"Cannabis the Evil Weed" You Tube BBC Horizon
by frankiespeakin 64 Replies latest jw experiences
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Satanus
I like the start of the vid, where the parents welcome the kid to smoke at home, instead of outside somewhere, which could be dangerous. I knew some people, xjw, who also did the same w their son. It turned out great. After a few yrs, the son stopped doing it entirely, cuz he started university. It does cut a persons sharpness, to an extent.
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frankiespeakin
Yeah, durring college or learning something requireing short term memory skills I would stick only to raw or high cbd strains only to keep mental sharpness and a occasional high thc one for some creativity sparks here and there.
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*lost*
bumped
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frankiespeakin
http://en.wikipedia.org/wiki/Cannabinoid_receptor
Cannabinoid receptor type 1 (CB 1 ) receptors are thought to be one of the most widely expressed G protein-coupled receptors in the brain. This is due to endocannabinoid-mediated depolarization-induced suppression of inhibition, a very common form of short-term plasticity in which the depolarization of a single neuron induces a reduction in GABA-mediated neurotransmission. Endocannabinoids released from the depolarized post-synaptic neuron bind to CB 1 receptors in the pre-synaptic neuron and cause a reduction in GABA release.
They are also found in other parts of the body. For instance, in the liver, activation of the CB 1 receptor is known to increase de novo lipogenesis. [ 11 ] Activation of presynaptic CB 1 receptors is also known to inhibit sympathetic innervation of blood vessels and contributes to the suppression of the neurogenic vasopressor response in septic shock. [ 12 ]
A study done on CB1 knockout mice (genetically altered mice that cannot produce CB1) showed an increase in mortality rate. They also displayed suppressed locomotor activity as well as hypoalgesia (decreased pain sensitivity). The CB1 knockout mice did respond to Delta9-Tetrahydrocannabinol THC. This shows that either CB2 or unknown cannabinoid receptors also have pharmacologic significance.[ CB 2
CB 2
Main article: Cannabinoid receptor type 2
CB 2 receptors are mainly expressed on T cells of the immune system, on macrophages and B cells, and in hematopoietic cells. They also have a function in keratinocytes, and are expressed on mouse pre-implantation embryos. They are also expressed on peripheral nerve terminals. These receptors play a role in antinociception, or the relief of pain. In the brain, they are mainly expressed by microglial cells, where their role remains unclear. While the most likely cellular targets and executors of the CB 2 receptor-mediated effects of endocannabinoids or synthetic agonists are the immune and immune-derived cells (e.g. leukocytes, various populations of T and B lymphocytes, monocytes/macrophages, dendritic cells, mast cells, microglia in the brain, Kupffer cells in the liver, etc.), the number of other potential cellular targets is expanding, now including endothelial and smooth muscle cells, fibroblasts of various origins, cardiomyocytes, and certain neuronal elements of the peripheral or central nervous systems. [ 7
Gastrointestinal activity
Inhibition of gastrointestinal activity has been observed after administration of Δ 9 -THC, or of anandamide. This effect has been assumed to be CB 1 -mediated since the specific CB 1 antagonist SR 141716A (Rimonabant) blocks the effect. Another report, however, suggests that inhibition of intestinalmotility may also have a CB 2 -mediated component. [ 23 ]
[edit] Cardiovascular activity
Cannabinoids are well known for their cardiovascular activity. Activation of peripheral CB1 receptors contributes to hemorrhagic and endotoxin-induced hypotension. Anandamide and 2-AG, produced by macrophages and platelets respectively, may mediate this effect.
The hypotension in hemorrhaged rats was prevented by the CB 1 antagonist SR 141716A. Recently the same group found that anandamide-induced mesentericvasodilation is mediated by an endothelially located SR 141716A-sensitive "anandamide receptor," distinct from the CB 1 cannabinoid receptor, and that activation of such a receptor by an endocannabinoid, possibly anandamide, contributes to endotoxin-induced mesenteric vasodilation in vivo. The highly potent synthetic cannabinoid HU-210, as well as 2-AG, had no mesenteric vasodilator activity. Furthermore it was shown that mesenteric vasodilation by anandamide apparently has 2 components, one mediated by a SR 141716-sensitive non-CB 1 receptor (located on the endothelium) and the other by an SR 141716A-resistant direct action on vascular smooth muscle.
The production of 2-AG is enhanced in normal, but not in endothelium-denuded rat aorta on stimulation with Carbachol, an acetylcholine receptor agonist. 2-AG potently reduces blood pressure in rats and may represent an endothelium-derived hypotensive factor.
Recent studies have also suggested that activation of CB 1 receptors in human and rodent cardiomyocytes, [ 24 ] [ 25 ] coronary artery endothelial and inflammatory cells [ 26 ] [ 27 ] [ 28 ] [ 29 ] promotes activation of mitogen-activated protein (MAP) kinases p38 and JNK, reactive oxygen species generation, cell death, and cardiovascular inflammatory response both in vitro, as well as in models of heart failure, atherosclerosis and vascular inflammation. [ 24 ] [ 25 ] [ 26 ] [ 28 ] [ 29 ]
[edit] Pain
Anandamide attenuates the early phase or the late phase of pain behavior produced by formalin-induced chemical damage. This effect is produced by interaction with CB 1 (or CB 1 -like) receptors, located on peripheral endings of sensory neurons involved in pain transmission. Palmitylethanolamide, which like anandamide is present in the skin, also exhibits peripheral antinociceptive activity during the late phase of pain behavior. Palmitylethanolamide, however does not bind to either CB 1 or CB 2 . Its analgesic activity is blocked by the substance that was once thought to be a specific CB 2 antagonist, SR 144528, though not by the specific CB 1 antagonist SR 141716A (rimonabant). Hence, a CB 2 -like receptor was postulated.
In experiments on mice, a chemical designated JZL184 that inhibits a naturally occurring enzyme MAGL from degrading a pain-relieving endocannabinoid called 2-arachidonoylglycerol (AG) increases the brain concentration of AG, thereby inducing analgesia. [ 30 ] [ 31 ]
[edit] Bone
The endocannabinoid system through CB2 signaling plays a key role in the maintenance of bone mass. CB2 is expressed in osteoblasts, osteocytes, and osteoclasts. CB2 agonists enhance endocortical osteoblast number and activity while restraining trabecular osteoclastogenesis. Another important effect is that CB2 agonists attenuates ovariectomy-induced bone loss while increasing cortical thickness. These findings suggest CB2 offers a potential molecular target for the diagnosis and treatment of osteoporosis. [ 32 ]
[edit] Cannabinoid treatments
Main article: Medical cannabis
Cannabis preparations have been known as therapeutic agents against various diseases for millennia. [ 33 ] The psychoactive compound tetrahydrocannabinol (THC) was found to be the principal mediator of the effects of cannabis. [ 34 ] Synthetic THC is prescribed today, under the INNdronabinol or the brand name Marinol, to treat vomiting and for enhancement of appetite, mainly in AIDS patients.
Several synthetic cannabinoids have been shown to bind to the CB 2 receptor with a higher affinity than to the CB 1 receptor. [ 35 ] Most of these compounds exhibit only modest selectivity. One of the described compounds, a classical THC-type cannabinoid, L-759,656, in which the phenolic group is blocked as a methylether, has a CB 1 /CB 2 binding ratio > 1000. [ 36 ] The pharmacology of these agonists has yet to be described.
Certain tumors, especially gliomas, express CB 2 receptors. Guzman and coworkers have shown that Δ 9 -tetrahydrocannabinol and WIN-55,212-2, two non-selective cannabinoid agonists, induce the regression or eradication of malignant brain tumors in rats and mice. [ 37 ] CB 2 selective agonists are effective in the treatment of pain, various inflammatory diseases in different animal models, [ 32 ] [ 38 ] osteoporosis [ 32 ] and atherosclerosis. [ 39 ] CB 1 selective antagonists have previously been used for weight reduction and smoking cessation (see Rimonabant). Activation of CB 1 provides neuroprotection after brain injury. [ 40 ]
Several studies, using animal models, have concluded that HU210 which is a cannabinoid 100 to 800 times more potent than marijuana compounds might have the ability to prevent Alzheimer's disease. [ 41 ] [ 42 ] But a more recent study using mice carrying human genetic mutations that cause Alzheimer's disease found that those same cannabinoides have no effect on Alzheimer's disease and have negative consequences for cognitive function, including causing brain cell death. [ 43 ]
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frankiespeakin
http://en.wikipedia.org/wiki/Cannabinoid_receptor_antagonist
The discovery of the endogenous cannabinoid system led to the development of CB 1receptorantagonists. The first cannabinoid receptor "antagonist," rimonabant, was described in 1994. Rimonabant blocks the CB 1 receptor selectively and it has been shown to decrease food intake and regulate body-weight gain. The prevalence of obesity worldwide is increasing dramatically and has a great impact on public health. The lack of efficient and well-tolerated drugs to cure obesity has led to an increased interest in research and development of cannabinoid antagonists. [ 1 ] [ 2 ] Cannabidiol, a naturally occurring cannabinoid, is a non-competitive CB1/2 antagonist.
Drug design
The first approach to develop cannabinoid antagonists in the late 1980s was to modify the structure of THC but the results were disappointing. In the early 1990s new family of cannabinoid agonists was discovered from the NSAID (non-steroidal anti-inflammatory) drug pravadoline which led to the discovery of aminoalkyl indole antagonists with some but limited success. As the search based on the structure of agonists was disappointing it was no surprise that the first potent and selective cannabinoid antagonist belonged to an entirely new chemical family. In 1994 the first selective cannabinoid antagonist, SR141716 (rimonabant), was introduced by Sanofi belonging to a family of 1,5-diarylpyrazoles. [ 8 ] [ 15 ]
Rimonabant, also known by the systematic name [N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1 H-pyrazole-3-carboxamidehydrochloride)], is a 1,5-diarylpyrazole CB 1 receptor antagonist (Figure 2). [ 15 ] Rimonabant is not only a potent and highly selective ligand of the CB 1 receptor, but it is also orally active and antagonizes most of the effects of cannabinoid agonists, such as THC, both in vitro and in vivo. Rimonabant has shown clear clinical efficacy for the treatment of obesity. [ 16 ]
Rimonabant (Acomplia) has been approved in the European Union (EU) since June 2006 for the treatment of obesity. On 23 October 2008 the European Medicines Agency (EMEA) has recommended the suspension of the marketing authorization across the EU for Acomplia from Sanofi-Aventis based on the risk of serious psychiatric disorders. [ 25 ] On 5 November 2008 Sanofi-Aventis announced discontinuation of rimonabant clinical development program. [ 26 ]
Sanofi-Aventis has also discontinued development of surinabant (SR147778), a CB 1 receptor antagonist for smoking cessation (31 October 2008). [ 27 ]
Merck has stated in its press release on 2 October 2008 that they will not seek regulatory approval for taranabant (MK-0364) to treat obesity and will discontinue its Phase III clinical development program. Data from Phase III clinical trial showed that greater efficacy and more adverse effects were associated with the higher doses of taranabant and it was determined that the overall profile of taranabant does not support further development for obesity. [ 28 ]
Another pharmaceutical company, Pfizer, terminated the Phase III development program for its obesity compound otenabant (CP-945,598), a selective antagonist of the CB 1 receptor. According to Pfizer their decision was based on changing regulatory perspectives on the risk/benefit profile of the CB 1 class and likely new regulatory requirements for approval. [ 29 ]
A number of initiatives have been published to develop CB1 antagonists that target only peripheral CB1 receptors by restricting their ability to cross the blood brain barrier. Among these initiatives 7TM Pharma [ 30 ] has reported the development of TM38837
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frankiespeakin
http://www.projectcbd.com/PTSD.Mikuriya.html#PTSD
Cannabis for Post Traumatic Stress
By Tod Mikuriya, MD
William Woodward, MD, of the American Medical Association, testify- ing before Congress in 1937 against the Prohibition of cannabis, paraphrased a French author (F. Pascal, 1934) to the effect that “Indian hemp has remarkable properties in revealing the subcon- scious.” A Congressman asked, “Are there any substitutes for that latter psychological use?” Woodward replied, “I know of none. That use, by the way, was recognized by John Stuart Mill in his work on psychol- ogy, where he referred to the ability of Cannabis or Indian hemp to revive old memories —and psychoanalysis de- pends on revivivification of hidden memories
Easement Effects of Cannabis.....
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frankiespeakin
http://www.nytimes.com/2013/04/25/us/colorado-considers-marijuana-tax.html?_r=0
DENVER — If marijuana is legalized and properly regulated, its proponents have long said, it could generate millions of dollars in state tax revenue. But how the drug should be taxed has proved to be a thorny question.
Ed Andrieski/Associated Press
Colorado proposes a 30 percent levy on recreational marijuana.
Enlarge This Image
Brennan Linsley/Associated Press
Ronald Kammerzell, center, was a chairman of a Colorado task force that was created to develop rules for legal marijuana.
In Colorado, where voters approved a measure in November legalizing small amounts of marijuana for recreational use, officials have been grappling with this issue for months as the state works to forge a cohesive regulatory code.
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frankiespeakin
http://www.cancer.gov/cancertopics/pdq/cam/cannabis/healthprofessional/page4
Laboratory/Animal/Preclinical Studies
Antitumor Effects
Appetite Stimulation
AnalgesiaCannabinoids are a group of 21-carbon–containing terpenophenolic compounds produced uniquely by Cannabis sativa and Cannabis indica species.[1,2] These plant-derived compounds may be referred to as phytocannabinoids. Although delta-9-tetrahydrocannabinol (THC) is the primary psychoactive ingredient, other known compounds with biologic activity are cannabinol, cannabidiol (CBD), cannabichromene, cannabigerol, tetrahydrocannabivarin, and delta-8-THC. CBD, in particular, is thought to have significantanalgesic and anti-inflammatory activity without the psychoactive effect (high) of delta-9-THC.
Antitumor Effects
One study in mice and rats suggested that cannabinoids may have a protective effect against the development of certain types of tumors.[3] During this 2-year study, groups of mice and rats were given various doses of THC by gavage. A dose-related decrease in the incidence of hepaticadenoma tumors and hepatocellular carcinoma was observed in the mice. Decreased incidences of benign tumors (polyps and adenomas) in other organs(mammary gland, uterus, pituitary, testis, and pancreas) were also noted in the rats. In another study, delta-9-THC, delta-8-THC, and cannabinol were found to inhibit the growth of Lewis lungadenocarcinomacellsin vitro and in vivo .[4] In addition, other tumors have been shown to be sensitive to cannabinoid-induced growth inhibition.[5-8]
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I OBJECT ................... TO THE USE OF THE WORD EVIL.
It's a miracle plant and should be legalised.
Haven't got around to reading this yet post yet. But happy to find it
