Chronic Fatigue Syndrome Research and autism
From:
Rich Van Konynenburg PhD
November 10, 2005
In the eight years during which I have been studying chronic fatigue syndrome,
I have not been as optimistic as I am right now about our prospects for
understanding the main subset of this disorder and learning how to treat it at
its roots. It isn't all "in the bag" yet, but I nevertheless
want to tell you why I feel this way.
Several significant things have come together relatively recently, not
necessarily in the order listed below:
1. The ability to characterize genetic variations (single nucleotide
polymorphisms) in an individual person's genome, and to do it at reasonable
cost.
2. The Swedish twin study in CFS published a few months ago, which gives
more support to the proposition that there is a significant genetic component
in an individual's vulnerability to developing CFS.
3. The study published about a year ago by S. Jill James and colleagues
on autistic children, showing the dysfunction in autism in the methionine (also
called the methylation) cycle and in the glutathione system, showing how these
are tied inextricably together, and also showing the genetic variations that
are at the basis of this disorder.
4. The aggregate of work performed by all those involved in the Defeat
Autism Now! Project of Bernie Rimland's Autism Research Institute, which I
believe, when compared with what we know of chronic fatigue syndrome, shows
that we are dealing with the same fundamental issues in these two disorders,
even though some of the manifestations are different because of the difference
in age and stage of brain development at onset, and because of differences in
the precipitating factors (mercury in the case of most of the autistic
children, a variety of other factors in CFS).
5. The new ATP profile test developed in the past few months by John
McLaren Howard at the Biolab Medical Unit in London, which is showing that
mitochondrial dysfunction is clearly present in CFS, and is helping to pinpoint
its origin.
6. Martin Pall's longstanding theory involving elevated peroxynitrite and
its effects on the mitochondria in CFS.
7. (with all due modesty!) My own elaboration at the most recent AACFS
meeting a year ago of the significant role of glutathione depletion in CFS
(starting with Paul Cheney's pre-1999 work on this), including its origins in
the variety of physical, chemical, biological and psychological stressors known
to be experienced
by PWCs prior to onset, and its effects, one of which is to raise peroxynitrite.
8. Arnold Peckerman et al.'s discovery some two years ago of low cardiac
output in CFS and its correlation with severity of disability.
9. Paul Cheney's grasp during the past year or so of the significance of
the Peckerman et al. work in terms of diastolic cardiomyopathy in late-stage
CFS, which can be explained by elevated peroxynitrite in the cardiac muscle
cells.
10. Sarah Myhill's longstanding determination to get to the root of the
mitochondrial problem in CFS, her collaboration with John Mc Laren Howard to
develop the ATP profile test, and her recent adoption of Stephen Sinatra's
supplemental support for heart failure, including D-ribose.
It is my hope and expectation that the above factors and many more that I have
not mentioned will soon be melded together to form a thoroughgoing explanation
of the etiology and pathogenesis of at least the major subset of CFS, and also
effective treatments aimed as closely as possible at its fundamental origins,
by which I mean supplements selected to compensate for the genetic variations
that are at the root of this disorder, and other treatments that will most
effectively help
PWCs to climb back out of the web of vicious circles and interactions that are
characteristic of CFS.
After learning less than two weeks ago in Long Beach, CA, about the wonderful
recent work of the Defeat Autism Now! project, I believe that I cannot
overemphasize the benefit that the CFS community will receive from what they
have already done, in terms of developing an understanding of the fundamental
dysfunctions in the sulfur metabolism (methionine cycle, transsulfuration
pathway, sulfoxidation, and the glutathione system) and in determining which
supplements will remedy them. If you want to see what I mean about this,
go to the website http://www.DANwebcast.com, register
(free), get your password (right away) and view some of the talks there.
I would especially recommend the talk by Jill James. If you want to know
more, go to the website http://www.autismresearchinstitute.com , click on the
underlined word "publications," and order a copy of the book
"Autism: Effective Biomedical Treatments," by Jon Pangborn and Sidney
Baker. In my opinion, this book is well worth it! s price, and I expect
that most of it will turn out to be directly applicable to CFS.
At this point, I think that the most important gap to be filled in CFS research
is the determination of the precise genetic variations (single nucleotide
polymorphisms) that are significant in predisposing a person to CFS, and
characterization of these genetic variations in a sizeable number of individual
PWCs. I
expect that they will turn out to be very similar to those found in autistic
children, because of the many parallels in biochemistry and symptomatology
between these two cohorts. If this is done soon, and if it comes out the
way I expect that it will, I think the prospects for an early end to the misery
of the main subset of
PWCs are excellent.
Rich Van Konynenburg, Ph.D.