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Liver the CBD and

lamoi1
27.07.2018

Content:

  • Liver the CBD and
  • CBD Oil: All the Rage, But Is It Really Safe and Effective?
  • What Is Alcohol Liver Disease (ALD)?
  • Keywords: hepatic encephalopathy, cannabidiol, cognition, liver enzymes, Cannabidiol (CBD) is a non-psychoactive ingredient of Cannabis sativa (Izzo et al. May 7, There also is some indication that CBD might harm the liver. About 10 percent of people taking CBD in studies had increases in liver enzymes. A collection of published research articles and other educational resources about liver disease and CBD (cannabidiol).

    Liver the CBD and

    One of over cannabinoids found within the marijuana plant, CBD is the non-psychoactive compound that has become so sought after in recent years for its incredible health benefits!

    Not only will CBD not get you high, but it also has the ability to provide a powerful treatment for a list of some of the most debilitating health conditions. Across certain states of America, you can obtain medical marijuana for the following conditions:. This list is by no means a reflection on the full extent of CBD , however. As more research is done into this incredible cannabinoid, we are finding even more situations where CBD may just be the best natural option for patients!

    It seems that there are many ways that CBD consumption can benefit the disease, both with the symptoms and also in terms of preventing it all together! We know from years of research, for example, that CBD is a potent anti-inflammatory compound, and it is this property in particular that has provided such a powerful effect on ALD.

    A study was done in that showed how CBD could help reduce inflammation in a chronically damaged liver. The study which was done on mice revealed a significant reduction in inflammation when administered with the non-psychoactive compound. CBD is a well-known anti-oxidant, for instance, and a study published in revealed that it could prevent oxidative stress, which ultimately results in further liver damage as a result of excess alcohol consumption.

    The group was split into three groups, and the results showed as follows:. The results from this study ultimately revealed that those most dependent on alcohol had the most significant protection from cannabis use.

    However, this is certainly not to say that people who abuse alcohol should also abuse cannabis. At the end of the day, the studies simply have provided a great eye-opener into the abilities of CBD and cannabis as a whole for treatment in this area! While marijuana advocates the world over continue to fight the good fight to make cannabis legal across the board, there are still many states that hold incredibly tight laws. As research plows on, though, we live in the hope that this will soon change!

    Leave a Reply Cancel reply. Your email address will not be published. Remember me Lost your password? Leave a Reply Cancel reply Your email address will not be published. What Does Weed Do to You? The hepatotoxicity of TAA is due to the generation of free radicals and oxidative stress Zimmermann et al. However, it is not clear whether TAA affects the brain directly or the liver Albrecht et al.

    Our results indicated that it has a neuroprotective role in HE induced by FHF; CBD was found to restore liver function, normalize 5-HT levels and improve the brain pathology in accordance with normalization of brain function. We also showed that CBD affects both central functions: Therefore, we conclude that it acts both centrally and peripherally. In addition, it has been shown that CBD can cross the blood — brain barrier and act centrally for review see Pertwee, Therefore, its effect may result from a combination of its actions in the liver and the brain.

    However, to elucidate its mechanism of action future experiments are needed to determine the effects of central administration of CBD. Previous work from our laboratory has demonstrated an impaired neurological and motor function 3 days, and impaired cognition 12 days after TAA injection to mice Avraham et al. These results were reproduced in the present study Figures 1—3. In a more recent study from our laboratory, cognitive and motor deficits were observed 21 days after bile duct ligation, a chronic model of liver disease Magen et al.

    The different durations of the development of HE symptoms in the two models apparently result from their different characteristics — an acute versus a chronic model of HE.

    In the latter model, CBD was found to improve cognition and locomotor activity, in accordance with our present data Magen et al. However, in sharp contrast to the findings reported here no evidence for astrogliosis was found in that study data not reported ; in our acute model induced by TAA we observed astrogliosis after 3 days Figure 4C.

    Similar results were reported by Jover et al. In the work of Jover et al. The reason for this may be that in chronic liver disease induced by bile duct ligation, compensation mechanisms are activated, which moderate the brain damage, while in the acute model induced by TAA, no such mechanisms can come into action because of the severity of the liver insult and the short interval of time between the induction of liver damage and the histopathological examination.

    Therefore, it is conceivable that such a mechanism was responsible for the astrogliosis observed in our study, since we found evidence of liver inflammation data not shown.

    As evident from the histopathology results, CBD did not appear to affect the development of TAA-induced necrotic lesions in the liver of mice. However, the levels of liver transaminases in the serum of CBD-treated mice were significantly reduced compared to their untreated counterparts, indicating that this substance contributed to a partial restoration of liver function.

    Recent evidence elucidating the complicated mechanisms involved in the release of hepatocyte cytosolic enzymes such as ALT and AST in the blood may explain the discrepancy between histopathology and serum biochemistry data observed in the present study.

    Indeed, it is now generally accepted that the release of cytosolic enzymes during both the reversible and irreversible phases of hepatocyte injury and therefore their appearance in blood does not necessarily indicate cell death and also that enzyme release during reversible cell damage occurs with an apparent lack of histological evidence of necrosis Solter, The interaction between hyperammonaemia and inflammation as a precipitating factor for HE has been discussed in two recent reviews Shawcross and Jalan, ; Wright and Jalan, Astrogliosis has also been shown to be involved in learning and memory deficits in a mouse model of Alzheimer's disease.

    In this study, astrogliosis was reduced by caloric restriction, which also reversed the cognitive deficits and increased the expression of neurogenesis in related genes Wu et al. Further studies, such as expression analysis of such genes using DNA microarray and evaluation of neurogenesis using BrdU staining, needs to be performed in order to explore the mechanisms through which TAA-induced astrogliosis impairs cognition, and through which CBD acts to improve it.

    Even though astrogliosis was found a week before cognitive function was observed, and it is not definite whether it was long-lasting, this mechanism seems, in our eyes, to account for the cognitive dysfunction, rather than the increase in 5-HT level Figure 5.

    The latter mechanism does not seem to be related to the cognitive dysfunction, even though this increase in 5-HT was reversed by CBD Figure 5 , as 5-HT depletion, not increase, has been shown to cause memory deficits in the eight arm maze Mazer et al. In addition, there is indirect evidence that this increase is related to decreased motor activity, as the nonselective 5-HT receptor antagonist methysergide increased motor activity in TAA-injected rats, while the selective 5-HT 2 receptor antagonist seganserin did not Yurdaydin et al.

    In parallel, motor activity was decreased following TAA injection and increased after CBD treatment, indicating a link between the increase in 5-HT and decrease in motor activity. In our previous studies we showed that cognition is multifactorial and not dependent only on 5-HT levels, and therefore there is no direct correlation between cognition and 5-HT levels.

    The reversal of astrogliosis was probably related to reduced hepatic toxin formation. Neurological and motor functions were improved 2 and 3 days, respectively, after induction of hepatic failure at the same time as a partial reversal of the astrogliosis and reduced levels of ammonia, bilirubin and liver enzymes were noticed. It seems that the behavioural effects of CBD are dramatic and occur within 3 days.

    It appears that this effect of CBD is multifactorial and involves cannabinoid Avraham et al. CBD improves the symptoms of FHF by affecting both brain histopathology and liver function, and thus may serve as therapeutic agent for treating human HE. Teaching Materials; Figs 1—6 as PowerPoint slide. National Center for Biotechnology Information , U. Journal List Br J Pharmacol v. Author information Article notes Copyright and License information Disclaimer.

    This article has been cited by other articles in PMC. Introduction Hepatic encephalopathy HE is a syndrome observed in patients with end-stage liver disease.

    Methods Mice Female Sabra mice 34—36 g , 8 to 10 weeks old, were assigned at random to different groups of 10 mice per cage and were used in all experiments. Induction of hepatic failure We adapted the rat model of acute liver failure induced by TAA to mice Zimmermann et al.

    Administration of CBD CBD was extracted from cannabis resin hashish and purified as previously reported Gaoni and Mechoulam, and was dissolved in a vehicle solution consisting of ethanol, emulphor and saline at a ratio of 1: Assessment of neurological function Neurological function was assessed by a point scale based on reflexes and task performance Chen et al.

    Assessment of activity The activity test was performed 2 days after the induction of hepatic failure. Cognitive function Cognitive function studies were performed 8 days after the induction of hepatic failure. Serum ammonia, liver enzymes and bilirubin levels Serum for alanine transaminase ALT , aspartate transaminase AST , bilirubin and ammonia measurements was obtained on day 3 in glass tubes, centrifuged, and analysed on the day of sampling using a Kone Progress Selective Chemistry Analyzer Kone Instruments, Espoo, Finland.

    Experiment 2 This was identical to experiment 1 on days 1—3, only the mice were not killed on day 3 but were evaluated for cognitive function using the eight-arm maze test, on days 8— Results Neurological score TAA significantly increased the neurological score of mice compared to the control group Figure 1 ; one-way anova: Open in a separate window.

    Activity TAA decreased the activity level of the mice Figure 2 ; anova: Acknowledgments We would like to thank the Israel Science Foundation for their support. Conflict of interest None. Supplementary material Supporting Information: Click here to view. Contrasting effects of thioacetamide-induced liver damage on the brain uptake indices of ornithine, arginine and lysine: Endocannabinoids affect neurological and cognitive function in thioacetamide-induced hepatic encephalopathy in mice.

    Cannabinoids and Capsaicin improve liver function following Thioacetamide — induced acute injury in mice. Prostaglandins Leukot Essent Fatty Acids.

    Capsaicin affects brain function in a model of hepatic encephalopathy associated with fulminant hepatic failure in mice. Inhibition of an equilibrative nucleoside transporter by cannabidiol: Neuroinflammation contributes to hypokinesia in rats with hepatic encephalopathy: An experimental model of closed head injury in mice: Cannabidiol, a nonpsychoactive Cannabis constituent, protects against myocardial ischemic reperfusion injury.

    Thioacetamide-induced liver regeneration involves the expression of cyclooxygenase 2 and nitric oxide synthase 2 in hepatocytes. Pharmacological activity of the cannabinoid receptor agonist, anandamide, a brain constituent. The isolation and structure of deltatetrahydrocannabinol and other neutral cannabinoids from hashish. J Am Chem Soc. Separation-induced body weight loss, impairment in alternation behavior, and autonomic tone: Interaction of oxidative stress, astrocyte swelling and cerebral ammonia toxicity.

    Leptin is required for fibrogenic responses induced by thioacetamide in the murine liver. Administration of 8-hydroxy Di-n-propylamino tetralin in raphe nuclei dorsalis and medianus reduces serotonin synthesis in the rat brain: Brain edema and inflammatory activation in bile duct ligated rats with diet-induced hyperammonemia: Separation as a new animal model for self-induced weight loss.

    Endocannabinoids in liver disease and hepatic encephalopathy. Cannabidiol ameliorates cognitive and motor impairments in mice with bile duct ligation. Cannabidiol ameliorates cognitive and motor impairments in bile-duct ligated mice via 5-HT 1A receptor activation. The nonpsychoactive cannabis constituent cannabidiol is an oral anti-arthritic therapeutic in murine collagen-induced arthritis. Cannabinoid receptors as therapeutic targets in the management of liver diseases.

    Serotonin depletion during synaptogenesis leads to decreased synaptic density and learning deficits in the adult rat: Remembrance of places passed: Emerging strategies for exploiting cannabinoid receptor agonists as medicines.

    Eight arm maze for mice. High prevalence of spontaneous portal-systemic shunts in persistent hepatic encephalopathy: Agonistic properties of cannabidiol at 5-HT 1A receptors.

    Thioacetamide-induced hepatic fibrosis in transforming growth factor beta-1 transgenic mice. Eur J Gastroenterol Hepatol. The pathophysiologic basis of hepatic encephalopathy: Cell Mol Life Sci.

    Systemic inflammatory response exacerbates the neuropsychological effects of induced hyperammonemia in cirrhosis. Clinical pathology approaches to hepatic injury. Studies of the blood ammonia in liver disease. Its diagnostic, prognostic, and therapeutic significance.

    CBD Oil: All the Rage, But Is It Really Safe and Effective?

    May 16, New studies are exploring how cannabis might help the liver . found that CBD is helpful in causing malignant cells found in liver fibrosis to. Jan 22, Here's what you need to know about cannabis and liver disease. In fact, CBD was able to restore normal liver functioning in the mice. MONDAY, May 7, (HealthDay News) -- Cannabidiol (CBD) oil has become the hot new . There also is some indication that CBD might harm the liver.

    What Is Alcohol Liver Disease (ALD)?



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    ffenohak

    May 16, New studies are exploring how cannabis might help the liver . found that CBD is helpful in causing malignant cells found in liver fibrosis to.

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