As for Shoemakers HLA-DR genes there is something that doesn't make sense to me.
If the "dreaded genotype" is as severe as he says and it makes the body completely unable to handle mycotoxins then why wouldn't it be producing fatal effects from birth (well before people develop CFIDS) and why are some carriers of this genotype unaffected?
We are all exposed to & absorb mycotoxins continually in our diets, in the air etc so it doesn't really make sense to me although I do find his theories interesting.
Redaxe, I did not have any of Shoemaker's genes tested. My history fits perfectly with Brewer's hypothesis, and since you can directly test for mycotoxins now, my doctor just had me do that. I responded very well to CSM and charcoal, and now am proving the sinus colonization by having so much die-off with the amphoB. The only gene testing he did was for the MTHFR, and I am double homozygous, so we know I don't methylate/detox well.
Shoemaker addressed this in one of his FAQ volumes that I purchased. Basically what he said is that they've seen that there is almost always some antecedent inflammatory illness that changes the expression of the gene. I found this very interesting as I, myself, do not have Lyme and yet had mononucleosis when I was 7 years old. Here's his full answer:
"
How long does exposure to water-damaged buildings have to occur before an
individual develops CIRS?
This question remains one of the most important in this entire field of medicine. We
know that people with HLA susceptibility and CIRS following exposure to water-
damaged buildings have that HLA from birth. What accounts for them developing a
CIRS illness, say in their 20’s but not in their teens and not in their early childhood?
We have attempted to answer this question by following people prospectively with
known susceptible HLA haplotypes but no illness. What we have seen repeatedly is that
an antecedent inflammatory illness, such as mononucleosis, Lyme disease, Coxsackie of
ECHO virus infections, intense inflammatory lung responses and unusual conditions such
as Kawasaki disease invariably occurs. These inflammatory responses predispose an
individual to have a change in antigen presentation such that an HLA that is “doing well,”
protecting an individual against a moldy building, no longer does so.
Please take a look at some of the HLA questions on this list to see further discussion of
HLA structure and antigen presentation.
The bottom line is that it makes sense for people to have an idea of what is their HLA,
what is their baseline C4a and TGF beta-1 are and to monitor MSH levels before and
after significant illnesses if the HLA is mold susceptible. Knowledge here is power. If no
illness develops then having the HLA becomes of no benefit. But if HLA is mold
susceptible and an intense illness occurs, follow MSH. When MSH falls, the HLA is
likely to be “primed,” increasing risk of acquisition of uncontrolled inflammatory illness.
If we have a CIRS in the early stage, and using the above approach makes detection easy,
the illness is far easier to treat early in the course then later."
