One of the ironies of these new developments in the behavioral and
brain sciences which will end up changing much of our understanding
of medical disease is that a fair amount of the research has appeared
in first class books and journals published by the Cambridge and Oxford
University Presses.
It is also interesting that three of the world's leading scientists
in molecular biology and immunology are now working on the brain -
James Watson - genetics of manic depression
Frances Crick - consciousness
Gerald Edelman - diseases of consciousness
There's a very simple quick and dirty way of determining the extent
of primary brain involvement in various diseases - epidemiological
correlates with ethnicity, socioeconomic status and personality. (The
Ancient Greeks had already figured some of this out in their thinking on
"hysteria".) This is because there are many thousands of genes which
in some way or another directly or indirectly affect the dopamine and
serotonin pathways in the brain, which in turn affect many different
aspects of personality and homeostatic control of the brain and body.
By this measure multiple sclerosis scores very high. This is the
disease
I have looked at most closely, partly because it appears to be very
closely related to Chronic Fatigue Syndrome. But I'm pretty sure that
there is also substantial involvement of several sorts in both Type I
and Type II diabetes.
Cloninger's biosocial model of the brain attributes somatic symptoms
with low basal firing rates of dopamine and serotonin neurons
(high novelty seeking and low harm avoidance.)
Once there is a substantial catalog of genetic polymorphisms growing out
of the Human Genome Project, it will be possible to carry out large
scale
statistical association studies of polymorphism-disease susceptibility.
The associations with individual genes are too small to show up in
conventional linkage studies. I wrote a letter to Science about this
in 1994, and just by another one of those strange coincidences a special
issue appeared later that year on behavioral genetics which specifically
addressed a number of the issues I had raised. (In particular, getting
rid of the OGOD model - one gene, one disease.)
All the evidence (of which there is plenty) for primary brain
involvement
in various diseases is so far indirect, a not entirely satisfactory
state
of affairs. But there's still no direct evidence for many fundamental
aspects of evolution either.
AJR
