The cannabis-derived chemical is non-psychoactive, and – while federally illegal – has been hailed as a cure for disease. Cannabidiol (CBD) is an active ingredient in cannabis derived from the Now I am not surprised they take this natural healing substance and. In just a few years, cannabidiol (CBD) has become immensely in a large survey among medicinal cannabis users published in .
cannabinoid CBD Healing
THC is the main psychoactive component of the cannabis plant. This compound works, in part, by mimicking the effects of anandamide and 2-AG. These neurotransmitters are produced naturally by the human body and help to modulate sleeping and eating habits, the perception of pain, and countless other bodily functions. Research studies indicate that THC may useful in helping with: Cannabidiol is one of the most critical cannabinoids contained in the cannabis plant.
It exists both in agricultural hemp, as well as medical cannabis. While cannabinoids are present within several plants in nature, cannabis is the only plant known to contain CBD.
This fact means that when you ingest CBD for medical purposes, you will more likely experience a relief of your unwanted discomfort, with little or no noticeable effect on your cognitive abilities. Research studies indicate that CBD may be useful in helping with: Research suggests CBD may be better for inflammation and neuropathic pain , while THC may excel with spasticity and cramp-related pain. It is worth noting that sometimes high doses of THC can exacerbate pain symptoms.
Meaning THC consumed in this capacity should be done in small amounts. Additionally, many individuals experience difficulty managing the side effects associated with THC, rendering useless any potential benefits. Some experts suggest that a combination of THC and CBD is the ideal way to approach pain, giving validity to something known as the entourage effect. For example, mg of isolated CBD may be substantially less effective at alleviating symptoms than mgs of a whole-plant, CBD-containing cannabis extract.
Many argue that consuming the plant in its whole form provides all the necessary cofactors to facilitate proper absorption. This argument is at the heart of the debate over CBD oil from hemp vs. CBD oil from cannabis. While it may be cheaper and more cost-effective to extract CBD from industrial hemp, users may ultimately experience less benefit due to the absence of clinically significant levels of terpenes and other compounds which occur in abundance in high-CBD marijuana.
While high-CBD cultivars of cannabis do contain much higher levels of various cannabinoids, terpenes, etc. Agricultural hemp is much closer to the kind of cannabis that one would find growing naturally in the wild, whereas high-CBD marijuana is hybridized and toyed with by growers to produce the highest levels of the desirable compounds. There is no hard science yet! It is up to each individual to decide which option is best for them.
THC is an illegal drug with considerable immediate and long-term cognitive side effects. These include impaired thinking and reasoning, a reduced ability to plan and organize, altered decision-making, and reduced control over impulses. Also, chronic use of THC correlates with significant abnormalities in the heart and brain.
Given the increasing popularity of medical cannabis, breeders are currently creating strains with higher CBD to THC ratios to minimize the psychoactive side effects. Overall, the lower health risks of CBD, combined with its efficacy, make it a better candidate for natural applications than THC. Your email address will not be published. What is CBD Oil? Is CBD for Pets? 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: 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. However, CB1 expression is predominant in the CNS, especially on presynaptic nerves, and CB2 is primarily expressed on immune cells [ 5 , 6 ]. Arachidonic acid metabolites have been shown to exhibit properties similar to compounds found in Cannabis sativa.
These metabolites are hence referred to as endocannabinoids. These ubiquitous endogenous cannabinoids act as natural ligands for the cannabinoid receptors expressed in mammalian tissue, thus constituting an important lipid-signaling system termed the endocannabinoid system. The endocannabinoid system is an important biological regulatory system that has been shown to be highly conserved from lower invertebrates to higher mammals [ 7 ].
Other than the lipid transmitters that serve as ligands for the cannabinoid receptors, the endocannabinoid family also comprises the enzymes for biosynthesis and degradation of the ligands.
The endocannabinoids include N -arachidonoylethanolamine, anandamide AEA , 2-arachidonoyl glycerol 2-AG , N -arachydonoyldopamine, noladin ether and virodhamine. AEA was discovered by Devane et al. It was found to exist in much higher concentration in serum and brain than AEA.
Endocannabinoids are derivatives of arachidonic acid conjugated with either ethanolamine or glycerol. They are synthesized on demand from phospholipid precursors residing in the cell membrane in response to a rise in intracellular calcium levels. Inside cells, endocannabinoids are catalytically hydrolyzed by the aminohydrolase fatty acid amide hydrolase FAAH , which degrades AEA into arachidonic acid and ethanolamine [ 11 ].
Fatty acid-binding proteins FABPs have been reported to play an important role as intracellular carriers in the transport of AEA from the plasma membrane to FAAH for their subsequent inactivation [ 12 ].
Studies to date indicate that the main pharmacological function of the endocannabinoid system is in neuromodulation: However, in the periphery, this system is an important modulator of the ANS, immune system and microcirculation [ 13 ]. Some well-known natural and synthetic cannabinoids and endocannabinoids are depicted in Table 1. Cannabinoids are potent anti-inflammatory agents and they exert their effects through induction of apoptosis, inhibition of cell proliferation, suppression of cytokine production and induction of T-regulatory cells Tregs.
In this review, we provide an in-depth description of all four different mechanisms and we further discuss the immunosuppressive properties of cannabinoids in the context of inflammatory and autoimmune disease states, triggered by cellular rather than humoral components of the immune system. One major mechanism of immunosupression by cannabinoids is the induction of cell death or apoptosis in immune cell populations. Under normal conditions, apoptosis is required in order to maintain homeostasis and it involves morphological changes i.
The extrinsic pathway of apoptosis is initiated with the ligation of death receptors i. The intrinsic pathway of apoptosis is initiated via mitochondria and caspase 9; cytochrome c and caspase 3 are the major players in the induction of cell death [ 14 , 15 ]. This study also showed that the process was mediated via activation of Bcl-2 and caspases [ 16 ].
It was difficult to demonstrate the apoptotic effects of THC on lymphocytes, in vivo , and our laboratory speculated that this might be due to rapid clearance of dead cells by phagocytic cells. The cells were incubated for 12—24 h ex vivo and, since the phagocytosis was excluded in the cultures, we detected significant levels of THC-induced apoptosis in T cells, B cells and macrophages [ 17 ].
We have also demonstrated that THC induced higher levels of apoptosis in naive lymphocytes, when compared with mitogen-activated lymphocytes, because activated cells downregulated the levels of CB2 on their cell surface [ 17 ]. Several studies also reported THC-induced apoptosis in antigen-presenting cells. Furthermore, THC increased Bcl-2 and caspase 1 activity in naive and lipopolysaccharide LPS -activated macrophages isolated from the peritoneal cavity of mice [ 16 ].
In addition, the use of synthetic CB2 agonist JWH treatment in vitro led to cell death via both the death-receptor pathway and the intrinsic pathway. When JWH was administered in vivo , the antigen-specific response to Staphylococcal enterotoxin A was inhibited significantly [ 22 ].
It is important to note that, unlike in immune cells, cannabinoids can protect from apoptosis in nontransformed cells of the CNS, which can play a protective role in autoimmune conditions such as multiple sclerosis. In a different study by Jackson et al. In addition, caspase 3 activation was higher in knockout cultures, indicating a protective role of CB1 in neuronal cells [ 24 ].
Cytokines are the signaling proteins synthesized and secreted by immune cells upon stimulation. They are the modulating factors that balance initiation and resolution of inflammation. One of the possible mechanisms of immune control by cannabinoids during inflammation is the dys-regulation of cytokine production by immune cells and disruption of the well-regulated immune response [ 25 ].
Furthermore, cannabinoids may affect immune responses and host resistance by perturbing the balance between the cytokines produced by T-helper subsets, Th1 and Th2.
However, the results were variable, depending on the cell line and the concentration used [ 26 ]. Both pro-inflammatory and anti-inflammatory effects of THC were demonstrated in this study, proposing that different cell populations have varied thresholds of response to cannabinoids. Interestingly, while the anti-inflammatory cytokine IL decreased following THC treatment, there was an increase in the proinflammatory cytokine IL In other studies, cannabinoid CP55, at nanomolar concentrations was shown to have a stimulatory effect on several cytokines in the human promyelocytic cell line HL [ 27 ].
In a different study, mice were challenged with Corynebacterium parvum, in vivo , following the administration of the synthetic cannabinoids WIN55, and HU The animals were then challenged with LPS. This effect was shown to be CB1 receptor dependent. During chronic inflammation, IL-6 suppression can decrease tissue injury [ 30 ]. AjA has been reported to prevent joint-tissue injury in animal models of adjuvant arthritis [ 31 ]. Recent studies showed that addition of AjA to human monocyte-derived macrophages in vitro reduced the secretion of IL-6 from activated cells, suggesting that AjA may have a value for treatment of joint inflammation in patients with systemic lupus erythematosus SLE , rheumatoid arthritis RA and osteoarthritis [ 32 ].
Recent in vitro studies have also shown the potent anti-inflammatory effect of synthetic cannabinoids CP55, and WIN55, Endocannabinoids have also been reported to affect the cytokine biology of various cell systems. Antiproliferative effects of endocannabinoids on cancer cell lines are well established and are discussed in the later section of the review.
However, AEA has also been reported to increase cytokine-induced proliferation. Mouse bone marrow cells, when cultured in the presence of IL-3 and AEA, were observed to produce more hematopoietic colonies than with IL-3 alone [ 35 ]. Furthermore, in undifferentiated and macrophage-like differentiated HL cells, 2-AG induced CB2-dependent acceleration in the production of IL-8 [ 37 ].
On a contrary note, cytokines have also been shown to affect the endocannabinoid system. Table 2 provides a summary of the effect of cannabinoids on cytokines and chemokines in various cell models [ 26 , 28 , 29 , 32 — 34 , 37 , 40 , 41 ]. CXC-chemokine ligand 8; ND: The action of these cells leads to the demyelination of nerve fibers and axons in the CNS of humans and results in many signs and symptoms, such as muscle spasms, tremor, ataxia, weakness or paralysis, constipation and loss of bladder control [ 42 ].
There is both anecdotal and clinical evidence to show the effectiveness of cannabinoids in the treatment of MS. In , a survey of MS patients 57 men and 55 women from the USA and UK was conducted; all of the patients were self-medicating with a form of cannabis. Use of cannabinoids also improved objective test results such as hand-writing tests and bladder control tests [ 43 , 44 ].
In general, cannabinoids are useful in treating MS because they have neuroprotective as well as immunosuppressive properties [ 44 , 45 ]. In this section, we will focus on the latter and discuss the action of endogenous, natural and synthetic cannabinoids on immune cells within the CNS during MS. 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 ]. 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. A CB1-mediated suppressive pathway has also been shown in myelin-specific T cells [ 24 ]. Microglial cells are the macrophages of the CNS and, during MS, they mediate tissue injury in two main ways: In the initial stages of inflammation, after activation, microglial cells present antigens to myelin-specific T cells, which results in the activation and proliferation of Th1 lineage cells.
The investigators confirmed this finding by studying the morphology of the cells reactive vs resting as well as by immunohistochemistry. In the later stages of disease, microglial cells secrete IL, IL and IL, nitric oxide and glutamate and contribute to myelin sheath destruction. IL drives the proliferation of Th1 cells while IL is important in the maintenance of Th17 cells.
A recent study by Correa et al. Cannabinoids also exert their immunosuppressive effects on astrocytes. During disease progression, astrocytes are activated to secrete cytokines, chemokines and nitric oxide, thereby contributing to the overall inflammatory response.
Because astrocytes express both CB1 and CB2 receptors, several studies investigated the inhibitory role of cannabinoids on this cell population in the context of MS. The precise role of IL-6 in the CNS is still unclear; however, it has been reported that IL-6 secretion potentiates neuronal growth factor production.
In , Sheng et al. The three main cell types that are involved in demyelination of the nerve fibers and axons in the CNS include activated T-cells, microglia and astrocytes. In activated T-cells, treatment with WIN 55,, AEA and JWH has been shown to inhibit cytokine production, infiltration of cells into the spinal cord and in vitro recall response to myelin oligodendrocyte glycoprotein by T-cells.
Cannabinoids also inhibit the antigen presenting abilities of microglia by downregulating MHCII expression, costimulatory molecule CD40 expression, as well as cytokine secretion. Astrocytes, the major cell population in the brain, are also affected, as cannabinoid binding to the receptors leads to inhibition of inflammatory molecules, such as nitric oxide, cytokines and chemokines.
In addition, anandamide binding leads to secretion of neural growth factor secretion and protection of the neurons in the CNS. During inflammation, several different cellular pathways are activated in the intestinal tract, leading to a pathological state [ 58 ].
Functional CB1 receptor has been shown to be expressed in the human ileum and colon and the number of CB1-expressing cells was found to be significantly increased after inflammation [ 59 , 60 ]. A protective role for these CB1 receptors during inflammation has been shown in a study analyzing the role of the endogenous cannabinoid system in the development of experimental colitis in mice, induced by intrarectal 2,4-dinitrobenzene sulfonic acid DNBS treatment or oral dextran sodium sulfate DSS administration [ 59 ].
The DSS model, originally reported by Okayasu et al. Furthermore, long-term DSS administration produces colorectal carcinoma, which is similar to the dysplasia—carcinoma sequence seen in the course of cancer development in human ulcerative colitis [ 62 ].
The involvement of the endogenous cannabinoid system in the modulation of the acute phase of DNBS-induced colitis was further supported by the increased levels of transcripts coding for CB1 in wild-type mice after induction of inflammation. It was observed that genetic ablation of CB1 receptors rendered mice more sensitive to inflammatory insults.
Furthermore, similar to results observed in CB1-deficient mice, pharmacological blockade of CB1 with the specific antagonist SRA led to a worsening of colitis [ 59 ]. The protective role of the endogenous cannabinoid system was observed 24 h after DNBS treatment and became more evident on days 2 and 3.
This gives further support to the notion that the endogenous cannabinoid system is protective against inflammatory changes. These data indicated that the activation of CB1 and the endogenous cannabinoid system is an early and important physiological step in self-protection of the colon against inflammation.
Pharmacological stimulation of cannabinoid receptors with the potent agonist HU also induced a reduction of experimental colitis. It has been reported that cannabinoid receptor stimulation could have a beneficial effect on experimental colitis [ 64 ]. Intraperitoneal application of ACEA, a CB1-selective agonist, and JWH, a CB2-selective agonist, inhibited oil of mustard OM -induced colitis and subsequent symptoms such as induced distal colon weight gain, colon shrinkage, inflammatory damage, diarrhea and histological damage.
This study demonstrated a role for CB2 activation in experimental colitis. The fact that both CB1 and CB2 agonists are active in colitis models lends additional support to the theory that signaling through cannabinoid receptors may mediate protective mechanisms in colitis.
In the small intestine, the involvement of CB1 receptors in the control of intestinal motility during croton oil-induced inflammation was recently demonstrated. It was further suggested that increased levels of CB1 receptor expression in inflamed jejuna may contribute to this protective effect. CB1 receptors were shown to modulate gastrointestinal motility during croton oil-induced inflammation in mice. Fatty acid amide hydrolase is the major enzyme involved in the degradation of several bioactive fatty amides, in particular anandamide [ 11 ], and its genetic deletion in mice leads to a strongly decreased ability to degrade this endocannabinoid and an increase of anandamide levels in several tissues [ 66 ].
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. During the past few years, awareness of the cannabinoid system in the pathophysiology of liver disease has gained momentum.
Both CB1 and CB2 receptors have been shown to be upregulated in the early stages of liver injury [ 68 — 72 ]. Although embryonic liver has been shown to express CB2 receptor mRNA, adult liver hepatocytes and endothelial cells displayed only a faint physiological level of expression of CB1 receptors and were shown to produce low levels of endocannabinoids. CB1 receptors have been found to be upregulated in the vascular endothelium and in myofibroblasts located in fibrotic bands of cirrhotic livers in human and rodents [ 72 ].
CB2 receptors are also expressed in myofibroblasts, inflammatory cells and biliary epithelial cells [ 69 ]. There has been growing evidence in recent years to suggest that endocannabinoids may regulate the pathophysiology of liver diseases, including both acute forms of hepatic injury, liver fibrosis and cirrhosis.
The endocannabinoids are found in low levels in normal liver, which may be due to high levels of expression of FAAH, which is responsible for the breakdown of AEA [ 11 ]. The levels of AEA have been shown to increase in the liver and serum during acute hepatitis and fatty liver disease [ 70 ].
Together, the above studies suggest that endocannabinoids and their receptors may play a critical role in regulating liver fibrogenesis; therefore, targeting the cannabinoid receptors may serve as a novel tool to prevent and treat liver injury.
While the mechanisms of inflammatory liver injury are unclear, they are accompanied by infiltration of activated polymorphonuclear leukocytes, activation of Kupffer cells, production of proinflammatory cytokines and generation of ROS. Many recent studies indicated strongly the increased upregulation of the endocannabinoid system during liver diseases involving hepatocyte injury, inflammation, fibrogenesis, hepatic encephalopathy, cirrhotic cardiomyopathy and portal hypertension [ 73 ].
Moreover, pretreatment of mice with JWH, a CB2 receptor agonist, was shown to decrease the degree of liver tissue injury and inflammatory cell infiltration and decrease serum levels of cytokines, chemokines and adhesion molecules [ 74 ]. The data also highlights the protective role of CB2 receptor activation in the inflammatory response associated with chronic liver diseases such as viral hepatitis and alcoholic or nonalcoholic fatty liver diseases.
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 ]. By contrast, activation of CB1 receptors was found to promote profibrotic response [ 72 ]. 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 ].
The abuse of cannabis has been shown to promote liver fibrosis in patients with chronic hepatitis C, indicating that cannabinoids may exacerbate liver fibrogenesis and that CB1 receptor antagonists may play a role as anti-fibrosing molecules [ 71 ].
However, an alternative explanation could be that marijuana can trigger immunosuppression. For example, CB2 activation in immune cells can trigger apoptosis and this, in turn, can have an immunosuppressive effect in patients with hepatitis C. As such patients require immunocompetent cells to keep hepatitis under control, chronic marijuana abuse may promote fibrogenesis through the activation of CB2 and consequent suppression of antiviral immunity [ 77 ]. Endocannabinoids may also regulate liver cirrhosis by acting as mediators of vascular and cardiac functions.
Endocannabinoids can trigger vasorelaxation, while an upregulated CB1-mediated cannabinoid tone causes enhanced mesenteric vasodialation leading to portal hypertension [ 73 , 75 ]. A recent in vivo study by Batkai et al.
Further improvement in contractile function of isolated papillary muscles was observed following treatment with AM, a CB1 receptor antagonist, suggesting therapeutic potential against cirrhotic cardiomyopathy [ 75 ]. There are limited, but reliable, data on the neuroprotective role of the endocannabinoid system in hepatic encephalopathy. It has been demonstrated in a murine model that, during fulminant hepatic failure, levels of 2-AG in the brain are elevated, potentially as a response to liver damage.
Thus, influencing the endocannabinoid system with exogenous cannabinoid derivates specific for the CB1 or CB2 receptor may have a beneficial therapeutic effect on neurological dysfunction in liver diseases [ 78 ]. Recently, we noted that both exogenous and endogenous cannabinoids protected mice from concanavalin-A ConA -induced acute hepatitis, a model that mimics viral or autoimmune hepatitis, in which T cells play a critical role in triggering liver injury.
We found that administration of a single dose of THC or anandamide could ameliorate Con-A-induced hepatitis. This overwhelming evidence shows that the cannabinoid system must play a major role in the pathophysiology of various liver diseases and its therapeutic potential should be exploited for the treatment of chronic liver injuries Figure 2. Endocannabinoids, CB1 antagonists and CB2 agonists as potential drugs for the treatment of liver injury.
The major immune cell populations involved in joint injury are macrophages, T cells, fibroblast-like synoviocytes and DCs. Cannabinoids and their anti-inflammatory properties have been studied in animal models of RA and on human cells from RA patients and these studies demonstrate the anti-arthritic properties of these natural plant compounds [ 32 , 82 — 84 ].
Interestingly, most of the studies on RA and cannabinoids focus on the use of nonpsychoactive cannabinoids. CBD is the major nonpsychoactive component of the cannabis plant and its protective effect has been shown in murine collagen-induced arthritis [ 85 ].
Lymph node cells from HUtreated mice showed decreased proliferative responses when the cells from 7-day post-inflammation mice were incubated with collagen II. In a different study, Parker et al. AjA also exerts its immunomodulatory effects by inducing apoptosis in mature osteoclast-like cells and, therefore, protecting the host from osteoclastogenesis.
The hallmarks of cancer-related inflammation include the presence of inflammatory cells in tumor tissue, and the regulation of tumor growth, metastasis and angiogenesis by inflammatory mediators e. The connection between inflammation and cancer is now generally accepted and nonsteroidal anti-inflammatory drugs have been shown to reduce varied cancer risk. Hence, inflammation can be considered as a therapeutic opportunity in certain types of cancer.
Recent applications of cannabinoids have been extended as antitumor agents [ 1 , 88 ], which relies on their ability to inhibit tumor angiogenesis [ 89 ] or induce direct apoptosis or cell cycle arrest in neoplastic cells [ 89 — 92 ]. A focus on the antiproliferative effects of these compounds in various tumors, such as breast and prostate cancers, pheochromocytoma and malignant gliomas, has been proposed [ 1 , 92 — 94 ].
Our laboratory reported that, in vitro , THC and other cannabinoids could induce apoptosis in transformed murine and human T cells [ 95 ], including primary acute lymphoblastic human leukemia cells. The role of endocannabinoids as potential endogenous tumor growth inhibitors has been suggested in a study where it was observed that levels of both AEA and 2-AG were higher in precancerous polyps than in fully developed carcinomas in the colon [ 98 ]. Recent in vivo studies proposed that selective targeting of CB2 receptors resulted in colorectal tumor growth inhibition via apoptosis, which was mediated through the stimulation of ceramide [ 98 ].
In a xenograft model of thyroid cancer, substances that blocked endocannabinoid degradation also increased the levels of AEA and 2-AG in the tissue and reduced tumor growth [ 99 ]. Various attempts have been made to inactivate cannabinoid-degrading enzymes, thereby increasing the local concentration of endocannabinoids at the tumor cell surface.
This leads to anti-tumor effects of CB receptor signaling in various cancer types, such as thyroid, brain and prostate cancer [ 99 — ]. Although the majority of the effects of cannabinoids are CB receptor mediated, AEA has been shown to induce its effects on cancerous cells by interacting with TRPV1 receptor [ , ] or cholesterol-rich lipid rafts [ ].
Furthermore, it has been reported that signaling pathways are differentially regulated by cannabinoids in normal cells versus cancer cells. In malignancies, such as thyroid cancer, lymphoma, melanoma, pancreas and breast cancer, the levels of cannabinoid receptors are often higher in the tumor compared with normal cells of the same origin, resulting in increased sensitivity to cannabinoids in the malignancies [ 89 , — ].
Moreover, many animal studies have reported antiproliferative and pro-apoptotic effects of cannabinoids on tumor cells but not on normal tissue [ 89 , 91 ]. Thus, the role of the cannabinoid system in cancer indicates that this system is involved in regulating many of the functions that are essential in cancer development. Allergic asthma is a complex inflammatory disorder characterized by airway hyper-responsiveness, elevated serum IgE, recruitment of eosinophils into the lung and mucus hypersecretion by goblet cells [ ].
While most studies have shown that cannabinoids, such as THC, facilitate a Th1 to Th2 cytokine switch, as discussed previously, it is surprising that cannabinoids can also suppress allergic asthma triggered primarily by Th2 cytokines.
What is CBD? The 'miracle' cannabis compound that doesn't get you high
Some patients believe CBD has the most medicinal benefit of all the cannabis compounds. But most of them do not realize that there are. The body of research on cannabidiol, CBD oil benefits, THC, and other . show that cannabis preparations have been used for wound healing in both animals. Hemp CBD oil might be different from cannabis CBD oil, but it's plants are used for a multitude of purposes, not just medicinal or recreational.