[There is evidence for the use of cannabinoids for symptomatic treatment of multiple sclerosis.]

“We identified 16 randomized placebo-controlled trials investigating cannabinoids as symptomatic treatment in multiple sclerosis (MS).

There is evidence that nabiximols (THC/CBD) oromucosal spray may reduce subjective symptoms of spasticity and that dronabinol (THC) is effective against neuropathic pain in patients with MS…”

http://www.ncbi.nlm.nih.gov/pubmed/25350886

http://www.thctotalhealthcare.com/category/multiple-sclerosis-ms/

The interface: marijuana and body weight.

“Acute marijuana use is classically associated with snacking behavior (colloquially referred to as “the munchies”). In support of these acute appetite-enhancing effects, several authorities report that marijuana may increase body mass index in patients suffering from human immunodeficiency virus and cancer…

Marijuana is a clinically controversial substance, but one potential medical benefit may be weight gain. According to available studies, appetite stimulation as well as weight gain may occur in patients with physical debilitation due to HIV/AIDS and/or cancer.

As for the effects of marijuana on body weight in the general population, use appears to be associated with a lower body mass index.

…marijuana may genuinely be a regulatory compound, increasing weight in those with low weight, but not in those who are normal or overweight.”

 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4204468/

Cannabidiol: promise and pitfalls.

“Over the past few years, increasing public and political pressure has supported legalization of medical marijuana.

One of the main thrusts in this effort has related to the treatment of refractory epilepsy-especially in children with Dravet syndrome-using cannabidiol (CBD).

Despite initiatives in numerous states to at least legalize possession of CBD oil for treating epilepsy, little published evidence is available to prove or disprove the efficacy and safety of CBD in patients with epilepsy. This review highlights some of the basic science theory behind the use of CBD, summarizes published data on clinical use of CBD for epilepsy, and highlights issues related to the use of currently available CBD products.

Cannabidiol is the major nonpsychoactive component of Cannabis sativa.

Over the centuries, a number of medicinal preparations derived from C. sativa have been employed for a variety of disorders, including gout, rheumatism, malaria, pain, and fever.

These preparations were widely employed as analgesics by Western medical practitioners in the 19(th) century.

More recently, there is clinical evidence suggesting efficacy in HIV-associated neuropathic pain, as well as spasms associated with multiple sclerosis.”

http://www.ncbi.nlm.nih.gov/pubmed/25346628

http://www.thctotalhealthcare.com/category/epilepsy-2/

Seizing an opportunity for the endocannabinoid system.

“Exogenous cannabinoids can limit seizures and neurodegeneration, and their actions are largely mimicked by endogenous cannabinoids (endocannabinoids).

Endocannabinoids are mobilized by epileptiform activity and in turn influence this activity by inhibiting synaptic transmission; both excitatory and some inhibitory synapses can be suppressed, leading to potentially complex outcomes.

Moreover, the endocannabinoid system is not a fixed entity, and its strength can be enhanced or reduced.

Endocannabinoids and their receptors are altered by epileptic seizures in ways that can reduce the efficacy of both exogenous and endogenous cannabinoids in sometimes unexpected ways.”

http://www.ncbi.nlm.nih.gov/pubmed/25346637

http://www.thctotalhealthcare.com/category/epilepsy-2/

Endocannabinoids, Related Compounds and Their Metabolic Routes.

“Endocannabinoids are lipid mediators able to bind to and activate cannabinoid receptors, the primary molecular targets responsible for the pharmacological effects of the Δ9-tetrahydrocannabinol.

These bioactive lipids belong mainly to two classes of compounds: N-acylethanolamines and acylesters, being N-arachidonoylethanolamine (AEA) and 2-arachidonoylglycerol (2-AG), respectively, their main representatives.

During the last twenty years, an ever growing number of fatty acid derivatives (endocannabinoids and endocannabinoid-like compounds) have been discovered and their activities biological is the subject of intense investigations.

Here, the most recent advances, from a therapeutic point of view, on endocannabinoids, related compounds, and their metabolic routes will be reviewed.”

http://www.ncbi.nlm.nih.gov/pubmed/25347455

Evaluation of the tolerability and efficacy of Sativex in multiple sclerosis.

“Refractory spasticity, central neuropathic pain and bladder dysfunction are common clinical problems in patients with multiple sclerosis (MS). None of the currently available oral medications has proven to be reliably effective and can be limited by toxicity.

Cannabinoids have shown therapeutic effects on those MS-associated symptoms.

Delta-9-tetrahydrocannabinol (THC)/cannabidiol (CBD) Sativex (nabiximols) is an oromucosal spray formulation that contains THC and CBD in an approximate 1:1 ratio and is described as an endocannabinoid system modulator.

The efficacy of THC/CBD on MS-associated spasticity, pain and bladder dysfunction has been studied in clinical trials as well as in clinical practice studies. Adverse effects are usually mild or moderate and the low rate of drug discontinuation provides good evidence of long-term tolerability. This article focuses on the pharmacological properties, clinical efficacy and tolerability of THC/CBD in MS patients.”

http://www.ncbi.nlm.nih.gov/pubmed/25331416

Cannabis, cannabidiol, and epilepsy – From receptors to clinical response.

“The use of cannabis for medicinal purposes is becoming more prevalent.

For this purpose, various preparations of cannabis of varying strengths and content are being used.

The recent changes in the legal environment have improved the availability of products with high cannabidiol (CBD) and low tetrahydrocannabinol (THC) concentrations.

There is some anecdotal evidence of their potential efficacy, but the mechanisms of such action are not entirely clear.

Some suspect an existence of synergy or “entourage effect” between CBD and THC.

There is strong evidence that THC acts via the cannabinoid receptor CB1.

The mechanism of action of CBD is less clear but is likely polypharmacological.

The scientific data support the role of the endocannabinoid system in seizure generation, maintenance, and control in animal models of epilepsy.

There are clear data for the negative effects of cannabis on the developing and mature brain though these effects appear to be relatively mild in most cases.

Further data from well-designed studies are needed regarding short- and long-term efficacy and side effects of CBD or high-CBD/low-THC products for the treatment of seizures and epilepsy in children and adults.”

http://www.ncbi.nlm.nih.gov/pubmed/25282526

http://www.thctotalhealthcare.com/category/epilepsy-2/

Type-2 cannabinoid receptor regulates proliferation, apoptosis, differentiation, and OPG/RANKL ratio of MC3T3-E1 cells exposed to Titanium particles.

“The type-2 cannabinoid receptor (CB2) is expressed in osteoblasts and plays a role in bone metabolism through regulation on bone mass and bone turnover, but the functional importance of CB2 in osteoblasts under Titanium (Ti) stimulation is incompletely understood.

This study aimed to investigate the CB2 expression in osteoblasts under Ti stimulation and the effects of CB2 activation on proliferation, apoptosis, differentiation, mineralization, OPG, and RANKL expression of MC3T3-E1 cells exposed to Ti particles…

In conclusion, CB2 activation has a favorable inhibitory effect on Ti-induced reactions in MC3T3-E1 cell through modulating proliferation, apoptosis, differentiation, and RANKL expression.

These findings suggest that activation of CB2 might be an effective therapeutic strategy to promote bone formation and reduce bone dissolution.”

http://www.ncbi.nlm.nih.gov/pubmed/25292314

Intraocular pressure, ocular toxicity and neurotoxicity after administration of cannabinol or cannabigerol.

“Cannabinol or cannabigerol was administered to cats topically in doses of 250, 500 and 1000 micrograms as a single drop or chronically via osmotic minipumps (20 micrograms hr-1) over a period of 9 days. While cannabinol had a modest effect on intraocular pressure after a single dose, it caused a more significant reduction in ocular tension during chronic administration. Cannabigerol had similar effects, but the magnitude of response to its chronic administration was greater. Cannabinol but not cannabigerol caused conjunctival erythema and hyperemia. After systemic administration of cannabinol (20, 40 or 80 mg kg-1) to rats, 8-13 Hz polyspike discharges appeared in the electrocorticogram during wakefulness and during rapid eye movement sleep episodes. Cannabigerol (10, 30 and 100 mg kg-1) lacked this effect.

These results indicate that chronic administration of these cannabinoids lowers ocular tension considerably.

Like marihuana and delta-9-tetrahydrocannabinol, cannabinol produced both ocular toxicity and neurotoxicity. As cannabigerol lacked these toxicities, it appears that the ocular hypotensive effect of this cannabinoid is somewhat dissociable from both the adverse central and ocular effects accompanying marihuana intake.”

http://www.ncbi.nlm.nih.gov/pubmed/6499952

A comparison of the ocular and central effects of delta 9-tetrahydrocannabinol and cannabigerol.

“Both delta 9-tetrahydrocannabinol (delta 9-THC) and cannabigerol, two naturally occurring marihuana cannabinoids, produced only a modest fall in intraocular pressure after acute topical application to the eyes of cats.

After chronic administration unilaterally to the cornea via Alzet osmotic minipumps and connecting extraocular cannulas, however, a considerable fall in ocular tension amounting to 4 to 7 mm Hg occurred. After systemic administration of delta 9-THC to rats, polyspike discharges appeared in the cortical electroencephalogram initially during wakefulness and behavioral depression. These polyspikes subsequently became evident within rapid eye movement sleep episodes. Cannabigerol was devoid of this effect. After removal of either sympathetic or parasympathetic input to the eyes of cats, the intraocular pressure lowering effect of delta 9-THC was not changed. Neither delta 9-THC nor cannabigerol altered the rate of formation of aqueous humor. On the other hand, both cannabinoids produced a two-to three-fold increase in aqueous outflow facility.

These results suggest that cannabigerol and related cannabinoids may have therapeutic potential for the treatment of glaucoma.”

http://www.ncbi.nlm.nih.gov/pubmed/1965836