The immunoreactive theory of selective male affliction.
The idea the general male preponderance of affliction could be caused by
maternal antibodies to male fetuses was first fully articulated by Thomas
Gualtieri and Robert Hicks in 1985.
Stated in simpler language, the
immunoreactive model proposes that some male fetuses come to be considered by
the mother’s body to be undesireable parasites and get attacked and damaged by
the mother’s immune system. There are
three major empirical arguments (sets of facts) in support of this general
model. 1) X-linked disorders are
insufficiently frequent to fully explain the greater male risk for
developmental disorders: many
male-prevalent disorders are known not to be X-linked. 2) Whereas developmental disorders seem to be
more often purely genetic in females,
they seem to depend more on gene-environment interactions in males: complications of pregnancy affect males more
than they do females and expression of the various disorders is more
heterogenous (variable) in males. 3)
Disorders which affect males more frequently clearly tend to be
congenital, their onset is earlier: a uterine influence can justifiably be
suspected.
The immunoreactive model proposes that maleness is a
complication of the basic (female) prototype,
making maleness a riskier trajectory:
more things can go wrong. And as
I articulate in chapter 6, this is
clearly reflected even in mortality rates.
What then is the main immunological argument in support of the model
? Gualtieri and Hicks proposed that
because maternal parity (number of previous offspring) increases risk for
congenital disorders, this suggests a
sort of «memory», or sensitization,
which the immune system is known to be capable of. In other words, the mother could develop a sort of «allergy»
to her own male fetuses. This is a
nearly gratuitous argument. After
all, parity, correlated with aging, are each known to cause a reduction of
endocrinological « competence » of the mother, and both could affect her reproductive
competence in many other non-immunological ways as well. But there are other indirect arguments in
favor of immune mother-son toxicity: 1)
male-to-male and female-to-female tissue grafts are less rejected than
male-to-female or female-to-male; 2) the mother seems to develop an auto immune
disorder (toxemia) more often when the fetus is male; 3) women with repeated miscarriages reject
tissue grafts from their husbands more than from third parties. Maternal immune rejection of the male
fetus should probably not be evoked as a major source of sex segregation of
pathology, and probably has nothing to
do with most pathologies. However, it may well have something to do with a few
specific pathologies. The likeliest
candidate, as far as I can tell, would
be autism. Indeed, the risk for autism seems seems to
depend, more than the other
sex-segregated disorders, upon sex
ratios of the mothers previous offspring.
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