Pot is good for you? Marijuana fights the superbugs
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Monthly Archives: August 2013
Fact: Cannabis Kills MRSA, Disrupts Prion Diseases
“Marijuana is a potent antibiotic that can kill methicillin-resistant Staphylococcus aureus and disrupt the progression of prion diseases such as Mad Cow disease and Creutzfeld-Jakob disease — just don’t expect the federal government to tell you any of this.”
“Scientists from Italy and the United Kingdom reported in the August 2007 issue of the Journal of Natural Products that the main active ingredient in weed, THC, as well as four other pot molecules “showed potent antibacterial activity against six different strains of MRSA of clinical relevance.”
Pot also stops prions, a type of protein that can cause neurodegenerative diseases that are invariably fatal. Once prions get into a brain they replicate rapidly and shred brain tissue “resulting in a ‘spongiform’ appearance on post-mortem histological examination of neural tissue.”
In 2007, American and French researchers reported that pot molecule cannabidiol “prevents prion accumulation and protects neurons against prion toxicity” in the Journal of Neuroscience.
Cannabidiol inhibited prion accumulation in mouse and sheep prion disease cell cultures and inhibited prion formation in the brain of infected mice given injections of CBD. “The authors conclude that CBD likely represents a new class of anti-prion drugs.””
“Antibacterial cannabinoids from Cannabis sativa: a structure-activity study.” http://www.ncbi.nlm.nih.gov/pubmed/18681481
“Nonpsychoactive Cannabidiol Prevents Prion Accumulation and Protects Neurons against Prion Toxicity” http://www.jneurosci.org/content/27/36/9537.full
Marijuana Kills MRSA and Inhibits Prions That Cause Neurodegenerative Disease; Still Recognized by Feds As a Dangerous Drug
“Research indicates that marijuana could effectively fight off MRSA, as well as prions — the proteins that cause mad cow disease and Creutzfeld-Jakob disease.”
“New research reveals that several marijuana ingredients exhibit a potent antibiotic capacity in cases of methicillin-resistant Staphylococcus aureus (MRSA) infections as well as the ability to fight off proteins called prions that can lead to Mad Cow disease and Creutzfeld-Jakob disease (CDJ).”
More: http://www.medicaldaily.com/articles/17941/20130730/marijuana-mrsa-prions-mad-cow-disease.htm
Cannabis abuse is associated with better emotional memory in schizophrenia: A functional magnetic resonance imaging study.
“…we performed a functional magnetic resonance imaging study of emotional memory in schizophrenia patients with cannabis abuse…
These results are consistent with previous findings showing that cannabis abuse is associated with fewer negative symptoms and better cognitive functioning in schizophrenia…”
Marijuana Cures Methadone and Heroin Addiction!
“It does it for all opiates.”
“I can already feel the first comment. What the hell is he talking about? Well, Okay. During the 1860’s Cannabis/Marijuana was used in the U.S. to get addicted people off alcohol, tobacco and opium, and it was very successful in doing so. Many Civil War veterans were addicted to all three of these.
About that time, Morphine and the hypodermic syringe were invented, which gave doctors real control of pain and brought about the concept that a physician’s first obligation to his patients was to control pain. It was far nicer and safer than opium or alcohol.
The chemists went to work on opium and synthesized many different compounds, several of which were found to be more powerful, and more addicting than Morphine, the original opiate. These more powerful drugs were Oxycodone, Hydrocodone, Dilaudid, and Heroin, which is diacetyl morphine. Codeine, another opiate, was a much weaker opiate and its use has been minimal in the face of these much stronger opiates.
With heavy advertising and mouth-to-ear gossip, patients demanded the strong opiates. This brought on a real problem for physicians — give the patients the strong opiates, or they will find another doctor who will.
These strong opiates are notorious for not only causing addictions but they can easily cause death from accidental overdose or suicides, which are in the thousands. So, Doctors will give you enough to turn you into an addict. 20 pills. Then they say no. But the patient is still in pain, so the patient changes doctors, and repeats the action. Soon they realize it is easier to get drugs on the street.
The state medical boards have jumped into this mess by ordering physicians to stop writing these strong opiate prescriptions.
What is a patient to do about this?”
More: http://salem-news.com/articles/july272013/pain-marijuana_pl.php
Cannabidivarin-rich cannabis extracts are anticonvulsant in mouse and rat via a CB1 receptor-independent mechanism.
“Epilepsy is the most prevalent neurological disease and is characterised by recurrent seizures. Here we investigate: (i) the anticonvulsant profiles of cannabis-derived botanical drug substances (BDS) rich in cannabidivarin (CBDV) and containing cannabidiol (CBD) in acute in vivo seizure models and (ii) the binding of CBDV BDSs and their components at cannabinoid CB1 receptors.
CDBV BDSs exerted significant anticonvulsant effects…
CONCLUSIONS AND IMPLICATIONS:
CBDV BDSs exerted significant anticonvulsant effects in three models of seizure that were not mediated by the CB1 cannabinoid receptor, and were of comparable efficacy to purified CBDV.
These findings strongly support the further clinical development of CBDV BDSs for treatment of epilepsy.”
http://www.ncbi.nlm.nih.gov/pubmed/23902406
“Cannabidivarin is anticonvulsant in mouse and rat… These results indicate that CBDV is an effective anticonvulsant in a broad range of seizure models.” http://www.ncbi.nlm.nih.gov/pubmed/22970845
Evaluation of the potential of the phytocannabinoids, cannabidivarin (CBDV) and Δ9 -tetrahydrocannabivarin (THCV), to produce CB1 receptor inverse agonism symptoms of nausea in rats.
“The cannabinoid 1(CB1 ) receptor inverse agonists/antagonists, rimonabant (SR141716, SR) and AM251, produce nausea and potentiate toxin-induced nausea by inverse agonism (rather than antagonism) of the CB1 receptor. Here, we evaluated two phytocannabinoids, cannabidivarin (CBDV) and Δ9 -tetrahydrocannabivarin (THCV) for their ability to produce these behavioural effects characteristic of CB1 receptor inverse agonism in rats.
…we investigated the potential of THCV and CBDV to produce conditioned gaping (measure of nausea-induced behaviour),..
THC, THCV and CBDV suppressed LiCl-induced conditioned gaping, suggesting anti-nausea potential…
The pattern of findings indicates that neither THCV nor CBDV produced a behavioural profile characteristic of CB1 receptor inverse agonists.
As well, these compounds may have therapeutic potential in reducing nausea.”
Peripherally restricted CB1 receptor blockers.
“Antagonists (inverse agonists) of the cannabinoid-1 (CB1) receptor showed promise as new therapies for controlling obesity and related metabolic function/liver disease.
These agents, representing diverse chemical series, shared the property of brain penetration due to the initial belief that therapeutic benefit was mainly based on brain receptor interaction. However, undesirable CNS-based side effects of the only marketed agent in this class, rimonabant, led to its removal, and termination of the development of other clinical candidates soon followed. Re-evaluation of this approach has focused on neutral or peripherally restricted (PR) antagonists.
Supporting these strategies, pharmacological evidence indicates most if not all of the properties of globally acting agents may be captured by molecules with little brain presence. Methodology that can be used to eliminate BBB penetration and the means (in vitro assays, tissue distribution and receptor occupancy determinations, behavioral paradigms) to identify potential agents with little brain presence is discussed.
Focus will be on the pharmacology supporting the contention that reported agents are truly peripherally restricted. Notable examples of these types of compounds are: TM38837 (structure not disclosed); AM6545 (8); JD5037 (15b); RTI-12 (19).”
Anandamide, Cannabinoid Type 1 Receptor, and NMDA Receptor Activation Mediate Non-Hebbian Presynaptically Expressed Long-Term Depression at the First Central Synapse for Visceral Afferent Fibers.
“Presynaptic long-term depression (LTD) of synapse efficacy generally requires coordinated activity between presynaptic and postsynaptic neurons and a retrograde signal synthesized by the postsynaptic cell in an activity-dependent manner.
In this study, we examined LTD in the rat nucleus tractus solitarii (NTS), a brainstem nucleus that relays homeostatic information from the internal body to the brain.
We found that coactivation of N-methyl-D-aspartate receptors (NMDARs) and type 1 cannabinoid receptors (CB1Rs) induces LTD at the first central excitatory synapse between visceral fibers and NTS neurons. This LTD is presynaptically expressed. However, neither postsynaptic activation of NMDARs nor postsynaptic calcium influx are required for its induction. Direct activation of NMDARs triggers cannabinoid-dependent LTD. In addition, LTD is unaffected by blocking 2-arachidonyl-glycerol synthesis, but its induction threshold is lowered by preventing fatty acid degradation.
Altogether, our data suggest that LTD in NTS neurons may be entirely expressed at the presynaptic level by local anandamide synthesis.”
Active Ingredient in Marijuana Kills Brain Cancer Cells – ABCNews
“New research out of Spain suggests that THC — the active ingredient in marijuana — appears to prompt the death of brain cancer cells.
The finding is based on work with mice designed to carry human cancer tumors, as well as from an analysis of THC’s impact on tumor cells extracted from two patients coping with a highly aggressive form of brain cancer.
Explaining that the introduction of THC into the brain triggers a cellular self-digestion process known as “autophagy,” study co-author Guillermo Velasco said his team has isolated the specific pathway by which this process unfolds, and noted that it appears “to kill cancer cells, while it does not affect normal cells…”
The findings were published in the April issue of The Journal of Clinical Investigation.”: http://www.jci.org/articles/view/37948
More: http://abcnews.go.com/Health/Healthday/story?id=7235037&page=1