Friday, November 11, 2011

Mount Sinai ME/CFS Research Center Meeting

Mount Sinai ME/CFS Research Center Meeting for patients and doctors
Sunday Nov 20, 2011 from 11am to 2pm

Information and registration available at:

Mount Sinai Medical Center Research Building
lcahn Institute
1425 Madison Avenue (at 98th St)
New York, NY 10029

First floor Seminar room.

New methods in diagnosis and treatment of ME/CFS

Participants include:
Dr. Eric Schadt
Dr. Derek Enlander
Dr. David Bell
Dr. Kenny DeMeirleir
Dr. Judy Mikovits [panel discussion]

Topics will include:

New Horizons in Genomics and Gene research
ME/CFS Treatment using
- Ampligen
- GcMaf, MAF 314, MAF 878
- Retuximab
- CMX 001
- Nexavir lotion and suppositories
- Hepapressing
- Methylation Cycle

There will be a panel discussion afterwards including all participants.


$30 in advance online
$40 at the door

Note: Once you purchase your tickets online, please email us your name or names of the people that are assisting to have your tickets ready the day of the meeting.

Sunday Nov 20, 2011 from 11am to 2pm

After registering please let us know by emailing:

ME/CFS Fundraising Group on ChaseGiving

(Please re-post)

The Chase Community Giving (CCG) Contest is underway, and we are
excited! This is an opportunity for us all to band together and help
some of our small US-based nonprofits to possibly win between
US$25,000 and US$250,000 each! US$3,000,000 will be distributed among
100 charities. In previous Chase CCG Contests, The CFIDS Association
of America, the WPI, and P.A.N.D.O.R.A. have all been winners.

Just to quickly introduce ourselves, we are part of the ME (ME/CFS)
Fundraising Group. This is an international group which was formed to
look for opportunities to help ME/CFS/CFIDS nonprofits raise money and
to support them during fund-raising efforts, as well as networking ME
advocates, group leaders, and organizations to coordinate our efforts.
The current focus is online contests sponsored by large corporations.
We interact through a facebook group (

Faith, from the fundraising group, sent out letters to the eligible
nonprofits asking certain questions to help the ME community
understand the orgs and decide how to vote. Cort Johnson, at Phoenix
Rising, is kindly posting these responses under his article about the
contest (

The fundraising group is composing a list of organizations thought to
be more engaged with the contest, based on the following:
    they have (or are working on producing) a profile at the CCG application,
    we think they are eligible to compete,
    they have (or are producing) a Facebook page (less important),
    they responded to us.

Other than the obvious (eligibility), we are using these criteria as
an indicator that the organization is ready and able to take an active
part in promoting itself to voters and able to complete the
considerable paperwork requirements for CCG (they must do
grant-writing twice).

The ME charities that have expressed interest and submitted the
necessary info to Chase are listed here:
American Association for Chronic Fatigue Syndrome, Inc. (=IACFS/ME)
Chicago, IL
Rocky Mountain CFS/ME and FM Association Denver, CO FB
Cfsknowledgecenter, Inc. Wellington, FL
Wisconsin Chronic Fatigue Syndrome Association, Inc. Sun Prairie, WI
New Jersey Chronic Fatigue Association, Inc. Florham Park, NJ FB

These two groups have expressed interest, but don't yet have their
profiles up on the Chase site:
Massachusetts CFIDS Association, Inc. Quincy, MA
Enterovirus Foundation, Inc. San Francisco, CA FB

Additional groups listed at Chase (but which we don't know to be
engaged with the contest):
CFIDS and Fibromyalgia Self-Help Program Palo Alto, CA
Chronic Fatigue Syndrome Fibromyalgia Org. of Georgia, Inc. Kennesaw,
Connecticut Chronic Fatigue and Immune Dysfunction Syndrome
Association, Inc. Milford, CT
American Fibromyalgia Syndrome Association, Inc. Tucson, AZ (Promotes
research, education, and advocacy for Fibromyalgia and CFS)
CFIDS Emergency Relief Services, Inc. Northport, AL
Chronic Fatigue Syndrome, Fibromyalgia & Chemical Sensitivity
Wilmette, IL
Fibromyalgia Coalition International Mission, KS (Provides support for
persons with Fibromyalgia and CFS)
National Chronic Fatigue Syndrome and Fibromyalgia Association Kansas
City, MO

Smaller groups listed at Chase (but which we don't know to be engaged
with the contest):
Black Hills Chronic Fatigue CFS and Fibromyalgia Syndrome FMS Support
Group Rapid City, SD
Tacoma Gig Harbor CFIDS and Fibromyalgia Support Group Gig Harbor, WA
Central Virginia Chronic Fatigue Syndrome & Fibromyalgia Association,
Inc. Charlottesville, VA
CFSFM Support Group of DFW, Inc. (Dallas Fort Worth) Euless, TX

Doesn't want to or can't take part this year (but listed at Chase):
RESCIND, Inc. Boca Raton, FL
National CFIDS Foundation, Needham, MA
Neuro Immune Disease Alliance, Inc. Agoura Hills, CA (Fund-raises for
Dr. Daniel Peterson's Simmaron Research)
Dr. A. Martin Lerner Chronic Fatigue Syndrome Foundation Beverly
Hills, MI (thought to be ineligible)

As we get status updates on these or any other orgs, we will post them
at the ME (ME/CFS) Fundraising Group ( and at
Phoenix Rising ( ).

Voters should, of course, do their own due diligence to ensure
organizations are eligible (there seems to be some confusion about
this in some cases), are behaving in a sportsmanlike manner, and are
organizations the voters want to support. The application is here: and
the rules are here:

We would like to ask your help in supporting ME/CFS organizations in
the contest. Could you please inform your members about the contest
and ask them and their family members to vote for the best positioned
ME/CFS organizations? We would genuinely appreciate it. And you will
be helping the ME/CFS community!

To vote, you must have a Facebook account, which is easy to set up if
you don't already have one ( Then go to: You must "Like" and
"Allow Access" to Chase Community Giving. That means you will go
unsecure to Chase Community Giving site, so they will know you are an
actual person. (You may need to click the "Like" button several times
throughout the program.) Click on "Chase Giving" at the left side of
the Chase Community Giving page.

To find the charities you wish to vote for, you can do a search for
each charity in the Search Box at the Chase contest site* or simply
use the URLs provided above, which will take you to the voting pages
for the various nonprofits. Each person gets 10 votes—which must each
be used for a different nonprofit.

Votes can be cast at any time November 8th-22nd, so this is easier
than a daily vote. When you vote, you can make a comment about the
organization, and you can also "Share" with your friends on Facebook
and/or Twitter that you have voted. These are great ways to spread the
word about your support for an organization.

We hope you will be interested in taking advantage of this opportunity
to support ME/CFS nonprofits and the ME community in the Chase
contest. Thank you very much for any help you and the members of your
organization can provide.


Helen Watkinson
Janelle Wiley
Faith Wong
Members, Board of Administrators
ME (ME/CFS) Fundraising Group

* Some groups can be a little hard to find using the search function.
Don't assume they're not there until you try the links above.


Dr. Vallings' notes on IACFS/ME Conference Presentations

Source: Rosamund Vallings
Date:   November 8, 2011

Summary of IACFS/ME conference, September 22-25,2011, Ottawa, Canada
by Rosamund Vallings MB BS

The conference opened with the keynote speaker, Christine Kozak
(Bethesda,USA), who discussed and clarified issues relating to
'Gammaretroviruses of mice and their links to Prostate cancer and
CFS/ME'. She described how MLVs cause leukaemias in mice, and
penetrate right into the cell nucleus, and can be transmitted
genomically. There are 3 categories:ectotropic, xenotropic and
polytropic. The latter two are distributed widely in house mice
species. Xenotropic viruses have a wide range of hosts, and there are
5 functional variants of receptors. XMRV can replicate in some species
of mice. Various host factors restrict XMRVs in mice, such as serum
factors, receptor block, receptor variation, Apobec 3 and Fv1 (both of
which can block viral replication at the reverse transcriptase stage)
and tetherin at the budding stage. Humans do not have Fv1, but have
TRIM5?a retrovirus restriction factor. The conclusion was that MLVs
and ERVs are found in house-mice worldwide. Receptor variants have
evolved in mice carrying XMRVs. XMRV has a distinct host range. XMRV
contributes to induced neoplastic diseases. Multiple host restriction
factors limit virus transmission. Contamination may be the reason we
see this virus in humans.

Virology research

G.Simmons (San Francisco,USA) discussed multi-laboratory evaluations
of XMRV detection assays. He presented work investigating the
prevalence of XMRV in blood donors. Published work on 22/9/11 in
Science Express showed a failure to detect XMRV in any sample. Only
one lab found clinical samples to be nucleic acid test (NAT) positive.
These positives were not reliable among replicates. Using a number of
techniques, there was very little correlation between positives from
the original WPI study and other assays. The conclusion was that
routine screening of blood donors for XMRV is not warranted. Meirleir (Brussels, Belgium) detected anti-XMRVantibodies in the
serum of patients and healthy blood donors. Of 84 Belgian CFS
patients, 21 had developed CFS after receiving a blood transfusion.
Controls were 44 healthy blood donors. 57% of CFS patients and 16% of
controls tested antibody positive. 10 of the 21 CFS patients who had
had a blood transfusion tested positive. PCR was not used. Western
blot was used to confirm the serology data. These results were
statistically significant. Samples were blinded and analysed at the WPI.

M.Hansen (NY,USA) presented work looking for MLV-like gag sequences in
blood and cell lines incubated with plasma from CFS patients and
controls. 30 were patients from D.Bell, 24 from S.Levine and 12
controls from Ithaca, NY. No XMRV was detected in the Bell group.
Cells were cultured for 30 days ? some gag sequences were found but no
other retroviral sequences could be found. There were no statistical
differences between patients and controls. Everything possible was
done to avoid contamination. The Levine samples were all negative for
gag sequences. This research is ongoing.

Post-SARS Syndrome was outlined by H.Moldofsky (Toronto, Canada). SARS
results from infection by a coronavirus A. It creeps into the brain
via the olfactory bulb in mice, and possibly via this route in humans.
250 cases occurred in Toronto, transmitted by one person who had been
in Hong Kong. There were 44 deaths and 50 cases who remained ill
post-SARS. These correlated with a diagnosis of CFS. Sleep was
disordered and this was similar to that seen in fibromyalgia syndrome
(FMS), but there was a lower rating of the alpha EEG sleep anomaly in
post-SARS as compared to FMS. The myalgia was also less severe.

J.Montoya (Stanford,USA) considered the role of the immune response in
CFS. Typical pathogens in CFS are involved, and are mostly
intracellular. There is initial tropism (e.g. respiratory or
GI)followed by involvement of target organs (eglymphatics)). Different
pathogens take similar pathways. CFS may be sustained for years, and
pathogens reactivate periodically. Reactivation tends to be at low
levels. This leads to an immune response, but this is not strong
enough to kill the organisms, so the bugs remain latent, and then
reactivate again leading to symptoms. CFS is a multi-system disease
with phases of immune response.

Peripheral blood studies are useful and convenient but imperfect.
Immune abnormalities have been inconsistent across labs, although some
are consistent. Inconsistency may be due to host variables, multiple
triggers, fluctuating nature of the disease, duration and severity.
There are also other non-CFS variables such as methodological
variables and statistical issues. There is a need to involve all
available data, apply new technology and coordinate research.

J.Mikovits (Reno,USA) and J.Coffin (Boston,USA) discussed the case for
and against human gammaretroviruses in CFS. Mikovits outlined her
earlier work involving detection of XMRV. As well as identifying the
virus in a significant number of patients, their lab have identified
an inflammatory cytokine and chemokinesignature that distinguishes
XMRV-infected patients from controls with 94% sensitivity and
specificity. Further tests are being developed for detection and
characterisation of XMRV. Coffin's lab had looked hard for XMRV in
mice, and did not find it in any mouse strain tested, but found an
XMRV ancestor in the mouse genome. A detection assay has been
developed. He pointed out that XMRV is a virus and MLV is not a virus,
but fragments.

Mice are extremely widespread, and mouse DNA can be found on
laboratory surfaces and can contaminate common reagents and materials.
Most virologists now consider XMRV to be a consequence of a collection
of artefacts originating from endogenous MLVs prevalent in the
laboratory. It is likely to be an accidental laboratory creation from
the 1990s. It is yet to be worked out how it has got into clinical
samples from CFS patients.

Treatment advances

D.Strayer (Philadelphia, USA) gave an update on the use of
Rintatolimod (previously known as Ampligen). They had studied the use
of the drug in XMRV/pMRV antibody positive patients. Of the patients
selected, 33.7% were antibody positive. The antibody negative group
had lower activity for daily living scores. Those who were
antibody-positive showed a significantly greater increase in exercise
treadmill tolerance when treated with the drug than those treated with
placebo and those who were antibody negative. The responding patients
also showed a decrease in use of other medication.

The use of Rifampicin was found to augment the effects of oxymatrine
(Equilibrant) in ME/CFS patients by J.Chia (Torrance,USA). Those with
chronic enterovirus infection had previously been shown to benefit
from oxymatrine (Equilibrant). 46 ME/CFS patients were treated with
Rifampicin 300mg bd for 7 days while taking oxymatrine and compared
with patients taking just oxymatrine, and a control group. Initially
flu-like symptoms occurred in those taking the rifampicin plus
oxymatrine, but subsequent symptomatic improvement was observed in
60%. Short courses of rifampicin may therefore be beneficial in
oxymatrine responders. Rifampicin induces nitric oxide from human
aveolar macrophages causing the initial flu-like symptoms. 2nd or
longer courses of rifampicin did not appear to help.

F.Friedberg (Stonybrook,NY) tested a brief self-management protocol
for unexplained chronic fatigue and ME/CFS in primary care. Two
self-management sessions focussing on CBT were undertaken in 3 study
conditions: 1) standard medical care alone, 2) standard medical care
plus nurse-delivered attention control condition of symptom monitoring
and 3) standard medical care plus nurse-delivered self-management CBT.
There was modest improvement in fatigue severity and patient global
impression of change (PGIC) ratings in the self-management programme.
Ratings tended to reflect different attitudes to the illness and/or
differential exposures to negative major life events. Improved
patients reported increased awareness of behaviour and affirmative
steps to pursue more healthy activities. Self-management can generate
improved outcomes.

Fibromyalgia (FM)

A lively debate followed between R.Staud (Florida,USA) and D.Clauw
(Ann Arbor,USA) entitled: 'Are tender points necessary?' Staud
outlined the American College of Rheumatology criteria for FM (1990)
which includes widespread body pain of 3 months duration and presence
of 11 out of 18 tender points. The tenderness should be with 4kg of
thumb pressure. In trials this has not been found to be reliable and a
more accurate diagnosis can be made using the 2010 provisional FM
criteria: 3/12 duration of pain with a widespread pain index in 19
areas with a severity scale of at least 9. This scoring system is
quite different, and additional symptoms include fatigue, unrefreshing
sleep, cognitive symptoms and somatic symptoms. (There is overlap with
CFS). Many different ways have been looked at for triggering pain for
measurement. Emotional 'windup' could be useful, but is not reliable.
Tonic heat and mechanical stimulation can be applied to painful and
non-painful areas. This can be used for assessment of pain or for
stimulating pain. Tenderness does correlate with pain and can be
measured by quantitative measurement of pain sensation (QST). For
clinical purposes, tender points provide little mechanistic
information about an individual's pain and associated symptoms.

Clauw feels that tender points in diagnosis are unnecessary, and
outlined 10 reasons why:
1. Convey inappropriate message about FM
2. Excludes males
3. Practitioners do not know how to do it, and often do not want to learn
4. Very few chronic pain states have a specific examination to diagnose pain
5. Tender points are an inadequate measure to assess experimental pain
6. There are better ways to assess pain threshold
7. Tender points are not normally distributed
8. Tender point count was never meant to be a 'physical exam' and
should not replace routine clinical examination
9. No evidence that they are necessary in diagnosis
10. Is the horse dead yet?!!

Case definitions

B.Carruthers (Canada) outlined the New International Criteria for ME.
The 2003 Canadian definition has been further defined. The 6 month
period is no longer required, but left to clinical judgement at 3
months. Post-Exertional Neuro-immune Exhaustion (PENE) was kept
criterial and further articulated. Modifications for paediatric cases
have been included. The illness is called ME rather than CFS. The
Canadian definition clearly separated out genuine cases, and this new
definition can be used clinically and in research and epidemiology.

L.Jason presented work contrasting case definitions. The Fukuda
definition has only 4 core symptoms, which do not include
post-exertional malaise. But this definition has been used by
researchers for over 15 years. He compared this definition with the
2003 ME/CFS Canadian criteria and the older Dowsett ME criteria. His
study suggests that the more recent criteria and the ME criteria could
be used to identify patients with more homogenous and severe
symptomatology and functional impairment.

His second paper describes Data Mining as being a useful tool in
aiding the diagnosis of ME/CFS. An objective computer-driven decision
is combined with a physician's medically influenced decision. The
Canadian criteria (compared to the Reeves 2005 criteria) were found to
have more construct validity and were more accurate, identifying 87%
of cases. Post-exertional malaise, neurocognitive symptoms and sleep
disorders were not identified as discriminating symptoms with the
Reeves criteria.

E.Unger (CDC Atlanta, USA) continued discussions about case
definitions. She explained that definitions are not specific to CFS.
They are used for epidemiological studies, clinical diagnosis and to
determine the biological basis of disease. She stressed the importance
of standardization. She asked the question 'Will refining lead to a
homogenous population?', and pointed out that heterogeneity is
challenging. Phenotypes are imperfect indicators of biology. Case
definitions may not be sufficient to discover pathways to
pathogenesis. Standardized measures will allow stratification and

Exercise challenge

B.Keller (New York,USA) studied the effects of fatigue on functional
capacity in patients with CFS. There is a need to quantify impairment.
The cardiopulmonary exercise test (CPET) measures functional
impairment and is an objective measure of energy expenditure and
physical work. It is validated and reliable in health and disease, but
she questioned whether it was useful in CFS. The purpose of the study
was to measure the effects of post-exertional malaise in CFS. She
concluded that patients' disability went from mild to moderate on
first test and from moderate to severe on second 24 hours later.
Looking at maximum exercise tests, it was shown that those with CFS
will exacerbate symptoms associated with post-exertional malaise
simply by completing normal daily activities.

C.Snell (Stockton,USA) then covered the importance of exercise
challenge, and the need for a standardised measured approach in
diagnosis and management. He described fatigue as a reduced efficiency
as a result of doing 'work'. Some measures can be indirect (e.g. heart
rate) or direct (e.g. gas exchange). Field tests are easy to
administer and require minimal equipment but are unmonitored and
therefore less likely to be accurate. Motivation and pacing both play
a big role in the results. He discussed the PACE trial and showed that
the results actually equate to 1.94 ? 2.35 mph and at 2 METS this
equates to 7ml/min/Kg oxygen. The NY Heart Association would classify
this as 'severely disabled'. Anything greater than 3mph is the
anaerobic threshold for most CFS patients. Direct assessment of
aerobic capcity should be the gold standard. CPET is uniquely able to
quantify efficiency with measures of workload and the metabolic cost
of the work. Healthy people do better on a second test, but in CFS
there is a massive drop. Post-exertional malaise (PEM) is an
exacerbation of symptoms after exertion. Most healthy people will
recover in 48 hours, but in the group studied, only one patient with
CFS recovered in 48 hours. The respiratory exchange rate (RER) is the
most reliable guage of subject effort ? it encompasses an analysis of
expired gases.


Natural killer cell (NK) function in a prospective cohort of
adolescents with CFS compared to controls following infectious
mononucleosis (IM) was discussed by B.Katz (Chicago,USA). He felt the
study was important because NK function has been much studied and
results are not always consistent. 9 with CFS and 9 matched controls
were studied. Blood was taken at 6, 12 and 24 months following IM. NK
quantification and function was measured. There was no difference in
NK cell numbers at each of the 3 points of analysis compared to
controls. However NK cell function was higher in cases than controls
at 6 months, with less differential at 12 and 24 months. The
conclusion was that there was no decrease in NK cell function in this

However, E.Brenu (Gold Coast,Australia) looked at cytotoxic function
of NK cells and CD8+T cells in CFS, and her findings showed
significant decreases in cytotoxic activity compared to controls at
baseline, at 6 and 12 months. NK CD56 bright cells remained decreased
in those with CFS. The study confirmed reduced immune function in CFS,
and she highlighted the possibility that NK cell cytotoxic function
could be a potential biomarker.

Her second study assessed proteins and receptors secreted and
expressed by CD4+T lymphocytes over time. At baseline IL-10, TNF? and
IFN? were increased in the CFS group. At 6 months, IL-2 was increased
and IL-10 and IL-!7a were significantly decreased in the CFS group,
and at 12 months only IL-2 was significantly increased in the CFS
group. The results suggest that the cytokine profile in CFS changes
over time during disease progression. Experimental findings need to be
matched with data on clinical disease progression.

The objectives of a study presented by V.Falkenberg (Atlanta, USA)
were to determine the pattern of perforin gene methylation in
conjunction with gene expression, and whether these features were
altered in CFS. Increased promoter DNA methylation correlated with
reduced perforin expression in the non-fatigued group, the
relationship was not seen in CFS. Small but significant differences in
methylation were detected over the day and there were differences
between both groups. Further studies are needed to help explain and
understand these differences.

N.Klimas (chairing this session) pointed out the importance of these
papers in helping us understand the nature of the immune response and
the variations over time.


G.Broderick (Edmonton, Canada) looked at the links between lymphocyte
metabolites and the clinical course of post-infectious fatigue in a
group of adolescents following infectious mononucleosis (IM). They
were followed over 2 years and 3 clinical courses were distinguished.
1) sustained increase in fatigue after early partial remission 2) a
monotonic decrease in fatigue and 3) slow decrease in fatigue after a
peak at 12 months. They surveyed lymphocyte gene expression. 107 genes
were differentially expressed. 40% were linked to immune metabolism
and 20% to immune signalling and cell functioning. Gene expression
supports directed functional interaction. Processes are linked to the
biochemistry of the stress response. Phenylalanine metabolic activity
supported the separation of the fatigue sub-groups. High activity was
linked to a more favourable prognosis. Results correlated with the
clinical course over 2 years.

T.Miike (Hyogo,Japan) presented a fascinating overview of the daily
life of children in Japan, with emphasis on their vulnerability for
developing CFS. These children are subject to sleep deprivation as a
result of modern daily life in Japan, and developed abnormal sleep
rhythms. He discussed the importance of reducing risk of developing
CFS by attention to children's daily life and lifestyle in Japan.

S.Tajema (Kobe,Japan) confirmed the relationship in Japan between the
abnormal biological clock system and childhood chronic fatigue. At
their newly-formed centre, they are now treating this disorder. In the
study, the treatment of children with CFS with bright light therapy,
thermal therapy (20 minutes of 60?C to the head), medication
(melatonin, clonidine and sedative psychotropics), CBT and lifestyle
training over 8 weeks was presented. Circadian rhythm and sleep
disorders were much improved, but other symptoms of CFS were not
significantly improved at this time. Recovery from the sleep
disturbances is looked on as the first stage of improvement for these

K.Rowe (Melbourne,Australia) had seen 788 paediatric patients (aged
6-18) between 1991 and 2009, and she presented follow-up to look at
the natural history of the illness. The average duration of the
illness was 5 years, with a range of 1-15 years. By 5 years, 60%
reported recovery. By 12 years 88% reported recovery, but in
approximately 1/3 of these they reported conscious monitoring of their
workload. Less than 5% were not working or studying, often due to
factors other than CFS, such as marrying or having children. 90%
completed or intended to complete post-secondary training. Treatments
used were studied and the only alternative practitioners who were
deemed helpful were those providing relief of muscle pain with massage
or who provided good dietary advice. Restrictive diets and supplements
did not reach placebo levels of response. The important issues were
balancing life to include social contact, physical activity,
educational input and a commitment to attend at least one activity
each week. Ability to engage in education was the best predictor of
functional outcome. She concluded that the outcomes for young people
in Australia with this illness are generally positive although


L.Jason (Chicago,USA) had looked at the natural history of the illness
over 10 years. His study's major finding was that rates of CFS appear
to have been relatively stable over the past decade. 67% of those with
CFS continued to have CFS over time. Some of those initially diagnosed
with Idiopathic Chronic Fatigue (ICF) had progressed to CFS,
suggesting that ICF is a group at higher risk of developing CFS. Of
those in remission, 50% went from a diagnosis of CFS to ICF,
indicating that while they no longer fitted the CFS criteria, they did
still suffer from fatigue. Post-exertional malaise is the cardinal
symptom. Of interest 29.4% of the CFS patients had had a blood

CFS knowledge and illness management among US healthcare providers was
reviewed by E.Unger (Atlanta,USA). When looking at results for health
practitioners, 94% of doctors had heard of CFS, 71% believed it was a
medical and psychological illness, 14% believed it was a psychiatric
illness, 37% had made a diagnosis. Studies of public knowledge
indicated that 57% had heard of CFS, 27% considered it a medical
condition and 2% believed it was a psychological illness. Nearly 10%
of the public knew of someone with CFS. The top 3 ways in which health
care providers manage CFS were: referral to a medical specialist
(35%), medication (29%), and referral to a psychologist/prescribing
graded exercise therapy (26%). The public sought information by
talking to family doctor (72%), searching the internet (54%) and
talking to a medical specialist (25%). Only 7% would join a support

J.Allegre (Barcelona,Spain) presented results of a study to determine
the sociodemographic, clinical and therapeutic characteristics of CFS
patients in Spain. The condition was found to affect mainly
middle-aged, educated women. Onset most often occurs following an
identifiable trigger, such as infection, delivery or stress, and was
sudden in 20%. At the time of diagnosis 62.5% were not working.
Treatments were: symptomatic medication (analgesics, antidepressants,
anxiolytics) in 78.3%, alternative treatments in 3% and physical
exercise and/or CBT in 5%.

Genomics and genetics

Expression patterns of genes relevant to immune function were
discussed by E. Brenu (Gold Coast, Australia). Her study confirmed
changes in microRNA expression in cytotoxic cells that may be related
to the poor function of these cells in CFS patients.

M.Rajeevan (Atlanta,USA) had looked at the immune and inflammatory
alterations in CFS to determine if genetic variants in inflammation
and immune pathways could be linked to CFS, as well as to quantitative
measures of functional impairment, fatigue and symptom inventory.
Compared to controls, CFS was associated with 34 functionally relevant
single nucleotide polymorphisms (SNPs). 12 of these are in pathways
related to complement cascade, chemokines and cytokines/cytokine
signalling and Toll-like receptor signalling. Differences in these
associations found for subjects with exclusionary conditions otherwise
meeting criteria for CFS, suggests important differences between these

L.Bateman (Salt lake City,USA) presented work to determine whether
baseline and/or post-exercise expression of genes involved in
signalling and modulating sensory fatigue and muscle pain are
potential biomarkers for distinguishing those with CFS and FM from
healthy controls. At least 2 sub-groups of patients were identified by
gene expression following exercise. The larger subgroup showed
increases in mRNA for sensory ion channels and adrenergic receptors
and a cytokine. Symptom severity was associated with greater
post-exercise increases in these genes. The smaller subgroup were
mainly patients with orthostatic intolerance and there was no
post-exercise increase in any gene, and was defined by decreases in
mRNA for ?2A adrenergic receptor. The FM only patients were identified
by baseline increases in 3 genes. Post-exercise increase in 4 genes
distinguished CFS from controls, and could be an objective biomarker
for CFS. Diagnosis based on gene expression may eventually be possible.

Following work with Gulf War veterans, L.Steele (Waco,USA)
investigated, with a small sample whether exposure to neurotoxicants
are risk factors for developing Gulf War Illness (GWI). Some troops
who were exposed however did not develop illness, so genetic
differences may have been implicated. Findings are supportive that GWI
may be associated with the PON1 genotype. PON1 is a detoxifying
enzyme. GW veterans whose PON1 genotype is known to provide slower
hydrolysis of some organophosphate pesticides are at greater risk of
GWI in relation to reported use of pesticides and prolonged use of
pyridostigmine. And GW veterans who carry the R allele PON1192, which
is known to provide inefficient hydrolysis of sarin were at increased
risk of GWI if they had heard chemical alarms, which indicated
potential exposure.

L.Garcia (Miami,USA) compared gene expression patterns in CFS and GWI.
Study was based on Jonathan Kerr's work which had identified 79 genes
associated with CFS with defined subgroups. Her group used gene
activation patterns in CFS and GWI during and after exercise challenge
to better understand the mediators of persistence and relapse. Kerr's
earlier findings were confirmed in the CFS group. There were
significant differences when compared to controls. There were
important overlaps with GWI. EB12 (an EBV induced gene) was 6-fold
higher in CFS than in controls, and 2-fold higher in GWI. ETS1 was
upregulated in both groups. Transcription factor 3 was markedly
elevated in GWI and less so in CFS, though was significant. Apoptosis
genes were markedly elevated in both groups though 400 fold higher in
GWI. The overall trend however was that most of the gene regulation
activities associated with CFS were not significantly different
between GWI and controls. Additional genes specific to GWI have
however been identified by the group. With exercise challenge, there
were changes in genes at peak of exercise which were unique to CFS.
This was accompanied by altered immune signalling pathways.

Brain and neuro-endocrine functioning

I.Treasaden (London,UK) looked at volumetric changes in regional grey
and white matter in CFS using Voxel 3D MRI techniques. He compared 26
CFS patients with controls. In the CFS patients there was reduced grey
matter in the occipital lobes (associated with visual processing), in
the right angular gyrus (involved in perceptual sequence learning,
conscious awareness of actions) and in the posterior division of the
left parahippocampalgyrus (associated with memory function and
retrieval). There was also reduction of white matter in the left
occipital lobe. This data helps to confirm a neurological diagnosis,
and needs to be correlated with biochemical changes.

That there is evidence for reduced aldosterone in those with CFS was
presented by R.Boneva (Atlanta,USA). Many of the symptoms in some CFS
patients do overlap with those of Addison's disease. These include
orthostatic intolerance, orthostatic tachycardia and heat/cold
intolerance. Maintenance of blood volume may be poor and this is
dependent on regulation by aldosterone and mineralocorticoid receptors
in the brain. In this study of 70 CFS patients and 212 controls, those
with CFS had comparatively lower aldosterone levels. A previous study
(Wichita) had reported higher plasma renin levels. Further studies
should measure aldosterone response to salt restriction and postural

A.Miller (Atlanta,USA) presented 2 papers. The first was on behalf of
J.Jones (Atlanta,USA) using functional MRI (fMRI). It has been
suggested that CFS symptoms may be linked to altered cognitive or
pre-cognitive processing in the CNS. This study investigated the sense
of 'self' and 'illness-related semantic information'. The focus was on
the right anterior insula, an area associated with awareness and
self-related processing. Conclusions were that there is a real
alteration of body physiology in CFS. The interoceptive landscape is
acquired cognitively and precognitively in an altered way, enhancing
the prominence of symptoms related to fatigue.

The second paper demonstrated decreased basal ganglia activity in CFS
associated with fatigue by fMRI. Results compared to controls, showed
decreased activation in the right caudate and right globuspallidus.
The decreased activation in the right globuspallidus was significantly
correlated with increased mental fatigue, general fatigue and reduced
activity. Dopamine has a central role in basal ganglia regulation, so
alterations in dopamine metabolism may be involved. Dopamine
transmission and metabolism in these areas may be due to activated
immune pathways. Pharmacologic strategies targeting dopamine and the
basal ganglia may be therapeutic possibilities.

J.Dyke (New York,USA) discussed a new brain imaging technique known as
arterial spin labelling MRI was used to compare regional cerebral
blood flow (rCBF) in CFS, patients with major depression (MDD) and
healthy controls. The 2 patient groups were psychotropic-medication
free for 1 week prior to scanning. rCBF was significantly decreased in
CFS in the left anterior cingulate cortex and the right lingual region
compared to controls, while those with MDD had a trend towards
significantly lower rCBF in the left anterior cingulate cortex. rCBF
for CFS and MDD did not differ significantly. It is unclear whether
the hypoperfusion in rCBF in CFS would account for previous
observation of increased ventricular lactate. This increase could be
due to oxidative stress, mitochondrial dysfunction or decreased rCBF.

Conference summary

The conference ended with an excellent over view by Anthony Komaroff
(Boston,USA). He mentioned an informal meeting which had taken place
to discuss multicentre research initiatives. He stressed the
importance of a variety of initiatives pulling clinicians and
researchers together. Forms, laboratory tests etc. need to be
standardised. He pointed out that 'Research Needs Money'.

(c) 2011 Rosamund Vallings

25% ME GROUP Support Group for Severe M.E. Sufferers

By Dr. Dowsett
What Are the Facts: the tools we can use today to study the brain offer possibilities which were unimaginable 50 years ago. These include Molecular Biology: for example PCR – a microbiological technique capable of amplifying and identifying minute fragments of viral genes, hidden away in internal organs (such as brain, heart or muscle) while a test for rapid diagnosis (within five hours) is currently available. These tests indicate that viruses from the polio group, or related to it, are involved both in the late effects of ME and the Post Polio Syndrome. Brain Imaging: the use of CT, MRI, SPECT and PET scans clearly indicates that metabolic dysfunction in the brain stem and the spinal nerve radiations which transverse it, are initially associated with viral (inflammatory) damage and are the major cause of the cardinal symptoms of ME – central fatigue, stress induced weakness, autonomic nervous dysfunction and the breakdown of homoeostasis over hormonal and other vital functions.

Conclusion: Modern technology has now served to confirm and to detail the meticulous clinical and scientific observations made about ME before 1988! We can rest assured that this serious disability can arise (like polio) from an initially trivial infection which has epidemic and pandemic potential but we need to give further thought to any name change. We should, instead, be making maximum use of modern and effective means of diagnosis, prevention and management.

Thursday, November 10, 2011

Letter for Christmas with M.E.


As I write, six weeks before Christmas, I have been running a
temperature for more than two weeks, am in bed or up, not washed or
dressed, only for essentials; the curtains are drawn against daylight; I
feel sickly and nauseous; I cannot concentrate for any time, nor hold my
head up to make conversation. My caring, supportive, doctor has nothing
to offer but genuine sympathy and advice of taking paracetamol, water
and rest. For those who say, when they see a person who suffers from
M.E. (Myalgic Encephalomyelitis) in the street, "You always seem all
right when I see you," this is what we are like, when unable to go out
and when you don't see us. I haven't been across the doors for 25
consecutive days this month for anyone to see.

Christmas, love it or hate it, is coming. It is a demanding time for
those with an abundance of health and wealth. It is a testing time for
all individuals and relationships, which is exacerbated to intolerable
when one is constantly ill. My experience, over 23 years, is quite
typical of hundreds of thousands in the UK, millions around the world.
There are tens of thousands, even more severely affected, who spend 365
days a year in an 8' x 10' space, bed bound, unable to speak, tube-fed,
blindfold, fans running, all possessions contained floor to ceiling, who
go nowhere unless on a stretcher. The majority are not entitled to care,
fuel allowance, or free prescriptions, as most people incorrectly assume
and, therefore, are left alone, unable to answer a door, raise a call
for help and, mostly, go without.

This appeal for understanding is not intended for those affected by
M.E., who are able to enjoy Christmas, or are prepared to suffer the
consequences afterwards but for those who dread it. If you love or care
for someone with M.E., think about it, put yourself in their position:
Would you welcome guests, in a party mood, if you were feeling as I have
described; wish them to enter your cold, house, neglected due to
inability; receive cards and gifts you have not the energy to return and
cannot afford without going further into debt? Would you want to receive
an invitation to a party of strangers, dependent on someone for
transport home; swap your own bed for a lilo on the floor of a spare
room, next to a loud gathering you cannot join?

Here is some advice, (1) for anyone who loves or cares for someone with
ME: ask them what would be best for them and then, unconditionally,
unquestioningly, do as they request; (2) for any M.E. sufferer, unable
to cope with Christmas: tell your relatives and friends the contents of,
or show them, this letter; (3) for any M.E. sufferer unable to deal
with, even bullied, by someone who doesn't understand: Contact us and we
will speak to them on your behalf.

We shall hear of more casualties in the New Year, from those who did not
heed this appeal and who will not be there 24 or 48 hours later to
witness the exhaustion, or the months of M.E. relapse, that ensue. I
don't know a single person affected by this awful illness who has not
additionally been touched by social isolation, fragmented relationships,
a broken heart or spirit and even death. Please take these tips for a
happier Christmas for all.

Yours sincerely
drjohngreensmith@mecommunitytrust. org
Dr John H Greensmith
ME Community Trust. org

I am sending this letter for publication to my local newspaper and some
other selected places.
If you would like it to appear in your local area newspaper, wherever
you live in the world, send an e-mail
to drjohngreensmith@mecommunitytrust. org with "My local newspaper" in
the subject line. If you don't know,
or can't find out the e-mail address for us to send it to (usually
something like letters(at), or editor (at), or firstname.secondname (at)
nameof, leave the message area blank and we'll reply with
the instructions how best to find it. It would be great if as many
people as can manage also write, separately, and/or in response to the
Christmas theme. You may also forward and re-post it wherever you
choose, such as online groups, forums, Facebook, Twitter and use in
newsletters for maximum impact of message.

Body Map No Help in Telling Where It Hurtss - Fibromyalgia Center -

5 Surprising Uses for Antidepressants

Wednesday, November 9, 2011

NIH Undiagnosed Diseases Program

 "A patient who cannot be diagnosed may cycle through the medical system with no satisfactory treatment plan or be abandoned by the medical system. Through the UDP, NIH provides a glimmer of hope to patients and their families, while at the same time gaining remarkable medical insights."

 More than half of the accepted patients had undiagnosed neurological problems. Other prominent disorder categories include gastrointestinal disease; fibromyalgia and chronic fatigue syndrome; immune-mediated and rheumatic illnesses; psychiatric conditions; pain; dermatologic disorders; and cardiovascular disease.

So far, most of the solved cases — 37 of 39 cases for which the UDP team arrived at a diagnosis — involved diseases previously encountered in the world of medicine

* * *

How many of these patients would've been undiagnosed if ME/CFS and fibromyalgia were taught in medical schools as something other than IAIYH?



Chase Community Giving is giving again

Less than 2 minutes of your time can significantly help those afflicted with
ME/CFS, Fibromyalgia, Gulf War Illness and other Neuro-Immune Disorders
from all over the world.

What's at stake:

The Chase Community Giving program will make a total of $3,025,000 in
donations to smaller non-profit organizations as follows:

*    $250,000 to the Charity receiving the most votes (rank 1);
*    $100,000 to the runner-up Charities (ranks 2-5); and
*    $25,000 to the next runner-up Charities (ranks 6-100).

From 12 noon (EDT) on November 8, 2011 to November 22, 2011, users can vote
for any charity that is authorized and registered with the Chase Community
Giving program on Facebook. On November 23, 2011, the votes will be tallied
and the 100 eligible Charities receiving the most votes will be considered
the top vote-getters of the Program and will share in $3,025,000 in
donations from Chase.

Participating and Voting:

No purchase necessary to participate or vote. You must, however, be
registered on Facebook. During the voting period, Participants who allow
"Access" and "Like" the Chase Community Giving application on the Facebook
platform, may vote for Charities. Each Participant will be limited to one
(1) vote per Charity with a total of ten (10) votes per valid user profile.

To Vote:

(1)   A Facebook page is required. If you don't have one - get a Facebook
<>  page. (You can easily delete it after the
contest if you wish.)

(2)   Sign into your Facebook Page and then go to the Chase Community
<>  Giving page and
click the "LIKE" button at the top of the page.)

(3)   Either type in the names of the orgs you want to vote for or use the
URLS posted below to vote for your favorite orgs.

The following ME/CFS organizations are in the contest, click on any of them
to view their contest page (several non-profits including Phoenix Rising,
Vermont CFIDS, OFFER and Simmaron Research are not eligible this year):

*    CFSKnowledgeCenter -- & (
*    Wisconsin Chronic Fatigue Syndrome Association
*    New Jersey Chronic Fatigue Syndrome Association
*    IACFS/ME (Named AACFS on Chase) (
*    The CFIDS and Fibromyalgia Self Help Program (
*    Rocky Mountain CFS Association Inc (
*    Mass CFIDS ME/FM Association
*    DR. A Martin Lerner Chronic Fatigue Sydrome Treatment
( <> )
*    The Chronic Fatigue Syndrome Fibromyalgia Org of Georgia Inc
*    Enterovirus Foundation (
*    The Connecticut CFIDS and FM Association (
*    The National CFIDS Foundation (

The following Fibromyalgia organizations are among those in the contest,
click on any of them to see their respective Chase contest page:


The following Gulf War Illness organizations are among those in the contest,
click on any of them to see their respective Chase contest page:


After You Vote:

(4)   After you vote for an organization spread the word by using the "LIKE"
buttons on the right hand side of each organizations' Chase Community Giving
profile page  and 'Like' the organization to give it more publicity.

(5)   In the comment section of the organizations' Facebook profile page and
ask others to vote for CFSKnowledgeCenter ( as well as
your other favorite charities.

(6)   Invite your Facebook Friends to  go to and  "Like" Chase Community
Giving and then vote for CFSKnowledgeCenter ( as well
as their favorite charities.

(7)   Come back to CFSKnowledgeCenter ( on Chase
throughout the contest and again share them on your Facebook and Twitter
pages using the "LIKE" buttons.

(8)   Ask your family and friends to vote in the Chase Community Giving

Daniel Moricoli <> <> <>

Practical Information, Community & Research Support for those afflicted with

PayPal button btn_donateCC_LG

To make a donation to support our work for those afflicted with ME/CFS,
please click:
4> &hosted_button_id=7561374

facebook logo_40P Find us on Facebook
<> .

What are the risk factors of fibromyalgia?

“Difficult” Patients Stay Sick

"Difficult" patients are characterized as having lots of unexplained physical symptoms, lots of stress, or extremes of pain and discomfort, or they may be struggling with anxiety and depression disorders.

How did being perceived as difficult affect the patients? They
were 2.4 times more likely to have worse symptoms two weeks
after their visit and to report that their expectations weren't met.

Not all this so-called difficulty rests with the patient, however. The researchers also found that physicians with fewer than 10 years of experience reported that almost one in four patient visits were difficult, while those with 20 or more years of experience ranked the number as just two percent.

Tuesday, November 8, 2011

How to Woo a Doctor

In crisis, always utter eight magical words. The once-off consultation with Dr. Conroy started out well. "You certainly have very good reflexes," he said, after hammering on my knee. "Oh, yes. Well, I've been working on that," I replied with a wince, instantly realizing how bad that lame flirtation sounded. Even worse, it didn't work. "I don't think there's anything else I can add here," he said as he closed my file and stood up. I tried to hide my shock and threw my eight-worded Hail Mary pass: "If you were me, what would you do?" He sat down and reopened the file.

Dr. Weil's Natural Approach to Happiness


MM: You mentioned you were on antidepressants for just a few days and [they] didn't agree with you. You say there are people out there being treated with antidepressants who might not actually be helped by them and actually may be worse off. Why do you think antidepressants sometimes don't help and why do so many people believe that they do?

AW: Well, there's an accumulating body of research that shows that SSRIs [selective serotonin reuptake inhibitors, a type of antidepressant medication] may not work any better than placebos, even for severe depression, and that maybe only in very, very severe depression is there in an advantage. One expert says that it may not matter what you do as long as you do something, and it doesn't matter WHAT you do — it could be going into therapy, taking antidepressants, making a lifestyle change — just doing something that shifts that mental energy. It changes your mood and that's what really produces a benefit.

* * *

Or maybe, people are made worse because they're being given anti-depressants when they don't actually have depression.  A-Ds make me sicker, because I'm not depressed -- I have a post-viral neurological condition.


5 Supplements for Fibroymalgia Pain - Chronic Pain

Monday, November 7, 2011

Bringing back an oldie but goodie

Since I just tracked down this post for someone, I thought it was worth a re-read (or a first-time read for those who are new subscribers).
I can't begin to tell you how many people over the years have told me to stop whining because they know someone with CFS (and a husband) and her house is always clean, she never complains about missing meals, she functions ever so much better than I claim to ... without these people ever catching the irony that the reason that Mary doesn't have to complain to other people in order to get sympathy (or help) is because John makes a point of telling people when she's in terrible pain, and because John sees to it that her needs are met, the house is clean, food appears at mealtime, etc. 
The last time anyone ever gave me a bedbath, I was 6 years old and in the hospital after surgery.  I can't remember the last time I had a meal brought to me in bed, because even if I call out for pizza, I still have to be able to drag myself to the front door to accept delivery.
When you're single -- voluntarily or involuntarily -- you can't count on anyone helping with those little niceties of life.  You learn to live with the clutter, to not fret too much about the same sheets having been on the bed for weeks, and that the nutritional value of PopTarts stashed under the bed is far superior to the nutritional value of organic veggies rotting in the fridge because you can't walk far enough to retrieve them from the kitchen to eat.

Sunday, November 6, 2011

Health Professionals Rate Lower Pain In Patients They Don't Like


Serious study should be undertaken into the long-term consequences of misreading the severity of a patient's pain, he said. Potential ramifications are that people won't get the care they require, or they won't follow the clinician's treatment prescriptions seriously, and therefore continue to suffer.

"Not getting the adequate or appropriate treatment is, in principle, harmful in itself," he said.

* * *

It is possible that inadequate pain relief is the ultimate cause of fibromyalgia. 

The Stigma Around Aging And Chronic Pain

The resulting care gap is serious enough that the Institute of Medicine (IOM) recently declared that we need a "transformation in how pain is perceived and judged both by people with pain and by the health care providers who help care for them."

Far from dismissing persistent pain as imagined, exaggerated or inevitable, the IOM report endorses the emerging view that, "because of the physiological and psychological changes that occur in people with chronic pain ... in many cases, chronic pain is a disease in its own right."

The International Association for the Study of Pain agrees, and last year declared access to pain management "a fundamental human right,"

What Are Autoimmune Diseases?

Your next question might be to ask why the body is attacking itself. The answer is simple: We don't know. There are theories that some bacteria or virii might trigger the autoimmune response in patients who are genetically predisposed, but nothing has been confirmed.
Because drug companies have not been able to target the specific characteristic of the immune system that makes it attack friendly cells, the treatment for autoimmune illness until as of late has been to, in effect, beat down the entire immune system -- good and bad parts alike. It's sort of like using a sledgehammer to put in a thumbtack.
Lately, though, there have been a slew of "bio-drugs," also called disease modifying agents, which target a very specific group of molecules in the body.

The Kafka Pandemic: A Machiavellian approach

you take steps to make it look like they are not suffering and dying.

Make sure their death certificates almost never show that they had anything underlying in common. Keep them out of official statistics. Keep them out of medical curricula.
* * *
Once again, Samuel hits the nail on the head.  Medical school teaches nothing at all about Myalgic Encephalomyelitis, and all they teach about CFS is that it's all in our heads.  As a result, it's almost impossible to find a doctor qualified to diagnose it -- I've seen people walking around with a CFS diagnosis who, in fact, have depression or anemia or food allergies because some doctors think any patient with fatigue has CFS.  And vice versa, patients who really do have what I have, who are misdiagnosed with something they don't have (often depression) because some doctors think any patient who sleeps a lot is depressed.
Some of my doctors ignored any objective symptoms of physical illness (like fever or rash) because they preferred a psychiatric explanation that absolved them of any further responsibility other than to nag me to get my head shrunk.  Blood tests I asked for were refused, because if the test was positive, not only would the doctor's ego be on the line (proving that the patient was right and the doctor was wrong) but he'd also have to spend more time trying to figure out what was really wrong.
Much easier to play Blame The Patient and refuse to look for a physical cause.