Can Medical Marijuana Help With Sleep Apnea

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“A medical disorder characterized by frequent interruptions in breathing of up to 10 seconds or more during sleep, sleep apnea, is associated with many physiological disorders, including fatigue, headaches, high blood pressure, irregular heartbeat, heart attack, and stroke…

In the June issue of the American Academy of Sleep Medicine Journal, researchers at the University of Illinois, Department of Medicine reported that sleep apnea in rats that received cannabinoids (natural chemicals of cannabis) was deleted. Doses of delta-9-THC and stabilized polyamide breathing during sleep and blocked serotonin-induced exacerbation of sleep apnea. Many patients who have used the ratio of medical cannabis improved sleep quality and less fatigue the next day.”

More: http://marijuanacalifornia.wordpress.com/2012/07/20/can-medical-marijuana-help-with-sleep-apnea/

Proof of Concept Trial of Dronabinol in Obstructive Sleep Apnea

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“… Δ9-TetraHydroCannabinol (Δ9THC) stabilizes autonomic output during sleep, reduces spontaneous sleep-disordered breathing, and blocks serotonin-induced exacerbation of sleep apnea. On this basis, we examined the safety, tolerability, and efficacy of dronabinol (Δ9THC), an exogenous Cannabinoid type 1 and type 2 (CB1 and CB2) receptor agonist in patients with Obstructive Sleep Apnea (OSA)…

Conclusion: Dronabinol treatment is safe and well-tolerated in OSA patients at doses of 2.5–10mg daily and significantly reduces AHI in the short-term. These findings should be confirmed in a larger study in order to identify sub-populations with OSA that may benefit from cannabimimetic pharmacologic therapy…

This proof of concept study demonstrates that dronabinol is safe, well-tolerated, and reduces AHI by approximately a third over 3 weeks of oral administration. Dronabinol treatment may be a viable alternative or adjunctive therapy in selected patients with OSA.”

Full text: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3550518/

Functional role for cannabinoids in respiratory stability during sleep.

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“Serotonin, acting in the peripheral nervous system, can exacerbate sleep-related apnea, and systemically administered serotonin antagonists reduce sleep-disordered respiration in rats and bulldogs. Because cannabinoid receptor agonists are known to inhibit the excitatory effects of serotonin on nodose ganglion cells, we examined the effects of endogenous (oleamide) and exogenous (delta9-tetrahydrocannabinol; delta9THC) cannabimimetic agents on sleep-related apnea…

Our data show that delta9THC and oleamide each stabilized respiration during all sleep stages… This observation suggests an important role for endocannabinoids in maintaining autonomic stability during sleep…

CONCLUSIONS:

This study demonstrates potent suppression of sleep-related apnea by both exogenous and endogenous cannabinoids. These findings are of relevance to the pathogenesis and pharmacological treatment of sleep-related breathing disorders.”

http://www.ncbi.nlm.nih.gov/pubmed/12071539

Circulating anandamide and blood pressure in patients with obstructive sleep apnea.

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” OBJECTIVE: Obstructive sleep apnea chronically increases blood pressure through sympathetic nervous system activation. In animals, hypertension and sympathetic activity are restrained by cannabinoid receptor activation. Therefore, we hypothesized that increased blood pressure in patients with obstructive sleep apnea is associated with increased circulating endocannabinoid concentrations.

 

CONCLUSION: Obstructive sleep apnea patients show positive correlations between blood pressure and venous anandamide concentrations independent of confounding factors. Our data suggest a previously not recognized role of the endocannabinoid system for blood pressure regulation in patients with high risk for hypertension and cardiovascular disease.”

http://www.ncbi.nlm.nih.gov/pubmed/23032139

Circulating endocannabinoids and N-acyl-ethanolamides in patients with sleep apnea–specific role of oleoylethanolamide.

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“OBJECTIVE:  The endocannabinoid system promotes diverse effects on fat and glucose metabolism as well as on energy balance and sleep regulation. The role of N-acylethanolamides like oleoylethanolamide (OEA) and other endocannabinoids such as anandamide (AEA) and 2-arachidonyl-glycerol (2-AG) has not yet been investigated in patients with sleep apnea.

 

CONCLUSIONS: These results indicate that among the three analyzed fatty acid derivatives, OEA plays a specific role in patients with sleep apnea. Together with animal data, the 2-fold elevation of OEA serum concentrations could be interpreted as a neuroprotective mechanism against chronic oxidative stressors and a mechanism to promote wakefulness in patients with nocturnal sleep deprivation and daytime hypersomnolence.”

http://www.ncbi.nlm.nih.gov/pubmed/20429051

 

[A study on the endogenous cannabinoid system synthetic and catabolic enzyme levels in patients with obstructive sleep apnea].

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“OBJECTIVE: To observe the differences of endogenous cannabinoid system (ECS) synthetic and catabolic enzyme levels between the obstructive sleep apnea syndrome (OSA) patients and the control subjects.

 

CONCLUSION: OSA altered the expression of the ECS synthetic and catabolic enzymes, leading to an increase in endogenous cannabinoid substances.”

 

http://www.ncbi.nlm.nih.gov/pubmed/21729625

Nuvilex Reports Cannabinoid-Based Pancreatic Cancer Treatments to be Developed by Its Subsidiary, Medical Marijuana Sciences, Inc.

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“Nuvilex, Inc. (OTCQB:NVLX), international biotechnology and clinical stage provider of natural products and cell and gene therapy solutions for the treatment of diseases, announced today its subsidiary, Medical Marijuana Sciences, Inc., is planning to develop treatments for pancreatic cancer based on cannabinoids from Cannabis sativa.

In 2006, in a publication in the prestigious scientific journal Cancer Research, cannabinoids were reported to cause the death of pancreatic cells in laboratory and animal studies; these results were also seen with human pancreatic cancer cells implanted in mice whose immune systems were suppressed. Since then, laboratory studies have shown that when gemcitabine (Gemzar®), the only drug approved by the FDA as a single agent for the treatment of advanced pancreatic cancer, was combined with three different cannabinoids (each used singly), the growth inhibition was more than additive for six different pancreatic cancer cell lines. When these studies were done with human pancreatic cancer cells in immunosuppressed mice, the antitumor effectiveness of gemcitabine was greatly enhanced. These results, combined with those from other studies not mentioned here, indicate the important potential for developing treatments for pancreatic cancer that include the use of cannabinoids.”

More: http://www.nasdaq.com/article/nuvilex-reports-cannabinoid-based-pancreatic-cancer-treatments-to-be-developed-by-its-subsidiary-medical-marijuana-sciences-inc-20130220-00761

Expression of the cannabinoid type I receptor and prognosis following surgery in colorectal cancer.

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“The cannabinoid system has been considered to be a potential target of colorectal carcinoma therapy. The aim of this study was to address the correlation between cannabinoid type 1 (CB1) receptor expression and disease severity/outcomes in patients with colorectal cancer (CRC).”

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 “…The high immunoreactivity of the cannabinoid type 1 receptor is a significant prognostic factor following surgery in stage IV CRC…

The effect of cannabinoids in colorectal cancer (CRC) has been demonstrated in in vitro experiments and animal models, which indicate the antiproliferative, apoptotic and antimetastatic actions of cannabinoid agonists…

Antineoplastic effects are mediated by the activation of cannabinoid type I (CB1), type 2 (CB2) or a non-cannabinoid receptor-mediated mechanism…”

Full text: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3576207/

AM404 attenuates reinstatement of nicotine seeking induced by nicotine-associated cues and nicotine priming but does not affect nicotine- and food-taking.

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“Multiple studies suggest a pivotal role of the endocannabinoid system in the regulation of the reinforcing effects of various substances of abuse. Different approaches have been used to modulate endocannabinoid neurotransmission including the use of endogenous cannabinoid anandamide reuptake inhibitors.

 Previously, the effects of one of them, N-(4-hydroxyphenyl)-arachidonamide (AM404), have been explored in rodents trained to self-administer ethanol and heroin, producing some promising results. Moreover, AM404 attenuated the development and reinstatement of nicotine-induced conditioned place preference (CPP). In this study, we used the nicotine intravenous self-administration procedure to assess the effects of intraperitoneal administration of 0, 1, 3 and 10 mg/kg AM404 on nicotine-taking and food-taking behaviors under fixed-ratio and progressive-ratio schedules of reinforcement, as well as on reinstatement of nicotine-seeking induced by nicotine priming and by presentation of nicotine-associated cues. The ability of AM404 to produce place preference was also evaluated. AM404 did not produce CPP and did not modify nicotine-taking and food-taking behaviors. In contrast, AM404 dose-dependently attenuated reinstatement of nicotine-seeking behavior induced by both nicotine-associated cues and nicotine priming.

Our results indicate that AM404 could be a potential promising therapeutic option for the prevention of relapse to nicotine-seeking in abstinent smokers.”

http://www.ncbi.nlm.nih.gov/pubmed/23427192

Cannabinoids ameliorate impairments induced by chronic stress to synaptic plasticity and short-term memory.

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“Repeated stress is one of the environmental factors that precipitates and exacerbates mental illnesses like depression and anxiety as well as cognitive impairments. We have previously shown that cannabinoids can prevent the effects of acute stress on learning and memory.

Here we aimed to find whether chronic cannabinoid treatment would alleviate the long-term effects of exposure to chronic restraint stress on memory and plasticity as well as on behavioral and neuroendocrine measures of anxiety and depression. Late adolescence rats were exposed to chronic restraint stress for two weeks followed each day by systemic treatment with vehicle or with the CB1/2 receptor agonist WIN55,212-2 (1.2 mg/kg). Thirty days after the last exposure to stress, rats demonstrated impaired long-term potentiation (LTP) in the ventral subiculum (vSub)-nucleus accumbens (NAc) pathway, impaired performance in the prefrontal cortex (PFC)-dependent object recognition task and the hippocampal-dependent spatial version of this task, increased anxiety levels, and significantly reduced expression of glucocorticoid receptors (GRs) in the amygdala, hippocampus, PFC and NAc. Chronic WIN55,212-2 administration prevented the stress-induced impairment in LTP levels and in the spatial task, with no effect on stress-induced alterations in unconditioned anxiety levels or GR levels. The CB1 antagonist AM251 (0.3 mg/kg) prevented the ameliorating effects of WIN55,212-2 on LTP and short-term memory. Hence, the beneficial effects of WIN55,212-2 on memory and plasticity are mediated by CB1 receptors and are not mediated by alterations in GR levels in the brain areas tested.

 Our findings suggest that cannabinoid receptor activation could represent a novel approach to the treatment of cognitive deficits that accompany a variety of stress-related neuropsychiatric disorders.”

http://www.ncbi.nlm.nih.gov/pubmed/23426383