Hypothesis for multiple chemical sensitivities (MCS)

[Guest guest]

Hi, all.

Here's a hypothesis that may explain at least some cases of MCS.

I think it can explain why Prof. Marty Pall and Dr. Grace Ziem have

had good results with nebulized glutathione and even glutathione

nasal spray. It can also explain why people with MCS are sensitive to

a whole variety of chemicals, and why symptoms appear so rapidly when

they are exposed to chemicals in the gaseous state (volatile

chemicals). Furthermore, I think it can explain why MCS is often

associated with CFS.

Here it is:

In the olfactory epithelium in the nose, there are olfactory neurons

and sustentacular (supporting) cells. The sustentacular cells have

been found to contain CYP450 enzymes at even higher concentration

than the liver. I suspect that their role is to break down chemicals

that are inhaled and that dissolve in the mucus overlaying the

olfactory epithelium, i.e. to perform Phase I detox on these

chemicals, just as this enzyme system does in the liver. It is known

that CYP450 enzymes generate superoxide ions, and that glutathione is

necessary to deal with the resulting hydrogen peroxide from the

superoxide dismutase reactions. If glutathione is depleted in the

sustentacular cells, I think we can expect not only the buildup of

reactive oxygen species, but also the survival of chemicals that

would normally be detoxed and removed, either in their unreacted

states or in their Phase I biotransformed states, which in some cases

are more toxic. This combination could be expected to produce damage

to cell membranes (both sustentacular cells and olfactory neurons),

due to the oxidative stress, and this would allow entry of toxic

chemicals into the olfactory neurons. From there, they have a short

path to the brain, and voila: MCS.

If this model is valid, it would seem that lifting the methylation

cycle block and thus allowing glutathione levels to come up to normal

would correct MCS along with correcting CFS.

I don't think this model explains why a large fraction of the people

with MCS can trace their onset to an acute high exposure to some

volatile chemical. This apparently caused damage that was not

repaired, presumably to a barrier in the olfactory epithelium that

normally prevents chemicals from entering the brain via the olfactory

epithelium. I don't understand this yet.

I think this model can account for the cases of MCS that did not

start with an acute exposure, howeever, and especially cases that are

associated with CFS, which in many cases seems to be associated

biochemically with a methylation cycle block.

I would appreciate comments on whether you think this model fits.

Thanks.

Rich