Solve ME/CFS Initiative 2014 Webinar Series

July 8, 2014

Workplace-WebinarBeginning in July and continuing through year-end, the Solve ME/CFS Initiative (SMCI) will be bringing you a free, monthly webinar series. Anyone that is interested can RSVP to participate live. Each webinar will be recorded and posted to our website and YouTube channel within a week of the live date, so if you miss it, don’t worry! You can still have access to the great content at your convenience.

Read more about the series and RSVP today!

 

Suzanne

Research Institute Without Walls – Progress and Promise

HELD on Thursday, July 31, 2014
Video Link

Suzanne D. Vernon, Ph.D., scientific director of the Solve ME/CFS Initiative will provide an update on the work being conducted through our Research Institute Without Walls. Participants can also expect to learn more about how the SolveCFS Biobank works and is attracting some of the brightest investigators from the best institutions to ME/CFS research.  You will leave with an understanding of what makes the SolveCFS BioBank unique, how to get enrolled and what to expect when you participate.  Vernon will also provide a sneak peek at some of the types of research being conducted on samples using the SolveCFS BioBank.

 

McGowan

Investigator Report: Epigenetics of ME/CFS

Thursday, August 21, 2014
2-3:00pm Eastern (1pm Central/Noon Mountain/11am Pacific)

Space is limited –  RSVP to Reserve Your Slot – Click HERE

Patrick O. McGowan, Ph.D., is one of the Solve ME/CFS Initiative 2011 funded investigators.  McGowan is an assistant professor in the Department of Biological Sciences, University of Toronto at Scarborough.  He will talk about his latest results from our grant funding.  McGowan used blood samples from the SolveCFS BioBank to identify the chemical modifications (e.g., methylation) to the DNA that is different in ME/CFS patients compared to healthy people.  This type of research will help explain the immune dysfunction of ME/CFS.

 

Dane-Cook

Investigator Report: Deciphering Post-Exertional Malaise

Thursday, September 18, 2014
2-3:00pm Eastern (1pm Central/Noon Mountain/11am Pacific)

Space is limited –  RSVP to Reserve Your Slot – Click HERE

Dane B. Cook, Ph.D. is assistant professor of Kinesiology at the University of Wisconsin, Madison.  Cook is one of the Solve ME/CFS Initiative’s 2011 funded investigators.  Cook will describe the system biology approach his team is taking to provide a clear picture as to what causes post-exertional malaise.  This is critically important research for ME/CFS because as Cook notes, “You can’t begin to fix a problem like post-exertional malaise until you can understand its underlying cause.”

 

unutmaz

Investigator Report: Decoding the Human Immune Response

Wednesday, October 1, 2014
2-3:00pm Eastern (1pm Central/Noon Mountain/11am Pacific)

Space is limited –  RSVP to Reserve Your Slot – Click HERE

Derya Unutmaz, MD, is Professor of Microbiology, Pathology and Medicine at NYU Langone Medical Center.  Unutmaz is using samples from the SolveCFS BioBank to understand the “Good, Bad and Ugly” aspects of the immune response in ME/CFS.  Unutmaz hypothesizes that a disproportionate immune response leads to damage in ME/CFS.   He will describe what the immune signature of ME/CFS looks like compared to a healthy immune response.

 

PeterRoweInvestigator Report: Neuromuscular Strain in ME/CFS

Thursday, October 23, 2014
2-3:00pm Eastern (1pm Central/Noon Mountain/11am Pacific)

Space is limited –  RSVP to Reserve Your Slot - Click HERE

Peter Rowe, MD, who directs the Chronic Fatigue Clinic at Johns Hopkins Children’s Center, will describe some novel observations about restrictions in range of motion in the limbs and spine in those with ME/CFS. Many affected individuals have restricted movements and increased mechanical tension in nerves. Applying a further mechanical strain to the nervous system can provoke increased symptoms in some patients. These concepts are starting to help explain the pathogenesis of some symptoms and neurological abnormalities in the illness—not only how they might arise but also how we might treat them more effectively.

 

 

November and December webinars to be announced at a later date.

 

 

Same Mission | New Name

May 30, 2014

Solve ME/CFS Initiative

We’re delighted to announce that The Solve ME/CFS Initiative has a new name – the Solve ME/CFS Initiative.   While our name has changed, our mission steadfastly remains the same:  We will make ME/CFS understood, diagnosable and treatable.

Why the change?  We recognize the many changes in our organization and our illness space since the organization was first named so long ago in 1987.  While the name of our illness continues to be controversial, “ME/CFS” better reflects today’s understanding. And we believe that the word “initiative” (defined as ‘leading action’), expresses our strong commitment to funding ground-breaking research.

Since our organization was founded and named in 1987, we have been the leading organization focused on this illness.  Over the years, we’re proud of our remarkable advances regarding this controversial and misunderstood disease.

  • Under the 22-year leadership of Kim McCleary, the organization’s first CEO, the Association played an integral part in developing a policy ruling for the Social Security Administration that recognized CFS as a disabling condition.
  • We are the leading private funder of ME/CFS research, directly funding $5.5 million in ground breaking research which has been leveraged into more than $12 million in additional ME/CFS research.
  • The organization fought to create and continues to advocate to sustain a dedicated federal advisory committee on ME/CFS research and education (CFSAC).
  • We helped expose the misappropriation of $12.9 million in CDC spending, restoring these funds to ME/CFS research.
  • We led the first-ever public awareness campaign for ME/CFS, led lobbying events, organized Congressional briefings and regularly deliver testimony at numerous federal hearings and meetings.

Four years ago, guided by a desire to move into a new era of scientific progress on ME/CFS, the Association made a strategic decision to heighten its focus on research.  Our thinking was simple – the best way to use our precious dollars is toward solving this despicable illness.

Today, led by President and CEO, Carol Head, the organization continues to drive its mission forward – to fund research that will make ME/CFS understood, diagnosable and treatable.  How do we do that? By providing more funding for high-quality ME/CFS studies, fostering increased collaboration among ME/CFS researchers and pushing the federal government to make ME/CFS research a higher priority.  We are working to leverage our experience, relationships and collective knowledge to propel the ME/CFS research field forward. We are a catalyst for scientific advances that translate into better care for ME/CFS patients. We are accelerating ME/CFS research.

As we continue our efforts to make ME/CFS widely understood, diagnosable, and treatable, it is fitting that we have a name that more accurately reflects who we are: The Solve ME/CFS Initiative. We trust that you will continue this journey with us as we work towards a day when ME/CFS is no more.

 

P2P Draft Evidence Review

October 20, 2014

Can a Process that is Inappropriate for ME/CFS Inform the Research Path Forward?P2P_title

Summary Overview

As a research focused organization, the Solve ME/CFS Initiative (SMCI) understands the impact a program like the Pathway to Prevention workshop (P2P) can have on the research landscape.  Because of its importance, we have utilized the collective brainpower of our Research Advisory Council, led by our scientific director, Suzanne D Vernon, PhD, to perform a careful review and response to the Evidence-Based Practice Centers’ draft evidence-based review for ME/CFS. (Read our official submission HERE)  We have concluded that:

  • It confirms what we and others have suspected: the Pathway to Prevention (P2P) process is not appropriate for ME/CFS.  Among other reasons, it uses comparative effectiveness methodology to review the evidence to inform healthcare; in the case of ME/CFS the evidence base is much too slim for this method to be effective.
  • The P2P systematic review of the ME/CFS evidence base illustrates the lack of rigor in crucial research design elements and the absence of high quality clinical trial data. The review shines a bright light on the need for well-designed, adequately powered studies to identify diagnostic gold standards and safe and effective treatments.

Furthermore, it is important to note that the vast majority of ME/CFS research studies were omitted from this evidence review due to their inability to meet the rigorous standards required for inclusion. Of all of ME/CFS research studies funded by the NIH since 1991 ($191.5 million spent), less than 1% of those studies were included. So, not only has the NIH egregiously underfunded this illness (based on prevalence), but the research NIH has funded has not contributed to an evidence base that has moved the science forward.

This review substantiates the negative cycle currently in play with ME/CFS research – Because there is little funding, there is little research. And because there is little research, there is little evidence to prompt additional funding. But the P2P process may be what is needed to break through that negative cycle and move us to a day when ME/CFS is appropriately funded. It’s existence demonstrates that there is increasing recognition of the clinically devastating nature of ME/CFS and recognition of the disease as an urgent area of future study.

 

Background – How did we get here?
To review what has led up to this NIH P2P workshop for ME/CFS:

  • The 2011 NIH State of the Knowledge Workshop for ME/CFS concluded that there were problems with definitions, gaps in study design, and a lack of studies on co-morbid conditions, biomarkers, or genetics.
  • A year later, at the CFS Advisory Committee meeting, Dr. Sandra Kweder, FDA Deputy Director of the Office of New Drugs tells us there are so few applications to the FDA because there is no accepted ME/CFS definition, no accepted method for measuring how patients feel or function and no accepted biomarker to provide a simple, quantitative measure of disease presence or activity.
  • In 2013, ME/CFS is the first “patient-focused drug development” workshop held by the FDA. The outcome of that meeting, as expressed in the Voice of the Patient report, is that ME/CFS is a serious disease with significant unmet medical need that requires comparative effectiveness research to generate the evidence to assess the effectiveness, benefits, and harms of different treatment options.
  • In 2014, Dr. Susan Maier, Deputy Director of the Office of Research on Women’s Health at the NIH, who oversees ME/CFS research at NIH, successfully garnered a Pathways to Prevention workshop titled, “Advancing the Research on Myalgic Encephalomyelitis/Chronic Fatigue Syndrome”.

For much of this year, the Solve ME/CFS Initiative (SMCI), as well as many other individual advocates and patient groups, has been talking about the National Institutes of Health (NIH) Pathways to Prevention (P2P) for ME/CFS workshop. In April, we first reported on the possibility of the P2P workshop, then in the approval process. Once it was approved, the NIH worked with the Agency for Healthcare Research and Quality (AHRQ) and their Evidence-Based Practice Centers to conduct this evidence-based review.

In June, SMCI expressed concerns that the search criteria used for the evidence-based literature review would bias the review toward studies on CBT and GET. On Sept. 22nd AHRQ published the draft systematic evidence review on the Diagnosis and Treatment of ME/CFS for comment.  Several members of our Research Advisory Council together with Suzanne D. Vernon, PhD reviewed the draft and have provided peer review comment directly to AHRQ. SMCI and our research advisors believe that this systematic review has identified important and significant gaps in research that have contributed to the dearth of evidence needed to diagnosis and treat ME/CFS. Indeed, it is almost all “gap” and almost no substance.

 

Dearth of Evidence
From 1991 to 2014, NIH Research Portfolio Online Reporting Tools (RePORT) indicates a total of $191.5 million has been awarded to investigators to directly study ME/CFS or conduct research relevant to ME/CFS.  Spending for other medically unexplained disorders that often occur with ME/CFS, like Fibromyalgia and irritable bowel syndrome (IBS), is about $400 million for each in the same time frame. This is in contrast to multiple sclerosis (MS) – a condition with objective diagnostic biomarkers and treatments – where NIH spending in the same period exceeds $4 billion.

Further, a search of PubMed.gov for anything published on ME/CFS finds 5,450 peer reviewed scientific articles; there are 8,000 articles for Fibromyalgia and 9,000 for IBS.  This is in contrast to the 55,500 articles found in PubMed that make up the MS evidence-base.  There is a direct correlation between funding levels and the breadth of the published evidence-base.

 

The One Percentexamine
Now, the NIH P2P draft systematic review is out. All told there were 5,901 papers considered by the Evidence-Based Practice Center in the comparative effectiveness systematic review. In the end, less than 1% of these 5,901 paper met criteria for inclusion in the systematic review process. Why? 

  • Because comparative effectiveness systematic reviews are based on evidence-based facts. The P2P uses a rigorous process to empirically identify methodological and scientific weaknesses in each published paper.
  • The investigators conducting these evidence-based reviews are experts in this review process and come to the task at hand without any bias or preconceived notion about the topic they are reviewing.
  • The procedures for these reviews are possible because there are standard methods and procedures in place for conducting research; especially human research intended to impact clinical care. They systematically reviewed the ME/CFS papers using specific research design criteria known as PICOTS – Populations, Interventions, Comparators, Outcomes, Timing, and Setting.

While the draft comparative effectiveness review on the Diagnosis and Treatment of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) may be a hard pill to swallow for patients and for the many ME/CFS scientists whose research studies were excluded from this review, it identifies vast research gaps and provides important information needed to chart the way forward.

The rationale for evidence-based reports makes sense:

  • “Systematic reviews are the building blocks underlying evidence-based practice; they focus attention on the strength and limits of evidence from research studies about the effectiveness and safety of a clinical intervention. In the context of developing recommendations for practice, systematic reviews can help clarify whether assertions about the value of the intervention are based on strong evidence from clinical studies.”

And …

  • “This review is not intended to address the question of etiology nor underlying factors that lead to the onset or perpetuation of ME/CFS but rather to focus on the diagnosis and treatment of this syndrome.”

With this is mind, the review identified only 64 studies that met evidence-based criteria to address the key questions; 1) ME/CFS diagnosis and 2) ME/CFS treatment. For a diagnosis study to be included it had to discriminate ME/CFS patients from healthy controls and (ideally) from other diseases with similar symptoms and if the study used biochemical marker it had to be in the context of treatment versus etiology. Twenty-eight studies addressed various aspects of diagnosis. Most of the studies pertaining to diagnosis were rated as fair quality (on a scale of “good”, “fair”, “poor”). These diagnosis studies showed that certain measures that assess function are able to distinguish between ME/CFS and healthy people reasonably well. The studies were rated “fair” because they were small and diseases similar to ME/CFS were seldom included. The lack of a gold standard for diagnosis of ME/CFS limits how broadly the limited evidence base can be generalized to the ME/CFS community as a whole. The review notes that clinical experts identify post-exertional malaise (PEM) as a cardinal feature of ME/CFS yet current methods of testing, comparing, and monitoring PEM are lacking.

 

So what few studies WERE included and do they shed light?
There were 36 randomized clinical trial studies for ME/CFS treatment; 9 for medications, 14 for counseling or behavioral therapies, 7 for complementary and alternative medicine, 6 for exercise, and 5 comparing therapies:

  • Seven were rated as “good-quality” trials: 5 counseling and behavioral therapies, 2 complementary and alternative medicine therapies
  • 24 were rated “fair-quality”
  • 5 were “poor-quality”
  • The phase III Ampligen trial was rated “fair to good-quality” and it was the only medication trial to get this rating; all other medication trials were fair and poor-quality.
  • The PACE trial was rated as “good-quality” for both counseling and behavioral and for exercise intervention but the strength of the evidence was moderate to low for cognitive behavioral therapy (CBT) and graded exercise therapy (GET).
  • The other 5 studies that used an exercise intervention were “fair-quality” and overall, exercise intervention trials showed moderate strength effect in function and well being and low-strength effect on fatigue. Importantly, the high rate of refusal in one study may indicate that patients are concerned the possible adverse effects of repeat exercise testing (e.g., the first exercise test may have caused PEM prohibiting the ability to do the second test). This deserves further study and consideration as a possible outcome.

All of the clinical trials were compromised because of small and heterogeneous patient populations, differences in inclusion criteria – including use of different case definitions, and measuring different outcomes (e.g., fatigue, function, etc). This is exactly what Dr. Peter Rowe reported at the 2013 FDA workshop on Development of Safe and Effective Drug Therapies for CFS and ME (http://www.tvworldwide.com/events/fda/130425/). Measuring the effect of an intervention was likely diminished by the above factors. Ways to better detect the effect of an intervention are to measure certain clinical features present before treatment starts compared to after treatment, such as severity and frequency of specific symptoms like brain fog or PEM. This is called subgroup analysis; not one of the intervention studies did a subgroup analysis.

 

Is there a Silver Lining?
Despite the lack of an evidence-base, this systematic review shines a light on important areas that must be pursued to build the ME/CFS comparative effectiveness research evidence base:

1.  Determine diagnostic criteria that can be used as the gold standard for ME/CFS diagnosis.

  • We note that the work of determining ME/CFS diagnostic criteria is currently underway at the Institute of Medicine (IOM)

2. Test gold standard diagnostic criteria in other populations with diseases similar to ME/CFS where diagnostic uncertainty exists so that the treatment is specific to ME/CFS vs another similar condition.

  • Determine the outcomes that are clinically meaningful and ensure standardized assessment so that the effect of interventions can be measured
  • Post-exertional malaise is a cardinal feature of ME/CFS and potentially one of the most important outcome measures; research should be conducted to determine what it is and how to measure it

3. The biomarker research and clinical trials conducted to date provide clues to the possible causes of ME/CFS and can serve as “disease models” for further study of ME/CFS pathophysiology

  • All basic and intervention research should use methodological standards to  ensure that it meaningfully contributes to the ME/CFS evidence-base

This analysis illustrates the lack of coherence in the field and the absence of high quality clinical trial data.  NIH, through the P2P workshop, set out to identify gaps in the research, and they found more gaps than substance. Yet the existence of this effort shows increased recognition that ME/CFS is an urgent area of future study and clearly implies that more resources need to be focused on well designed, adequately powered studies. We believe that it is NIH’s responsibility to address their own finding.

 

What Happens Now?
The P2P panel will review this evidence-based report, including the comments and feedback now being submitted, in advance of the meeting that will take place on December 9 & 10, 2014. At that two-day workshop in Washington DC, the P2P panel will hear from the expert speakers and be able to ask clarifying questions in a town-hall-like Q&A that will take place after each session.

Experts in ME/CFS are being invited to address each agenda item. They will speak to their personal experience and expertise as a patient, caregiver, researcher, etc. The slate of speakers has not yet been released.

The day after the P2P meeting, the P2P Panel will write a draft report which will be published and the public will have time for comment on the final report, just as we are now commenting on the draft evidence review. The comment period is 30 days; the deadline should be around January 12th, 2015. Once the comment period closes, the report will be finalized and NIH will organize a plan to disseminate it widely.

The goal, as we understand it, is a report that contains a set of recommendations based on the totality of the evidence, in the hopes of having said recommendations carried out by Federal partners in 2015. These recommendations are aimed at improving the nature of the research being conducted in ME/CFS. The Solve ME/CFS Initiative will pass along additional information as it is received and when the opportunity for public comment is scheduled, we will report that and share the means by which you can participate.

For far too long, ME/CFS has been underfunded, misunderstood, and even disbelieved. Our community has been pushing a very heavy fly-wheel aimed at increasing understanding, acceptance and progress toward treatments and cure. Now there is federal activity, all aimed at moving the needle for ME/CFS – FDA Voice of the Patient, IOM activity on creating clean diagnostic tools and other much-needed tasks, and this P2P. What this evidence based report shows is that the status quo must change. We hope P2P will illuminate the clear need for more funding, increased research activity and faster progress.

 

What Can You Do?
Registration is now open for the Pathways to Prevention workshop for Advancing the Research on ME/CFS taking place on December 9 & 10. You can register to attend live or participate via webcast. It is our hope that many stakeholders will participate in this process in order to ensure the patients have a strong presence and a voice.

To register to attend live click HERE 

To register for the webcast click HERE

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Many other patients and advocates are also weighing in on the P2P and the draft evidence review. Read what just a few others are saying:

Medscape Medical News – a log in is required to view the article, but it is free and anyone can create an account.

Jenny Spotila, Mary Dimmock & others via Occupy  CFS

Cort Johnson via HealthRising

 

P2P Releases Systematic Evidence Review

October 1, 2014

P2POn Sept. 22nd, the Association for Health Research and Quality (AHRQ) released the draft systematic evidence review on the Diagnosis and Treatment of ME/CFS NIH requested the literature review for the purposes of the Pathways to Prevention (P2P) Workshop, and the Agency for Healthcare Research and Quality contracted with the Oregon Health & Sciences University to perform it. 

We first wrote about the P2P workshop program in April (http://solvecfs.org/pathways-to-prevention-for-mecfs/) and have been working with the advocacy community since then to stay abreast of the P2P process and assess its impact on ME/CFS. The NIH Office of Disease Prevention Pathway to Prevention (P2P) program approved the ME/CFS workshop earlier this summer and in June SMCI expressed its concerns about the protocol for the evidence-based literature review. (http://solvecfs.org/solve-mecfs-initiative-smci-position-on-p2p/)  

The draft report is an extensive review on ME/CFS literature covering diagnosis and treatment and is but one element of the NIH Pathways to Prevention (P2P) process. On December 9 & 10, the Pathways to Prevention workshop for Advancing the Research on ME/CFS will take place in Washington, D.C. and the panel will hear expert testimony at that time. Also, during the workshop stakeholders/patients will have the opportunity to participate in the discussion both in person and online by asking questions or making comments via microphones or computer; webcast viewers can type in comments and questions in a comment box on the webpage. There is a total of 3.5 hours of “Discussion” time noted on the draft agenda, where public input will be addressed. Interested individuals may register to attend live or participate via webcast.  It is our hope that many stakeholders will participate in this process in order to ensure the patients have a strong presence and a voice.

Learn more about how to register for the December 9 & 10 P2P Workshop in this earlier post: http://solvecfs.org/p2p-workshop-registration-now-open/

Comments on the draft systematic evidence review can be made until October 20 – Learn more about that process HERE.

scrutinizeThe Solve ME/CFS Initiative is in the process of reviewing the draft report more thoroughly with members of its Research Advisory Council in order to provide the most informed comments prior to the deadline of October 20, 2014.

We will keep you informed and share our thorough review once completed.

Guest Blog: Laurie – Hope Springs Eternal

September 22, 2014

hope2

 

The year was 1989, six years after giving birth to my son and nine years into a career as the head of a private school. I was a single parent, in a serious relationship, active in volunteering, loved working out and had just finished overseeing a major construction project at the school.

One afternoon during a lunch meeting I started to feel like my equilibrium was off. Thinking I might be coming down with something, I returned to my office to lie down, hoping to feel better. I felt like the room was going to spin, my body ached all over and I broke into a cold sweat. I was so nauseous I thought I would throw up. I laid down on the floor and closed my eyes. I could not make sense of what was happening to me. I felt like my limbs and body were going to lose control. I was afraid to move. I laid on the floor for the remainder of the afternoon until I felt that I could go home.

My list of symptoms increased – among them, swollen glands and a chronic low grade fever – so I went to see my doctor.  Luckily, he was familiar with Chronic Epstein Barr and with my lab tests to prove it I didn’t have to go through the ugly maze of doctors telling me that there was nothing wrong with me.  However, my doctor had no idea of how to treat it. His best advice was “to continue working and ignore my symptoms”.  Since my initial symptoms would come and go, I took his advice. I thought I could navigate my illness and still handle the demands of my job. That lasted for two years and then I crashed.

Hoping that I would rebound, I took a 7 month leave of absence figuring that it would make a difference. Seven months later my symptoms had not gotten better, instead they exacerbated.  I had to write a letter of resignation.

This loss was devastating. It was the beginning of a thirteen year struggle in my quest to become an active working member of society again. I had always been successful at overcoming difficulties… mostly through keeping a positive attitude and pushing forward. I could not understand why I could not improve or overcome this illness.

My life slowed down. I was having to sleep 16-18 hours a day; a challenge since I was a single mother who wanted to be there for her son. I tried numerous alternative treatments and traditional therapies. Then a friend who had been diagnosed with the same illness died after receiving a new experimental treatment. I never knew if the treatment caused her death.

Given this and my own reactions to many of the medications and treatments, I became cautious. Eventually I learned to trust my body, navigate how it reacted, and go with what I felt would make a difference.  Through trial and error I learned that making adjustments to my diet, getting lots of rest, avoiding stress of any kind (even good) and not overdoing it helped.

Thirteen years later I was able to return to work. My high functioning abilities had returned and I was excited about using them. I took a Head of School position out of state, but immediately discovered that the school had more difficulties than revealed. The demands of the job were more than anticipated. After three months I started to experience mild symptoms but chose to ignore them hoping to succeed at all costs.

I was renting my house, knowing I would return to Colorado someday. My plans were to work until retirement age or beyond. Moving back and having to pack an entire household after only working three months was not an option that I wanted to court so I continued to push myself. I had forgotten how devastating my illness could be and my desire to fulfill my dreams of working again was strong.

Being high functioning again after thirteen years of being ill, I made sure to give my all. The fear of having to pack up and move back to Colorado led me to take an anti-depressant, hoping that it would make a difference.  It took away some of the emotional aspects that surrounded my fears but it did very little for my physical symptoms. The only thing that helped was rest and sleep which I did whenever I was not at work, leaving me with no social life.

Again, I started seeing an array of doctors and doing alternative therapies, hoping to find something that would help. I operated in that vein for 3 years doing my best to ignore my symptoms but they continued to get worse. Two and a half years later I crashed and could no longer work. For the second time this illness stripped me of my profession. This time I did not feel like a failure; instead I had finally learned the anatomy of an illness that would not allow me to be a working member of society. I was able to my new life.

There is an expression, “Hope Springs Eternal.”  I believe this applies to me as I continue my search for help.

  • I have learned that I know my body better than anyone else.
  • I will not allow someone to tell me it is all in my head or just depression “so just take a little pill”.
  • When I feel sad I know it is because my illness has flared up causing me to become more limited in my activities.  When my body is “depressed” for an extended period of time due to relapse I feel sad or depressed… and when the symptoms diminish the sadness and/or depression lifts.
  • Overall I am a positive person so when there are relapses I know in my heart of hearts that they will eventually pass.

hopeThe claims that doctors and alternative practitioner make I now approach cautiously. Even though their intentions are good and they have had success with a number of patients, I know that my body can react negatively to many of their pills or treatments causing a downward spiral. This is why I am so glad that the Solve ME/CFS Initiative is there.

They are “Working to make ME/CFS widely understood, diagnosable and treatable”.  We are so fortunate to have a team like this working on our behalf. By pooling the information they have received from doctors, researchers, and professionals in the field, I believe they will find something that will help each of us on our journey to wellness. I encourage everyone that has ME/CFS and their healthy friends and family members to help the incredible team at Solve ME/CFS Initiative by signing up for their SolveCFS BioBank, following their progress by signing up for their newsletter, and supporting their work financially.

 

Research Digest – September 2014: Cortisol in ME/CFS

September 15, 2014

Cortisol is a hormone that is produced in the adrenal glands where it enters into the circulation to dampen inflammation. It does this by entering into the cytoplasm of cells, binding to the cortisol receptor (called the glucocorticoid receptor) and then moving into the cell nucleus to bind to DNA and regulate the expression of inflammatory molecules.

Cortisol is an essential hormone for immune function and many studies have shown that cortisol is low in ME/CFS patients – known as hypocortisolism.  Recent articles find increased cortisol receptor expression is associated with post-exertion malaise (PEM), low cortisol is associated with more severe PEM and a return of cortisol to normal levels is associated with recovery.

In this month’s research digest, we review three studies that look at the effect of cortisol on function and post-exertional malaise in ME/CFS.

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In a Solve ME/CFS Initiative funded study published in Fatigue: Biomedicine, Health & Behavior Jacob Meyer, a PhD candidate at the University of Wisconsin, worked with a team of investigators from the University of Wisconsin, Madison, Marshfield Clinic Research Foundation and the University of Utah to study gene expression using an exercise challenge.  Thirteen ME/CFS patients and 11 healthy controls had blood samples taken before and after a maximal exercise challenge.  Compared to controls, ME/CFS patients had increased expression of 2 genes – the glucocorticoid receptor and the adrenergic alpha 2a receptor.  This increased gene expression was associated with PEM symptoms.  The authors suggest that these finding, particularly as they relate to cortisol, may lead to an understanding of the biological mechanism of PEM.  http://www.tandfonline.com/doi/full/10.1080/21641846.2013.838444#.U9gd-qgox4I

 

A short communication titled “Stress management skills, cortisol awakening response, and post-exertional malaise in Chronic Fatigue Syndrome” was published online in the journal Psychoneuroendocrinology.  Daniel L. Hall and Michael Antoni from the Department of Psychology at the University of Miami together with Mary Ann Fletcher and Nancy Klimas from the Institute for Neuro Immune Medicine, Nova Southeastern University found that greater stress management skills was associated with higher cortisol levels upon wakening and less PEM severity.  The investigators recommend that similar research be conducted over longer periods of time to determine if by improving stress management skills, cortisol regulation improves and ME/CFS patients experience less PEM.
http://www.ncbi.nlm.nih.gov/pubmed/25049069

 

In another study published earlier this year in Psychoneuroendocrinology titled “The role of hypocortisolism in chronic fatigue syndrome”, investigators from the Netherlands examined cortisol levels in young ME/CFS patients participating in the FITNET (Fatigue In Teenagers on the interNET) trial.  FITNET, an internet-based cognitive behavioral therapy program for young ME/CFS patients. These investigators found that the cortisol levels in patients that improved after 6 months of treatment returned to normal levels.  ME/CFS patients that did not respond to treatment had slight increases in cortisol levels but still below normal.  The investigators conclude that the return of cortisol levels to normal is associated with treatment success and that poor functioning of the hypothalamic-pituitary-adrenal (HPA) axis that regulates cortisol levels plays a role in ME/CFS symptoms.  Understanding what contributes to HPA axis dysfunction could help improve ME/CFS treatment.
http://www.ncbi.nlm.nih.gov/pubmed/24636516

 

Guest Blog: Dr. Peter Rowe – Is The Physical Examination Normal in CFS? Part 3

September 11, 2014

In this 3rd piece of our three-part blog series Dr. Peter Rowe discusses range of motion in ME/CFS patients.

In the first post in the series, Dr Rowe discussed orthostatic heart rate and blood pressure changes. Read Part 1 HERE

In the second post, Dr Rowe discussed joint hypermobility. Read Part 2 HERE

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Postural dysfunctions and movement restrictions

Some of those with joint hypermobility also have postural abnormalities that are thought to be a consequence of the effect of gravitational loading of the spine, including a head-forward posture, a rounded appearance of the thoracic spine, and increased lumbar curvature. My physical therapist colleague, Rick Violand, had originally identified a number of associated areas of reduced movement of the spine and limbs during his examination of those with CFS. These observations describing adverse neural tension (also termed neurodynamic dysfunction) have been reported elsewhere.1-3 During the clinical care of patients over the last decade, we had been struck by how many individuals with CFS had focal areas of restricted range of motion, and how adding an elongation strain to nerves and soft tissues could aggravate their typical CFS symptoms. With other co-investigators, we recently published a large study showing that reduced range of motion of the limbs and spine was significantly more common in adolescents and young adults with CFS than in carefully matched controls, and that adding a longitudinal strain to the nerves and soft tissues was another way of provoking common CFS symptoms.18 These examination abnormalities can be detected most readily by physical therapists and other manual practitioners. Physicians and nurse practitioners can become adept at screening for these problems if provided with extra training.

Why does the detection of movement restrictions matter? Our experience leads us to believe that the areas of adverse neural tension are treatable. In clinical care we have noted that improvement in the range of motion is usually accompanied by improvement in daily function for those with CFS. Much more work needs to be done to characterize these abnormalities further, to determine whether the same changes are also present in adults with CFS, and to identify the optimal treatment approaches. These observations open up new avenues for understanding the pathogenesis of CFS symptoms, and for further individualized approaches to treatment. We hypothesize that treating the movement restrictions first using gentle manual therapy techniques will help the most impaired CFS patients begin to tolerate exercise better.

Conclusion    

These three related areas of dysfunction—circulatory disturbances, joint hypermobility, and movement restrictions—emphasize that there is much to be gained from the performance of a careful clinical examination in those with CFS. Given that aspects of each abnormality are treatable, their identification has the potential to improve the daily symptoms and function for those with CFS. We recommend the more widespread adoption of maneuvers to ascertain for these abnormalities in the clinical and research evaluation of those with CFS.

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 As medicine becomes more and more dependent on sophisticated technology, the physical exam is in danger of becoming a lost art.  As Dr. Peter Rowe, Johns Hopkins University, has laid out in this three-part series, there is much to be learned in a physical exam in CFS. Our hope is that this information will be of great value to both you and your doctor. We believe it clearly illustrates the value of laying on of hands in the physical examination of ME/CFS.

Suzanne D Vernon, PhD
Solve ME/CFS Initiative Scientific Director

 

References

  1. Rowe PC, Fontaine KR, Violand RL. Neuromuscular strain as a contributor to cognitive and other symptoms in chronic fatigue syndrome. Frontiers in Integrative Physiology 2013; Front Physiol 2013;4:115. doi: 10.3389/fphys. 2013.00115
  2. http://www.research1st.com/2013/01/25/manual-therapy-1-of-2/
  3. http://www.research1st.com/2013/02/01/manual-therapy-2-of-2/
  4. Rowe PC, Marden CL, Flaherty M, Jasion SE, Cranston EM, Johns AS, Fan J, Fontaine KR, Violand RL. Impaired range of motion of limbs and spine in chronic fatigue syndrome. J Pediatrics 2014 (in press).

 

Guest Blog: Dr. Peter Rowe – Is The Physical Examination Normal in CFS? Part 2

September 9, 2014

In the 2nd part of this three-part blog series on physical examination in ME/CFS, Dr. Peter Rowe discusses joint hypermobility.  You can read the first blog post in the series where Dr Rowe discussed orthostatic heart rate and blood pressure changes HERE.

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Joint hypermobility

Some patients meeting the criteria for CFS have a genetic disorder of connective tissue known as Ehlers-Danlos syndrome (EDS). Those with EDS have stretchy skin, very loose, hypermobile joints that often dislocate easily, along with delayed wound healing, fragile skin, and a tendency to develop an early onset of varicose veins. Those with EDS have chronic fatigue and widespread pain of uncertain cause, which of course overlaps with the central features of CFS.

We first drew attention to this association in 1999, noting that those with CFS and orthostatic intolerance had a much higher prevalence of EDS than expected.1 We then went on to examine whether those with CFS had a higher prevalence of joint hypermobility. Although we might expect less flexibility in a population that has had at least 6 months of reduced activity, in that study, 60% of new adolescent patients with CFS met criteria for joint hypermobility, compared to just 24% of healthy controls.2

Slide2Slide1

The assessment of joint hypermobility takes only a couple of minutes, and can easily be performed using a goniometer for accurate measurement of joint angles. The most commonly used series of maneuvers is the 9 point Beighton score, as shown in the pictures above. It should be noted that the Beighton score does not do a good job of evaluating for laxity in the hips and shoulders, but it is a useful screening tool.

CFIDS PE article Fig 4

Other findings on the examination in those with EDS can include increased extensibility of the skin, abnormally widened and thin (“papyraceous”) scars, easy eversion of the eyelids, and stretch marks (striae) even in the absence of excessive changes in weight. Examples of these findings are shown in the pictures to the right.

Since the publication of these results, a number of studies have confirmed that those with joint hypermobility have more orthostatic symptoms and a reduced tolerance of upright posture,3 and that fatigue is a prominent contributor to lower quality of life in EDS.4 New work from investigators in Belgium confirms that those with hypermobile EDS have high rates of autonomic symptoms, abnormal heart rate responses to upright posture, and other features of autonomic dysfunction.5,6

Why does the assessment for joint hypermobility matter? Joint hypermobility is associated with other co-morbid disorders such as temporomandibular joint dysfunction, and the laxity in ligaments often contributes to arthralgias and myalgias. Better ascertainment of these problems can lead to more focused therapy directed at pain, and physical treatments directed at biomechanical dysfunctions.7 Beyond the effects on joints, connective tissue laxity also affects the blood vessel walls. The increased distensibility in blood vessels may be a factor in the early development of varicose veins in those with EDS. Vascular stretch also is thought to allow increased blood pooling in the dependent circulation during upright posture, leading to diminished blood return to the heart, and thus to orthostatic intolerance symptoms. Given the high prevalence of skin and joint laxity in those with CFS, and the contribution of connective tissue abnormalities to the development of orthostatic intolerance, we recommend that all those with CFS undergo screening with a Beighton score, and that clinicians look carefully for the skin changes of EDS in their patients with CFS.

 

References

  1. Rowe PC, Barron DF, Calkins H, Maumenee IH, Tong PY, Geraghty MT. Orthostatic intolerance and chronic fatigue syndrome associated with Ehlers-Danlos syndrome. J Pediatr 1999;135:494-9.
  2. Barron DF, Cohen BA, Geraghty MT, Violand R, Rowe PC. Joint hypermobility is more common in children with chronic fatigue syndrome than in healthy controls. J Pediatr 2002;141:421-5.
  3. Gazit Y, Nahir AM, Grahame R, Jacob G. Dysautonomia in the joint hypermobility syndrome. Am J Med 2003;115:33-40.
  4. Voermans NC, Knoop H, van de Kamp H, et al. Fatigue is a frequent and clinically relevant problem in Ehlers-Danlos syndrome. Semin Arthritis Rheum 2010;40:267-274.
  5. de Wandele I, Calders P, Peersman W, et al. Autonomic symptom burden in the        hypermobile type of Ehlers-Danlos syndrome: a comparative study with two other EDS types, fibromyalgia, and healthy controls. Semin Arthritis Rheum 2014 (in press).
  6. de Wandele I, Rombaut L, Leybaert L, et al. Dysautonomia and its underlying mechanisms in the hypermobility type of Ehlers-Danlos syndrome. Semin Arthritis Rheum 2014; (in press).
  7. Simmonds JV, Keer RJ. Hypermobility and the hypermobility syndrome, part 2: assessment and management of hypermobility syndrome: illustrated via case studies. Man Ther 2008;13:e1-e11.

 

Figure Legends

Fig 3a: The Beighton score. Possible scores are 0-9, with scores ≥ 4 indicating joint hypermobility. On each side, score 1 point for > 90o of hyperextensibility of the 5th finger, 1 point for the ability to appose the thumb to the forearm, and 1 point for > 10o of hyperextensibility at the elbow.

Fig 3b: On each side, score 1 point for >10o of hyperextensibility at the knee, and 1 point for the ability to place the palms on the floor.

Fig 4: Other features of EDS: clockwise from the top left, stretch marks (striae) in a non-obese individual who has not had excessive weight change, easy eversion of the upper eyelids and Gorlin’s sign (the ability to touch the tongue to the tip of the nose, increased extensibility of the skin of the upper eyelid, and wide, thin scarring at the site of wound dehiscence after a simple laparoscopy incision.

 

Guest Blog: Dr. Peter Rowe – Is The Physical Examination Normal in CFS? Part 1

September 5, 2014

The Laying on of Hands: Recently I read with great interest a Medscape article titled, “Patients Lose When Doctors Can’t Do Good Physical Exams”.  You can read the article here: http://www.medscape.com/viewarticle/825442 but the crux is that as medicine becomes more and more dependent on sophisticated technology, the physical exam is in danger of becoming a lost art.

This Medscape article made me think about the experiences of our ME/CFS patient community and the frequency of physical examination. I reached out to Dr. Peter Rowe whose research we have funded that deals with neuromuscular strain and range of motion. This is the first in a series of blog posts from Dr. Peter Rowe of Johns Hopkins University titled “Is the physical exam in CFS normal?” We are certain that this information will be of great value to both you and your doctor and will clearly illustrate the value of laying on of hands in the physical examination of ME/CFS.

Suzanne D Vernon, PhD
Solve ME/CFS Initiative Scientific Director

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Is the physical examination normal in CFS?

Papers in the early 1990s described a low yield of physical examinations in patients with chronic fatigue and CFS.1 Although there were some notable counter-arguments made by Komaroff—describing sore throat and swollen lymph nodes, as well as a 10-20% prevalence of abnormal Romberg tests (Romberg test is a neurological exam that assesses balance while standing)2—most reviews of CFS included statements like the one that appeared in the 2002 Australian CFS Guidelines: “Characteristically, there are no abnormal physical findings in people with CFS.”3

The absence of abnormalities on the physical examination, especially when contrasted with the profound functional impairment in CFS, was often interpreted to be consistent with a largely psychosomatic origin of the illness. Research in the past 20 years, however, provides a decidedly different view.  In this three-part blog post, Dr. Peter Rowe will describe three groups of abnormalities found on physical examination.

Orthostatic heart rate and blood pressure changes

One of the most readily apparent abnormalities on the examination of those with CFS is that heart rate and blood pressure abnormalities are present, sometimes at rest, and more consistently during relatively brief periods of upright posture. In response to standing or upright tilt table testing, individuals with CFS have a higher prevalence of neurally mediated hypotension (NMH) and postural tachycardia syndrome (POTS), or both (Figure 1). The prevalence of these and other blood pressure and heart rate abnormalities is higher in adolescent than in adults, but even in the absence of objective changes in blood pressure or heart rate, orthostatic (upright) stress in individuals with CFS of all ages provokes characteristic daily symptoms of increased fatigue, lightheadedness, mental fog, or headache. In adolescents, all published controlled studies have shown a numerically higher prevalence of orthostatic intolerance in CFS than in healthy individuals (4 of 5 reporting statistically significantly differences), and all studies looking at autonomic tone show a sympathetic predominance of heart rate variability, especially in response to orthostatic stress.

Slide1   Slide2

NMH occasionally can be provoked by a brief standing test, but more commonly requires a more prolonged head-up tilt table test. The median time to provoke a drop in blood pressure in our tilt laboratory in the mid-1990s was 28 minutes,4 although symptoms are usually exacerbated shortly after the patient is tilted upright.

The diagnosis of POTS in adults requires a ≥ 30 beat per minute (bpm) increase in heart rate (HR) during 10 minutes upright when compared to baseline supine values, or a HR increase to ≥ 120 bpm, together with the reproduction of typical orthostatic symptoms. Normative data on healthy young people showed that the adult HR criteria overdiagnosed POTS, so in adolescents the diagnosis now requires a ≥ 40 bpm HR increase in the first 10 minutes of head-up tilt or standing, or a HR ≥ 120 bpm.5 Some individuals with POTS at an early point of tilt testing subsequently develop a more profound drop in BP, consistent with delayed orthostatic hypotension or with NMH.

CFIDS PE article Fig 2Along with the changes in heart rate and blood pressure, a striking physical finding among those with CFS and orthostatic intolerance is a purple discoloration in the dependent limbs termed acrocyanosis (Figure 2). Acrocyanosis is readily apparent if the patient is examined in shorts, seated on the examination table, with the legs hanging down. This finding can be differentiated from Raynaud’s phenomenon by the absence of blanching of the fingers or toes, and by the fact that hands and feet are diffusely discolored.

Why does recognition of orthostatic physical examination findings matter? Open treatment studies show that people with CFS can enjoy improved function with standard measures to manage orthostatic intolerance. That management involves lifestyle adjustments, compression garments, and increased salt and fluid intake, along with judicious use of medications. These treatments provide another avenue for a pragmatic, individualized approach to symptoms in those with CFS.

Studies by MacLean and Allen in the 1940s had drawn attention to the similarity between the symptoms of neuromyasthenia (an older term for what we now call CFS) and the symptoms of patients who experienced orthostatic tachycardia and hypotension after assuming an upright posture. Most of the latter group experienced orthostatic exhaustion, blurring of vision, weakness on exercise, and syncopal episodes,6,7 familiar problems for those with CFS. Although these observations were neglected for several decades, the weight of the evidence now suggests that all subjects with CFS deserve careful assessment of their heart rate, blood pressure, and symptomatic responses to at least 10 minutes of quiet upright posture. The British NICE guidelines that strongly recommend against the routine use of orthostatic testing8 need to be revised in light of the available and compelling data.

 

References

  1. Lane TJ, Matthews DA, Manu P. The low yield of physical examinations and laboratory investigations of patients with chronic fatigue. Am J Med Sci 1990;299:313-318.
  2. Chronic fatigue syndrome: clinical practice guidelines—2002. Medical J Australia 2002; 176:S24.
  3. Komaroff AL, Buchwald D. Symptoms and signs of chronic fatigue syndrome. Rev Infect Dis 1991;13(Suppl 1): S8-11.
  4. Bou-Holaigah I, Rowe PC, Kan J, Calkins H. Response to upright tilt testing in 100 consecutive patients with chronic fatigue syndrome. Circulation 1995;92(8S): I-414.
  5. Freeman R, Wieling W, Axelrod FB, Benditt DG, Benarroch E, Biaggioni I, et al. Consensus statement on the definition of orthostatic hypotension, neurally mediated syncope and the postural tachycardia syndrome. Clin Auton Res 2011;21:69–72
  6. MacLean AR, Allen EV. Orthostatic hypotension and orthostatic tachycardia: with the “head-up” bed. JAMA 1940;115:2162-7.
  7.  MacLean AR, Allen EV, Magath TB. Orthostatic hypotension and orthostatic tachycardia: defects in the return of venous blood to the heart. Am Heart J 1944;27:145-63.
  8. National Institute for Health and Clinical Excellence. Clinical guideline CG53. Chronic fatigue syndrome/myalgic encephalomyelitis (or encephalopathy): diagnosis and management. London, NICE, 2007. http://guidance.nice.org.uk/CG53.

 

Figure Legends

Fig 1a. NMH. The hemodynamic response to upright tilt testing in an individual with CFS. Note the early onset of orthostatic symptoms of lightheadedness (LH) and pallor, without early HR elevations, following at a relatively early point by profound hypotension and relative bradycardia, consistent with NMH.

Fig 1b. POTS. The hemodynamic response to quiet standing in an individual with CFS. Note the normal supine heart rate and the dramatic 51 beat per minute change in heart rate with standing, accompanied by lightheadedness, fatigue, and headache, without major changes in blood pressure.

Fig 2: Acrocyanosis (left) and delayed capillary refill (right) appearing within 5 minutes of quiet standing in an adolescent with chronic fatigue syndrome and low orthostatic tolerance.

P2P Workshop – Registration Now Open

September 3, 2014

P2P_title Registration is now open for the Pathways to Prevention workshop for Advancing the Research on ME/CFS. Interested individuals may register to attend live or participate via webcast. It is our hope that many stakeholders will participate in this process in order to ensure the patients have a strong presence and a voice.

Our understanding is that stakeholders/patients will have the opportunity to participate in the discussion both in person and online by asking questions or making comments via microphones or computers in the room. Webcast viewers can type in comments and questions in a comment box on the webpage. There is a total of 3.5 hours of “Discussion” time noted on the draft agenda, where public input will be addressed.

To register to attend live click HERE 

To register for the webcast click HERE

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More About the P2P: The National Institutes of Health (NIH), through the Office of Disease Prevention (ODP) has a program called the Pathways to Prevention. The goal is to host workshops that identify research gaps in a selected scientific area, identify methodological and scientific weaknesses in that scientific area, suggest research needs, and move the field forward through an unbiased, evidence-based assessment of a complex public health issue. You can read more about the P2P Workshop for ME/CFS HERE In June of 2012, the NIH launched the process of including ME/CFS in the P2P program. Several departments within the federal government came together to recommend ME/CFS for a P2P workshop. In November of 2012, the ODP received the recommendation to consider ME/CFS and approved the submission of a full proposal in December of 2012 based on “necessity, urgency and the identification of ME/CFS as a serious unmet medical need and a public health issue and that proposal was accepted then later approved. The workshop will take place on December 9 & 10, 2014. Topics for the two-day workshop agenda were defined by questions that formed the evidence review. Speakers have been recruited for the workshop for each question/agenda item. The speakers are all to be experts in ME/CFS and are able to speak to their personal experience and expertise as a patient, caregiver, researcher, etc. The evidence review is a concise presentation of the ‘evidence’ and literature in ME/CFS (that relates to the study questions), boiled down and presented to the panel. There is opportunity for the P2P panel to review unpublished data as well. The Solve ME/CFS Initiative submitted additional evidence for their review, as well as encouraged our funded investigators, colleagues and peers to do the same. The P2P panel will review the evidence-based report in advance of the meeting and the report will be released to the public at that time. There will be opportunity to comment and offer feedback on this report. We anticipate the report’s release in early October and will alert you to its publishing as soon as we hear more. At the two-day workshop, the P2P panel will hear from the expert speakers and be able to ask clarifying questions in a town-hall-like Q&A that will take place after each session during the meeting.  The P2P Panel will be made up of experts in areas or topics that have relevance to ME/CFS and the evidence based report, but they are not to be ME/CFS experts by design – an effort to avoid bias and produce a report based on the facts presented in the evidence-based report and through the speakers. We do not know if patients in the gallery will be able to engage in the Q&A. The day after the P2P meeting, the P2P Panel will write a draft report which will be published and the public will have time for comment. Originally the comment period was slated for 15 days. SMCI, along with other organizations and advocates, reached out to the P2P and asked that this comment period be extended in order to accommodate patient’s needs. We have received word that the comment period has been extended to 30 days, meaning the new deadline should be around January 12th, 2015. Once the comment period closes, the report will be finalized and NIH will organize a robust plan to disseminate it widely. The goal, as we understand it, is to have a report that contains a set of recommendations based on the totality of the evidence, in the hopes of having said recommendations carried out by Federal partners in one-nine months. These recommendations are aimed at improving the robust nature of the research being conducted in ME/CFS. The Solve ME/CFS Initiative will pass along additional information as it is received and when the opportunity for public comment is scheduled, we will report that and share the means by which you can effectively participate.

Research Digest – August 2014: More Results from the SolveCFS BioBank

August 22, 2014

The Solve ME/CFS Initiative established the SolveCFS BioBank in 2010.  Over the past 4 years clinical information and samples from the first 240 ME/CFS patients and 87 controls have been used by more than ten researchers – most new to ME/CFS research.   Right after we established the SolveCFS BioBank, Science magazine published the results that described a new virus in ME/CFS patients called XMRV.  This research caught the attention of many scientists and the pharmaceutical industry – immediately investigators needed samples to try to further these XMRV results.

The timing was perfect for the then-new SolveCFS BioBank.  In collaboration with GlaxoSmithKline (GSK) and four expert ME/CFS physicians, the SolveCFS BioBank collected information and samples from ME/CFS patients and healthy controls.  We are pleased to now report the publication of this SolveCFS BioBank “founding” study and some of the results from the first study of epigenetics in ME/CFS. Both used the clinical information and samples that were collected in 2010 through the SolveCFS BioBank.

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The study that helped us establish the SolveCFS BioBank titled No association found between the detection of either xenotropic murine leukemia virus-related virus (XMRV) or polytropic murine leukemia virus and chronic fatigue syndrome in a blinded, multi-site, prospective study by the establishment and use of the SolveCFS BioBank was recently published in the open access journal BMC Research Notes. The authors are from GSK, the Solve ME/CFS Initiative and several ME/CFS clinics – a great example of partnership and collaboration.  Like the many studies that have been published following the initial description of XMRV in ME/CFS, this research also found that the XMRV was found in both ME/CFS patients and healthy controls.  XMRV was detected in 6.7% (5/72) of ME/CFS patients and 5.4% (2/37) healthy controls.  Since these detection rates were so similar, it indicated that XMRV was a contaminant rather than a virus associated with the disease.  By comparing the XMRV detected here to the XMRV described in other studies, it was clear that XMRV was a contaminant from a reagent(s) used in the laboratory test. The finding that XMRV is a “contaminant” in the reagents we use in these very sensitive laboratory tests was an important discovery and has improved the way we test for viruses and interpret results.  This study was also the only one related to XMRV that used a biobank and collaborated with a patient-centered research organization.
You can read the full text of this open access article here: http://www.ncbi.nlm.nih.gov/pubmed/25092471

 

 

Wilfred de Vega, PhD candidate at the University of Toronto and his mentor Dr. Patrick McGowan together with Suzanne D. Vernon, scientific director of the Solve ME/CFS Initiative and the SolveCFS BioBank conducted the first ME/CFS epigenetic study. The results have just recently been published in the open access and highly regarded journal PLOS ONE.  The title of this paper is “DNA methylation modifications associated with chronic fatigue syndrome”.  Methylation modifies DNA without changing the genetic sequence and this chemical change affects the way the gene is expressed.  Lots of methylation corresponds to less gene expression – possibly even silencing the gene; less or no methylation corresponds to increased expression.  de Vega and his team found genes important for the immune response had different methylation patterns in ME/CFS patients compared to matched healthy controls.  Many of the methylation differences were in parts of the gene important for regulating gene expression.  These novel findings provide further evidence of immune response abnormalities contributing to ME/CFS pathophysiology.
You can read the full text of this open access article here: http://www.ncbi.nlm.nih.gov/pubmed/25111603

Read more about this study in a recent blog post HERE 

And watch McGowan’s webinar on this topic HERE

 

CFSAC Charter Up for Renewal

August 21, 2014

The Solve ME/CFS Initiative is involved in advocacy efforts aimed at improving the research landscape for the early detection, objective diagnosis and effective treatment of ME/CFS.  As part of this effort, we work to validate the burden of illness imposed by ME/CFS in agencies where national policy is made and executed.

The Chronic Fatigue Syndrome Advisory Committee (CFSAC) provides advice and recommendations to the Secretary of Health and Human Services (HHS) through the Assistant Secretary for Health on issues related to myalgic encephalomyelitis and chronic fatigue syndrome (ME/CFS).  In addition to sitting on the CFSAC as a non-voting liaison member, SMCI has been involved in the CFSAC through encouraging patient involvement in meetings, by providing public testimony, and through serving on various sub-committees.

Every two years, the charter for the CFSAC must be renewed. With the last renewal being filed September 5, 2012, the charter is again up for renewal. SMCI understands the importance of having a federal advisory committee focused on issues related to ME/CFS and so on August 1, 2014 we wrote to the Secretary of Health and Human Services urging her to renewal the CFSAC charter.

We will keep you posted on the results of this request, a copy of which is posted below.

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CFSME_logomain_fkacfids

 

 

 

Sylvia Mathews Burwell
Secretary of Health and Human Services
U.S. Department of Health and Human Services
200 Independence Avenue, SW
Washington, D.C. 20201

August 1, 2014

Dear Secretary Burwell:

We are writing to urge you to renew the charter and fully fund the Department of Health and Human Services (DHHS) Chronic Fatigue Syndrome Advisory Committee (CFSAC). The charter is set to expire on September 5, 2014.

The CFSAC was established to provide evidence-based advice and recommendations to you and the Assistant Secretary of Health on issues related to chronic fatigue syndrome (CFS). The issues can include factors affecting access and care for persons with CFS; the science and definition of CFS; and broader public health, clinical, research and educational issues related to CFS.

Chronic Fatigue Syndrome (CFS), also known as myalgic encephalomyelitis (ME), is a complex and severely debilitating chronic illness that affects up to 4 million Americans, according to the CDC. ME/CFS is now recognized by most authorities, including CDC and NIH, as a severe and debilitating disease. Unrelenting exhaustion, widespread muscle and joint pain, cognitive impairments (particularly problems with memory and concentration), unrefreshing sleep, sore throat, headache, and a constellation of other symptoms are debilitating enough to dismantle careers and destroy active lifestyles. Its hallmark, post-exertional malaise, is a return or worsening of all symptoms following even modest physical or mental activity which can last for days or weeks.

Alarmingly, less than 20 percent of ME/CFS patients have been diagnosed, yet early detection and symptom management have been shown to improve the patient’s long-term outlook. The high prevalence of ME/CFS, its low rate of diagnosis and the annual economic toll of up to $25 billion demonstrates the need for increased public and policy-maker awareness and a more potent research effort.

Meetings of the CFSAC provide a vital opportunity for experts selected by the Department to listen to and exchange information with representatives of DHHS agencies, including the National Institutes of Health, Centers for Disease Control and Prevention, Health Resources and Services Administration, Agency for Healthcare Research & Quality, Food and Drug Administration and Social Security Administration. The CFSAC meetings also provide opportunities for patients and advocates to express support for or concerns about ME/CFS programs through public testimony. The CFSAC allows for greater transparency and accountability for ME/CFS programs, helping to ensure the most effective policies and utilization of federal resources dedicated to ME/CFS.

We urge you to renew the CFSAC charter before its September 5, 2014 expiration and to fully support its important work. We appreciate your consideration and look forward to receiving your response.

Sincerely,

Carol E Head
President and CEO, Solve ME/CFS Initiative

 

cc: Dr. Nancy C. Lee, Deputy Assistant Secretary for Health – Women’s Health
Designated Federal Officer for CFSAC