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CBD deter 6. diseases can neurodegenerative

inflames
25.01.2019

Content:

  • CBD deter 6. diseases can neurodegenerative
  • CBD oil for Parkinson’s Disease
  • Cannabidiol (CBD)
  • Learn about the massive impact CBD can have on the seniors in our lives. 6. CBD can deter neurodegenerative diseases. Because CBD can. PD is among the most common neurodegenerative with CBD for 6 weeks improves PD's patients quality of life (Chagas et al., b). The protective effects of CBD in this model do not seem. In Parkinson's disease patients, CBD is able to attenuate the psychotic symptoms . On day 6, all the reserpine-treated groups displayed diminished locomotor .. et al., ), and neurodegenerative disorders (Fagherazzi et al., ). In summary, we showed here that CBD can attenuate the motor and.

    CBD deter 6. diseases can neurodegenerative

    The mechanisms whereby CBD exerts these beneficial effects are beyond the scope of this work. Previous data from our group show that the effects of reserpine are potentiated by a pro-oxidant compound Calvente et al. In accordance, CBD has been described to present antioxidant, anti-inflammatory, and neuroprotective actions. The antioxidant effects of CBD are seen in rat models of binge alcohol consumption Hamelink et al.

    CBD administration in this model up-regulates the mRNA levels for the antioxidant enzyme copper-zinc superoxide dismutase Garcia-Arencibia et al. Aiming to diminish the amount of animals used in the study, we did not include groups treated with CBD and vehicle. Nonetheless, multiple studies show that CBD does not induce catalepsy or oral dyskinesia per se , even at high doses Zuardi et al. In summary, we showed here that CBD can attenuate the motor and cognitive impairments induced by reserpine.

    FP and VCA wrote the first draft of the manuscript. All authors contributed to and have approved the final manuscript. The other authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

    We thank Maria Vieira Seles for the capable assistance. National Center for Biotechnology Information , U. Journal List Front Pharmacol v. Published online Sep Peres , 1, 2 Raquel Levin , 1, 2 Mayra A. Suiama , 1, 2 Mariana C. Diana , 1, 2 Douglas A. Zuardi , 4, 5 Jaime E. Silva , 2 and Vanessa C. Author information Article notes Copyright and License information Disclaimer. This article was submitted to Neuropharmacology, a section of the journal Frontiers in Pharmacology.

    Received Jul 18; Accepted Sep The use, distribution or reproduction in other forums is permitted, provided the original author s or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice.

    No use, distribution or reproduction is permitted which does not comply with these terms. This article has been cited by other articles in PMC. Abstract Cannabidiol CBD is a non-psychotomimetic compound from Cannabis sativa that presents antipsychotic, anxiolytic, anti-inflammatory, and neuroprotective effects.

    Catalepsy Catalepsy behavior Fernandes et al. Vacuous Chewing Movements Vacuous chewing movements Abilio et al. Plus-Maze Discriminative Avoidance Task Plus-maze discriminative avoidance task allows the simultaneous evaluation of learning, memory, anxiety, and locomotor activity Fernandes et al.

    Open in a separate window. Acknowledgments We thank Maria Vieira Seles for the capable assistance. Effects of melatonin on behavioral dopaminergic supersensitivity. Important role of striatal catalase in aging- and reserpine-induced oral dyskinesia.

    Effects of melatonin on orofacial movements in rats. Psychopharmacology Berl — Cannabidiol exhibits anxiolytic but not antipsychotic property evaluated in the social interaction test. Effects of cannabinoid and vanilloid drugs on positive and negative-like symptoms on an animal model of schizophrenia: Cannabidiol reduces host immune response and prevents cognitive impairments in Wistar rats submitted to pneumococcal meningitis.

    Coexistence of severe parkinsonism and tardive dyskinesia as side effects of neuroleptic therapy. A different marker profile in four neurodegenerative diseases. Ebselen attenuates reserpine-induced orofacial dyskinesia and oxidative stress in rat striatum. The mitochondrial toxin 3-nitropropionic acid aggravates reserpine-induced oral dyskinesia in rats. Cannabidiol increases survival and promotes rescue of cognitive function in a murine model of cerebral malaria. Differential effects of limbic versus striatal dopamine loss on motoric function.

    Effects of reserpine on the plus-maze discriminative avoidance task: Treatment with cannabidiol reverses oxidative stress parameters, cognitive impairment and mortality in rats submitted to sepsis by cecal ligation and puncture. Drug Targets 10 — Open label evaluation of cannabidiol in dystonic movement disorders. Tardive dyskinesia and new antipsychotics. Behavioral and neurochemical effects induced by reserpine in mice. Increased levels of lipid hydroperoxides in the parkinsonian substantia nigra: Antidepressant-like effect of delta9-tetrahydrocannabinol and other cannabinoids isolated from Cannabis sativa L.

    Memory-rescuing effects of cannabidiol in an animal model of cognitive impairment relevant to neurodegenerative disorders. On the coexistence of parkinsonism and tardive dyskinesia.

    Beneficial effects of vitamin C and vitamin E on reserpine-induced oral dyskinesia in rats: Memory impairment induced by low doses of reserpine in rats: Extrapyramidal symptoms and cognitive test performance in patients with schizophrenia.

    There was no significant reduction in the chorea indicators, but no toxicity was observed Consroe et al. The protective effects of CBD and other cannabinoids were also evaluated in a cell culture model of HD, with cells expressing mutated huntingtin. In this model, the induction of huntingtin promotes rapid and extensive cell death Aiken et al.

    These effects seem to be independent of CB 1 activation, since absence of CB 1 receptors has been reported in PC12, the cell line used Molderings et al. The authors suggest that the cannabinoids exert this protective effect by antioxidant mechanisms Aiken et al.

    Regarding studies with animal models, treatment with 3-nitropropionic acid 3-NP , an inhibitor of complex II of the respiratory chain, induces striatal damage—mainly by calpain activation and oxidative injury —, being suggested as relevant to study HD Brouillet et al.

    In accordance with what previously seen with CBD alone, Sativex administration attenuates all the 3-NP induced neurochemical, histological and molecular alterations Sagredo et al. Authors also observed a protective effect of Sativex in reducing the increased expression of iNOS gene induced by malonate Sagredo et al. Malonate administration leads to striatal damage by apoptosis and inflammatory events related to glial activation, being used as an acute model for HD Sagredo et al.

    In a subsequent study, it was observed that the administration of a Sativex-like combination attenuates all the malonate-induced alterations, namely: Although the beneficial effects of Sativex on cell survival are blocked by both CB 1 or CB 2 antagonists, CB 2 receptors seem to have a greater role in the protective effect observed Valdeolivas et al. Treatment with a Sativex-like combination, although not reversing animal's deterioration in rotarod performance, attenuates the elevated clasping behavior, that reflects dystonia Valdeolivas et al.

    More recently, one study described the results of administering cannabinoid drugs to 7 patients 2 of them were treated with Sativex; the others received dronabinol or nabilone, agonists of the cannabinoid receptors: Dystonias are the result of abnormal muscles tone, causing involuntary muscle contraction, and resulting in repetitive movements or abnormal posture Breakefield et al.

    Dystonias can be primary, for instance paroxysmal dyskinesia, or secondary to other conditions or drug use, such as tardive dyskinesia after prolonged treatment with antipsychotic drugs Breakefield et al. However, it should be noted that in two more recent studies with PD patients no worsening of motor function was seen Zuardi et al.

    In accordance, Sandyk et al. The effects of CBD on dystonic movements were also evaluated in pre-clinical studies. In a hamster model of idiopathic paroxysmal dystonia, the higher dose of CBD showed a trend to delay the progression of dystonia Richter and Loscher, In addition, CBD prevents the increase in vacuous chewing movements, i. In addition, treatment with capsazepine and CBD decreases the expression of inflammatory markers, reinforcing the suggestion that the anti-inflammatory actions of CBD may be beneficial to the treatment of dyskinesia Dos-Santos-Pereira et al.

    Moreover, Sativex has been used in the treatment of spasticity in multiple sclerosis. A significant portion of patients does not respond to the conventional anti-spasmodic therapies, and some strategies are invasive, posing risks of complications Flachenecker et al. Recent data point to Sativex as a valid and well-tolerated therapeutic option. Sativex is able to treat the spasms, improving the quality of life, and displays a low incidence of adverse effects Giacoppo et al.

    One important concern is whether CBD is a safe therapeutic strategy. Several preclinical and clinical reports show that CBD does not alter metabolic and physiological parameters, such as glycemia, prolactin levels, blood pressure, and heart rate. In addition, CBD does not modify hematocrit, leukocyte and erythrocyte counts, and blood levels of bilirubin and creatinine in humans. CBD also does not affect urine osmolarity, pH, albumin levels, and leukocyte and erythrocyte counts.

    Moreover, in vitro studies demonstrate that CBD does not alter embryonic development nor the vitality of non-tumor cell lines. The most reported side effects of CBD are tiredness, diarrhea, and changes on appetite. CBD does not seem to induce tolerance. For a broad review of CBD's side effects, see Bergamaschi et al. In the context of movement disorders with concomitant cognitive symptoms, as the ones discussed here, it is crucial to evaluate the potential motor and cognitive side effects of CBD.

    CBD does not induce catalepsy behavior in rodents—being even able to attenuate the effects of several cataleptic agents, as discussed above El-Alfy et al. In accordance, CBD does not induce extrapyramidal effects in humans Leweke et al.

    With respect to cognitive effects, studies report that CBD does not impair cognition, being even able to improve it in some conditions. Pre-clinical data show that CBD restores the deficit in the novel object recognition task in mice treated with MK a protocol used to model schizophrenia Gomes et al. CBD also reverses impaired social recognition in a murine model for Alzheimer's disease Cheng et al. In addition, studies demonstrate that CBD per se does not modify animals' performance in cognitive tasks Osborne et al.

    CBD also improves facial emotion recognition in cannabis users Hindocha et al. It is noteworthy that in some cases, particularly concerning multiple sclerosis and HD clinical studies, CBD per se does not seem to be beneficial. Multiple clinical studies with Sativex have not observed motor or cognitive adverse effects Aragona et al. Nevertheless, one recent open-label study compared multiple sclerosis patients who continued the treatment with Sativex to those who quitted and reported worse balance and decrease in cognitive performance in the continuers Castelli et al.

    Although the studies are scarce, CBD seems to be effective on treating dystonic movements, both primary and secondary. Data regarding HD are scarce, but the results of using Sativex in multiple sclerosis are encouraging. Reviews of the clinical use of this compound in the last decade point to effectiveness in the treatment of spasticity as well as improvement in quality of life, with low incidence of adverse effects Giacoppo et al.

    In respect to PD, although the pre-clinical studies are promising, the few studies with patients failed to detect improvement of the motor symptoms after treatment with CBD. There is a significant difference between the clinical and pre-clinical PD studies. In animals, the beneficial effects are seen when CBD is administered prior to or immediately after the manipulation that induces the PD-like symptoms. In clinical practice, PD is diagnosed subsequently to the emergence of motor symptoms—that appear up to 10 years after the beginning of neurodegeneration and the onset of non-motor symptoms Schrag et al.

    The fact that in clinical trials CBD is administered only after this substantial progression of the disease might explain the conflicting results. Unfortunately, the early diagnosis of PD remains a challenge, posing difficulty to the implementation of preventive strategies.

    The development of diagnosis criteria able to detect PD in early stages would probably expand the CBD's applications in this disease. The molecular mechanisms associated with CBD's improvement of motor disorders are likely multifaceted.

    Moreover, all movement disorders are in some extent linked to oxidative stress and inflammation, and CBD has been reported to display an antioxidant and anti-inflammatory profile, in vitro and in animal models for movement abnormalities.

    The studies investigating the role of CBD on the treatment of movement disorders are few. Notwithstanding, the beneficial neuroprotective profile of CBD added to the preliminary results described here are encouraging.

    All authors listed have made substantial, direct and intellectual contribution to the work, and approved it for publication. The other authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

    National Center for Biotechnology Information , U. Journal List Front Pharmacol v. Published online May Crippa , 2, 3 Regina H.

    Silva , 1 and Vanessa C. Author information Article notes Copyright and License information Disclaimer. This article was submitted to Neuropharmacology, a section of the journal Frontiers in Pharmacology.

    Received Dec 23; Accepted Apr The use, distribution or reproduction in other forums is permitted, provided the original author s and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. This article has been cited by other articles in PMC. Abstract Movement disorders such as Parkinson's disease and dyskinesia are highly debilitating conditions linked to oxidative stress and neurodegeneration.

    CBD's mechanisms of action CBD has several molecular targets, and new ones are currently being uncovered. Open in a separate window. Table 1 Clinical studies investigating the effects of CBD on movement disorders. Treatment with CBD for 4 weeks diminished the psychotic symptoms.

    CBD did not worsen the motor function or induce adverse effects. Patients were in stable doses of anti-PD medication for at least 7 days. Treatment with CBD did not improve the symptoms, but it was not toxic.

    Sativex did not induce severe adverse effects or clinical worsening. However, Sativex did not improve patients' symptoms or promoted molecular changes on biomarkers. THC in approximately 1: Duration of the disease: CBD improved the dystonic symptoms without inducing adverse effects.

    One administration CBD mg. Table 2 Pre-clinical studies investigating the effects of CBD on movement disorders. Model Main findings References Hamster model of idiopathic paroxysmal dystonia The higher dose of CBD shows a trend to delay the progression of dystonia.

    These protective effects seem to be independent of CB 1 receptors. These protective effects do not seem to depend on activation of CB 1 receptors.

    CBD reverses or attenuates the 3-NP-induced alterations. This effect is not blocked by antagonists of CB 1 or CB 2 receptors. In addition, rats treated with malonate display increased expression of the iNOS gene, reversed by the administration of Sativex. Sativex-like combination attenuates all malonate-induced alterations. Sativex effect seems to depend on both CB 1 and CB 2 receptors. CBD's effects on neuritogenesis seem to depend on trkA receptors. Concomitant treatment with CBD prevents the increase in catalepsy behavior, the oral dyskinesia and the memory deficit.

    CBD also reverses the increase in catalepsy behavior induced by haloperidol. Sativex also reversed some of animals' alterations in markers of brain integrity, but not the deterioration in rotarod performance. Huntington's disease HD HD is a fatal progressive neurodegenerative disease characterized by motor dysfunctions, cognitive loss and psychiatric manifestations McColgan and Tabrizi, Other movement disorders Dystonias are the result of abnormal muscles tone, causing involuntary muscle contraction, and resulting in repetitive movements or abnormal posture Breakefield et al.

    Safety and side effects One important concern is whether CBD is a safe therapeutic strategy. Author contributions All authors listed have made substantial, direct and intellectual contribution to the work, and approved it for publication. Structure of cannabidiol, a product isolated from the marihuana extract of Minnesota wild hemp.

    In accordance with a second aspect of the present invention there is provided the use of one or more of the phytocannabinoids: In accordance with a third aspect of the present invention there is provided a method of preventing or treating neurodegenerative diseases or disorders which comprises administering to a subject in need thereof a therapeutically effective amount of one or more of the phytocannabinoids: Neurodegenerative diseases or disorders arise when degeneration of the neural pathway occurs as a result of a specific disease.

    Ischemic diseases arise when degeneration of the neural pathway occurs as a result of lack of oxygen. Brain injury or damage occurs when degeneration of the neural pathway occurs as a result of an injury to the brain itself. Age-related or autoimmune neural degeneration arise when degeneration of the neural pathway occurs as a result of the patient's age or due to an autoimmune disease. Preferably the neurodegenerative disease or disorder is taken from the group: Alzheimer's disease; Parkinson's disease; amyotrophic lateral sclerosis; or Huntington's disease.

    Alternatively the neurodegenerative disease or disorder is taken from the group: Preferably the one or more of the cannabinoids are present in a daily dose effective to prevent or treat neurodegenerative diseases or disorders.

    In a further embodiment of the present invention the one or more of phytocannabinoids are used in combination with one or more other medicinal substances. Preferably the one or more cannabinoids are in the form of a botanical drug substance BDS. It is prepared from botanical raw materials by one or more of the following processes: Thus, in the case of cannabis, BDS derived from cannabis plants do not include highly purified Pharmacopoeial grade cannabinoids.

    In the present invention a BDS is considered to have two components: The actual amount is likely to depend on the starting material used and the method of extraction used.

    Some BDS's will have two or more secondary phytocannabinoids that are present in significant amounts. However not all BDS's will have a secondary phytocannabinoid. Typically the non-phytocannabinoid containing component of the BDS comprises terpenes, sterols, triglycerides, alkanes, squalenes, tocopherols and carotenoids. These compounds may play an important role in the pharmacology of the BDS either alone or in combination with the phytocannabinoid.

    These terpene components can be further defined in a similar manner to the cannabinoids. In a further embodiment of the present invention there is provided a composition comprising one or more of the phytocannabinoids: Embodiments of the invention are further described hereinafter with reference to the accompanying drawings, in which:. The Examples below demonstrate the results obtained using six different which have not previously been demonstrated as having the ability to prevent or treat neurodegenerative diseases or disorders.

    In addition Example 2 also includes data for CBD, a known neuroprotectant, for comparison purposes. The cannabinoids were isolated from cannabis plant material and purified.

    Neuronal cells were differentiated with retinoic acid. Cell viability was determined using 3 4,5-dimethylthiazol-2yl 2,5-diphenyl-2H-tetrazolium bromide MTT assay which is an assay based on the ability of viable cells to convert MTT in formazan salt. Thereafter, the medium was replaced with fresh medium and the cells were treated as above described. For example, the ability of these cannabinoids to decrease the amount of nitrite produced in the glial cells which had undergone treatment to simulate neurodegeneration means that these cannabinoids are effective neuroprotectants.

    Reduction in the level of nitrite produced is a key parameter in the study of many neurological diseases and disorders including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, Huntington's disease, stroke or heart disease Kuiper et al.

    Similarly the ability of CBC and CBDV to prevent neuronal cell death provides credible evidence that these cannabinoids act as neuroprotectants in a model of neurodegeneration. It is clear that an increase in glial cell viability is vitally important in the prevention or treatment of diseases and disorders including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, Huntington's disease, stroke or heart disease.

    After this time, the cytoplasmic fractions were then obtained by centrifugation at g for 10 min and protein concentration in the samples was determined with Bio-Rad assay kit according to the manufacturer's instructions.

    The proteins were transferred onto nitrocellulose membrane according to the manufacturer's instructions Bio-Rad Laboratories, Hercules, Calif. The immune complexes were developed using enhanced chemiluminescence detection reagents Amersham, Italy , according to the manufacturer's instructions and developed by Image-Quant Apparatus GE Healthcare. The protein bands were scanned and densitometrically analyzed with a GS imaging densitometer Bio-Rad Laboratories, Calif.

    ELISA essay was performed on supernatants of cultured cells. The wells were washed three times and then blocked with phosphate-buffered saline PBS containing 0. The standard curve was generated using 0. Following four washes in ELISA buffer, monoclonal antibodies were diluted and added to the wells for 1 h.

    The wells were washed four more times and then incubated with the secondary antibody: The colour reaction was stopped by addition of HCl and optical densities at nm were measured using a microplate reader.

    CBD oil for Parkinson’s Disease

    Alzheimer's disease progresses in patients until they can no longer Cannabidiol (CBD) comes in various forms, including the oil mentioned above. Neurodegenerative diseases, such as Parkinson's, Multiple Dear CBD International Staff, although my nana was given days to live she lasted 6 weeks. Can smoking marijuana prevent Alzheimer's disease? Both CBD and THC are capable of interacting with the brain, however, they do not do. “high” similar to that of D9-THC; however, CBD can have some . He returned to the hospital in 6 months' time, and on Indian hemp passed. 2 months and CBD, relieves spasticity and pain in multiple sclerosis more effectively .. prevent toxic intracellular Ca2+ buildup and reduce gluta- mate release

    Cannabidiol (CBD)



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