- CBD Oil For Lupus
CBD Oil For Lupus
CBD Oil For Lupus
Lupus, also known as Systemic Lupus Erythematosus, is an autoimmune disorder that results in sometimes severe inflammation, swelling, pain (typically from tissue damage), and other harm to a variety of body parts. This condition is a chronic disease, meaning there is no known cure. It occurs when a patient’s confused, hyperactive immune system attacks their tissues and organs. Inflammation and swelling caused by lupus can affect many different body systems, including one’s joints, skin, kidneys, blood cells, brain, heart, and lungs.
Lupus medical forums, websites, and directories and are very active with personal testimonials from people with lupus and treatments they are personally using with CBD oil. These testimonials from lupus sufferers report their experiences with high quality Cannabidiol oil (CBD), CBD oil with little to no THC like what is sold in our store with ZERO THC. Perhaps even more important, many people claim that CBD oil helps reduce their flare ups and chronic lupus symptoms among other triggers and health conditions without any issues, side effects, or reactions they may have or have had with their prescriptions ordered by their doctors.
Web MD and other reputable sources like Mayo Clinic and others report many side effects for prescription medications given for lupus. Some of the medication vary on the severity of the case but can include:
- Acetaminophen or nonsteroidal anti-inflammatory drugs (NSAIDs), sometimes in combination with antimalarial drugs. Acetaminophenand NSAIDS are often enough to reduce symptoms.
- Antimalarial drugs such as hydroxychloroquine (Plaquenil).
- Low-dose corticosteroids and/or corticosteroid creams or ointments.
- Corticosteroids, such as prednisone.
- Immunosuppressive medicines, such as azathioprine, belimumab, cyclophosphamide, methotrexate, or mycophenolate mofetil.
- Some people with lupus are sensitive to antibiotic medicines called sulfonamides (sulfa medicines). These includeBactrim, Septra, and many others. Your doctor can prescribe medicines that don’t contain sulfa, if needed.
- People with lupus can go into spontaneous remission. If this happens to you, your doctor may cut back your medicine over time or stop your medicine.
– higher risk of infection
– stomach bleeding
– heart problems
– weight gain
– high blood pressure
– easy bruising of the skin
– liver damage
– reduces fertility
– higher risk of cancer
CBD Oil For Lupus
So per Lupus.org:
Anti-inflammatory medications help to relieve many of the symptoms of lupus by reducing inflammation and pain. Anti-inflammatories are the most common drugs used to treat lupus, particularly symptoms such as fever, arthritis or pleurisy, which generally improve within several days of beginning treatment.
For many people with lupus, an anti-inflammatory drug may be the only medication they need to control their lupus.
So Does CBD help with Anti inflammatory health conditions?
Aon an article posted by NCBI HERE it states the following:
Cannabinoids & other inflammatory diseases
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 . Murine models of allergic airway disease, employing ovalbumin (OVA) as an aeroallergen, indicated that CD4+ Th2 cells (IL-4, IL-5 and IL-13) played a pivotal role in the pathophysiology of the allergic airway response . Intraperitoneal administration of THC or cannabinol (CBN) in OVA-sensitized and challenged A/J mice led to attenuation of serum IgE, IL-2, IL-4, IL-5 and IL-13 mRNA expression and decreased allergen-induced mucus production, indicating that cannabinoid-based compounds may represent a novel class of therapeutic agents for the treatment of allergic airway diseases . 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. It is possible that THC may affect other cells such as DCs and B cells directly in this model. Previous findings indicated that aerosolized THC was capable of causing significant bronchodilatation with minimal systemic side effects, but had a local irritating effect on the airways . Further bronchodilator effects of cannabinoids administered orally or by aerosol to asthmatic patients have also been reported [115,116]. Similarly, endogenous cannabinoids have been shown to regulate airway responsiveness. In rodent lungs, a Ca2+-activated mechanism for the biosynthesis of anandamide was observed and CB1 receptors were found predominantly on axon terminals of airway nerves, indicating that endocannabinoids may regulate bronchial smooth muscle tone . It was reported that activation of CB1 receptors by locally released anandamide may participate in the control of bronchial contractility. Blocking of AEA-induced CB1 activity can enhance capsaicin-induced bronchospasm. However, the authors further suggested that the effects of AEA may depend on the state of the bronchial muscle. During capsaicin-evoked bronchospasm, AEA may reduce the muscle contraction, whereas AEA may cause bronchoconstriction in the absence of vagus nerve-constricting tone .
Cannabidiol has been shown to be effective in protecting endothelial function and integrity in human coronary artery endothelial cells (HCAECs). The study demonstrated that CBD reversed the harmful effects of high glucose on HCAECs by inhibiting :
- Reactive oxygen species production by mitochondria
- NF-κB activation
- Transendothelial migration of monocytes
- Monocyte–endothelial adhesion in HCAECs
In a different experiment, HCAECs were stimulated with TNF-α in order to mimic the inflammatory processes during atherosclerosis, and the effect of different CB2 receptor agonists on the activated cells was studied. It was demonstrated that activation of cells with TNF-α led to increased expression of CB2 and activation of Ras, p38, MAPK, JNK and AKT pathways. In addition, proliferation and migration was markedly increased in activated cell populations. The use of CB2 agonists JWH-133 and HU-308 inhibited all activated pathways in a dose-dependent manner, establishing a novel use for these cannabinoid compounds .
Experimental autoimmune uveoretinitis (EAU), is a CD4+ T-cell-mediated autoimmune disease, which can be induced in rodents by challenge with retinal antigens or their peptides . In a recent study, it was observed that the CB2-selective agonist JWH-133 had a high in vivo immunosuppressive effect in EAU model. EAU was strongly inhibited when the CB2 was engaged and the effects of CB2 engagement appeared to be mediated predominantly through downregulation of T-cell function with a less-marked effect on antigen presentation . An impaired T-cell-proliferative response in leukocytes from JWH-133-treated mice was also accompanied by marked reductions in cytokine production. A more recent study showed that JWH-133 (10 nM–5 μM) suppressed IL-12p40 and enhanced IL-10 production in mouse macrophages induced by LPS . As IL-12p40 is critical for the development of EAU and IL-10 could suppress EAU [123,124], the authors suggested that this may also be one of the possible mechanisms responsible for the effect of JWH-133 on EAU.
Insulin-dependent Type 1 diabetes mellitus (T1DM) is an autoimmune disease resulting in destruction of insulin-producing pancreatic β cells, a process that is assumed to be mediated mainly by CD4 Th1 and CD8 T lymphocytes . In rodents, T1D is induced by administration of multiple low doses of streptozotocin (MLDSTZ). This model is used for studying autoimmune processes associated with pancreatic β-cell pathogenesis. A study performed by Li et al. indicated that Δ9-THC could exert a transient attenuation of MLDSTZ-induced autoimmune diabetes. Δ9-THC treated (150 mg/kg) CD-1 mice exhibited reduced hyperglycemia and a significant decrease in the loss of pancreatic insulin. MLDSTZ-induced insulitis was also significantly attenuated by decreases in CD3+ inflammatory cells in the pancreatic islets and in mRNA expression for IL-12, IFN-γ and TNF-α. It was suggested that in this model, the autoimmune component was most effectively modulated by Δ9-THC treatment . Similarly, CBD treatment has been shown to significantly inhibit and delay destructive insulitis and inflammatory Th1-associated cytokine production in nonobese diabetes-prone (NOD) female mice. CBD-treated mice exhibited significant reduction of plasma levels of the proinflammatory cytokines IFN-γ and TNF-α, whereas production of the Th2-associated cytokines IL-4 and IL-10 was increased when compared with untreated control mice, thus shifting the immune response from Th1 to Th2 dominance . A recent study indicated that treatment of 11–14-week-old female NOD mice, either in a latent diabetes stage (after 14 weeks) or with initial symptoms of diabetes (appearing up to 14 weeks) with CBD for 4 weeks, could lead to sustained inhibition of insulitis . CBD treatment inhibited specific destruction of the islets and reduced the infiltrates by mononuclear cells into the islets, thus preventing diabetes. Furthermore, cannabinoids have also been demonstrated to possess additional beneficial effects in animal models of diabetes. It has been reported that rats treated with CBD for periods of 1–4 weeks experienced significant protection from diabetic retinopathy . Cannabinoids have also been shown to alleviate neuropathic pain associated with the disease. Mice injected with a cannabis receptor agonist experienced a reduction in diabetic-related tactile allodynia compared with nontreated controls . Thus, cannabinoids can be considered useful for controlling T1D due to their anti-inflammatory properties.
CBD Oil For Lupus
Below is a list of studies done on Inflammation and CBD:
- Cannabidiol as an emergent therapeutic strategy for lessening the impact of inflammation on oxidative stress
- The endocannabinoid system: an emerging key player in inflammation
- Cannabinoids suppress inflammatory and neuropathic pain by targeting α3 glycine receptors
- Cannabinoids in clinical practice
- Cannabinoids, inflammation, and fibrosis
- Cannabidiol reduces intestinal inflammation through the control of neuroimmune axis
- Diabetic retinopathy: Role of inflammation and potential therapies for anti-inflammation
- Cannabidiol reduces Aβ-induced neuroinflammation and promotes hippocampal neurogenesis through PPARγ involvement
- Cannabidiol attenuates high glucose-induced endothelial cell inflammatory response and barrier disruption
- Vanilloid TRPV1 receptor mediates the antihyperalgesic effect of the nonpsychoactive cannabinoid, cannabidiol, in a rat model of acute inflammation
- Anti-inflammatory role of cannabidiol and O-1602 in cerulein-induced acute pancreatitis in mice
- Cannabinoids, endocannabinoids, and related analogs in inflammation
- Cannabidiol, a non-psychotropic plant-derived cannabinoid, decreases inflammation in a murine model of acute lung injury: role for the adenosine A(2A) receptor
- Cannabidiol attenuates cisplatin-induced nephrotoxicity by decreasing oxidative/nitrosative stress, inflammation, and cell death