Cannabinoid 2 (CB2) receptor agonism reduces lithium chloride-induced vomiting in Suncus murinus and nausea-induced conditioned gaping in rats.

“We aimed to investigate the potential anti-emetic and anti-nausea properties of targeting the cannabinoid 2 (CB2) receptor.

We investigated the effect of the selective CB2 agonist, HU-308, on lithium chloride- (LiCl) induced vomiting in Suncus murinus (S. murnius) and conditioned gaping (nausea-induced behaviour) in rats.

These findings are the first to demonstrate the ability of a selective CB2 receptor agonist to reduce nausea in animal models, indicating that targeting the CB2 receptor may be an effective strategy, devoid of psychoactive effects, for managing toxin-induced nausea and vomiting.”

http://www.ncbi.nlm.nih.gov/pubmed/27263826

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The Antitumor Activity of Plant-Derived Non-Psychoactive Cannabinoids.

“As a therapeutic agent, most people are familiar with the palliative effects of the primary psychoactive constituent of Cannabis sativa (CS), Δ9-tetrahydrocannabinol (THC), a molecule active at both the cannabinoid 1 (CB1) and cannabinoid 2 (CB2) receptor subtypes.

Through the activation primarily of CB1 receptors in the central nervous system, THC can reduce nausea, emesis and pain in cancer patients undergoing chemotherapy.

During the last decade, however, several studies have now shown that CB1 and CB2 receptor agonists can act as direct antitumor agents in a variety of aggressive cancers.

In addition to THC, there are many other cannabinoids found in CS, and a majority produces little to no psychoactivity due to the inability to activate cannabinoid receptors.

For example, the second most abundant cannabinoid in CS is the non-psychoactive cannabidiol (CBD). Using animal models, CBD has been shown to inhibit the progression of many types of cancer including glioblastoma (GBM), breast, lung, prostate and colon cancer.

This review will center on mechanisms by which CBD, and other plant-derived cannabinoids inefficient at activating cannabinoid receptors, inhibit tumor cell viability, invasion, metastasis, angiogenesis, and the stem-like potential of cancer cells.

We will also discuss the ability of non-psychoactive cannabinoids to induce autophagy and apoptotic-mediated cancer cell death, and enhance the activity of first-line agents commonly used in cancer treatment.”

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Effects of cannabinoids on lithium-induced conditioned rejection reactions in a rat model of nausea.

“Marijuana has been reported to suppress nausea produced by chemotherapy treatment in human cancer patients.

… there is abundant evidence that cannabinoid agonists attenuate vomiting in emetic species…

The present experiments evaluated the potential of low doses of the cannabinoid agonists, delta-9-tetrahydrocannabinol (THC; 0.5 mg/kg, i.p.), and HU-210 (0.001 mg/kg and 0.01 mg/kg, i.p.), and the CB(1) antagonist SR-141716A in modulating the establishment and the expression of lithium-induced conditioned rejection reactions in rats.

These results indicate that the establishment and the expression of lithium-induced conditioned rejection reactions are suppressed by pretreatment with cannabinoid agents.”

http://www.ncbi.nlm.nih.gov/pubmed/12528012

http://www.thctotalhealthcare.com/category/nauseavomiting/

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Cannabinoids suppress acute and anticipatory nausea in pre-clinical rat models of conditioned gaping.

“The sensation of nausea is one of the most debilitating human experiences. Current anti-emetic therapies are effective in reducing vomiting, but are less effective in reducing acute and delayed nausea and are completely ineffective in reducing anticipatory nausea.

Recent pre-clinical evidence using a selective rat model of nausea (conditioned gaping reactions) has revealed that cannabinoids have great promise as treatments for nausea and that their anti-nausea effects may be mediated by the interoceptive insular cortex.”

http://www.ncbi.nlm.nih.gov/pubmed/25691302

http://www.thctotalhealthcare.com/category/nauseavomiting/

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Protective effects of cannabidiol on lesion-induced intervertebral disc degeneration.

“Disc degeneration is a multifactorial process that involves hypoxia, inflammation, neoinnervation, accelerated catabolism, and reduction in water and glycosaminoglycan content…

Cannabidiol (CBD) is the major nonpsychotropic phytocannabinoid of Cannabis sativa (up to 40% of Cannabis extracts). Contrary to most cannabinoids, CBD does not produce psychotomimetic or cognitive effects. Interesting, in the last years it has been suggest that CBD produces a plethora of others pharmacological effects, including antioxidant, neuroprotective, anti-proliferative, anti-anxiety, hypnotic and antiepileptic, anti-nausea, anti-ischemic, anti-hyperalgesic, and anti-inflammatory…

The present study investigated the effects of cannabidiol intradiscal injection in the coccygeal intervertebral disc degeneration induced by the needle puncture model using magnetic resonance imaging (MRI) and histological analyses…

 Cannabidiol significantly attenuated the effects of disc injury induced by the needle puncture. Considering that cannabidiol presents an extremely safe profile and is currently being used clinically, these results suggest that this compound could be useful in the treatment of intervertebral disc degeneration.

 In summary our study revealed anti-degenerative effects of intradiscal microinjection of CBD 120 nmol. CBD represents one of the most promising candidates present in the Cannabis sativa plant for clinical use due to its remarkable lack of cognitive or psychotomimetic actions.”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4269422/

http://www.thctotalhealthcare.com/category/spinal-cord-injury/

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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.”

http://www.ncbi.nlm.nih.gov/pubmed/23902479

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Medical Marijuana Is Safe for Children

“Numerous cases show clinical cannabis is effective on illnesses in children”

By  William Courtney, M.D. is CEO of Cannabis International.

“The courage and fortitude of parents who have chosen cannabis compounds to treat their children facing life-threatening illness have raised eyebrows. Some live in terror that their government will take their child away, since medical marijuana is only legal in some states. However, there are numerous cases demonstrating the benefits of clinical cannabis, which happen to threaten a very profitable healthcare industry that relies on conventional drugs, as well as political agendas.

The cannabinoid acids in cannabis have been found to have anti-proliferative, anti-neoplastic, anti-inflammatory, anti-epileptic, anti-ischemic, anti-diabetic, anti-psychotic, anti-nausea, anti-spasmodic, antibiotic, anti-anxiety, and anti-depressant functions. The anti-neoplastic action of cannabis—inhibiting development of malignant cells—was recognized in the 1970s and patented by the U.S. Department of Health and Human Services in 2003.

Out of 7,000 patients, my youngest, an 8-month-old, was diagnosed with a massive midbrain tumor. Pediatric oncologists recommended chemotherapy and radiation. Instead, the parents applied a cannabinoid concentrate to their son’s pacifier twice a day, which resulted in a significant reduction in the size of the tumor in 30 days. The response prevented a million-dollar chemo-radiation hospitalization. The child’s oncologist calls the infant a ‘miracle baby,’ but most medical experts would discount the case as anecdotal, unacceptable in a peer-reviewed journal. But the real peers are other parents reluctant to consent to the devastation of surgery, chemotherapy, and radiation—not those benefiting from the $2.6 trillion healthcare industry.

A 2-year-old spent a year in a pediatric oncology ward, endured 39 hours of brain surgery, received chemotherapy, a bone marrow transplant, and radiation under general anesthesia for 42 days, only to be discharged home on hospice and morphine. The child’s local pediatrician started to treat her with juiced raw cannabis leaf. Two years later, she is still alive, now free of cancer and scar tissue.

A 6-year-old patient with a severe, intractable form of childhood epilepsy, was tried on 11 anti-epileptics, including experimental European drugs. He was finally placed on a drug commonly used to prevent seizures, but continued having 300-400 seizures a day. An ointment produced from cannabis with an increased amount of cannabidiol, a compound patented by HHS, has reduced his seizures to one every 3-4 days.

Several years ago, I proposed that cannabis be recognized as an essential nutrient in the diet of individuals in their 30s and older. Children were excluded out of fear of backlash but it is now my incontrovertible opinion that the immune system of the 8-month-old would never have allowed the tumor to gain a foothold if supported with dietary cannabis, or Vitamin F.

We know Vitamin C deficiency results in scurvy and Vitamin D deficiency results in rickets. Vitamin F, the previous label for Omega-3 and -6 essential fatty acids, is an appropriate appellation for the cannabinoid acids found in cannabis. Vitamin F deficiency allows the cell proliferation found in tumors and cancer. Three studies of over 24,000 children have shown no adverse effects from use of cannabis in pregnancy.

There is no other area in medicine where the heavy hand of federal funding and political agenda compromise valid and reproducible findings to this extent. To advance disease prevention and benign therapy, we must re-examine our preconceptions.”

http://www.usnews.com/opinion/articles/2013/01/07/medical-marijuana-is-safe-for-children

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Cannabidiol: an overview of some chemical and pharmacological aspects. Part I: chemical aspects.

“Over the last few years considerable attention has focused on cannabidiol (CBD), a major non-psychotropic constituent of Cannabis. In Part I of this review we present a condensed survey of the chemistry of CBD; in Part II, to be published later, we shall discuss the anti-convulsive, anti-anxiety, anti-psychotic, anti-nausea and anti-rheumatoid arthritic properties of CBD. CBD does not bind to the known cannabinoid receptors and its mechanism of action is yet unknown. In Part II we shall also present evidence that it is conceivable that, in part at least, its effects are due to its recently discovered inhibition of anandamide uptake and hydrolysis and to its anti-oxidative effect.”

http://www.ncbi.nlm.nih.gov/pubmed/12505688

http://www.scribd.com/doc/52920296/Cannabidiol-an-Overview-of-Some-Chemical-and-Pharmacological-Aspects-Part-I-Chemical-Aspects

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Cannabidiol in vivo blunts beta-amyloid induced neuroinflammation by suppressing IL-1beta and iNOS expression.

“Pharmacological inhibition of beta-amyloid (Aβ) induced reactive gliosis may represent a novel rationale to develop drugs able to blunt neuronal damage and slow the course of Alzheimer’s disease (AD). Cannabidiol (CBD), the main non-psychotropic natural cannabinoid, exerts in vitro a combination of neuroprotective effects in different models of Aβ neurotoxicity. The present study, performed in a mouse model of AD-related neuroinflammation, was aimed at confirming in vivo the previously reported antiinflammatory properties of CBD.

Cannabidiol (CBD), the main non-psychotropic component of the glandular hairs of Cannabis sativa, exhibits a plethora of actions including anti-convulsive, sedative, hypnotic, anti-psychotic, anti-nausea, anti-inflammatory and anti-hyperalgesic properties. CBD has been proved to exert in vitro a combination of neuroprotective effects in Aβ-induced neurotoxicity, including anti-oxidant and anti-apoptotic effects, tau protein hyperphosphorylation inhibition through the Wnt pathway, and marked decrease of inducible nitric oxide synthase (iNOS) protein expression and nitrite production in Aβ-challenged differentiated rat neuronal cells.

In spite of the large amount of data describing the significant neuroprotective and anti-inflammatory properties of CBD in vitro, to date no evidence has been provided showing similar effects in vivo. To achieve this, the present study investigated the potential anti-inflammatory effect of CBD in a mouse model of AD-related neuroinflammation induced by the intrahippocampal injection of the human Aβ (1–42) fragment.

The results of the present study confirm in vivo anti-inflammatory actions of CBD, emphasizing the importance of this compound as a novel promising pharmacological tool capable of attenuating Aβ evoked neuroinflammatory responses.

 …on the basis of the present results, CBD, a drug well tolerated in humans, may be regarded as an attractive medical alternative for the treatment of AD, because of its lack of psychoactive and cognitive effects.”

Read more: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2189818/

 

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