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cannabis anti inflammatory properties

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."

CBD has been touted for a wide variety of health issues, but the strongest scientific evidence is for its effectiveness in treating some of the cruelest childhood epilepsy syndromes, such as Dravet syndrome and Lennox-Gastaut syndrome (LGS), which typically don’t respond to antiseizure medications. In numerous studies, CBD was able to reduce the number of seizures, and, in some cases, it was able to stop them altogether. Videos of the effects of CBD on these children and their seizures are readily available on the Internet for viewing, and they are quite striking. Recently the FDA approved the first ever cannabis-derived medicine for these conditions, Epidiolex, which contains CBD.

How is cannabidiol different from marijuana?

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.

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.

Cannabidiol (CBD) has been recently covered in the media, and you may have even seen it as an add-in booster to your post-workout smoothie or morning coffee. What exactly is CBD? Why is it suddenly so popular?

Reviewed studies categorized by the Oxford Centre for Evidence-Based Medicine – Levels of Evidence in the order from highest to lowest levels A, B, C, and D

We found 2 studies conducted in healthy volunteers’ samples, conducted by the same research team, Pacifi et al. [23, 24], in 2003 [23] and 2006 [24]. Both were longitudinal observational studies. On the 2003 article [23], 61 volunteers were included and 3 distinct groups were analyzed: polydrug users, cannabis users, and a control group with no drug use. The aim was to compare the cell-mediated immune response and cytokine release in cannabis users in relation to the control group. The major finding was that cannabis users had lower function on immune response, with a considerable decrease in inflammatory cytokine serum levels. The authors state that the small sample size might have been a limitation of that study. On the 2006 article [24], 94 volunteers were included and divided into the same 3 groups of the 2003 article [23]. The article analyzed the cell-mediated immune function and the occurrence of mild infectious diseases. It reported 3 important findings: (i) polydrug users had a big decrease in immune response and a considerable increase in anti-inflammatory transforming growth factor β1; therefore, (ii) polydrug users had an increase in mild common infections; finally, (iii) cannabis users had an intermediate decrease in immune response in relation to the control group. This article also had the small sample size limitation, and it did not consider the possible effect of lifestyle on immune function. Detailed information is presented in Table 2.

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.

Table 3.

The aim of this study was to review the literature about the effect of cannabis use on inflammatory markers. The main findings were as follows: (i) among healthy volunteers and among cannabis users, cannabinoids seemed to decrease the inflammatory response, thus decreasing the immune response leading in turn to a higher risk of infections; (ii) among patients with MS, cannabinoids seemed to have little impact on the inflammatory markers’ levels.

These findings must be interpreted in light of some limitations. One of them is that we included only publications in English and Portuguese. Although this is a limitation, a previous study has stated that language restriction does not usually alter the main findings of systematic reviews [35]. Moreover, this review focused only on human studies, and the percentage of the CBD/THC relation in each study was not provided. This CBD/THC relation is important because the THC-rich compounds have serious limitations such as unpredictable gastrointestinal absorption and potential intoxication and disorientating central nervous system effects at the higher doses [36]. The addition of CBD to THC should ameliorate the intoxicating effects of THC, paranoia, and euphoria associated with THC, with diminished potential for abuse [37].

Sexton et al. [25] performed a cross-sectional study, evaluating 10 cannabis users. The aim of this study was to evaluate the migratory potential of isolated monocytes from cannabis users. It found that cannabinoids inhibited the migration of monocytes in both groups (naïve and nonnaïve to cannabis), and the monocytes from subjects nonnaïve to cannabis expressed more CB1 messenger ribonucleic acid (mRNA). Although the authors report no limitations, we can infer that unknowing about the acute and long-term effects of phytocannabinoid (pCB) on human circulating monocytes limits the comprehension of the study findings.

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TNFα in the sera of mice treated with zymosan and essential oils. Twenty-four hours after injecting zymosan and/or an intraperitoneal dose of CBD (5 mg/kg) or essential oils (10, 25, or 50 mg/kg) dissolved in vehicle containing ethanol:Cremophore:saline at a ratio of 1:1:18, the TNFα concentration in the serum was determined by ELISA. N=3 for each treatment group. **p<0.01. TNFα, tumor necrosis factor alpha.

Introduction: Cannabinoids are well known to have anti-inflammatory effects in mammalians; however, the Cannabis plant also contains other compounds such as terpenoids, whose biological effects have not yet been characterized. The aim of this study was to compare the anti-inflammatory properties of terpenoids with those of cannabidiol (CBD).

2 Department of Medicinal and Natural Products, Institute for Drug Research, The Hadassah Medical School, The Hebrew University of Jerusalem, Jerusalem, Israel.

Anti-inflammatory and antinociceptive effects of terpenoid-rich essential oils

RAW 264.7 cells were seeded at a density of 1×10 5 cells/well in 24-well plates and incubated overnight at 37°C and 5% CO2. On the following day, the medium was changed to fresh DMEM without FCS, containing various concentrations of the essential oils. The cells were then stimulated by the addition of lipopolysaccharide (LPS) to a concentration of 1 μg/mL. Cell supernatants (SNs) were harvested after 24 h for nitric oxide radical (NO • ) assay by addition of 100 μL SN to an equal volume of Griess reagent (1% sulfanilamide, 0.1% naphthalene diamine, and 2% H3PO4). After 10 min of incubation, the resultant color was measured at 550 nm. The amount of NO • produced, and any inhibition by the test materials, was calculated from a standard curve prepared with NaNO2.

Calibrated calipers were used to measure paw swelling (thickness) 2, 6, and 24 h after injection of zymosan. 20

To study the effects of terpenoids on essential macrophage functions, the RAW 264.7 macrophage cell line was either untreated or incubated with the essential oils at indicated concentrations, before stimulation with zymosan to induce ROIs or LPS to induce NO • production. The ROI production was measured by luminol chemiluminescence, while NO • production was measured by resulting nitrite concentration in the supernatant. The generation of ROI by RAW 264.7 macrophages was significantly suppressed following a short 5 min-incubation with 40 μg/mL terpenoids from chemotypes T1 and T2 ( Fig. 2 ), while lower concentrations had barely any effect. T3 terpenoids, however, showed only a moderate inhibition at 40 μg/mL ( Fig. 2 ). When the macrophages were incubated with terpenoids for 24 h before zymosan induction of ROI, the terpenoids had barely any inhibitory effect ( Fig. 2 ). This observation suggests for a transient inhibitory effect of terpenoids.

In contrast, only a moderate pain inhibition could be achieved with the T2 and T3 terpenoid preparations ( Fig. 4B ). No correlative dose–response could be seen for T2 and T3, suggesting for having reached a maximum effect. The more potent pain-relieving effects of T1 in comparison to T2 and T3 is correlative to the better prevention of paw swelling by T1 (compare Fig. 4B with 4A). Of note, the antinociceptive effects of all compounds, including CBD, were most prominent at 6 h.