Medical Marijuana Zone

HERBAL CBD says:

Valleylabz from the 559 makes it in front of you and let's you know all the information how cannabis helps are receptors and how it can help build immune system I trust his cbd he has been doing before it was legal but cbd helps if it's made right

xxnike629xx says:

Given that CBD use is still a new thing we need more time to see if it’s effect and use is effective and safe.
For those that use it regularly, if it helps you then I’m glad it’s helping.

If CBD helped this former military man prevent committing suicide and getting back to living then good for him.
Whatever helps people bad long as it’s not an illegal drug or has negative effects on your physical and mental health then why not use it?

seeking wisdom says:

Snake oil, poisons is what comes out of the normal medical system. No healing

Lori Touma says:

Very very good video and hoping that more people get well with this type of drug… i believe in the benefits in CBD FOR SOME people and children who can defenitely benefit for a better life!!

Justin Norton says:

This is why you can't trust corporations. They will cut corners and quality to maximize profits. Use only growers, because you can see how your product is made. Compassion Centers around my part of the US, is ran and owned by slimy politicians and law enforcement, who only care about profit, not the People.

Ominous Cloud says:

Beware of cbds if you are on depakote.The combo can blow out your liver.Why is this not common knowledge?

Daughter Of Zion, iron, like a lion, in zion says:

It's not produced from the cannabis plant though…lying twat!…its produced from the hemp plant, cannabis's cousin…which is legal to grow

Colleen Osullivan says:

CBD doesn’t make you high, but it does work. I use CBD gummy bears. It doesn’t kill the pain, but it makes it tolerable

Idylchatter says:

The FDA recently came out with a warning re: CBD and liver damage. If you are on a plethora of drugs, it would be unwise to heavily dose CBD due to P450 enzyme reduced activity, other than that? They need to explain just exactly what it is they are getting at.

Sci Rep. 2017 Sep 21;7(1):12064. doi: 10.1038/s41598-017-10924-8.
Cannabidiol attenuates alcohol-induced liver steatosis, metabolic dysregulation, inflammation and neutrophil-mediated injury.
Wang Y1,2, Mukhopadhyay P1, Cao Z1, Wang H3, Feng D3, Haskó G4, Mechoulam R5, Gao B3, Pacher P6.
Author information
Abstract

Cannabidiol (CBD) is a non-psychoactive component of marijuana, which has anti-inflammatory effects. It has also been approved by FDA for various orphan diseases for exploratory trials. Herein, we investigated the effects of CBD on liver injury induced by chronic plus binge alcohol feeding in mice. CBD or vehicle was administered daily throughout the alcohol feeding study. At the conclusion of the feeding protocol, serums samples, livers or isolated neutrophils were utilized for molecular biology, biochemistry and pathology analysis. CBD significantly attenuated the alcohol feeding-induced serum transaminase elevations, hepatic inflammation (mRNA expressions of TNFα, MCP1, IL1β, MIP2 and E-Selectin, and neutrophil accumulation), oxidative/nitrative stress (lipid peroxidation, 3-nitrotyrosine formation, and expression of reactive oxygen species generating enzyme NOX2). CBD treatment also attenuated the respiratory burst of neutrophils isolated from chronic plus binge alcohol fed mice or from human blood, and decreased the alcohol-induced increased liver triglyceride and fat droplet accumulation. Furthermore, CBD improved alcohol-induced hepatic metabolic dysregulation and steatosis by restoring changes in hepatic mRNA or protein expression of ACC-1, FASN, PPARα, MCAD, ADIPOR-1, and mCPT-1. Thus, CBD may have therapeutic potential in the treatment of alcoholic liver diseases associated with inflammation, oxidative stress and steatosis, which deserves exploration in human trials.

https://www.ncbi.nlm.nih.gov/m/pubmed/25595882/?i=2&from=Fatty%20liver%20cannabidiol 

Two non-psychoactive cannabinoids reduce intracellular lipid levels and inhibit hepatosteatosis.
Silvestri C, et al. J Hepatol. 2015.
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Abstract

BACKGROUND & AIMS: Obesity and associated metabolic syndrome have quickly become a pandemic and a major detriment to global human health. The presence of non-alcoholic fatty liver disease (NAFLD; hepatosteatosis) in obesity has been linked to the worsening of the metabolic syndrome, including the development of insulin resistance and cardiovascular disease. Currently, there are few options to treat NAFLD, including life style changes and insulin sensitizers. Recent evidence suggests that the cannabinoids Δ(9)-tetrahydrocannabivarin (THCV) and cannabidiol (CBD) improve insulin sensitivity; we aimed at studying their effects on lipid levels.

METHODS: The effects of THCV and CBD on lipid levels were examined in a variety of in vitro and in vivo systems, with special emphasis on models of hepatosteatosis. Transcriptional, post-translational and metabolomic changes were assayed.

RESULTS: THCV and CBD directly reduce accumulated lipid levels in vitro in a hepatosteatosis model and adipocytes. Nuclear magnetic resonance- (NMR) based metabolomics confirmed these results and further identified specific metabolic changes in THCV and CBD-treated hepatocytes. Treatment also induced post-translational changes in a variety of proteins such as CREB, PRAS40, AMPKa2 and several STATs indicating increased lipid metabolism and, possibly, mitochondrial activity. These results are supported by in vivo data from zebrafish and obese mice indicating that these cannabinoids are able to increase yolk lipid mobilization and inhibit the development of hepatosteatosis respectively.

CONCLUSIONS: Our results suggest that THCV and CBD might be used as new therapeutic agents for the pharmacological treatment of obesity- and metabolic syndrome-related NAFLD/hepatosteatosis.

Idylchatter says:

Fibromyalgia, or myofascial pain syndrome, is an extremely common but controversial condition, whose very basis has been questioned, particularly among neurologists [65]. Even this author must admit to past prejudice in labeling it a “semi mythical pseudo-disease.”  Notwithstanding these opinions, the condition is the most frequent diagnosis in American rheumatology practices. Bennett has provided an excellent review [66], emphasizing new insights into fibromyalgia as a condition indicative of “central sensitization” and amplification of somatic nociception. While no clear chemical or anatomical pathology has been clarified in tender muscle points, these present a self-sustaining and amplifying influence on pain perception in the brain over time, and lead to a concomitant disturbances in restful sleep, manifestations of dysautonomia, and prevalent secondary depression. Interestingly, the application of standard antidepressant medication to the latter, and pharmacotherapy in general, provide disappointing results in fibromyalgia treatment. Has a promising therapeutic avenue been missed? Returning to the work of Nicolodi and Sicuteri, the  “secondary hyperalgesia” manifested by an increased response to noxious stimuli in areas adjacent to the pain is common to migraine and fibromyalgia (see below). 

These authors suggested NMDA blockade as an approach to pain in defects of serotonergic analgesia in fibromyalgia [67]. Several studies of Richardson and her group provide key support for a relation of fibromyalgia and similar conditions to a clinical endocannabinoid deficiency. An initial study [68] demonstrated that intrathecal injection of SR141716A, a powerful cannabinoid antagonist/inverse agonist, resulted in thermal hyperalgesia in mice. This suggests  that the endocannabinoid system regulates nociceptive thresholds, and that absence of such regulation, or endocannabinoid hypofunction, underlies hyperalgesia and related chronic pain conditions. In a subsequent study [69], oligonucleotides directed against CB1 mRNA produced significant hyperalgesia. Additionally, the hyperalgesic effect of SR141716A was blocked in a dose-dependent manner by co-administration of two NMDA receptor antagonists, again sup-porting tonic activity of the endocannabinoid system under normal conditions. 

On this basis, it was suggested that cannabinoid agonists would be applicable to treatment of chronic pain conditions unresponsive to opioid analgesics. Further investigation demonstrated that intrathecal AEA totally blocked carrageenan-induced spinal thermal hyperalgesia, while having no effect on normal thermal sensory and antinociceptive thresholds [70]. Additionally, AEA inhibited K+ and capsaicin-evoked calcitonin gene-related peptide (CGRP) release, and CB1 receptors were identified in rat sensory neurons and trigeminal ganglion. On this basis, the authors recommended cannabinoids for disorders driven by a primary afferent barrage (e.g., allodynia, visceral hyperalgesia, temporomandibular joint pain (TMJ), and reflex sympathetic dystrophy (RSD)), and that such treatment could be effective a sub-psychoactive dosages. 

Another study examined peripheral mechanisms [71], wherein AEA acted on CB1 to reduce hyperalgesia and inflammation via inhibition of CGRP neurosecretion in capsaicin activated nerve terminals. This is akin to mechanisms of “sterile inflammation” observed centrally in migraine, where CGRP is felt to be an important mediator [5]. Overall the results supported the notion that endocannabinoids modulate neurogenic inflammation through inhibition of peripheral terminal neurosecretion in capsaicin-sensitive fibers. AEA demonstrated anti-edema effects in addition to anti-hyperalgesia. Similar implications were provided by another study [72], in which WIN 55,212–2, a powerful  CB1 agonist, blocked capsaicin-induced hyperalgesia in rat paws. Once more, the benefit occurred at a dosage that did not produce analgesia or motor impairment, suggesting therapeutic benefit of cannabinoids without adverse effects. Similarly, lo-cal THC administration was evaluated in capsaicin-induced pain in rhesus monkeys [73], where, once more, pain was effectively reduced at low dosage, and was blocked by a CB1 antagonist.