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causing accute pain/nausea? stomach CBD oil



  • causing accute pain/nausea? stomach CBD oil
  • Cannabinoid Hyperemesis Syndrome
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  • Nausea. Some people have found that ingesting CBD oil can cause mild stomach discomfort. At low doses, CBD oil causes relaxation and diminished pain or anxiety — both conditions that can contribute to insomnia. Acute CBD administration by the oral, inhalatory or intravenous route did not induce. Cannabis has been shown to be effective at helping to repair the gut when it CBD oil · More CBD · Growing · Companion Planting · Vaporizers is gastritis, a group of symptoms, that are all caused by inflammation of the gut. that are similar to the symptoms of gastritis itself, such as nausea, vomiting. She'd get nauseous and a feel like the room was spinning, which was followed by violent vomiting and severe stomach pains. syndrome characterised by nausea and vomiting after smoking cannabis and was thought to be.

    causing accute pain/nausea? stomach CBD oil

    Upon continuation of his complaints, the patient had presented to our Emergency Unit. At the time of presentation, the patient had epigastric tenderness, but the other systemic findings were normal. His blood tests were as follows: The patient gave no history of a chronic disease, regularly medications used, alcohol consumption, or trauma. He had no history of a recent febrile disease, either. However, one of the family members stated that the patient was regularly taking cannabis powder that he had been preparing for a long time and stopped cannabis when his pains began.

    On the abdominal computed tomography scan performed to determine the etiology and pancreas damage, there were no abnormalities in the pancreas, no peripancreatic fluid Balthazar grade A acute pancreatitis , no gall stones, and no dilation in the biliary system. Following a consultation, the patient was hospitalized in the Clinic of Gastroenterology. The computed tomography showed no penetration of the duodenal ulcer to the pancreas. Cannabis is a plant belonging to the Cannabaceae family.

    The active substances of cannabis are cannabinoids in resin, which are obtained through dried and then powdered leaves of the plant. The major cannabinoid in hashish is tetrahydrocannabinol THC , which is responsible for the pharmacological effect of hashish. Powder hashish is obtained by drying the high THC-containing parts of female cannabis in the shade and then by grinding and sifting the dried parts.

    The mechanism by which THC causes acute pancreatitis has not been fully clarified [ 4 , 6 ]. These two receptors are also present in the pancreatic tissue [ 6 ].

    The receptors affect the gastrointestinal system both positively and negatively [ 7 , 8 ]. By decreasing gastric acid and intestinal secretions, they delay the gastric emptying [ 6 , 9 ]. Studies on mice with cerulein-induced pancreatitis have shown that administration of anandamide, a cannabinoid receptor agonist, to mice increases the severity of pancreatitis, but the reason for this effect is not clearly explained [ 10 , 11 ].

    The effect of cannabinoids on gastric secretions and emptying can be the cause of gastric and duodenal ulcers present in our patient. We achieved this score from the answers of the questions shown below. In conclusion, patients may not give a history of cannabinoid use which is illegal.

    In order to determine the etiology in patients with acute pancreatitis attacks, the use of hashish should also be questioned. Unfortunately, many of these patients relapse upon resuming cannabis [ 6 , 59 , 61 , 62 ]. It has been suggested that many of these patients increase or continue their cannabis use because of their perception that it will have beneficial effects on nausea [ 52 ].

    Patient education should therefore be provided with emphasis on the paradoxical nature of the symptoms of CHS. Furthermore, some authors have reported referring patients to drug rehabilitation programs in an attempt to raise the likelihood of long-term cannabis cessation [ 54 , 71 ]. Studies have demonstrated the efficacy of outpatient treatment options such as cognitive behavioral therapy and motivational enhancement therapy for marijuana dependence [ 73 ].

    There are several shortcomings in our understanding of CHS. There exists no epidemiological data regarding the incidence and prevalence of CHS among chronic marijuana users. The syndrome is likely underreported given its recent recognition [ 74 , 75 ]. With the large prevalence of marijuana use in the world, why does it appear that so few patients develop CHS?

    Certain individuals may have a genetic polymorphisms in the cytochrome P enzymes responsible for the metabolism of the cannabinoids [ 62 , 72 ]. This could result in excessive levels of pro-emetic cannabinoids or emetogenic metabolites. Such genetic variations have yet to be studied in patients diagnosed with CHS and represent an area for future research.

    The mechanism by which cannabis induces hyperemesis is presently unknown. A recent review has explored numerous potential explanations regarding various pharmacokinetic and pharmacodynamic factors of the cannabinoids [ 72 ]. The cannabis plant contains over four hundred different chemicals, with sixty possessing cannabinoid structures [ 76 ]. Additional pharmacological research is needed regarding the pro-emetic effects of additional cannabinoids and their metabolites.

    Another proposed explanation is that in susceptible individuals the pro-emetic effect of cannabis on the gut e. This hypothesis is supported by the demonstration of delayed gastric emptying on gastric emptying scintigraphy in some cases [ 6 , 55 , 62 ]. Further research is required to investigate the gastrointestinal physiology in these patients during both the acute attacks of hyperemesis and between episodes.

    A lack of long-term follow-up is also a major shortcoming in our knowledge of CHS. The majority of reported cases that have provided follow-up included a period of less than one year [ 6 , 52 , 54 , 56 — 60 , 62 , 68 , 71 ]. A greater understanding of the natural course of the syndrome and response to marijuana cessation may be gained with longer lengths of follow-up. Future studies following patients longitudinally for extended periods of time are needed.

    Cannabinoid Hyperemesis Syndrome is a new and under recognized clinical entity. Although its prevalence is unknown, numerous publications have preliminarily established its unique clinical characteristics. CHS should be considered as a plausible diagnosis in the setting of patients with recurrent intractable vomiting and strong history of cannabis abuse.

    Further initiatives are needed to determine this disease prevalence and its other epidemiological characteristics, natural history, and pathophysiology. Additional treatments are needed and efforts to discontinue cannabis abuse are paramount. National Center for Biotechnology Information , U. Curr Drug Abuse Rev. Author manuscript; available in PMC Feb Author information Copyright and License information Disclaimer.

    The publisher's final edited version of this article is available at Curr Drug Abuse Rev. See other articles in PMC that cite the published article. Abstract Coinciding with the increasing rates of cannabis abuse has been the recognition of a new clinical condition known as Cannabinoid Hyperemesis Syndrome.

    Epidemiology and Introduction Cannabis is the most commonly used illicit drug in the United States with over The Endogenous Cannabinoids Endocannabinoids Along with the discovery of the CB 1 and CB 2 receptors has been the identification of endogenous arachidonic acid derivatives that bind to these receptors Figure 1.

    Open in a separate window. The Effects of Cannabinoids in the Gastrointestinal System The gastrointestinal actions of cannabinoids are mediated chiefly by CB 1 receptors Figure 2. Table 1 Epidemiology, clinical presentation and follow up of patients with Hyperemesis Cannabis Syndrome - Longitudinal case series and individual case reports.

    The Cannabis Hyperemesis Syndrome characterized by persistent nausea and vomiting, abdominal pain, and compulsive bathing associated with chronic marijuana use: Cannabinoid Hyperemesis and compulsive bathing: Cannabinoid Hyperemesis relieved by compulsive bathing US 2 - 16 14—18 Daily 17 14—20 8. Table 2 Comparison of cyclic vomiting syndrome in adults and cannabis hyperemesis syndrome. Treatment The treatment of Cannabinoid Hyperemesis Syndrome can be divided into therapy for the hyperemetic phase and the prevention of relapse.

    Conclusion Cannabinoid Hyperemesis Syndrome is a new and under recognized clinical entity. Office of Applied Studies. National Survey on Drug Use and Health. Inter-university Consortium for Political and Social Research [distributor]; Adolescent use and misuse of marijuana. Prevalence of marijuana use disorder in the United States: Cannabis use disorders in the USA: Nonclassical Cannabinoid analgetics inhibit adenylate cyclase: Cannabis and the brain.

    Izzo AA, Camilleri M. Emerging role of cannabinoids in gastrointestinal and liver diseases: Pharmacology of cannabinoid CB1 and CB2 receptors. Pharmacology of cannabinoid receptor ligands. Differential expression of cannabinoid receptors in the human colon: Cannabinoid CB 2 receptors in the gastrointestinal tract: Effects of cannabinoid receptor-2 activation on accelerated gastrointestinal transit in lipopolysaccharide-treated rats.

    Occurrence and biosynthesis of endogenous cannabinoid precursors, N-arachidonoyl phosphatidylethanolamine, in rat brains. Formation and inactivation of endogenous cannabinoid anandamide in central neurons.

    Mechanisms of endocannabinoid inactivation: J Pharmacol Exp Ther. Involvement of CYP2C in the metabolism of cannabinoids by human hepatic microsomes from an old woman. Pharmacokinetics and pharmacodynamics of cannabinoids. Metabolism, disposition, and kinetics of delta-9 tetrahydrocannabinol, in men and women.

    Kreuz DS, Axelrod J. Comparative in vitro metabolism of the cannabinoids. Intravenous injection in man of deltatetrahydro-cannabinol and OH-deltatetrahydrocannabinol. Agonistic properties of Cannabidiol at 5-HT1a receptors.

    Effect of cannabinoids on lithium-induced vomiting in the Suncus murinus house musk shrew Psychopharmacology. A comparative analysis of the potential of cannabinoids and ondansetron to suppress cisplatin-induced emesis in the Suncus murinus house musk shrew Psychopharmacology.

    Evidence that the plant cannabinoid cannabigerol is a highly potent alpha 2-adrenoceptor agonist and moderately potent 5HT1A receptor antagonist. Interaction between non-psychotropic cannabinoids in marihuana: Effect of rimonabant, a cannabinoid-1 receptor blocker, on weight and cardiometabolic risk factors in overweight or obese patients: The potent emetogenic effects of the endocannabinoid, 2-AG 2-arachidonoylglycerol , are blocked by delta 9 -tetrahydrocannabinol and other cannabinoids.

    Cannabinoids inhibit emesis through CB1 receptors in the brainstem of the ferret. Established and potential therapeutic applications of cannabinoids in oncology. The emerging role of the endocannabinoid system in endocrine regulation and energy balance.

    Requirement of cannabinoid receptor type 1 for the basal modulation of hypothalamic-pituitary-adrenal axis function. Cannabinoid receptor agonism inhibits transient lower esophageal sphincter relaxation and reflux in dogs. Cannabinoid 1 CB1 receptors coupled to cholinergic motorneurones inhibit neurogenic circular muscle contractility in the human colon. Effects of a cannabinoid receptor agonist on colonic motor and sensory functions in humans: Cannabinoids and the gastrointestinal tract.

    Delta9-tetrahydrocannabinol inhibits gastric motility in the rat through cannabinoid CB1 receptors. Inhibitory effect of cannabinoid agonists on gastric emptying in the rat. Naunyn Schmiedebergs Arch Pharmacol. Deltatetrahydrocannabinol delays the gastric emptying of solid food in humans: Effect of a cannabinoid agonist on gastrointestinal transit and postprandial satiation in healthy human subjects: Selective lack of tolerance to delayed gastric emptying after daily administration of WIN 55, in the rat.

    Cannabinoid-induced delayed gastric emptying is selectively increased upon intermittent administration in the rat: Treatment of patients with diabetic gastroparesis. Roche E, Foster PN. Singh E, Coyle W. Chang YH, Windish D. Cannabinoid hyperemesis relieved by compulsive bathing. Sannarangappa V, Tan C. Cannabinoid hyperemesis presenting to a New Zealand hospital. Cannabinoid hyperemesis and compulsive bathing: J Am Board Fam Med.

    The cannabis hyperemesis syndrome characterized by persistent nausea and vomiting, abdominal pain, and compulsive bathing associated with chronic marijuana use: AGA Technical review on nausea and vomiting. Idiopathic cyclic nausea and vomiting—a disorder of gastrointestinal motility. Clinical, psychiatric and manometric profile of cyclic vomiting syndrome in adults and response to tricyclic therapy. Efficacy of tricyclic antidepressant therapy in adults with cyclic vomiting syndrome: Porreca F, Ossipov MH.

    Nausea and vomiting side effects with opioid analgesics during treatment of chronic pain: Side effects of opioids during short-term administration: Chepyala P, Olden KW. Cyclic vomiting and compulsive bathing with chronic cannabis abuse.

    A conundrum-from clinical recognition to basic science mechanisms. Marijuana dependence and its treatment. Addict Sci Clin Pract. Confirming the diagnosis of cannabinoid hyperemesis syndrome.

    Cannabis hyperemesis causation questioned. Support Center Support Center. Please review our privacy policy. A report of eight cases in the United States. A case series and paradoxical pathophysiological explanation. Cannabinoid Hyperemesis relieved by compulsive bathing.

    Cannabinoid Hyperemesis Syndrome

    Experts believe that periods of vomiting are caused when there is a loss of While it is theoretically possible, a severe electrolyte abnormality. Upset stomach, diarrhea, and gastrointestinal distress are not typically caused by cannabinoid oil itself, but Many people can experience abdominal cramping and stomach pain, especially when consuming large quantities. characterized by a history of chronic cannabis use followed by a cyclic pattern of nausea, vomiting and colicky abdominal pain. Interestingly.

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    Experts believe that periods of vomiting are caused when there is a loss of While it is theoretically possible, a severe electrolyte abnormality.


    Upset stomach, diarrhea, and gastrointestinal distress are not typically caused by cannabinoid oil itself, but Many people can experience abdominal cramping and stomach pain, especially when consuming large quantities.


    characterized by a history of chronic cannabis use followed by a cyclic pattern of nausea, vomiting and colicky abdominal pain. Interestingly.

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