Research on CBD Oil for Diabetes
Research on CBD Oil for Diabetes is ongoing, but has already revealed some noteworthy discoveries. Related research shows that plant cannabinoids have an immune tempering effect on the TH-1 lymphocyte, a type of immune cell responsible for the destruction of the beta cells while simultaneously causing the more beneficial helper and anti- inflammatory immune cell TH-2, to positively alter the size of the beta cell toward growth. CBD can create endogenous precursor cells in the pancreas to slowly give rise to increased beta cell mass and volume in the early stages of Type 1 diabetes, thereby maintaining normal blood sugar levels. CBD has been shown to decrease the need for insulin in type 1 diabetes by a significant number – 58%. CBD has also successfully reversed type 2 diabetes; it causes glucose breakdown, lipid breakdown, and increases insulin sensitivity. According to Raphael Mechoulam, PhD., Professor of Medical Chemistry and Natural Products, at Hebrew University in Jerusalem, and world renown for his expertise on the Cannabis Sativa plant, “CBD did not only prevent the onset (of diabetes), it blocked the development of diabetes.” The significance of this is beyond measure for America is in the midst of a diabetes epidemic.
Cannabis-derived CBD Oil in treating Diabetic Nephropathy
Diabetes is a leading cause of renal failure, accounting for 44% of all new cases in 2008. Hyperglycemia stimulates ROS generation, which ultimately leads (via diverse pathways) to diabetic nephropathy characterized by mesangial expansion, thickening of the glomerular basement membrane, and glomerular sclerosis. There is strong evidence that both the synthetic and degradative pathways of the ECS are present in the kidney, and the CB1 receptor is expressed in both glomeruli and tubular epithelial cells.72In intrarenal arteries, the CB1 receptor is present in the endothelium, and the CB2 receptor is present in mesangial cells.71 Cannabinoid receptors play opposing roles in the regulation of oxidative stress in the kidney, as observed in a murine nephropathy model induced by cisplatin. The CB1 receptor promotes inflammation, oxidative/nitrative stress, and cell death through the activation of the p38-MAPK pathway. In contrast, CB2 receptor agonists limit damage after cisplatin administration by reducing oxidative stress, inflammation, and apoptosis.74 For therapeutic purposes, it is important that plant-derived CBD is also able to ameliorate cisplatin-induced nephrotoxicity.
Cannabis-derived CBD Oil in treating Diabetic Retinopathy
Diabetes is the leading cause of new cases of blindness and preventable blindness among adults. Vascular inflammation and endothelial cell death caused by oxidative and nitrative stress are characteristics of diabetic retinopathy. In the early stages, retinopathy is characterized by microaneurysm formation and microvascular lesions and later by extensive intraretinal hemorrhage that culminates in proliferative diabetic retinopathy with neovascularization and either preretinal or vitreous hemorrhage.
The ECS is present in the retina as shown by the presence of AEA, 2-AG, and the metabolizing enzymes FAAH and MAGL. CB1 receptors are expressed in the layers of the retina, ciliary body, iris, and choroid, whereas CB2 receptors are localized to the retina. It has been shown that EC levels are elevated in the eyes of patients with diabetic retinopathy. 2-AG levels are elevated in the iris, whereas AEA levels are increased in the cornea, ciliary body, retina, and the choroid. The role of such an increase gained importance when we received insight into the role of CB1 receptor activation in diabetic retinopathy. Deletion of the CB1 receptor or treatment with a CB1 receptor antagonist prevented retinal cell death in a murine diabetes model. Treatment of diabetic mice or human retinal cells with CB1 receptor antagonists after exposure to high glucose levels attenuated oxidative/nitrative stress, reduced NF-κB activation and adhesion molecule levels, and attenuated MAPK activation. These observations were supported by the fact that hyperglycemia up-regulated CB1 receptor expression and induced apoptosis in retina pigment epithelial cells, effects that were preventable with a CB1 receptor antagonist. Interestingly, hyperglycemia also decreased FAAH expression, leading to a locally increased concentration of AEA and thereby increasing apoptosis via CB1 receptor signaling.
The effect of CBD was also examined in experimental diabetic retinopathy. CBD was able to reduce oxidative stress, inflammation, cell death, and vascular hyperpermeability associated with diabetes. Consistent with these findings, CBD also inhibited p38-MAPK signaling. Furthermore, CBD also attenuated high glucose–induced endothelial cell dysfunction, ROS generation, and barrier disruption in primary human coronary artery endothelial cells. The protective effects of CBD on retinal cell death were, at least in part, due to the reduction of tyrosine nitration of glutamine synthase in macroglial cells, thereby preventing the accumulation and excitotoxicity of glutamine through N-methyl-D-aspartate receptors.
Cannabis-derived CBD Oil in treating Diabetic Neuropathy
Approximately 60% to 70% of people with diabetes have some kind of nervous system damage. The typical presentation is chronic, length-dependent sensorimotor neuropathy, which develops in a background of long-standing hyperglycemia and is associated with alterations of microvessels; it can be stabilized with rigorous glycemic control. Autonomic dysfunction and pain may develop over time as well.
CB1 receptors are widely expressed throughout the central and peripheral nervous systems, whereas CB2receptors are primarily restricted to the cells of the peripheral nervous system, microglia, and dorsal horn neurons. ECs are retrograde messengers with agonistic activity on presynaptic CB1 receptors, slowing neurotransmission. A good example of this effect is the suppression of nociceptive transmission in the periphery at the level of the posterior horn of the spinal cord. It has been proven that these peripheral CB1 receptors play a key role in cannabinoid-induced analgesia. Interestingly, although CB1 and CB2 agonists are effective in animal models of acute and chronic pain, in clinical trials, they only perform well in patients with chronic pain syndrome. Sativex spray containing THC and CBD is already approved for the treatment of pain in patients with multiple sclerosis and cancer pain unresponsive to opioid therapy in Canada, the United Kingdom, and Spain.
The first indication of the role of the ECS in diabetic neuropathy came from a murine diabetes model. A dual CB1/CB2 receptor agonist inhibited capsaicininduced calcitonin gene–related peptide release, a measure of sensory neuron function, which was prevented by a CB1 antagonist. AEA also inhibited capsaicininduced calcitonin gene–related peptide release in a non-CB1/CB2 receptor– dependent fashion, which was interestingly lacking in diabetic mice. Mechanical allodynia in diabetic rats can also be attenuated by treatment with a nonselective cannabinoid agonist. A highly significant finding was that both CB1 and CB2 agonists demonstrated antinociceptive effects in mice with streptozotocininduced diabetes, and there were no pronociceptive effects for either CB1 or CB2 antagonists. Even more promising is (in terms of developing and using CB1 antagonists in the treatment of primary diabetes and diabetic complications) that subchronic CB1 receptor antagonism has been shown to evoke a κ-opiate– dependent analgesia by increasing the transcription of genes encoding the opioid system in the spinal cord.
In summary, CB1 receptor antagonism appears to be a viable option for halting the progression of diabetic neuropathy and may provide some analgesic effects through a κ-opiate–dependent pathway. The natural cannabinoid CBD offers a further possible therapeutic advantage because it was able to attenuate the development of neuropathic pain. This effect was associated with the restriction in the elevations of microglial density in the spinal cord and of phosphorylated p38-MAPK. The first clinical trial with Sativex has already been conducted in patients with painful diabetic neuropathy. Although the trial failed to show any advantage compared with placebo treatment, further analysis is needed because several confounding factors were present.
What is Diabetes?
Diabetes is a disease that occurs when your blood glucose, also called blood sugar, is too high. Blood glucose is your main source of energy and comes from the food you eat. Insulin, a hormone made by the pancreas, helps glucose from food get into your cells to be used for energy. Sometimes your body doesn’t make enough—or any—insulin or doesn’t use insulin well. Glucose then stays in your blood and doesn’t reach your cells.
Over time, having too much glucose in your blood can cause health problems. Although diabetes has no cure, you can take steps to manage your diabetes and stay healthy.
What are the different types of diabetes?
The most common types of diabetes are type 1, type 2, and gestational diabetes.
Type 1 diabetes
If you have type 1 diabetes, your body does not make insulin. Your immune system attacks and destroys the cells in your pancreas that make insulin. Type 1 diabetes is usually diagnosed in children and young adults, although it can appear at any age. People with type 1 diabetes need to take insulin every day to stay alive.
If you have type 2 diabetes, your body does not make or use insulin well. You can develop type 2 diabetes at any age, even during childhood. However, this type of diabetes occurs most often in middle-aged and older people. Type 2 is the most common type of diabetes.
Gestational diabetesdevelops in some women when they are pregnant. Most of the time, this type of diabetes goes away after the baby is born. However, if you’ve had gestational diabetes, you have a greater chance of developing type 2 diabetes later in life. Sometimes diabetes diagnosed during pregnancy is actually type 2 diabetes.
Other types of diabetes
Symptoms & Causes of Diabetes
What are the symptoms of diabetes?
- increased thirst and urination
- increased hunger
- blurred vision
- numbness or tingling in the feet or hands
- sores that do not heal
- unexplained weight loss
Symptoms of type 1 diabetes can start quickly, in a matter of weeks. Symptoms of type 2 diabetes often develop slowly—over the course of several years—and can be so mild that you might not even notice them. Many people with type 2 diabetes have no symptoms. Some people do not find out they have the disease until they have diabetes-related health problems, such as blurred vision or heart trouble.
What causes type 1 diabetes?
Type 1 diabetes occurs when your immune system, the body’s system for fighting infection, attacks and destroys the insulin-producing beta cells of the pancreas. Scientists think type 1 diabetes is caused by genesand environmental factors, such as viruses, that might trigger the disease. Studies such as TrialNetare working to pinpoint causes of type 1 diabetes and possible ways to prevent or slow the disease.
What causes type 2 diabetes?
Type 2 diabetes—the most common form of diabetes—is caused by several factors, including lifestyle factors and genes.
Overweight, obesity, and physical inactivity
You are more likely to develop type 2 diabetes if you are not physically active and are overweight or obese. Extra weight sometimes causes insulin resistance and is common in people with type 2 diabetes. The location of body fat also makes a difference. Extra belly fat is linked to insulin resistance, type 2 diabetes, and heart and blood vessel disease.
Type 2 diabetes usually begins with insulin resistance, a condition in which muscle, liver, and fat cells do not use insulin well. As a result, your body needs more insulin to help glucoseenter cells. At first, the pancreas makes more insulin to keep up with the added demand. Over time, the pancreas can’t make enough insulin, and blood glucose levels rise.
What health problems can people with diabetes develop?
Over time, high blood glucose leads to problems such as
- heart disease
- kidney disease
- eye problems
- dental disease
- nerve damage
- foot problem
Articles on Medical Marijuana, Cannabis Hemp Oil and Cannabidiol (CBD) to treat Diabetes
- How do I find the right dosage of CBD for diabetes-related symptoms?
- What is CBD and how does it work?
- What is the endocannabinoid system and why it matters to your health?
Research Studies on the effects of CBD oil to treat Diabetes:
- The impact of marijuana use on glucose, insulin, and insulin resistance among US adults
- CBDattenuates cardiac dysfunction, oxidative stress, fibrosis, and inflammatory and cell death signaling pathways in diabetic cardiomyopathy
- CBDlowers incidence of diabetes in non-obese diabetic mice
- Neuroprotective and blood-retinal barrier-preserving effects of CBDin experimental diabetes
- Cannabidiol arrests onset of autoimmune diabetes in NODmice
- Diabetic retinopathy: Role of inflammation and potential therapies for anti-inflammation
- Cannabinoids alter endothelial function in the Zucker rat model of type 2 diabetes
- The endocannabinoid system in obesity and type 2 diabetes
- Cannabinoids and endocannabinoids in metabolic disorders with focus on diabetes
- The endocannabinoid system and plant-derived cannabinoids in diabetes and diabetic complications
- Cannabinoid-mediated modulation of neuropathic pain and microglial accumulation in a model of murine type I diabetic peripheral neuropathic pain
- Biochemical and immunohistochemical changes in delta-9-tetrahydrocannabinol-treated type 2 diabetic rats
- Efficacy and Safety of CBDand THC-V on Glycemic and Lipid Parameters in Patients With Type 2 Diabetes
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