Hello greetings from California I'm Ronald Davis at Stanford University.
We work extensively on ME/CFS. We've recently published a paper on a biomarker that may be used to diagnose patients, however we are also working on a number of other biomarker techniques which we might find necessary to use in combination to distinguish the patients from other diseases.
We're also working extensively on all the pathways in patients that seem to be disrupted. This effort is to hope to find new treatments that may help the patients. However I think our biggest effort is to try to understand the cause of the disease. If we can understand the cause of the disease we have a chance of curing it.
Our major hypothesis currently is called the metabolic trap. So far we have been unable to show that it's not correct and that's the way you do science. We are continuing to work on this but more of the evidence now is that it is probably correct.
When we are convinced that this is the correct problem at least for most of the patients we will then work on how to get you out of the trap.
So I'm very optimistic that what we're doing as well as researchers all over the world are extensively working on this in major collaborations and I'm hoping that we'll be able to come up with better treatments and hopefully a cure for this disease.
There are a number of people researching the metabolic trap hypothesis but I'm going to talk specifically about Robert Phair's version of it because it's what I understand the best.
ELI5: The basic idea behind a metabolic trap is that your body falls ill in a way that you don't produce enough energy any more, and that lack of energy causes a feedback loop that prevents you from getting better without intervention.
More detail: In Dr Phair's research he's been looking at the IDO2 protein and has found that there is some genetic problem with it in all of the Stanford ME/CFS patients he's looked at. The human body processes tryptophan in a few ways, with the IDO1 and IDO2 pathways being part of the energy metabolism. We almost always rely on IDO1, but when under high stress we may be kicked into a situation where we need IDO2 to do work. If IDO2 is broken in some way, then the body can't process the tryptophan fast enough to get back into the zone where IDO1 works, which causes a build up of tryptophan and a lack of energy, which further pushes the body to a place where IDO2 has to do all the work. It's a negative feedback loop and we get stuck there.
Some of the practical implications of this hypothesis are interesting. It implies that ME/CFS could be very common, because IDO2 gene problems seem common. The only reason that a quarter of the population isn't sick is because it takes a really big trigger to get and stay in a broken state. With modelling he found that being sick for 10 days would take 30 weeks to recover, and being sick for 8 weeks meant no automatic recovery at all. So it fits well with so many of us experiencing an initial infection or stressor.
Also I'm going to reiterate one of the warnings he and Ron Davis have given. Do not try to self experiment on this. There was a wave of deaths associated with tryptophan supplementation back around 1990, so these are tricky pathways to muck around with on your own.
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Transcript: courtesy of ljimbo423 on the forums.
Hello greetings from California I'm Ronald Davis at Stanford University.
We work extensively on ME/CFS. We've recently published a paper on a biomarker that may be used to diagnose patients, however we are also working on a number of other biomarker techniques which we might find necessary to use in combination to distinguish the patients from other diseases.
We're also working extensively on all the pathways in patients that seem to be disrupted. This effort is to hope to find new treatments that may help the patients. However I think our biggest effort is to try to understand the cause of the disease. If we can understand the cause of the disease we have a chance of curing it.
Our major hypothesis currently is called the metabolic trap. So far we have been unable to show that it's not correct and that's the way you do science. We are continuing to work on this but more of the evidence now is that it is probably correct.
When we are convinced that this is the correct problem at least for most of the patients we will then work on how to get you out of the trap.
So I'm very optimistic that what we're doing as well as researchers all over the world are extensively working on this in major collaborations and I'm hoping that we'll be able to come up with better treatments and hopefully a cure for this disease.
Thank you.
Is there an ELI5 for that?
There are a number of people researching the metabolic trap hypothesis but I'm going to talk specifically about Robert Phair's version of it because it's what I understand the best.
ELI5: The basic idea behind a metabolic trap is that your body falls ill in a way that you don't produce enough energy any more, and that lack of energy causes a feedback loop that prevents you from getting better without intervention.
More detail: In Dr Phair's research he's been looking at the IDO2 protein and has found that there is some genetic problem with it in all of the Stanford ME/CFS patients he's looked at. The human body processes tryptophan in a few ways, with the IDO1 and IDO2 pathways being part of the energy metabolism. We almost always rely on IDO1, but when under high stress we may be kicked into a situation where we need IDO2 to do work. If IDO2 is broken in some way, then the body can't process the tryptophan fast enough to get back into the zone where IDO1 works, which causes a build up of tryptophan and a lack of energy, which further pushes the body to a place where IDO2 has to do all the work. It's a negative feedback loop and we get stuck there.
Some of the practical implications of this hypothesis are interesting. It implies that ME/CFS could be very common, because IDO2 gene problems seem common. The only reason that a quarter of the population isn't sick is because it takes a really big trigger to get and stay in a broken state. With modelling he found that being sick for 10 days would take 30 weeks to recover, and being sick for 8 weeks meant no automatic recovery at all. So it fits well with so many of us experiencing an initial infection or stressor.
Also I'm going to reiterate one of the warnings he and Ron Davis have given. Do not try to self experiment on this. There was a wave of deaths associated with tryptophan supplementation back around 1990, so these are tricky pathways to muck around with on your own.
Thanks for taking the time to write a great answer and thinking to reiterate the warning along with it.
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