Why does sulfur sensitivity sometimes develop in CFS?

[Guest guest]

Hi, all.

Ever since trying to understand the case of Thorstenson on

this list six years ago, I've been puzzled by the above question.

Since then, we've been hearing from several other PWCs who developed

sensitivity to foods and supplements that contain sulfur, after they

had developed CFS. Before they had CFS, they could tolerate sulfur-

containing foods well, which tells us that there wasn't a very

serious genetic problem involved.

Since I had become convinced that glutathione depletion was involved

in many cases of CFS by the time I encountered 's case, this

seemed like a particularly perverse feature of her case. She

clearly needed more chemically reduced sulfur, but she couldn't

tolerate it. As my kids say, " What's up with that? "

Now that I've been learning more about sulfur metabolism, I have

come up with an idea about what might be at the root of this

problem, and I want to suggest it here.

As you may know, all the sulfur compounds in our bodies, with the

exceptions of sulfate and taurine, must eventually pass through

sulfoxidation to become sulfate, the excess of which is excreted in

the urine. The key step is the reaction that converts sulfite to

sulfate, and this reaction is catalyzed by the enzyme sulfite

oxidase. Sulfite oxidase is one of the three enzymes in the human

body that require molybdenum as a cofactor. (The other two are

xanthine oxidase, which produces uric acid from purines, and

aldehyde oxidase, which is involved in the metabolism of alcohol.)

In order to be in the active form needed by these enzymes,

molybdenum must be incorporated in a substance called

molybdopterin. Here's the key point: The synthesis of

molybdopterin requires two SULFUR atoms, and they have to come from

CYSTEINE! So...there's the vicious circle. Cysteine goes down

(because of a set of genetic factors together with some combination

of physical, chemical, biological and/or psychological/emotional

stressors, which together result in depletion of glutathione, which

produces oxidative stress and puts a block into the methylation

cycle and/or the transsulfuration pathway), and now you can't make

enough molybdopterin, so now you develop a sensitivity to reduced

sulfur containing substances, and you can't tolerate ingesting

cysteine, which is what you really need!

was able to climb out of her vicious circle by taking

supplementary molybdenum and Epsom salts and starting with small

amounts of reduced sulfur compounds and working up as she could

tolerate it. In view of the above, I think I now understand why

that worked. (Now I would suggest adding taurine, also.) It is

basically a pump-priming operation, as we would call it in

engineering. In order to get the pump to pump water, you have to

put some water in it. Fortunately, this is possible to do. It

isn't easy, and it doesn't happen right away, but I think it will

work, at least for many PWCs who have sulfur sensitivity.

Now I have to rethink my longstanding explanation for alcohol

sensitivity in most PWCs. Is it really due to NAD+ depletion in the

liver, producing a combination of hypoglycemia and lactic acidosis,

or is it actually due to buildup of acetaldehyde because of a block

at aldehyde oxidase as a result of inability to make molybdopterin

fast enough? Hmmmmm. Maybe both are involved. The first mechanism

would also involve aldehyde buildup, but for a different reason. I

guess the way to tell would be to run a blood test for glucose and

lactic acid on a PWC who is alcohol-intolerant and has just drunk

some alcohol, but I think there would be some ethical issues

involved with doing that, aside from the difficulty in recruiting a

volunteer! So I guess we'll have to leave that unresolved for now!

Rich