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Hepatic encephalopathy is a syndrome seen in patients with severe liver cirrhosis. Our gut has urease-producing bacteria so naturally ammonia is formed. This is absorbed into blood vessels called the hepatic portal veins which then lead to the liver. The role of the liver is to detoxify (among many other things) blood before its onward journey to the rest of the body. With regards to ammonia, the liver converts this back to urea which is excreted via the kidneys in urine.
In liver cirrhosis where the liver has become scarred, which is most commonly due to hepatitis B and C viruses, alcoholic liver disease or non-alcoholic fatty liver disease, the compensatory mechanisms of the liver are overcome, and the liver is unable remove all of the ammonia and other toxins. Over time and with an increasingly failing liver, the blood ammonia levels rise. Ammonia and other toxins cross the blood-brain barrier and cause hepatic encephalopathy. There are a wide range of symptoms from mild confusion, all the way up to coma and death.
Current treatments include antibiotics such as Rifaximin which preferentially targets urease-producing bacteria, as well as the laxative lactulose which increases gut transit speed and this itself reduces ammonia production. Lactulose also alters the gut microbiome by promoting proliferation of bacteria such as Lactobacillus which do not produce a urease enzyme.
We hope we can use our urease-inhibiting Watercress Tonic, as a natural alternative to lower ammonia production in the gut. But we need to investigate the extent to which some/all inhibitors within our Watercress Tonic are absorbed and metabolised (biochemically changed to other non-inhibitory molecules) before reaching the gut.