The Amazing Health Benefits of Juicing Raw Cannabis (Marijuana) Leaves

“Contrary to popular belief, the marijuana plant is a whole lot more than just a psychoactive drug that “stoners” use to get high.

In raw form, marijuana leaves and buds are actually loaded with a non-psychoactive, antioxidant, anti-inflammatory, and anti-cancer nutrient compound known as cannabidiol (CBD) that is proving to be a miracle “superfood” capable of preventing and reversing a host of chronic illnesses…


“There’s a tendency to discount claims when something appears to be good for everything, but there’s a reason this is the case. The endogenous cannabinoid system acts as a modulator in fine-tuning a lot of these systems, and if something is deranged biochemically in a person’s body, it may well be that a cannabinoid system can bring things back into balance.””

Read More: http://www.whydontyoutrythis.com/2013/02/health-benefits-of-juicing-raw-cannabis.html#sthash.Zgix94HO.dpbs

The nonpsychoactive Cannabis constituent cannabidiol is a wake-inducing agent.

“Cannabidiol (CBD) is a constituent of Cannabis sativa that induces nonpsychotropic effects, and some of its biological actions in sleep have been described by the authors’ group.

 Here, the authors report that when administered 10 or 20 microg/1 microl during the lights-on period directly into either lateral hypothalamus (LH) or dorsal raphe nuclei (DRN), which are wake-inducing brain areas, CBD enhanced wakefulness and decreased slow wave sleep and REM sleep. Furthermore, CBD increased alpha and theta power spectra but diminished delta power spectra. Additionally, CBD increased c-Fos expression in LH or DRN.

These findings suggest that this cannabinoid is a wake-inducing compound that presumably activates neurons in LH and DRN.”

http://www.ncbi.nlm.nih.gov/pubmed/19045957

Cannabidiol, a constituent of Cannabis sativa, modulates sleep in rats.

“Delta(9)-tetrahydrocannabinol (Delta(9)-THC) and cannabidiol (CBD) are two major constituents of Cannabis sativa. Delta(9)-THC modulates sleep, but no clear evidence on the role of CBD is available.

In order to determine the effects of CBD on sleep, it was administered intracerebroventricular (icv) in a dose of 10 microg/5 microl at the beginning of either the lights-on or the lights-off period. We found that CBD administered during the lights-on period increased wakefulness (W) and decreased rapid eye movement sleep (REMS). No changes on sleep were observed during the dark phase. Icv injections of CBD (10 microg/5microl) induced an enhancement of c-Fos expression in waking-related brain areas such as hypothalamus and dorsal raphe nucleus (DRD). Microdialysis in unanesthetized rats was carried out to characterize the effects of icv administration of CBD (10 microg/5 microl) on extracellular levels of dopamine (DA) within the nucleus accumbens. CBD induced an increase in DA release. Finally, in order to test if the waking properties of CBD could be blocked by the sleep-inducing endocannabinoid anandamide (ANA), animals received ANA (10 microg/2.5 microl, icv) followed 15 min later by CBD (10 microg/2.5 microl). Results showed that the waking properties of CBD were not blocked by ANA.

 In conclusion, we found that CBD modulates waking via activation of neurons in the hypothalamus and DRD. Both regions are apparently involved in the generation of alertness. Also, CBD increases DA levels as measured by microdialysis and HPLC procedures.

Since CBD induces alertness, it might be of therapeutic value in sleep disorders such as excessive somnolence.”

http://www.ncbi.nlm.nih.gov/pubmed/16844117

Effects of acute systemic administration of cannabidiol on sleep-wake cycle in rats.

“Cannabidiol (CBD) is one of the main components of Cannabis sativa and has a wide spectrum of action, including effects in the sleep-wake cycle. Objective: The objective of this paper is to assess the effects on sleep of acute systemic administration of CBD.

 Method: Adult male Wistar rats were randomly distributed into four groups that received intraperitoneal injections of CBD 2.5 mg/kg, CBD 10 mg/kg, CBD 40 mg/kg or vehicle (n=seven animals/group). Sleep recordings were made during light and dark periods for four days: two days of baseline recording, one day of drug administration (test), and one day after drug (post-test). Results: During the light period of the test day, the total percentage of sleep significantly increased in the groups treated with 10 and 40 mg/kg of CBD compared to placebo. REM sleep latency increased in the group injected with CBD 40 mg/kg and was significantly decreased with the dose of 10 mg/kg on the post-test day. There was an increase in the time of SWS in the group treated with CBD 40 mg/kg, although this result did not reach statistical significance.

 Conclusion: The systemic acute administration of CBD appears to increase total sleep time, in addition to increasing sleep latency in the light period of the day of administration.”

http://www.ncbi.nlm.nih.gov/pubmed/23343597

The effects of cannabidiol on the antigen-induced contraction of airways smooth muscle in the guinea-pig.

“(-)-Δ(9)-Tetrahydrocannabinol has been demonstrated to have beneficial effects in the airways, but its psychoactive effects preclude its therapeutic use for the treatment of airways diseases. In the present study we have investigated the effects of (-)-cannabidiol, a non-psychoactive component of cannabis for its actions on bronchial smooth muscle in vitro and in vivo.

 Guinea-pig bronchial smooth muscle contractions induced by exogenously applied spasmogens were measured isometrically. In addition, contractile responses of bronchial smooth muscle from ovalbumin-sensitized guinea-pigs were investigated in the absence or presence of (-)-cannabidiol. Furthermore, the effect of (-)-cannabidiol against ovalbumin-induced airway obstruction was investigated in vivo in ovalbumin-sensitized guinea pigs. (-)-Cannabidiol did not influence the bronchial smooth muscle contraction induced by carbachol, histamine or neurokinin A. In contrast, (-)-cannabidiol inhibited anandamide- and virodhamine-induced responses of isolated bronchi. A fatty acid amide hydrolase inhibitor, phenylmethanesulfonyl fluoride reversed the inhibitory effect of (-)-cannabidiol on anandamide-induced contractions. In addition, (-)-cannabidiol inhibited the contractile response of bronchi obtained from allergic guinea-pigs induced by ovalbumin. In vivo, (-)-cannabidiol reduced ovalbumin-induced airway obstruction.

 In conclusion, our results suggest that cannabidiol can influence antigen-induced airway smooth muscle tone suggesting that this molecule may have beneficial effects in the treatment of obstructive airway disorders.”

http://www.ncbi.nlm.nih.gov/pubmed/23428645

[Cannabinoids for symptomatic therapy of multiple sclerosis].

“Spasticity represents a common troublesome symptom in patients with multiple sclerosis (MS). Treatment of spasticity remains difficult, which has prompted some patients to self-medicate with and perceive benefits from cannabis. Advances in the understanding of cannabinoid biology support these anecdotal observations.

Various clinical reports as well as randomized, double-blind, placebo-controlled studies have now demonstrated clinical efficacy of cannabinoids for the treatment of spasticity in MS patients. Sativex is a 1:1 mix of delta-9-tetrahydocannabinol and cannabidiol extracted from cloned Cannabis sativa chemovars, which recently received a label for treating MS-related spasticity in Germany.

The present article reviews the current understanding of cannabinoid biology and the value of cannabinoids as a symptomatic treatment option in MS.”

http://www.ncbi.nlm.nih.gov/pubmed/22080198

Symptomatic therapy in multiple sclerosis: the role of cannabinoids in treating spasticity

“Anecdotal evidence suggests a beneficial effect of cannabis on spasticity as well as pain. Recently, randomized, double-blind, placebo-controlled studies have confirmed the clinical efficacy of cannabinoids for the treatment of spasticity in patients with MS. Based on these data, nabiximols (Sativex), a 1:1 mix of Δ-9-tetrahydrocannabinol and cannabidiol extracted from cloned Cannabis sativa chemovars, received approval for treating MS-related spasticity in various countries around the globe. In this article we review the current understanding of cannabinoid biology and the value of cannabinoids as a symptomatic treatment option addressing spasticity in patients with MS.

Based on individual case reports, the consumption of plant parts, specifically, the resin of the Cannabis sativa hemp plant, has, for years, been attributed to the capacity to reduce the symptoms of multiple sclerosis (MS), such as spasticity, neuropathic pain, tremor, and disturbed bladder function. As characterization of the endocannabinoid system and its role in the motor system and pain processing continue to advance, there is increasing evidence of a scientific basis for the postulated therapeutic effect of cannabis derivatives.

The oromucosal administration of THC and CBD in a 1:1 ratio has proven to be a well tolerated therapeutic option for treating spasticity in patients with MS who respond poorly to conventional antispastic drugs. Assessment of the efficacy is limited by the fact that spasticity as a symptom is very difficult to measure reliably, objectively, and validly. Current study data support the position that the beneficial effects of nabiximols on subjective and objective endpoints in a selected patient sample outweigh the adverse pharmaceutical effects. The effects of long-term nabiximols treatment on neuropsychological processes and the structure of the endocannabinoid system need to be further characterized.”

Full text: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3437528/

Sativex® in multiple sclerosis spasticity: a cost-effectiveness model.

“Multiple sclerosis (MS) is a chronic, progressive disease that carries a high socioeconomic burden. Spasticity (rigidity and spasms) is common in MS and a key contributor to MS-related disability.

This study evaluated the cost-effectiveness of Sativex®, a 9-d-tetrahydrocannabinol/cannabidiol-based oromucosal spray that acts as an endocannabinoid system modulator. Sativex was recently approved for the management of resistant MS spasticity as add-on medication.

CONCLUSION:

Despite having a relatively high acquisition cost, Sativex was shown to be a cost-effective treatment option for patients with MS-related spasticity.”

http://www.ncbi.nlm.nih.gov/pubmed/22681512

A new multiple sclerosis spasticity treatment option: effect in everyday clinical practice and cost-effectiveness in Germany.

“Sativex(®) (GW Pharmaceuticals PLC, Porton Down, UK; Laboratorios Almirall, SA, Barcelona, Spain), a cannabinoid oromucosal spray containing a 1:1 ratio of 9-δ-tetrahydrocannabinol and cannabidiol, has been licensed in Germany since July 2011 as add-on therapy for moderate-to-severe multiple sclerosis (MS) treatment-resistant spasticity symptoms.

The ‘MOVE 2′ study evaluated clinical outcomes, treatment satisfaction, quality of life (QoL) and provision of care in MS patients with spasticity receiving Sativex in everyday clinical practice. Data from 300 patients were collected from 42 specialized MS centers across Germany and were available for this analysis. Assessments, including the MS spasticity 0-10 numerical rating scale, modified Ashworth scale, patients’ and physicians’ clinical impressions, and QoL scales were rated at baseline and at 1 and 3 months after starting treatment with Sativex.

 Sativex provided relief of MS-related spasticity in the majority of patients who were previously resistant to treatment. In addition, clear improvements were noted in MS spasticity-associated symptoms (e.g., sleep quality, bladder function and mobility), activities of daily living and QoL. Sativex was generally well tolerated. The majority of patients (84%) reported no adverse events, and there was only a limited risk of serious adverse reactions.

Furthermore, based on data from Sativex clinical trials, a Markov model-based analysis has shown that Sativex is a cost-effective treatment option for patients with MS spasticity in Germany.”

http://www.ncbi.nlm.nih.gov/pubmed/23369055

Endocannabinoid system modulator use in everyday clinical practice in the UK and Spain.

“Spasticity is a disabling complication of multiple sclerosis. Some commonly used oral medications include baclofen, tizanidine, anticonvulsants and benzodiazepines, but their benefits are modest.

Sativex(®) (GW Pharmaceuticals PLC, Porton Down, UK; Laboratorios Almirall, SA, Barcelona, Spain) is a unique cannabinoid-based medicine with two main active ingredients; 9-δ-tetrahydrocannabinol, which acts mainly on cannabinoid 1 receptors in the CNS and plays a key role in the modulation of spasticity and spasms, and cannabidiol, which has different properties, including minimization of the psychoactivity associated with 9-δ-tetrahydrocannabinol. Sativex is indicated for symptomatic improvement in adult patients with moderate-to-severe multiple sclerosis-related spasticity who have not responded adequately to other first- or second-line antispasticity medications, and who demonstrate clinically significant improvement in spasticity-related symptoms during an initial trial of therapy.

Over the past couple of years, Sativex has been approved for use in a number of European countries and ongoing postmarketing studies are evaluating the possible risks associated with Sativex treatment by systematically collecting all suspected adverse reactions that occur in patients from the start of treatment. Interim data from the UK as well as Spanish Sativex safety registries confirm that clinical benefit is maintained over the longer term despite the expected trend for deterioration owing to disease progression.

 Even after more than 2 years of use, no new safety/tolerability signals have emerged with Sativex, including no evidence of driving impairment and no relevant incidence of falls or other adverse events of concern, such as psychiatric or nervous system events.

Sativex appears to be a well-tolerated and useful add-on therapy in patients who have not achieved an adequate response with traditional antispastic agents.”

http://www.ncbi.nlm.nih.gov/pubmed/23369054