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cannabis anti inflammatory

CBD is readily obtainable in most parts of the United States, though its exact legal status is in flux. All 50 states have laws legalizing CBD with varying degrees of restriction, and while the federal government still considers CBD in the same class as marijuana, it doesn’t habitually enforce against it. In December 2015, the FDA eased the regulatory requirements to allow researchers to conduct CBD trials. Currently, many people obtain CBD online without a medical cannabis license. The government’s position on CBD is confusing, and depends in part on whether the CBD comes from hemp or marijuana. The legality of CBD is expected to change, as there is currently bipartisan consensus in Congress to make the hemp crop legal which would, for all intents and purposes, make CBD difficult to prohibit.

Some CBD manufacturers have come under government scrutiny for wild, indefensible claims, such that CBD is a cure-all for cancer, which it is not. We need more research but CBD may be prove to be an option for managing anxiety, insomnia, and chronic pain. Without sufficient high-quality evidence in human studies we can’t pinpoint effective doses, and because CBD is currently is mostly available as an unregulated supplement, it’s difficult to know exactly what you are getting. If you decide to try CBD, talk with your doctor — if for no other reason than to make sure it won’t affect other medications you are taking.

Is cannabidiol legal?

CBD may offer an option for treating different types of chronic pain. A study from the European Journal of Pain showed, using an animal model, CBD applied on the skin could help lower pain and inflammation due to arthritis. Another study demonstrated the mechanism by which CBD inhibits inflammatory and neuropathic pain, two of the most difficult types of chronic pain to treat. More study in humans is needed in this area to substantiate the claims of CBD proponents about pain control.

CBD is commonly used to address anxiety, and for patients who suffer through the misery of insomnia, studies suggest that CBD may help with both falling asleep and staying asleep.

CBD stands for cannabidiol. It is the second most prevalent of the active ingredients of cannabis (marijuana). While CBD is an essential component of medical marijuana, it is derived directly from the hemp plant, which is a cousin of the marijuana plant. While CBD is a component of marijuana (one of hundreds), by itself it does not cause a "high." According to a report from the World Health Organization, "In humans, CBD exhibits no effects indicative of any abuse or dependence potential…. To date, there is no evidence of public health related problems associated with the use of pure CBD."

MS is an autoimmune inflammatory disease with several physical and mental symptoms, which affects deeply the patient’s quality of life [30-33]. These MS-associated symptoms can be treated by current drug therapies that cause considerable side effects, including hallucinations, hypotension, seizures, anxiety, weakness, and nausea [34]. According to Goodin et al. [34], the effectiveness of the disease-modifying therapeutics agents in reducing disability progression in relapsing-remitting MS patients is unclear. The articles analyzed in this study, on the contrary, reveal that cannabis extracts and cannabinoids promote improvement in MS symptoms and seemed to have little impact on the serum inflammatory markers’ levels [26, 27], which suggests that improvements may occur through different mechanisms involving the cannabinoids. Considering that immune diseases, such as MS, systemic lupus erythematosus, and rheumatoid arthritis are considerably disabling both physically and mentally, the potential of decrease in the immune function caused by cannabis extracts and cannabinoids could provide a pathway through which inflammatory diseases could be addressed by reducing disease immune activity.

Among the cannabis extracts, the THC is the main psychoactive component due to the lipophilic structure that allows the molecule to cross the blood-brain barrier [3]. Once in the central nervous system, the THC acts as a cannabinoid agonist, and its modulation of cannabinoid receptor 1 (CB1) is linked to pleasurable sensations. Such sensations are achieved because the CB1 is heterogeneously distributed around the brain, modulating the dopaminergic transmission in the limbic cortex and the association cortices [4]. The most commonly reported pleasure sensations are feeling of well being, calmness, relaxation, and hilarity [5]. Furthermore, according to Carlini et al. [5], the most common physical symptoms are xerostomia, red eyes, polyphagia, and tachycardia. Medical properties of cannabis extracts, however, are due to the several neurotransmitters involved on CB1 and CB2 (cannabinoid receptor 2) receptors [6].

Five out of the 6 papers in our review were longitudinal studies. In 4 of the papers, cannabis or its extracts were found to be negatively associated with immunity status, indicating that the higher the cannabis consumption, the lower the immunity cytokine levels went. The remaining 2 articles showed no association between cannabis use and serum immunity cytokine levels. The most commonly reported exposure covariates were age, sex, cannabis use, alcohol use, and tobacco use.


The correlation between immune response and cannabis use has been explored, as in the longitudinal study performed by Kagen et al. [7], which aimed to evaluate the role of cannabis use on inducing sensitization to Aspergillus. It was important to find that cannabis users had a higher risk of fungal exposure and infection, increasing the variety of immunologic lung disorders presented by the subjects. Roth et al. [8] performed a study aiming to analyze the production of nitric oxide (NO) on cannabis users and the role of NO as an antimicrobial agent. The study provides the role of cannabis use decreasing NO production, which acts as an important mediator of antibacterial effects. So, these studies illustrate direct and indirect impact of cannabis use on the susceptibility to infections.

Introduction: Although the recreational cannabis use is expressive worldwide, the literature about medical potential of cannabis extracts, including its anti-inflammatory properties, remains inconclusive. Methods: We screened all articles, published on the PubMed database, on inflammatory mediators and any information about cannabis use from 1980 to March 2019. Results: Six studies were included, and the main findings were as follows: (i) among healthy volunteers and cannabis users, cannabinoids seemed to decrease the inflammatory response, thus decreasing the immune response, which led to a higher risk of infections; (ii) among patients with multiple sclerosis, cannabinoids seemed to have little impact on the inflammatory markers’ levels. Discussion: Although cannabis use can produce immune inflammatory suppression in healthy people, this effect is not robust enough to change inflammatory mediators’ levels in situations of highly dysfunctional inflammatory activation. Nevertheless, the impact of cannabinoids in clinical outcomes of these conditions remains to be determined.

The authors have no conflicts of interest to declare.

Although these data indicate the use of cannabis worldwide is expressive, the literature about medical properties of cannabis is inconclusive and lacks literature reviews. Schlicker [2] revealed that cannabis derivatives, such as delta-9-tetrahydrocanabinol (delta-9-THC) and cannabidiol (CBD), are involved in several neurotransmitters systems, such as glutamatergic, serotonergic, noradrenergic, and dopaminergic systems, which are responsible for the therapeutic and recreational effects of cannabis.

ACEA: Arachidonyl-2-ethylamide; NGF: Neuronal growth factor.

Cannabinoids are a group of compounds that mediate their effects through cannabinoid receptors. The discovery of Δ 9 -tetrahydrocannabinol (THC) as the major psychoactive principle in marijuana, as well as the identification of cannabinoid receptors and their endogenous ligands, has led to a significant growth in research aimed at understanding the physiological functions of cannabinoids. Cannabinoid receptors include CB1, which is predominantly expressed in the brain, and CB2, which is primarily found on the cells of the immune system. The fact that both CB1 and CB2 receptors have been found on immune cells suggests that cannabinoids play an important role in the regulation of the immune system. Recent studies demonstrated that administration of THC into mice triggered marked apoptosis in T cells and dendritic cells, resulting in immunosuppression. In addition, several studies showed that cannabinoids downregulate cytokine and chemokine production and, in some models, upregulate T-regulatory cells (Tregs) as a mechanism to suppress inflammatory responses. The endocannabinoid system is also involved in immunoregulation. For example, administration of endocannabinoids or use of inhibitors of enzymes that break down the endocannabinoids, led to immunosuppression and recovery from immune-mediated injury to organs such as the liver. Manipulation of endocannabinoids and/or use of exogenous cannabinoids in vivo can constitute a potent treatment modality against inflammatory disorders. This review will focus on the potential use of cannabinoids as a new class of anti-inflammatory agents against a number of inflammatory and autoimmune diseases that are primarily triggered by activated T cells or other cellular immune components.

In conclusion, cannabinoids have been shown to regulate the tissue response to excessive inflammation in the colon, mediated by both dampening smooth-muscular irritation caused by inflammation and suppressing proinflammatory cytokines, thus controlling the cellular pathways leading to inflammatory responses. These results strongly suggest that modulation of the physiological activity of the cannabinoid system during colonic inflammation might be a promising therapeutic tool for the treatment of several diseases characterized by inflammation of the GI tract.

Cannabinoids & multiple sclerosis

The destruction of the blood–brain barrier in MS is initiated by myelin-specific self-reactive T cells. Infiltration of these cells into the spinal cord and CNS, and their subsequent activation, leads to the elimination of the myelin sheath around the nerves and axons [46,47]. The myelin- specific T cells are usually CD4 + , IL-2R + or MHCII-restricted Th1 cells and they secrete proinflammatory cytokines such as IFN-γ and TNF-α [47]. More recently, Th17 cells have been shown to be involved in the pathogenesis of MS [48,49]. One mechanism of immunosuppression by cannabinoids is the induction of apoptosis and Sanchez et al. demonstrated that WIN55,212-2 blocks a passive form of experimental authoimmune encephalomyelitis (EAE) by inducing apoptosis in encephalitogenic cells through partial activation of the CB2 receptor [50]. A CB1-mediated suppressive pathway has also been shown in myelin-specific T cells [24]. This study demonstrated that ex vivo WIN55,212-2 inhibited T-cell recall response to myelin oligodendrocyte glycoprotein (MOG) peptide, as well as decreasing IL-2, IFN-γ and TNF-α production by MOG-activated T cells. Other synthetic cannabinoids, such as JWH-015 and ACEA, also decreased the number of CD4 + infiltrates in the spinal cord of Theiler’s murine encephalomyelitis virus (TMEV)-infected mice [51]. Mestre et al. showed that decreased infiltration of CD4 + T cells upon WIN55,212-2 treatment in EAE mice is due to decreased intercellular and vascular cell adhesion molecules (ICAM-1 and VCAM-1) expression by endothelial cells. Another novel finding of this study demonstrated that WIN55,212-2 exerted its effects by acting through nuclear receptor PPAR-γ [52].

Cannabis, commonly known as marijuana, is a product of the Cannabis sativa plant and the active compounds from this plant are collectively referred to as cannabinoids. For several centuries, marijuana has been used as an alternative medicine in many cultures and, recently, its beneficial effects have been shown in: the treatment of nausea and vomiting associated with cancer chemotherapy; anorexia and cachexia seen in HIV/AIDS patients; and in neuropathic pain and spasticity in multiple sclerosis [1–4]. Cannabinoid pharmacology has made important advances in recent years after the discovery of the cannabinoid receptors (CB1 and CB2). Cannabinoid receptors and their endogenous ligands have provided an excellent platform for the investigation of the therapeutic effects of cannabinoids. It is well known that CB1 and CB2 are heterotrimeric Gi/o-protein-coupled receptors and that they are both expressed in the periphery and the CNS. However, CB1 expression is predominant in the CNS, especially on presynaptic nerves, and CB2 is primarily expressed on immune cells [5,6].

Viral hepatitis, alcohol abuse and nonalcoholic fatty liver are some of the conditions that can induce chronic liver injury and inflammation, leading to activation of fibrogenesis as a wound-healing mechanism. However, persistence of fibrogenic stimuli can enhance deposition of the extracellular matrix by hepatic myofibroblasts, thus disrupting normal liver architecture and, ultimately, leading to cirrhosis and liver failure. CB1 and CB2 receptors are shown to be markedly upregulated in cirrhotic human liver samples, demonstrating the impact of endocannabinoids in liver fibrogenesis. In addition, increases in circulating levels of anadamide and hepatic 2-AG have also been reported in cirrhosis and liver fibrosis, respectively [73]. CB2 −/− mice exposed to CCl4 showed enhanced liver fibrosis when compared with wild-type mice, thereby suggesting a protective role for CB2 receptor activation in liver fibrosis. By contrast, activation of CB1 receptors was found to promote profibrotic response [72]. The pharmacological inactivation of CB1 with rimonabant ® (SR141716) results in the reduction of obesity and hepatic steatosis in rodents [75], demonstrating that CB1 and CB2 receptors exert opposite effects on liver fibrosis and further suggesting that endocannabinoid system regulates both pro- and anti-fibrogenic responses in the liver. Further effects of the endocannabinoids have also been shown to be receptor independent. AEA and 2-AG have been shown to induce necrosis and apoptosis, respectively, in activated hepatic stellate cells, through increased generation of ROS [76].

Other natural and synthetic cannabinoid compounds (CBD, AEA, ajulemic acid [AjA] and JWH-015), whose structures are depicted in Table 1 , have also been shown to induce apoptosis in murine and human T lymphocytes. Cannabidiol, the nonpsychoactive ingredient in cannabis, induced apoptosis in CD4 + and CD8 + T cells at 4–8-μM concentrations by increasing reactive oxygen species (ROS) production as well as caspase 3 and 8 activity [20].