Combined Grey Matter VBM and White Matter TBSS ... [Brain Topogr. 2013] - PubMed - NCBI

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,                                       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.

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Translational Psychiatry - Cannabidiol enhances anandamide signaling and alleviates psychotic symptoms of schizophrenia

The cannabinoid cannabidiol, (CBD)--found in marijuana--has remarkable effects against schizophrenic psychosis. It also shows great promise for treating breast cancer and diabetes. The only place you can get medications, i.e. cannabis and cannabis remedies with CBD, is from dispensaries in states with medical marijuana laws. Dispensaries contract with growers to purchase high CBD strains and the products are then tested by analytical labs to ascertain the levels of CBD and THC. The availability of these products has salvaged many, many patients' health and relieved an immense amount of suffering. Why are politicians who claim to be compassionate and concerned about citizens' health care working so hard to close down dispensaries? Terrible, terrible politicians like Dianne Feinstein remain arrogantly and smugly ignorant and cling to out-dated reefer-madness based policies with their greedy blood-stained talons not giving a damn about the misery of cancer, AIDS, Alzheimer's disease, diabetes and mental illness patients. Citation: Translational Psychiatry 2012 2, e94; doi:10.1038/tp.2012.15Published online 20 March 2012Cannabidiol enhances anandamide signaling and alleviates psychotic symptoms of schizophreniaF M Leweke1,2, D Piomelli3,4, F Pahlisch1,3, D Muhl2,3, C W Gerth2, C Hoyer1,2, J Klosterkötter2, M Hellmich5 and D Koethe1,2 1Department of Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany 2Department of Psychiatry and Psychotherapy, University of Cologne, Cologne, Germany 3Department of Pharmacology and Biological Chemistry, University of California, Irvine, CA, USA 4The Unit of Drug Discovery and Development, Italian Institute of Technology, Genova, Italy 5Institute for Medical Statistics, Informatics, and Epidemiology, University of Cologne, Cologne, GermanyCorrespondence: Professor FM Leweke, Department of Psychiatry and Psychotherapy, Central Institute of Mental Health, University of Heidelberg, Medical Faculty Mannheim, J5, 68159 Mannheim, Germany. E-mail:; D Piomelli, Department of Pharmacology and Biological Chemistry, University of California, Irvine, 3101 Gillespie Neuroscience Facility, Irvine, CA 91697-4625, USA. E-mail: piomelli@uci.eduReceived 13 October 2011; Revised 9 January 2012; Accepted 30 January 2012Top of pageAbstractCannabidiol is a component of marijuana that does not activate cannabinoid receptors, but moderately inhibits the degradation of the endocannabinoid anandamide. We previously reported that an elevation of anandamide levels in cerebrospinal fluid inversely correlated to psychotic symptoms. Furthermore, enhanced anandamide signaling let to a lower transition rate from initial prodromal states into frank psychosis as well as postponed transition. In our translational approach, we performed a double-blind, randomized clinical trial of cannabidiol vs amisulpride, a potent antipsychotic, in acute schizophrenia to evaluate the clinical relevance of our initial findings. Either treatment was safe and led to significant clinical improvement, but cannabidiol displayed a markedly superior side-effect profile. Moreover, cannabidiol treatment was accompanied by a significant increase in serum anandamide levels, which was significantly associated with clinical improvement. The results suggest that inhibition of anandamide deactivation may contribute to the antipsychotic effects of cannabidiol potentially representing a completely new mechanism in the treatment of schizophrenia.Keywords:anandamide; cannabidiol; endocannabinoid; fatty acid amide hydrolase; human; schizophrenia

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