Hi, all.
Here's a press release about a newly patented diagnostic for ME/CFS:
http://www.marketwatch.com/story/ri...ents-with-chronic-fatigue-syndrome-2012-04-11
Note that low NADPH has a lot of ramifications: NADPH is normally used to convert folic acid to THF. It is also used to reduce oxidized glutathione. It also supports Phase I detox by the CYP450 enzymes. It does other good things, also.
I think that the reason it is low in ME/CFS is that the main source of it is the pentose phosphate shunt on the glycolysis pathway. When the mitochondria become dysfunctional in ME/CFS, the cells are forced to ramp up glycolysis to try to make up the shortfall in ATP production. This is done primarily by the enzyme phosphofructokinase, which is upregulated by low ATP and high AMP. When this occurs, more of the flow goes through the main glycolysis chain, and less is available to enter the pentose phosphate shunt, so less NADP+ gets reduced to NADPH, and therefore, NADPH goes down.
Best regards,
Rich
Here's a press release about a newly patented diagnostic for ME/CFS:
http://www.marketwatch.com/story/ri...ents-with-chronic-fatigue-syndrome-2012-04-11
Note that low NADPH has a lot of ramifications: NADPH is normally used to convert folic acid to THF. It is also used to reduce oxidized glutathione. It also supports Phase I detox by the CYP450 enzymes. It does other good things, also.
I think that the reason it is low in ME/CFS is that the main source of it is the pentose phosphate shunt on the glycolysis pathway. When the mitochondria become dysfunctional in ME/CFS, the cells are forced to ramp up glycolysis to try to make up the shortfall in ATP production. This is done primarily by the enzyme phosphofructokinase, which is upregulated by low ATP and high AMP. When this occurs, more of the flow goes through the main glycolysis chain, and less is available to enter the pentose phosphate shunt, so less NADP+ gets reduced to NADPH, and therefore, NADPH goes down.
Best regards,
Rich