Posted on Feb. 15, 2016, 6 a.m. in Brain and Mental Performance Botanical Agents Environment Marijuana can reverse cognitive decline…as long as it’s not laced with toxic pesticides. Notably, there are moderate advantages to be garnered from medicinal cannabis. Unfortunately, it also possess some disadvantages which should be considered. Marijuana can reverse cognitive decline…as long as it’s not laced with toxic pesticides. One of the most surprising and recent revelations about cannabinoids are their capability to perform as antioxidants in the brain. German experts have found that the brain’s cannabinoid system has the capability of restoring impaired brain cells, while developing new ones. Cannabinoids may curb the effects of Alzheimer’s, Parkinson’s, Huntington’s disease and possibly more. The news was revealed in the journal Philosophical Transactions of the Royal Society B. The researchers discovered that natural marijuana, that is marijuana devoid of pesticides, can curb brain inflammation behind an onslaught of cognitive disorders, including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease and other similar diseases. “I’ve been trying to find a drug that will reduce brain inflammation and restore cognitive function in rats for over 25 years; cannabinoids are the first and only class of drugs that have ever been effective,” notes Gary Wenk, a professor of neuroscience, immunology and medical genetics at Ohio State University (OSU), who contributed to the study. “I think that the perception about this drug is changing and in the future people will be less fearful.” Not all states have permitted marijuana for recreational use. Just as users who purchase marijuana illegally can’t be sure whether their stash has been laced with drugs, users who purchase marijuana legally can’t be sure whether their stash has been laced with pesticides. The general agreement among those who run the legal marijuana industry, is that there hasn’t been enough research that determines which chemicals are best to grow, smoke or eat marijuana with. “We have an industry that’s been illegal for so many years that there’s no research,” observed Frank Conrad, director of the marijuana testing laboratory Colorado Green Lab. “There’s no guidelines. There’s nothing.” Lack of federal regulation enables growers to disregard pesticide laws. Moreover, even though the state limitation of marijuana has decreased, the federal government continues to analyze cannabis as an illicit drug, meaning, they have no interest in funding research about chemical use for marijuana crops. “There is no federal agency that will recognize this as a legitimate crop,” said pesticide expert Whitney Cranshaw of Colorado State University. “Regulators just bury their heads, and as a result, pest-management information regarding this crop devolves to Internet chats and hearsay.” Since marijuana is a low priority at the federal level, it can take years for the Environmental Protection Agency (EPA) to respond to state requests about which pesticides are approved for marijuana crops. As a result, it’s easy for marijuana growers to disregard rules that limit or ban certain pesticides. In Denver, for example, a chemical called Eagle 20 EW was found to be in marijuana circulating the market. Although the chemical, technically a fungicide, is approved for grapes and hops, it’s banned for use on tobacco plants, because it can become hazardous when heated. Oregon faced a similar hurdle in June, after an investigation by The Oregonian unearthed residues surpassing legal limits for edible marijuana products. Other pesticides, which are linked to cancer, nerve damage and neural degeneration, were found as well. Since these pesticides are not state-regulated, their use is legal. A strong case can be made for the medicinal benefits of cannabis. There is plenty of marijuana in circulation harboring pesticides unfit for human consumption today. Therefore, in reaping the benefits of medicinal cannabis, it’s important for users to remember that not all cannabis plants are created equal.
Patent US6630507 - Cannabinoids as antioxidants and neuroprotectants Filing dateApr 21, 1999 They have been lying to us the entire time. Good post Waterhead.
Great post! We really need to be certain what our medicine is coming in contact with! Sent from my iPhone using Grasscity Forum mobile app
Damn, this is some scary shit. It has me wondering about the bud I buy. I need to start asking questions about how the bud I buy is grown. I doubt the budtenders would know, but hopefully I find someone with the right answers. I guess growing it yourself would be the best option.
More on mental performance/Alzheimer's and cannabis. Marijuana May Slow Alzheimer's (news - 2006) Marijuana May Slow Alzheimer's “THC blocks an enzyme called acetylcholinesterase, which speeds the formation of amyloid plaque in the brains of people with Alzheimer's disease. The Alzheimer's drugs Aricept and Cognex work by blocking acetylcholinesterase. When tested at double the concentration of THC, Aricept blocked plaque formation only 22% as well as THC, and Cognex blocked plaque formation only 7% as well as THC.” From “Marijuana May Slow Alzheimer's” WebMD. That article is based on this study- A Molecular Link between the Active Component of Marijuana and Alzheimer’s Disease Pathology (full - 2006) http://www.ukcia.org/research/AlzheimersDiseasePathology.pdf “It is noteworthy that THC is a considerably more effective inhibitor of AChE-induced A‚ deposition than the approved drugs for Alzheimer’s disease treatment, donepezil and tacrine, which reduced A‚ aggregation by only 22% and 7%,respectively, at twice the concentration used in our studies. Therefore, AChE inhibitors such as THC and its analogues may provide an improved therapeutic for Alzheimer’s disease, augmenting acetylcholine levels by preventing neurotransmitter degradation and reducing A‚ aggregation, thereby simultaneously treating both the symptoms and progression of Alzheimer’s disease.” (FYI- AChE= acetylcholinesterase, that speeds the formation of amyloid plaque in your brain; A, = amyloid plaque; donepezil and tacrine = Aricept and Cognex) But it gets even BETTER! THC activates both the CB1 receptors (the high and some healing) and the "no high" CB2 receptors that control inflammation and MUCH more. At times, CB2s can work minor miracles- (FYI- macrophages are "cleanup crew" cells; in vitro means in a test tube; in situ means "on site" in this case in a brain) The activation of cannabinoid CB2 receptors stimulates in situ and in vitro beta-amyloid removal by human macrophages. (abst - 2009) The activation of cannabinoid CB2 receptors stimulates in situ and in vitro beta-amyloid removal by human macrophages. - PubMed - NCBI Activation of the CB(2) receptor system reverses amyloid-induced memory deficiency. (abst – 2013) Activation of the CB2 receptor system reverses amyloid-induced memory deficiency. - PubMed - NCBI And then there's this one- Can the benefits of cannabinoid receptor stimulation on neuroinflammation, neurogenesis and memory during normal aging be useful in AD prevention? (AD = Alzheimer’s Disease) (full – 2012) Journal of Neuroinflammation “The chronic administration of non-selective cannabinoids may delay the onset of cognitive deficits in AD patients; this will dramatically reduce the socio-economic burden of AD and improve the quality of life of the patients and their families.” THC is a non-selective cannabinoid meaning it activates both CB1 and CB2 receptors (and a few others besides). For the "Tauists", THC goes after Tau proteins, too! FYI- There is a big argument among Alzheimer's scientists about the roles of Tau proteins and amyloid plaque in Alzheimers! But either way, THC helps! Sativex is a simple 50/50 THC/ CBD tincture derived from cannabis plants. It is illegal in the US, but legal in Canada and much of Europe. Natural Cannabinoids Improve Dopamine Neurotransmission and Tau and Amyloid Pathology in a Mouse Model of Tauopathy. (full – 2013) Metapress “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.” “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.” However, the changes cannabis causes in brain function is not limited to just the old! See Rough childhood? Cannabis may help! Also, a synthetic (strictly lab use only) cannabinoid, WIN, acts much like THC. It can provide some protection against the effects of organophosphate poisoning, so THC should have a similar effect on a low dose pesticide exposure. But I'll stick with my organic home-grown, anyway! And "Apoptosis" means cell death. Cannabinoid Receptor Agonist WIN-55,212-2 Protects Differentiated PC12 Cells From Organophosphorus- Induced Apoptosis (abst – 2010) Cannabinoid Receptor Agonist WIN-55,212-2 Protects Differentiated PC12 Cells From Organophosphorus- Induced Apoptosis And one last FYI- I am 68 and do NOT fear Alzheimer's! My brain should be fairly clear of amyloid plaque and Tau proteins! Granny
OMG....Granny you're the best. This is GREAT info. Blows me away. The benefits of Cannabis are just staggering. It's no wonder at all why it's so tightly controlled. H
Researchers led by Andreas Zimmer of the University of Bonn in Germany gave low doses of delta-9 tetrahydrocannabinol, or THC, marijuana’s main active ingredient, to young, mature and aged mice. As expected, young mice treated with THC performed slightly worse on behavioral tests of memory and learning. For example, after receiving THC, young mice took longer to learn where a safe platform was hidden in a water maze, and they had a harder time recognizing another mouse to which they had previously been exposed. Without the drug, mature and aged mice performed worse on the tests than young ones did. But after the elderly animals were given THC, their performances improved to the point that they resembled those of young, untreated mice. “The effects were very robust, very profound,” Zimmer says. Other experts praised the study but cautioned against extrapolating the findings to humans. “This well-designed set of experiments shows that chronic THC pretreatment appears to restore a significant level of diminished cognitive performance in older mice, while corroborating the opposite effect among young mice,” wrote Susan Weiss, director of the Division of Extramural Research at the National Institute on Drug Abuse, who was not involved in the study, in an e-mail. Nevertheless, she added, “while it would be tempting to presume the relevanceof these findings [extends] to aging humans ... further research will be critically needed.”
