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THCV, CBDV, CBD can treat diabetes so says the research

TYPES OF MARIJUANA THAT TREAT DIABETES - 15 CLINICAL STUDIES

THCV, CBDV, CBD can treat diabetes so says the research

A somewhat rare cannabinoid, THC-V was shown in the clinic to lower blood glucose-sugar in both animals and humans. This and other research findings presented here explains how the ingredients of marijuana may benefit those with diabetes, blood sugar issues or weight issues.  

 

A rare form of THC called THCV, found in South African strains. has been shown in the clinic to energise, suppresses appetite and improve the condition of both diabetic animals and humans. Test groups of diabetics also benefited by Cannabidiol-CBD and THC-V in combination to protect from insulin high-blood sugar damage to cells, to the lowering or food cravings and overall balance behavior that complicates and worsens diabetic conditions.

In diabetes, inflammation and prostaglandins play a causative role. Cannabinoids, THC, CBD and THCV may normalize the production and action of prostaglandins, which are all important in inflammation and healing, among other important processes.  Prostaglandins are powerful locally acting vasodilators - blood vessels dialators that inhibit the aggregation - clotting - of blood platelets.  Prostaglandins are synthesized in the walls of blood vessels and also regulate the contraction of smooth muscle tissue.  The normalizing of prostaglandin function by phyto-cannabinoids may explain why it works to alleviate so many conditions.  

 

ARTICLES FROM 2017 - DIABETES AND CANNABIS

 

*SKINNY MARIJUANA STRAINS & WEIGHT LOSS  THC-V strains that suppress appetite and balances blood sugar levels,... little known strains of marijuana that, dials down overactive "appetite receptors" by tapping into a natural endocannabinoid system that regulates many bodily functions.

*BONUS SIDES EFFECTS OF Cannabidiol  In dramatic contrast to most drugs, CBD has many side effects, but they are mostly good, like reducing craving for drugs, food, cigarettes, while it balances the body in more ways than previously thought possible.

*Diabetes M. - Medical Cannabis Research Papers Worldwide - 2000 to 2017

*EVEN MORE EFFECTIVE THAN CBD? - CBD-V is under intense investigation in Epilepsy, Parkinson's, Multiple Sclerosis ,seizure, spasm and tremor

 

 

DEEP RESEARCH - MARIJUANA AND DIABETES

*A multicentre, open-label, follow-on scientific, medical inquiry to take a look at the long-term maintenance of effect, tolerance and safety of d9THC/CBD oromucosal (tincture under tongue)  spray in the management of neuropathic chronic-pain.

*Peripheral neuropathic pain -PNP  poses a notable clinical challenge. The long-term efficacy of d9THC:CBD oromucosal (tincture under tongue)  spray was investigated in this 38-week open-label extension scientific medical inquiry. In total, 380 subjects with PNP often comes  with diabetes or allodynia entered this medical inquiry from two parent randomised, controlled trials. Patients received THC/CBD spray for a further 38 weeks in addition to their current analgesic therapy.

*Neuropathic chronic-pain severity was the primary effectiveness measure using a pain 0-10 numerical rating scale - NRS. Additional effectiveness, safety and tolerability outcomes were also investigated. In total, two hundred and thirty four subjects completed the medical inquiry - sixty two  percent. The chronic-pain NRS showed a lower in score over time in subjects from a mean of 6.9 points

*The ratio of subjects who reported at least a clinically relevant thirty percent improvement in chronic-pain continued to increase with time - up to nine months; at least half of all subjects reported a thirty percent improvement at all time points. Improvements were observed for all secondary effectiveness outcomes, including sleep quality 0-10 NRS scores, neuropathic chronic-pain scale scores, subject global impression of change and EQ-5D questionnaire scores. THC/CBD spray was well tolerated for the scientific medical inquiry duration and subjects did not seek to increase their dose with time, with no new safety concerns arising from long-term use.

*In this previously difficult to manage patient population, THC/CBD spray was beneficial for the majority of subjects with PNP often comes  with diabetes or allodynia.

 

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*Cannabidiol improves vasorelaxation in Zucker diabetic fatty rodents through cyclooxygenase activation.

 *Cannabidiol - CBD lowers insulitis (kills insulin creating cells), chronic inflammation, neuropathic chronic-pain, and myocardial dysfunction in preclinical models of diabetes. We recently showed that Cannabidiol-CBD also improves vasorelaxation in the Zucker diabetic fatty -ZDF rat, and the objective of the present scientific medical inquiry was to establish the biological workings underlying this effect.

*Femoral blood vessels from ZDF rodents and ZDF lean controls were isolated, mounted on a myograph, and incubated with Cannabidiol-CBD -10  micromolar or vehicle for two hours. Subsequent vasorelaxant responses were measured in combination with various interventions. Prostaglandin metabolites were detected using enzyme immunoassay.

*Direct effects of Cannabidiol-CBD on cyclooxygenase - COX (inflammation) enzyme activity were measured by oxygraph assay. Cannabidiol-CBD enhanced the maximum vasorelaxation to acetylcholine -ACh in femoral blood vessels from ZDF lean rodents and especially ZDF rodents. In ZDF blood vessels, this enhancement persisted after cannabinoid receptor - CB1 type, endothelial CB, or peroxisome proliferator-activated receptor-γ antagonism but was inhibited by CB2 receptor type antagonism. Cannabidiol-CBD also uncovered a vasorelaxant response to a CB2 agonist (dials up) not previously observed.

*The Cannabidiol-CBD enhanced ACh response was endothelium-, nitric oxide-, and hydrogen peroxide-independent.  However, COX-1/2- and superoxide dismutase-dependent, and Cannabidiol-CBD enhanced the activity of both purified COX-1 and COX-2 (enzymes associated with inflammation). The Cannabidiol-CBD enhanced ACh response in the blood vessels was inhibited by a prostanoid EP4 receptor antagonist (blocker) .

*Prostaglandin E2 metabolite levels were below the limits of detection, but 6-keto prostaglandin F1 α was lowered after Cannabidiol-CBD incubation. These data show that Cannabidiol-CBD exposure enhances the ability of blood vessels to relax via enhanced production of vasodilator COX-1/2-derived products acting on EP4 receptors.

 

*Efficacy and Safety of Cannabidiol and Tetrahydrocannabivarin on Glycemic and Lipid Parameters in Patients With Type two Diabetes: A Randomized, Double-Blind, Placebo-Controlled, Parallel Group Pilot scientific medical inquiry.

*OBJECTIVE: Cannabidiol-CBD and d9THC-V are non psychoactive phytocannabinoids affecting lipid and glucose metabolism in animal models. This scientific medical inquiry set out to study and document the effects of these compounds in subjects with type two diabetes.
*RESEARCH DESIGN AND PROTOCOL: In this randomized, double-blind, placebo-controlled medical inquiry, sixty two patients with noninsulin-treated type two diabetes were randomized to five treatment arms: Cannabidiol- CBD - 100 milligram twice per day, THCV  5 milligram twice per day, 1:1 ratio of CBD and THCV  5 milligram/5 milligram, twice per day, 20:1 ratio of CBD and THCV  100 milligram/5 milligram, twice per day, or matched placebo for 13 weeks.

*The primary end point was a change in HDL-cholesterol concentrations from baseline. Secondary/tertiary endpoints included changes in glycemic control, lipid profile, insulin sensitivity, body weight, liver triglyceride content, adipose tissue distribution, appetite, markers of chronic chronic inflammation, markers of vascular function, gut hormones, circulating endocannabinoids, and adipokine concentrations. Safety and tolerability endpoints were also evaluated.
*DATA AND FINDINGS: Compared with placebo, THCV notably lowered fasting plasma glucose. Compared with baseline , Cannabidiol-CBD lowered resistin and increased glucose-dependent insulinotropic peptide. None of the combination treatments had a notable impact on end points. CBD and THCV were well tolerated.
*TAKE AWAYS: THCV could represent a new therapeutic agent in glycemic control in patients with type two diabetes.


 

*Cannabidiol-CBD dials down cardiac dysfunction, oxidative stress, fibrosis, and inflammatory and cell death signaling pathways in diabetic cardiomyopathy

*OBJECTIVES: In this scientific medical inquiry, we have investigated the effects of Cannabidiol -CBD on myocardial dysfunction, chronic chronic inflammation, oxidative/nitrative stress, cell death, and interrelated signaling pathways, using a mouse model of type I diabetic cardiomyopathy and primary human cardiomyocytes exposed to high glucose.
*HISTORY: Cannabidiol, the most abundant non psychoactive constituent of Cannabis sativa - marijuana plant, exerts anti-inflammatory effects in various condition models and alleviates chronic-pain and spasticity often comes with multiple sclerosis in humans.
*PROTOCOL: Left ventricular function was measured by the pressure-volume system. Oxidative stress, cell death, and fibrosis markers were evaluated by molecular biology/biochemical techniques, electron spin resonance spectroscopy, and flow cytometry.
*DATA AND FINDINGS: Diabetic cardiomyopathy was characterized by declined diastolic and systolic myocardial performance often comes  with increased oxidative-nitrative stress, nuclear factor-κB and mitogen-activated protein kinase activation, enhanced expression of adhesion molecules , tumor necrosis factor-α, markers of fibrosis, enhanced cell death polymerase activity, chromatin fragmentation, and terminal deoxynucleotidyl transferase dUTP nick end labeling, and diminished Akt phosphorylation.

*Remarkably, Cannabidiol-CBD dial down myocardial dysfunction, cardiac fibrosis, oxidative/nitrative stress, chronic inflammation, cell death, and interrelated signaling pathways. Furthermore, Cannabidiol-CBD also dial down the high glucose-induced increased reactive oxygen species generation, nuclear factor-κB activation, and cell death in primary human cardiomyocytes.
*TAKE AWAYS: Collectively, these results coupled with the excellent safety and tolerability profile of Cannabidiol-CBD in humans, strongly suggest that it may have great therapeutic potential in the treatment of diabetic complications, and perhaps other cardiovascular disorders, by attenuating oxidative/nitrative stress, chronic inflammation, cell death and fibrosis.


 

*Cannabidiol-CBD lowers rate of diabetes in nonobese diabetic rodents  

*Cannabinoids are components of the Cannabis sativa -marijuana plant that have been shown capable of suppressing chronic inflammation and various properties of cell-mediated immunity. Cannabidiol -CBD, a non-psychoactive cannabinoid has been previously shown by us to suppress cell-mediated autoimmune joint destruction in an animal model of rheumatoid arthritis.

*We now report that Cannabidiol-CBD treatment notably reduces the rate of diabetes in NOD rodents from an rate of 86 percent in non-treated control rodents to an rate of thirty percent in Cannabidiol-CBD treated rodents. Cannabidiol-CBD treatment also resulted in the notable reduction of plasma levels of the pro-inflammatory cytokines, IFN-gamma and TNF-alpha. Th1-associated cytokine production of in vitro activated T-cells and peritoneal macrophages was also notably reduced in Cannabidiol-CBD treated rodents, whereas production of the Th2-associated cytokines, IL-4 and IL-10, was increased when compared to untreated control rodents.

*Histological examination of the pancreatic islets (insulin producing) of Cannabidiol-CBD treated rodents revealed notably reduced insulitis (kills insulin creating cells). Our results indicate that Cannabidiol-CBD may inhibit and delay destructive insulitis (kills insulin creating cells) and inflammatory Th1-associated cytokine production in NOD rodents, resulting in a lowered rate of diabetes possibly through an immunomodulatory mechanism shifting the immune response from Th1 to Th2 dominance.

 

*Neuroprotective and blood-retinal barrier-preserving effects of Cannabidiol-CBD in experimental diabetes

*Diabetic retinopathy is characterized by blood-retinal barrier -BRB breakdown and neurotoxicity. These pathologies often come with oxidative stress and proinflammatory cytokines, which may operate by activating their downstream target p38 MAP kinase. In the present scientific medical inquiry, the protective effects of a nonpsychotropic cannabinoid.

*Cannabidiol -CBD, were studied and documented in streptozotocin-induced diabetic rodents after 1, 2, or 4 weeks. Retinal cell death was determined by terminal dUTP nick-end labeling assay; BRB function by quantifying extravasation of bovine (pig) serum (blood) albumin-fluorescein; and oxidative stress by assays for lipid peroxidation, dichlorofluorescein fluorescence, and tyrosine nitration.

*Experimental diabetes induced notable increases in oxidative stress, retinal neuronal cell death, and vascular permeability. These effects often come with increased levels of tumor necrosis factor-alpha, vascular endothelial growth factor, and intercellular adhesion molecule-1 and activation of p38 MAP kinase, as assessed by enzyme-linked immunosorbent assay, immunohistochemistry, and/or Western blot. Cannabidiol-CBD treatment notably reduced oxidative stress; lowered the levels of tumor necrosis factor-alpha, vascular endothelial growth factor, and intercellular adhesion molecule-1; and prevented retinal cell death and vascular hyperpermeability in the diabetic retina.

*Consistent with these effects, Cannabidiol-CBD treatment also notably inhibited p38 MAP kinase in the diabetic retina. These results demonstrate that Cannabidiol-CBD treatment reduces neurotoxicity, chronic inflammation, and BRB breakdown in diabetic animals through activities that may involve inhibition of p38 MAP kinase.

 

*Cannabidiol arrests onset of autoimmune diabetes in NOD rodents  

*We have previously reported that Cannabidiol -CBD lowers the rate of diabetes in young non-obese diabetes-prone  NOD female rodents. In the present scientific medical inquiry, we show that administration of Cannabidiol-CBD to 11-14 week old female NOD rodents, which are either in a latent diabetes stage or with initial symptoms of diabetes, ameliorates the manifestations of the condition.

*Diabetes was diagnosed in only 32 percent of the rodents in the Cannabidiol-CBD treated group, compared to 86 percent and 100 percent in the emulsifier-treated and untreated groups, respectively. In addition, the level of the proinflammatory cytokine IL-12 produced by splenocytes was notably reduced, whereas the level of the anti-inflammatory IL-10 was notably elevated following

*Cannabidiol-CBD treatment. Histological examination of the pancreas of Cannabidiol-CBD treated rodents revealed more intact islets (insulin producing) than in the controls. Our data strengthen our previous assumption that Cannabidiol-CBD, known to be safe in man, may possibly be used as a therapeutic agent for treatment of type one diabetes.

 

*Diabetic retinopathy: Role of chronic inflammation and potential therapies for anti-inflammation  

*Diabetic retinopathy is a leading cause of blindness among working-age adults. Despite many years of research, treatment options for diabetic retinopathy remain limited and with adverse effects. Discovery of new molecular entities with adequate clinical activity for diabetic retinopathy remains one of the key research priorities in ophthalmology.

*This review is focuses on the therapeutic effects of Cannabidiol  CBD, a non-psychoactive native cannabinoid, as an emerging and novel therapeutic modality in ophthalmology based on systematic studies in animal models of inflammatory retinal conditions including diabetic retinopathy - a retinal condition often comes  with vascular-neuroinflammation. Special emphasis is placed on novel biological workings which may shed light on the pharmacological activity often comes  with Cannabidiol-CBD preclinically.

*These include a self-defence system against chronic inflammation and neurodegeneration mediated by inhibition of equilibrative nucleoside transporter and activation of adenosine receptor by treatment with Cannabidiol-CBD.

 

*Cannabinoids alter endothelial function in the Zucker rat model of type two diabetes  

*Circulating levels of anandamide are increased in diabetes, and Cannabidiol ameliorates a number of pathologies often comes  diabetes. The aim of the present medical inquiry was to study and document how exposure to anandamide or Cannabidiol might affect endothelial dysfunction often comes with with Zucker Diabetic Fatty rodents.

*Age-matched Zucker Diabetic Fatty and Zucker lean rodents were killed by cervical dislocation and their blood vessels mounted on a myograph at 37 °C. Arteries were incubated for 2 hours with anandamide, Cannabidiol or vehicle, contracted, and cumulative concentration-response curves to acetylcholine were constructed. Anandamide  -10  micromole , 2 hour notably improved the vasorelaxant responses to acetylcholine in aortae and femoral blood vessels from Zucker Diabetic Fatty rodents but not Zucker lean rodents.

*By contrast, anandamide  -1  micromole , 2 hours notably blunted acetylcholine-induced vasorelaxation in third-order mesenteric blood vessels  - G3 from Zucker Diabetic Fatty rodents. Cannabidiol incubation  - 10  micromole, 2 hour improved acetylcholine responses in the blood vessels of Zucker Diabetic Fatty rodents  -aorta and femoral and Zucker lean  -aorta, femoral and G3 mesenteric, and this effect was greater in the Zucker Diabetic Fatty rat.

*These studies suggest that increased circulating endocannabinoids may alter vascular function both positively and negatively in type two diabetes, and that part of the beneficial effect of Cannabidiol in diabetes may be due to improved endothelium-dependent vasorelaxation.

 

*The endocannabinoid system in obesity and type two diabetes  

*Endocannabinoids  -ECs are defined as endogenous agonists of cannabinoid receptors type one and two  - CB1 and CB2. ECs, EC anabolic and catabolic enzymes and cannabinoid receptors constitute the EC signalling system. This system participates in the control of lipid and glucose metabolism at a handful of levels, with the possible endpoint of the accumulation of energy as fat.

*Following unbalanced energy intake, however, the EC system becomes dysregulated, and in most cases overactive, in a handful of organs participating in energy homeostasis, particularly, in intra-abdominal adipose tissue. This dysregulation might contribute to excessive visceral fat accumulation and reduced adiponectin release from this tissue, and to the onset of a handful of cardiometabolic risk factors that are often comes with with obesity and type two diabetes.

*This discovery might form the basis of the mechanism of action of CB1 antagonist (blocker) s/inverse agonists, recently developed by a handful of pharmaceutical companies as adjuvants to lifestyle changes for weight reduction, glycaemic control and dyslipidemia in obese and type two diabetes subjects. It also helps to explain why some of the beneficial actions of these new therapeutics appear to be partly independent from weight loss.

 

*Cannabinoids and endocannabinoids in metabolic disorders with focus on diabetes  

*The cannabinoid receptors for d9THC, and particularly, the CB-1 type receptor, as well as its endogenous ligands, the endocannabinoids anandamide and 2-arachidonoylglycerol, are deeply involved in all properties of the control of energy balance in mammals. While initially it was believed that this endocannabinoid signaling system would only facilitate energy intake, we now know that perhaps even more important functions of endocannabinoids and CB-1 type receptors in this context are to enhance energy storage into the adipose tissue and reduce energy expenditure by influencing both lipid and glucose metabolism.

*Although normally well controlled by hormones and neuropeptides, both central and peripheral properties of endocannabinoid regulation of energy balance may become dysregulated and contribute to obesity, dyslipidemia, and type two diabetes, thus raising the possibility that CB1 type antagonists (blocker) might be used for the treatment of these metabolic disorders.

*On the other hand, evidence is emerging that some nonpsychotropic plant cannabinoids, such as Cannabidiol, may be employed to slowβ-cell damage in type one diabetes. These novel properties of endocannabinoid research are reviewed in this chapter, with emphasis on the biological effects of cannabinoids and endocannabinoid receptor antagonists in diabetes.

 

*The endocannabinoid system and phyto-cannabinoids (plant)in diabetes and diabetic complications  

*Oxidative stress and chronic inflammation play critical roles in the development of diabetes and its complications. Recent studies provided compelling evidence that the newly discovered lipid signaling system may notably influence reactive oxygen species production, chronic inflammation, and subsequent tissue injury, in addition to its well-known metabolic effects and functions.

*The modulation of the activity of this system holds tremendous therapeutic potential in a wide range of conditions, ranging from cancer, chronic-pain, neurodegenerative, and cardiovascular conditions to obesity and metabolic syndrome, diabetes, and diabetic complications. This review focuses on the role of the endocannabinoid system in primary diabetes and its effects on various diabetic complications, such as diabetic cardiovascular dysfunction, nephropathy, retinopathy, and neuropathy, particularly highlighting the biological workings beyond the metabolic consequences of the activation of the endocannabinoid system.

*The therapeutic potential of targeting the endocannabinoid system and certain plant-derived cannabinoids, such as Cannabidiol and d9-tetrahydrocannabivarin, which are devoid of psychotropic effects and possess potent anti-inflammatory and/or antioxidant properties, in diabetes and diabetic complications is also discussed.

 

*Cannabinoid-mediated modulation of neuropathic pain and microglial accumulation in a model of murine type I diabetic peripheral neuropathic chronic-pain  

*HISTORY: Despite the frequency of diabetes mellitus and its relationship to diabetic peripheral neuropathy - DPN and neuropathic pain - NeP, our understanding of underlying biological workings leading to chronic pain in diabetes remains poor. Recent evidence has demonstrated a prominent role of microglial cells in neuropathic pain states. One potential therapeutic option gaining clinical acceptance is the cannabinoids, for which cannabinoid receptors - CB are expressed on neurons and microglia.

*We studied the accumulation and activation of spinal and thalamic microglia in streptozotocin - STZ-diabetic CD1 rodents and the impact of cannabinoid receptor agonism/antagonism during the development of a chronic NeP state. We provided either intranasal or intraperitoneal cannabinoid agonists/antagonists (blocker) at multiple doses both at the initiation of diabetes as well as after the establishment of diabetes and its related NeP state.
*DATA AND FINDINGS:  Tactile allodynia and thermal hypersensitivity were observed over 8 months in diabetic rodents without intervention. Microglial density increases were seen in the dorsal spinal cord and in thalamic nuclei and were accompanied by elevation of phosphorylated p38 MAPK, a marker of microglial activation. When initiated coincidentally with diabetes, moderate-high doses of intranasal Cannabidiol - cannabinoid receptor ii agonist (dials up) and intraperitoneal Cannabidiol dialed down the development of an NeP state, even after their discontinuation and without changes of the diabetic state.

*Cannabidiol was also often comes  with a restriction in elevation of microglial density in the dorsal spinal cord and elevation in phosphorylated p38 MAPK. When initiated in an established DPN NeP state, both CB1 and CB2 agonists demonstrated an antinociceptive effect until their discontinuation. There were no pronociceptive effects demonstrated for either CB1 or CB2 antagonists.
*TAKE AWAYS: The prevention of microglial accumulation and activation in the dorsal spinal cord was often comes  with limited development of a neuropathic chronic-pain state. Cannabinoids demonstrated antinociceptive effects in this mouse model of DPN. These results suggest that such interventions may also benefit humans with DPN, and their early introduction may also modify the development of the NeP state

 

*Biochemical and immunohistochemical changes in delta-9-tetrahydrocannabinol-treated type two diabetic rodents   The regulation of glucose, lipid metabolism and immune reactivities of insulin and glucagon peptides by delta-9-tetrahydrocannabinol -d9THC in diabetes were studied and documented in an experimental rat model. Male Sprague-Dawley rodents were divided into four groups: control, d9THC treated, diabetic, and diabetic+d9THC.

*The type two diabetic rat model was established by intraperitoneal injection of nicotinamide -85 milligram/kilogram body weight followed after 15 minutes by i.p. injection of streptozotocin -STZ at 65 milligram/kilogram of body weight. d9THC and d9THC treated diabetic groups received 3 milligram/kilogram/day of d9THC for seven days. The immunolocalization of insulin and glucagon peptides was investigated in the pancreas using a streptavidin-biotin-peroxidase technique. High density lipoprotein cholesterol - HDL, low density lipoprotein cholesterol - LDL, very low density lipoprotein cholesterol - VLDL, triglycerides -TG, total cholesterol -TC and total protein -TP levels were measured in serum.

*Total islet (insulin producer cells) area percent of insulin immunoreactive cells slightly changed in diabetic+d9THC rodents compared to diabetic animals. However, the area percent of glucagon immunoreactive cells showed a lower in diabetic+d9THC rodents compared to that of diabetic animals alone. Serum (blood) TC, HDL (cholesterol) and LDL (cholesterol) levels of diabetes+d9THC group showed a lower compared to the diabetic group. These results indicate that d9THC may serve a protective role against hyperlipidemia and hyperglycemia in diabetic rodents.

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