Marijuana Use Reduces Obesity » Marijuana Gateway to Health

Marijuana use is significantly protective against obesity as well as the harmful illnesses that accompany the syndrome. This is because THC and other cannabinoids work as systemic biological health regulators, the are key to our ability to survive and thrive. We really do need to encourage more adults to use marijuana in some form to improve their health and guard against degenerative illnesses. Science continues to affirm this position.                       Med Hypotheses. 2013 Feb 11. Cannabis and Δ9-tetrahydrocannabinol THC for weight loss?Le Foll B, Trigo JM, et al.Abstract: Obesity is one of the highest preventable causes of morbidity and mortality in the developed world [1]. 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 [2]. 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 Δ9-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.via Cannabis and Δ9-tetrahydrocannabinol THC … [Med Hypotheses. 2013] – PubMed – NCBI. via Marijuana Use Reduces Obesity » Marijuana Gateway to Health.

Marijuana's cannabinoids protect the brain from Alzheimer's disease

Here is more evidence that THC and CBD, cannabinoids from marijuana, can effectively protect us from the damage that leads to the development of Alzheimer's disease as well as other neurological ailments. The cannabinoid THC stimulates both the CB1 and CB2 receptors, but the cannabinoid CBD steers THC away from the CB1 receptor and over to the CB2 receptors, thus possibly activating the neuroprotective effects described in this study. With the trillion dollar threat that Alzheimer's disease poses to our national health care budget, isn't it critical that we recruit more adults to use some form of marijuana? Tell you friends and family that the most effective thing they can do to protect themselves from Alzheimer's disease is to start using cannabis--either smoking or vaporizing a small amount a few times a week, or taking some drops of a cannabis tincture before bedtime or eating a low-dose edible. What we want to do is increase the regular consumption of cannabinoids in our society because the evidence is in: using some form of marijuana regularly lowers our risks for developing numerous, serious illnesses. J Alzheimers Dis. 2013 Jan 1;354:847-58. doi: 10.3233/JAD-130137.CB2 Cannabinoid Receptor Agonist Ameliorates Alzheimer-Like Phenotype in AβPP/PS1 Mice.Aso E, Juvés S, Maldonado R, Ferrer I.SourceInstitut de Neuropatologia, Servei d'Anatomia Patològica, Abstract: The specific CB2 cannabinoid receptor agonist JWH-133 induced cognitive improvement in double AβPP/PS1 transgenic mice, a genetic model of Alzheimer's disease. This effect was more pronounced when administered at the pre-symptomatic rather than the early symptomatic stage. The cognitive improvement was associated with decreased microglial reactivity and reduced expression of pro-inflammatory cytokines IL-1β, IL-6, TNFα, and IFNγ. In addition, JWH-133 reduced the expression of active p38 and SAPK/JNK, increased the expression of inactive GSK3β, and lowered tau hyperphosphorylation at Thr181 in the vicinity of amyloid-β plaques. Moreover, JWH-133 produced a decrease in the expression of hydroxynonenal adducts, and enhanced the expression of SOD1 and SOD2 around plaques. In contrast, the chronic treatment with JWH-133 failed to modify the amyloid-β production or deposition in cortex and hippocampus. In conclusion, the present study lends support to the idea that stimulation of CB2 receptors ameliorates several altered parameters in Alzheimer's disease such as impaired memory and learning, neuroinflammation, oxidative stress damage and oxidative stress responses, selected tau kinases, and tau hyperphosphorylation around plaques.

via CB2 Cannabinoid Receptor Agonist Ameliorate... [J Alzheimers Dis. 2013] - PubMed - NCBI.

THC could be a chemotherapeutic agent for treating stomach cancer

Cannabinoids, such as THC, which activate the CB1 and CB2 cannabinoid receptors are more effective against stomach cancer than the main chemotherapy treatment. Using marijuana protects us from so many cancers and other illnesses, aren't you mad that it's still illegal? Anticancer Res. 2013 Jun;33(6):2541-7.

Cannabinoid Receptor Agonist as an Alternative Drug in 5-Fluorouracil-resistant Gastric Cancer Cells.

Xian XS, Park H, Choi MG, Park JM.

Source

Division of Gastroenterology, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, 505, Banpo-Dong, Seocho-Gu, Seoul, 137-070, Korea. parkjerry@catholic.ac.kr.

Abstract

Fluorouracil is the main chemotherapeutic drug used for gastrointestinal cancers, which suffers the important problem of treatment resistance. There is little information whether cannabinoid agonists can be used as an alternative drug for fluorouracil-resistant gastric cancer cells. In this study, we investigated the effects of a cannabinoid agonist, WIN-55,212-2, on 5-fluorouracil (5-FU)-resistant human gastric cancer cells, to examine whether the cannabinoid agonist may be an alternative therapy. Survival of the 5-FU-resistant gastric cancer cell line, SNU-620-5FU/1000, was not significantly reduced even by a high dose of 5-FU treatment. However, WIN-55,212-2 inhibited the proliferation of SNU-620-5FU/1000 and enhanced their apoptosis, as indicated by an increase of apoptotic cell proportion, activated caspase-3 and Poly (ADP-ribose) polymerase cleavage. Furthermore, WIN-55,212-2 reduced phospho-extracellular-signal-regulated kinases (ERK) 1/2, phospho-Akt (protein kinase B), B-cell lymphoma-2 (BCL2) and BCL2-associated X (BAX) protein expression in 5-FU-resistant gastric cancer cells. These results indicate that a cannabinoid agonist may, indeed, be an alternative chemotherapeutic agent for 5-FU-resistant gastric cancer.

KEYWORDS:

Gastric cancer, apoptosis, cannabinoids, drug resistance, fluorouracil

via Cannabinoid Receptor Agonist as an Alternativ... [Anticancer Res. 2013] - PubMed - NCBI.

THC from Marijuana Protects the Brain from Injury

Once again we see that using (even very small amounts of) marijuana improves our health by shielding the brain from the damage that follows a head injury. These same actions protect the brain from the age-related changes that lead to Alzheimer's disease and other forms of dementia. We need to recruit more people to use marijuana on a regular basis to lower our national health-care expenditures. Marijuana use is good for you! Tell someone today! Long-term behavioral and biochemical effects of an ultra-low dose of Δ9-tetrahydrocannabinol THC: neuroprotection and ERK signaling Miriam Fishbein, Sahar Gov, Fadi Assaf, Mikhal Gafni, Ora Keren, Yosef Sarne                                                                              Abstract: We have previously reported that a single injection of an ultra-low dose of delta-9-tetrahydrocannabinol THC; the psychoactive ingredient of marijuana protected the brain from pentylenentetrazole PTZ-induced cognitive deficits when applied 1–7 days before or 1–3 days after the insult. In the present study we expanded the protective profile of THC by showing that it protected mice from cognitive deficits that were induced by a variety of other neuronal insults, including pentobarbital-induced deep anesthesia, repeated treatment with 3,4 methylenedioxymethamphetamine MDMA; “ecstasy” and exposure to carbon monoxide. The protective effect of THC lasted for at least 7 weeks. The same ultra-low dose of THC 0.002 mg/kg, a dose that is 3–4 orders of magnitude lower than the doses that produce the known acute effects of the drug in mice induced long-lasting 7 weeks modifications of extracellular signal–regulated kinase ERK activity in the hippocampus, frontal cortex and cerebellum of the mice. The alterations in ERK activity paralleled changes in its activating enzyme MEK and its inactivating enzyme MKP-1. Furthermore, a single treatment with the low dose of THC elevated the level of pCREB phosphorylated cAMP response element–binding protein in the hippocampus and the level of BDNF brain-derived neurotrophic factor in the frontal cortex. These long-lasting effects indicate that a single treatment with an ultra-low dose of THC can modify brain plasticity and induce long-term behavioral and developmental effects in the brain.

via Long-term behavioral and biochemical effects of an ultra-low dose of Δ9-tetrahydrocannabinol THC: neuroprotection and ERK signaling - Springer.

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.

A Response to “Going to Pot” by Roxanne Khamsi

By Clint Werner, author of “Marijuana Gateway to Health”

In the June 2013 issue of Scientific American, “Science of Health” columnist Roxanne Khamsi wrote a surprisingly unscientific and biased piece on the health ramifications of legalizing marijuana that was sadly tainted with residue from last century’s reefer madness campaign. The title of the piece itself, “Going to Pot” is a loaded term that confers a negative association on the subject via cultural symbolism having nothing to do with the reality of what science is telling us about marijuana and how it affects the human organism and society. First, Ms. Khamsi is mistaken when she writes that doctors “may prescribe marijuana to treat or manage ailments.” In states with medical marijuana provisions, physicians write recommendations for their patients that allow access to dispensaries or cultivation cooperatives. Ms. Khamsi then asserts that “the safety of recreational use is poorly understood” and that “researchers worry that both short- and long-term use of the drug may harm the body and mind.” Researchers who are up-to-date on the science of marijuana have no such concerns regarding adult use. In terms of harming the body, recent research has revealed that regular use of marijuana actually seems to improve physical health. Population studies have shown that regular marijuana users have a reduced risk for developing lung cancer (Hashibe, Cancer Epidemiological, Biomarkers and Prevention, 2006), head and neck cancers (Liang, Cancer Prevention Research, 2009), bladder cancer (Thomas, American Urological Association meeting, 2013), lymphomas (Holly, American Journal of Epidemiology, 1999), as well as diabetes (Rajavashisth, BMJ Open, 2012). The diabetes protection data from the enormous NHANES report also revealed that subjects who smoked marijuana three times per week had a profound (> 50%) reduction in their blood levels of C reactive protein, a inflammation marker for heart disease, indicating that they experienced significant protection from developing cardiac disease. Research also revealed that regular, moderate marijuana smokers have improved lung function compared to non-marijuana smokers with no risk for developing COPD (Pletcher, JAMA, 2012). National Institute of Drug Abuse pulmonary researcher, Dr. Donald Tashkin has said that he now endorses legalization since there is no basis for concern about the substance’s negative effects on lung function. Given the nearly century-long reefer madness campaign waged with untold billions of government dollars, it is hard for people to grasp that a denigrated and criminalized substance could have such positive health effects, especially when smoked, but science trumps myth and superstition with evidence. In terms of mental health, a just-published paper reports that “marijuana use consistently buffered people from the negative consequences associated with loneliness and social exclusion” (Deckman, Social Psychological and Personality Science, 2013), which could be one of the reasons that researchers found a truly startling drop in suicides, especially among young adult men, following the enactment of state medical marijuana laws (Anderson, IDEAS, 2012). Other research has shown that marijuana’s anti-depressant effects could be the result of neurogenesis, the production of healthy and functional new brain cells, which is promoted by the cannabinoids in marijuana (Jiang, Journal of Clinical Investigation, 2005). Another recently-published study found that “mortality risk was lower in cannabis users than in non-cannabis users with psychotic disorders” (Koola, Journal of Psychiatric Research, 2013), indicating that marijuana is a beneficial treatment for mental problems rather than, as increasingly inferred, a causative agent. In attempting to explain the activity of marijuana’s cannabinoid molecules on the endocannabinoid receptors, Ms. Khamsi once again employs loaded language to imply a negative effect, writing that THC “triggers domino chains” which implies a collapse of order and function rather than an alteration in order and function, which is what is truly occurring. Ms. Khamsi then frets that using marijuana impairs “working memory.” Yes marijuana alters mental functioning; it shifts the mind into a blissful euphoria that redirects thought from the ordered and analytical to the relaxed and free-association style of thought that characterizes relaxation and insight. And unlike alcohol, which serves a similar function of quieting the work day mental noise, marijuana is not carcinogenic or lethal. Ms. Khamsi expresses the understandable concern that marijuana users will make our roadways more dangerous but this is not supported by data that shows us what actually happens when legal restrictions are eased. A comprehensive review of data from states with medical marijuana laws found that enactment of the laws led to a significant drop in traffic accident deaths by allowing for marijuana to substitute for alcohol, a far more impairing substance. Traffic accident fatalities dropped by 9 percent in medical marijuana states. (Anderson, pending publication in the Journal of Law and Economics, 2013). That is essentially the same level of protection afforded by the passage of mandatory sea belt laws and by increasing the age for alcohol consumption from 18 to 21 years. According to research conducted by the automobile insurance company 4autoinsurance.com, marijuana users are safe drivers because, unlike alcohol drinkers, they are aware of their level of impairment and either refuse to drive, delay driving or drive more carefully than normal by reducing speed and not changing lanes. Regular marijuana users showed far less evidence of impairment than did novice and occasional users. Impairment testing is the only way to effectively police for marijuana-impaired drivers without ruining the lives of people who pose no threat on the roadways. The cannabinoid CBD steers THC away from the CB1 receptor, thus dulling or nullifying the mind-altering effects, but CBD does not reduce THC levels in the blood. Therefore, a driver using a high CBD strain of marijuana could test over the THC limit while experiencing no psychoactive effects whatsoever. Consequently, effective and fair impairment assessment techniques will need to be developed. Ms. Khamsi then returns to the health effects of marijuana, but ignores the previously cited benefits of reduced risks for developing numerous cancers, diabetes and other inflammation- and oxidation-based degenerative illnesses, such as Alzheimer’s disease and arthritis. She then refers to the recent study of data from New Zealand that indicates that teenagers who use marijuana heavily have up to an 8 percent drop in IQ points. Those results were called into question upon review but still indicate a disturbing effect of heavy marijuana use on the developing adolescent brain. Neurologist Dr. Gary Wenk, who has written “a puff is enough” to protect the adult brain from age-related dementia, says that the effect of marijuana on a developing brain, especially in those under 15 years of age, is impairing. Regular use of marijuana by teens may also interfere with social and professional skill development by monopolizing the time and consciousness of teens that enjoy it. Ms. Khamsi correctly notes that black market marijuana is sometimes contaminated with “sand or glass beads” which are far more harmful to the user than cannabis itself. Black market marijuana is also frequently contaminated with insecticides not intended for use on plants that are consumed. Some of these products are neurotoxic and, ironically, may induce neurodegenerative illnesses by interfering with the functions of the endocannabinoid system. (Casida, Annual Review of Entomolgy, 2013) Smuggled marijuana is also stale and often riddled with mold. Given these threats to heavy teenage users, the question needs to be asked: How do we best reduce access to marijuana, especially the most harmful forms of marijuana, by teenagers? One study suggests that multidimensional family therapy (MDFT) is the most effective approach for treating teenagers with what is termed “cannabis use disorder” (Rigter, Drug and Alcohol Dependence, 2012). MDFT essentially reestablishes parental authority and time management in teens’ lives. If parents remain involved in all aspects of their teenage children’s lives, MDFT would not be necessary to correct a deficit in parenting. The best way to prevent teenage substance abuse is for parents to rigorously monitor and guide their children’s activities. By doing this, parents might not prevent experimentation but they can create an environment where regular access to and use of marijuana is impossible. Shrinking and killing off the black market via legalization and regulation can assist parents in this task, by making marijuana more difficult for teens to obtain. Dealers do not card and taking marijuana away from the illicit drug black market will also protect teens from the multiple drug offerings of those dealers. If teens do obtain marijuana on the sly, at least, having been diverted from legal and tested supplies, it will be less likely to be contaminated with more harmful substances. Commercial medical marijuana venders such as Harborside Health Center, which Khamsi mentioned, contract with growers and test their marijuana for safety and potency. Legalization transforms marijuana cultivators from shady criminals into proud artisans. And despite the possible risk of heavy marijuana use to teenagers’ cognition, a study of adolescent binge drinkers found that those who used marijuana suffered significantly less alcohol-related brain damage than the booze-only drinkers (Jacobus, Neurotoxicology and Teratology, 2009). Consider the irony: Marijuana protects the brains of booze binge drinkers. Ms. Khamsi also mentions increases in emergency room visits and those seeking treatment for marijuana use. The emergency room statistic most frequently cited by opponents of legalization involve the detection of marijuana use via urinalysis, a method that only indicates if marijuana has been used within the last two to four weeks, therefore the data does not indicate that marijuana use caused the emergency room visit. It merely indicates that more people seem to be using marijuana overall (DAWN Drug Abuse Warning Network, HHS, 2008). In fact, two studies have found direct associations between marijuana use and a decrease in emergency room visits (Vinson, Missouri Medicine, 2006 and Gmel, BMC Public Health 9, 2009). The BMC study found that “relative risks decreased with increasing levels of use,” in other words, when more marijuana was used, fewer injuries occurred. This might seem odd until one recalls that a cannabinoid-blocking drug (rimonabant) was rejected for approval by the FDA due to its side-effects, which included an increase in accidents and injuries. Given that smoking marijuana reduces our risks for developing various cancers, diabetes, heart disease, COPD, Alzheimer’s disease, and other inflammation-based illnesses along with depression, suicidal tendencies and alcohol-caused traffic accidents, shouldn’t it’s use by adults be encouraged and safe, legal outlets be established? Science has spoken.

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A Response to “Going to Pot” by Roxanne Khamsi

By Clint Werner, author of “Marijuana Gateway to Health” In the June 2013 issue of Scientific American, “Science of Health” columnist Roxanne Khamsi wrote a surprisingly unscientific and biased piece on the health ramifications of legalizing marijuana that was sadly tainted with residue from last century’s reefer madness campaign. The title of the piece itself, “Going to Pot” is a loaded term that confers a negative association on the subject via cultural symbolism having nothing to do with the reality of what science is telling us about marijuana and how it affects the human organism and society. First, Ms. Khamsi is mistaken when she writes that doctors “may prescribe marijuana to treat or manage ailments.” In states with medical marijuana provisions, physicians write recommendations for their patients that allow access to dispensaries or cultivation cooperatives. Ms. Khamsi then asserts that “the safety of recreational use is poorly understood” and that “researchers worry that both short- and long-term use of the drug may harm the body and mind.” Researchers who are up-to-date on the science of marijuana have no such concerns regarding adult use. In terms of harming the body, recent research has revealed that regular use of marijuana actually seems to improve physical health. Population studies have shown that regular marijuana users have a reduced risk for developing lung cancer (Hashibe, Cancer Epidemiological, Biomarkers and Prevention, 2006), head and neck cancers (Liang, Cancer Prevention Research, 2009), bladder cancer (Thomas, American Urological Association meeting, 2013), lymphomas (Holly, American Journal of Epidemiology, 1999), as well as diabetes (Rajavashisth, BMJ Open, 2012). The diabetes protection data from the enormous NHANES report also revealed that subjects who smoked marijuana three times per week had a profound (> 50%) reduction in their blood levels of C reactive protein, a inflammation marker for heart disease, indicating that they experienced significant protection from developing cardiac disease. Research also revealed that regular, moderate marijuana smokers have improved lung function compared to non-marijuana smokers with no risk for developing COPD (Pletcher, JAMA, 2012). National Institute of Drug Abuse pulmonary researcher, Dr. Donald Tashkin has said that he now endorses legalization since there is no basis for concern about the substance’s negative effects on lung function. Given the nearly century-long reefer madness campaign waged with untold billions of government dollars, it is hard for people to grasp that a denigrated and criminalized substance could have such positive health effects, especially when smoked, but science trumps myth and superstition with evidence. In terms of mental health, a just-published paper reports that “marijuana use consistently buffered people from the negative consequences associated with loneliness and social exclusion” (Deckman, Social Psychological and Personality Science, 2013), which could be one of the reasons that researchers found a truly startling drop in suicides, especially among young adult men, following the enactment of state medical marijuana laws (Anderson, IDEAS, 2012). Other research has shown that marijuana’s anti-depressant effects could be the result of neurogenesis, the production of healthy and functional new brain cells, which is promoted by the cannabinoids in marijuana (Jiang, Journal of Clinical Investigation, 2005). Another recently-published study found that “mortality risk was lower in cannabis users than in non-cannabis users with psychotic disorders” (Koola, Journal of Psychiatric Research, 2013), indicating that marijuana is a beneficial treatment for mental problems rather than, as increasingly inferred, a causative agent. In attempting to explain the activity of marijuana’s cannabinoid molecules on the endocannabinoid receptors, Ms. Khamsi once again employs loaded language to imply a negative effect, writing that THC “triggers domino chains” which implies a collapse of order and function rather than an alteration in order and function, which is what is truly occurring. Ms. Khamsi then frets that using marijuana impairs “working memory.” Yes marijuana alters mental functioning; it shifts the mind into a blissful euphoria that redirects thought from the ordered and analytical to the relaxed and free-association style of thought that characterizes relaxation and insight. And unlike alcohol, which serves a similar function of quieting the work day mental noise, marijuana is not carcinogenic or lethal. Ms. Khamsi expresses the understandable concern that marijuana users will make our roadways more dangerous but this is not supported by data that shows us what actually happens when legal restrictions are eased. A comprehensive review of data from states with medical marijuana laws found that enactment of the laws led to a significant drop in traffic accident deaths by allowing for marijuana to substitute for alcohol, a far more impairing substance. Traffic accident fatalities dropped by 9 percent in medical marijuana states. (Anderson, pending publication in the Journal of Law and Economics, 2013). That is essentially the same level of protection afforded by the passage of mandatory sea belt laws and by increasing the age for alcohol consumption from 18 to 21 years. According to research conducted by the automobile insurance company 4autoinsurance.com, marijuana users are safe drivers because, unlike alcohol drinkers, they are aware of their level of impairment and either refuse to drive, delay driving or drive more carefully than normal by reducing speed and not changing lanes. Regular marijuana users showed far less evidence of impairment than did novice and occasional users. Impairment testing is the only way to effectively police for marijuana-impaired drivers without ruining the lives of people who pose no threat on the roadways. The cannabinoid CBD steers THC away from the CB1 receptor, thus dulling or nullifying the mind-altering effects, but CBD does not reduce THC levels in the blood. Therefore, a driver using a high CBD strain of marijuana could test over the THC limit while experiencing no psychoactive effects whatsoever. Consequently, effective and fair impairment assessment techniques will need to be developed. Ms. Khamsi then returns to the health effects of marijuana, but ignores the previously cited benefits of reduced risks for developing numerous cancers, diabetes and other inflammation- and oxidation-based degenerative illnesses, such as Alzheimer’s disease and arthritis. She then refers to the recent study of data from New Zealand that indicates that teenagers who use marijuana heavily have up to an 8 percent drop in IQ points. Those results were called into question upon review but still indicate a disturbing effect of heavy marijuana use on the developing adolescent brain. Neurologist Dr. Gary Wenk, who has written “a puff is enough” to protect the adult brain from age-related dementia, says that the effect of marijuana on a developing brain, especially in those under 15 years of age, is impairing. Regular use of marijuana by teens may also interfere with social and professional skill development by monopolizing the time and consciousness of teens that enjoy it. Ms. Khamsi correctly notes that black market marijuana is sometimes contaminated with “sand or glass beads” which are far more harmful to the user than cannabis itself. Black market marijuana is also frequently contaminated with insecticides not intended for use on plants that are consumed. Some of these products are neurotoxic and, ironically, may induce neurodegenerative illnesses by interfering with the functions of the endocannabinoid system. (Casida, Annual Review of Entomolgy, 2013) Smuggled marijuana is also stale and often riddled with mold. Given these threats to heavy teenage users, the question needs to be asked: How do we best reduce access to marijuana, especially the most harmful forms of marijuana, by teenagers? One study suggests that multidimensional family therapy (MDFT) is the most effective approach for treating teenagers with what is termed “cannabis use disorder” (Rigter, Drug and Alcohol Dependence, 2012). MDFT essentially reestablishes parental authority and time management in teens’ lives. If parents remain involved in all aspects of their teenage children’s lives, MDFT would not be necessary to correct a deficit in parenting. The best way to prevent teenage substance abuse is for parents to rigorously monitor and guide their children’s activities. By doing this, parents might not prevent experimentation but they can create an environment where regular access to and use of marijuana is impossible. Shrinking and killing off the black market via legalization and regulation can assist parents in this task, by making marijuana more difficult for teens to obtain. Dealers do not card and taking marijuana away from the illicit drug black market will also protect teens from the multiple drug offerings of those dealers. If teens do obtain marijuana on the sly, at least, having been diverted from legal and tested supplies, it will be less likely to be contaminated with more harmful substances. Commercial medical marijuana venders such as Harborside Health Center, which Khamsi mentioned, contract with growers and test their marijuana for safety and potency. Legalization transforms marijuana cultivators from shady criminals into proud artisans. And despite the possible risk of heavy marijuana use to teenagers’ cognition, a study of adolescent binge drinkers found that those who used marijuana suffered significantly less alcohol-related brain damage than the booze-only drinkers (Jacobus, Neurotoxicology and Teratology, 2009). Consider the irony: Marijuana protects the brains of booze binge drinkers. Ms. Khamsi also mentions increases in emergency room visits and those seeking treatment for marijuana use. The emergency room statistic most frequently cited by opponents of legalization involve the detection of marijuana use via urinalysis, a method that only indicates if marijuana has been used within the last two to four weeks, therefore the data does not indicate that marijuana use caused the emergency room visit. It merely indicates that more people seem to be using marijuana overall (DAWN Drug Abuse Warning Network, HHS, 2008). In fact, two studies have found direct associations between marijuana use and a decrease in emergency room visits (Vinson, Missouri Medicine, 2006 and Gmel, BMC Public Health 9, 2009). The BMC study found that “relative risks decreased with increasing levels of use,” in other words, when more marijuana was used, fewer injuries occurred. This might seem odd until one recalls that a cannabinoid-blocking drug (rimonabant) was rejected for approval by the FDA due to its side-effects, which included an increase in accidents and injuries. Given that smoking marijuana reduces our risks for developing various cancers, diabetes, heart disease, COPD, Alzheimer’s disease, and other inflammation-based illnesses along with depression, suicidal tendencies and alcohol-caused traffic accidents, shouldn’t it’s use by adults be encouraged and safe, legal outlets be established? Science has spoken.

Marijuana use fights diabetes and lowers waist fat

The irrational opponents of marijuana legalization are having a harder and harder time of making the case that using it is harmful when we see that marijuana smokers suffer from less obesity and have significant protection from developing diabetes. Therefore, encouraging adult use of marijuana will work to lower our national health-care costs. Am J Med. 2013 May 9. The Impact of Marijuana Use on Glucose, Insulin, and Insulin Resistance among US Adults. Penner EA, Buettner H, Mittleman MA.SourceUniversity of Nebraska College of Medicine, Omaha; Department of Epidemiology, Harvard School of Public Health, Boston, Mass.AbstractBACKGROUND:There are limited data regarding the relationship between cannabinoids and metabolic processes. Epidemiologic studies have found lower prevalence rates of obesity and diabetes mellitus in marijuana users compared with people who have never used marijuana, suggesting a relationship between cannabinoids and peripheral metabolic processes. To date, no study has investigated the relationship between marijuana use and fasting insulin, glucose, and insulin resistance.METHODS:We included 4657 adult men and women from the National Health and Nutrition Examination Survey from 2005 to 2010. Marijuana use was assessed by self-report in a private room. Fasting insulin and glucose were measured via blood samples after a 9-hour fast, and homeostasis model assessment of insulin resistance HOMA-IR was calculated to evaluate insulin resistance. Associations were estimated using multiple linear regression, accounting for survey design and adjusting for potential confounders.RESULTS:Of the participants in our study sample, 579 were current marijuana users and 1975 were past users. In multivariable adjusted models, current marijuana use was associated with 16% lower fasting insulin levels 95% confidence interval [CI], -26, -6 and 17% lower HOMA-IR 95% CI, -27, -6. We found significant associations between marijuana use and smaller waist circumferences. Among current users, we found no significant dose-response.CONCLUSIONS:We found that marijuana use was associated with lower levels of fasting insulin and HOMA-IR, and smaller waist circumference.

via The Impact of Marijuana Use on Glucose, Insulin, an... [Am J Med. 2013] - PubMed - NCBI.

The relationships between sugar-sweetened b... [J Acad Nutr Diet. 2013] - PubMed - NCBI

Sugar creates pro-disease environments and effects. Why don't the prohibitionists work against the "Big Sugar" industry that is addicting kids into seriously self-destructive life-styles? Although teens should not use marijuana, it is interesting that using the plant regularly reduces obesity and the incidence of diabetes. Maybe obese teens could benefit from a marijuana pill that has less THC than CBD and is therefore not psychoactive. J Acad Nutr Diet. 2013 Feb                                                              The relationships between sugar-sweetened beverage intake and cardiometabolic markers in young children.                               Kosova EC, Auinger P, Bremer AA.SourceDepartment of Medicine, Brigham and Women’s Hospital, Boston, MA, USA.               Abstract: BACKGROUND:The consumption of sugar-sweetened beverages has been implicated as a major contributor to the development of obesity and cardiometabolic disease.OBJECTIVE:To evaluate the relationships between sugar-sweetened beverage intake and cardiometabolic markers in young children.DESIGN:A cross-sectional analysis of the National Health and Nutrition Examination Survey data collected by the National Center for Health Statistics.PARTICIPANTS:A total of 4,880 individuals aged 3 to 11 years from nationally representative samples of US children participating in the National Health and Nutrition Examination Survey during 1999-2004 were studied.MAIN OUTCOME MEASURES:Concentrations of total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, triglyceride, and C-reactive protein as well as waist circumference and body mass index percentile for age-sex.STATISTICAL ANALYSES PERFORMED:Multivariate linear regression analyses were performed to determine independent associations between each outcome variable and the number of serving equivalents of sugar-sweetened beverages consumed after adjusting for age, sex, race, poverty status, physical activity, and energy intake.RESULTS:Increased sugar-sweetened beverage intake was independently associated with increased C-reactive protein concentrations P=0.003, increased waist circumference P=0.04, and decreased high-density lipoprotein cholesterol concentrations P<0.001. Subgroup analyses demonstrated differences in the association of sugar-sweetened beverage intake with metabolic markers and anthropometric measurements among age ranges, sex, and racial/ethnic groups.CONCLUSIONS:In this cross-sectional analysis of children's dietary data, sugar-sweetened beverage intake was independently associated with alterations in lipid profiles, increased markers of inflammation, and increased waist circumference in children. Prospective studies are needed, but awareness of these trends is essential in combating the growing metabolic and cardiovascular disease burden in the pediatric population.Copyright © 2013 Academy of Nutrition and Dietetics. Published by Elsevier Inc. All rights reserved.PMID: 23351625 [PubMed - indexed for MEDLINE] Publication Types, MeSH Terms, Substances, Grant Support

via The relationships between sugar-sweetened b... [J Acad Nutr Diet. 2013] - PubMed - NCBI.

Bladder Cancer Risk Lower in Pot Smokers - Renal and Urology News

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.

via Bladder Cancer Risk Lower in Pot Smokers - Renal and Urology News.

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Bladder Cancer Risk Lower in Pot Smokers - Renal and Urology News

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. via Bladder Cancer Risk Lower in Pot Smokers - Renal and Urology News.

Marijuana relieves symptoms of Crohn's disease

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.

Source

Department of Gastroenterology and Hepatology, Meir Medical Center and Sackler Faculty of Medicine, Tel Aviv University, Kfar Saba, Israel. Electronic address: naftali@post.tau.ac.il.

Abstract

BACKGROUND:

& 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.

METHODS:

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.

RESULTS:

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.

CONCLUSION:

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.

via Cannabis Induces a Clinical Respo... [Clin Gastroenterol Hepatol. 2013] - PubMed - NCBI.

Marijuana for psoriasis

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.

via A novel control of human keratin expression: cannabino... [PeerJ. 2013] - PubMed - NCBI.

THC/Marijuana fights liver cancer

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.

via Involvement of PPARγ in the antitumoral actio... [Cell Death Dis. 2013] - PubMed - NCBI.

THC and similar compounds suppress HIV infection and spread

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: yuri.persidsky@tuhs.temple.edu or servio.ramirez@temple.edu                                                     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.

via Attenuation of HIV-1 replication in macrophages by cannabinoid receptor 2 agonists.

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, sven.haller@hcuge.ch.                                       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.

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

Natural Cannabinoids Improve Dopamine Neuro... [J Alzheimers Dis. 2013] - PubMed - NCBI

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.

via Natural Cannabinoids Improve Dopamine Neuro... [J Alzheimers Dis. 2013] - PubMed - NCBI.

Promotion of β-amyloid production by C-reactiv... [Neurochem Int. 2012] - PubMed - NCBI

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.

via Promotion of β-amyloid production by C-reactiv... [Neurochem Int. 2012] - PubMed - NCBI.

Obesity and cannabis use: results from 2 repr... [Am J Epidemiol. 2011] - PubMed - NCBI

Smoking marijuana significantly protects users from obesity and related diseases. Tell someone today! Am J Epidemiol. 2011 Oct 15;1748:929-33.  2011 Aug 24.

Obesity and cannabis use: results from 2 representative national surveys.                                                                                              Le Strat Y, Le Foll B.SourceTranslational Addiction Research Laboratory, Centre for Addiction and Mental Health, Toronto, Ontario, Canada.                                                                                   Abstract: The role of cannabis and endocannabinoids in appetite regulation has been extensively studied, but the association of cannabis use with weight in the general population is not known. The authors used data from 2 representative epidemiologic studies of US adults aged 18 years or older, the National Epidemiologic Survey on Alcohol and Related Conditions NESARC; 2001-2002 and the National Comorbidity Survey-Replication NCS-R; 2001-2003, to estimate the prevalence of obesity as a function of cannabis use. The adjusted prevalences of obesity in the NESARC and the NCS-R were 22.0% and 25.3%, respectively, among participants reporting no use of cannabis in the past 12 months and 14.3% and 17.2%, respectively, among participants reporting the use of cannabis at least 3 days per week. These differences were not accounted for by tobacco smoking status. Additionally, after adjustment for sex and age, the use of cannabis was associated with body mass index differences in both samples. The authors conclude that the prevalence of obesity is lower in cannabis users than in nonusers.

via Obesity and cannabis use: results from 2 repr... [Am J Epidemiol. 2011] - PubMed - NCBI.