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AACFS Disappoints

By Jill McLaughlin

    The sixth biannual AACFS Conference was held in Chantilly, VA from January 31-February
2, 2003. Due to a family emergency, I was unable to attend; however, this is a brief overview
from reports done by Dr. Vallings and several others.

    There were under 200 people in attendance. This is very low as at the previous two
conferences (Seattle and Boston), there were around 4-500. Also, there was no patient
conference, and very few patients were in attendance. (The AACFS decided to have patient
meetings in the years that the AACFS does not have their conference. The last meeting was in
Minnesota, and the next patient conference will be in Chicago in Oct 2003.)

    Dr. Hanna (NIH) was unable to attend, but no one knew of any others from HHS in
attendance (other than Dr. William Reeves and a few others from the CDC). The fact that there
were so few HHS people is disturbing as this would indicate that there is little interest in CFS,
either on the research front or the name change effort.

    Dr. Dharam Ablashi is the new President of the AACFS. He specializes in microbiology and
virology and is an internationally recognized herpesvirus expert. He previously worked at the
NCI and co-discovered HHV-6 while working with Dr. Robert Gallo. He has also worked with
animal and human retroviruses including HIV, HTLV-I, and HTLV-II. His background may be a
definite plus in the field, since things have been stagnating.

     A major concern with this conference was the labeling of the topic titles. In many cases, CFS
was replaced by "medically unexplained illnesses," an utterly false and disingenuous
representation which set a rather bad "tone" for the conference. We can certainly explain most, if
not all, of the pathophysiology of ME/CFIDS, called CFS for this report as they referred to the
disease. We can't explain the causes or precise pathogenesis although the NCF funding has
broken into this realm.. On the other hand, we can't do this for MS, Lupus, Parkinson's Disease,
and many other diseases, yet have never seen them referred to as "medically unexplained

    "Medically unexplained illness" has real overtones of the Functional Somatic Syndrome (FSS)
category. It is different in theory from Functional Somatic Syndromes, which are perceived to be
emotionally-based (and, therefore, explained) illnesses. However, on face value many presume
that the lack of medical explanation means psychological. Another problem is that people
think "medically unexplainable" when they read "medically unexplained" (meaning it simply
cannot be as it simply hasn't been). Funny how medical ignorance can masquerade as a virtue.
The reality is that an explanation is possible if we get our scientific act together to do so. But
even at this conference it actually was done - many of the presentations gave sound credible
medical explanations for the illness.

    Dr. Lapp of North Carolina presented a fairly thorough overview of diagnosis, treatment,
management and disability evaluation. Dr. Leonard Jason of DePaul University in Chicago
presented most of the epidemiology and reviewed the problems with the definition. Dr. Akemi
Todoma (Kumamoto University School of Medicine, Japan), reported that 2% of Junior High
School students and 5% of High School students in Japan are disabled by CFS.

    Dr. Reeves discussed the CFS definition and the fact that it is under review. He suggested that
temporary exclusions may include sleep disorders, hypothyroidism, diabetes and morbid obesity.
(This was taken from Dr. Vallings report and she has been quite accurate and thorough in her
summaries over the years.) However, it has been well established that sleep disorders and
hypothyroidism are part of CFS and many people gain considerable weight. In fact, in a study of
symptom prevalence and severity by De Becker et al., 94.8% of 951 patients meeting the Holmes
criteria, and 91.9% of 1,578 patients meeting the Fukuda criteria, reported sleep disturbance with
an average severity of 2.5 and 2.4, respectively, out of 3. When sleep disturbance is such an
integral part of ME/CFS, would excluding it apply to CFS as it has come to be recognized or do
anything to clarify the definition or help to select patients? It also appears that many patients
develop diabetes, at least as the illness progresses. So typically the CDC tends to consider
anything exclusionary other than fatigue. Again, the CDC has been reviewing these ambiguities
of the definition (that they created) and problems with exclusionary and comorbid conditions ad
infinitum, pretty much the same as was presented at the case definition session in Seattle two
years ago, so would not count on any real solutions from the CDC in this area anytime soon.

    From the information we have received, the best presentation was by Dr. Robert Suhadolnik.
He seems to be moving forward in his RNase-L work, which has profound implications for the
pathophysiology of the illness. His main topics were oxidative stress, 2-5A synthetase/RNase-L,
protein kinase pathway, apoptosis, mitochondrial function. These well documented
abnormalities lead to a chain of events which cause problems such as endocrine dysfunction,
reduced glutathione levels, oxidative stress, and mitochondrial dysfunction, accounting for many
of the symptom manifestations.

    Dr. Suhadolnik discovered a close association between the upregulated RNase-L pathway and
the clinical presentation of CFS. These markers can be used with clinical parameters to identify
CFS patients and to identify homogeneous subsets with the population. This would prove useful
in studying and identifying patient groups and in studying treatment methodologies for various
subsets. He also referred to the work of Dr. Martin Pall, who also has a poster presentation on his
NO/peroxynitrate theory, who seems to be gaining credibility. Dr. Snell used exercise testing to show
that oxygen consumption and exercise duration were lowest in patients who had highest elevations of RNase-L.

    Dr. Daniel Peterson and Dr.Benjamin Natelson each gave good presentations on Central
Nervous System (CNS) involvement in CFS. Dr. Peterson discussed the role of the brain, and
described structural and functional abnormalities. Dr. Peterson discovered that a large cohort of
children had evidence of HHV6A (using culture and PCR) in their spinal fluid. He thus
recommended spinal taps for patients who have prominent CNS symptoms. Dr. Natelson
presented evidence of covert encephalopathy in some patients, as demonstrated by MRI and
measurement of ventricular volume. The size of the ventricular volumes positively correlated
with severity of the illness. 44% of CFS patients were found to have abnormal amounts of
protein or wbc's in their spinal fluid, supporting the hypothesis that some patients have an
underlying pathological brain process which can cause their symptoms. 29% of patients with
normal spinal fluid showed signs of depression within a few weeks, while those with CSF
abnormalities did not. CFS patients without comorbid psychological disorders had more
neuropsychological dysfunction than those with psychological dysfunction or controls. Further
studies are needed to investigate correlation between those with CSF abnormalities and
psychological and cognitive status.

    Dr. Julian Stewart demonstrated that POTS, a common autonomic abnormality in CFS, was
related to decreased arterial vasoconstriction in the lower extremities. This means that blood flow
to the lower extremities is low and venous resistance is high, resulting in blood pooling in the
lower extremities on standing. Such patients frequently have acrocyanosis (skin turns blue) upon
prolonged standing.

    Three groups, including the CDC, reported on the utility of gene expression by microarray,
which was able to distinguish CFS patients from healthy controls. The purpose is to compare the
amount of messenger RNA (which in turn produces various proteins or enzymes) within cells
from PWCs and cells from either healthy controls or from people with other disorders, to see
which genes are being transcribed into RNA at higher or lower rates in CFS. There were quite a
number of genes that were being either under or over expressed in CFS. It is known what
proteins some genes code for, but there are also many genes that code for unknown proteins.
This technique may produce some insight into the pathophysiology, i.e. the way the cells are
operating abnormally on the metabolic level in CFS patients. The use of this technique in CFS
research is in its infancy at present and seems premature to draw conclusions right now without
running many more samples and doing more statistical analysis of the results. For example, one
paper reported that the level of expression of the IL-1 (interleukin-1) gene in white blood cells
was elevated in CFS. (This is consistent with the fact that IL-1 is known to upregulate the
RNase-L pathway, which is known to be upregulated in CFS.) However, there are more direct
methods currently available to measure IL-1 and other cytokines, which are more readily
available and easier to perform.

    Dr. John Hay gave a presentation on the status of infectious and immunological hypotheses,
but no one seems to know what if anything he has done in CFS. Dr. Gold presented on "HPA
axis abnormalities are different from depression" (as if we haven't known this for 10 years). He
did also present the biochemical response of PWC's to exercise, which would indicate that CFS
patients do not respond well to stress which is not new to patients.

    There was really very little that was new. There were a few poster presentations on treatment.
A small study by Dr. Jhodoi (Japan) showed some clinical improvement with low dose gamma
globulin. Dr. Brewer (Kansas City, MO) found that patients with documented HHV6 viremia
improved symptomatically and immunologically with the administration of transfer factor.

    There were many presentations and discussions of the same aspects of sleep, exercise, goal
setting, counseling, and CBT that we've all heard over and over.  Trudy Chalder of the UK, a
Wessely colleague, gave a talk on CBT. From reports I've seen, her presentation made very little
scientific sense. While she apparently states that CFS is a physical rather than psychological
illness, she then goes on to present CBT and exercise as the way to overcome
symptoms and thus achieve normality -- which requires little more than sleep management,
keeping regular hours, avoiding naps and a realistic exercise plan - even if it results in worsening
of symptoms. This is absurd and contradictory and, and more to the point, harmful, to patients
who are very ill. To ignore the patient's experience and tell them to ignore their symptoms - not
only if they do not improve but even - especially - if they are worsened, is abusive. She further
claims that patients should concentrate on overcoming symptoms rather than looking for a
cause of symptoms. This presumptive, value-laden, arrogant approach is the ultimate in "blame
the victim" - not only for their symptoms but their inability to overcome them.

    The complexity of CBT studies, variability of the interpretation and application, their varied
inclusion and exclusion criteria, the logistical difficulties in ensuring that they are properly
blinded, the high drop out rates, and the subjective means used for most evaluations, raises
serious doubt as to the validity of any of them.

    Unfortunately, patients for whom these interventions do help can also fit into the broad
definition of CFS, right along with those suffering from a serious neurological illness such as ME
- yet another example of different illness, same name. Even though it has been well established
that CFS is heterogeneous, it has become allowable to generalize these dubious, superficial
conclusions of the effectiveness of CBT and exercise to the entire population, which has gained
far too much credence and acceptance in media articles and by the medical community.

    Compare and contrast even some of the good serious research that was presented here, some
of which has been well documented elsewhere -indicating pathological multisystemic
dysfynction - CNS abnormalities, immune system abnormalities, endocrine dysfunction,
autonomic nervous system disorders, cardiocascular abnormalities. Can anyone consider that
what was just described, which has come to be known as CFS, to be "medically unexplained"
or believe that CBT and exercise will really improve it?

    It is a poor reflection on our health agencies, professional societies, and even some rank and
file clinicians and scientists who, (pardon the expression) should damn well know better, that this
has been allowed to continue all this time. (That said, we should thank the Name Change
Workgroup along those lines, for being the first officially charged body to recognize these
problems and take the steps necessary to rectify the situation. This is why it is important to
support that the proposal by the Name Change Workgroup be accepted and implemented as a
subgroup proposal, which splits off ME from CFS - by name and definition - rather than just
having a name change.)

    The name change session was held at the end, but very few attended. Unfortunately it was
never added to the agenda prior to the conference, and even though the time was listed on the
program that was distributed at the conference, perhaps many had already made travel
arrangements or other plans. There were members of both the Name Change Workgroup as well
as members of the Board of Directors of AACFS but ended up as a general discussion. We would
like to thank Tom Hennessy for attending the name change session and presenting the ME
petition and reinforcing patient's consistent requests for the recognition of myalgic
encephelomyelitis. (The petition can be found at   )
We believe the NCW proposal represents some good, solid potential for progress.

The National CFIDS Foundation * 103 Aletha Rd, Needham Ma 02492 * (781) 449-3535 Fax (781) 449-8606