Thursday, November 8, 2012

Ampligen Review in December

REMINDER: Ampligen costs about $20,000 a year and is not likely to be covered by either insurance or Medicare.  In fact, someone with Medicare had made the explicit statement a couple years ago that it would NOT be paid for, even if it was approved.  If it returned me to full-time employment as a paralegal, I would be earning enough to pay for it myself (and have a huge medical deduction on my tax return every year), but the catch is that you can't work full-time while taking Ampligen  because two days a week you have to spend several hours hooked up to an IV drip.
 
 
http://www.thestreet.com/story/11720256/1/hemispherxs-ampligen-rehash-unlikely-to-impress-fda.html

Hemispherx's Ampligen Rehash Unlikely to Impress FDA
By Adam Feuerstein 09/27/12 - 07:00 AM EDT


PHILADELPHIA (TheStreet) --Three years after being rejected by U.S.
Food and Drug Administration, Hemispherx Biopharma (HEB) is back
seeking regulatory approval for Ampligen, its controversial therapy
for chronic fatigue syndrome.

Everyone loves a comeback story with a happy ending, but Hemispherx's
second attempt won't turn out any happier than the first. FDA is
likely to reject Ampligen again because Hemispherx ignored the
agency's demand to run a new clinical trial in chronic fatigue
syndrome.

Instead, Hemipsherx has spent the past three years doing essentially
nothing but re-analyzing data from the old Ampligen phase III trial
completed in 2004. FDA reviewed the original study already, deeming it
"lacking credible evidence of efficacy of Ampligen."

It would be highly unusual -- unprecedented, even -- for FDA to
reverse itself and find a retrospective rehash of old Ampligen data
more compelling this time around. FDA has been facing political
pressure to speed new drugs to market, particularly for diseases like
chronic fatigue syndrome with no current treatments. But this hardly
means FDA is going to throw out its drug-review rulebook.

FDA has scheduled an advisory panel for Dec. 20 to review Hemispherx's
Ampligen resubmission. The agency is expected to issue a final
approval decision on or before Feb. 2, 2013.

Ampligen's long odds haven't deterred speculators from bidding up
Hemispherx's stock price, just like they did in 2009. At Wednesday's
close of 90 cents, Hemispherx shares are up more than 220% since July
11 when the company announced plans to resubmit Ampligen for FDA
approval.

For those that don't remember, the phase III study enrolled 234
patients with chronic fatigue syndrome, randomized to treatment with
Ampligen or a placebo. The study's primary endpoint was improvement in
treadmill exercise tolerance at week 40.

Hemispherx announced positive results from the Ampligen study in May
2004, claiming that Ampligen patients demonstrated a 17.4% improvement
in treadmill exercise tolerance compared to a 4.3% improvement for
placebo patients -- a net difference of 13.1%. The result was
statistically significant with a p value of 0.047.

However, in May 2006, results from this same study were presented at a
medical meeting showing a 12.9% difference in treadmill exercise
performance between Ampligen and placebo that was not statistically
significant.

Depending on which data presentation you believe, the Ampligen study
was either a success or a failure. By rejecting Ampligen in 2009, FDA
clearly sided with the latter view.

In March, Hemispherx published the full data from the Ampligen trial
in the open-access science journal PLOS One. Once again, the study
results changed and got worse.

Ampligen-treated patients with chronic fatigue syndrome entered the
study with a mean, baseline treadmill exercise duration of 576
seconds. After 40 weeks of treatment, mean exercise duration rose to
672 seconds, or a 16.7% improvement.

The placebo patients began the study with a mean, baseline treadmill
exercise duration of 588 seconds and ended at 616 seconds, or an
improvement of 4.8%.

That works out to a placebo-adjusted improvement in exercise duration
for Ampligen of 11.9%. This benefit doesn't appear to be statistically
significant, however. The study, as published in PLOS One, makes no
mention of this intra-group comparison reaching statistical
significance.

The Ampligen study appears to have failed -- which gibes with the
FDA's decision to reject the drug and call for a new study to be
conducted.

Hemispherx has not invested the money and time necessary to run a new
Ampligen study, choosing instead to change the way the primary
endpoint of treadmill exercise duration was measured. Instead of
comparing the two groups of Ampligen and placebo patients, Hemispherx
switched to analyzing the exercise data using each individual patient
as their own comparator.

On this "intra-patient" basis, Ampligen improved exercise duration by
36.5% compared to a 15.2% improvement for placebo patients. The net
difference of 21.3% was "statistically significant" with a p value of
0.047, according to the PLOS One study. Hemispherx CEO William Carter
and Medical Director David Strayer were lead authors of the study.
William Mitchell, a Hemispherx director, is also listed as a study
author.

Hemispherx also conducted other, post-hoc analyses claiming to show
that patients who were able to exercise longer following Ampligen
therapy had improved quality of life and reduced dependency on
concomitant medications compared to Ampligen patients who couldn't
exercise longer.

All of these new analyses of the Ampligen data were done
retrospectively, or long after the study was completed. Hemispherx has
made no effort to confirm any of these findings with new clinical
trials.

Following a meeting with FDA officials in June, Hemispherx claims the
agency agreed to review the new analyses of the Ampligen study in lieu
of data from a new clinical trial. However, Hemispherx also warned
that, "Whether these data provide adequate evidence of efficacy will
ultimately be a review issue, and there can be no assurance the FDA
will conclude the data are adequate to support approval of the
Ampligen NDA."

Investors would be wise to take that warning seriously.

A postscript: Omitted from this column is a retelling or discussion of
Hemispherx management's questionable actions and misleading statements
made during the previous Ampligen review cycle in 2009. I covered
Hemispherx extensively during this period, so feel free to go back and
read my prior stories:

Hemispherx's CFS Drug Is a Long Shot
http://www.thestreet.com/story/10506671/1/hemispherxs-cfs-drug-is-a-long-shot.html

--Written by Adam Feuerstein in Boston.

A treatable auto-immune disease?

Note: Rituximab works by knocking out the immune system. Although
Rituximab has a good history for a drug (the European patent for Roche
expires next year and GenTech in the U.S. loses their patent in 2015)
for patients who have latent and or active microbial infections the
side effects can be severe including death.

Also, the one person in the placebo arm of the trial who showed marked
long term improvement may have had an affective disorder only
according to the study authors as that person did not meet the
Canadian Consensus Criteria although they met the international 1994
Fukuda criteria which does not require post exertional malaise or
cognitive problems. This highlights the problems inherent with being
unable or unwilling to separate those who have a disease from those
who do not.

Chronic Fatigue Syndrome -- A Treatable Autoimmune Disease
Matthew Edlund, M.D./ Huffington Post
Posted: 10/26/11 11:22 AM ET

Chronic fatigue syndrome wrecks people's lives. It does so
physicially, socially and economically. Appearing "normal" yet not
being able to think or work causes enormous hardship compounded by
many doctors who think the illness does not really exist -- a position
health and disability insurance companies are more than happy to
endorse. And those who firmly believe it exists are often stumped by
how to treat it -- beyond stretching, physical activity and
psychotherapy.

Now a new study out of Bergen, Norway adds much to the data that
chronic fatigue is an autommune disease. If not entirely definitive,
it points in the direction that many CFS sufferers and clinicians have
argued for decades -- that the illness is a disorder of the immune
system, is preceded in most cases by some kind of infection and
continues to provoke multiple debilities for a long time.

The Haukelund Study:

Many ideas for clinical treatment occur from observing the clinically
unexpected. In this case, the Haukelund Hospital researchers were
struck by a patient with lymphoma and CFS whose fatigue also improved
with treatment. They decided to treat 30 people with CFS, mainly young
(average age 37.3 for those treated and 31.5 years for placebo) and
female (80 percent) with rituximab, a potent anti-inflammatory
monoclonal antibody that markedly depletes B cells. None of the
patients allowed into the study were suffering from endogenous
depression, which afflicts a large number of CFS sufferers. None of
them showed evidence of the XMRV virus, which previously had been
reported as more common in some CFS sufferers, though critics felt
such studies were methodologically flawed.

Results:

Some major findings were:

1. About two-thirds of the study group saw their fatigue (self-rated)
as considerably improved compared to only 13 percent of the placebo
group. Cognitive and other functions also improved, though not
necessarily as much.

2. Effects were delayed. Some patients only showed improvement 6-7
months after treatment with the drug, and none quickly.

3. Some people showed marked long term improvement, but only a few
(more or less complete in 2/15 on rituximab and 1/15 on placebo at
30-33 months.)

Problems:

A. This is a small study. The number of people treated was not large,
the placebo group had the disease longer, and as the authors are very
aware, this study needs replication and expansion with ongoing
treatment arms.

B. The study group may not be reflective of the majority of CFS
patients, many of whom are older, have other intercurrent autoimmune
problems (about one-fifth of the study group also did) and who often
suffer from depression and sleep disorders.

C. Though the authors believe this study shows rituximab is moderating
a long term immunological effect through B cells and autoantibodies,
nobody has a clear sense of why it works.

D. Rituximab is expensive and has lots of side effects, including
infusion reactions, renal failure, immunological disorders and
possible death.

Implications:

Despite the problems, there is much cheering in the Bergen study.
First, something seems to work. Most clinical trials of CFS patients,
like with acyclovir, show only subsets of patients who experience real
improvement.

Second, this study goes a fair way to knocking off the strong belief
in the medical community that CFS is "only in people's heads." Many
with CFS are told that they are depressed -- they know that, but also
know very well something else is going on that causes that depression.

Third, if something works, further treatment along the lines of
oncology/rheumatologic trials may now get funded. Ritixumab and other
monoclonal antibodies may be tried, alone or in combination.

The biggest change may occur with public acceptance and awareness.
It's one thing to live with a chronic disease that controls much of
your life; it's another to live with an illness many do not believe
exists.

I think the Bergen study will provoke many more arguments about CFS,
particularly what its main manifestations really are and what to do
about it. Many sufferers will want immediate treatment with rituximab
or other monoclonal antibodies, which may be clinically premature.
Immunity is fiendishly complicated, and the effects of monoclonal
antibodies on immunity profound. But the argument that CFS is not
related to the immune system may now be less stridently asserted. That
would be real progress.

http://www.huffingtonpost.com/matthew-edlund-md/chronic-fatigue-syndrome_b_1028341.html?
 

The greater social question

 
Llewellyn King asks:
These drugs, Ampligen and Retuxin, with their hint of hope in a dark sky, raise a basic societal issue: Is it better for society to pay to make hundreds of thousands of citizens well enough to work, or is the externality of lost work too hard to figure into public health policy and budgeting?
 
* * *
Dr. Jason estimates the loss to the US economy from CFS is $26B per year.  If we could devote just 1% of that ($260M) to CFS research each year, the taxes paid by those who return to the workforce as a result of treatment would quickly return that to the treasury.
 

CFS and the CDC: A Long, Tangled Tale (excerpts)

A good concise history of CFS -- "concise" only in that it's shorter than Osler's Web -- the full article is about 10,000 words.
 
 
David Tuller writes a guest post in Virology Blog about the CDC's CFS
research program.

-------------------------------------------------------------------

http://www.virology.ws/2011/11/23/chronic-fatigue-syndrome-and-the-cdc-a-long-tangled-tale/

Chronic Fatigue Syndrome and the CDC: A Long, Tangled Tale
23 November 2011

by David Tuller

Note: This account draws from interviews, a close reading of a
fraction of the 4608 epidemiologic studies that pop up (as of today;
yesterday it was 4606) on a PubMed search
for "chronic fatigue
syndrome," and a review of many pages of government documents–in
particular the minutes and testimony from meetings of the Chronic
Fatigue Syndrome Advisory Committee to the U.S. Department of Health
and Human Services, one of many such panels established to provide
guidance to federal health officials. Not much here will be a surprise
to anyone who has read the better ME/CFS blogs
, or Hillary Johnson's
authoritative and prodigiously researched 1996 account, Osler's Web:
Inside the Labyrinth of the Chronic Fatigue Syndrome Epidemic. Some
readers might know that I have written a number of articles on chronic
fatigue syndrome as a freelance contributor to The New York Times, so
I want to be clear: The Times has nothing to do with this piece. I
want to thank Professor Racaniello for letting me invade his space to
post this very long story.

David Tuller is coordinator of a new concurrent masters degree in
public health and journalism at UC Berkeley. He was a guest on TWiV
119.


Dr. Racaniello said that when he used to question colleagues about
chronic fatigue syndrome, they would argue that it was an imaginary
illness. "Every time I asked someone about it, they would say it
doesn't exist, it isn't a real disease, even as recently as the past
year," he said. "But once you start paying attention and reading papers, this looks like a chronic or hyper-immune activation. These patients have a lot of signs that their immune systems are firing almost constantly."
...
There is no dispute that exercise can be a very effective treatment
for depression. But people with chronic fatigue syndrome generally
suffer from a distinctive symptom known as "post-exertional malaise"—a
disproportionate depletion of energy following minimal activity that
is not a typical feature of depression. (However, the word 'malaise,'
like the word 'fatigue,' is a complete misnomer; post-exertional
malaise is much closer to a serious crash or relapse than a Victorian
fainting spell.) An emerging field of research—much of it taking place
at the University of Utah and University of the Pacific in Stockton,
California–indicates that people with CFS suffer from problems with oxygen consumption, energy production and muscle recovery. So it's not surprising that increasing activity levels could lead in some or many cases to a prolonged resurgence of their symptoms rather than the
improvement predicted by proponents of graded exercise therapy.





Significant neuroanatomical changes occur in CFS

British Journal of Radiology 2011, doi:10.1259/bjr/93889091


Full Text (PDF): http://bjr.birjournals.org/cgi/reprint/93889091v1


Regional grey and white matter volumetric
changes in myalgic encephalomyelitis
(chronic fatigue syndrome): a voxel-based
morphometry 3-T MRI study

B K Puri, PhD, FRCPsych1, P M Jakeman, MSc, PhD2,
M Agour, MB, MRCPsych3, K D R Gunatilake, MD,
MRCPsych4, K A C Fernando, MBBS, MRCPsych5, A I
Gurusinghe, MBBS, PGDPsych6, I H Treasaden, MRCS,
FRCPsych7, A D Waldman, PhD, MRCP1,8 and P
Gishen, DMRD, FRCR1

1 Department of Imaging, Hammersmith Hospital, London,
UK 2 Department of Physical Education and Sport
Sciences, University of Limerick, Republic of Ireland 3
University of Hertfordshire, and Care Principles, Rose
Lodge, Langley, West Midlands, UK 4 The Ridge Hill
Centre, Dudley, UK 5 Brooklands Hospital, Birmingham,
West Midlands, UK 6 Broadmoor Hospital, Berkshire, UK
7 Three Bridges Unit, WLMHT, Middlesex, UK 8 National
Hospital for Neurology and Neurosurgery, Queen Square,
London, UK


Objective:

It is not established whether myalgic
encephalomyelitis/chronic fatigue syndrome (CFS) is
associated with structural brain changes. The aim of this
study was to investigate this by conducting the largest
voxel-based morphometry study to date in CFS.

Methods:
High-resolution structural 3-T cerebral MRI scanning was
carried out in 26 CFS patients and 26 age- and
gender-matched healthy volunteers. Voxel-wise
generalised linear modelling was applied to the processed
MR data using permutation-based non-parametric testing,
forming clusters at t > 2.3 and testing clusters for
significance at p < 0.05, corrected for multiple
comparisons across space.

Results:

Significant voxels (p < 0.05, corrected for multiple
comparisons) depicting reduced grey matter volume in the
CFS group were noted in the occipital lobes (right and left
occipital poles; left lateral occipital cortex, superior
division; and left supracalcrine cortex), the right angular
gyrus and the posterior division of the left
parahippocampal gyrus. Significant voxels (p < 0.05,
corrected for multiple comparisons) depicting reduced
white matter volume in the CFS group were also noted in
the left occipital lobe.

Conclusion:

These data support the hypothesis that significant
neuroanatomical changes occur in CFS, and are
consistent with the complaint of impaired memory that is
common in this illness; they also suggest that subtle
abnormalities in visual processing, and discrepancies
between intended actions and consequent movements,
may occur in CFS.

Rituximab Reduced Fatigue in 67% of Patients in Study

WARNING: costs about $70,000 a year, and probably will not be covered by your insurance at this time
 
 
http://www.webmd.com/chronic-fatigue-syndrome/news/20111020/cancer-drug-may-also-treat-chronic-fatigue-syndrome

Cancer Drug May Also Treat Chronic Fatigue Syndrome
Rituximab Reduced Fatigue in 67% of Patients in Study
By Brenda Goodman, MA
WebMD Health News


Oct. 19, 2011 -- Researchers in Norway say they've been able to treat
symptoms of chronic fatigue syndrome by giving patients a biologic
drug that affects the immune system.

The drug, rituximab (Rituxan), works by depleting immune cells called
B-cells. It is FDA approved to treat non-Hodgkin's lymphoma, chronic
lymphocytic leukemia, rheumatoid arthritis, and two kinds of
vasculitis.

For the study, researchers recruited 30 people with chronic fatigue
syndrome (CFS). Half got two infusions of rituximab given two weeks
apart. The other half got infusions of saline solution as a placebo.

Ten patients in the rituximab group (67%) and two patients in the
placebo group (13%) saw at least moderate reductions in fatigue.

In most of the patients, improvements were transient and faded within
eight to 44 weeks.

But three patients, two in the rituximab group and one that got the
placebo, continue to be symptom free 2 1/2 years after their
treatments. Those three patients have all returned to full-time jobs,
researchers say.

The study is published in the journal PLoS One.

"Our thought is that in fact CFS is an autoimmune disease in most
patients," says study researcher Olav Mella, MD, PhD, an oncologist at
Haukeland University Hospital in Bergen, Norway.

Mella and his colleague, Oystein Fluge, MD, PhD, say they accidentally
discovered that rituximab might help chronic fatigue syndrome after
they used it to treat three patients who suffered from both CFS and
non-Hodgkin's lymphoma. All three patients reported significant
improvements in fatigue after rituximab infusions. They eventually
relapsed and were given more doses of rituximab. All three again had
improvements in their CFS, though those eventually faded.

Their cases were reported in BioMedCentral Neurology in 2009.

Is Chronic Fatigue Syndrome an Autoimmune Disease?

Researchers say they aren't sure why the drug is working.

"We cannot know for sure, but what we see is that there's a delay from
the rapid B-cell depletion after rituximab treatment to the clinical
response. The delay can be from three to perhaps eight months before
the response is thought to occur," says Fluge, who is an oncologist
and medical physicist at Haukeland Hospital.

B-cells are part of the immune system. They roam the body in
relatively small numbers searching for foreign invaders. When a B-cell
finds one, it springs into action, becoming an infection-fighting
chemical factory.

In some diseases, like leukemia, B-cells may go haywire and cause
cancer. In rheumatoid arthritis, B-cells may attack the body's own
tissues.

In CFS, however, it's unclear why killing off B-cells might help.

One theory, held by researchers who believe CFS may be caused by an
infection, suggests that retroviruses may hide out in dormant B-cells,
only becoming active when the cell is triggered and rapidly
multiplies.

But Fluge thinks if that's the case, patients would see quicker
improvements after taking the rituximab.

"We think what we see could be best explained with an autoimmune
mechanism and gradual elimination of auto-antibodies," he says.

Other, more circumstantial evidence supports the idea that CFS may be
an autoimmune disease.

Like other autoimmune conditions, it tends to be much more common in
women than in men, for example. Many people report getting CFS after a
bout with triggering illness. The risk of getting chronic fatigue
appears be similar to the risk for getting other kinds of immune
disorders.

More Research Needed

Despite the positive results of the study, researchers stressed that
it was far too early for people with chronic fatigue to seek treatment
with rituximab.

"For the time being, this is a clinical trial. It is not for routine
use. We need at least one more large study, partly here and partly
somewhere else, to confirm the results," Mella says.

Rituximab is expensive. A single course of treatment for cancer can
cost more than $20,000. Rarely, fatal reactions have been reported
after infusions of the drug, although no significant adverse events
were reported in the current study.

"The most exciting news from the study is the possibility of
disease-modifying treatment for at least some people with CFS," Kim
McCleary, president and chief executive officer of the CFIDS
Association of America, says in an email. "This study also provides
support for other possible approaches to repair immune abnormalities
that have been identified in CFS patients."
 
 

CDC Refuses to remove Toolkit, despite CFSAC

Interview with CDC, in which the agency claims that the CDC¹s CFS Toolkit is
accurate. This despite the fact that CFSAC voted to remove the Toolkit.
The Toolkit encourages CBT and GET and states there are no diagnostic tests
for ME. According to CDC, "The information in the Toolkit is not
inaccurate, and we have verified this repeatedly in discussions with
clinicians who care for CFS patients."

More at CFS Central
www.cfscentral.com

As you can tell.....

I've been having a "bed day" -- this time without brain fog -- and catching up on my reading, having gotten well behind on it due to real life getting in the way for a while. 
 
The good news is, I am now able to have a bit of a "real life" and not spend all day every day in bed with nothing better to do than read and post CFS articles!
 
This means that some items that I might have posted, had I read them at the time I received them, have become outdated or superseded (e.g., XMRV has now been declared, even by Dr. Judy, to be a red herring, so that information is no longer essential to CFS patients).  So, instead of a hundred or more postings, there are only a couple of dozen for you to read.
 
One thing that I noticed helped a lot was that a friend moved to the mountains and invited me to visit for a few weeks -- above the pollution that is a constant factor in the valley where I live.  That I detoxed the pollution-related crud while there was obvious: near the end of my visit, my friend said "you don't smell nearly as bad as you did" -- when I'm detoxing, the nasties coming out of my system reek to high heaven.  Despite the lower oxygen level at that altitude, I was actually able to do things without the repercussions I get at home near sea level, which tells me the pollution I've been breathing daily for 20+ years is part of the problem.
 
The cold weather on the mountain isn't good for my arthritis and fibro, but the experience has convinced me that I need to investigate moving somewhere that the pollution blows out to sea.  That won't make me 100%, but apparently it does help a lot.  And anything that helps enough that I can work a few more hours every week justifies the financial cost (e.g., the first year that I had my Sleep Number bed, I was able to work enough additional hours to pay off the bed entirely).
 
I'd discovered last winter that setting the thermostat a few degrees above where I normally keep it also had a good effect on my health, and decided the extra few dollars a month was worth it for the improved functioning.  I was up and dressed at least a portion of most days, rather than spending most of the winter horizontal.
 
 

CFSAC Testimony re HIV, CFS and AIDS

~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
{This was also submitted to the CFSAC (June 2012) and is formal public record.}
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

The medical establishment will have you believe that Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME) is some sort of mysterious illness, but it's no mystery to me; CFS/ME leads to NON-HIV AIDS, idiopathic CD lympocytopena (ICL), a clinical diagnosis I possess.

How can the AIDS establishment continue with a stale "it's caused by HIV" theory when there are ICL cases cited in medical journals dating back to 1992? While millions of ailing immunodeficient CFS/ME patients get belittled and neglected, perfectly healthy HIV+ people are allocated billions of dollars in taxpayer money. How can it make sense to anyone?

In the U.S. last year, the NIH spent $3.1 Billion of our tax money drugging perfectly healthy HIV+ people. Sick, ailing immunodeficienct (some of us dying) CFIDS patients received $6 Million. How can it make sense to you? source: report.nih.gov/categorical_spending.aspx

It's so easy to see that the medical establishment simply has these paradigms (CFIDS, HIV) inverted. AIDS patients are simply more CFIDS patients, who also happen to harbor a seemingly harmless virus, HIV. AIDS patients are just the tip of the CFIDS iceberg, and it's already well-documented that HIV is not the cause.

How else do you explain why there is no CFS/ME pandemic in the HIV+ population? CFS/ME does not discriminate.

The answer is that there is!

Any otherwise perfectly healthy HIV+ person that is:

1) symptomatic,
2) better on ARV's, and/or
3) severely immunosuppressed (AIDS)...

...is a CFIDS patient.

Putting causal pathogens aside, simply rename CFIDS, ME, and AIDS all to be "low natural killer cell disease" and only diagnosis patients with "low NK cells" with it. Everyone would clearly see that:

CFIDS + ME + AIDS = low NK cell disease = one catastrophic pandemic *

* not caused by HIV

Allied government sold-out global public health for sake of profit --> industry, oil, and Orwellian greed.

Now that the mystery has been solved, could we please stop wasting time and re-allocate all HIV funding into CFIDS/ME/AIDS research?

7 Step Plan to resolving our World's catastrophic public health disaster:

1. Demand research funding parity for CFIDS with AIDS.
2. Suggest that CFIDS & AIDS be researched together by scientists rather than as separate entities.
3. Urge the CDC to move their AIDS division under the CFS umbrella so they research all the infections that AIDS and CFIDS have in common.
4. Urge that AIDS organizations (like AmfAR) include CFS under their umbrellas so that CFS advocates don't have to reinvent the wheel.
5. Demand that the White House, Fauci and the Director of NIH make a public statement that (just from what we know today) in terms of the immune dysfunction and human suffering, CFIDS/ME is just as serious a public health problem as AIDS.
6. Request that an annual international joint CFIDS/AIDS conference be held by the WHO.
7. Suggest that next December 1st be declared the first "World CFIDS/AIDS Day."


For more about NON HIV AIDS: www.cfsstraighttalk.blogspot.com


{or simply google "non hiv aids"}


SIGN THE PETITION HERE: http://www.change.org/petitions/hiv-negative-aids


My 5min testimony about NON HIV AIDS at the June 2012 CFSAC committee meeting:
http://www.youtube.com/watch?v=ubjGm5dILpY&list=PL600CB038194B4593&index=11&feature=plpp_video/

Katrina Berne Interview

Medical Mystery Of Chronic Fatigue Syndrome Returns

JOANNE SILBERNER
September 5, 2011, 5:58 AM


Several months ago, researchers proved wrong the 2009 finding that
chronic fatigue syndrome is caused by a bacteria. Now, without a cause
to focus on, patients and doctors are back in a medical limbo.

Transcript

STEVE INSKEEP, host:

It's MORNING EDITION from NPR News. I'm Steve Inskeep. Good morning.

Today, on Your Health, we have two reports on Chronic Fatigue
Syndrome. We'll hear about possible treatments in a moment. First,
we'll ask some questions about the cause. Researchers still are not
sure why people suffer pain, exhaustion, anxiety, insomnia and other
symptoms, sometimes for years. They have suspected viruses but have
not proven which one. Joanne Silberner reports on what that
uncertainty means for people living with the disease.

JOANNE SILBERNER: Clinical psychologist Katrina Byrne of Seattle used
to run, play racquetball, see patients, and teach courses. That was
before she developed Chronic Fatigue Syndrome.

Ms. KATRINA BYRNE (Clinical Psychologist): There are days when I'm
bedfast and I get up only to use to the bathroom or get something to
eat or drink. There are days when I'm housebound, and that's the most
typical day for me right now.

SILBERNER: For the past 27 years, she's been prone to severe crashes
where she's sensitive to light and noise and unable to read or watch
TV.

Ms. BYRNE: Ill, like the way you feel when you have the flu, an
unrelenting, unremitting flu.

SILBERNER: The first doctors Byrne went to weren't much help.

Ms. BYRNE: One doctor told me it was related to anxiety; another one
said it was dehydration; a third one said it was hormonal; a fourth
one said it was stress-related and I needed to exercise.

SILBERNER: The problem back then was that no one much knew what was
going on. With no known cause, there was no definitive lab test there
still isn't.

And Anthony Komaroff, a professor of medicine at Harvard Medical
School, says that troubled doctors.

Mr. ANTHONY KOMAROFF (Harvard Medical School Medical Professor): I
would say most doctors were very, very skeptical. First, this illness
is defined, predominantly, by a group of symptoms, and so doctors were
asking what's the evidence - objective evidence - that there's
something physically wrong with these people?

SILBERNER: Over the years, researchers have identified various brain,
immune system and energy metabolism irregularities. Komaroff points to
a study done a couple of years ago by the Centers for Disease Control
and Prevention. It showed that the majority of doctors now recognize
Chronic Fatigue Syndrome as an illness. Today, an estimated one
million Americans are thought to have it.

But lots of regular folks are still doubters, at least in the
experience of Cynthia Johnson of Lake Oswego, Oregon. She says the
disbelief makes the disease worse. Johnson is a breast cancer
survivor, but in October 2009, she was hit with a bad flu that hasn't
go away.

Ms. CYNTHIA JOHNSON: People really admire you for fighting cancer, and
they're very excited that you survived. They congratulate you for
surviving. Nobody does that, day to day, for CFS. They are just like,
oh.

SILBERNER: Just as she was diagnosed a couple of years ago, a report
came out in a scientific journal linking a virus called XMRV to
Chronic Fatigue Syndrome. But 14 months later, four scientific papers
claimed the virus was just a lab contaminant. Few in the field are
hopeful that the cause has been discovered. The federal government is
sponsoring two large studies that should answer the question once and
for all.

For Katrina Byrne in Seattle and Cynthia Johnson in Portland, the
initial report, even if it turns out to be a blind alley, did some
good. Cynthia Johnson.

Ms. JOHNSON: I was happy to see all the attention in the press to
XMRV, simply to give attention to the disease. So my first thought was
at least people are writing about it.

SILBERNER: Johnson has been given a 50-50 chance by her doctor of
throwing off the symptoms in a couple of years. She knows what she'll
do if an effective treatment comes along.

Ms. JOHNSON: I'd like to make plans, you know, plan for the future,
plan for tomorrow, and know that it would go well, to make an
appointment for the doctors, or a haircut, or to meet friends and be
confident that I would feel reasonably well. You know, walk as far as
I could and go to the beach.

SILBERNER: Some changes are coming soon. The results of those two
studies on whether there's an XMRV connection may be released at a
meeting in Canada at the end of the month. Meanwhile, advocates for
people with Chronic Fatigue Syndrome are pushing for a name change to
make the name sound like more than a description of someone who just
needs a nap. For NPR News, I'm Joanne Silberner. Transcript provided
by NPR, Copyright National Public Radio.

A Tale of Two Viruses

http://bit.ly/zBgXXD


DISCOVER
M A G A Z I N E

The Crux


A Tale of Two Viruses: Why AIDS
Was Pinned to HIV, but Chronic
Fatigue Remains a Mystery


Vincent Racaniello is Higgins Professor of Microbiology &
Immunology at Columbia University, where he oversees
research on viruses that cause common colds and
poliomyelitis. He teaches virology to graduate, medical,
dental, and nursing students, and writes about viruses at
virology.ws


The detection of a new virus called XMRV
(http://bit.ly/x5WHir) in the blood of patients with chronic
fatigue syndrome (CFS) in 2009 raised hope that a
long-sought cause of the disease, whose central
characteristic is extreme tiredness that lasts for at least six
months, had been finally found.

But that hypothesis has dramatically (http://bit.ly/w4sHj2)
fallen apart (http://bit.ly/xhQJiT) in recent months.

Its public demise brings to mind an instance when a virus
*was* successfully determined to be behind a mysterious
scourge: the case of HIV and AIDS. How are these two
diseases different – how was it that stringent lab tests and
epidemiology ruled one of these viruses out, and one of
them in?


The first inklings of the disease now called AIDS surfaced in
Los Angeles in the summer of 1981. The 5 June 1981 issue
(http://1.usa.gov/x97mzV) of Morbidity and Mortality
Weekly Report described 5 homosexual men with
Pneumocystis carinii pneumonia (abbreviated PCP),
normally only observed in individuals with weakened
immune systems.

The article suggested the possibility of an immune
dysfunction related to exposure to something that would
make individuals vulnerable to opportunistic infections. Soon
clusters of PCP and Kaposi's sarcoma, a rare skin cancer,
were observed in gay men in other urban centers.

The Centers for Disease Control and Prevention established
a simple case definition – Kaposi's sarcoma or
opportunistic infections – and began scouring hospital
records. Over time this definition was modified, but its early
use identified an ongoing epidemic, and identified groups at
risk for the disease as men who have sex with men and
injection drug users.


The next year the new disease was called AIDS, and soon
the U.S. Public Health Service recommended that members
of risk groups not donate blood or plasma.


Soon came reports that the disease could be acquired by
newborn babies from their mothers, and also by
heterosexual contact.

By the fall there were nearly 700 people who had been
diagnosed with AIDS in the U.S., of whom almost 300 had
died. The CDC and World Health Organization worked
together to publish global data on the disease, and issue
recommendations to prevent its spread.


During the early years, the epidemiology of AIDS suggested
an infectious cause, and in 1983, just two years after the
disease was identified, a novel retrovirus
(http://bit.ly/zJkSGS) was isolated from a patient at risk for
AIDS.

A year later a commercial blood test was developed, which
allowed comprehensive studies to be done that showed
clearly that the virus, later named human immunodeficiency
virus type I (HIV-1), was the cause of AIDS. This conclusion
was strengthened by the transmission of AIDS to hospital
workers when they inoculated themselves with
HIV-containing blood by accidental needle sticks.


By 1987 the first anti-HIV drug, azidothymidine or AZT, was
licensed for the treatment of AIDS. Today over 20 anti-HIV
drugs have been approved. When given in combinations of
three, the emergence of drug-resistant viral variants is
minimized, transforming AIDS from a death sentence to a
life-long chronic disease.


The story of CFS, generally defined as persistent fatigue of
six months or greater not relieved by rest and accompanied
by other specific symptoms, is markedly different.

This syndrome was first reported in Los Angeles as well, but
in 1934. There were subsequent sporadic outbreaks, some
of which were reviewed by DA Henderson in 1959
(http://bit.ly/xYHOq4), who noted that females were more
frequently affected, and suggested that a virus might be
involved.

In the 1980s Daniel Peterson identified antibodies against
Epstein-Barr virus (EBV) in the blood of a group of CFS
patients in Incline Village, Nevada (http://1.usa.gov/zzgs3q).

The CDC entered the investigation but was unable to confirm
that antibodies to the virus were consistently present in
patient blood. A subsequent case-control study failed to
identify EBV as the causative agent of the disease, which
was subsequently named chronic fatigue syndrome.


The search for that agent of CFS has continued to be
fruitless. In addition to EBV, a host of other viruses have
been found in CFS patients, including enteroviruses,
measles virus, herpesviruses, and human T-lymphotropic
virus type II. However, none have been consistently
detected in CFS patients and therefore are not considered
to cause the disease.

The possibility of a viral cause of CFS re-emerged in 2009
with the detection of a retrovirus called XMRV
(http://1.usa.gov/zT9NKI) in the blood of a substantial
fraction of CFS patients.

A second laboratory (http://1.usa.gov/x47VLE) subsequently
identified sequences related to murine leukemia viruses,
also retroviruses, in the blood of CFS patients. However,
many other laboratories were unable to replicate these
findings, and both papers have been retracted
(http://bit.ly/xhQJiT).


Why do the stories of AIDS and CFS have such different
outcomes? One reason is that it has been difficult to reach
a consensus on a clinical definition of CFS.

At the onset the case definition of AIDS was simple -
-"Kaposi's sarcoma or opportunistic infections "– which
made it possible to rapidly and accurately identify new
cases, especially among different research groups around
the country.

This led to the establishment of risk factors, and the
epidemiological data obtained from this work made it highly
likely that an infectious agent was involved, spurring the
search for the causative pathogen.

The case definition for CFS has undergone a number of
revisions over the years. When different research groups
use different definitions of the disease, it becomes difficult
to compare findings.

Most importantly, there is no indicator or diagnostic test that
can be used to identify CFS, and since diagnosing CFS is a
long and difficult process, cohorts established by different
investigators vary, leading to different findings, confusion,
and contention.

In contrast, AIDS was readily identifiable and easily
diagnosed once a blood test for HIV was developed.

Another problem is that in contrast to their excellent work on
AIDS, the CDC has stumbled when tackling CFS
(http://bit.ly/usLskj).

The CDC has dismissed evidence that CFS is an organic
disease, and spent funds on investigating psychiatric and
trauma-related causes, rather than infectious origins.

The agency also diverted funds designated for CFS to other
programs. These and other missteps alienated the CFS
patient community – the opposite of what the agency
accomplished with the AIDS community.


In part due to the standardized case definition of AIDS,
identification of a candidate virus was relatively rapid.
Determining its role in the disease was facilitated by the
development of a blood test, which could be used to prove
that HIV-1 caused AIDS.

The relationship between HIV and AIDS was further
confirmed by the development of antiviral drugs that
inhibited viral replication and helped alleviate the symptoms
of the disease.


Why have investigators failed to identify a virus behind CFS?
(It is not due to the lack of appropriate technology; this has
improved substantially since the 1980s with the
development of polymerase chain reaction and rapid DNA
sequencing.)

One explanation for this dilemma is that an infectious agent
does not cause CFS. However, there is plausible evidence
for an infectious etiology, including observations that the
disease is known to occur in outbreaks.

Furthermore, in many cases the onset of symptoms appears
to begin with a flu-like illness.

Additionally, CFS is a heterogeneous disease, and may be
caused by several different agents or a combination of
viruses and non-infectious conditions.

Another possibility is that an infection initiates an immune
response that spirals out of control, leading to CFS
symptoms.

This scenario implies that at least some CFS patients have
underlying deficits in immune regulation. If that's true, it will
be very difficult to identify the virus involved because it will
likely have been eliminated from patients' systems by the
time CFS symptoms become apparent.


In retrospect, it is clear that the properties of AIDS made it
an easy disease to understand. While the path to
understanding CFS has been clouded by non-scientific
issues, in the end the main reason why we do not
understand this disease is because it is extraordinarily
complex.

But that never stopped a good scientist.

October CFSAC Review

Another CFSAC Done Gone

October 6th, 2012
Jennie Spotila J.D.

The CFS Advisory Committee held its second meeting of the year on
October 3-4, 2012. Last time, I organized my summary around the good,
the bad, and the WTF moments. This time, I am organizing around the
discussion themes. Overall, I felt this meeting was more substantive
than in the past. There were even hints of introspection and data
driven discussion.

Agency Updates

Assistant Secretary Dr. Howard Koh attended the opening of the
meeting, and provided an update on the Department's efforts since the
last meeting. I was watching the meeting via webcast, and my feed
froze during Dr. Koh's comments. However, the portion I did see
contained nothing new. Dr. Koh did not provide any details on the Ad
Hoc Working Group beyond what we already know. Unlike previous
meetings, he did not take questions from the members. Although he said
"the committee has gotten stronger," he did not announce the
appointment of a new member to replace Dr. Rose. The committee bylaws
require vacancies to be filled within 90 days, so the failure to
appoint a replacement is a violation of the bylaws.

Both the FDA and Social Security Administration gave substantive
presentations to the Committee. In my opinion, this was the high point
of the meeting. Both Dr. Sandra Kweder (FDA) and Arthur Spencer (SSA)
provided detailed information about their agencies and CFS related
data. Dr. Kweder reported on the status of nine investigative new drug
applications for CFS. Mr. Spencer provided disability data that the
committee has been requesting for years. The overall approval rate for Social Security disability among cases where CFS is the primary diagnosis is 21%, in contrast to a national overall rate of 30%. I'm
looking forward to seeing the slides from both these presentations
because there was a lot of good information in them.

NIH and CDC also gave detailed updates. Dr. Susan Maier (NIH) reported
that several new members were added to the Trans-NIH ME/CFS Working
Group, including Dr. Harvey Alter. It's very good news that Dr. Alter
is staying involved in CFS despite the end of XMRV. Dr. Maier also
provided (for the first time) data on the acceptance rates for
CFS-related grant applications. The overall success rate is 25%, and
in FY2012 the success rate is 18%. These rates are higher than the
overall rate across NIH. Most of CDC's report was focused on various
education initiatives including CMEs offered through Medscape and CDC,
as well as video of patient vignettes for the MedEd Portal that will
be finished next year.

The full post can be found here:
http://www.occupycfs.com/2012/10/06/another-cfsac-done-gone/

Mary Schweitzer and Pat Fero's latest testimony on funding

Mary Schweitzer
Oral Testimony to the Chronic Fatigue Syndrome Advisory Committee to the
U.S. Department of Health and Human Services
Washington, D.C.
October 3, 2012

-----------------------

Peanuts cartoon [courtesy of the Charles M. Schultz Museum, Santa Rosa, California] -

Charlie Brown is watching Lucy and Linus.
Lucy: OK, Linus. Now we put on our dark glasses and we look at the sun.
Charlie Brown: ?
Lucy: Do you see it? It's eclipsing! It's eclipsing! Isn't that marvelous?
Charlie Brown: Oh good grief!
Lucy: Now, when you take off your glasses, the eclipse stops. See?
Charlie Brown, turing away: I can't stand it!
Lucy: Now put 'em on again … See? It's eclipsing! It's eclipsing!
Charlie Brown to Patty: Poor Linus. He'll have to go to school twice as long as everybody else. It'll take him twelve years to UNLEARN everything Lucy's been teaching him!

-----------------------

Thank you for allowing me time to testify.

[I also want to thank FDA for the meetings they are holding on developing pharmaceutical treatments for ME and CFS. I have been on Ampligen since 1999, except for three or four years. Please don't take it away from me again. (Added in oral testimony.)]

I want to point out several issues that have come up since the last meeting of CFSAC.

FIRST, I'm glad that CFS is going to be coded in G93.3 in ICD-10-CM, but why is NCHS determined to add "NOS" to CFS in ICD-10-CM?

At the last meeting of NCHS, Donna Pickett stated that in this case, we should take NOS to signify the default designation for the code. That doesn't make sense – NOS would be expected to appear in every code if that were true. And it most certainly doesn't.

Accompanying material for ICD-9-CM tells us that NOS (not otherwise specified) stands for cases where there is not enough evidence to give a more specific diagnosis. That makes more sense – but it leaves us even more confused as to what NCHS intends by the designation "CFS NOS" - because if there's not enough evidence for a CFS diagnosis, the CDC website says to use CF, or chronic fatigue, which is coded at R53.8 (where they wanted to code CFS).

ICD-10 has been out for two decades. It is in use by over 100 nations. Several use clinical modifications, like we do, but they adopted theirs a decade ago.

"CFS NOS" does not occur in any other nation's version of ICD-10. Period. Why has it suddenly appeared in ours? Get rid of it.

[There was more on this subject in the version handed in to the committee.]

SECOND, do something about CDC. Shut down the website, throw away the "toolkit" and the pamphlet, and while you're at it, shut down the studies in conjunction with Emory Universities section on factitious illnesses within their department of psychiatry.

It's funny - I find the Emory studies laughable - the entire idea of a million Americans having a "factitious" illness is laughable - but your people find them convincing. At the same time, the virus studies seem to come much closer to fitting the symptoms we actually have, but you find the virus studies laughable.

I don't want to be rude, but let's look at the institutions involved. CDC is infatuated with Emory University (because it's nearby, I guess) and, in particular, Emory's unit on factitious illness. The virus studies are being conducted by Ivy League institutions and others, such as Stanford and Mt. Sinai, that are of that stature. Please. Get us somebody to deal with this disease who knows what they are doing. Factitious illness is – frankly – a crackpot idea. You've spent enough time on it, and since Dr. Reeves is no longer with us to defend it, let's move on.

If CDC refuses to move on, then I turn to Secretary Sebelius and ask that the entire section on CFS at CDC be shut down now, along with the website and current publications.

As Charlie Brown observed, poor Linus would have to go to school twice as long to unlearn everything Lucy had taught him. Those new to the disease CFS who have turned to CDC for information, including family doctors and anyone in the media, will have to re-learn everything they think they know after having read what's been on that website for 25 years.

THIRD, I have explained at length in other testimony and in an essay on my blogsite how the Wichita study that supposedly verified the accuracy of the "empirical definition" by the late William Reeves of CDC for CFS was a sham. I think that article should be retracted, but that is probably a subject for another day. In the meantime, return to Fukuda (1994) and dispense with any references to the Reeves definition, which also means get rid of the questionnaires and any studies conducted with them.

FINALLY, when is something going to be done about the absence of funding for our disease by NIH? At the most, NIH has allocated $6 million a year to this disease, which is $6 per person. All we ask for is parity. Multiple Sclerosis, hardly an overfunded disease, has allocated an average of $350 a year per person since 2000 to a disease with half as many patients. By that standard, NIH should be spending at least $700 million a year on CFS.

I was on the planning committee for NIH's CFS State of the Knowledge Workshop, and thought it went off very well. However, I was a little concerned by a statement Dr. Coffin made towards the end of his presentation. He said that too much time and money had already been wasted on the connection between [the apparent lab contaminant] XMRV and CFS.

Too much money?? Too much money had been spent trying to determine whether a retrovirus was present in a disease that could affect at least one million adult Americans?

Is that the attitude of NIH?

For years, NIH has stated that the reason there is not more funding for CFS research is that CFS researchers do not turn in good enough proposals. Aside from the overt insult to researchers around the nation, many connected with top research departments, who have ventured into the CFS arena, with such a disparity in funding it would seem that NIH would do a better job of finding the projects instead of clearing itself of an obligation to fund the projects that are out there.

When I was at the NIH workshop, during a break I had planned to ask Dr. Coffin what he thought of the question of whether chromosomally integrated HHV-6A actually has been found. It had sparked a heated debate at the HHV-6 Research Conference held in Reston, VA, a month earlier. But I foolishly began by saying I fought for years a persistent infection with HHV-6A. Coffin chuckled and told me I did not have HHV-6A. Having been in a published study conducted by Dr. Dharam Ablashi, I was fairly certain I did have HHV-6A. The only thing that held it back was that I was on Ampligen most of the past 14 years.

I never got to ask Dr. Coffin about ciHHV-6. He walked off chuckling at the absurdity of my remark.

Later, during another break, I turned to Dr. Stephen Collins of CDC. I wanted to discuss the other viruses associated with CFS. I began with EBV, and again, I made the mistake of starting by commenting that I had problems with recurring Epstein-Barr. He did not chuckle. He put his hand up (as in "talk to the hand") and said, simply, "No you don't. It's a problem with your testing. It's a false echo." Then he turned and walked away.

So twice I had asked a question having to do with a research program of which I was a part, and twice I had ended up staring at a man's back as he walked away from me.

[Then, at today's meeting of CFSAC, the topic was biomarkers. Apparently unaware that researchers have been working on a number of biomarkers in this disease for almost thirty years, they brought in someone from a different disease. Once again, the biomarkers I have weren't mentioned.]

What concerns me here is that Dr. Colllins is in charge of the division at CDC where CFS resides. And Dr. Coffin is a highly respected virologist who might well be asked to review a research proposal for NIH.

Apparently the new narrative we are supposed to accept is that CFS is an autoimmune disease. It just LOOKS like we have viruses because our immune systems are hyper-activated.

I had the same EBV testing that college students get. Nobody says they don't have EBV when the tests show them positive for active EBV. I had the same CMV and HHV-6 testing that AIDS patients get. Nobody says they don't have active CMV or HHV-6 when the tests show them positive for those viruses.

Why is it different for me?

And that brings us back to the basic problem: lack of funding.

If these gentlemen thought the very idea of persistent infections with HHV-6A or recurring infections with EBV was ridiculous, how would they judge a research program on that very subject?

What must their reaction be to Dr. Montoya, who has been studying EBV and beta herpesviruses in CFS at Stanford University for at least six years? Are they funding studies of the types of testing for natural killer cell function used by Dr. Klimas or Dr. Peterson? What of Dr. Lipkin's promise to look at the other viruses (besides retroviruses) implicated in CFS? What about the Mt. Siniai initiative, and projects at Cornell, Harvard, USC, and many other reputable research institutions that at this very moment are studying the interrelationship of a number of viruses, including not only the herpesviruses, but also enteroviruses?

Could this prejudice account for the denial of research funding by NIH? Could this problem – that there are people in a position of power over who receives funding think it is ridiculous that we could actually be suffering from long-term viral infections, that we could be immune deficient – could that have something to do with the paucity of NIH funding? It's not the research PROPOSALS - it is the research TOPICS that are "unacceptable" - unacceptable because they refute the current pet theory at CDC and most likely at NIH.

Let me suggest that if researchers at Ivy League and comparable institutions are working on these projects, they deserve funding by NIH. The problem is with the evaluators, not the researchers.

And we certainly don't deserve ridicule for bringing the subject up.

Thank you.

Mary M. Schweitzer, Ph.D.

* * *
Note: Ms. Fero's testimony refers to several charts that I was unable
to attach to the post.

Fall 2012 Testimony CFSAC
Pat Fero

For almost 10 years, I have tracking NIH CFS funding patterns. What I
will present today is evidence that patients
are worse off in 2012 than in 1993. I expect you to look at these
graphs. I expect you to walk away with some
history of NIH activity. My hope is to further your understanding of
the need for fundamental change within the NIH.

THE EVIDENCE:
1. General Accounting Office,(GAO) graph This graph shows intramural
and extramural funding as well as
cooperative agreements. On pages 46 – 52 of the GAO report,
investigators present a rationale for why some
projects were excluded from CFS expenditures and why other projects
should have been included.

Overall, the GAO concluded that the NIH was actively pursuing CFS
research despite near flat line spending from
1996 though 1999. In addition, investigators state, "Despite its
varied efforts, the intramural program on CFS in
NIAID is currently inactive. NIAID's primary CFS investigator has
recently moved elsewhere in the agency, and we
were told that no one else has yet indicated an interest in developing
work in this area." (Pg. 22)

2. Line graph two The blue line indicates NIH reported levels of CFS
expenditures from 2000 through 2010. In
1999, GAO reports research funding close to 7 million dollars. Within
the next 11 years, funding spiraled downward
to a low of 3.5 million dollars in 2008. From 2002 through 2008 with
no intramural CFS expenditures, it appears
that the CFS intramural program remained inactive. The bounce in 2009
to over 6 million is due to intramural and
extramural research on pathogens to include XMRV.

The black line shows NIH levels of CFS expenditures once adjusted
through FOIA data. I DID EVERYTHING
HUMANLY POSSIBLE TO MEET THE STANDARDS OF THE GAO. If CFS was not the
primary focus of the grant,
the GAO investigators did not include it in their report and I did not
include it in this report either.
On May 30, 2002, the National Advisory Allergy and Infectious Disease
Council (NAAIDC) voted to "not renew
CFS research centers and to give the money that NIAID had set aside
for their concept to the NIH ORWH which
coordinates CFS research for the entire NIH…" (5.30.02 NAAIDC meeting
minutes) Note: Intramural funding for
CFS stopped in 2002. Note: From 2002 through 2005, six renewed
unrelated projects show as CFS expenditures.
(FOIA 32335 ) NOTE: 2002 – 2007 gap between reported and actual CFS. I
do not blame ORWH.

3. Bar graph three Blue bars show NIH reported CFS spending. Red bars
have a number inside showing the
number of new grants funded. Again, look at 2002 through 2005. The
problem is arithmetic )), but illusive.

2010. Under ME/CFS categorical spending, the NIH REPORTER excludes at
least one CFS primary research
grant - $700,000 a year, 5 year, to a PI from Ohio State. This grant
shows under the search terms "chronic fatigue
syndrome." In 2010, an NIH FOIA officer said that the NIH Reporter is
an accurate reporting of CFS spending. Is it?

4. NIH Activities This chart is copied the GAO report page 56 and 57.
The NIH reported a long list of ongoing
Congressionally Requested CFS projects. What Happened?

There is a pattern in NIH CFS funding. Despite the development of
extraordinary research techniques and
technology, patients are on the curb. We have no evidence from the NIH
that we, the people, are being taken
seriously. We MUST continue to promote fairness. We must continue to
ask for fundamental change. I want all of
us to look at the truth. Do not sugar coat this NIH "lack of interest"
in CFS as poor grant writing, a systems error,
misstatements, and lack of funds. I may be sick, but I am not stupid.
We need a strategic and fully funded 5 year
plan. Don't be selling me a bill of goods about planning "new action,
if it does not cost anything." I am a human
being. These sick adults, and our sick children will show you we matter.
 

CFS and Impaired Cardiac Function -- MRI tagging

http://www.ncbi.nlm.nih.gov/pubmed/21793948


J Intern Med. 2011 Jul 27. doi:
10.1111/j.1365-2796.2011.02429.x.
[Epub ahead of print]

Impaired Cardiac Function in
Chronic Fatigue Syndrome
measured using Magnetic
Resonance Cardiac Tagging.


Hollingsworth KG, Hodgson T,
Macgowan GA, Blamire AM, Newton JL.


Newcastle Magnetic
Resonance Centre, Institute of
Cellular Medicine, Newcastle
University, Campus for Ageing
and Vitality, NE4 5PL, UK
Institute for Ageing and
Health, Newcastle University,
Campus for Ageing and
Vitality, NE4 5PL, UK

Department of Cardiology,
Freeman Hospital, Newcastle
upon Tyne, NE7 7DN and
Institute of Human Genetics,
Newcastle University, NE2
4HH, UK


Abstract


Objectives:

Impaired cardiac function has
been confirmed in patients
with chronic fatigue syndrome
(CFS).

Magnetic resonance cardiac
tagging is a novel technique
that assesses myocardial wall
function in vivo.

We hypothesized that CFS
patients may have impaired
development and release of
myocardial torsion and strain.


Methods:

Cardiac morphology and
function was assessed using
magnetic resonance imaging
and cardiac tagging
methodology in 12 CFS
(Fukuda) and 10 matched
controls.


Results:

Compared to controls the CFS
group had substantially
reduced LV mass (reduced by
23%), end diastolic volume
(30%), stroke volume (29%),
and cardiac output (25%).

Residual torsion at 150% of
the end-systolic time was
found to be significantly
higher in the CFS patients
(5.3±1.6(o) ) compared to the
control group (1.7±0.7(o),
p=0.0001).

End diastolic volume index
correlated negatively with
both torsion to endocardial
strain ratio (TSR) (r =-0.65,
p=0.02) and the residual
torsion at 150% end systolic
time (r=-0.76, p=0.004), so
decreased end diastolic
volume is associated with
raised TSR and torsion
persisting longer into
diastole.

Reduced end diastolic volume
index also correlated
significantly with increased
radial thickening (r=-0.65,
p=0.03) and impaired
diastolic function represented
by the ratio of early to late
ventricular filling velocity (E/A
ratio, r=0.71, p=0.009) and
early filling percentage
(r=0.73, p=0.008).


Conclusion:

CFS patients have markedly reduced cardiac mass and
blood pool volumes, particularly end diastolic volume:
this results in significant impairments in stroke volume and cardiac output compared to controls.

The CFS group appeared to have a delay in the release of torsion.




Copyright © 2011 The
Association for the
Publication of the Journal of
Internal Medicine.

PMID: 21793948 [PubMed -
as supplied by publisher]
 

January 2013 Conference: Primer for Clinical Practitioners

APTA=American Physical Therapy Association

--------
http://www.apta.org/CSM/Programming/2013/CardiovascularPulmonary/

Tuesday, January 22

Best Practices Update for Chronic Fatigue Syndrome/Myalgic
Encephalomyelitis: The IACFS/ME Primer for Clinical Practitioners

Time: 8:00 am–10:00 am (See Program for Room)

Speakers: Todd E. Davenport, PT, DPT; Staci R. Stevens, MA; Daniel L.
Peterson, MD; Kenneth J. Friedman, PhD

Level: Multiple Level

Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is one
cause of clinically debilitating fatigue. Its features have been
related to Gulf War syndrome and post-9/11 syndrome. CFS/ME may
present a spectrum of symptoms, providing multiple reasons for entry
to physical therapy. Physical therapists are in a unique position to
identify CFS/ME and to direct appropriate management through both
physical therapist interventions and referral to other health care
providers. Over the past 2 years, an international working group of
the International Association for Chronic Fatigue Syndrome/Myalgic
Encephalomyelitis (IACFS/ME) has developed a document that describes
current clinical best practices for the diagnosis, medical and
psychological management, and physical rehabilitation for people with
CFS/ME.

This session will provide leading-edge information about physical
therapy management of patients with CFS/ME from a group of recognized
clinicians and researchers, including participants of the guideline
development committee. In this session, the speakers will discuss the
development of the IACFS/ME Primer for Clinical Practitioners;
summarize the clinical features and patho-etiology of CFS/ME with
respect to optimal identification, differential diagnosis, and
clinical management by physical therapists; discuss current medical
and psychological management for people with CFS/ME; and describe
current concepts in physical rehabilitation for people with CFS/ME.

Upon completion of this course, you'll be able to:
•Define CFS/ME according to current classification models.
•Discuss the evidence regarding the physical and cognitive
pathophysiological processes that underlie the clinical presentation
of CFS/ME.
•Appraise a patient/client's case for the diagnostic features of CFS/ME.
•Compare and contrast the clinical presentation of CFS with other
health conditions that cause persistent pain and fatigue.
•Summarize current medical and psychological management for CFS/ME.
•Design and implement an evidence-based physical therapy management
program for patients with CFS/ME.

-------
http://www.apta.org/CSM/Overview/

The Combined Sections Meeting (CSM) focuses on programming designed by
all 18 of APTA's specialty sections.

CSM 2013 will bring together more than 9,000 physical therapy
professionals from around the nation for several stimulating days of
exceptional programming, networking opportunities, and an exhibit hall
filled with products and services in San Diego. Here's an overview:
etc.
 

XMRV: It's simply not there

Final Study Confirms: Virus Not Implicated in Chronic Fatigue Syndrome
by Martin Enserink on 18 September 2012, 2:08 PM

Coming around. "It's simply not there," Judy Mikovits said at a press
conference this morning.
Credit: Columbia University

You could be forgiven for thinking that the story of XMRV, a mouse
retrovirus implicated in chronic fatigue syndrome (CFS), is over.
After all, study after study has failed to replicate the XMRV-CFS
link, and last year, Science retracted the 2009 paper in which XMRV
was first fingered as a cause of the elusive syndrome. Most
researchers concluded long ago that those findings resulted from an
accidental contamination of patient samples in the lab.

But until now, the biggest study on the topic still hadn't been
wrapped up: a project funded by the U.S. National Institutes of Health
(NIH) and led by Ian Lipkin of Columbia University that brought
together supporters and skeptics of the theory that XMRV plays a role
in chronic fatigue. Today, mBio published the results of the study,
which proves that, as most scientists suspected, the XMRV theory is
most definitely dead.

This time, even Judy Mikovits, the chief author of the 2009 study and
the main protagonist in the twisted scientific saga, agrees. Mikovits,
formerly at the Whittemore Peterson Institute (WPI) in Reno, Nevada,
participated in Lipkin's study and concedes that it is "the definitive
answer. … There is no evidence that XMRV is a human pathogen."

Three research groups took part in the mBio study: Mikovits, along
with her collaborators Francis Ruscetti at the National Cancer
Institute and Maureen Hanson at Cornell University; a team led by
Shyh-Ching Lo at the Food and Drug Administration, which linked CFS to
a related group of viruses called MLVs in a study that was also
retracted; and a group at the Centers for Disease Control and
Prevention, which had failed to find the virus in CFS patient samples.
Each group was presented with samples from 147 patients and 146
healthy controls from six U.S. cities. Each was free to analyze
samples using its own techniques; that way, no one could complain that
the right methods weren't used, Lipkin says. The samples were blinded
until all the analyses were done.

Live Chat: Do Hungry Primates Live Longer? Thursday 3 p.m. EDT
Mikovits's participation in the study was complicated by the fact that
she was fired by WPI in September of 2011 and later arrested, jailed,
and charged with illegally taking data and related property from WPI.
(The criminal charges, which came on top of a civil suit by WPI, were
dropped in June.) Antibody testing for Mikovits's share of the study
was done at Ruscetti's lab and PCR tests at Hanson's lab.

None of the groups found any trace of XMRV or MLVs whatsoever—neither
in patients nor controls. Mikovits and Ruscetti did find that about 6%
of patients and controls had antibodies that reacted to XMRV—a result
that they chalk up to aspecific binding instead of XMRV infection.

As to XMRV, "it's simply not there," Mikovits said at a press
conference this morning to announce the results of the new study. No
previous study had tried to replicate her findings using her exact
methods, Mikovits says. "I'm forever grateful to Ian Lipkin for making
it possible to participate," she says. Lipkin says he is "proud" of
Mikovits for accepting the outcome and asked the audience at the press
conference to give her a round of applause.

The outcome isn't surprising, says Vinay Pathak of the National Cancer
Institute, one of the authors of a key study last year that showed
XMRV was accidentally created in the lab. Still, Pathak says, Lipkin's
study is a "model" for how similar disputes can be resolved in the
future. Kim McCleary, the head of the CFIDS Association of America, a
CFS advocacy group, hopes the study will finally bring closure to the
debate about XMRV.

Samples gathered for the new study will also be available for other
researchers, which is a "silver lining for an ultimately disappointing
outcome," McCleary says. "We hope that people from all over the world
will use these samples," Lipkin said this morning.

http://news.sciencemag.org/sciencenow/2012/09/final-study-confirms-virus-not-i.html
 

EEGs differentiate CFS from Depression

Note: A Case-control study is a type of epidemiological study design.
Case-control studies are used to identify factors that may contribute
to a medical condition by comparing subjects who have that condition
(the 'cases') with patients who do not have the condition but are
otherwise similar (the 'controls'). Obviously how you define those
with and those without a disease or disorder substantially contributes
to the results and conclusions of any study. One of the major pluses
of this study, which has been in the works for several years, is the
size of the study.

EEG spectral coherence data distinguish chronic fatigue syndrome
patients from healthy controls and depressed patients – A case control
study

Previous studies suggest central nervous system involvement in chronic
fatigue syndrome (CFS), yet there are no established diagnostic
criteria. CFS may be difficult to differentiate from clinical
depression.

The study's objective was to determine if spectral coherence, a
computational derivative of spectral analysis of the
electroencephalogram (EEG), could distinguish patients with CFS from
healthy control subjects and not erroneously classify depressed
patients as having CFS.

Methods: This is a study, conducted in an academic medical center
electroencephalography laboratory, of 632 subjects: 390 healthy normal
controls, 70 patients with carefully defined CFS, 24 with major
depression, and 148 with general fatigue. Aside from fatigue, all
patients were medically healthy by history and examination.

EEGs were obtained and spectral coherences calculated after extensive
artifact removal. Principal Components Analysis identified coherence
factors and corresponding factor loading patterns.

Discriminant analysis determined whether spectral coherence factors
could reliably discriminate CFS patients from healthy control subjects
without misclassifying depression as CFS.

Results: Analysis of EEG coherence data from a large sample (n=632) of
patients and healthy controls identified 40 factors explaining 55.6%
total variance. Factors showed highly significant group
differentiation (p<.0004) identifying 89.5% of unmedicated female CFS
patients and 92.4% of healthy female controls.

Recursive jackknifing showed predictions were stable. A conservative
10-factor discriminant function model was subsequently applied, and
also showed highly significant group discrimination (p<.001),
accurately classifying 88.9% unmedicated males with CFS, and 82.4%
unmedicated male healthy controls.

No patient with depression was classified as having CFS. The model was
less accurate (73.9%) in identifying CFS patients taking psychoactive
medications.

Factors involving the temporal lobes were of primary importance.

Conclusions: EEG spectral coherence analysis identified unmedicated
patients with CFS and healthy control subjects without misclassifying
depressed patients as CFS, providing evidence that CFS patients demonstrate brain physiology that is not observed in healthy normals or patients with major depression. Studies of new CFS patients and
comparison groups are required to determine the possible clinical
utility of this test.

The results concur with other studies finding neurological abnormalities in CFS, and implicate temporal lobe involvement in CFS pathophysiology.

Author: Frank DuffyGloria McAnultyMichelle McCrearyGeorge
CuchuralAnthony Komaroff
Credits/Source: BMC Neurology 2011, 11:82
 
Free (provisional) full text at:
http://bit.ly/js0SQl i.e.
http://www.biomedcentral.com/content/pdf/1471-2377-11-82.pdf

Final version will be available at:
http://www.biomedcentral.com/1471-2377/11/82

International Consensus Criteria for ME/CFS

Source: Journal of Internal Medicine
Preprint
Date: July 2011
URL: http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2796.2011.02428.x


Myalgic Encephalomyelitis: International Consensus Criteria
-----------------------------------------------------------
Bruce M Carruthers MD, CM, FRCP(C), Marjorie I van de
Sande BEd, Kenny L De Meirleir MD, PhD, Nancy G Klimas
MD, Gordon Broderick PhD, Terry Mitchell MA, MD, FRCPath,
Don Staines MBBS, MPH, FAFPHM, FAFOEM, AC Peter Powles
MRACP, FRACP, FRCP(C), ABSM, Nigel Speight MA, MB, BChir,
FRCP, FRCPCH, DCH, Rosamund Vallings MNZM, MB, BS, MRCS,
LRCP, Lucinda Bateman MS, MD, Barbara Baumgarten-
Austrheim MD, David S Bell MD, FAAP, Nicoletta Carlo-
Stella MD, PhD, John Chia MD, Austin Darragh MA, MD,
FFSEM. (RCPI, RCSI), FRSHFI Biol I (Hon), Daehyun Jo MD,
PhD, Don Lewis MD, Alan R Light PhD, Sonya Marshall-
Gradisbik PhD, Ismael Mena MD, Judy A Mikovits PhD,
Kunihisa Miwa MD, PhD, Modra Murovska MD, PhD, Martin L
Pall PhD, Staci Stevens MA


Abstract

The label 'chronic fatigue syndrome' (CFS) has persisted
for many years because of lack of knowledge of the
etiological agents and of the disease process. In view of
more recent research and clinical experience that strongly
point to widespread inflammation and multisystemic
neuropathology, it is more appropriate and correct to use
the term 'myalgic encephalomyelitis' (ME) because it
indicates an underlying pathophysiology. It is also
consistent with the neurological classification of ME in
the World Health Organization's International
Classification of Diseases (ICD G93.3). Consequently, an
International Consensus Panel consisting of clinicians,
researchers, teaching faculty and an independent patient
advocate was formed with the purpose of developing
criteria based on current knowledge. Thirteen countries
and a wide range of specialties were represented.
Collectively, members have approximately 400 years of
both clinical and teaching experience, authored hundreds
of peer reviewed publications, diagnosed or treated
approximately 50,000 ME patients, and several members
coauthored previous criteria. The expertise and experience
of the panel members as well as PubMed and other medical
sources were utilized in a progression of suggestions/
drafts/reviews/revisions. The authors, free of any
sponsoring organization, achieved 100% consensus through
a Delphi type process.

The scope of this paper is limited to criteria of ME and
their application. Accordingly, the criteria reflect the
complex symptomatology. Operational notes enhance
clarity and specificity by providing guidance in the
expression and interpretation of symptoms. Clinical and
research application guidelines promote optimal
recognition of ME by primary physicians and other health
care providers, improve consistency of diagnoses in
adult and paediatric patients internationally, and
facilitate clearer identification of patients for
research studies.

--------
(c) 2011 The Association for the Publication of the Journal of
Internal Medicine
 
TRANSLATION INTO OTHER LANGUAGES AVAILABLE:
Here you can find European translations of the International Consensus
ME Document, Journal of Internal Medicine, July 2011. With thanks to
Plataforma para la Fibromialgia, Síndrome de Fatiga Crónica y SSQM,
Reivindicación de Derechos for Spain, the Norwegian ME organisation for
Norway and ME/CVS-Net and Esther for the Netherlands and ME/CVS in
Belgium for Belgium, CFS -aktuelle for Germany. You can print the ME
document for your own doctor.

Spanish translation of the International Consensus ME Document:
http://esme-eu.com/getfile.php/Files/536_Criterios%20ICC-EM%20Julio%202011.pdf
Norwegian translation of the International Consensus ME Document:
http://esme-eu.com/getfile.php/Files/Norwegian%20ME%20ICC%281%29.pdf
German translation of the International Consensus ME Document:
http://www.cfs-aktuell.de/ICC.pdf
 
 

Misinformation on the internet

Many Internet sites contain considerable misinformation when it comes
to health and medicine. Make sure the information you find can be
independently and factually verified. Always check with your own
physician before adding herbs/supplements to your diet (natural
doesn't mean it's not a drug), purchasing expensive "cures" or
treatments and when requiring a medical diagnosis.

Potential problem sites:

*Any site promising to "cure" CFS, or any other disease for that
matter - particularly when the disease is included along with a long
laundry list of other unrelated diseases. Such sites should probably
best be avoided. There is no cure for ME and CFS as well as many other
organic diseases at this time. Many such sites are financial scams
targeting desperate people and they dress the site up to look like the
"cure" comes from a "doctor" or other "expert."

*Some so-called health forums or sites on the Internet prohibit
posting of legitimate links to sources of accurate information such as
the PubMed - the site for the U.S. National Library of Medicine;
medical citations and/or scientific papers - thus limiting posts to
poster "opinion" only. Although most likely the advice and opinions
found on such sites are well-intentioned, "opinion" should not be a
substitute for factual medical or scientific information or access to
such information.

*As well, other sites post inaccurate, cobbled together articles - not
to give accurate information, - but in order to get "clicks" on their
site in order boost their own rankings in the algorithms of search
engines such as Google. Such sites use "popular" and other often
queried topics as bait. A common tip off to such sites may be the word
admin in place of an actual authors name as well as a URL that has
nothing to do with the topic at hand..
 
 
(Thanks to Kelly Latta for this one!)
 
 
"The trouble with quotes on the Internet is that you can never know if they are genuine." - Abraham Lincoln 

Scientific Research Fraud

URL: http://www.cbsnews.com/8301-204_162-57523932/study-scientific-research-fraud-on-the-rise/
Ref: http://www.pnas.org/content/by/year


Study: Scientific research fraud on the rise
--------------------------------------------

* Red wine researcher Dr. Dipak K. Das published fake data: UConn
* Study linking chronic fatigue syndrome to virus retracted by journal

WASHINGTON - Fraud in scientific research, while still rare, is
growing at a troubling pace, a new study finds. A review of
retractions in medical and biological peer-reviewed journals finds the
percentage of studies withdrawn because of fraud or suspected fraud
has jumped substantially since the mid-1970s. In 1976, there were
fewer than 10 fraud retractions for every 1 million studies published,
compared with 96 retractions per million in 2007. The study authors
aren't quite sure why this is happening. But they and outside experts
point to pressure to hit it big in science, both for funding and
attention, and to what seems to be a subtle increase in deception in
overall society that science may simply be mirroring.

Fraud in life sciences research is still minuscule and committed by
only a few dozen scientific scofflaws. However, it causes big
problems, said Arturo Casadevall, a professor of microbiology at the
Albert Einstein College of Medicine in New York. Casadevall is the
lead author of the study which looked at the reasons for 2,047
retractions among many millions of studies published in journals and
kept in a government database for medically focused research. Fraud
was the No. 1 cause of retractions, accounting for 43 percent of them.
When fraud was combined with other areas of misconduct, such as
plagiarism, it explained about 2 out of 3 retractions, the study
found. 'Very few people are doing it, but when they do it, they are
doing it in areas that are very important,' Casadevall said. 'And when
these things come out, society loses faith in science.'

Prominent retractions that Casadevall cited for fraud include a
notorious British study that wrongly linked childhood vaccines to
autism, nine separate studies on highly touted research at Duke
University about cancer treatment, and work by a South Korean cloning
expert who later was convicted in court of embezzlement and illegally
buying human eggs for research. Casadevall said he was surprised
because he didn't set out to study fraud. His plan was to examine the
most common avoidable errors that caused retractions. What he found
was that 889 of the more than 2,000 retractions were due to fraud or
suspected fraud.

While other studies have shown a rise in retractions, no previous
study has found scientific misconduct as the leading cause, said
Nicholas Steneck, director of the research ethics program at the
University of Michigan, who wasn't involved in the Casadevall study.
That shows a need for better, more honest reporting of retractions by
the science journals themselves, he said. He and others also said the
findings suggest there may just be better detection of scientific
fraud overall.

Most 'scientists out there are well meaning and honest people who are
going to be totally appalled by this,' Casadevall said. The study was
published online Monday in the Proceedings of the National Academy of
Sciences, which had the second most retracted articles for all
reasons, behind only the journal Science. The publication with the
most fraud-based retractions was the Journal of Biological Chemistry.
PNAS ranked fifth.

Casadevall said that even if society as a whole has become more
deceptive, 'I used to think that science was on a different plane. But
I think science is like everybody else and that we are susceptible to
the same pressures.' In science, he said, 'there's a disproportionate
reward system' so if a researcher is published in certain prominent
journals they are more likely to get jobs and funding, so the
temptations increase.

'Bigger money makes for bigger reasons for fraud,' said New York
University bioethicist Arthur Caplan. 'More fame, more potential for
profit... Some of the cheating and fraud is not too dissimilar to the
cheating and fraud we've seen in banking.'

Science historian Marcel LaFollette, author of a book about science
fraud 'Stealing into Print,' said researchers can't prove that more
people are lying in general in society, but they get the distinct
feeling it's happening more. And in 2006 an Associated Press-Ipsos
poll found that while most people say they don't approve of lying, 65
percent of those questioned said it is OK to lie in certain
situations. The world has become accustomed to lying and forgives
politicians when they do it in relationships, LaFollette said. But
it's different when it's a doctor, scientist or an engineer because
people can get hurt, she said.

Casadevall and Caplan pointed to the 1998 study in Lancet by Andrew
Wakefield temporarily linking childhood vaccines to autism - a study
later retracted because it was found to be what another scientific
journal called 'an elaborate fraud.' 'Think about the damage society
took when mothers started to question vaccines,' Casadevall said.
'That's damage and it's still going on.' Reached at home in Texas,
Wakefield, who was banned from practicing medicine in his native Great
Britain and whose claims are contrary to what prevailing established
medical research shows about vaccine and autism, said: 'There was no
fraud and to use this and to use me as a poster child of fraud really
compounds that error.'

Casadevall said his work is about science trying to clean its own
house. And because it's about fraud, he said he did one extra thing
with his study: He sent reviewers not just a summary of their work,
but all the data, 'so they can check on us.'

--------
(c) 2012 The Associated Press

UNUM's Chronic Fatigue Syndrome Management Program circa 1995

UNUM's Chronic Fatigue Syndrome Management Program circa 1995

----------------------------------------------------------------------------------------

pdf file- http://www.mediafire.com/?g5eh1cq5ssqbse3

UNUM
Life Insurance Company
Southern Regional Benefits
Chronic Fatigue Syndrome Management Program

Carolyn L. Jackson M.D.
Revised April 4, 1995

Contents

1.0 Executive Summary
1.1 Objective
1.2 Definition
1.3 Evolution
1.4 Risks, Opportunities, & Benefits
1.5 Premise and Approach
1.6 Program Reviews

2.0 Key Roles and Responsibilities
2.1 OSP/RN
2.2 DBS
2.3 Attending Physician
2.4 Claimant
2.5 Employers
2.6 UNUM Rehab
2.7 Social Security Specialist

3.0 Program Plan
4.0 Process Detail
5.0 Pilot

1.0 Executive Summary

1.1 Objective
The objective of the Chronic Fatigue Syndrome Management Program
(CFSMP) is to effectively address the growing number of Chronic
Fatigue Syndrome claims through collaboration with attending
physicians, claimants, employers, and inteinal UNUM groups, thereby
reducing UNUM's financial exposure while simultaneously motivating
claimants to gradually and willingly return to work.

1.2 Definition
The definitions for CFS ase as variable and numerous as its symptoms,
below is one selected definition:
"Chronic fatigue syndrome is a clinically defined condition
characterized by severe disabling fatigue and a combination of
symptoms that prominently features self-reported impairments in
concentration and short term memory, sleep disturbances, and
musculoskeletal pain." (Annals of Internal Medicine, December, 1994;
121:953-959)

1.3 Evolution
The etiology of CFS is unknown. It is still being argued whether CFS
is a true physical illness vs an atypical depression. Whatever its
cause, studies indicate that less than 5% of patients who carry this
diagnosis actually have CFS. What, then, do the other 95% of this
group truly have?

Many believe that internal and external environmental factors are
contributing to CFS. Increasing demands are being placed upon
individuals in the workplace. Economic recession, corporate
downsizings, high -tech complexities, the 'do more with less'
philosophy are contributing to great stress for most American workers.
Many professionaIs are struggling in very competitive positions, each
person now doing the work of 1.3 people and bringing much of that work
home. The American Dream is well out of reach for many. These societal
and economic ills have played a key role in the increasing rise of the
diagnosis of CFS, a rise incumbent upon the popularity of this
"medical" diagnosis rather than a "psychiatric" one to explain this
disorder.

0 can conveniently abbreviate the above statements into a "formula" for CFS:
CFS = Negative External Factors (recession, downsizing, etc.) +
Negative Internal Factors (stress, conflict, failure of coping
mechanisms, etc.) + Entitlement Philosophy = LTD

In six years of managing medical disability claims; 1 have seen a
precipitous rise in the number of CFS claims. Since joining UNUM in
August, 1994, the number of CFS claims refelred into Medical Resources
at SRB has more than doubled. Although CFS claims may represent a
small percentage of the total claim volume, the dollar exposure is
significant. These claims also result in substantial time commitment
by the OSP/RN as well as the DBS group. The increasing level of
frustration generated by their management impacts overall productivity
and effectivity.

1.4 UNUM's Risk and Opportunity
UNUM stands to lose millions if we do not move quickly to address this
increasing problem The subjective nature of CFS leaves us highly
exposed to the self -diagnosis of cIaimants, some of whom take
advantage of doctors and the entire insurance industry. On the other
hand, there are claimants who have legitimate disability related to
CFS. Both groups must be effectively managed. UNUM can position itself
on the leading edge of disability management by developing and
implementing a program to properly manage this most cllallenging area
of LTD claims.

1.5 Premise and Approach
The CFSMP is based on the premise that CFS impacts more than just
LNUM. Employers, attending physicians, and claimants are at risk. Many
attending physicians are having a difficult time managing through the
subjective nature of CFS. Group policyholders (employers) are paying
higher premiums and losing valued employees. Many highly educated and
trained professionals are losing motivation and slipping into
self-imposed oblivion because of CFS.

UNUM Southern Region has developed a program that involves all of the
key groups that are impacted by and that can produce an impact on this
phenomenon. The program intends to develop a collaborative strategy
with all the parties involved to ensure the recovery of the
patientlclaimant, to restore their motivation/incentive, and to effect
their eventual return to full or partial work capacity.

Due to the program complexjty and newness, a pilot approach will be
used, approaching one CSF physician at a time to make him/her aware of
this collaborative strategy and the ways in which it can enhance their
management of the CFS patient. As this pilot progresses, from one CFS
physician to another, best practices will be identified, developed and
implemented utilizing the philosophy and spirit of Continuous
Improvement.

1.6 Program Reviews
Ongoing program reviews will be held periodically to facilitate
strategic management, information sharing, continuous improvement and
total involvement. Attending CFS physicians, UNUM management,
employers, and other key contributors will be invited to attend. Guest
speakers will be brought in to enhance the value of the program
reviews. DBS's will have the opportunity to pose questions and
highlight concerns to help with the overall program. The program
reviews will be held at the SRB office in Atlanta.

2.0 Roles and Responsibilities
Although the following groups are responsible for many activities, the
roles and responsibilities listed are only those relevant to the
support of the CFSMP.

2.1 On Site Physician/Registered Nurse (OSP/RN)
-Early intervention in all CSF claims
-Establishment of an on-going partnership with the attending physician
-Timely collaboration with the DBSs in setting claim direction
-Identification of opportunities for claim resolution
-Ongoing identification and implementation of best practices for
claims management

3.2 Disability Benefits Specialist (DBS)
-Manage these files more aggressively and in a proactive rather than a
reactive fashion
-Identify opportunities to implement early intervention as soon as
possible by having them identified by the policyholder during the STD
period
-develop improved claims management skills
-work more closely and more frequently with the claimant and the
attending physician
-Frequently update medical information from the claimant and the
attending physician
-Identify opportunities to capitalize on any improvement in the
claimant's functionality or significant change in his/her medical
status

2.3 Attending Physicians
-Support realistic therapeutic regiment, recovery time and return to work goals
-Work with UNUM OSP/RN to establish interim recovery objectives for
returning to work
-Cooperate and collaborate with UNUM OSP/RN in helping claimant to
overcome disability and return to work
-Collaborate with UNUJM OSP/RN to determine the appropl-iate juncture
to evaluate claimant's medical statuslfunctional capacity via IME,
FDE, neuropsychiatric testing, etc.
-Open and objective discussion on interpretation of results of these evaluations
-Support plan to gradually increase claimant's functionality, using
graded exercise programs, work conditioning programs and psychotherapy
when and where appropriate
-Work with UNUM rehabilitation services or an outside vendor in an
effort to retuin the patient/claimant back to maximum functionality
with or without symptoms

2.4 Claimant
-Increase motivation to return to work
-Work with attending physician to establish and meet recoveiy goals
-Work with UNUM rehab and be open to recommendations
-Cooperate with effo~tso f graded increase in functionality

2.5 Employers
-Hold claimant's job open for as long as possible
Work with UNUM rehab to modify job or work schedule for early return to work

2.6 UNUM Rehab
-Clarify the job function of claimants
-Work with cmployers to modify jobs where appropriate
-Perform transferable skills analysis when indicated
-Provide direct and indirect vocational counseling
-Coordinate Work Incentive Benefit program

2.7 Social Security Specialist
Assist the OSP/RN and/or DBS determine SSDI feasibility when appropriate
-Work with the claimant when SSDI is feasible

3.0 Program Plan

3.1 Understand and define the problern
3.2 Establisli Guidelines for Managing the Problem
3.3 Idenify Key Players and Stakeholders
3.4 Gain Support and Buy-in from Key Players & Stakeholders
3.5 Finalize Operational Process
3.6 Pilot Implementation
3.7 Pilot Evaluation and Feedback
3.8 Implement Continuous Improvement steps
3.90 Implementation with sequential physicians
3.91 Evaluation, Feedback, Enhancements through On-going Program Reviews
3.92 Eventually expand this project to be used in all "subjective" claims

4.0 Chronic Fatigue Syndrome
Process Detail

3.1 Claim received

3.2 DBA/DBS marks up the claim arid begins initial claim work-up. This
step includes a detailed call to the claimant ( addendum A),
discussion with employer ( addendum B ), and a letter to the attending
physician (see addendum C) requesting the claimant's medical records
(to include all office notes, consult notes and diagnostic tests).

4.1 Claim is referred to the OSP/RN for the initial medical review.
This step includes a call to the attending physician to establish a
paitnering relationship and to set expectations and return to work
goals. Recovery goals for the claimant are agreed upon by the UNUM
OSP/RN and the attending physician.

4.4 Joint claim review by both the DBS and UNUM medical. All pertinent
information and data are shared at this point, enabling the DBS to
make and informed decision about the next step in management of the
claim.

4.5 DBS decision to accept or deny claim.

3.6 If DBS accepts claim, then the ongoing CFS claim management
process is initialized.
(steps 4.7 through 4.9)

4.7 DBS establishes a claim review schedule, whlch should be at least
evely three months, or sooner if there is a change in the claimant's
functionality or medical status.

4.8 At each sequential review, the first level of the review is
pelformed by the DBS and should include the following:
-Review of office notes
-Review of all diagnostic tests
-Review of referrals to other physicians
-Telephone discussion with the claimant to assess changes in functionality
-Telephone call to employer to assess job status ( Is there still a
position open? Has the person been terminated?)
-An RBR visit early in the process is encouraged to give us an
accurate assessment/objectification of the claimant's condition

4.9 At each sequential review, the second level of the review is
pelformed by OSP/RN and should include the following:
-Discussion with the attending physician to review claimant's progress
against recovery goals.
-Strategizing with the attending physician to get or keep the claimant
on track for recovery.
-A determination of the need for diagnostic tests that evaluate
physical and cognitive functionality
-discussion of need for specialty consult or IME
-A determination of the need to involve UNUM rehab, psychotherapists,
employers and other groups that can help the claimant increase
functionality.

5.0 Pilot Strategy
Due to the complexity and newness of the program the CFSMP utilizes a
pilot strategy. To help "sell" the program on a large scale, a track
record of wins must be established.

A list of attending physicians who handle CFS cases frequently seen by
the Southern Regional Benefits office has been compiled. From that
list, the attending physician with the highest volume of claims was
chosen.

Dr. Salvato, a widely-known CFS physician in Houston, Texas was
carefully approached, first by telephone, which led to a scheduled
visit to her office and lab. Highlights of that initial,
groundbreaking visit are as follows:

Objectives of the Visit:
-This fist objective was to get into her office and get past the
presumed initial barriers.
-The second objective was to give her a clear picture of how we can
work together for the mutual benefit of the patienuclaimant resulting
in a successful outcome for all involved, i.e., a win-win situation.
-There was a strong effort to avoid the development of an adversarial
relationship, and to smooth over any existing rough edges between her
office and UNUM-SRB.
-Convince her to "buy-in" to the collaborative approach

Results of the visit to Dr Salvato's office:
-Dr. Salvato now has a much clearer picture of ways in whlch UNUM
could contribute to and enhance the management of the CFS
patienuclaimant
-In particular, she was very interested in the OSPIRN partnering
concept and the many ways that our Rehab services could impact the
patient's functional/vocational outcome
-She was surprised to how that we had a social security specialist to
help with SSDI applications (aiding her patients with SSDI
applications has been a Problem area for her)
-She was also not aware of and was very interested in our WIB program
-She was enthusiastic in a collaborative approach to evaluating
functional capacity and working together on an incremental return to
work (She expressed past difficulty in getting employers to accept
modified work schedules/duties)
-Specifically, we arranged that all UNUM files that involved her CST
patient's would be channeled through the OSP or the Rehab specialist
for discussions with her. A specific time and date would be
pre-arranged for these discussions on an ongoing basis
-We could channel CFSF claims from other UNUM offices through the SRB
OSP/RN or Rehab specialist
-Overall, she expressed an enthusiasm about working with LNUM and
encouraged us to speak with some of her peers about a similar
arrangement

Update on Atlanta CFS Pilot
July 25, 1995

Background
Chronic Fatigue Syndrome Management Program (CFSMP)
Key participants:
Dr Carolyn Jackson and Sally Fowler
(Southern Regional Benefits)
Dr Don Abbott (Portland) and UNUM medical staff
(Unknown role): Susan Steele/Anne Dinsmore

Key Premise: CFS Impacts MORE than Just UNUM

EMPLOYERS
Paying Higher Premiums
Losing Valued Employees

ATTENDING PHYSICIANS
Difficulty With Subjectivity of CFS

CLAIMANT
Highly educated professionals slipping into self-imposed oblivion!

CFSMP
Approach one CFS physician at a time and make him/her aware of our
collaborative strategy

As this pilot progresses, from one CFS physician to another, best
practices will be identified, developed, and implemented.


Roles and Responsibilities

WHO? WHAT?

On-Site Physician Early intervention on all CFS claims
Establish partnership with AP

DBS Manage CFS files more aggressively,
proactively, and more frequently.
Identify/notify during STD period

Attending Physician Support realistic therapeutic regimen,
recovery time and RTW goals

Everyone Partnership/collaboration on
establishing, monitoring and meeting RTW goals


Roles and Responsibilities

WHO? WHAT?

Claimant Increase motivation to RTW -- cooperate
on efforts for graded increase in functionality

Employers Hold claimants job open for as long as
possible -- modify job or work schedule to allow early RTW

UNUM Rehab Clarify the job function of claimants; work
with ERs to modify jobs when indicated

CHRONIC FATIGUE SYNDROME
CURRENT THINKING AT UNUM

Diagnosis
- Neurosis with a new banner

Claimant Profile
- Professional working women ages 30-50
- Susceptible to doctor's power of suggestion
- Self-reports symptoms
- Longer claim duration
- Difficult return to work (recovery claims)

Condition Profile
- Burnout: loss of concentration, memory, sleep
- Sensitive immune system
- CFS is symptom, not cause
- Cause involves other psychological, psychosomatic issues
- Often linked to soft tissue conditions

Treatment Protocol
- Eliminated all other conditions before giving CFS diagnosis