Marijuana Gateway to Health: How Cannabis Protects Us from Cancer and Alzheimer's Disease

Marijuana reduces users' risks for developing cancer, diabetes and Alzheimer's disease because THC and other cannabinoids produced by the plant effectively reduce the harmful inflammation and oxidative damage that promote these ailments. Yes, it is true, marijuana smokers have significantly lower rates of bladder cancer, lung cancer, head and neck cancer, lymphoma, other cancers, Type 1 and 2 diabetes, age and injury-related dementia. That is why we need to discard last century's reefer madness myths and deal with science. And the science indicates that we should begin promoting adult marijuana use to reduce human misery and save health-care costs. We also see that marijuana protects the brains of binge drinkers from the damage caused by alcohol and that alcohol promotes dating violence while marijuana does not. In medical marijuana states, traffic accident fatalities plunged following implementation of the laws. Suicides also dropped significantly. Let's stop this sadistic insanity of ruining marijuana users' and growers' lives by arresting them. Arrest causes far more trauma and damage to both the individual and society than marijuana use ever could. Being arrested for marijuana devastates one's finances, sense of security, respect for the authority of law, employment status and opportunity, autonomy and generates untold levels of stress, stress promotes inflammation and inflammation promotes the diseases that marijuana use fights. Being arrested and jailed or imprisoned also subjects one to psychological brutalization and possible physical and sexual abuse. All for using a plant that causes laughter, hunger and discourages diseases formation? That is immoral.

Clint Werner at the San Francisco Public Library

Marijuana has anti-tumor properties and prevents the brain from injury and aging, according to local author Clint Werner. The Main Library's Business, Science & Technology Center presented this evening with the acclaimed activist on January 22, 2014 while he was promoting "Marijuana Gateway to Health."

The impact of marijuana use on glucose, insulin, and insulin resistance among US adults. [Am J Med. 2013] - PubMed - NCBI

Sometimes I just want to hold my head and weep at the terrible suffering caused by marijuana prohibition (pretty much every day). I'm looking at a study and it really is clear that using marijuana is one of the best things a diabetic can do for their health. The cannabinoids in marijuana seem to protect the pancreatic insulin-producing cells and improve glucose metabolism. Diabetics need marijuana products, NOW! They don't have time to wait for big pharma to produce an over-priced cannabis treatment. Start telling your diabetic friends and family to support legalization so that they can grow their best medicine, after insulin, for free and make it into tincture, oil or capsules.

Link: http://www.ncbi.nlm.nih.gov/pubmed/23684393

Delta9-tetrahydrocannabinol (THC) can reduce brain damage from stroke 2007

This study presents further evidence that THC can protect the brain following a stroke.

CONCLUSIONS AND IMPLICATIONS:

Our findings demonstrate that AM 404 and THC reduce neuronal damage caused by bilateral carotid occlusion in gerbils and that this protection is mediated through an interaction with CB1 and opioid receptors. Endocannabinoids might form the basis for the development of new neuroprotective drugs useful for the treatment of stroke and other neurodegenerative pathologies.

Marijuana's THCA relieves nausea

Nonpsychoactive THCA from unheated marijuana reduced nausea in lab animals more effectively than THC (from heated marijuana), legalize! How many dealers sell THCA? None. Support dispensary rights.

Br J Pharmacol. 2013 Jul 25. doi: 10.1111/bph.12316. [Epub ahead of print]

Tetrahydrocannabinolic acid reduces nausea-induced conditioned gaping in rats and vomiting in Suncus murinus.

Rock E, Kopstick R, Limebeer C, Parker L.

Source

Department of Psychology, University of Guelph, Guelph, ON, Canada.

Abstract

BACKGROUD AND PURPOSE:

We evaluated the anti-emetic and anti-nausea properties of the acid precursor of Δ9 -tetrahydrocannabinol (THC), tetrahydrocannabinolic acid (THCA), and to determine its mechanism of action in these animal models.

EXPERIMENTAL APPROACH:

We investigated the effect of THCA on lithium chloride- (LiCl) induced conditioned gaping (nausea-induced behaviour) to a flavour, and context (a model of anticipatory nausea, AN) in rats, and on LiCl-induced vomiting in Suncus murinus. Furthermore, we investigated THCA's ability to induce hypothermia and suppress locomotion [rodent tasks to assess cannabinoid1 (CB1 ) receptor agonist-like activity], and measured plasma and brain THCA and THC levels. We also determined whether THCA's effect could be blocked by pretreatment with SR141716 (SR, a CB1 receptor antagonist).

KEY RESULTS:

In rats, THCA (0.05 and/or 0.5 mg/kg) suppressed LiCl-induced conditioned gaping to a flavour and context; the latter effect blocked by the CB1 receptor antagonist, SR, but not by the 5-HT1A receptor antagonist, WAY100635. In S. murinus, THCA (0.05 and 0.5 mg/kg) reduced LiCl-induced vomiting; an effect that was reversed with SR. A comparatively low dose of THC (0.05 mg/kg) did not suppress conditioned gaping to a LiCl-paired flavour or context. THCA did not induce hypothermia or reduce locomotion, indicating non-CB1 agonist-like effects. THCA, but not THC was detected in plasma samples.

CONCLUSIONS AND IMPLICATIONS:

THCA potently reduced conditioned gaping in rats and vomiting in S. murinus; effects that were blocked by SR.. These data suggest that THCA may be a more potent alternative to THC in the treatment of nausea and vomiting.

via Tetrahydrocannabinolic acid reduces nausea-in... [Br J Pharmacol. 2013] - PubMed - NCBI.

Marijuana increases positivity

A just-published study found that THC from marijuana increased activity for positive emotional content. Marijuana enhances happiness which could explain the enormous drop in suicides, especially among young adult men, in medical marijuana states.

Eur Neuropsychopharmacol. 2013 Aug 5. pii: S0924-977X(13)00195-8. doi: 10.1016/j.euroneuro.2013.06.009. [Epub ahead of print]

The endocannabinoid system and emotional processing: A pharmacological fMRI study with ∆9-tetrahydrocannabinol.

Bossong MG, van Hell HH, Jager G, Kahn RS, Ramsey NF, Jansma JM. Abstract

Various psychiatric disorders such as major depression are associated with abnormalities in emotional processing. Evidence indicating involvement of the endocannabinoid system in emotional processing, and thus potentially in related abnormalities, is increasing. In the present study, we examined the role of the endocannabinoid system in processing of stimuli with a positive and negative emotional content in healthy volunteers. A pharmacological functional magnetic resonance imaging (fMRI) study was conducted with a placebo-controlled, cross-over design, investigating effects of the endocannabinoid agonist ∆9-tetrahydrocannabinol (THC) on brain function related to emotional processing in 11 healthy subjects. Performance and brain activity during matching of stimuli with a negative ('fearful faces') or a positive content ('happy faces') were assessed after placebo and THC administration. After THC administration, performance accuracy was decreased for stimuli with a negative but not for stimuli with a positive emotional content. Our task activated a network of brain regions including amygdala, orbital frontal gyrus, hippocampus, parietal gyrus, prefrontal cortex, and regions in the occipital cortex. THC interacted with emotional content, as activity in this network was reduced for negative content, while activity for positive content was increased. These results indicate that THC administration reduces the negative bias in emotional processing. This adds human evidence to support the hypothesis that the endocannabinoid system is involved in modulation of emotional processing. Our findings also suggest a possible role for the endocannabinoid system in abnormal emotional processing, and may thus be relevant for psychiatric disorders such as major depression.

via The endocannabinoid system and emot... [Eur Neuropsychopharmacol. 2013] - PubMed - NCBI.

Cannabinoids Decrease the Th17 Infla... [J Neuroimmune Pharmacol. 2013] - PubMed - NCBI

Marijuana's cannabinoids improve human health by reducing systemic inflammation which is a root cause for many degenerative diseases. J Neuroimmune Pharmacol. 2013 Jul 28. [Epub ahead of print]

Cannabinoids Decrease the Th17 Inflammatory Autoimmune Phenotype.

Kozela E, Juknat A, Kaushansky N, Rimmerman N, Ben-Nun A, Vogel Z.

Source

The Dr Miriam and Sheldon G. Adelson Center for the Biology of Addictive Diseases, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel, ewa.kozela@weizmann.ac.il.

Abstract

Cannabinoids, the Cannabis constituents, are known to possess anti-inflammatory properties but the mechanisms involved are not understood. Here we show that the main psychoactive cannabinoid, Δ-9-tetrahydrocannabinol (THC), and the main nonpsychoactive cannabinoid, cannabidiol (CBD), markedly reduce the Th17 phenotype which is known to be increased in inflammatory autoimmune pathologies such as Multiple Sclerosis. We found that reactivation by MOG35-55 of MOG35-55-specific encephalitogenic T cells (cells that induce Experimental Autoimmune Encephalitis when injected to mice) in the presence of spleen derived antigen presenting cells led to a large increase in IL-17 production and secretion. In addition, we found that the cannabinoids CBD and THC dose-dependently (at 0.1-5 μM) suppressed the production and secretion of this cytokine. Moreover, the mRNA and protein of IL-6, a key factor in Th17 induction, were also decreased. Pretreatment with CBD also resulted in increased levels of the anti-inflammatory cytokine IL-10. Interestingly, CBD and THC did not affect the levels of TNFα and IFNγ. The downregulation of IL-17 secretion by these cannabinoids does not seem to involve the CB1, CB2, PPARγ, 5-HT1A or TRPV1 receptors. In conclusion, the results show a unique cannabinoid modulation of the autoimmune cytokine milieu combining suppression of the pathogenic IL-17 and IL-6 cytokines along with boosting the expression of the anti-inflammatory cytokine IL-10.

via Cannabinoids Decrease the Th17 Infla... [J Neuroimmune Pharmacol. 2013] - PubMed - NCBI.

Marijuana Use Reduces Obesity » Marijuana Gateway to Health

Marijuana use is significantly protective against obesity as well as the harmful illnesses that accompany the syndrome. This is because THC and other cannabinoids work as systemic biological health regulators, the are key to our ability to survive and thrive. We really do need to encourage more adults to use marijuana in some form to improve their health and guard against degenerative illnesses. Science continues to affirm this position.                       Med Hypotheses. 2013 Feb 11. Cannabis and Δ9-tetrahydrocannabinol THC for weight loss?Le Foll B, Trigo JM, et al.Abstract: Obesity is one of the highest preventable causes of morbidity and mortality in the developed world [1]. It has been well known for a long time that exposure to cannabis produces an increase of appetite a phenomenon referred to as the ‘munchies’. This phenomenon led to an exploration of the role of the endocannabinoid system in the regulation of obesity and associated metabolic syndrome. This effort subsequently led to the development of a successful therapeutic approach for obesity that consisted of blocking the cannabinoid CB1 receptors using ligands such as Rimonabant in order to produce weight loss and improve metabolic profile [2]. Despite being efficacious, Rimonabant was associated with increased rates of depression and anxiety and therefore removed from the market. We recently discovered that the prevalence of obesity is paradoxically much lower in cannabis users as compared to non-users and that this difference is not accounted for by tobacco smoking status and is still present after adjusting for variables such as sex and age. Here, we propose that this effect is directly related to exposure to the Δ9-tetrahydrocannabinol THC present in cannabis smoke. We therefore propose the seemingly paradoxical hypothesis that THC or a THC/cannabidiol combination drug may produce weight loss and may be a useful therapeutic for the treatment of obesity and its complications.via Cannabis and Δ9-tetrahydrocannabinol THC … [Med Hypotheses. 2013] – PubMed – NCBI. via Marijuana Use Reduces Obesity » Marijuana Gateway to Health.

Marijuana's cannabinoids protect the brain from Alzheimer's disease

Here is more evidence that THC and CBD, cannabinoids from marijuana, can effectively protect us from the damage that leads to the development of Alzheimer's disease as well as other neurological ailments. The cannabinoid THC stimulates both the CB1 and CB2 receptors, but the cannabinoid CBD steers THC away from the CB1 receptor and over to the CB2 receptors, thus possibly activating the neuroprotective effects described in this study. With the trillion dollar threat that Alzheimer's disease poses to our national health care budget, isn't it critical that we recruit more adults to use some form of marijuana? Tell you friends and family that the most effective thing they can do to protect themselves from Alzheimer's disease is to start using cannabis--either smoking or vaporizing a small amount a few times a week, or taking some drops of a cannabis tincture before bedtime or eating a low-dose edible. What we want to do is increase the regular consumption of cannabinoids in our society because the evidence is in: using some form of marijuana regularly lowers our risks for developing numerous, serious illnesses. J Alzheimers Dis. 2013 Jan 1;354:847-58. doi: 10.3233/JAD-130137.CB2 Cannabinoid Receptor Agonist Ameliorates Alzheimer-Like Phenotype in AβPP/PS1 Mice.Aso E, Juvés S, Maldonado R, Ferrer I.SourceInstitut de Neuropatologia, Servei d'Anatomia Patològica, Abstract: The specific CB2 cannabinoid receptor agonist JWH-133 induced cognitive improvement in double AβPP/PS1 transgenic mice, a genetic model of Alzheimer's disease. This effect was more pronounced when administered at the pre-symptomatic rather than the early symptomatic stage. The cognitive improvement was associated with decreased microglial reactivity and reduced expression of pro-inflammatory cytokines IL-1β, IL-6, TNFα, and IFNγ. In addition, JWH-133 reduced the expression of active p38 and SAPK/JNK, increased the expression of inactive GSK3β, and lowered tau hyperphosphorylation at Thr181 in the vicinity of amyloid-β plaques. Moreover, JWH-133 produced a decrease in the expression of hydroxynonenal adducts, and enhanced the expression of SOD1 and SOD2 around plaques. In contrast, the chronic treatment with JWH-133 failed to modify the amyloid-β production or deposition in cortex and hippocampus. In conclusion, the present study lends support to the idea that stimulation of CB2 receptors ameliorates several altered parameters in Alzheimer's disease such as impaired memory and learning, neuroinflammation, oxidative stress damage and oxidative stress responses, selected tau kinases, and tau hyperphosphorylation around plaques.

via CB2 Cannabinoid Receptor Agonist Ameliorate... [J Alzheimers Dis. 2013] - PubMed - NCBI.

Cannabidiol from marijuana reduces cigarette consumption

As misguided politicians move to eradicate medical marijuana dispensaries, we are learning more and more about the benefits of the nonpsychoactive cannabinoid, CBD, which dealers don't sell but dispensaries do. Fight the ignorance and fight the repression! Educate the public and promote marijuana as a health-building supplement.

Addict Behav. 2013 Sep; .Cannabidiol reduces cigarette consumption in tobacco smokers: Preliminary findings. Morgan CJ, Das RK, Joye A, Curran HV, Kamboj SK.SourceClinical Psychopharmacology Unit, University College London, London, UK. .Abstract: The role of the endocannabinoid system in nicotine addiction is being increasingly acknowledged. We conducted a pilot, randomised double blind placebo controlled study set out to assess the impact of the ad-hoc use of cannabidiol CBD in smokers who wished to stop smoking. 24 smokers were randomised to receive an inhaler of CBD n=12 or placebo n=12 for one week, they were instructed to use the inhaler when they felt the urge to smoke. Over the treatment week, placebo treated smokers showed no differences in number of cigarettes smoked. In contrast, those treated with CBD significantly reduced the number of cigarettes smoked by ~40% during treatment. Results also indicated some maintenance of this effect at follow-up. These preliminary data, combined with the strong preclinical rationale for use of this compound, suggest CBD to be a potential treatment for nicotine addiction that warrants further exploration.

via Cannabidiol reduces cigarette consumption in to... [Addict Behav. 2013] - PubMed - NCBI.

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Cannabidiol from marijuana reduces cigarette consumption

As misguided politicians move to eradicate medical marijuana dispensaries, we are learning more and more about the benefits of the nonpsychoactive cannabinoid, CBD, which dealers don't sell but dispensaries do. Fight the ignorance and fight the repression! Educate the public and promote marijuana as a health-building supplement. Addict Behav. 2013 Sep; .Cannabidiol reduces cigarette consumption in tobacco smokers: Preliminary findings. Morgan CJ, Das RK, Joye A, Curran HV, Kamboj SK.SourceClinical Psychopharmacology Unit, University College London, London, UK. .Abstract: The role of the endocannabinoid system in nicotine addiction is being increasingly acknowledged. We conducted a pilot, randomised double blind placebo controlled study set out to assess the impact of the ad-hoc use of cannabidiol CBD in smokers who wished to stop smoking. 24 smokers were randomised to receive an inhaler of CBD n=12 or placebo n=12 for one week, they were instructed to use the inhaler when they felt the urge to smoke. Over the treatment week, placebo treated smokers showed no differences in number of cigarettes smoked. In contrast, those treated with CBD significantly reduced the number of cigarettes smoked by ~40% during treatment. Results also indicated some maintenance of this effect at follow-up. These preliminary data, combined with the strong preclinical rationale for use of this compound, suggest CBD to be a potential treatment for nicotine addiction that warrants further exploration.

via Cannabidiol reduces cigarette consumption in to... [Addict Behav. 2013] - PubMed - NCBI.

CBD from marijuana protects the brain from Alzheimer's disease and triggers the production of new brain cells

Like THC, the cannabinoid CBD from marijuana protects the brain from the damage that leads to Alzheimer's disease and other forms of dementia. CBD, which lacks the psychoactive effects of THC, is only available from cannabis products sold by dispensaries, dealers do not sell marijuana that doesn't get you high. Why are communities shortsightedly moving to close dispensaries? Reefer madness residue and marijuanaphobia. Speak out for medical marijuana! Cannabidiol reduces Aβ-induced neuroinflammation and promotes hippocampal neurogenesis through PPARγ involvement.       Esposito G, Scuderi C, Valenza M, Togna GI, Latina V, De Filippis D, Cipriano M, Carratù MR, Iuvone T, Steardo L.SourceDepartment of Physiology and Pharmacology Vittorio Erspamer, Sapienza University of Rome, Rome, Italy.                                                                               Abstract: Peroxisome proliferator-activated receptor-γ PPARγ has been reported to be involved in the etiology of pathological features of Alzheimer's disease AD. Cannabidiol CBD, a Cannabis derivative devoid of psychomimetic effects, has attracted much attention because of its promising neuroprotective properties in rat AD models, even though the mechanism responsible for such actions remains unknown. This study was aimed at exploring whether CBD effects could be subordinate to its activity at PPARγ, which has been recently indicated as its putative binding site. CBD actions on β-amyloid-induced neurotoxicity in rat AD models, either in presence or absence of PPAR antagonists were investigated. Results showed that the blockade of PPARγ was able to significantly blunt CBD effects on reactive gliosis and subsequently on neuronal damage. Moreover, due to its interaction at PPARγ, CBD was observed to stimulate hippocampal neurogenesis. All these findings report the inescapable role of this receptor in mediating CBD actions, here reported.

via Cannabidiol reduces Aβ-induced neuroinflammation an... [PLoS One. 2011] - PubMed - NCBI.

THC from marijuana is an anticancer drug

How long will this government-perpetrated fraud that there is no such thing as medical marijuana endure in the face of an overwhelming tsunami of science which proves that marijuana delivers health-building and protecting cannabinoids which fight disease and enhance our vitality? Promote adult marijuana use! From the following report, "THC has shown therapeutic potential as an anticancer drug." J Drug Target. 2013 Jun 18. [Epub ahead of print]

Preparation and characterization of Δ9-tetrahydrocannabinol-loaded biodegradable polymeric microparticles and their antitumoral efficacy on cancer cell lines.

de la Ossa DH, Gil-Alegre ME, Ligresti A, Aberturas MD, Molpeceres J, Torres AI, Di Marzo V.

Source

Department of Pharmacy and Pharmaceutical Technology, School of Pharmacy, Complutense University of Madrid , Madrid , Spain .

Abstract

Abstract: Cannabinoids present an interesting therapeutic potential as antiemetics, appetite stimulants in debilitating diseases (cancer, AIDS and multiple sclerosis), analgesics, and in the treatment of multiple sclerosis and cancer, among other conditions. However, despite their high clinical potential, only few dosage forms are available to date. In this paper, the development of Δ9-tetrahydrocannabinol (THC) biodegradable microspheres as an alternative delivery system for cannabinoid parenteral administration is proposed. Tetrahydrocannabinol was encapsulated into biodegradable microspheres by the oil-in-water (o/w) emulsion solvent evaporation method. Several formulations were prepared using different drug:polymer ratios. The influence of antioxidant (α-tocopherol acetate) concentration on the release of THC from the microparticles was studied. Elevated process yield and entrapment efficiencies were achieved. The in vitro drug release studies showed that the encapsulated drug was released over a two week period. As THC has shown therapeutic potential as anticancer drug, the efficacy of the microspheres was tested on different cancer cell lines. Interestingly, the microspheres were able to inhibit cancer cell proliferation during the nine-day study period. All the above results suggest that the use of biodegradable microspheres would be a suitable alternative delivery system for THC administration.

via Preparation and characterization of Δ9-tetrahy... [J Drug Target. 2013] - PubMed - NCBI.

Acute Δ9-tetrahydrocannabinol blocks gastric... [Eur J Pharmacol. 2013] - PubMed - NCBI

THC blocks stomach damage from NSAIDs (nonsteroidal anti-inflammatory drugs) with doses that do not cause mind-altering effects. Marijuana, it's not just about getting high anymore!. Eur J Pharmacol. 2013 Jun 11. pii: S0014-29991300461-5. doi: 10.1016/j.ejphar.2013.06.001. [Epub ahead of print]Acute Δ9-tetrahydrocannabinol blocks gastric hemorrhages induced by the nonsteroidal anti-inflammatory drug diclofenac sodium in mice.Kinsey SG, Cole EC.SourceDepartment of Psychology, West Virginia University, Morgantown, WV USA. Electronic address: sgkinsey@mail.wvu.edu.AbstractNonsteroidal anti-inflammatory drugs NSAIDs, which are among the most widely used analgesics in the world, cause gastrointestinal inflammation that is potentially life-threatening. Although inhibitors of endocannabinoid catabolic enzymes protect against gastropathy in fasted NSAID-treated mice, the gastroprotective effects of Δ9-tetrahydrocannabinol THC, the primary psychoactive component of marijuana, have yet to be investigated. Male C57BL/6J mice were fasted, administered vehicle or Δ9-THC .01-50mg/kg; oral or intraperitoneal, and then treated with the NSAID diclofenac sodium 100mg/kg, p.o. to induce gastric lesions. In separate groups of mice, the cannabimimetic behavioral effects of Δ9-THC given via each route of administration were compared using a battery of tests, consisting of assessment of locomotor activity, nociception in the tail withdrawal test, catalepsy in the bar test, and hypothermia. Δ9-THC dose-dependently attenuated diclofenac-induced gastric hemorrhagic streaks through both p.o. and i.p. routes of administration ED50 95% confidence interval=0.64 0.26-1.55 mg/kg and 0.06 0.01-0.34 mg/kg, respectively. Δ9-THC given i.p. was 2-3 orders of magnitude more potent in reducing diclofenac-induced gastric ulcers than in producing locomotor immobility, antinociception, hypothermia, and catalepsy, while the potency of ratio of p.o. Δ9-THC between each behavior measure was 7-18. These data indicate that the phytocannabinoid Δ9-THC protects against diclofenac-induced gastric inflammatory tissue damage at doses insufficient to cause common cannabinoid side effects.

via Acute Δ9-tetrahydrocannabinol blocks gastric... [Eur J Pharmacol. 2013] - PubMed - NCBI.

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Acute Δ9-tetrahydrocannabinol blocks gastric... [Eur J Pharmacol. 2013] - PubMed - NCBI

THC blocks stomach damage from NSAIDs (nonsteroidal anti-inflammatory drugs) with doses that do not cause mind-altering effects. Marijuana, it's not just about getting high anymore!. Eur J Pharmacol. 2013 Jun 11. pii: S0014-29991300461-5. doi: 10.1016/j.ejphar.2013.06.001. [Epub ahead of print]Acute Δ9-tetrahydrocannabinol blocks gastric hemorrhages induced by the nonsteroidal anti-inflammatory drug diclofenac sodium in mice.Kinsey SG, Cole EC.SourceDepartment of Psychology, West Virginia University, Morgantown, WV USA. Electronic address: sgkinsey@mail.wvu.edu.AbstractNonsteroidal anti-inflammatory drugs NSAIDs, which are among the most widely used analgesics in the world, cause gastrointestinal inflammation that is potentially life-threatening. Although inhibitors of endocannabinoid catabolic enzymes protect against gastropathy in fasted NSAID-treated mice, the gastroprotective effects of Δ9-tetrahydrocannabinol THC, the primary psychoactive component of marijuana, have yet to be investigated. Male C57BL/6J mice were fasted, administered vehicle or Δ9-THC .01-50mg/kg; oral or intraperitoneal, and then treated with the NSAID diclofenac sodium 100mg/kg, p.o. to induce gastric lesions. In separate groups of mice, the cannabimimetic behavioral effects of Δ9-THC given via each route of administration were compared using a battery of tests, consisting of assessment of locomotor activity, nociception in the tail withdrawal test, catalepsy in the bar test, and hypothermia. Δ9-THC dose-dependently attenuated diclofenac-induced gastric hemorrhagic streaks through both p.o. and i.p. routes of administration ED50 95% confidence interval=0.64 0.26-1.55 mg/kg and 0.06 0.01-0.34 mg/kg, respectively. Δ9-THC given i.p. was 2-3 orders of magnitude more potent in reducing diclofenac-induced gastric ulcers than in producing locomotor immobility, antinociception, hypothermia, and catalepsy, while the potency of ratio of p.o. Δ9-THC between each behavior measure was 7-18. These data indicate that the phytocannabinoid Δ9-THC protects against diclofenac-induced gastric inflammatory tissue damage at doses insufficient to cause common cannabinoid side effects.

via Acute Δ9-tetrahydrocannabinol blocks gastric... [Eur J Pharmacol. 2013] - PubMed - NCBI.

THC could be a chemotherapeutic agent for treating stomach cancer

Cannabinoids, such as THC, which activate the CB1 and CB2 cannabinoid receptors are more effective against stomach cancer than the main chemotherapy treatment. Using marijuana protects us from so many cancers and other illnesses, aren't you mad that it's still illegal? Anticancer Res. 2013 Jun;33(6):2541-7.

Cannabinoid Receptor Agonist as an Alternative Drug in 5-Fluorouracil-resistant Gastric Cancer Cells.

Xian XS, Park H, Choi MG, Park JM.

Source

Division of Gastroenterology, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, 505, Banpo-Dong, Seocho-Gu, Seoul, 137-070, Korea. parkjerry@catholic.ac.kr.

Abstract

Fluorouracil is the main chemotherapeutic drug used for gastrointestinal cancers, which suffers the important problem of treatment resistance. There is little information whether cannabinoid agonists can be used as an alternative drug for fluorouracil-resistant gastric cancer cells. In this study, we investigated the effects of a cannabinoid agonist, WIN-55,212-2, on 5-fluorouracil (5-FU)-resistant human gastric cancer cells, to examine whether the cannabinoid agonist may be an alternative therapy. Survival of the 5-FU-resistant gastric cancer cell line, SNU-620-5FU/1000, was not significantly reduced even by a high dose of 5-FU treatment. However, WIN-55,212-2 inhibited the proliferation of SNU-620-5FU/1000 and enhanced their apoptosis, as indicated by an increase of apoptotic cell proportion, activated caspase-3 and Poly (ADP-ribose) polymerase cleavage. Furthermore, WIN-55,212-2 reduced phospho-extracellular-signal-regulated kinases (ERK) 1/2, phospho-Akt (protein kinase B), B-cell lymphoma-2 (BCL2) and BCL2-associated X (BAX) protein expression in 5-FU-resistant gastric cancer cells. These results indicate that a cannabinoid agonist may, indeed, be an alternative chemotherapeutic agent for 5-FU-resistant gastric cancer.

KEYWORDS:

Gastric cancer, apoptosis, cannabinoids, drug resistance, fluorouracil

via Cannabinoid Receptor Agonist as an Alternativ... [Anticancer Res. 2013] - PubMed - NCBI.

Cannabinoids fight pancreatic cancer

Cannabinoids which work via the CB1 and CB2 receptor, as does THC from marijuana, interfere with pancreatic cancer's cellular metabolism, causing the cancer cells to die off. The following abstract is quite technical but what you need to consider is the final line which reports that cannabinoids killed off and stunted the growth of pancreatic cancer cells. Cell Death Dis. 2013 Jun 13;4:e664. doi: 10.1038/cddis.2013.151.Cannabinoids inhibit energetic metabolism and induce AMPK-dependent autophagy in pancreatic cancer cells.Dando I, Donadelli M, Costanzo C, Dalla Pozza E, D'Alessandro A, Zolla L, Palmieri M.SourceDepartment of Life and Reproduction Sciences, Biochemistry Section, University of Verona, Verona, Italy. Abstract: The anti-tumoral effects of cannabinoids have been described in different tumor systems, including pancreatic adenocarcinoma, but their mechanism of action remains unclear. We used cannabinoids specific for the CB1 ACPA and CB2 GW receptors and metabolomic analyses to unravel the potential pathways mediating cannabinoid-dependent inhibition of pancreatic cancer cell growth. Panc1 cells treated with cannabinoids show elevated AMPK activation induced by a ROS-dependent increase of AMP/ATP ratio. ROS promote nuclear translocation of GAPDH, which is further amplified by AMPK, thereby attenuating glycolysis. Furthermore, ROS determine the accumulation of NADH, suggestive of a blockage in the respiratory chain, which in turn inhibits the Krebs cycle. Concomitantly, inhibition of Akt/c-Myc pathway leads to decreased activity of both the pyruvate kinase isoform M2 PKM2, further downregulating glycolysis, and glutamine uptake. Altogether, these alterations of pancreatic cancer cell metabolism mediated by cannabinoids result in a strong induction of autophagy and in the inhibition of cell growth.

via Cannabinoids inhibit energetic metabolism and... [Cell Death Dis. 2013] - PubMed - NCBI.

Marijuana can relieve chemotherapy-induced pain

Another study finds that cannabinoids, like those found in marijuana, suppress the pain resulting from chemotherapy-induced neuropathy. And the Feds continue to claim that there is no medical use for marijuana. J Pain Symptom Manage. 2013 Jun 4. pii: S0885-39241300238-8. doi: 10.1016/j.jpainsymman.2013.02.018. [Epub ahead of print]A Double-Blind, Placebo-Controlled, Crossover Pilot Trial With Extension Using an Oral Mucosal Cannabinoid Extract for Treatment of Chemotherapy-Induced Neuropathic Pain.Lynch ME, Cesar-Rittenberg P, Hohmann AG.SourcePain Management Unit, Queen Elizabeth II Health Sciences Centre, Dalhousie University, Halifax, Nova Scotia, Canada; Department of Anesthesia, Psychiatry and Pharmacology, Dalhousie University, Halifax, Nova Scotia, Canada. Electronic address: mary.lynch@dal.ca.                                  Abstract: Neuropathic pain caused by chemotherapy limits dosing and duration of potentially life-saving anti-cancer treatment and impairs quality of life. Chemotherapeutic neuropathy responds poorly to conventional treatments, and there is an urgent medical need for new treatments. Recent preclinical studies demonstrate that cannabinoid agonists suppress established chemotherapy-evoked neuropathy.OBJECTIVES:This was a pilot trial to begin to investigate a currently available cannabinoid agent, nabiximols oral mucosal spray containing cannabinoids, in the treatment of chemotherapy-induced neuropathic pain.METHODS:A randomized, placebo-controlled crossover pilot study was done in 16 patients with established chemotherapy-induced neuropathic pain. A 0-10 point numeric rating scale for pain intensity NRS-PI was used as the primary outcome measure.RESULTS:When examining the whole group, there was no statistically significant difference between the treatment and the placebo groups on the NRS-PI. A responder analysis demonstrated that there were five participants who reported a two-point or greater reduction in pain that trended toward statistical significance and the number needed to treat was five.CONCLUSION:Chemotherapy-induced neuropathic pain is particularly resistant to currently available treatments. This pilot trial found a number needed to treat of five and an average decrease of 2.6 on an 11-point NRS-PI in five "responders" as compared with a decrease of 0.6 with placebo and supports that it is worthwhile to study nabiximols in a full randomized, placebo-controlled trial of chemotherapy-induced neuropathic pain.

via A Double-Blind, Placebo-Controlled, Cr... [J Pain Symptom Manage. 2013] - PubMed - NCBI.

Medical marijuana ingredient prevents brain damage

The words “marijuana” and “brain damage” usually go in that order in medical literature. An Israeli researcher has flipped them around, finding that THC, the active ingredient in marijuana, may arrest some forms of brain damage in mice.The loco weed already is favored by those who suffer from chronic diseases, not to mention fans of Cypress Hill, Bob Marley and the Grateful Dead.But pharmacologist Josef Sarne of Tel Aviv University found that a minuscule amount of tetrahydrocannabinol may protect the brain after injuries from seizures, toxic drug exposure or a lack of oxygen. via Medical marijuana ingredient prevents brain damage in mice - latimes.com.