finally, AJA, administered p.o. to nude mice at a dosage several orders of magnitude below that which produces toxicity, inhibited the growth of subcutaneously implanted U87 human glioma cells modestly but significantly. We conclude that AJA acts to produce significant antitumor activity and effects its actions primarily via CB(2) receptors. Its very favorable toxicity profile, including lack of psychoactivity, makes it suitable for chronic usage. Further studies are warranted to determine its optimal role as an antitumor agent.
A pilot clinical study of 9-tetrahydrocannabinol in patients with recurrent glioblastoma multiforme

Tetrahydrocannabinol (THC) and other cannabinoids inhibit tumour growth and angiogenesis in animal models, so their potential application as antitumoral drugs has been suggested. However, the antitumoral effect of cannabinoids has never been tested in humans. Here we report the first clinical study aimed at assessing cannabinoid antitumoral action, specifically a pilot phase I trial in which nine patients with recurrent glioblastoma multiforme were administered THC intratumoraly. The patients had previously failed standard therapy (surgery and radiotherapy) and had clear evidence of tumour progression. The primary end point of the study was to determine the safety of intracranial THC administration. We also evaluated THC action on the length of survival and various tumour-cell parameters. A dose escalation regimen for THC administration was assessed. Cannabinoid delivery was safe and could be achieved without overt psychoactive effects. Median survival of the cohort from the beginning of cannabinoid administration was 24 weeks (95% confidence interval: 15-33). Delta9-Tetrahydrocannabinol inhibited tumour-cell proliferation in vitro and decreased tumour-cell Ki67 immunostaining when administered to two patients. The fair safety profile of THC, together with its possible antiproliferative action on tumour cells reported here and in other studies, may set the basis for future trials aimed at evaluating the potential antitumoral activity of cannabinoids.
Cannabidiol as a novel inhibitor of Id-1 gene expression in aggressive breast cancer cells -- McAllister et al. 6 (11): 2921 -- Molecular Cancer Therapeutics

Invasion and metastasis of aggressive breast cancer cells is the final and fatal step during cancer progression, and is the least understood genetically. Clinically, there are still limited therapeutic interventions for aggressive and metastatic breast cancers available. Clearly, effective and nontoxic therapies are urgently required. Id-1, an inhibitor of basic helix-loop-helix transcription factors, has recently been shown to be a key regulator of the metastatic potential of breast and additional cancers. Using a mouse model, we previously determined that metastatic breast cancer cells became significantly less invasive in vitro and less metastatic in vivo when Id-1 was down-regulated by stable transduction with antisense Id-1. It is not possible at this point, however, to use antisense technology to reduce Id-1 expression in patients with metastatic breast cancer. Here, we report that cannabidiol (CBD), a cannabinoid with a low-toxicity profile, could down-regulate Id-1 expression in aggressive human breast cancer cells. The CBD concentrations effective at inhibiting Id-1 expression correlated with those used to inhibit the proliferative and invasive phenotype of breast cancer cells. CBD was able to inhibit Id-1 expression at the mRNA and protein level in a concentration-dependent fashion. These effects seemed to occur as the result of an inhibition of the Id-1 gene at the promoter level. Importantly, CBD did not inhibit invasiveness in cells that ectopically expressed Id-1. In conclusion, CBD represents the first nontoxic exogenous agent that can significantly decrease Id-1 expression in metastatic breast cancer cells leading to the down-regulation of tumor aggressiveness.

and FINALLY, to coincide with the numerous reported cases displayed in the video, the even more numerous peer reviewed studies also stipulating that THC is an effective tool in combating cancer cells i have this

Medical Marijuana: Unpublished Federal Study Found THC- Treated Rats Lived Longer, Had Less Cancer

the canadian government deined Rick simpson's petition for clinical studies on THC vs cancer, and it seems in america, they just bury the truth.

Wow bro.. thats some post man.. we have to push this .. I'm going to e mail cancer wards with this info.. there is some thing to all of this..
what we need is more clinical studies done on humans, the majority of these are on lab rats, with two exceptions. More clinical studies on humans, with a much larger sample, we need in the hundreds 1st, then hopefully in the thousands. after thet ther is no more denile.
Cannabinoid action induces autophagy-mediated cell death through stimulation of ...

...ER stress in human glioma cells

Autophagy can promote cell survival or cell death, but the molecular basis underlying its dual role in cancer remains obscure. Here we demonstrate that Δ9-tetrahydrocannabinol (THC), the main active component of marijuana, induces human glioma cell death through stimulation of autophagy. Our data indicate that THC induced ceramide accumulation and eukaryotic translation initiation factor 2α (eIF2α) phosphorylation and thereby activated an ER stress response that promoted autophagy via tribbles homolog 3–dependent (TRB3-dependent) inhibition of the Akt/mammalian target of rapamycin complex 1 (mTORC1) axis. We also showed that autophagy is upstream of apoptosis in cannabinoid-induced human and mouse cancer cell death and that activation of this pathway was necessary for the antitumor action of cannabinoids in vivo. These findings describe a mechanism by which THC can promote the autophagic death of human and mouse cancer cells and provide evidence that cannabinoid administration may be an effective therapeutic strategy for targeting human cancers.
AWESOME Post Sativaindica !!! If only humanity would just drop all the bullshit about cannabis and realize it for the wonderful gift that it is !!!-------------SS

Rolln J

whats really the pisser in all this is in 72 nixon had a study done to prove that pot is bad for you and they found out then that not only is it NOT bad for you but it that may aid curing of cancer and they suppressed that info - that is truly some fucked up shit!
whats really the pisser in all this is in 72 nixon had a study done to prove that pot is bad for you and they found out then that not only is it NOT bad for you but it that may aid curing of cancer and they suppressed that info - that is truly some fucked up shit!
Yeap they have know for along time, that's why they pharmaceutical companies jumped on board with the anti-cannabis politicians.

I think using food grade ethanol for ricks oil is safer ...

also I believe cannabis milk is very medicinal ...

Rubbig Alcohol 91% about $1.50 a quart at Wal Mart...

The Pharmaceutical companies have known this since the 1930's when Doctors were regularly using cannabis for just about everything, as well as opium and other "PLANTS." During that time the pharmaceutical companies were attempting to synthesize the active compounds so that they could patent them. Plants cannot be patented and so the birth of pharmaceuticals happened.

It will do no good to show this to the pharmaceutical companies but individuals willing to listen should be told. Spread the word through friends and family and show them the Run From the Cure videos. Show your Doctors as well. Don't allow them (doctors) to be ignorant.
Great post! Thanks for all the useful info, its crazy what people with ignore when they risk losing money. I was wondering if anyone knows how Rick Simpson makes his oil? I read the high times article on him and I saw that he ONLY uses the best flowers on the plants but does he use any different methods or is it the same as making oridinary oil, just not with the trimmings? Thnks again for the post!
Sorry guys i found it haha. I used this magical new invention called the search function and what do ya know? I found it lol. Thanks
AWESOME Post Sativaindica !!! If only humanity would just drop all the bullshit about cannabis and realize it for the wonderful gift that it is !!!-------------SS
Oh my so well sad and my feelings exactly.....when when when ???????

What a fantastic post the op has made. Thanks for all that work you have done.

God Bless you for doing that


Premium Member
Farmers, Check my post in this forum! Quite a read but Wow! What a read! guineapig is the poster..i just linked it up for you all to read! monkey5
thats some great referencing and some amazing points,

May i first point out "the big C" is not a singular disease or condition but a grouping of many undefined conditions resulting in a proliferation of cells, i.e. a tumor. the majority of cells could begin dividing at an abnormally fast rate (proliferation) resulting in a large collections of cells which may not be undertaking apoptosis (killing themselves). Now there are millions of "factors" which could be telling these cells to replicate and/or not to kill themselves. Some tumors have even been linked to viruses tricking the cells into diviiding so the virus can use the cells "machinery" to replicate itself while others have proven to be more likely faults in cell signalling processes (cytokines). YES THIS DOES REQUIRE MORE RESEARCH, YES THERE IS SOME EVIDENCE, AND NO WE CANNOT STATE ANY FACTS ABOUT THIS AT THIS TIME.

The amount of people that smoke pot is ridiculously high, all we would need to do is put clinical data together with an honestly answered questionaire on our selective intake of illicit substances and we may be able to state even better statistical information. but the problem here is human nature and fear of persecution by the relevant authorities/laws.

i really found this one of interest.........................
We're all human and are fully aware of troubles of growing up, some of us will have exhibited anger, distress, anxiety, and many more expressions of our neurology.

Cannabis useage has for a long time been some what of a "right of passage" for adolescents and I think that the quoted research above may give us some idea into why.

After reaching pubity most people go through a stage of turmoil as their frontal lobe finishes developing, this is the neurons(brain cells) sorting their shit out into a complex and diverse rationalizing machine, and is suggested to complete its task for most individuals around the age of 21/23.

this turmoil COULD likely be result of these changes and I have observed many of my peers and myself, deal with this by smoking a few doobs, after which a coversation is alot more applicable, personal offense is rarely taken, and "the pain" of the mind physically rearranging itself is alot more manageable.

Now comes the hard part..................Is this due to the inhibitory factors from the THC acting on these neurons or the general sedative effect of smoking pot?

Does this suggest the idea that pot causes mental conditions is correct? or is it the use of other substances at the same time? the statement i hear that "pot causes mental illness in later life" seems stupid to me as most these "potheads" in later life that are being referred to are from the acid/coke/pill generations and probably pushed it to the point they were on verge of a lethal dose.

The isolationism and fear of said substances pushes people who choose to do these things away from society. i think that fact is horrible to experience and is really the another persons idea being forced upon the individual which can make anyone go insane!!!

cheers guys been fun reading and ranting. x

Green Supreme

Pot Shrinks Tumors; Government Knew in '74

In 1974 researchers learned that THC, the active chemical in marijuana, shrank or destroyed brain tumors in test mice. But the DEA quickly shut down the study and destroyed its results, which were never replicated -- until now.
May 31, 2000 |

The term medical marijuana took on dramatic new meaning in February, 2000 when researchers in Madrid announced they had destroyed incurable brain tumors in rats by injecting them with THC, the active ingredient in cannabis.

The Madrid study marks only the second time that THC has been administered to tumor-bearing animals; the first was a Virginia investigation 26 years ago. In both studies, the THC shrank or destroyed tumors in a majority of the test subjects.

Most Americans don't know anything about the Madrid discovery. Virtually no major U.S. newspapers carried the story, which ran only once on the AP and UPI news wires, on Feb. 29, 2000.

The ominous part is that this isn't the first time scientists have discovered that THC shrinks tumors. In 1974 researchers at the Medical College of Virginia, who had been funded by the National Institute of Health to find evidence that marijuana damages the immune system, found instead that THC slowed the growth of three kinds of cancer in mice -- lung and breast cancer, and a virus-induced leukemia.

The DEA quickly shut down the Virginia study and all further cannabis/tumor research, according to Jack Herer, who reports on the events in his book, "The Emperor Wears No Clothes." In 1976 President Gerald Ford put an end to all public cannabis research and granted exclusive research rights to major pharmaceutical companies, who set out -- unsuccessfully -- to develop synthetic forms of THC that would deliver all the medical benefits without the "high."

The Madrid researchers reported in the March issue of "Nature Medicine" that they injected the brains of 45 rats with cancer cells, producing tumors whose presence they confirmed through magnetic resonance imaging (MRI). On the 12th day they injected 15 of the rats with THC and 15 with Win-55,212-2 a synthetic compound similar to THC. "All the rats left untreated uniformly died 12-18 days after glioma (brain cancer) cell inoculation ... Cannabinoid (THC)-treated rats survived significantly longer than control rats. THC administration was ineffective in three rats, which died by days 16-18. Nine of the THC-treated rats surpassed the time of death of untreated rats, and survived up to 19-35 days. Moreover, the tumor was completely eradicated in three of the treated rats." The rats treated with Win-55,212-2 showed similar results.

The Spanish researchers, led by Dr. Manuel Guzman of Complutense University, also irrigated healthy rats' brains with large doses of THC for seven days, to test for harmful biochemical or neurological effects. They found none.

"Careful MRI analysis of all those tumor-free rats showed no sign of damage related to necrosis, edema, infection or trauma ... We also examined other potential side effects of cannabinoid administration. In both tumor-free and tumor-bearing rats, cannabinoid administration induced no substantial change in behavioral parameters such as motor coordination or physical activity. Food and water intake as well as body weight gain were unaffected during and after cannabinoid delivery. Likewise, the general hematological profiles of cannabinoid-treated rats were normal. Thus, neither biochemical parameters nor markers of tissue damage changed substantially during the 7-day delivery period or for at least 2 months after cannabinoid treatment ended."

Guzman's investigation is the only time since the 1974 Virginia study that THC has been administered to live tumor-bearing animals. (The Spanish researchers cite a 1998 study in which cannabinoids inhibited breast cancer cell proliferation, but that was a "petri dish" experiment that didn't involve live subjects.)

In an email interview for this story, the Madrid researcher said he had heard of the Virginia study, but had never been able to locate literature on it. Hence, the Nature Medicine article characterizes the new study as the first on tumor-laden animals and doesn't cite the 1974 Virginia investigation.

"I am aware of the existence of that research. In fact I have attempted many times to obtain the journal article on the original investigation by these people, but it has proven impossible." Guzman said.

In 1983 the Reagan/Bush Administration tried to persuade American universities and researchers to destroy all 1966-76 cannabis research work, including compendiums in libraries, reports Jack Herer, who states, "We know that large amounts of information have since disappeared."

Guzman provided the title of the work -- "Antineoplastic activity of cannabinoids," an article in a 1975 Journal of the National Cancer Institute -- and this writer obtained a copy at the University of California medical school library in Davis and faxed it to Madrid.

The summary of the Virginia study begins, "Lewis lung adenocarcinoma growth was retarded by the oral administration of tetrahydrocannabinol (THC) and cannabinol (CBN)" -- two types of cannabinoids, a family of active components in marijuana. "Mice treated for 20 consecutive days with THC and CBN had reduced primary tumor size."

The 1975 journal article doesn't mention breast cancer tumors, which featured in the only newspaper story ever to appear about the 1974 study -- in the Local section of the Washington Post on August 18, 1974. Under the headline, "Cancer Curb Is Studied," it read in part:

"The active chemical agent in marijuana curbs the growth of three kinds of cancer in mice and may also suppress the immunity reaction that causes rejection of organ transplants, a Medical College of Virginia team has discovered." The researchers "found that THC slowed the growth of lung cancers, breast cancers and a virus-induced leukemia in laboratory mice, and prolonged their lives by as much as 36 percent."

Guzman, writing from Madrid, was eloquent in his response after this writer faxed him the clipping from the Washington Post of a quarter century ago. In translation, he wrote:

"It is extremely interesting to me, the hope that the project seemed to awaken at that moment, and the sad evolution of events during the years following the discovery, until now we once again Œdraw back the veil‚ over the anti-tumoral power of THC, twenty-five years later. Unfortunately, the world bumps along between such moments of hope and long periods of intellectual castration."

News coverage of the Madrid discovery has been virtually nonexistent in this country. The news broke quietly on Feb. 29, 2000 with a story that ran once on the UPI wire about the Nature Medicine article. This writer stumbled on it through a link that appeared briefly on the Drudge Report web page. The New York Times, Washington Post and Los Angeles Times all ignored the story, even though its newsworthiness is indisputable: a benign substance occurring in nature destroys deadly brain tumors.

Raymond Cushing is a journalist, musician and filmmaker. This article was named by Project Censored as a "Top Censored Story of 2000."

Peace GS