Stephan ChoMay 06, 2013 Bladder Cancer Risk Lower in Pot Smokers SAN DIEGO—For the first time, a study has found that cannabis use may be associated with a decreased risk of bladder cancer, researchers reported at the American Urological Association 2013 annual meeting.In a study of nearly 82,000 men, bladder cancer developed in 279 over an 11-year period. Subjects who smoked marijuana, but not tobacco, had a significant 45% decreased risk of bladder cancer compared with those who did not, after adjusting for age, body mass index, and race and ethnicity, according to lead investigator Anil A. Thomas, MD, a researcher with Southern California Permanent Medical Group in Los Angeles. Men who smoked tobacco, but not marijuana, had a significant 52% increased risk, a finding that is consistent with numerous previous studies. Men who smoked both had a 28% increased risk.Of the 82,000 men, 41% reported ever using marijuana and 57% reported tobacco use; 27% reported used both tobacco and marijuana.
Marijuana is effective for relieving the misery that is Crohn’s disease as well as other bowel disease symptoms.
Clin Gastroenterol Hepatol. 2013 May 3. pii: S1542-3565(13)00604-6. doi: 10.1016/j.cgh.2013.04.034. [Epub ahead of print]
Cannabis Induces a Clinical Response in Patients with Crohn’s Disease: a Prospective Placebo-Controlled Study.
Naftali T, Bar Lev L, Dotan I, Lansky EP, Sklerovsky BF, Konikoff FM.
Department of Gastroenterology and Hepatology, Meir Medical Center and Sackler Faculty of Medicine, Tel Aviv University, Kfar Saba, Israel. Electronic address: firstname.lastname@example.org.
& Aims: The marijuana plant Cannabis sativa has been reported to produce beneficial effects for patients with inflammatory bowel diseases, but these have not been investigated in controlled trials. We performed a prospective trial to determine whether cannabis can induce remission in patients with Crohn’s disease.
We studied 21 patients (mean age 40±14 years, 13 male) with Crohn’s Disease and activity index (CDAI) scores >200 who did not respond to therapy with steroids, immunomodulators, or anti-tumor necrosis factor-α agents. Patients were randomly assigned to groups given cannabis, twice daily, in the form of cigarettes containing 11.5 mg of tetrahydrocannabinol (THC) or placebo containing cannabis flowers from which the THC had been extracted. Disease activity and laboratory tests were assessed during 8 weeks of treatment and 2 weeks thereafter.
Complete remission (a CDAI score <150) was achieved by 5/11 subjects in the cannabis group (45%) and 1/10 in the placebo group (10%; P=.43). A clinical response (a decrease in CDAI score of >100) was observed in 10/11 subjects in the cannabis group (90%; from 330±105 to 152±109) and 4/10 in the placebo group (40%; from 373±94 to 306±143; P=.028). Three patients in the cannabis group were weaned from steroid dependency. Subjects receiving cannabis reported improved appetite and sleep, with no significant side effects.
Although the primary endpoint of the study (induction of remission) was not achieved, a short course (8 week) of THC-rich cannabis produced significant clinical, steroid-free benefits to 11 patients with active CD, compared to placebo, without side effects. Further studies, with larger patient groups and a non-smoking mode of intake, are warranted. ClinicalTrials.gov NCT01040910.
Copyright © 2013 AGA Institute. Published by Elsevier Inc. All rights reserved.
When we passed the first medical marijuana laws in CA and AZ, opponents mocked the movement saying that doctors would be writing recommendations for people with psoriasis. Guess what, here is evidence that activating the CB1 receptor, as triggered by THC in marijuana, inhibits the inflammation and cell proliferation that cause the disease’s miserable and disfiguring side effects.
PeerJ. 2013 Feb 19; .A novel control of human keratin expression: cannabinoid receptor 1-mediated signaling down-regulates the expression of keratins K6 and K16 in human keratinocytes in vitro and in situ.Ramot Y, Sugawara K, Zákány N, Tóth BI, Bíró T, Paus R.SourceDepartment of Dermatology, University of Luebeck , Luebeck , Germany ; Department of Dermatology, Hadassah-Hebrew University Medical Center , Jerusalem , Israel. Abstract: Cannabinoid receptors CB are expressed throughout human skin epithelium. CB1 activation inhibits human hair growth and decreases proliferation of epidermal keratinocytes. Since psoriasis is a chronic hyperproliferative, inflammatory skin disease, it is conceivable that the therapeutic modulation of CB signaling, which can inhibit both proliferation and inflammation, could win a place in future psoriasis management. Given that psoriasis is characterized by up-regulation of keratins K6 and K16, we have investigated whether CB1 stimulation modulates their expression in human epidermis. Treatment of organ-cultured human skin with the CB1-specific agonist, arachidonoyl-chloro-ethanolamide ACEA, decreased K6 and K16 staining intensity in situ. At the gene and protein levels, ACEA also decreased K6 expression of cultured HaCaT keratinocytes, which show some similarities to psoriatic keratinocytes. These effects were partly antagonized by the CB1-specific antagonist, AM251. While CB1-mediated signaling also significantly inhibited human epidermal keratinocyte proliferation in situ, as shown by K6/Ki-67-double immunofluorescence, the inhibitory effect of ACEA on K6 expression in situ was independent of its anti-proliferative effect. Given recent appreciation of the role of K6 as a functionally important protein that regulates epithelial wound healing in mice, it is conceivable that the novel CB1-mediated regulation of keratin 6/16 revealed here also is relevant to wound healing. Taken together, our results suggest that cannabinoids and their receptors constitute a novel, clinically relevant control element of human K6 and K16 expression.
First we learned that the cannabinoids produced by the cannabis plant fight and kill cancer cells now we are beginning to uncover the mechanisms by which cannabinoids target and kill cancer cells. Alcohol promotes cancer while marijuana suppresses cancer, what’s wrong with this picture? I could go buy gallons and gallons of booze legally, but the government will destroy your life if you market marijuana.
Cell Death Dis. 2013 May 2;4:e618. doi: 10.1038/cddis.2013.141.Involvement of PPARγ in the antitumoral action of cannabinoids on hepatocellular carcinoma.Vara D, Morell C, Rodríguez-Henche N, Diaz-Laviada I.SourceBiochemistry and Molecular Biology Unit, Department of System Biology, School of Medicine, University ofAlcala, 28871 Madrid, Spain.AbstractCannabinoids exert antiproliferative effects in a wide range of tumoral cells, including hepatocellular carcinoma HCC cells. In this study, we examined whether the PPARγ-activated pathway contributed to the antitumor effect of two cannabinoids, Δ9-tetrahydrocannabinol THC and JWH-015, against HepG2 and HUH-7 HCC cells. Both cannabinoids increased the activity and intracellular level of PPARγ mRNA and protein, which was abolished by the PPARγ inhibitor GW9662. Moreover, genetic ablation with small interfering RNA siRNA, as well as pharmacological inhibition of PPARγ decreased the cannabinoid-induced cell death and apoptosis. Likewise, GW9662 totally blocked the antitumoral action of cannabinoids in xenograft-induced HCC tumors in mice. In addition, PPARγ knockdown with siRNA caused accumulation of the autophagy markers LC3-II and p62, suggesting that PPARγ is necessary for the autophagy flux promoted by cannabinoids. Interestingly, downregulation of the endoplasmic reticulum stress-related protein tribbles homolog 3 TRIB3 markedly reduced PPARγ expression and induced p62 accumulation, which was counteracted by overexpression of PPARγ in TRIB3-knocked down cells. Taken together, we demonstrate for the first time that the antiproliferative action of the cannabinoids THC and JWH-015 on HCC, in vitro and in vivo, are modulated by upregulation of PPARγ-dependent pathways.
Here is more evidence that using marijuana can improve the health of and increase the long-term survival of people with AIDS. THC and similar synthetic compounds block the ability of HIV to infect cells and to replicate. Recall that the Bush Sr. Administration denied medical marijuana to the numerous AIDS patients who were seeking it and ended the Compassionate Use Act rather than help the suffering. How many people died prematurely because of you old buzzard Bush? Blood drips from your mangled talons you evil vulture.
Attenuation of HIV-1 replication in macrophages by cannabinoid receptor 2 agonists Servio H. Ramirez,†,1, Nancy L. Reichenbach, Shongshan Fan, Slava Rom, Steven F. Merkel, Xu Wang, Wen-zhe Ho,† and Yuri Persidsky,†,1+ Author Affiliations Department of Pathology and Laboratory Medicine and †Center for Substance Abuse Research, Temple University School of Medicine, Philadelphia, Pennsylvania, USA ↵1.Correspondence: Dept. of Pathology and Laboratory Medicine, Temple University School of Medicine, 3401 N. Broad St., Philadelphia, PA 19140, USA. E-mail: email@example.com or firstname.lastname@example.org Abstract: Infiltrating monocytes and macrophages play a crucial role in the progression of HIV-1 infection in the CNS. Previous studies showed that activation of the CB2 can attenuate inflammatory responses and affect HIV-1 infectivity in T cells and microglia. Here, we report that CB2 agonists can also act as immunomodulators on HIV-1-infected macrophages. First, our findings indicated the presence of elevated levels of CB2 expression on monocytes/macrophages in perivascular cuffs of postmortem HIV-1 encephalitic cases. In vitro analysis by FACS of primary human monocytes revealed a step-wise increase in CB2 surface expression in monocytes, MDMs, and HIV-1-infected MDMs. We next tested the notion that up-regulation of CB2 may allow for the use of synthetic CB2 agonist to limit HIV-1 infection. Two commercially available CB2 agonists, JWH133 and GP1a, and a resorcinol-based CB2 agonist, O-1966, were evaluated. Results from measurements of HIV-1 RT activity in the culture media of 7 day-infected cells showed a significant decrease in RT activity when the CB2 agonist was present. Furthermore, CB2 activation also partially inhibited the expression of HIV-1 pol. CB2 agonists did not modulate surface expression of CXCR4 or CCR5 detected by FACS. We speculate that these findings indicate that prevention of viral entry is not a central mechanism for CB2-mediated suppression in viral replication. However, CB2 may affect the HIV-1 replication machinery. Results from a single-round infection with the pseudotyped virus revealed a marked decrease in HIV-1 LTR activation by the CB2 ligands. Together, these results indicate that CB2 may offer a means to limit HIV-1 infection in macrophages.
Marijuana is a gateway to health!
Med Hypotheses. 2013 May;80(5):564-7. doi: 10.1016/j.mehy.2013.01.019. Epub 2013 Feb 11.
Cannabis and Δ(9)-tetrahydrocannabinol (THC) for weight loss?
Le Foll B, Trigo JM, Sharkey KA, Le Strat Y.
Translational Addiction Research Laboratory, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health (CAMH), Toronto, Ontario, Canada; Addictions Program, CAMH, Toronto, Ontario, Canada; Departments of Psychiatry, Pharmacology, Family and Community Medicine, Institute of Medical Sciences, University of Toronto, Toronto, Ontario, Canada. Electronic address: email@example.com.
Obesity is one of the highest preventable causes of morbidity and mortality in the developed world . 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 . 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 Δ(9)-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.
Copyright © 2013 Elsevier Ltd. All rights reserved.
Marijuana legalization will eradicate the illegal markets which distribute marijuana that has been cut or weighted with far more harmful compounds than the weed itself. Here is a case of lung damage from marijuana contaminated with silicon dioxide particles which add weight and make low grade cannabis sparkle like high grade product. Talc and ground glass have also been used in this manner. Once again we see how prohibition is far more harmful on all levels than is legalization, unless one is a drug war/treatment industry misery profiteer. Also notice the first line in the abstract report and how it promotes disinformation as accepted fact: “the respiratory toxicity of cannabis is well known today” is a falsehood, in fact the bulk of research on marijuana-only smokers finds that they have superior lung function compared to nonsmokers and a reduction in the likelihood of developing lung cancer, again, compared to nonsmokers! How is this possible? Because the cell-nurturing and protective effects of cannabinoids in marijuana are vastly more beneficial than the by products of combustion are harmful. Cannabinoids reduce inflammation, oxidation and attack and kill cancer cells thereby improving lung health. It is quite amazing.
Arch Pediatr. 2013 Apr 22. pii: S0929-693X1300224-8. doi: 10.1016/j.arcped.2013.03.008. [Epub ahead of print] [Hemoptysis in a young man smoking cannabis.][Article in French]Monfort M, Larakeb A, Gouraud F.SourceService de pédiatrie générale, hôpital de Meaux, 6-8, rue Saint-Fiacre, BP 218, 77104 Meaux cedex, France. Electronic address: firstname.lastname@example.org. Abstract: The respiratory toxicity of cannabis is well known today. (Editor note: This assertion is not supported by evidence, it is an unscientific statement of bias not fact) Along with the classic cannabis ‘joint’, there are other ways of consuming it, which should be known. Smoking cannabis that has been cut with micro-particles of silicon dioxide may cause hemoptysis. We will describe here the case of a young 16-year-old man who was in the hospital because of hemoptic expectoration. The etiologic investigation was negative, in particular a thoracic scan and a bronchial fiberscope. Questioning the patient afterwards allowed us to discover the inhalation of cannabis 2 h before the hemoptysis, cannabis mixed with micro-particles of silicon dioxide. Stopping inhalation stopped the symptoms. Pediatricians should be familiarized with such practices. Silicon dioxide particles cause ENT problems or bronchial ones coughing, spitting, hemoptysis, wheezing. Over the long term, the risk of silicosis cannot be excluded, although a longer and more complete exposure is necessary.Copyright © 2013 Elsevier Masson SAS. All rights reserved.
This just in: No difference was found in the brains of very heavy marijuana smokers compared to nonusers. More evidence that nullifies the neoprohibitionists’ assertions that THC is “neurotoxic” and causes “brain changes” associated with “mental illness.” Science slays reefer madness once again.
Brain Topogr. 2013 Apr 19. [Epub ahead of print]Combined Grey Matter VBM and White Matter TBSS Analysis in Young First Episode Psychosis Patients With and Without Cannabis Consumption.Haller S, Curtis L, Badan M, Bessero S, Albom M, Chantraine F, Alimenti A, Lovblad KO, Giannakopoulos P, Merlo M.SourceService neuro-diagnostique et neuro-interventionnel DISIM, University Hospitals of Geneva, Rue Gabrielle Perret-Gentil 4, 1211, Geneva 14, Switzerland, email@example.com. Abstract: Cannabis consumption is temporally associated with the development of first episode psychosis FEP. Whether or not the chronic use of this substance induces structural brain changes that may be responsible for the cognitive and psychological disturbances in this disorder is still matter of debate. To address this issue, we compared the magnetic resonance imaging MRI-assessed grey GM and white matter WM changes in young FEP patients between users versus non-users of cannabis. This prospective study included 50 consecutive FEP subjects: 33 users 22.7 ± 4.1 years, 4 women and 17 non-users 23.9 ± 4.2 years, 10 women. Users were further divided into 15 heavy 23.3 ± 4.5 years, 2 women and 18 light users 22.2 ± 3.8 years, 2 women according to their lifetime cannabis use. Voxel-based-morphometry VBM analysis of GM and tract-based-spatial-statistics TBSS analysis of WM were performed. Age and gender were used as non-explanatory co-regressors. There were no supra-threshold differences between user and non-user groups for both GM and WM parameters. This was also the case when only heavy users were compared to non-users. Multivariate models controlling for age and gender confirmed these findings. We found no evidence for cannabis consumption related alterations in GM or WM in FEP subjects. Due to the strict correction for multiple comparisons and sample size, we cannot formally exclude subtle morphometric changes associated with cannabis consumption. However, even if present, such potential alterations would be of low magnitude.
Cannabis protects us from Alzheimer’s and other forms of dementia and natural cannabis from a dispensary is far less expensive than Sativex and keeps money in the community and away from big pharma and foreign profiteers. There is a role for Sativex as a prescribed drug, possibly compounded with other treatments, but not as a monopoly.
Natural Cannabinoids Improve Dopamine Neurotransmission and Tau and Amyloid Pathology in a Mouse Model of Tauopathy.Casarejos MJ, Perucho J, Gomez A, Muñoz MP, Fernandez-Estevez M, Sagredo O, Fernandez Ruiz J, Guzman M, de Yebenes JG, Mena MA.SourceDepartments of Neurobiology, Ramon y Cajal University Hospital, Madrid, Spain CIBERNED, Spain.AbstractCannabinoids are neuroprotective in models of neurodegenerative dementias. Their effects are mostly mediated through CB1 and CB2 receptor-dependent modulation of excitotoxicity, inflammation, oxidative stress, and other processes. We tested the effects of Sativex®, a mixture of Δ9-tetrahydrocannabinol and cannabidiol, acting on both CB1 and CB2 receptors, in parkin-null, human tau overexpressing PK-/-/TauVLW mice, a model of complex frontotemporal dementia, parkinsonism, and lower motor neuron disease. The animals received Sativex®, 4.63 mg/kg, ip, daily, for one month, at six months of age, at the onset of the clinical symptoms. We evaluated the effects of Sativex® on behavior, dopamine neurotransmission, glial activation, redox state, mitochondrial activity, and deposition of abnormal proteins. PK-/-/TauVLW mice developed the neurological deficits, but those treated with Sativex® showed less abnormal behaviors related to stress, less auto and hetero-aggression, and less stereotypy. Sativex® significantly reduced the intraneuronal, MAO-related free radicals produced during dopamine metabolism in the limbic system. Sativex® also decreased gliosis in cortex and hippocampus, increased the ratio reduced/oxidized glutathione in the limbic system, reduced the levels of iNOS, and increased those of complex IV in the cerebral cortex. With regard to tau and amyloid pathology, Sativex® reduced the deposition of both in the hippocampus and cerebral cortex of PK-/-/TauVLW mice and increased autophagy. Sativex®, even after a short administration in animals with present behavioral and pathological abnormalities, improves the phenotype, the oxidative stress, and the deposition of proteins in PK-/-/TauVLW mice, a model of complex neurodegenerative disorders.
The inflammatory compound, C-reactive protein, is involved in the development of Alzheimer’s disease, other forms of dementia, heart disease, diabetes and most likely cancer and arthritis. A solid study of a large population sample found that people who smoked marijuana at least three times per week had half of the blood levels of C-reactive protein as those who did not use marijuana (Decreased prevalence of diabetes in marijuana users, 2012). This is more evidence that responsible marijuana use benefits human health by preventing disease-friendly internal environments, interrupting disease processes. and triggering repair mechanisms.
Neurochem Int. 2012 Feb Promotion of β-amyloid production by C-reactive protein and its implications in the early pathogenesis of Alzheimer’s disease. Bi BT, Lin HB, Cheng YF, Zhou H, Lin T, Zhang MZ, Li TJ, Xu JP.SourceDepartment of Pharmacology, School of Pharmaceutical Sciences, Southern Medical University, Guangzhou, Guangdong 510515, China. Abstract: C-reactive protein CRP and β-amyloid protein Aβ are involved in the development of Alzheimer’s disease AD. However, the relationship between CRP and Aβ production is unclear. In vitro and in vivo experiments were performed to investigate the association of CRP with Aβ production. Using the rat adrenal pheochromocytoma cell line PC12 cells to mimic neurons, cytotoxicity was evaluated by cell viability and supernatant lactate dehydrogenase LDH activity. The levels of amyloid precursor protein APP, beta-site APP cleaving enzyme BACE-1, and presenilins PS-1 and PS-2 were investigated using real-time polymerase chain reaction and Western blotting analysis. Aβ1-42 was measured by enzyme-linked immunosorbent assay. The relevance of CRP and Aβ as well as potential mechanisms were studied using APP/PS1 transgenic Tg mice. Treatment with 0.5-4.0 μM CRP for 48 h decreased cell viability and increased LDH leakage in PC12 cells. Incubation with CRP at a sub-toxic concentration of 0.2 μM increased the mRNA levels of APP, BACE-1, PS-1, and PS-2, as well as Aβ1-42 production. CRP inhibitor reversed the CRP-induced upregulations of the mRNA levels of APP, BACE-1, PS-1, and PS-2, and the protein levels of APP, BACE-1, PS-1, and Aβ1-42, but did not reversed Aβ1-42 cytotoxicity. The cerebral levels of CRP and Aβ1-42 in APP/PS1 Tg mice were positively correlated, accompanied with the elevated mRNA expressions of serum amyloid P component SAP, complement component 1q C1q, and tumor necrosis factor-α TNF-α. These results suggest that CRP cytotoxicity is associated with Aβ formation and Aβ-related markers expressions; CRP and Aβ were relevant in early-stage AD; CRP may be an important trigger in AD pathogenesis.