alex3619
Senior Member
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- Logan, Queensland, Australia
The debate on this issue of NADH, NAD etc is raging in several threads on PR, mostly threads started by Radio, but there are some good points there. Its also a case that the argument so far mostly consists of throwing up reams of possibly relevant information and saying there must be something there. Its a model, not yet shown to be substantially important for most patients, but interesting. There is no doubt some will benefit from the approach though, the question is who, in what doses of what supplements, under what conditions, and what are the long term issues? As always my mantra applies: we need more research.
NAD and alpha lipoic acid seem to be the key players, but other supplements may vary patient by patient. NADH by itself is likely to be toxic, and NAD is rapidly destroyed and needs to be recycled from NADH, so alpha lipoic acid is essential. However there is some concern by some researchers this can mobilize too much mercury, and that mercury can cross the blood brain barrier.
One of the hypotheses that Sarah Myhill put forward in her mitochondrial investigation was as the ATP dwindles we can start cannibalizing the AMP (or ADP?) for energy as an emergency pathway (iirc), but synthesizing more takes a lot of time and the mitochondria will be in crisis until that happens. This is one of her hypotheses about PEM. If ATP is in very short supply after excessive activity then it will set off a chain reaction of consequences.
We know that iodine is needed for thyroid hormone, but proper thyroid functioning also requires selenium and a great many other factors. As nearly always when hormonal issues are involved, there are nutritional factors that should possibly be considered.
On T4 affecting biochemical processes, I have not investigated this. However the body has many enzymes that require cofactors, and their presence or lack can affect various pathways. This is part of how the body creates complex webs of reactions needed for biochemical homeostasis (or chemical balance). If something is out of whack there might not actually be a problem with that thing, but with something else that influences another thing, then another, which then causes the problem with the first thing.
So much of what we see in ME and CFS appear to be secondary or tertiary effects. We need to understand the core mechanisms. We are not there yet. However many different lines of investigation now seem to be merging. Give it a few years and a more complete model may emerge.
NAD and alpha lipoic acid seem to be the key players, but other supplements may vary patient by patient. NADH by itself is likely to be toxic, and NAD is rapidly destroyed and needs to be recycled from NADH, so alpha lipoic acid is essential. However there is some concern by some researchers this can mobilize too much mercury, and that mercury can cross the blood brain barrier.
One of the hypotheses that Sarah Myhill put forward in her mitochondrial investigation was as the ATP dwindles we can start cannibalizing the AMP (or ADP?) for energy as an emergency pathway (iirc), but synthesizing more takes a lot of time and the mitochondria will be in crisis until that happens. This is one of her hypotheses about PEM. If ATP is in very short supply after excessive activity then it will set off a chain reaction of consequences.
We know that iodine is needed for thyroid hormone, but proper thyroid functioning also requires selenium and a great many other factors. As nearly always when hormonal issues are involved, there are nutritional factors that should possibly be considered.
On T4 affecting biochemical processes, I have not investigated this. However the body has many enzymes that require cofactors, and their presence or lack can affect various pathways. This is part of how the body creates complex webs of reactions needed for biochemical homeostasis (or chemical balance). If something is out of whack there might not actually be a problem with that thing, but with something else that influences another thing, then another, which then causes the problem with the first thing.
So much of what we see in ME and CFS appear to be secondary or tertiary effects. We need to understand the core mechanisms. We are not there yet. However many different lines of investigation now seem to be merging. Give it a few years and a more complete model may emerge.
