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.

Marijuana-safe and effective for treating sleep apnea

Here is evidence that THC, the psychotropic cannabinoid found in marijuana, can benefit people suffering from sleep apnea. If you have sleep apnea, a toke or two of vaporized or smoked marijuana (or some tincture or an edible) could significantly improve your quality of life. Also, if there is some oxygen deprivation resulting from apnea, the cannabinoids will shield the brain and likely reduce the resulting damage. Front Psychiatry.  Epub 2013 Jan 22.

Proof of concept trial of dronabinol in obstructive sleep apnea.Prasad B, Radulovacki MG, Carley DW.SourceDepartment of Medicine, University of Illinois at Chicago Chicago, IL, USA.AbstractStudy Objective: Animal data suggest that Δ9-TetraHydroCannabinol Δ9THC stabilizes autonomic output during sleep, reduces spontaneous sleep-disordered breathing, and blocks serotonin-induced exacerbation of sleep apnea. On this basis, we examined the safety, tolerability, and efficacy of dronabinol Δ9THC, an exogenous Cannabinoid type 1 and type 2 CB1 and CB2 receptor agonist in patients with Obstructive Sleep Apnea OSA. Design and Setting: Proof of concept; single-center dose-escalation study of dronabinol. Participants: Seventeen adults with a baseline Apnea Hypopnea Index AHI ≥15/h. Baseline polysomnography PSG was performed after a 7-day washout of Continuous Positive Airway Pressure treatment. Intervention: Dronabinol was administered after baseline PSG, starting at 2.5 mg once daily. The dose was increased weekly, as tolerated, to 5 mg and finally to 10 mg once daily. Measurements and Results: Repeat PSG assessments were performed on nights 7, 14, and 21 of dronabinol treatment. Change in AHI ΔAHI, mean ± SD was significant from baseline to night 21 -14.1 ± 17.5; p = 0.007. No degradation of sleep architecture or serious adverse events was noted. Conclusion: Dronabinol treatment is safe and well-tolerated in OSA patients at doses of 2.5-10 mg daily and significantly reduces AHI in the short-term. These findings should be confirmed in a larger study in order to identify sub-populations with OSA that may benefit from cannabimimetic pharmacologic therapy.PMID: 23346060 [PubMed] PMCID: PMC3550518Free PMC Article

via Proof of concept trial of dronabinol in obs... [Front Psychiatry. 2013] - PubMed - NCBI.

Marijuana and the Teen Brain: How Prohibition Encourages Kids to Use Cannabis

By Clint Werner The opponents of marijuana legalization are running out of justifications for using the power of law enforcement to ruin the lives of those who enjoy the substance but they continue to fan the dying embers of reefer madness hysteria with alarms about how policy reform will lead to an epidemic of teen brain degeneration. And yet, if their true goal is to reduce the prevalence of marijuana use among adolescents, standing firm against legalization could undermine the success of their efforts by affording marijuana the type of novel and manageable risk status that has strong appeal to the teen brain. Many of the assumptions held by theorists on how the teenage brain develops have been proven incorrect or incomplete by a series of MRI scans conducted by the National Institutes of Health on over one hundred adolescents in the 1990s. Although the brain has reached 90 percent of its physical size by about the age of 6 years-old, the internal structure of the brain undergoes dynamic changes during the adolescent years. The imaging has shown that the adolescent brain does not develop in a linear and balanced manner but that there is a disparity of maturation between the prefrontal and subcortical regions of the organ. It seems that maturation proceeds from back to front during the teenage years which explains the frequently irrational behavior that puzzles and vexes adults during this time. As teens mature, they experience a rapid development and activation of the region of the brain that governs rewards and emotions while the region that regulates our sense of impulse control, gratification delay and rational thinking remains immature. The angst of adolescence is largely a result of the awkward and difficult effort to coordinate emotions and behavior into the greater social and intellectual environment. This behavior involves irregular development between emotional impulsivity and impulse control that frequently appears to mimic psychopathology. These awkward feelings and impulses serve to trigger independence and novelty-seeking behaviors that too frequently result in suboptimal decisions that can lead to injuries, violence, unintended pregnancies, STDs and substance abuse. While developments that increase these kinds of risks might seem to defeat the evolutionary drive for survival, they actually serve the valuable purpose of propelling young people out of the family home into independence in society. The impulsivity and increase in risk taking serve a purpose because “leaving home is a high-risk behavior.” There seems to be universality to this behavior because, according to the researchers who conducted the NIH study, “during adolescence, independence-seeking behaviors are prevalent across species.” Unfortunately, for those who cite concerns over adolescent marijuana use as a reason to maintain criminalization or to move toward a Cold War on pot in which everyone is screened and forced into “treatment,” this type of response may very well prime young people to seek out marijuana. The laws against marijuana make it a more novel substance than products that have been integrated into our culture such as alcohol, tobacco and caffeine. The efforts to segregate cannabis out of our society in order to protect children apparently has the opposite effect, giving it an outlaw appeal that is reinforced by the appeal of violating parental approval in independence-seeking behavior. According to the NIH experts, teens are to oblivious to the serious hazards posed by their behavioral choices but their impulse control is over-ridden by emotion and rewards of peer-approval. Using marijuana appeals to this mentality because there is plenty of evidence that the risks are comparatively minor and the novelty appeal is great. The larger marijuana culture, also fostered by criminalization, has a draw for the teen that is looking for a means of expressing independence from the parents. For the thrill-seeking teen, smoking marijuana has outlaw appeal but less risk than stealing a car or picking a fight. A number of papers have asserted that the Netherlands where marijuana distribution is treated as a quasi-legal enterprise, use by teenagers is significantly lower than teen use in the U.S. recent data also shows a drop in teen marijuana use in Arizona since the passage of a medical cannabis law. When marijuana is legalized, the forbidden fruit nature of the substance is mitigated by cultural familiarity. Of course, sensible age restrictions on alcohol maintain an appeal that drives teens to seek them out for abuse, so there is no assertion that legalization would eradicate youthful marijuana use but it would dampen the allure of the forbidden. Many longtime, high profile marijuana advocates have found that their kids have no interest in using marijuana because it is completely novelty-free for them. Ed Rosenthal, the guru of ganja, his son has never been interested in what is his father’s lifelong passion. Keith Stroup, the founder of the National Organization for the Reform of Marijuana Laws (NORML), says that his daughter never smokes cannabis so he has to get high with his son-in-law. The residual reefer madness hysteria that sustains an irrational and counterproductive policy of marijuana criminalization is a self-defeating situation in terms of protecting the kids. Limiting teen access to marijuana is a worthy effort because, despite the lack of harm—and indeed possible benefits—to the adult brain from marijuana use, there may indeed be some impairment to cognition for the rapidly-developing adolescent brain. Julie Holland, M.D., author of The Pot Book, once described teen brain development as similar to a tree that is branching out, expanding connections which then undergo a pruning back phase to tighten up connections. The NIH research reveals that the dendrites—signal-receiving structures—do branch out and the frequently-used synapses grow vital while the lesser-used synapses begin to wither away in a process called “synaptic pruning” which serves the speed and efficiency of the brain. Researchers in Australia, hoping to find some form of brain damage caused by chronic cannabis use, instead were surprised to discover that regular, long-term marijuana smokers experienced a significant increase in functional connectivity in the brain, specifically “greater connectivity between the prefrontal cortex and the occipitoparietal cortex was evident in cannabis users, as compared with controls.” Is it possible that this cannabinoid-driven enhancement of functional connectivity in adult brains impairs synaptic pruning in teens? Neurologist Gary Wenk, Ph.D. has researched the effects of cannabinoids, such as are found in marijuana, on the brain and found positive effects in adults but he cautions that research has shown that “using marijuana prior to age 15 performed more poorly on all aspects of executive function tasks years compared with those who started using marijuana after age 15 or those who had never used marijuana.” Executive function is controlled by the frontal lobes, the ones that mature last and control complex thought, reasoning, planning and impulse control over emotional reactivity. It is encouraging that “scientists did not find differences in executive functioning abilities of people who started smoking marijuana after age 15 as compared to people who had never smoked marijuana.” Unfortunately, the novelty appeal of marijuana’s criminality lures the most vulnerable set of youth into using it when they are most susceptible to habituation. Cannabis is not physically addictive in the way that other drugs such as cocaine and heroin are but one of its great appeals is its ability to heighten the sense of novelty, to alleviate the sense of the mundane and make everyday objects seem fascinating. Raphael Mechoulam, M.D., the Israeli researcher who discovered the structure of the cannabinoids, suggests that one of their functions is to assist the mind in beneficial forgetting so that one does not become overwhelmed by the memories of every face seen and every word heard. This effect contributes to the “Oh wow” effect that marijuana use evokes, wherein everyday objects seem novel and fascinating. For the as-yet-undeveloped adolescent brain which is geared to seek novelty in order to propel the youth into an independent life away from the parental home, marijuana can become a cul-de-sac, a cloister of easily accessed novelty which sabotages the intent of the novelty-seeking brain. If everything in the surrounding environment is transformed into novelty the impulse to seek novelty can be stunted. This could be an underlying explanation for the not entirely unjustified stereotype of the 20 or 30-something stoner living at his parents’ home in the basement. On the other hand, in 2009, researchers published a study which was intended to find out how much harm alcohol and marijuana cause to the brain when used together. The scientists were surprised to discover that binge-drinking teens who smoked marijuana had significant protection from alcohol’s damage to the white matter of their brains when compared to binge drinkers who did not use marijuana. It is clear that any deficit that might occur to the teenage brain from chronic marijuana use does not compare to the devastating damage done by alcohol-poisoning. Another harmful aspect of prohibition is that the threat of imprisonment and the irrational stigma grafted to marijuana through years of propaganda serves to reduce the social contacts of young marijuana users at a time when such experiences are vital for the development social skills. Teenage marijuana users often form cliques that alienate them from the larger arena of social interaction. Some schools conduct marijuana screening and ban users from extracurricular activities, which only compound these problems. Once again, prohibition only serves to aggravate problems with teen marijuana use. The most rational way to approach teen marijuana use is to legalize and normalize adult use, thus making it less appealing as a novel, risk-taking behavior. Also, placing barriers to teen acquisition of marijuana by permitting commercial distribution to adults with penalties for diversion will make marijuana less easily available and will also reduce teen exposure to the illegal polydrug marketplace. One reason that teen cannabis use is lower in the Netherlands, along with the lack of outlaw novelty appeal, is the tight regulation that keeps youngsters out of cannabis shops and eradicates demand for black market street sales of marijuana and hashish. The prohibition zealots are apoplectic that two U.S. states have legalized marijuana and they rail about the threat that this liberalization means to children and warn of a generation of brain dead youth, but sadly, they may be their own worst enemies when it comes to discouraging adolescent use of marijuana.

Marijuana protects drunkards' brains during booze withdrawal

The following data is pretty academic but what it essentially says is that withdrawal from alcohol so severely disrupts brain chemistry that it kills brain cells and that there is some solid evidence that using marijuana can reduce the severity of the damage. Put that in your pipe and smoke it! Isn't it amazing that alcohol addiction so completely sabotages and rewires brain chemistry that suddenly stopping drinking it can kill brain cells? And then when you consider that activating the CB1 receptor, as using marijuana does, shields the brain from the booze damage, you just have to shake your head at the injustice of cannabis prohibition and vow to work harder to tell the general public the truth that the drug warriors want to keep buried. Pharmacological activation/inhibition of the cannabinoid system affects alcohol withdrawal-induced neuronal hypersensitivity to excitotoxic insults.Rubio M, Villain H, Docagne F, Roussel BD, Ramos JA, Vivien D, Fernandez-Ruiz J, Ali C.SourceINSERM U919 Serine Protease and Pathophysiology of the Neurovascular Unit, UMR CNRS 6232 CINAPS, Caen, France. rubio@cyceron.frAbstractCessation of chronic ethanol consumption can increase the sensitivity of the brain to excitotoxic damages. Cannabinoids have been proposed as neuroprotectants in different models of neuronal injury, but their effect have never been investigated in a context of excitotoxicity after alcohol cessation. Here we examined the effects of the pharmacological activation/inhibition of the endocannabinoid system in an in vitro model of chronic ethanol exposure and withdrawal followed by an excitotoxic challenge. Ethanol withdrawal increased N-methyl-D-aspartate NMDA-evoked neuronal death, probably by altering the ratio between GluN2A and GluN2B NMDA receptor subunits. The stimulation of the endocannabinoid system with the cannabinoid agonist HU-210 decreased NMDA-induced neuronal death exclusively in ethanol-withdrawn neurons. This neuroprotection could be explained by a decrease in NMDA-stimulated calcium influx after the administration of HU-210, found exclusively in ethanol-withdrawn neurons. By contrast, the inhibition of the cannabinoid system with the CB1 receptor antagonist rimonabant SR141716 during ethanol withdrawal increased death of ethanol-withdrawn neurons without any modification of NMDA-stimulated calcium influx. Moreover, chronic administration of rimonabant increased NMDA-stimulated toxicity not only in withdrawn neurons, but also in control neurons. In summary, we show for the first time that the stimulation of the endocannabinoid system is protective against the hyperexcitability developed during alcohol withdrawal. By contrast, the blockade of the endocannabinoid system is highly counterproductive during alcohol withdrawal.

via Pharmacological activation/inhibition of the cannab... [PLoS One. 2011] - PubMed - NCBI.