Tag Archives: cannabis

Self-reported efficacy of cannabis and other complementary medicine modalities by Parkinson’s disease patients in colorado.

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“Complementary and alternative medicine (CAM) is frequently used by Parkinson’s disease (PD) patients. We sought to provide information on CAM use and efficacy in PD patients in the Denver metro area with particular attention to cannabis use given its recent change in legal status.

Self-reported improvement related to the use of CAM was highest for massage, art therapy, music therapy, and cannabis.

While only 4.3% of our survey responders reported use of cannabis, it ranked among the most effective CAM therapies.

Conclusions. Overall, our cross-sectional study was notable for a high rate of CAM utilization amongst PD patients and high rates of self-reported efficacy across most CAM modalities.

Cannabis was rarely used in our population but users reported high efficacy, mainly for nonmotor symptoms.”

http://www.ncbi.nlm.nih.gov/pubmed/25821504

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4363882/

http://www.thctotalhealthcare.com/category/parkinsons-disease/

Association of single nucleotide polymorphisms in catechol-O-methyltransferase and serine-threonine protein kinase genes in the Pakistani schizophrenic population: a study with special emphasis on cannabis and smokeless tobacco.

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“Schizophrenia is a neuropsychiatric disorder in which abnormalities in the prefrontal cortex lead to impaired synthesis of dopamine. It is associated with hallucination, psychosis and hearing impairments. Many susceptible genes have been identified in schizophrenia such as catechol-O-methyltransferase (COMT) and serine/threonine kinase (AKT1).

Moreover, a study based on a single family showed COMT Met allele inheritance in schizophrenic offspring. This suggested that COMT allele alteration influences susceptibility to at least some forms of psychosis…

Interestingly, according to our socio-economic survey, COMT genotype has no association with cannabis but it is strongly associated with tobacco.”

http://www.ncbi.nlm.nih.gov/pubmed/25801838

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

 

Cannabidiol, a Major Non-Psychotrophic Cannabis Constituent Enhances Fracture Healing and Stimulates Lysyl Hydroxylase Activity in Osteoblasts.

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“Cannabinoid ligands regulate bone mass, but skeletal effects of cannabis (marijuana and hashish) have not been reported. Bone fractures are highly prevalent, involving prolonged immobilization and discomfort.

Here we report that the major non-psychoactive cannabis constituent, cannabidiol (CBD), enhances the biomechanical properties of healing rat mid-femoral fractures.

Using Fourier Transform Infrared Spectroscopy we confirmed the increase in collagen crosslink ratio by CBD, which is likely to contribute to the improved biomechanical properties of the fracture callus.

Taken together, these data show that CBD leads to improvement in fracture healing and demonstrate the critical mechanical role of collagen crosslinking enzymes.”

http://www.ncbi.nlm.nih.gov/pubmed/25801536

Δ9-Tetrahydrocannabinol alone and combined with cannabidiol mitigate fear memory through reconsolidation disruption.

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“Δ9-tetrahydrocannabinol (THC) and cannabidiol (CBD) are the major constituents of the Cannabis sativa plant, which is frequently consumed by subjects exposed to life-threatening situations to relief their symptomatology.

It is still unknown, however, whether THC could also affect the maintenance of an aversive memory formed at that time when taken separately and/or in conjunction with CBD. The present study sought to investigate this matter at a preclinical level.

We report that THC (0.3-10mg/kg, i.p.) was able to disrupt the reconsolidation of a contextual fear memory, resulting in reduced conditioned freezing expression for over 22 days. This effect was dependent on activation of cannabinoid type-1 receptors located in prelimbic subregion of the medial prefrontal cortex and on memory retrieval/reactivation.

Since CBD may counteract the negative psychotropic effects induced by THC and has been shown to be a reconsolidation blocker, we then investigated and demonstrated that associating sub-effective doses of these two compounds was equally effective in attenuating fear memory maintenance in an additive fashion and in a dose ratio of 10 to 1, which contrasts with that commonly found in C. sativa recreational samples.

Of note, neither THC alone nor CBD plus THC interfered with anxiety-related behaviors and locomotor activity, as assessed in the elevated plus-maze test, at a time point coinciding with that used to evaluate their effects on memory reconsolidation.

Altogether, present findings suggest a potential therapeutic value of using THC and/or CBD to mitigate a dysfunctional aversive memory through reconsolidation disruption in post-traumatic stress disorder patients.”

http://www.ncbi.nlm.nih.gov/pubmed/25799920

http://www.thctotalhealthcare.com/category/post-traumatic-stress-disorder-ptsd/

Endocannabinoid signaling at the periphery: 50 years after THC.

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“In 1964, the psychoactive ingredient of Cannabis sativa, Δ9-tetrahydrocannabinol (THC), was isolated. Nearly 30 years later the endogenous counterparts of THC, collectively termed endocannabinoids (eCBs), were discovered: N-arachidonoylethanolamine (anandamide) (AEA) in 1992 and 2-arachidonoylglycerol (2-AG) in 1995.

Since then, considerable research has shed light on the impact of eCBs on human health and disease, identifying an ensemble of proteins that bind, synthesize, and degrade them and that together form the eCB system (ECS). eCBs control basic biological processes including cell choice between survival and death and progenitor/stem cell proliferation and differentiation.

Unsurprisingly, in the past two decades eCBs have been recognized as key mediators of several aspects of human pathophysiology and thus have emerged to be among the most widespread and versatile signaling molecules ever discovered.

Here some of the pioneers of this research field review the state of the art of critical eCB functions in peripheral organs. Our community effort is aimed at establishing consensus views on the relevance of the peripheral ECS for human health and disease pathogenesis, as well as highlighting emerging challenges and therapeutic hopes.”

http://www.ncbi.nlm.nih.gov/pubmed/25796370

The potential of inhibitors of endocannabinoid metabolism as anxiolytic and antidepressive drugs-A practical view.

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“The endocannabinoid system, comprising cannabinoid CB1 and CB2 receptors, their endogenous ligands anandamide and 2-arachidonoylglyerol, and their synthetic and metabolic enzymes, are involved in many biological processes in the body, ranging from appetite to bone turnover.

Compounds inhibiting the breakdown of anandamide and 2-arachidonoylglycerol increase brain levels of these lipids and thus modulate endocannabinoid signalling.

In the present review, the preclinical evidence that these enzymes are good targets for development of novel therapies for anxiety and depression are discussed from a practical, rather than mechanistic, point of view.

It is concluded that the preclinical data are promising, albeit tempered by problems of tolerance as well as effects upon learning and memory for irreversible monoacylglycerol lipase inhibitors, and limited by a focus upon male rodents alone.

Clinical data so far has been restricted to safety studies with inhibitors of anandamide hydrolysis and a hitherto unpublished study on such a compound in elderly patients with major depressive disorders, but under the dose regimes used, they are well tolerated and show no signs of “cannabis-like” behaviours.”

http://www.ncbi.nlm.nih.gov/pubmed/25791296

Cannabinoids in late-onset Alzheimer’s disease.

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“Given the lack of effective treatments for late-onset Alzheimer’s disease (LOAD) and the substantial burden on patients, families, healthcare systems, and economies, finding an effective therapy is one of the highest medical priorities.

The past few years have seen a growing interest in the medicinal uses of cannabinoids, the bioactive components of the cannabis plant, including the treatment of LOAD and other physical conditions that are common in older people.

Several in vitro and in vivo studies have demonstrated that cannabinoids can reduce oxidative stress, neuroinflammation, and the formation of amyloid plaques and neurofibrillary tangles, the key hallmarks of LOAD.

Also, in population-based studies, cannabinoids reduced dementia-related symptoms (e.g., behavioral disturbances).

The current article provides an overview of the potential of cannabinoids in the treatment of LOAD and related neuropsychiatric symptoms in older people.

We also discuss the efficacy, safety and pharmacokinetics of cannabinoid-based drugs in older people with dementia.”

http://www.ncbi.nlm.nih.gov/pubmed/25788394

http://www.thctotalhealthcare.com/category/alzheimers-disease-ad/

NEUROPROTECTIVE EFFECTS OF CANNABIS SATIVA ALCOHOLIC EXTRACT AGAINST SPINAL ALPHA MOTONEURONS DEGENERATION IN MALE TYPE II DIABETIC RATS

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“Diabetic neourophaty is one of the long-term usual outcomes of diabetes.

According to anti-tumor, anti-diabetic and anti-oxidant effects of Cannabis sativa, the aim of this research was to investigate the effect of Cannabis sativa alcoholic extract on Alpha motoneurons degeneration after sciatic nerve compression in diabetic rats…

Conclusion: Using alcoholic extract of Cannabis sativa as a neuroprotective agent can prevent the progression of neural system disorders as a result of hyperglycemia.”

http://en.journals.sid.ir/ViewPaper.aspx?ID=278407

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

Cannabidiol, a non-psychoactive cannabinoid, leads to EGR2-dependent anergy in activated encephalitogenic T cells.

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“Cannabidiol (CBD), the main non-psychoactive cannabinoid, has been previously shown by us to ameliorate clinical symptoms and to decrease inflammation in myelin oligodendrocyte glycoprotein (MOG)35-55-induced mouse experimental autoimmune encephalomyelitis model of multiple sclerosis as well as to decrease MOG35-55-induced T cell proliferation and IL-17 secretion. However, the mechanisms of CBD anti-inflammatory activities are unclear…

Our data suggests that CBD exerts its immunoregulatory effects via induction of CD4(+)CD25(-)CD69(+)LAG3(+) cells in MOG35-55-activated APC/TMOG co-cultures. This is accompanied by EGR2-dependent anergy of stimulated TMOG cells as well as a switch in their intracellular STAT3/STAT5 activation balance leading to the previously observed decrease in Th17 activity.”

http://www.ncbi.nlm.nih.gov/pubmed/25779454