We're only speculating here, but one of my favorite ideas is that the stressors we all talk about as initiating the first crash do so by inhibiting IDO1 for long enough to build up the substrate Trp beyond the critical point. For example, nitric oxide is a potent inhibitor of IDO1. This could be combined with excess Trp in the diet, which some of you know is my hypothesis for how so many athletes and body builders have contracted ME/CFS.
In the Australian Dubbo study of infections, I think it was 9% had ME/CFS symptoms 6 months post-infection. These tended to be those who had the most severe infections, so we're thinking that's the immediate cause of increasing cellular Trp.
Then, of course, after cellular Trp increases beyond the critical point (defined in the paper), you can be cured of the precipitating infection, but you are still in the IDO metabolic trap.
In the Australian Dubbo study of infections, I think it was 9% had ME/CFS symptoms 6 months post-infection. These tended to be those who had the most severe infections, so we're thinking that's the immediate cause of increasing cellular Trp.
Then, of course, after cellular Trp increases beyond the critical point (defined in the paper), you can be cured of the precipitating infection, but you are still in the IDO metabolic trap.