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.

THC from Marijuana Protects the Brain from Injury

Once again we see that using (even very small amounts of) marijuana improves our health by shielding the brain from the damage that follows a head injury. These same actions protect the brain from the age-related changes that lead to Alzheimer's disease and other forms of dementia. We need to recruit more people to use marijuana on a regular basis to lower our national health-care expenditures. Marijuana use is good for you! Tell someone today! Long-term behavioral and biochemical effects of an ultra-low dose of Δ9-tetrahydrocannabinol THC: neuroprotection and ERK signaling Miriam Fishbein, Sahar Gov, Fadi Assaf, Mikhal Gafni, Ora Keren, Yosef Sarne                                                                              Abstract: We have previously reported that a single injection of an ultra-low dose of delta-9-tetrahydrocannabinol THC; the psychoactive ingredient of marijuana protected the brain from pentylenentetrazole PTZ-induced cognitive deficits when applied 1–7 days before or 1–3 days after the insult. In the present study we expanded the protective profile of THC by showing that it protected mice from cognitive deficits that were induced by a variety of other neuronal insults, including pentobarbital-induced deep anesthesia, repeated treatment with 3,4 methylenedioxymethamphetamine MDMA; “ecstasy” and exposure to carbon monoxide. The protective effect of THC lasted for at least 7 weeks. The same ultra-low dose of THC 0.002 mg/kg, a dose that is 3–4 orders of magnitude lower than the doses that produce the known acute effects of the drug in mice induced long-lasting 7 weeks modifications of extracellular signal–regulated kinase ERK activity in the hippocampus, frontal cortex and cerebellum of the mice. The alterations in ERK activity paralleled changes in its activating enzyme MEK and its inactivating enzyme MKP-1. Furthermore, a single treatment with the low dose of THC elevated the level of pCREB phosphorylated cAMP response element–binding protein in the hippocampus and the level of BDNF brain-derived neurotrophic factor in the frontal cortex. These long-lasting effects indicate that a single treatment with an ultra-low dose of THC can modify brain plasticity and induce long-term behavioral and developmental effects in the brain.

via Long-term behavioral and biochemical effects of an ultra-low dose of Δ9-tetrahydrocannabinol THC: neuroprotection and ERK signaling - Springer.

Majority of Doctors Would Recommend Medical Marijuana

Most Docs OK With Medical Marijuana: SurveyMajority would give a prescription to an advanced cancer patient in pain

By Serena Gordon HealthDay Reporter

WEDNESDAY, May 29 (HealthDay News) -- Three-quarters of doctors who responded to a survey about medical marijuana said they would approve the use of the drug to help ease pain in an older woman with advanced breast cancer.

In a February issue of the New England Journal of Medicine, doctors were presented with a case vignette, as well as arguments both for and against the use of medical marijuana. Doctors were then asked to decide whether or not they would approve such a prescription for this patient.

The results now appear in the May 30 edition of the journal.

Seventy-six percent of the 1,446 doctors who responded said they would give the woman a prescription for medical marijuana. Many cited the possibility of alleviating the woman's symptoms as a reason for approving the prescription.

"The point of the vignette was to illustrate the kinds of patients that show up on our doorstep who need help. This issue is not one you can ignore, and some states have already taken matters into their own hands," said Dr. J. Michael Bostwick, a professor of psychiatry at the Mayo Clinic in Rochester, Minn.

Bostwick wrote the "pro" side for the survey, but said he could've written the "con" side as well, because there are valid arguments on both sides of the issue.

"There are no 100 percents in medicine. There's a lot of anecdotal evidence that this is something we should study more. Forgive the pun, but there's probably some fire where there's smoke, and we should investigate the medicinal use of marijuana or its components," Bostwick said.

Marijuana comes from the hemp plant Cannabis sativa. It's a dry, shredded mix of the plant's leaves, flowers, stems and seeds. It can be smoked as a cigarette or in a pipe, or it can be added to certain foods, such as brownies.

The case presented to the doctors was Marilyn, a 68-year-old woman with breast cancer that had spread to her lungs, chest cavity and spine. She was undergoing chemotherapy, and said she had no energy, little appetite and a great deal of pain. She had tried various medications to relieve her pain, including the narcotic medication oxycodone. She lives in a state where the use of medical marijuana is legal, and asks her physician for a prescription.

Dr. Bradley Flansbaum, a hospitalist at Lenox Hill Hospital, in New York City, said he sided with the majority for this particular case.

"I think there's some context that needs to be considered," Flansbaum said. "This was a woman with stage 4 cancer who wasn't responding to [anti-nausea medications]. I'm not saying let's legalize marijuana, but this is a woman at the end of her life, so what's the downside, given that there might be a benefit. In a different situation, medical marijuana might not be so well embraced."

For his part, Bostwick said that while he approved the use of medical marijuana in this case, he feels it's important that the prescription of marijuana as medicine only be done within the confines of an already-established doctor-patient relationship.

"My concern is doctors who see someone once and give them a prescription for medical marijuana. That's bad medicine," Bostwick said.

While many physicians felt as if there was no harm in allowing the breast cancer patient to try marijuana to see if it helped, Dr. Gary Reisfield, who co-wrote the "against" side for survey, expressed concern about a patient with lung disease smoking marijuana.

"Marijuana smoke irritates the airways," he said. The smoke can also cause airway inflammation and symptoms of bronchitis, and decreases the ability of the lungs to fight off fungal and bacterial infections, said Reisfield, chief of pain management services at the University of Florida's department of psychiatry.

What's more, marijuana isn't as safe a drug as many believe it to be. "Heavy marijuana use is associated with numerous adverse health and societal outcomes including psychomotor, memory and executive function impairments; marijuana use disorders; other psychiatric conditions such as psychosis; poor school and work performance and impaired driving performance," he said.

Many of the physicians who responded pointed out that drugs already approved and in use also have the potential for addiction, such as narcotics. "Similar arguments could be made against alcohol, opiates and stimulants," Bostwick said.

For his part, Reisfield pointed out that there are two FDA-approved prescription cannabinoid pills -- dronabinol (Marinol) and nabilone (Cesamet) -- that don't begin working as quickly as smoked marijuana, but provide longer symptom relief without the high of marijuana. They also don't appear to have any addictive properties, he said.

What many doctors would like to see, according to the survey, is more evidence on the use of marijuana as medicine, so they could make a better-informed decision one way or the other.

More information

Learn more about marijuana and its potential for medical use from the U.S. National Cancer Institute.

SOURCES: J. Michael Bostwick, M.D., professor, psychiatry, Mayo Clinic, Rochester, Minn.; Bradley Flansbaum, M.D., hospitalist, Lenox Hill Hospital, New York City; Gary Reisfield, M.D., chief, pain management services, department of psychiatry, University of Florida College of Medicine, Gainesville; May 30, 2013, New England Journal of Medicine

Marijuana protects the brain from alcohol damage

Here is evidence that using marijuana shields the brain from a significant amount of the damage that alcohol causes. If you are drinking, you should probably be toking. Also recall that a recent study concluded that: "There is no safe threshold for alcohol consumption with regards to cancer," and recall that ample evidence shows that using marijuana causes cancer cells to die off thus lowering the risk for everything from lung to head and neck to bladder cancers as well as lymphoma. Prohibition is carcinogenic. White Matter Integrity in Adolescents with Histories of Marijuana Use and Binge Drinking  J. Jacobus,a,b T. McQueeny,g S. Bava,b,c B. C. Schweinsburg,e,f L.R. Frank,d T. T. Yang,c and S. F. Tapertb,c, Abstract: Structural brain abnormalities have been observed in adolescents with alcohol use disorders but less is known about neuropathological brain characteristics of teens with subdiagnostic binge drinking or the common pattern of binge drinking combined with marijuana use. The goal of this study was to examine white matter integrity in adolescents with histories of binge drinking and marijuana use.Diffusion tensor imaging DTI was conducted with 42 adolescents ages 16−19 classified as controls, binge drinkers, or binge drinkers who are also heavy marijuana users. Tract based spatial analysis identified shared fiber structure across individuals and facilitated voxelwise comparisons of fractional anisotropy FA and mean diffusivity MD between groups.Significant between group differences were found in FA in eight white matter regions ps ≤ .016 between the binge drink-only group and controls, including superior corona radiata, inferior longitudinal fasciculus, inferior fronto-occipital fasciculus, and superior longitudinal fasciculus. Interestingly, in 4 of these same regions, binge drinkers who are also heavy marijuana users had higher FA than binge drinkers who did not use marijuana ps < .05. MD did not differ between groups. Findings are largely consistent with research suggesting less neuropathology in adolescents without histories of substance use. However, binge drinkers who also use marijuana did not show as consistent a divergence from non-users as did the binge drink-only group. Detection of white matter alterations may have implications in identifying early cognitive dysfunction in substance using adolescents.Keywords: Adolescence, Brain Imaging, Marijuana Abuse, Alcohol Abuse, White Matter, Diffusion Tensor Imaging

via White Matter Integrity in Adolescents with Histories of Marijuana Use and Binge Drinking.

CBD protects pig brains--new hope for politicians

CBD protects pig brains in a model of stroke. Cannabinoids, such as THC and CBD, protect the brain. Neuropharmacology. 2013 Aug;71C:282-291. doi: 10.1016/j.neuropharm.2013.03.027. Epub 2013 Apr 12.Mechanisms of cannabidiol neuroprotection in hypoxic-ischemic newborn pigs: Role of 5HT1A and CB2 receptors.Pazos MR, Mohammed N, Lafuente H, Santos M, Martínez-Pinilla E, Moreno E, Valdizan E, Romero J, Pazos A, Franco R, Hillard CJ, Alvarez FJ, Martínez-Orgado J.SourceExperimental Unit, Pediatric Department, University Hospital Puerta de Hierro Majadahonda, 28222 Madrid, Spain.AbstractThe mechanisms underlying the neuroprotective effects of cannabidiol CBD were studied in vivo using a hypoxic-ischemic HI brain injury model in newborn pigs. One- to two-day-old piglets were exposed to HI for 30 min by interrupting carotid blood flow and reducing the fraction of inspired oxygen to 10%. Thirty minutes after HI, the piglets were treated with vehicle HV or 1 mg/kg CBD, alone HC or in combination with 1 mg/kg of a CB2 receptor antagonist AM630 or a serotonin 5HT1A receptor antagonist WAY100635. HI decreased the number of viable neurons and affected the amplitude-integrated EEG background activity as well as different prognostic proton-magnetic-resonance-spectroscopy H±-MRS-detectable biomarkers lactate/N-acetylaspartate and N-acetylaspartate/choline ratios. HI brain damage was also associated with increases in excitotoxicity increased glutamate/N-acetylaspartate ratio, oxidative stress decreased glutathione/creatine ratio and increased protein carbonylation and inflammation increased brain IL-1 levels. CBD administration after HI prevented all these alterations, although this CBD-mediated neuroprotection was reversed by co-administration of either WAY100635 or AM630, suggesting the involvement of CB2 and 5HT1A receptors. The involvement of CB2 receptors was not dependent on a CBD-mediated increase in endocannabinoids. Finally, bioluminescence resonance energy transfer studies indicated that CB2 and 5HT1A receptors may form heteromers in living HEK-293T cells. In conclusion, our findings demonstrate that CBD exerts robust neuroprotective effects in vivo in HI piglets, modulating excitotoxicity, oxidative stress and inflammation, and that both CB2 and 5HT1A receptors are implicated in these effects.

via Mechanisms of cannabidiol neuroprotection ... [Neuropharmacology. 2013] - PubMed - NCBI.

A Response to “Going to Pot” by Roxanne Khamsi

By Clint Werner, author of “Marijuana Gateway to Health”

In the June 2013 issue of Scientific American, “Science of Health” columnist Roxanne Khamsi wrote a surprisingly unscientific and biased piece on the health ramifications of legalizing marijuana that was sadly tainted with residue from last century’s reefer madness campaign. The title of the piece itself, “Going to Pot” is a loaded term that confers a negative association on the subject via cultural symbolism having nothing to do with the reality of what science is telling us about marijuana and how it affects the human organism and society. First, Ms. Khamsi is mistaken when she writes that doctors “may prescribe marijuana to treat or manage ailments.” In states with medical marijuana provisions, physicians write recommendations for their patients that allow access to dispensaries or cultivation cooperatives. Ms. Khamsi then asserts that “the safety of recreational use is poorly understood” and that “researchers worry that both short- and long-term use of the drug may harm the body and mind.” Researchers who are up-to-date on the science of marijuana have no such concerns regarding adult use. In terms of harming the body, recent research has revealed that regular use of marijuana actually seems to improve physical health. Population studies have shown that regular marijuana users have a reduced risk for developing lung cancer (Hashibe, Cancer Epidemiological, Biomarkers and Prevention, 2006), head and neck cancers (Liang, Cancer Prevention Research, 2009), bladder cancer (Thomas, American Urological Association meeting, 2013), lymphomas (Holly, American Journal of Epidemiology, 1999), as well as diabetes (Rajavashisth, BMJ Open, 2012). The diabetes protection data from the enormous NHANES report also revealed that subjects who smoked marijuana three times per week had a profound (> 50%) reduction in their blood levels of C reactive protein, a inflammation marker for heart disease, indicating that they experienced significant protection from developing cardiac disease. Research also revealed that regular, moderate marijuana smokers have improved lung function compared to non-marijuana smokers with no risk for developing COPD (Pletcher, JAMA, 2012). National Institute of Drug Abuse pulmonary researcher, Dr. Donald Tashkin has said that he now endorses legalization since there is no basis for concern about the substance’s negative effects on lung function. Given the nearly century-long reefer madness campaign waged with untold billions of government dollars, it is hard for people to grasp that a denigrated and criminalized substance could have such positive health effects, especially when smoked, but science trumps myth and superstition with evidence. In terms of mental health, a just-published paper reports that “marijuana use consistently buffered people from the negative consequences associated with loneliness and social exclusion” (Deckman, Social Psychological and Personality Science, 2013), which could be one of the reasons that researchers found a truly startling drop in suicides, especially among young adult men, following the enactment of state medical marijuana laws (Anderson, IDEAS, 2012). Other research has shown that marijuana’s anti-depressant effects could be the result of neurogenesis, the production of healthy and functional new brain cells, which is promoted by the cannabinoids in marijuana (Jiang, Journal of Clinical Investigation, 2005). Another recently-published study found that “mortality risk was lower in cannabis users than in non-cannabis users with psychotic disorders” (Koola, Journal of Psychiatric Research, 2013), indicating that marijuana is a beneficial treatment for mental problems rather than, as increasingly inferred, a causative agent. In attempting to explain the activity of marijuana’s cannabinoid molecules on the endocannabinoid receptors, Ms. Khamsi once again employs loaded language to imply a negative effect, writing that THC “triggers domino chains” which implies a collapse of order and function rather than an alteration in order and function, which is what is truly occurring. Ms. Khamsi then frets that using marijuana impairs “working memory.” Yes marijuana alters mental functioning; it shifts the mind into a blissful euphoria that redirects thought from the ordered and analytical to the relaxed and free-association style of thought that characterizes relaxation and insight. And unlike alcohol, which serves a similar function of quieting the work day mental noise, marijuana is not carcinogenic or lethal. Ms. Khamsi expresses the understandable concern that marijuana users will make our roadways more dangerous but this is not supported by data that shows us what actually happens when legal restrictions are eased. A comprehensive review of data from states with medical marijuana laws found that enactment of the laws led to a significant drop in traffic accident deaths by allowing for marijuana to substitute for alcohol, a far more impairing substance. Traffic accident fatalities dropped by 9 percent in medical marijuana states. (Anderson, pending publication in the Journal of Law and Economics, 2013). That is essentially the same level of protection afforded by the passage of mandatory sea belt laws and by increasing the age for alcohol consumption from 18 to 21 years. According to research conducted by the automobile insurance company 4autoinsurance.com, marijuana users are safe drivers because, unlike alcohol drinkers, they are aware of their level of impairment and either refuse to drive, delay driving or drive more carefully than normal by reducing speed and not changing lanes. Regular marijuana users showed far less evidence of impairment than did novice and occasional users. Impairment testing is the only way to effectively police for marijuana-impaired drivers without ruining the lives of people who pose no threat on the roadways. The cannabinoid CBD steers THC away from the CB1 receptor, thus dulling or nullifying the mind-altering effects, but CBD does not reduce THC levels in the blood. Therefore, a driver using a high CBD strain of marijuana could test over the THC limit while experiencing no psychoactive effects whatsoever. Consequently, effective and fair impairment assessment techniques will need to be developed. Ms. Khamsi then returns to the health effects of marijuana, but ignores the previously cited benefits of reduced risks for developing numerous cancers, diabetes and other inflammation- and oxidation-based degenerative illnesses, such as Alzheimer’s disease and arthritis. She then refers to the recent study of data from New Zealand that indicates that teenagers who use marijuana heavily have up to an 8 percent drop in IQ points. Those results were called into question upon review but still indicate a disturbing effect of heavy marijuana use on the developing adolescent brain. Neurologist Dr. Gary Wenk, who has written “a puff is enough” to protect the adult brain from age-related dementia, says that the effect of marijuana on a developing brain, especially in those under 15 years of age, is impairing. Regular use of marijuana by teens may also interfere with social and professional skill development by monopolizing the time and consciousness of teens that enjoy it. Ms. Khamsi correctly notes that black market marijuana is sometimes contaminated with “sand or glass beads” which are far more harmful to the user than cannabis itself. Black market marijuana is also frequently contaminated with insecticides not intended for use on plants that are consumed. Some of these products are neurotoxic and, ironically, may induce neurodegenerative illnesses by interfering with the functions of the endocannabinoid system. (Casida, Annual Review of Entomolgy, 2013) Smuggled marijuana is also stale and often riddled with mold. Given these threats to heavy teenage users, the question needs to be asked: How do we best reduce access to marijuana, especially the most harmful forms of marijuana, by teenagers? One study suggests that multidimensional family therapy (MDFT) is the most effective approach for treating teenagers with what is termed “cannabis use disorder” (Rigter, Drug and Alcohol Dependence, 2012). MDFT essentially reestablishes parental authority and time management in teens’ lives. If parents remain involved in all aspects of their teenage children’s lives, MDFT would not be necessary to correct a deficit in parenting. The best way to prevent teenage substance abuse is for parents to rigorously monitor and guide their children’s activities. By doing this, parents might not prevent experimentation but they can create an environment where regular access to and use of marijuana is impossible. Shrinking and killing off the black market via legalization and regulation can assist parents in this task, by making marijuana more difficult for teens to obtain. Dealers do not card and taking marijuana away from the illicit drug black market will also protect teens from the multiple drug offerings of those dealers. If teens do obtain marijuana on the sly, at least, having been diverted from legal and tested supplies, it will be less likely to be contaminated with more harmful substances. Commercial medical marijuana venders such as Harborside Health Center, which Khamsi mentioned, contract with growers and test their marijuana for safety and potency. Legalization transforms marijuana cultivators from shady criminals into proud artisans. And despite the possible risk of heavy marijuana use to teenagers’ cognition, a study of adolescent binge drinkers found that those who used marijuana suffered significantly less alcohol-related brain damage than the booze-only drinkers (Jacobus, Neurotoxicology and Teratology, 2009). Consider the irony: Marijuana protects the brains of booze binge drinkers. Ms. Khamsi also mentions increases in emergency room visits and those seeking treatment for marijuana use. The emergency room statistic most frequently cited by opponents of legalization involve the detection of marijuana use via urinalysis, a method that only indicates if marijuana has been used within the last two to four weeks, therefore the data does not indicate that marijuana use caused the emergency room visit. It merely indicates that more people seem to be using marijuana overall (DAWN Drug Abuse Warning Network, HHS, 2008). In fact, two studies have found direct associations between marijuana use and a decrease in emergency room visits (Vinson, Missouri Medicine, 2006 and Gmel, BMC Public Health 9, 2009). The BMC study found that “relative risks decreased with increasing levels of use,” in other words, when more marijuana was used, fewer injuries occurred. This might seem odd until one recalls that a cannabinoid-blocking drug (rimonabant) was rejected for approval by the FDA due to its side-effects, which included an increase in accidents and injuries. Given that smoking marijuana reduces our risks for developing various cancers, diabetes, heart disease, COPD, Alzheimer’s disease, and other inflammation-based illnesses along with depression, suicidal tendencies and alcohol-caused traffic accidents, shouldn’t it’s use by adults be encouraged and safe, legal outlets be established? Science has spoken.

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