Cannabinoid hyperemesis syndrome, explained

It is generally administered at 0.5 to 2 mg intravenously every six hours, as needed 77,78. Additionally, interactions between dopamine and CB1 signaling pathways may contribute to haloperidol’s effectiveness in treating CHS 79. Both CVS and CHS are complex gastrointestinal conditions influenced by several entities, including genetic, environmental, and lifestyle factors. While their genetic underpinnings are still not fully understood, research has suggested potential genetic predispositions for each. The CVS has strong links to mitochondrial dysfunction and neurobiological pathways related to migraine, while CHS is primarily influenced by chronic cannabis use and endocannabinoid system dysfunction.

Recovery stage

Among these cannabinoids, tetrahydrocannabinol (THC) is the most well-known for its ability to induce euphoria, alter perception, and stimulate appetite. Cannabidiol (CBD), another major cannabinoid, has gained attention for its potential therapeutic properties, including anti-inflammatory, anxiolytic, and neuroprotective effects 1. CHS is a condition caused by chronic and repeated cannabis use that leads to severe nausea and vomiting. In one 2018 study, a group of researchers surveyed 2,127 U.S. adults between the ages of 18 and 49 at an emergency department in New York. Of those surveyed, 155 met the criteria of smoking cannabis at least 20 days per month. In two case reports, doctors used lorazepam (Ativan) to manage CHS-related nausea and vomiting.

Table 1. Characteristics of Cannabinoid Hyperemesis Syndrome (CHS) and Cyclic Vomiting Syndrome (CVS).

The recent 2024 American Gastroenterology Association (AGA) clinical practice update recommended combining evidence-based psychosocial interventions and pharmacological treatments for the successful long-term management of CHS 63. If you need help quitting, speak to a healthcare provider or connect with your local addiction treatment services. Understanding the ECS and its effects on the vomiting center of the brain are fundamental to explain the effect of cannabis for this biphasic response 21. The ECS is composed of ligands, receptors, signaling, and enzymes (its regulators and inhibitors) 22. It is difficult to quantify the precise amount of cannabis consumed by cannabinoid hyperemesis syndrome patients who manifest CHS. Reporting is often subjective and qualitative, and there is no metric for how much physiologically active compounds are contained in one joint, cone, bong, etc.

3. Recovery Phase

• In this context a comprehensive history along with initial screening tests should be performed to exclude acute conditions and emergencies (e.g pancreatobiliary disease, intestinal obstruction, pregnancy, etc).
• Finally, there have been anecdotal reports that changing the variety or strain of botanical marijuana can mitigate or even alleviate CHS.
• As recovery progresses, patients are initially given clear liquids and gradually advance to a regular diet as tolerated.
• Among the leading suspects, he says, are lack of sleep and intense stress.

Anandamide and 2-AG possess similar biochemical structures, but each has a distinct pathway for biosynthesis and degradation. Anandamide is synthesized from the precursor N-arachidonoyl phosphatidylethanolamine, while 2-AG is produced from an inositol-1,2-diacylglycerol precursor 8,16,17. The metabolism of anandamide is principally carried out via fatty acid amide hydrolase (FAAH), whereas the major enzyme metabolizing 2-AG is monoacylglycerol lipase (MAGL) 18.

• In a study of the treatment of neuropathic pain with topical capsaicin, the most common adverse effect was a burning sensation upon application, localized erythema, and nonproductive cough 106.
• CHS is also underdiagnosed because people sometimes use marijuana to suppress nausea and vomiting.
• A key focus was on studies that included detailed demographic information such as age, gender, and cannabis usage patterns, as well as data regarding co-morbidities, substance use history, and prior treatments.
• CHS patients generally do not experience significant weight loss, as periods of regular oral intake often compensate for the days of vomiting.

Δ9-tetrahydrocannabinol (THC) has several well-established effects in the central nervous system, such as alteration of psychomotor behavior, impairment in short-term memory, stimulation of appetite, and analgesia 8. Rimonabant, a CB1 antagonist, blocks the appetite stimulating qualities of the cannabinoids in the hypothalamus and has been marketed for the treatment of obesity and metabolic dysfunction 34. In animal models, CB1 receptor activation in the dorsal vagal complex of the brainstem mediates this effect 35,36. Dronabinol (synthetic THC) and nabilone (a CB1 receptor agonist) are two commercially available cannabinoids for the treatment of chemotherapy-induced nausea and vomiting 37.

The Effects of Cannabinoids in the Gastrointestinal System

Lidocaine patches have been proposed as a means to relax the rectus muscle, potentially alleviating abdominal pain during acute flares 91. TRPV1, transient receptor potential cation channel subfamily V member 1; TCA, tricyclic antidepressant; CB, cannabinoid; CTZ, chemoreceptor trigger zone. Drug rehabilitation In patients with CHS, elevated urinary concentrations of the cannabis metabolite carboxy-THC (THC-COOH) exceeding 100 ng/mL are indicative of significant chronic cannabis exposure. The only known treatment to permanently get rid of CHS is to stop cannabis use completely. You may have symptoms and side effects of CHS for a few weeks after quitting cannabis. The pathophysiology of CHS is unclear secondary to a dearth of research dedicated to explicitly investigating its underlying mechanism.