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Post by beebs on Jun 14, 2012 17:25:51 GMT -5
Copied and pasted my post on FB: Look up suppression of info on curative "Hemp Oil" with Rick Simpoon and others, THC, CBDs, species, and Big Pharma Pharmacia & Johnson produced at a secret location in the South of the UK. Its produced from Cannabis Stavia L, + synthetics. Unpleasant side effects, Sativa stimulates, helps with focus, but can trigger paranoia & tachycardia, due to the high content of THC and other unknown compounds. No wonder patients complain of nasty side effects. Indica OTOH, is not psychoactive, contains better ratio of THC to CBD compound, "cures" cancers, and other diseases, helps with insomnia, and CNS symptoms. The ratio of THC and CBD should be appropriate depending on treatment. Neuroscientists and other scientists in Belgium, Spain, UK and USA, researching for CNS symptoms, cancer and other diseases. Unfortunately, those two known compounds are being extracted and mixed with synthetics. CBC and THC are patented. Do your homework being gulping down the oil... More posts will follow.
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Post by beebs on Jun 15, 2012 4:11:29 GMT -5
I was unsure about vested interests, a closer look leads me to believe, that Cannabis has merit for health benefits. Reading up yielded evidence that Cannabis has been used by various models of medicine for centuries which adds more credibility. Big Pharma know the therapeutic effects for cancer for many years, the snag - it would destroy the "Cancer Industry" continue to decimate entire cancer population with chemo/radiation, known to have less than 3% success rate and yields billions per year!! There are thousands of other compounds working in synergy in cannabis, which are unidentified. THC & CBD compounds have been patented. Altering its molecular structure by adding synthetics, will undoubtedly reduce its therapeutic effects and/or cause unnecessary side effects. The article mentions THC compounds kills cancer cells Active Ingredient in Marijuana Kills Brain Cancer Cells Experts say finding worth further study, but patients shouldn't light up just yet.By Alan Mozes HealthDay Reporter WEDNESDAY, April 1 (HealthDay News) -- New research out of Spain suggests that THC -- the active ingredient in marijuana -- appears to prompt the death of brain cancer cells. The finding is based on work with mice designed to carry human cancer tumors, as well as from an analysis of THC's impact on tumor cells extracted from two patients coping with a highly aggressive form of brain cancer. Explaining that the introduction of THC into the brain triggers a cellular self-digestion process known as "autophagy," study co-author Guillermo Velasco said his team has isolated the specific pathway by which this process unfolds, and noted that it appears "to kill cancer cells, while it does not affect normal cells." Cont/.... health.usnews.com/health-news/family-health/cancer/articles/2009/04/01/active-ingredient-in-marijuana-kills-brain-cancer
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Post by beebs on Jun 15, 2012 5:35:12 GMT -5
The article is an easy read, from the International Journal of Oncology. Many have "cured" their cancers by taking the oil version, reported the cure, were shunned by the establishment. Look up Rick Simpson on YT. Int J Oncol. 2012 Aug;41(2):407-13. doi: 10.3892/ijo.2012.1476. Epub 2012 May 14. Cannabinoid-associated cell death mechanisms in tumor models (Review). Calvaruso G, Pellerito O, Notaro A, Giuliano M. Source Department of Experimental Biomedicine and Clinical Neuroscience, Section of Biochemical Sciences, University of Palermo, 90129 Palermo, Italy. Abstract In recent years, cannabinoids (the active components of Cannabis sativa) and their derivatives have received considerable interest due to findings that they can affect the viability and invasiveness of a variety of different cancer cells. Moreover, in addition to their inhibitory effects on tumor growth and migration, angiogenesis and metastasis, the ability of these compounds to induce different pathways of cell death has been highlighted. Here, we review the most recent results generating interest in the field of death mechanisms induced by cannabinoids in cancer cells. In particular, we analyze the pathways triggered by cannabinoids to induce apoptosis or autophagy and investigate the interplay between the two processes. Overall, the results reported here suggest that the exploration of molecular mechanisms induced by cannabinoids in cancer cells can contribute to the development of safe and effective treatments in cancer therapy .http://www.ncbi.nlm.nih.gov/pubmed/22614735
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Post by beebs on Jun 15, 2012 6:18:12 GMT -5
The study below, appears promotional, patients who took www.neurosoup.com/sativex.htm reported dizziness, vomiting, tachycardia, and other unpleasant side effects. Not mentioned in the article. Also reported, negligible benefits. In contrast, those who juice the leaves, take the oil, report sleeping well. Others, who didn't do their homework, reported tachycardia, due to the high THC content. If I was to take it for health benefits, I would approach an Ayurvedic doctor or TCM, find out about various species, juice the leaves, eat in salads, take the oil, ensuring its purity, and trying various combos of THC and CBD ratio. Its about experimenting and find what is the right combo (as with everything else, including vits and supps). Apparently, hundreds of hybrids are being developed, sadly, some companies are focusing on THC and CBDs.. Br J Clin Pharmacol. 2012 Jul;74(1):42-53. doi: 10.1111/j.1365-2125.2012.04164.x. Novel Δ(9) -tetrahydrocannabinol formulation Namisol® has beneficial pharmacokinetics and promising pharmacodynamic effects.Klumpers LE, Beumer TL, van Hasselt JG, Lipplaa A, Karger LB, Kleinloog HD, Freijer JI, de Kam ML, van Gerven JM. Source Centre for Human Drug Research, Zernikedreef 10, 2333 CL Leiden Echo Pharmaceuticals, 14thFloor Unit A1, Jonkerbosplein 52, 6534 AB Nijmegen, the Netherlands. Abstract WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT • Cannabis based medicines are registered as a treatment for various indications, such as pain and spasms in multiple sclerosis (MS) patients, and anorexia and nausea in patients with HIV or receiving cancer treatment. • the pharmacokinetics of the various administration routes of cannabis and cannabis based medicines are variable and dosing is hard to regulate. WHAT THIS STUDY ADDS • Namisol is a new tablet containing pure THC (>98%) that has a beneficial pharmacokinetic profile after oral administration. • Namisol gives a quick onset of pharmacodynamic effects in healthy volunteers, which implies a rapid initiation of therapeutic effects in patients. AIMS Among the main disadvantages of currently available Δ(9) -tetrahydrocannabinol (THC) formulations are dosing difficulties due to poor pharmacokinetic characteristics. Namisol® is a novel THC formulation, designed to improve THC absorption. The study objectives were to investigate the optimal administration route, pharmacokinetics (PK), pharmacodynamics (PD) and tolerability of Namisol®. METHODS This first in human study consisted of two parts. Panel I included healthy males and females (n = 6/6) in a double-blind, double-dummy, randomized, crossover study with sublingual (crushed tablet) and oral administration of Namisol® (5 mg THC). Based on these results, male and female (n = 4/5) participants from panel I received oral THC 6.5 and 8.0 mg or matching placebo in a randomized, crossover, rising dose study during panel II. PD measurements were body sway; visual analogue scales (VAS) mood, psychedelic and heart rate. THC and 11-OH-THC population PK analysis was performed. RESULTS Sublingual administration showed a flat concentration profile compared with oral administration. Oral THC apparent t(1/2) was 72-80 min, t(max) was 39-56 min and C(max) 2.92-4.69 ng ml(-1) . THC affected body sway (60.8%, 95% CI 29.5, 99.8), external perception (0.078 log mm, 95% CI 0.019, 0.137), alertness (-2.7 mm, 95% CI -4.5, -0.9) feeling high (0.256 log mm, 95% CI 0.093, 0.418) and heart rate (5.6 beats min(-1) , 95% CI 2.7, 6.5). Namisol® was well tolerated. CONCLUSIONS Oral Namisol® showed promising PK and PD characteristics. Variability and t(max) of THC plasma concentrations were smaller for Namisol® than reported for studies using oral dronabinol and nabilone. This study was performed in a limited number of healthy volunteers. Therefore, future research on Namisol® should study clinical effects in patient populations. www.ncbi.nlm.nih.gov/pubmed/22680341
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Post by beebs on Jun 15, 2012 6:46:26 GMT -5
See article below. J Mol Med (Berl). 2012 Jan 10. [Epub ahead of print] Chemopreventive effect of the non-psychotropic phytocannabinoid cannabidiol on experimental colon cancer.Aviello G, Romano B, Borrelli F, Capasso R, Gallo L, Piscitelli F, Di Marzo V, Izzo AA. Source Department of Experimental Pharmacology, Endocannabinoid Research Group, University of Naples Federico II, Naples, Italy. Abstract Colon cancer affects millions of individuals in Western countries. Cannabidiol, a safe and non-psychotropic ingredient of Cannabis sativa, exerts pharmacological actions (antioxidant and intestinal antinflammatory) and mechanisms (inhibition of endocannabinoid enzymatic degradation) potentially beneficial for colon carcinogenesis. Thus, we investigated its possible chemopreventive effect in the model of colon cancer induced by azoxymethane (AOM) in mice. AOM treatment was associated with aberrant crypt foci (ACF, preneoplastic lesions), polyps, and tumour formation, up-regulation of phospho-Akt, iNOS and COX-2 and down-regulation of caspase-3. Cannabidiol-reduced ACF, polyps and tumours and counteracted AOM-induced phospho-Akt and caspase-3 changes. In colorectal carcinoma cell lines, cannabidiol protected DNA from oxidative damage, increased endocannabinoid levels and reduced cell proliferation in a CB(1)-, TRPV1- and PPARγ-antagonists sensitive manner. It is concluded that cannabidiol exerts chemopreventive effect in vivo and reduces cell proliferation through multiple mechanisms. www.ncbi.nlm.nih.gov/pubmed/22231745
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Post by beebs on Jun 16, 2012 13:21:22 GMT -5
Will put up more vids -
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Post by beebs on Jun 26, 2012 10:06:40 GMT -5
See the cute rabbit vid below the article. Arthritis Res Ther. 2008;10(2):R43. Epub 2008 Apr 16. Characterisation of the cannabinoid receptor system in synovial tissue and fluid in patients with osteoarthritis and rheumatoid arthritis.Richardson D, Pearson RG, Kurian N, Latif ML, Garle MJ, Barrett DA, Kendall DA, Scammell BE, Reeve AJ, Chapman V. Source Centre for Analytical Bioscience, School of Pharmacy, University of Nottingham, Nottingham, NG7 2RD, UK. denise.richardson@pfizer.com Abstract INTRODUCTION: Cannabis-based medicines have a number of therapeutic indications, including anti-inflammatory and analgesic effects. The endocannabinoid receptor system, including the cannabinoid receptor 1 (CB1) and receptor 2 (CB2) and the endocannabinoids, are implicated in a wide range of physiological and pathophysiological processes. Pre-clinical and clinical studies have demonstrated that cannabis-based drugs have therapeutic potential in inflammatory diseases, including rheumatoid arthritis (RA) and multiple sclerosis. The aim of this study was to determine whether the key elements of the endocannabinoid signalling system, which produces immunosuppression and analgesia, are expressed in the synovia of patients with osteoarthritis (OA) or RA. METHODS: Thirty-two OA and 13 RA patients undergoing total knee arthroplasty were included in this study. Clinical staging was conducted from x-rays scored according to Kellgren-Lawrence and Larsen scales, and synovitis of synovial biopsies was graded. Endocannabinoid levels were quantified in synovial fluid by liquid chromatography-mass spectrometry. The expression of CB1 and CB2 protein and RNA in synovial biopsies was investigated. Functional activity of these receptors was determined with mitogen-activated protein kinase assays. To assess the impact of OA and RA on this receptor system, levels of endocannabinoids in the synovial fluid of patients and non-inflamed healthy volunteers were compared. The activity of fatty acid amide hydrolase (FAAH), the predominant catabolic endocannabinoid enzyme, was measured in synovium. RESULTS: CB1 and CB2 protein and RNA were present in the synovia of OA and RA patients. Cannabinoid receptor stimulation of fibroblast-like cells from OA and RA patients produced a time-dependent phosphorylation of extracellular signal-regulated kinase (ERK)-1 and ERK-2 which was significantly blocked by the CB1 antagonist SR141716A. The endocannabinoids anandamide (AEA) and 2-arachidonyl glycerol (2-AG) were identified in the synovial fluid of OA and RA patients. However, neither AEA nor 2-AG was detected in synovial fluid from normal volunteers. FAAH was active in the synovia of OA and RA patients and was sensitive to inhibition by URB597 (3'-(aminocarbonyl) [1,1'-biphenyl]-3-yl)-cyclohexylcarbamate). CONCLUSION: Our data predict that the cannabinoid receptor system present in the synovium may be an important therapeutic target for the treatment of pain and inflammation associated with OA and RA. www.ncbi.nlm.nih.gov/pubmed/18416822More studies: www.ncbi.nlm.nih.gov/pubmed?term=arthropathy%20arthritis%20indica%20%20cannabis www.youtube.com/watch?v=YCttegJ2rTM
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