Why Choose CBD Oil? How Does CBD Work?
The USA is in the grips of an opioid epidemic which kills over 130 people every day. Opioid painkillers are widely prescribed but are very addictive, and users often end up dependant on them. Sufferers of chronic pain have started to rely on CBD oil to take the edge off of their symptoms, through its interaction with pain receptors in your brain and immune system.
CBD is short for cannabidiol. Your body actually produces its own cannabinoids as part of the endocannabinoid system which helps to regulate mood, sleep and relaxation. There are endocannabinoid receptors all throughout your body. CBD binds to your body’s CB1 and CB2 receptors, helping them to function more effectively. Though research into the endocannabinoid system (which was only discovered in the 1990s) and the effects of CBD are in their infancy, several studies have shown CBD to produce promising results. It has been seen to reduce pain and inflammation in animal and pre-clinical studies. It could be the natural, non-addictive alternative we desperately need! Read on below for a brief review of current research literature on CBD and pain/inflammation relief. Studies are in descending order.
(2019) In a study of mice with chemotherapy-induced neurotoxicity, CBD was found to reduce the oxidative stress, inflammation and cell death commonly associated with the treatment.
The platinum compound cisplatin is one of the most potent chemotherapy agents available to treat various malignancies. Nephrotoxicity is a common complication of cisplatin chemotherapy, which involves increased oxidative and nitrosative stress, limiting its clinical use. In this study, we have investigated the effects of a nonpsychoactive cannabinoid cannabidiol, which was reported to exert antioxidant effects and has recently been approved for the treatment of inflammation, pain, and spasticity associated with multiple sclerosis in patients in a mouse model of cisplatin-induced nephropathy. Cisplatin induced increased expression of superoxide-generating enzymes RENOX (NOX4) and NOX1, enhanced reactive oxygen species generation, inducible nitric-oxide synthase expression, nitrotyrosine formation, apoptosis (caspase-3/7 activity, DNA fragmentation, and terminal deoxynucleotidyl transferase dUTP nick-end labeling staining), poly(ADP-ribose) polymerase activity, and inflammation (tumor necrosis factor-α and interleukin-1β) in the kidneys of mice, associated with marked histopathological damage and impaired renal function (elevated serum blood urea nitrogen and creatinine levels) 72 h after the administration of the drug. Treatment of mice with cannabidiol markedly attenuated the cisplatin-induced oxidative/nitrosative stress, inflammation, and cell death in the kidney, and it improved renal function. Thus, our results suggest that cannabidiol may represent a promising new protective strategy against cisplatin-induced nephrotoxicity.
(2017) In a study using rats with osteoarthritis, prophylactic CBD treatment was found to prevent the later development of pain and nerve damage in the affected joints.
Osteoarthritis (OA) is a multifactorial joint disease, which includes joint degeneration, intermittent inflammation, and peripheral neuropathy. Cannabidiol (CBD) is a noneuphoria producing constituent of cannabis that has the potential to relieve pain. The aim of this study was to determine whether CBD is anti-nociceptive in OA, and whether inhibition of inflammation by CBD could prevent the development of OA pain and joint neuropathy. Osteoarthritis was induced in male Wistar rats (150-175 g) by intra-articular injection of sodium monoiodoacetate (MIA; 3 mg). On day 14 (end-stage OA), joint afferent mechanosensitivity was assessed using in vivo electrophysiology, whereas pain behaviour was measured by von Frey hair algesiometry and dynamic incapacitance. To investigate acute joint inflammation, blood flow and leukocyte trafficking were measured on day 1 after MIA. Joint nerve myelination was calculated by G-ratio analysis. The therapeutic and prophylactic effects of peripheral CBD (100-300 μg) were assessed. In end-stage OA, CBD dose-dependently decreased joint afferent firing rate, and increased withdrawal threshold and weight bearing (P < 0.0001; n = 8). Acute, transient joint inflammation was reduced by local CBD treatment (P < 0.0001; n = 6). Prophylactic administration of CBD prevented the development of MIA-induced joint pain at later time points (P < 0.0001; n = 8), and was also found to be neuroprotective (P < 0.05; n = 6-8). The data presented here indicate that local administration of CBD blocked OA pain. Prophylactic CBD treatment prevented the later development of pain and nerve damage in these OA joints. These findings suggest that CBD may be a safe, useful therapeutic for treating OA joint neuropathic pain.
(2014) In a rat model of arthritis, the topical application of CBD as found to have the potential to relieve arthritis-related pain and inflammation without significant side effects.
Background: Current arthritis treatments often have side‐effects attributable to active compounds as well as route of administration. Cannabidiol (CBD) attenuates inflammation and pain without side‐effects, but CBD is hydrophobic and has poor oral bioavailability. Topical drug application avoids gastrointestinal administration, first pass metabolism, providing more constant plasma levels.
Methods: This study examined efficacy of transdermal CBD for reduction in inflammation and pain, assessing any adverse effects in a rat complete Freund’s adjuvant‐induced monoarthritic knee joint model. CBD gels (0.6, 3.1, 6.2 or 62.3 mg/day) were applied for 4 consecutive days after arthritis induction. Joint circumference and immune cell invasion in histological sections were measured to indicate level of inflammation. Paw withdrawal latency (PWL) in response to noxious heat stimulation determined nociceptive sensitization, and exploratory behaviour ascertained animal’s activity level.
Results: Measurement of plasma CBD concentration provided by transdermal absorption revealed linearity with 0.6–6.2 mg/day doses. Transdermal CBD gel significantly reduced joint swelling, limb posture scores as a rating of spontaneous pain, immune cell infiltration and thickening of the synovial membrane in a dose‐dependent manner. PWL recovered to near baseline level. Immunohistochemical analysis of spinal cord (CGRP, OX42) and dorsal root ganglia (TNFα) revealed dose‐dependent reductions of pro‐inflammatory biomarkers. Results showed 6.2 and 62 mg/day were effective doses. Exploratory behaviour was not altered by CBD indicating limited effect on higher brain function.
Conclusions: These data indicate that topical CBD application has therapeutic potential for relief of arthritis pain‐related behaviours and inflammation without evident side‐effects.
(2013) In a study of chemotherapy-induced neuropathic pain, CBD was found to protect against associated neurotoxicity. The study suggests that use of CBD during Paclitaxel chemotherapy treatment is safe and affective in its prevention of or attenuation of neuropathic pain.
Background and Purpose: Paclitaxel (PAC) is associated with chemotherapy‐induced neuropathic pain (CIPN) that can lead to the cessation of treatment in cancer patients even in the absence of alternate therapies. We previously reported that chronic administration of the non‐psychoactive cannabinoid cannabidiol (CBD) prevents PAC‐induced mechanical and thermal sensitivity in mice. Hence, we sought to determine receptor mechanisms by which CBD inhibits CIPN and whether CBD negatively effects nervous system function or chemotherapy efficacy.
Experimental Approach: The ability of acute CBD pretreatment to prevent PAC‐induced mechanical sensitivity was assessed, as was the effect of CBD on place conditioning and on an operant‐conditioned learning and memory task. The potential interaction of CBD and PAC on breast cancer cell viability was determined using the MTT assay.
Key Results: PAC‐induced mechanical sensitivity was prevented by administration of CBD (2.5 – 10 mg·kg−1) in female C57Bl/6 mice. This effect was reversed by co‐administration of the 5‐HT1A antagonist WAY 100635, but not the CB1 antagonist SR141716 or the CB2 antagonist SR144528. CBD produced no conditioned rewarding effects and did not affect conditioned learning and memory. Also, CBD + PAC combinations produce additive to synergistic inhibition of breast cancer cell viability.
Conclusions and Implications: Our data suggest that CBD is protective against PAC‐induced neurotoxicity mediated in part by the 5‐HT1A receptor system. Furthermore, CBD treatment was devoid of conditioned rewarding effects or cognitive impairment and did not attenuate PAC‐induced inhibition of breast cancer cell viability. Hence, adjunct treatment with CBD during PAC chemotherapy may be safe and effective in the prevention or attenuation of CIPN.
(2013) This study using a viral model of multiple sclerosis showed that by several mechanisms, CBD has significant anti-inflammatory effects.
Inflammation in the central nervous system (CNS) is a complex process that involves a multitude of molecules and effectors, and it requires the transmigration of blood leukocytes across the blood–brain barrier (BBB) and the activation of resident immune cells. Cannabidiol (CBD), a non-psychotropic cannabinoid constituent of Cannabis sativa, has potent anti-inflammatory and immunosuppressive properties. Yet, how this compound modifies the deleterious effects of inflammation in TMEV-induced demyelinating disease (TMEV-IDD) remains unknown. Using this viral model of multiple sclerosis (MS), we demonstrate that CBD decreases the transmigration of blood leukocytes by downregulating the expression of vascular cell adhesion molecule-1 (VCAM-1), chemokines (CCL2 and CCL5) and the proinflammatory cytokine IL-1β, as well as by attenuating the activation of microglia. Moreover, CBD administration at the time of viral infection exerts long-lasting effects, ameliorating motor deficits in the chronic phase of the disease in conjunction with reduced microglial activation and pro-inflammatory cytokine production. Adenosine A2A receptors participate in some of the anti-inflammatory effects of CBD, as the A2A antagonist ZM241385 partially blocks the protective effects of CBD in the initial stages of inflammation. Together, our findings highlight the anti-inflammatory effects of CBD in this viral model of MS and demonstrate the significant therapeutic potential of this compound for the treatment of pathologies with an inflammatory component.
Acute lung injury is an inflammatory condition for which treatment is mainly supportive because effective therapies have not been developed. Cannabidiol, a non-psychotropic cannabinoid component of marijuana (Cannabis sativa), has potent immunosuppressive and anti-inflammatory properties. Therefore, we investigated the possible anti-inflammatory effect of cannabidiol in a murine model of acute lung injury. Analysis of total inflammatory cells and differential in bronchoalveolar lavage fluid was used to characterize leukocyte migration into the lungs; myeloperoxidase activity of lung tissue and albumin concentration in the bronchoalveolar lavage fluid were analyzed by colorimetric assays; cytokine/chemokine production in the bronchoalveolar lavage fluid was also analyzed by Cytometric Bead Arrays and Enzyme-Linked Immunosorbent Assay (ELISA). A single dose of cannabidiol (20 mg/kg) administered prior to the induction of LPS (lipopolysaccharide)-induced acute lung injury decreases leukocyte (specifically neutrophil) migration into the lungs, albumin concentration in the bronchoalveolar lavage fluid, myeloperoxidase activity in the lung tissue, and production of pro-inflammatory cytokines (TNF and IL-6) and chemokines (MCP-1 and MIP-2) 1, 2, and 4 days after the induction of LPS-induced acute lung injury. Additionally, adenosine A2A receptor is involved in the anti-inflammatory effects of cannabidiol on LPS-induced acute lung injury because ZM241385 (4-(2-[7-Amino-2-(2-furyl)[1,2,4]triazolo[2,3-a][1,3,5]triazin-5-ylamino]ethyl)phenol) (a highly selective antagonist of adenosine A2A receptor) abrogated all of the anti-inflammatory effects of cannabidiol previously described. Thus, we show that cannabidiol has anti-inflammatory effects in a murine model of acute lung injury and that this effect is most likely associated with an increase in the extracellular adenosine offer and signaling through adenosine A2A receptor.
(2011) This study aimed to investigate the effect of CBD on inflammation caused by ulcerative colitis. Using samples from human ulcerative colitis patients and inflamed intestinal segments from mice, CBD was found to reduce inflammation in both.
Enteric glial cells (EGC) actively mediate acute and chronic inflammation in the gut; EGC proliferate and release neurotrophins, growth factors, and pro-inflammatory cytokines which, in turn, may amplify the immune response, representing a very important link between the nervous and immune systems in the intestine. Cannabidiol (CBD) is an interesting compound because of its ability to control reactive gliosis in the CNS, without any unwanted psychotropic effects. Therefore the rationale of our study was to investigate the effect of CBD on intestinal biopsies from patients with ulcerative colitis (UC) and from intestinal segments of mice with LPS-induced intestinal inflammation. CBD markedly counteracted reactive enteric gliosis in LPS-mice trough the massive reduction of astroglial signalling neurotrophin S100B. Histological, biochemical and immunohistochemical data demonstrated that S100B decrease was associated with a considerable decrease in mast cell and macrophages in the intestine of LPS-treated mice after CBD treatment. Moreover the treatment of LPS-mice with CBD reduced TNF-α expression and the presence of cleaved caspase-3. Similar results were obtained in ex vivo cultured human derived colonic biopsies. In biopsies of UC patients, both during active inflammation and in remission stimulated with LPS+INF-γ, an increased glial cell activation and intestinal damage were evidenced. CBD reduced the expression of S100B and iNOS proteins in the human biopsies confirming its well documented effect in septic mice. The activity of CBD is, at least partly, mediated via the selective PPAR-gamma receptor pathway. CBD targets enteric reactive gliosis, counteracts the inflammatory environment induced by LPS in mice and in human colonic cultures derived from UC patients. These actions lead to a reduction of intestinal damage mediated by PPARgamma receptor pathway. Our results therefore indicate that CBD indeed unravels a new therapeutic strategy to treat inflammatory bowel diseases.
(2008) This review of recent research on the utilization of CBD and the endocannabinoid system found an equal-part CBD/THC spray to be safe and effective in treating central and peripheral neuropathic pain, rheumatoid arthritis and cancer-related pain.
This article reviews recent research on cannabinoid analgesia via the endocannabinoid system and non-receptor mechanisms, as well as randomized clinical trials employing cannabinoids in pain treatment. Tetrahydrocannabinol (THC, Marinol®) and nabilone (Cesamet®) are currently approved in the United States and other countries, but not for pain indications. Other synthetic cannabinoids, such as ajulemic acid, are in development. Crude herbal cannabis remains illegal in most jurisdictions but is also under investigation. Sativex®, a cannabis derived oromucosal spray containing equal proportions of THC (partial CB1 receptor agonist ) and cannabidiol (CBD, a non-euphoriant, anti-inflammatory analgesic with CB1 receptor antagonist and endocannabinoid modulating effects) was approved in Canada in 2005 for treatment of central neuropathic pain in multiple sclerosis, and in 2007 for intractable cancer pain. Numerous randomized clinical trials have demonstrated safety and efficacy for Sativex in central and peripheral neuropathic pain, rheumatoid arthritis and cancer pain. An Investigational New Drug application to conduct advanced clinical trials for cancer pain was approved by the US FDA in January 2006. Cannabinoid analgesics have generally been well tolerated in clinical trials with acceptable adverse event profiles. Their adjunctive addition to the pharmacological armamentarium for treatment of pain shows great promise.
(2007) An analysis of three studies into the effects of oral CBD on pain found that low doses were effective in treating the pain of chronic sufferers. Sample sizes are small and the follow-up period for each study was relatively short, limiting broader generalization, but it’s an interesting early result which merited further investigation.
Purpose of review: The aim of this article is to assess the role of cannabinoids in the treatment of acute and chronic pain in humans.
Recent findings: Very few clinical trials looking at the analgesic effects of cannabinoids in the acute pain settings have been performed. Three recent studies have evaluated the oral administration of synthetic cannabinoids in postoperative pain. At low doses cannabinoids are not different from placebo, whereas at high doses they may be associated with adverse effects or even worsening of pain intensity. In chronic pain patients, the safety and analgesic efficacy of a number of cannabinoid compounds have recently been evaluated in several clinical trials in several chronic pain conditions. While the small size of the trials and the relatively short duration of follow-up limits broad generalization, to date there is increasing evidence that cannabinoids are safe and effective for refractory chronic pain conditions including neuropathic pain associated with multiple sclerosis, rheumatoid arthritis, and peripheral neuropathy associated with HIV/AIDS.
Summary: The precise role of cannabinoids in pain treatment still needs further evaluation. Cannabinoid compounds may be more effective in the context of chronic neuropathic pain than for the management of acute pain.
(2006) In this meta-analysis, several studies of CBD treatments for pain management of multiple sclerosis patients were examined. The studies sought to determine how effective CBD treatments were in treating neuropathic pain. It concluded that CBD, along with a CBD/THC spray, is effective in treating MS-related pain.
Objective: Debilitating pain, occurring in 50–70% of multiple sclerosis (MS) patients, is poorly understood and infrequently studied. We summarized efficacy and safety data of cannabinoid-based drugs for neuropathic pain.
Data sources: Studies were identified from Medline, Embase, and Cochrane databases; Bayer Healthcare provided additional trials.
Study selection: Accepted were randomized, double-blinded placebo-controlled trials of cannabinoid-based treatments for MS-related/neuropathic pain in adults ≥ 18 years of age.
Data extraction: Two reviewers identified studies and extracted data; a third adjudicated disagreements. Data included baseline and endpoint pain scores on visual analog or 11-point ordinal scales.
Data synthesis: Of 18 articles and three randomized controlled trial (RCT) reports identified, 12 articles and two reports were rejected (9 = inappropriate disease or outcome, 1 = duplicate, 1 = review, and 1 = abstract); six accepted articles and one RCT-report involved 298 patients (222 treated, 76 placebo); four examined Sativex (a cannabidiol/delta-9-tetrahydrocannabinol (THC) buccal spray) (observations = 196), five cannabidiol (n = 41), and three dronabinol (n = 91). Homogeneity χ2 values were non-significant, allowing data combination. Analyses focused on baseline-endpoint score differences. The cannabidiol/THC buccal spray decreased pain 1.7 ± 0.7 points ( p = 0.018), cannabidiol 1.5 ± 0.7 ( p = 0.044), dronabinol 1.5 ± 0.6 ( p = 0.013), and all cannabinoids pooled together 1.6 ± 0.4 ( p < 0.001). Placebo baseline-endpoint scores did not differ (0.8 ± 0.4 points, p = 0.023). At endpoint, cannabinoids were superior to placebo by 0.8 ± 0.3 points ( p = 0.029). Dizziness was the most commonly observed adverse event in the cannabidiol/THC buccal spray arms (39 ± 16%), across all cannabinoid treatments (32.5 ± 16%) as well as in the placebo arms (10 ± 4%).
Conclusion: Cannabinoids including the cannabidiol/THC buccal spray are effective in treating neuropathic pain in MS.
Limitations: This review was based on a small number of trials and patients. Pain related to MS was assumed to be similar to neuropathic pain.
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