Dr Jernigan once asked me where the excess ammonia in Lyme patients came from and although I had an answer, it wasn't a good answer. We both knew that. It just didn't account for the volume of ammonia seen in this group of patients. I still feel the ammonia increase is from a combination of places, but I have found a better answer.
My earlier posts about dysbiosis showed where an increase in gram negative anaerobes of the Bacteriodetes phylum could increase ammonia production. This is just part of the ammonia increase. Looking at what can happen, as we treat with antibiotics, or have a bacterial toxin that alters GI bacterial levels, or have an condition that affects GI bacterial nutrient absorption, the levels of certain bacteria change. What we see is an increase in Bacteriodetes (nitrogen fixing meat loving bacteria) and a decrease in Firmicutes (Lactobacillus). Lactobacillus forms spores to keep from being eradicated and that leaves a void in our microbiome. Each phylum of bacteria adds something to help the other phyla. When the Lactobacillus level drops, the hydrogen peroxide it makes decreases and candida increases. Another potential problem arises. With a decrease in the gram positive bacteria Lactobacillus, other gram positive bacteria increase to fill the void. Enter into the equation Enterococcus. Enterococcus is mostly drug resistant and antibiotics often only reduce its competition. At normal levels, enterococcus is not a pathogen but as its numbers increase, it becomes problematic. Enterococcus, a biofilm producer, makes phenylethylamine and those with alcohol sensitivities most likely have issues with it. Without going into too much detail, phenylalanine and phenylethylamine are major players in the games that Lyme patients play. There are over six enzymes that break down phenylethylamine which indicates to me the variability and importance in its breakdown.
A Lactobacillus increase can decrease enterococcus levels but if manganese levels are low, lactobacillus will stay in spore form. When we supplement with manganese, we can increase lactobacillus levels but the enterococcal die off is often too harsh. Low and slow applies here.
How does this apply to ammonia production? If enterococcus levels remain high and lactobacillus can't control them, the body will try to "right the ship" so to speak. Enterococcus grows best at a pH of between 9.0 and 9.5. I've found research that shows an ammonia increase in the small intestine increases pH to 11.0 to 11.5 and reduces enterococcus growth. The body absorbs up to 40 grams of ammonia from the intestines into the portal vein per day. So the body can reduce enterococcus growth for a price. The price is elevated ammonia levels.
Physicians can perform an Indole test. It can show the increased presence of E coli, H flu, some Klebsiella, and Enterococcus. If you don't have ample Vitamin B6 and other cofactors like manganese, you won't show positive on this test even if you have an increase in some of these bacteria.
This is just another piece of our puzzle.