“Some US states have created de facto legal supply of cannabis for medical use. So far this policy does not appear to have increased cannabis use or cannabis-related harm.”
http://www.ncbi.nlm.nih.gov/pubmed/25777798
“Some US states have created de facto legal supply of cannabis for medical use. So far this policy does not appear to have increased cannabis use or cannabis-related harm.”
http://www.ncbi.nlm.nih.gov/pubmed/25777798
“Natural cannabis was preferred to synthetic cannabis by 93% of users, with natural cannabis rated as having greater pleasurable effects when high and being more able to function after use. Synthetic cannabis was associated with more negative effects, hangover effects, and greater paranoia…
Users report a strong preference for natural over synthetic cannabis…”
“Synthetic cannabinoids (SCs) have become increasingly popular in recent years. Often marketed to reflect their similar effects to cannabis, their use has been associated with a range of negative health effects. We sought to determine the relative risk of seeking emergency medical treatment (EMT) following use of SCs and natural cannabis.
The relative risk associated with the use of SCs was 30 (95% CI 17.5-51.2) times higher than that associated with cannabis. Significantly more symptoms (p=0.03) were reported by respondents seeking treatment for SCs than for cannabis.
Whilst these findings must be treated with caution, SCs potentially pose a greater risk to users’ health than natural forms of cannabis. Regulation is unlikely to remove SCs from the market, so well-informed user-focused health promotion messages need to be crafted to discourage their use.”
“Acute rejection of cardiac allografts is a major risk factor limiting survival of heart transplant recipients. Rejection is triggered by dendritic cell (DC) mediated activation of host T cells, amongst others CD4+ T helper (TH)1- and TH17 cells.
The cannabinoid receptor 2 (CB2) is an important modulator of cellular immune responses…
These results demonstrate that CB2 modulates in vitro cytokine responses via DCs and directly via its influence on TH1/TH17 differentiation.
These findings and the fact that allograft rejection is enhanced in Cnr2-/- mice suggest that CB2 may be a promising therapeutic target in organ transplantation.”
“One of the most promising potential medical applications of cannabinoids involves their ability to protect cells from a variety of toxic events.
Cannabinoids have been reported to protect neurons from death…
Cannabinoids, such as the pharmacologically active component of marijuana (-)Δ9-tetrahydrocannabinol (THC)…
The neuroprotective effects of Δ9-tetrahydrocannabinol (THC) were examined…
Protective effects of Delta(9)-tetrahydrocannabinol… THC may function as an antioxidant to increase cell survival…
THC can produce receptor-independent neuroprotective or cellular protective effects at micromolar concentrations as a result of its antioxidant properties…
In conclusion, THC produces a potent neuroprotective effect…”
“Excitotoxic neuronal death underlies many neurodegenerative disorders…
Delta9-tetrahydrocannabinol protects hippocampal neurons from excitotoxicity…
…desensitization of CB(1) receptors diminishes the neuroprotective effects of cannabinoids.
This study demonstrates the importance of agonist efficacy and the duration of treatment on the neuroprotective effects of cannabinoids.
It will be important to consider these effects on neuronal survival when evaluating pharmacologic treatments that modulate the endocannabinoid system.”
http://www.ncbi.nlm.nih.gov/pubmed/17140550
“Molecular Mechanisms of Cannabinoid Protection from Neuronal Excitotoxicity” http://molpharm.aspetjournals.org/content/69/3/691.long
“Cannabinoids protect neurons from excitotoxic injury…
Endogenous or exogenous cannabinoids have shown neuroprotective effects…
The main finding reported here is that cannabinoids protect neurons from excitotoxic injury by a mechanism that involves the activation of CB1R and inhibition of NOS and PKA….
Cannabinoid receptor agonist drugs protect neurons…
By identifying the signaling pathways responsible for cannabinoid effects in animal models of disease and their human counterparts, it may be possible to design more specific and therefore more efficacious cannabinoid-based therapies.”
http://molpharm.aspetjournals.org/content/69/3/691.long
“Hypothalamic pro-opiomelanocortin (POMC) neurons promote satiety. Cannabinoid receptor 1 (CB1R) is critical for the central regulation of food intake.
Here we test whether CB1R-controlled feeding in sated mice is paralleled by decreased activity of POMC neurons.
We show that chemical promotion of CB1R activity increases feeding, and notably, CB1R activation also promotes neuronal activity of POMC cells…
Together, these results uncover a previously unsuspected role of POMC neurons in the promotion of feeding by cannabinoids.”
http://www.ncbi.nlm.nih.gov/pubmed/25707796
“The opioid system consists of three receptors, mu, delta, and kappa, which are activated by endogenous opioid peptides (enkephalins, endorphins, and dynorphins).
The endogenous cannabinoid system comprises lipid neuromodulators (endocannabinoids), enzymes for their synthesis and their degradation and two well-characterized receptors, cannabinoid receptors CB1 and CB2.
These systems play a major role in the control of pain as well as in mood regulation, reward processing and the development of addiction.
Both opioid and cannabinoid receptors are coupled to G proteins and are expressed throughout the brain reinforcement circuitry.
A better understanding of opioid-cannabinoid interactions may provide novel strategies for therapies in addicted individuals.”
“To investigate the regulation of cannabinoid receptors CB1 and CB2 on immune cells by proinflammatory cytokines and its potential relevance to the inflammatory neurological disease, multiple sclerosis (MS).
CB1 and CB2 signalling may be anti-inflammatory and neuroprotective in neuroinflammatory diseases.
Cannabinoids can suppress inflammatory cytokines…
The levels of CB1 and CB2 can be up-regulated by inflammatory cytokines, which can explain their increase in inflammatory conditions including MS”
http://www.ncbi.nlm.nih.gov/pubmed/25704169
http://www.thctotalhealthcare.com/category/multiple-sclerosis-ms/