Seven
genomic
subtypes
of
chronic
fatigue
syndrome/myalgic
encephalomyelitis:
a
detailed
analysis
of gene
networks
and
clinical
phenotypes
J R
Kerr1,2,
B
Burke1,
R
Petty1,
J
Gough1,2,
D
Fear3,
D L
Mattey4,
J S
Axford1,2,
A G
Dalgleish1,
D J
Nutt5
Abstract
Aim:
Chronic fatigue syndrome/myalgic
encephalomyelitis (CFS/ME) is a
multisystem disease, the
pathogenesis of which remains
undetermined. The authors have
recently reported a study of gene
expression that identified
differential expression of 88 human
genes in patients with CFS/ME.
Clustering of quantitative PCR (qPCR)
data from patients with CFS/ME
revealed seven distinct subtypes
with distinct differences in Medical
Outcomes Survey Short Form-36
scores, clinical phenotypes and
severity.
Methods:
In this study, for each CFS/ME
subtype, those genes whose
expression differed significantly
from that of normal blood donors
were identified, and then gene
interactions, disease associations
and molecular and cellular functions
of those gene sets were determined.
Genomic analysis was then related to
clinical data for each CFS/ME
subtype.
Results:
Genomic analysis revealed some
common (neurological, haematological,
cancer) and some distinct (metabolic,
endocrine, cardiovascular,
immunological, inflammatory) disease
associations among the subtypes.
Subtypes 1, 2 and 7 were the most
severe, and subtype 3 was the
mildest. Clinical features of each
subtype were as follows:
subtype 1 (cognitive,
musculoskeletal, sleep, anxiety/depression);
subtype 2 (musculoskeletal, pain,
anxiety/depression);
subtype 3
(mild);
subtype 4 (cognitive);
subtype 5 (musculoskeletal,
gastrointestinal);
subtype 6 (postexertional);
subtype 7 (pain, infectious,
musculoskeletal, sleep, neurological,
gastrointestinal, neurocognitive,
anxiety/depression).
Conclusion:
It was particularly interesting that
in the seven genomically derived
subtypes there were distinct
clinical syndromes, and that those
which were most severe were also
those with anxiety/depression, as
would be expected in a disease with
a biological basis.
cfs-research.org/pdf
CFS Genes Research
Scientists have discovered
that people with chronic fatigue syndrome (CFS)
have certain genes and gene activities that
reduce their body’s ability to deal with
physical and psychological stress.
“It really is the first
credible evidence of a biological basis for
chronic fatigue syndrome,” said Dr. Julie
Gerberding, director of the Center for Disease
Control (CDC) at a press briefing held to
announce the results of the largest-ever
clinical trial focusing on chronic fatigue
syndrome. The research has been published in a
set of 14 articles appearing in the April, 2006
issue of the scientific journal
Pharmacogenomics.
The Project
The $2 million research
project examined 227 people with CFS in Wichita,
Kan. Volunteers spent two full days in the
hospital undergoing detailed clinical
evaluations which included: sleep studies,
cognitive functioning measurements, autonomic
nervous system evaluations, extensive blood work
and genetic testing. The activity levels of
20,000 genes were assessed.
Once the data was
gathered, it was turned over to
multidisciplinary teams of experts in medicine,
molecular biology, epidemiology, genomics,
mathematics, engineering and physics to be
analyzed and interpreted. Dr. William C. Reeves,
principal CFS investigator at the CDC, described
the results as “groundbreaking.”
The Results
At the press briefing, Dr.
Reeves stated, “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…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.”
Dr. Suzanne Vernon, who
oversaw the project along with Dr. Reeves,
added, “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.”
Why Is This Research So
Important?
This study should put to rest
any lingering doubts about the validity of CFS.
It is a very real illness with an identifiable
biologic basis. Besides confirming its validity,
Reeves and Vernon agree that having a biologic
basis for CFS will also help scientists and
researchers identify better ways to diagnose the
illness and develop more effective treatments.
Source: Center for
Disease Control, Press Briefing on Chronic
Fatigue Syndrome, 4/20/06
The VDR Gene
On the patient
forum Phoenix Rising, there’s been discussion recently about
mutations in the Vitamin D Receptor (VDR) gene predicting
patient response to the experimental drug GcMAF. GcMAF
(pronounced G C “MAF”) is believed to work on HIV, cancer and,
now, ME/CFS. These diseases turn off white cells called
macrophages whose job is to ingest pathogens, and GcMAF
presumably turns macrophages back on. (See YouTube video at the
bottom of this post for more information on GcMAF.)
Kenny de
Meirleir
Belgian physician Kenny de
Meirleir has been using GcMAF, coupled with an old antiviral,
the injectable Nexavir (formerly called Kutapressin), on ME/CFS
patients and reports that 80 percent are improving. Derived from
pig liver, Kutapressin was first used as an anti-inflammatory
for skin conditions. In the 1980s, when doctors began using
Kutapressin to treat ME/CFS—the drug is particularly effective
against herpes viruses—it acquired the moniker “mini Ampligen.”
cfscentral gene-pool.
Video
GcMaf explained
|