Glutathione is one of the most important end products of the methylation pathway. It's anti-oxidant capability comes from it's thiol composition containing sulfur molecules. Sulfur is like an electrophillic sponge and binds free radicals and helps the immune system function appropriately. Glutathione is recycled in most people, we Lyme patients aren't so lucky. Over time, constant inflammation takes its toll and our glutathione levels are reduced. Our methylation pathway function and glutathione production decrease because of epigenetic shifts, decreased catalysts and substrates for the methylation pathway, direct metal blockade, and less glutathione recycling because of free radical interaction.
There are other potential causes of glutathione deficiency. Glycine deficiency from a decrease in CGAT or SHMT2 gene function can lead to lower glutathione levels. Many bacteria and pathogens utilize glycine during their life cycle because it is the simplest of the amino acids. This can lead to glycine deficiency. People with CBS mutations don't recycle homocysteine which will decrease glutathione production. These people don't tolerate sulfur or thiol levels very well either so supplementing with glutathione precursors like NAC or cysteine can cause problems. This often occurs because of or in conjunction with a molybdenum deficiency. Molybdenum or other mineral deficiencies often occur because of MTRR mutations and are often seen in individuals with increased pathogens. A couple examples would be how a chronic Candida infection can lower molybdenum levels or increased sulfur intake can lower molybdenum levels. When molybdenum is low, copper levels often increase and concentrate in macrophages to increase oxidative stress on pathogens. It is all interconnected and the root or base of everything appears to be pathogens.
A potential issue is that the production of glutathione requires so many things that we take for granted. Glutathione can not be made without serine, glycine, ATP, or glutamate. Many of these items are created under an optimal pH and patients with chronic inflammation do not have an optimal pH. Glutamate is a good example. The glutamate/GABA cycle is responsible for ammonia homeostasis and the inflammatory conditions we often face are a very acidic environment. This leads to more ammonia production and as the hydrogen ions get used to convert ammonia to ammonium, that leaves less hydrogen ions that can be utilized. This can create a cellular pH gradient IMO. That is another topic.
I don't advocate eating less animal protein because I want to, I do it because all of my research has pointed in that direction.
Post Edited (Georgia Hunter) : 3/30/2016 4:42:19 AM (GMT-6)