I posted this a couple of years ago. I'll put it here because they'd just move it anyway.
I was discussing ammonia and a CBS mutation with a Lyme patient and thought this may be relevant to someone.
A CBS mutation isn't the problem with ammonia, it's part of the solution. Sulfur laden protein like cysteine and methionine are the real problem. There are bacteria in our GI tract called Desulfuromonas and they are gram negative sulfur reducing bacteria. They are Proteobacteria and are a separate genera from the other Proteobacteria like Salmonella, E coli, H pylori, Vibrio, etc. When these Proteobacteria levels increase, our Desulfuromonas levels decrease. This decreases your ability to reduce sulfur in the GI tract. Most of the other Proteobacteria are pathogens and many have flagella (41 kDa band). This greatly alters one's immune response because the immune system is directly reducing their levels in the GI tract and has less immune allocation for other bacteria/pathogens. The Proteobacteria are mostly nitrogen fixing bacteria so this increases nitrogen levels which increases ammonia levels. Ammonia is the ultimate feedback loop to inhibit pathogenic growth in the proximal colon. I always say a reduction of animal protein is beneficial long term because it limits nitrogen and sulfur intake which among other things, decreases Protebacteria levels.
An epigenetic shift or CBS mutation just allows for more transsulfuration to occur and more glutathione (antioxidant) production. A problem can occur if/when P-5-P and molybdenum levels decrease because this alters the transulfuration pathway and shunts it towards ammonia production and less glutathione. You increase P-5-P or molybdenum levels, you increase your antioxidant capabilities. But be careful what you wish for, it also can cause more oxidative stress. The oxidative stress load increase is almost always greater than the antioxidant increase.
I was discussing ammonia and a CBS mutation with a Lyme patient and thought this may be relevant to someone.
A CBS mutation isn't the problem with ammonia, it's part of the solution. Sulfur laden protein like cysteine and methionine are the real problem. There are bacteria in our GI tract called Desulfuromonas and they are gram negative sulfur reducing bacteria. They are Proteobacteria and are a separate genera from the other Proteobacteria like Salmonella, E coli, H pylori, Vibrio, etc. When these Proteobacteria levels increase, our Desulfuromonas levels decrease. This decreases your ability to reduce sulfur in the GI tract. Most of the other Proteobacteria are pathogens and many have flagella (41 kDa band). This greatly alters one's immune response because the immune system is directly reducing their levels in the GI tract and has less immune allocation for other bacteria/pathogens. The Proteobacteria are mostly nitrogen fixing bacteria so this increases nitrogen levels which increases ammonia levels. Ammonia is the ultimate feedback loop to inhibit pathogenic growth in the proximal colon. I always say a reduction of animal protein is beneficial long term because it limits nitrogen and sulfur intake which among other things, decreases Protebacteria levels.
An epigenetic shift or CBS mutation just allows for more transsulfuration to occur and more glutathione (antioxidant) production. A problem can occur if/when P-5-P and molybdenum levels decrease because this alters the transulfuration pathway and shunts it towards ammonia production and less glutathione. You increase P-5-P or molybdenum levels, you increase your antioxidant capabilities. But be careful what you wish for, it also can cause more oxidative stress. The oxidative stress load increase is almost always greater than the antioxidant increase.