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Hepatic encephalopathy, or HE, is a potentially reversible loss of brain function caused by liver dysfunction. Plant-based pharmaceutical company KannaLife Sciences is currently developing a cannabinoid-based medication that will reduce oxidative stress caused by the disease and thereby assists in both prevention and treatment.
What is Hepatic Encephalopathy (HE)?
Hepatic encephalopathy (HE) is when the liver is unable to remove toxins from the blood, causing a loss of brain function. The liver damage can cause sudden hepatic encephalopathy. In most cases, it occurs in people with chronic liver disease, but in some cases hepatic encephalopathy occurs in people unaware of their liver problems.
The liver is responsible for managing toxic substances that have been ingested. When liver damage occurs, its functionality is compromised and toxins, such as ammonia, can build up in the bloodstream, create oxidative stress and therefore damage to the body’s nervous system.
While the exact cause of HE is not yet known, the disease is brought on by liver disorders, like cirrhosis or hepatitis, and conditions that prevent the blood to properly circulate to the liver. It can be triggered by dehydration, consuming too much protein, electrolyte abnormalities, intestinal bleeding, infections, kidney problems, low oxygen levels, shunt complications, surgery and medications that suppress the central nervous system.
Symptoms of HE can begin slowly and gradually worsen, or they can begin suddenly and immediately be severe. Early symptoms commonly include a musty or sweet-odor breath, sleep pattern changes, thinking changes, mild confusion or fogginess, forgetfulness, personality or mood changes, and poor concentration or judgment. Severe symptoms can include abnormal shaking of the hands or arms, agitation or excitement, disorientation, drowsiness or confusion, severe personality changes, strange behavior, slurred speech and slowed or sluggish movements. It’s also not uncommon for those with HE to become unconscious and unresponsive, or even enter a coma.
Treating HE first requires dealing with any factors that may have caused the condition, such as gastrointestinal bleeding. Life support to facilitate breathing or blood circulation may be needed. Lactulose may be administered to prevent the creation of ammonia and help remove blood from the intestines. Antibiotic medications can also help. Some cases of HE are a short-term problem that can be treated and corrected. Others, however, occur due to a chronic liver disease and will worsen over time. HE is considered a medical emergency and both acute and chronic versions can cause an irreversible coma and death.
KannaLife Science’s Cannabinoid-Based Treatment for HE
Both HE and chronic traumatic encephelopathy (CTE) are oxidative stress-related diseases and research indicates that cannabinoids could be effective for reducing oxidative stress. Cannabinoids demonstrated it also reduces inflammation and neurological impairment, thereby serving as neuroprotectants and facilitating recovery from oxidative stress-related conditions (Lopez-Rodriguez, et al., 2013) (Shohami, et al., 2011).
KannaLife Sciences, Inc. holds an exclusive license with the National Institutes of Health (NIH) for the Commercialization of U.S. Patent #6630507, “Cannabinoids as Antioxidants and Neuroprotectants.” The plant-based pharmaceutical company is actively developing a novel compound based on cannabinoids to treat HE, as well as chronic traumatic encephalopathy (CTE).
Currently, KannaLife Sciences is conducting research and development on sustainable cannabis oil that they believe will eventually serve as a preventative and therapeutic modality for HE.
- Hepatic encephalopathy. (2013, October 13). MedlinePlus. Retrieved from https://www.nlm.nih.gov/medlineplus/ency/article/000302.htm.
- Hepatic Encephalopathy. (2014, June). Cleveland Clinic. Retrieved from http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/hepatology/hepatic-encephalopathy/.
- Lopez-Rodriguez, A.B., Siopi, E., Finn, D.P., Marchand-Leroux, C., Garcia-Segura, L.M., Jafarian-Tehrani, M.H., and Viveros, M.P. (2013). CB1 and CB2 cannabinoid receptor antagonists prevent minocycline-induced neuroprotection following traumatic brain injury in mice. Cerebral Cortex. Retrieved from https://academic.oup.com/cercor/article-lookup/doi/10.1093/cercor/bht202.
- Shohami, E., Cohen-Yeshurun, A., Magid, L., Algali, M., & Mechoulam, R. (2011). Endocannabinoids and traumatic brain injury. British Journal of Pharmacology, 163(7), 1402–1410. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3165950/.