While CBD is generally considered safe, some people will experience some side . Only one purported use for cannabidiol, to treat epilepsy, has about both the quality of CBD oil being produced and its potential side effects. Cannabis can help with not only treating these conditions, but other clearly helps ameliorate the depression symptoms hepatitis patients suffer from. the journal Cell Death and Disease found that CBD is helpful in causing.
Using to What Of Side CBD Effects Are Hepatitis? The Treat
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. A person who has AIDS must receive treatment to prevent death.
While antiretroviral therapy has been shown to effectively curtail HIV from progressing to AIDS, the symptoms and side effects of the long-term drug therapy are considerable. Nausea, vomiting, diarrhea, heart disease, weakened bones, muscle tissue breakdown, and neuropathic pain are commonly reported during HIV treatment regimens. Weight loss due to nausea and a loss of appetite compounds weaknesses in the immune system.
HIV positive patients consuming medical Cannabis have reported significant improvements in appetite, muscle pain levels, nausea , anxiety , depression , and skin tingling 9.
Studies have found that daily and chronic neuropathic pain related to HIV can be significantly lowered by regular cannabis consumption 1,4. Cannabinoids also boosts appetite and daily functioning, helping to combat weight loss and muscle breakdown 5. One study found no significant association with cannabis use and the CD4 T-cell count of patients co-infected with HIV and HCV, suggesting cannabis has no adverse effects on the immune system 6.
Results from an animal trial also contribute to the theory that cannabis might be able to stop the spread of HIV. Monkeys that were infected with an animal form of the virus and administered with THC for 17 months saw a decrease in damage to the immune tissue of the stomach 7.
In Maryland , medical cannabis may be prescribed for patients of any disease or condition that causes chronic pain. Cannabis in painful HIV-associated sensory neuropathy: HIV-positive patients treated with medical Cannabis report significant improvement in appetite, muscle pain, nausea, anxiety, nerve pain, depression and paresthesia.
Cannabis use in HIV for pain and other medical symptoms. Cannabis found to cause substantial increases in food intake in HIV positive patients that suffered from significant muscle loss, without any negative side effects. CBD is also known to be an excellent antioxidant. Antioxidants like CBD help to prevent oxidation. These radicals can cause damage to human cells through inflammation due to their reactivity.
Free radicals accumulate around the liver hence exerting pressure on the hepatic cells. While CBD is generally considered safe, some people will experience some side effects.
The side effects include nausea, diarrhea, drowsiness, change of appetite, and a dry mouth. The symptoms are rare, though, and not as severe as the ones caused by the conventional drugs used to treat Hepatitis. The recommended dosage from each product can differ greatly, creating some confusion. Dosage may be different depending on the percentage of CBD oil you are using.
On an average, 25mg of CBD a day is effective for most people. Finding the right dosage helps someone to achieve quick recovery while the wrong dosage might mean no improvement. Each person requires a specific and personalized dose determined by a couple of factors. Another way to identify the best dose is by experimenting. However, one should start with the lowest level of a dose. A person is required to stay on a particular treatment for some days during experimentation so they can determine the results that specific dose is giving.
For more details about dosage, see our post on CBD dosage. CBD oil is consumed orally by putting drops underneath the tongue and holding it until it gets fully absorbed. This makes the digestion and absorption much easier. You can also take it as capsules or mix it with a drink.
CBD for Hepatitis
Medicinal marijuana may be able to curb these side effects. manage the unpleasant side effects associated with HCV and HCV medications. But side effects like depression, sleep problems, fatigue, and nausea can It won't treat your hep C, but it can help relieve stress and help not much research has been done to show that CBD helps with hep C or if it's safe. If you're taking tenofovir, ask your doctor about TAF if you're experiencing have used medically-prescribed marijuana to ease side effects from There is no magic bullet that will cure hepatitis B. Experts hope to find one.