Here are seven health benefits of CBD oil that are backed by scientific evidence. Studies have shown that CBD may help reduce chronic pain by may be effective in reducing pain associated with diseases like multiple. CBD, or cannabidiol, oil is currently being studied for its health benefits. that CBD could help people with neurodegenerative disorders, which are diseases. Last month, a U.S. Food and Drug Administration advisory panel unanimously recommended approval of the CBD medication Epidiolex to treat.
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Cannabis has been used for millennia as a pain-relieving substance. Evidence suggests that cannabinoids may prove useful in pain modulation by inhibiting neuronal transmission in pain pathways. Considering the pronounced antinociceptive effects produced by cannabinoids, they were proposed to be a promising therapeutic approach for the clinical management of trigeminal neuralgia.
These results do not support an overall benefit of THC in pain and quality of life in patients with refractory neuropathic pain. Other studies show much better results of pain relief. When THC was given to a patient with familial Mediterranean fever, with chronic relapsing pain and gastrointestinal inflammation, a highly significant reduction in pain was noted.
Nabilone is a synthetic cannabinoid approved for treatment of severe nausea and vomiting associated with cancer chemotherapy. A significant decrease in disabling spasticity-related pain of patients with chronic upper motor neuron syndrome UMNS was found with nabilone.
Cannabimimetic effects with ajulemic acid in rodents have also been recorded. It is efficacious and well tolerated in the treatment of symptoms of multiple sclerosis, notably spasticity and neuropathic pain. Inflammation, autoimmune response, demyelination, and axonal damage are thought to participate in the pathogenesis of MS. Increasing evidence supports the idea of a beneficial effect of cannabinoid compounds for the treatment of this disease. In clinical trials, it has been shown that cannabis derivatives are active on the pain related to MS, 84 , 85 , 95 , 97 , 98 However, this is not the only positive effect of cannabinoids in this disease.
Reduction in the inflammatory response in the brain and spinal cord was also noted in animals treated with dexanabinol HU a nonpsychoactive synthetic cannabinoid. These observations may explain the efficacy of cannabinoid agonists in improving motor symptoms spasticity, tremor, ataxia typical of MS in both humans and animal models. Marijuana was suggested as treatment of muscle spasticity as early as the s.
Responses varied, but benefit was seen in patients with tonic spasms. Improved motor coordination was seen when patients with MS, seriously disabled with tremor and ataxia, were given oral THC. MS is not the only disease state where the neuroprotective potential of cannabinoids can be seen. In animal experiments, 2 weeks after the application of 6-hydroxydopamine, a significant depletion of dopamine contents and a reduction in tyrosine hydroxylase activity in the lesioned striatum were noted, and were accompanied by a reduction in tyrosine hydroxylase-messenger ribonucleic acid mRNA levels in the substantia nigra.
Daily administration of THC over 2 weeks produced a significant irreversible waning in the magnitude of these changes, which may be relevant in the treatment of Parkinson's disease see below The cannabinoids have a neuroprotective activity not only in vitro but also in vivo: HU, a potent synthetic analog of THC, increases survival of mouse cerebellar granule cells exposed to 6-hydroxydopamine.
Rimonabant exerted neuroprotection independently of its cannabinoid receptor-blocking effect. A trend toward faster and better neurologic outcome was also observed. Atherosclerosis is a chronic inflammatory disease, and is the primary cause of heart disease and stroke in Western countries.
Oral treatment with a low dose of THC inhibits atherosclerosis progression in an apolipoprotein E knockout mouse model, through pleiotropic immunomodulatory effects on lymphoid and myeloid cells.
Thus, THC may be a valuable target for treating atherosclerosis. Its concentrations are significantly increased in three different inflammatory and neuropathic conditions. The enhanced levels may possibly be related to a protective local anti-inflammatory and analgesic action. In experiments with obese vs lean rats, rimonabant was found to be a potent inhibitor of sensory hypersensitivity associated with CFA-induced arthritis in obese rats, in which the inflammatory reaction is more severe than in lean rats.
It may thus have therapeutic potential in obesity-associated inflammatory diseases. Parkinson's disease PD is a chronic, progressive neurodegenerative disorder. The main pathological feature of PD is the degeneration of dopamine DA -containing neurons of the substantia nigra, which leads to severe DAergic denervation of the striatum.
The irreversible loss of the DA-mediated control of striatal function leads to the typical motor symptoms observed in PD, ie, bradykinesia, tremor, and rigidity.
It has been proposed that cannabinoids may have some beneficial effects in the treatment of PD. The majority of PD patients undergoing levodopa therapy develop disabling motor complications dyskinesias within 10 years of treatment. Recent studies in animal models and in the clinic suggest that CB1 receptor antagonists could prove useful in the treatment of both parkinsonian symptoms and levodopa-induced dyskinesia, whereas CB1 receptor agonists could have value in reducing levodopa-induced dyskinesia.
This effect was significantly reduced by coinjection with the cannabinoid receptor agonist WIN 55, The simultaneous administration of the CB1 antagonist rimonabant with quinpirole and WIN 55, blocked the effect of WIN 55, on quinpirole-induced alleviation of akinesia. This effect was also reversed by rimonabant. The injection of 0. In clinical trials, the cannabinoid receptor agonist nabilone significantly reduced levodopainduced dyskinesia in PD.
Advanced grades of HD showed an almost total loss of CB1 receptors and a further depletion of Dl receptors in the caudate nucleus, putamen, and globus pallidus internus, and an increase in GABA A receptor binding in the globus pallidus internus.
Indeed, arvanil, a hybrid endocannabinoid and vanilloid compound, behaves as an antihyperkinetic agent in a rat model of HD generated by bilateral intrastriatal application of 3-nitropropionic acid 3-NP. However, both capsaicin VR1 agonist and CP55, an CB1 agonist had antihyperkinetic activity Quinolinic acid QA is an excitotoxin which, when injected into the rat striatum, reproduces many features of HD by stimulating glutamate outflow.
Perfusion with WIN 55, significantly and dose-dependently prevented the increase in extracellular glutamate induced by QA. Thus, the stimulation of CB1 receptors might lead to neuroprotective effects against excitotoxic striatal toxicity. Tourette syndrome TS is a complex inherited disorder of unknown etiology, characterized by multiple motor and vocal tics. Anecdotal reports have suggested that the use of cannabis might improve tics and behavioral problems in patients with TS. There was a significant improvement of motor tics, vocal tics and obsessive-compulsive behavior after treatment with THC.
Amyotrophic lateral sclerosis ALS is a fatal neurodegenerative disorder characterized by a selective loss of motor neurons in the spinal cord, brain stem, and motor cortex. Many effects of marijuana may be applicable to the management of ALS.
These include analgesia, muscle relaxation, bronchodilation, saliva reduction, appetite stimulation, and sleep induction. In addition, its strong antioxidative and neuroprotective effects may prolong neuronal cell survival. Furthermore, genetic ablation of the FAAH enzyme, which results in raised levels of the endocannabinoid anandamide, prevented the appearance of disease signs in these mice.
Ablation of the CB1 receptor, in contrast, had no effect on disease onset in these mice, but significantly extended life span. Together these results show that cannabinoids have significant neuroprotective effects in this model of ALS, and suggest that these beneficial effects may be mediated by nonCB1 receptor mechanisms. Administration at the onset of tremors delayed motor impairment in treated mice when compared with vehicle controls ; moreover, AM prolonged survival in these mice.
Studies on cannabinoid anticonvulsant activity began in , when CBD, and four CBD derivatives, CBD-aldehyde-diacetate, 6-oxo-CBD-diacetate, 6-hydroxy-CBD-tri-acetate and 9-hydroxy-CBD-triacetate were shown to protect against maximal electroshock convulsions in mice, to potentiate pentobarbital sleeping-time and to reduce spontaneous motor activity. Furthermore, it appears that CBD enhances the anticonvulsant effects of drugs in major seizures and reduces their effects in minor seizures.
The induction of status epilepticus-like activity by CB1 receptor antagonists was reversible and could be overcome by maximal concentrations of CB1 agonists. Cannabis use is common in patients with bipolar disorder, and anecdotal reports suggest that some patients use marijuana to alleviate symptoms of both mania and depression.
The effect of cannabinoids on schizophrenia is controversial. Neuropsychological results in THC-intoxicated normal volunteers exhibit strong similarities with data acquired from patients suffering from productive schizophrenic psychoses, as regards disturbances in internal regulation of perceptual processes. Data from experimental-psychological tests show that personality changes generated by schizophrenia progression are comparable to psychopathological phenomenon due to cannabis intoxication.
This argues against a distinct schizophrenia-like psychosis caused by cannabis. The group receiving the CB1 antagonist did not differ from the group receiving placebo on any outcome measure. CBD causes antipsychotic effects. Posttraumatic stress disorder PTSD is a term for severe psychological consequences of exposure to, or confrontation with, stressful, highly traumatic events. Cannabinoids are believed to help in such cases. AMtreated animals showed decreased shock-induced reinstatement of fear.
SRI blocked the effects of OL, suggesting that endogenous anandamide plays a facilitator role in extinction through a CB1 receptor mechanism of action. However, upon repeated stress or acute severe stress, CB1 receptor deficiency causes persistent behavioral inhibition. Repeated bell stress seemed to cause a cumulative fear in CB1 receptor knockout mice.
CB1 receptor gene polymorphism is known to modify transcription of the gene. In patients with Parkinson's disease, the presence of two long alleles, with more than 16 repeated AAT trinucleotides in the CNR1 gene, was associated with a reduced prevalence of depression. CBD, and some derivatives, were found to cause a selective anxiolytic effect in the elevated plus-maze, within a limited range of doses. The effects of marijuana on human sleep patterns were noticed long ago.
Asthma is a chronic disease of the respiratory system in which the airway occasionally constricts, becomes inflamed, and is lined with excessive amounts of mucus. In animal experiments, after methacholine-induced or exercise-induced bronchospasm, marijuana caused a prompt improvement of the bronchospasm and associated hyperinflation. The daily use of THC was not associated with clinical tolerance.
Maximal bronchodilatation was achieved more rapidly with salbutamol, but at 1 hour both drugs were equally effective. No cardiovascular or mood disturbance was detected, and plasma total cannabinoids at 15 minutes were not detected by radioimmunoassay.
The mode of action of THC differed from that of sympathomimetic drugs. In another study, THC induced sympathetic stimulation and parasympathetic inhibition of cardiovascular control pathways. The peak heart rate rise after THC was attenuated by atropine and by propranolol, and nearly abolished by atropine-propranolol pretreatment.
With repetitive dosing supine bradycardia and decreased blood pressure with tolerance to orthostatic hypotension were observed. A number of studies suggest that there is a correlative, but not necessarily causal, relationship between glaucoma and systemic hypertension. Ocular hypertension OHT refers to any situation in which intraocular pressure is higher than normal, and is the most important risk factor for glaucoma.
In contrast, noladin ether decreased IOP immediately after topical administration, and no initial IOP increase was observed. CB2 mRNA was undetectable. Ocular toxicity was seen after THC treatment, consisting of conjunctival erythema and chemosis as well as corneal opacification. Although these changes also occurred with marijuana extract, their intensity was much reduced. In contrast, no ocular toxicity was apparent during administration of plant cannabinoids other than THC.
The results indicate that THC may have value as a hypotonizing ocular drug. The intensity and duration of the arterial and ocular pressure responses to THC were greater in hypertensives than in normotensive patients; the changes in ocular pressure paralleled the changes in blood pressure in glaucoma patients. The antiproliferative action of cannabinoids on cancer cells was first noticed in the s.
Since then cannabinoids were found to act on various cancer cell lines, through various mechanisms. Moreover, cannabinoid challenge decreased the efficiency of glioma stem-like cells to initiate glioma formation in vivo. Activation of these receptors decreased growth, proliferation, angiogenesis, and metastasis, and increased apoptosis, of melanomas in mice. These effects were prevented by blockade of the CB2 cannabinoid receptor or by pharmacologic inhibition of ceramide synthesis de novo.
THC inhibited tumor-cell proliferation in vitro, decreased tumor-cell Ki67 immunostaining and prolonged the survival time of two of the patients. Many drugs used today can cause addiction and are misused and abused, for example opiates, cocaine, benzodiazepines, barbiturates, cholinergic agonists, ketamine, , dopaminergic agonists, amphetamines, and others.
Nevertheless they are still an important part of our pharmacopeia. Marijuana was used for centuries as a medicinal plant, but during the last century, because of its abuse and addictive potential it was taken out of clinical practice. Now, we believe that its constituents and related compounds should be brought back to clinical use. The endocannabinoid system is a very complex one and regulates numerous processes, in parallel with other wellknown systems, such as the adrenergic, cholinergic, and dopaminergic systems.
National Center for Biotechnology Information , U. Journal List Dialogues Clin Neurosci v. Kogan , MSc Natalya M. Author information Copyright and License information Disclaimer. This is an open-access article distributed under the terms of the Creative Commons Attribution License http: This article has been cited by other articles in PMC.
Abstract Cannabis sativa L. Abstract Las preparaciones de Cannabis sativa L. Addiction to canabis, and the influence of cannabis on addiction to other substances Marijuana may produce mild dependence in humans. Negative effects of cannabis other than addiction There are some negative effects of cannabis use other than addiction, most of them related to alterations of attentional and cognitive functions or other neuropsychological and behavioral effects.
Therapeutic uses of cannabinoids Obesity, anorexia, emesis Cannabis has been known for centuries to increase appetite and food consumption. Pain Cannabis has been used for millennia as a pain-relieving substance. Multiple sclerosis, neuroprotection, inflammation Inflammation, autoimmune response, demyelination, and axonal damage are thought to participate in the pathogenesis of MS.
Parkinson's disease, Huntington's disease, Tourette's syndrome, Alzheimer's disease, epilepsy Parkinson's disease PD is a chronic, progressive neurodegenerative disorder. Bipolar disorder, schizophrenia, post-traumatic stress disorder PTSD , depression, anxiety, insomnia Cannabis use is common in patients with bipolar disorder, and anecdotal reports suggest that some patients use marijuana to alleviate symptoms of both mania and depression.
Asthma, cardiovascular disorders, glaucoma Asthma is a chronic disease of the respiratory system in which the airway occasionally constricts, becomes inflamed, and is lined with excessive amounts of mucus.
Cancer The antiproliferative action of cannabinoids on cancer cells was first noticed in the s. Conclusion Many drugs used today can cause addiction and are misused and abused, for example opiates, cocaine, benzodiazepines, barbiturates, cholinergic agonists, ketamine, , dopaminergic agonists, amphetamines, and others. Early medical use of cannabis.
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Ann N Y Acad Sci. Treatment of cannabis use disorders: Cannabis addiction and Telic Dominance Scale. Clinical trial of abstinencebased vouchers and cognitive-behavioral therapy for cannabis dependence.
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SR, a central cannabinoid CB 1 receptor antagonist, blocks the motivational and dopaminereleasing effects of nicotine in rats. The diagnosis of alcohol and cannabis dependence addiction in cocaine dependence addiction. Behavioral effects of cocaine alone and in combination with ethanol or marijuana in humans.
Marihuana smoking increases plasma cocaine levels and subjective reports of euphoria in male volunteers. Involvement of cannabinoid CB1 receptors in drug addiction: Rimonabant, a CB1 antagonist, blocks nicotineconditioned place preferences.
Nicotine-associated cues maintain nicotine-seeking behavior in rats several weeks after nicotine withdrawal: The role of the cannabinoid system in nicotine addiction.
Successful control of lipids, kilos and cigarettes]. Advances in pharmacotherapy for tobacco dependence. Expert Opin Emerg Drugs. Expert Opin Investig Drugs. Adenosine A2a blockade prevents synergy between mu-opiate and cannabinoid CB1 receptors and eliminates heroin-seeking behavior in addicted rats.
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J Clin Endocrinol Metab. Lack of tolerance to the suppressing effect of rimonabant on chocolate intake in rats. The role of CB1 receptors in sweet versus fat reinforcement: SR , a CB1 cannabinoid receptor antagonist, selectively reduces sweet food intake in marmoset. Efficacy of rimonabant and other cannabinoid CB1 receptor antagonists in reducing food intake and body weight: Fighting obesity and associated risk factors by antagonising cannabinoid type 1 receptors.
Effects of rimonabant on metabolic risk factors in overweight patients with dyslipidemia. N Engl J Med. Effect of rimonabant, a cannabinoid-1 receptor blocker, on weight and cardiometabolic risk factors in overweight or obese patients: Effects of the cannabinoid-1 receptor blocker rimonabant on weight reduction and cardiovascular risk factors in overweight patients: Clinical trials update and cumulative meta-analyses from the American College of Cardiology: Eur J Heart Fail.
Rimonabant improves cardiometabolic risk profile in obese or overweight subjects: Rimonabant in obese patients with type 2 diabetes. Am J Health Syst Pharm. Long-term efficacy and safety of dronabinol for acquired immunodeficiency syndrome-associated anorexia.
J Pain Symptom Manage. Dronabinol as a treatment for anorexia associated with weight loss in patients with AIDS. Dronabinol effects on weight in patients with HIV infection.
The safety and pharmacokinetics of single-agent and combination therapy with megestrol acetate and dronabinol for the treatment of HIV wasting syndrome. Cannabinoids in the treatment of the cachexiaanorexia syndrome in palliative care patients.
A phase II study of deltatetrahydrocannabinol for appetite stimulation in cancer-associated anorexia. Mechanism of action of cannabinoids: An efficient new cannabinoid antiemetic in pediatric oncology. Cannabinoids for control of chemotherapy induced nausea and vomiting: Therapeutic potential of cannabinoids in trigeminal neuralgia. Cannabinoids block release of serotonin from platelets induced by plasma from migraine patients.
Int J Clin Pharmacol Res. Are oral cannabinoids safe and effective in refractory neuropathic pain? Lack of analgesic efficacy of oral deItatetrahydrocannabinol in postoperative pain. Pain relief with oral cannabinoids in familial Mediterranean fever. Efficacy of two cannabis based medicinal extracts for relief of central neuropathic pain from brachial plexus avulsion: Does the cannabinoid dronabinol reduce central pain in multiple sclerosis?
Randomised double blind placebo controlled crossover trial. Effect of the synthetic cannabinoid dronabinol on central pain in patients with multiple sclerosis - secondary publication.
The analgesic properties of deItatetrahydrocannabinol and codeine. Analgesic effect of deItatetrahydrocannabinol. Cannabis use for chronic non-cancer pain: Cannabis use in HIV for pain and other medical symptoms. Experience with the synthetic cannabinoid nabilone in chronic noncancer pain. Low dose treatment with the synthetic cannabinoid Nabilone significantly reduces spasticity-related pain: Analgesic effect of the synthetic cannabinoid CT-3 on chronic neuropathic pain: Cannabimimetic properties of ajulemic acid.
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