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.
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.
Study Says Cannabis May Help Reverse Dementia From Alzheimer’s February 14, 2013 Toke up for the sake of your brain? The Sydney Morning Herald reports: A team from Neuroscience Research Australia is in the early stages of research examining if one of the main active ingredients in cannabis, called cannabidiol, could reverse some of the symptoms of memory loss in animals. Tim Karl, a senior research fellow with the group, said cannabidiol has been found to have anti-inflammatory, antioxidant and other effects that could be beneficial for the brain. His study involved injecting cannabidiol into mice that had symptoms similiar to those seen in Alzheimer’s, as well as examining what would happen to brain cells treated with the drug. Dr Karl found that when the mice were given the cannabidiol they showed drastic improvement on parts of the tests that were related to recognising and remembering objects and other mice: “You could say it cured them.”
Now we see that the so-called research that the opponents of marijuana legalization were touting as "definitive proof" that marijuana use damages teen brains has been revealed as bogus with flawed methodology and deceptive causal inference drawn from premature evidence. The review of the pseudo-scientific deceit found that "the true effect (of marijuana on teen cognition) could be zero." So how did the original research team come up with such flawed results? By tailoring the study's parameters and subject population and protocol to give them the results they wanted. Why? Because bad science on marijuana gets excellent funding. With the turn in public opinion and the move by the first two states to legalize marijuana, be prepared to hear more and more desperate assertions drawn from bogus research in a pitiful effort to hide the truth about marijuana and how it benefits human health. 2013 Jan 14. [Epub ahead of print]
Correlations between cannabis use and IQ change in the Dunedin cohort are consistent with confounding from socioeconomic status.
Does cannabis use have substantial and permanent effects on neuropsychological functioning? Renewed and intense attention to the issue has followed recent research on the Dunedin cohort, which found a positive association between, on the one hand, adolescent-onset cannabis use and dependence and, on the other hand, a decline in IQ from childhood to adulthood [Meier et al. (2012) Proc Natl Acad Sci USA 109(40):E2657-E2664]. The association is given a causal interpretation by the authors, but existing research suggests an alternative confounding model based on time-varying effects of socioeconomic status on IQ. A simulation of the confounding model reproduces the reported associations from the Dunedin cohort, suggesting that the causal effects estimated in Meier et al. are likely to be overestimates, and that the true effect could be zero. Further analyses of the Dunedin cohort are proposed to distinguish between the competing interpretations. Although it would be too strong to say that the results have been discredited, the methodology is flawed and the causal inference drawn from the results premature.
So much for the scary IQ "study" that claimed teens are vulnerable to an 8-point IQ loss if they use marijuana frequently. The findings were discredited by a thorough review of the data by an outside investigator. There are solid reasons that teens should not be using marijuana regularly, unless they are ill, and these horror stories only muddy the water. Whenever you see a report on a study that claims terrible harm from marijuana, be suspicious, very suspicious. There are numerous so-called clinical investigators who I call researchstitutes (prostituting researchers) who have access to hundreds of millions of dollars from the federal health bureaucracy to fund studies designed and calculated to find harm from marijuana. This is not honest research and the sad thing is that the investigators who pull these scams justify their dishonesty with 20th century reefer madness fallacies, they believe that the end goal of discouraging marijuana use justifies them torturing data and shading results to conform to their expectations. They conduct small studies with patients populations at risk for the maladies they want to associate with marijuana and they ignore contradictory evidence and highlight insubstantial evidence, taken out of context, that seems to offer confirmation of their beliefs. When one conducts small studies, confounding variables sometimes appear and stand out because of the small number of other subjects. When larger studies are done these anomalies disappear. The dishonest researchstitutes who promote disinformation about marijuana take the unusual results when they happen to appear and assert their importance in the face of contrary evidence. Unfortunately, most news reporters are not scientifically literate enough, or even curious enough to look at the actual studies behind the scary press releases. Thank goodness there are other more honest scientists willing to devote the time and resources to double check spurious claims by sleazy, money-grubbing federal henchmen. Oh, another way bogus results are generated is by injecting rats and mice with synthetic cannabinoids (similar to the "bath salts" marketed to avoid marijuana laws) and then claiming the negative results apply to human use of marijuana.
The mainstream media is finally recognizing what an amazing story it is that cannabinoids, just like the ones in marijuana, protect and improve our health. The latest from TIME magazine: The latest review, published in Philosophical Transactions of the Royal Society B, suggests that activating the brain’s cannabinoid system may trigger a sort of anti-oxidant cleanse, removing damaged cells and improving the efficiency of the mitochrondria, the energy source that powers cells, ultimately leading to a more robustly functioning brain.Previous studies have linked cannabinoids to increased amounts of brain-derived neurotrophic factor BDNF, a substance that protects brain cells and promotes the growth of new ones. Since new cell growth slows or stops during aging, increasing BDNF could potentially slow the decline in cognitive functions.
Once again we see no harm to the brain from regular marijuana use, in fact this study presents evidence that connectivity in the brain is enhanced by long-term, chronic marijuana smoking. Unfortunately, hobbled by euphoranoia and marijuanaphobia, the authors speculate that these improvements in brain structure result from compensatory actions resulting from impairment by euphoria when in reality the improvement in brain structure is more likely the result of direct actions triggered by cannabinoids, especially THC. We know that THC has the amazing ability to stimulate the production of healthy new brain cells, a process known as neurogenesis, therefore it is not unreasonable to speculate that the improved connections in the brain result from the positive biochemical effects of this neuroprotective, neuroreparative cannabinoid. The powerful stigma associated with marijuana that was brainwashed into two generations with reefer madness campaigns supported by reams of pseudo-scientific data continues to blind researchers to the reality that cannabinoids are health-building and health-regulating compounds and that supplementing our naturally-produced supply of these vital compounds with cannabis or cannabis products vastly improves all aspects of human health. Functional Connectivity in Brain Networks Underlying Cognitive Control in Chronic Cannabis Users
Ian H Harding1, Nadia Solowij2,3, Ben J Harrison1, Michael Takagi1, Valentina Lorenzetti1, Dan I Lubman4, Marc L Seal5,6, Christos Pantelis1 and Murat Yücel1
1Department of Psychiatry, Melbourne Neuropsychiatry Centre, University of Melbourne and Melbourne Health, Melbourne, VIC, Australia
2School of Psychology, University of Wollongong, Wollongong, NSW, Australia
3Schizophrenia Research Institute, Sydney, NSW, Australia
4Turning Point Alcohol and Drug Centre, Eastern Health and Monash University, Melbourne, VIC, Australia
5Murdoch Childrens Research Institute, Melbourne, VIC, Australia
6Department of Paediatrics, University of Melbourne, Melbourne, VIC, Australia
Correspondence: Dr IH Harding and Professor M Yücel, Department of Psychiatry, Melbourne Neuropsychiatry Centre, Alan Gilbert Building, University of Melbourne, 3/161 Barry Street, Carlton, Melbourne, VIC 3053, Australia, Tel: (+61 3) 8344 1861, Fax: (+61 3) 9348 0469, E-mail: firstname.lastname@example.org and email@example.com
Received 21 September 2011; Revised 13 February 2012; Accepted 1 March 2012
Advance online publication 25 April 2012
Top of page
The long-term effect of regular cannabis use on brain function underlying cognitive control remains equivocal. Cognitive control abilities are thought to have a major role in everyday functioning, and their dysfunction has been implicated in the maintenance of maladaptive drug-taking patterns. In this study, the Multi-Source Interference Task was employed alongside functional magnetic resonance imaging and psychophysiological interaction methods to investigate functional interactions between brain regions underlying cognitive control. Current cannabis users with a history of greater than 10 years of daily or near-daily cannabis smoking (n=21) were compared with age, gender, and IQ-matched non-using controls (n=21). No differences in behavioral performance or magnitude of task-related brain activations were evident between the groups. However, greater connectivity between the prefrontal cortex and the occipitoparietal cortex was evident in cannabis users, as compared with controls, as cognitive control demands increased. The magnitude of this connectivity was positively associated with age of onset and lifetime exposure to cannabis. These findings suggest that brain regions responsible for coordinating behavioral control have an increased influence on the direction and switching of attention in cannabis users, and that these changes may have a compensatory role in mitigating cannabis-related impairments in cognitive control or perceptual processes.
attention; brain; cannabis; cognitive control; functional connectivity