lydiajen at LiveJournal’s CFIDS and M.E. Support Community points to a very interesting CDC press briefing on their recent CFS research. I’ve selected some comprehensible to non-scientist me excerpts [all emphases mine]:

With us today is the director of the CDC, Dr. Julie Gerberding,
and two of our principle chronic fatigue syndrome researchers here at
CDC, Dr. William Reeves and Dr. Suzanne Vernon.
 

DR. GERBERDING:  . . . It really
is the first credible evidence of a biological basis for chronic
fatigue syndrome, that’s come out in 14 articles, simultaneously, in
the journal
Pharmacogenomics. And I think it really reflects a remarkable
confluence
of a number of scientific advances really coming to bear on a problem
of great importance to many people around the United States and one
that’s had controversies in the past…

. . . by identifying specific genes and gene activities associated
with people who have chronic fatigue syndrome, we’re really beginning
to tease out the biological foundations of the manifestation of a
disease in the population, not just at the individual level

DR. REEVES: . . For the first time ever, we have
documented that people with CFS have certain genes that are related to
those parts of brain activity that mediate the stress response.
 

And that they have different gene activity levels, this is outside
which genes are there, that are related to their body’s ability to
adapt to challenges and stresses that occur throughout life, such as
infections, injury, trauma or various adverse events.

Why is it important?  Well, knowing that there is now a biologic
basis for CFS will help us identify better ways to more effectively
diagnose the illness and to come up with more effective treatments,
including cognitive behavioral therapy, medications or a combination of
both….
 

DR. VERNON: I think what we’ve been able to show is that
CFS is very heterogeneous, it’s not just one thing, so there’s probably
not just one diagnostic marker.

We’ve actually demonstrated that there are probably at least four
or
five molecular profiles or groups of people that make up this complex
of CFS, implicating perhaps subtle alterations in the system, that
person’s, that is affected, more or less. . .      
 

QUESTION: So is the idea here then that people who are
susceptible to CFS encounter stresses in their everyday lives, like an
infection, and they are less able to fight off that stress?

DR. REEVES: That is correct, and one of the things we have
not mentioned in this, we’ve mainly focused this talk on the gene
activity. One of the groups approached this through the concept of
allostatic load, which is a physiologic marker, it’s a complex one,
it’s put together of accumulated wear and tear on the body through
continued adaptation to stress.

Those people with chronic fatigue syndrome have significantly
increased allostatic load indices and there is a significantly
increasing risk of that with normal medium level and high-level
allostatic load indices. . .

QUESTION: Thanks. I was curious whether you know anything
about how this particular genetic makeup that you identified as being
associated with the disease occurs.    

Is this something that can occur through, you know, environmental factors?   

DR. REEVES: The genetic makeup–no. Our hypothesis that
the HPA axis is involved in this, which is very clear in this
allostatic load, is a physiologic marker of one’s accumulated
adaptation to stress.
 

The working hypothesis is that the HPA axis and the brain is a
plastic organ which changes its actual physical architecture depending
on stresses that are accumulated over the lifetime.
      

So as people experience stress, and that can be childhood
abuse, it can be childhood infections, it can be multiple injuries–all
the stresses that we experience as these are experienced throughout the
lifespan, to some extent the genetics determine how you are going to react to
them, they determine how your allostatic load may accumulate, and more
importantly, they actually determine your subsequent reaction to stress
applied at a later time during the lifespan. . .

It’s well worth going to read the entire transcript (especially, I
expect, if you have some scientific training) — and there is also an audio file that’s about 45 minutes long.

Just one observation — while it’s certainly true that I’m now highly reactive to stress, before I was ill I could manage high-stress situations without (it seemed) consequence. Could, and did.

Are they just saying we are worn out, like that tired old bear?