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!



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.



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.



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.”



Investigator Report: Decoding the Human Immune Response

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

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

Derya Unutmaz, MD, is associate professor of Microbiology and Pathology 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.


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.


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:



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:

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.






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.


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


Guest Blog: Roger Dodd, PhD – Retrovirus Testing in Retrospect

August 21, 2014

On August 13, 2014, Suzanne D. Vernon Ph.D., Scientific Director for the Solve ME/CFS Initiative (SMCI), held a webinar that provided an overview of the work done through SMCI’s Research Institute Without Walls and SolveCFS BioBank, as well as a glimpse of what’s ahead.  (Watch it HERE) During the Q&A portion of that webinar she received a question from someone concerning XMRV, wondering if they should be concerned that they tested positive. Realizing that others may have similar lingering questions or concerns about XMRV, she reached out to Roger Dodd, PhD, Vice President of Biomedical Services Research and Development at the American Red Cross, and asked him to provide this guest post on the topic.

“I met Roger in 2010 when I was asked to be on the Blood XMRV Scientific Research Working Group. The situation with XMRV was being taken very seriously and companies like Gen-Probe were developing the most sensitive diagnostic tests to detect the virus.  Roger told me a story about HIV testing that I asked him to share with you, as it applies to our XMRV situation.  It is a great example of the rigor needed for diagnostic tests.”, says Suzanne.


Dodd2-249x300Guest Blog – Retrovirus Testing in Retrospect
By Roger Y. Dodd, PhD
Vice President of Biomedical Services Research and Development at the American Red Cross
Member of SMCI’s Research Advisory Council

Around the world, donated blood had been tested for HIV antibodies since 1985 – in the US alone, about 400 million tests – and we still have not perfected the process.  Certainly, there is essentially no risk of transmission of HIV by transfusion, but thousands of blood donors are uncertain about their test results even though we now use the most sensitive and specific tests available, from top flight manufacturers, intensively regulated by the FDA.  How can this be?  Simply put, it is a result of complexity, caution and simple mathematics.

The term complexity covers a tremendous range of issues, but suffice it to say that developing a test for antibodies to retroviruses is not at all simple.  The virus itself has many components that can react with antibodies, but it also has proteins that are similar to human proteins (human antigens).  Originally, the virus used to develop tests was grown in cells in the lab and some of the components of these cells were carried over into the test.  Also no retrovirus is totally unique and may share antigens with other retroviruses that humans may be exposed to but which do not cause any problems.    The tests themselves might react in unexpected ways – for example, some human antibodies react with the plastics in the test kits.  Not all of these complex issues are understood, and the outcome is that a test may give a result that looks positive, but has nothing to do with HIV infection.  This kind of event is called a false positive.  The term “specificity” is a measure that defines how often false positives occur (although its definition is actually the proportion of negative results when the test is used on people who are absolutely negative for the virus).  The ideal value for specificity is 100%, of course.  Because false-positives occur, it is always important to check reactive test results using a different test method, but even this is not perfect.

Caution has been a very important component of testing programs for HIV.  This caution is expressed in two directions: firstly, as pointed out to be sure that results are confirmed, but more importantly in the ways in which uncertainties have been handled.  So, even though a false positive result may be identified by a second test, no blood is used if the first test gives reactive results after the test is repeated.  So donors may be told that they cannot give blood, but that additional testing indicates that they are not infected.  Not a very encouraging message.

Where does simple mathematics fit into the equation?  It is a matter of understanding what the actual meaning of a reactive result is.  In collecting blood, very few of our donors are infected with HIV (actually, about 3 in every 100,000).  The test that we use has a specificity of about 99.9%.  That means that there is one false positive result for every 1000 donations tested.  So, in 100,000 donations, there might be three people with HIV and 100 with a false positive.  So a positive result with the very good test that we use only has one chance in about 33 of being right.  No wonder we have to do careful confirmatory tests and scrupulous counseling of our donors.  All of this with the very best of retrovirus tests used and refined over 30 years. Imagine how difficult it was in 1985.

The blood bank community took XMRV seriously, but were fully aware of the pitfalls of retrovirus tests and found little to encourage them about the validity of the XMRV testing that was being offered to the public.  What works in the research lab is not appropriate for mass testing without extensive validation and a clear, proven rationale.  XMRV itself was a laboratory artifact, and the so-called antibody tests were not credible.  This means the test that was being used to test the blood samples that ME/CFS patients sent to the testing laboratory were false positive.  If you were one of those who received a report indicating you tested positive for XMRV, you should rest assured that you are not. It is to be hoped that nobody carries lingering concern about XMRV and any test results associated with it.

CDC Stakeholder Call – Open Invitation

August 18, 2014

CDCIn the fall of 2012, the U.S. Centers for Disease Control and Prevention (CDC) began a new series of conference calls to update stakeholders about ME/CFS-related research activities and other topics of interest. Information on the next call, scheduled for Tuesday, September 9, 2014, is provided below from their listserv and website.  

There is no need to RSVP for this call, simply dial in. To join the listserv, please send an email message directly to CDC at



Tuesday, September 9, 2014

3:00 pm - 4:00 pm EDT

CDC CFS Patient-centered outreach and communication activity (PCOCA) Conference Call

Call number: 1-800-857-5128

Participant Code: 4459244

Please mark your calendars for the next CDC Chronic Fatigue Syndrome (CFS) Patient-Centered Outreach and Communication Activity (PCOCA) Conference Call.


Meeting Agenda

3:00pm    Welcome and Telephone Overview

3:05pm   Updates from CDC – Elizabeth Unger, PhD, MD

Branch Chief, Chronic Viral Diseases Branch

Centers for Disease Control and Prevention


3:15pm  “Can ME/CFS and FM Sleep Research Help You Sleep?”

Lucinda Bateman MD

Director, Fatigue Consultation Clinic

Adjunct Assistant Professor, Anesthesiology – Operations, University of Utah

Adjunct Instructor, Family and Preventive Medicine, University of Utah

3:45pm   Questions from CFSPCOCACall Mailbox for Guest Speaker and CDC


 Disclaimer: Although the content of calls is directed to patients, caregivers, health care professionals, and other interested parties, CDC has no control over who participates on the conference call.  Therefore please exercise discretion on sensitive content and material, as confidentiality during these calls cannot be guaranteed. 


Please note that questions for the Guest Speakers and CDC can be submitted only via email at This mailbox cannot respond to inquires received and is in use only for the scheduled CFS PCOCA calls. If you would like to be added to the call list, please send an email to


Contact for CFSPCOCA Conference Call:


For some additional resources and information on the biology of sleep, CLICK HERE



Breaking News: Chemical Changes in Immune Cell DNA from ME/CFS Patients

August 12, 2014

SMCI Funded Research Results Announced!

We are pleased to announce the first study to report epigenetic modifications throughout the genome in female ME/CFS patients compared to a matched sample of healthy controls.  This research conducted in partnership and funded by the Solve ME/CFS Initiative (SMCI) was published today in the high impact and open access journal PLOS ONE (

McGowanThe Solve ME/CFS Initiative launched our Research Institute Without Walls in 2010 and Dr. Patrick McGowan was one of our first grantees to use this innovative infrastructure. Together with his graduate student, Will de Vega and SMCI’s Scientific Director, Suzanne D. Vernon, they found evidence of distinct epigenetic profiles in immune and other physiologically relevant genes in a selected group of female ME/CFS patients. Will de Vega, who performed much of the work, is a PhD candidate in the department of Cell and Systems Biology at the University of Toronto. His thesis research concerns how environmental factors and ME/CFS impact immunological processes, and their effects on clinically relevant phenotypes. 

Epigenetic modifications affect the way genes are turned on or off without changing the inherited gene sequences. “Knowledge about the epigenetics of ME/CFS could potentially lead to alternative treatment options for sufferers, from targeted lifestyle interventions to new pharmacological treatments”, notes McGowan. There were many epigenetic modifications in and around immune genes that affect the way these genes are regulated and expressed. These types of changes would be expected to affect immune cell function in ME/CFS patients. “This is the first in a series of exciting results coming from McGowan’s lab at the University of Toronto”, says Suzanne D. Vernon. “By understanding these epigenetic differences in the immune cells of ME/CFS patients, we can begin to decipher the molecular mechanisms of the immune dysfunction that we suspect is at the root of ME/CFS”.

McGowan started this ME/CFS epigenetic research in 2012. His quick success is a testament to the power of patient-centered research approach used by the Solve ME/CFS Initiative. “Our study would not have been possible without the funding provided by the Solve ME/CFS Initiative, patient samples from the SolveCFS BioBank, and the collaborative support of the Initiative’s scientific director Dr. Suzanne D. Vernon” says McGowan.

The Solve ME/CFS Initiative will continue to partner with McGowan and his team at the University of Toronto to further this exciting work of epigenetics and ME/CFS. This field of research holds promise for identification of diagnostic biomarkers and potential treatment and interventions for ME/CFS. For right now it is further demonstration of the indisputable biological basis of ME/CFS.


Learn More about McGowan’s work and results through our Webinar Series

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.

Guest Blog: Mark A. Demitrack, MD, FAPA – Neurobiology of ME/CFS

July 17, 2014

Far too often, myalgic encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) patients are met with healthcare providers who do not believe in the biological nature of the disease. Patients have an understandable reticence when it comes to psychologists and psychiatrists because of the fear that their ME/CFS will be labeled as a psychological disorder rather than treated as the very real debilitating disease that it is. Yet, the medical disciplines of psychology and psychiatry have a tremendous amount to contribute to the ME/CFS community, because of their extensive knowledge of how the central nervous system works.integrated

In this guest blog post, Mark Demitrack, MD, FAPA describes how for a long time he has advocated for and used an integrated approach to understand how the brain is involved in the biology of ME/CFS.


Neurobiology of ME/CFS
by Mark A. Demitrack, MD, FAPA
Member, Research Advisory Council, Solve ME/CFS Initiative

In 1991, I co-authored an editorial in the journal Biological Psychiatry, entitled, “Chronic Fatigue Syndrome: The Need for an Integrative Approach”.  The topic of that manuscript was an appeal to the medical community to expand and recast the research investigation of Chronic Fatigue Syndrome into a more integrative framework.  In such a broader framework, I suggested that any advances in scientific research for the pathophysiologic underpinnings of this disabling illness were unlikely to be helped without taking a comprehensive view of the clinical reality of the illness.  In my view, at that time there was an urgency to this issue, since there were few studies that had examined illness models that fully accounted for the observation that central nervous system symptoms (e.g., alterations in symptom domains such as cognition, behavior, sleep, pain sensitivity) were core aspects of the patient’s experience of this perplexing illness.  Moreover, I had recently reported the observation that patients with this illness experienced an apparent disruption in the central nervous system regulation of the body’s stress response system, the hypothalamic-pituitary-adrenal axis.  This finding opened an avenue of research investigation in ME/CFS that has only expanded in the past decades.

For example, in a recent blog post in June 2014 on the Solve ME/CFS Initiative website, neuroimaging research from the laboratories of Dr. Andrew Miller at Emory University and Dr. Dikoma Shungu at Weill Cornell Medical College emphasized that the central nervous system is not a silent bystander in this illness.  Abnormalities in dopamine metabolism in the basal ganglia were noted by Dr. Miller’s group, while Dr. Shungu and colleagues reported significant disturbances in brain lactate and glutathione metabolism.

Experimental observations such as these and others are essential in expanding our understanding of how ME/CFS develops.  While the immediate significance of these findings for treatment of a patient are far from clear, and that can be undeniably frustrating, they are necessary and essential building blocks in helping to establish a clear appreciation of the fact that ME/CFS has an underlying biology.  In particular, these findings underscore that the central nervous system is a critical part of that biological reality, indeed there is a neurobiology to this illness.  While some of these observations may not be unique to ME/CFS, they are nonetheless critical observations on the path toward a more comprehensive understanding of the pathobiology of this illness.  In fact, the use of appropriate, other disease state control populations, as was done in these studies, is an essential component to future research.

Psychologists and psychiatrists have a unique and in-depth understand of how the central nervous system works. Research has consistently shown that the central nervous system plays a role in ME/CFS. For too long, the study of causes and treatments for ME/CFS has been held hostage to an unfortunate tendency for the scientific debate to be forced into an unnecessary and unproductive dualism, namely that it is either “psychological” or “biological”.  It is now abundantly clear that replicated observations of both peripheral and central nervous system biological disturbances are seen in patients with ME/CFS.  The challenge ahead will be to maintain this broader, integrative view.


Research Digest – July 2014: Define & Diagnose

July 16, 2014

puzzleIn order for patients to be diagnosed, a disease must be defined.  Chronic Fatigue Syndrome, also referred to as myalgic encephalomyelitis (ME/CFS) is currently defined by excluding other medical and psychiatric diseases that explain the symptoms.  Biomarkers – or an objective and measurable indicator of a biological state – would take the “process of elimination” out of ME/CFS and therefore provide objective criteria to define and diagnose ME/CFS.  Not only do disease states need to be defined but recovery from disease states also require definition.

The core signs, symptoms and decrements in specific functioning can and should be used to define what ME/CFS is and what it means to recover from ME/CFS.  Signs are objective measures – think of these like biomarkers.  Symptoms are how and what a patient feels.  Specific functioning varies depending on the patient.  Bottom line – all of these “core” components are important to defining and diagnosing ME/CFS.

This month we highlight three recent publications tackling the “core” components of ME/CFS.


Dr. Peter Rowe and his team at Johns Hopkins University School of Medicine have reported on increased prevalence of Ehlers-Danlos and hypermobile joints in ME/CFS patients.  Over the years he has also made (seemingly paradoxical) observations of restricted range of motion (ROM) during the clinical care of ME/CFS patients.  In a study funded in part by SMCI in 2012, Rowe studied 48 ME/CFS patients and 48 matched, healthy controls to determine if there was an association between ROM and symptoms.  They found that impaired ROM was more common ME/CFS patients and that certain types of movements (called neuromuscular strain) could induce ME/CFS symptoms.  This novel and important study, published online June 11, 2014 in The Journal of Pediatrics, points ROM and neurodynamics as potential objective measures that warrant further study and validation.


Jordan Dimitrakoff, M.D., a former member of the CFS Advisory Committee, is the corresponding author on a paper reviewing the evidence for neurological and immunological biomarkers in ME/CFS.  He teamed up with investigators at Harvard, Dartmouth, DePaul, University of Mississippi, Johns Hopkins and CDC to conduct this review. Potential neurological biomarkers included brain anatomy using neuroimaging, brain blow flow, brain function (as measured by functional neuroimaging), brain chemistry and cognition.  Potential immunological biomarkers included cytokines, NK cell markers, humoral immunity and inflammation characteristics.   The authors discussed the limitations of these potential biomarkers and some reasons why none have been validated.  They recommended that because ME/CFS is heterogeneous that these biomarkers be used to define subtypes.  This important paper is published in the June 2014 issue of Fatigue:


Investigators from Stony Brook University including Jenna L. Adamowicz, Indre Caikauskaite and Fred Friedberg teamed up to review the literature on how recovery in ME/CFS is defined.  This paper was published in the journal Quality of Life Research in May 2014.  The investigators identified 22 studies on ME/CFS recovery and found that each defined recovery differently – which could explain the range in recovery rates of 0-66% described in these studies.  They concluded that a consistent definition for recovery – one that captures a return to health and includes assessments of fatigue and function – is needed. Ways to think about recovery were provided including concepts such as recovery time following physical and mental exertion. Importantly, they note that patients’ perspectives on recovery could help inform treatment, education and outcome studies.



Breaking Down the Complexities of ME/CFS – Part 3

July 9, 2014

divide and conquerQuantifying Complexities

Since the Internet’s earliest days, patients have used online resources to share experiences, learn about diseases and treatments, and become advocates. In recent years we have seen these online communities evolve into centers of patient-driven research. Modern day, patient-driven research has the potential to be used as meaningful evidence as larger sets of data are gathered.

Datafication = the process of using technology
to turn many aspects of our lives into data.

With few researchers and clinicians specializing in myalgic encephalomyelitis (ME)/Chronic Fatigue Syndrome (CFS), many patients have become experts in ME/CFS specific research by doing their own online study of published literature. In addition, you make important observations about your own condition by living with it every day.

With the advent of personal tracking and monitoring devices, you now have tremendous resources to track your own data:iBand

  • UP band helps you understand how you sleep, move and eat
  • Mio band, continuously tracks heart rate
  • iFit Active band tracks everyday activity, sleep and nutrition
  • … just to name a few

Though they are largely marketed as fitness or workout devices, they can be used to readily track things like sleep, activity, what you eat, heart rate and more.  They typically come with an app for your Smartphones, which can be used to track and monitor many things using other apps or passively using the GPS.  This translates to a lot of data; in some cases 24 hours, 7 days a week.  This allows you to be the researcher, tracking and monitoring the things that are meaningful to you.

Now there are emerging ways for you to incorporate this data with important biological data. We are working on ways to collate all of this information; integrate it with your biological data (e.g., your gut microbiome), share it (if you want to) with others like you, and analyze it so that patterns can emerge.

Currently, there is no other experimental platform that allows for this type of discovery with and by the patients. But at the Solve ME/CFS Initiative we understand that you are critical to effective research. We must actively engage YOU – the patient – in our research efforts if we are to cure ME/CFS sooner rather than later.


Read the other blogs in this series on Breaking Down the Complexities of ME/CFS:

Part 1: Clinical Intuition

Part 2:  Solve CFS BioBank & Registry


Breaking Down the Complexities of ME/CFS – Part 2

July 7, 2014

divide and conquerSolve CFS BioBank & Registry

“Complex” is a word that is frequently used to describe the myalgic encephalomyelitis (ME)/Chronic Fatigue Syndrome (CFS) disease state.  Here are some of the reasons why:

  • Many body systems are affected
  • People are sick for varying lengths of time
  • Symptom type and severity vary from person to person
  • A variety of medications are used to treat symptoms
  • The environment that ME/CFS patients live in varies, and that can affect their health
  • Many people experience other “overlapping” conditions in addition to ME/CFS

ME/CFS is a diagnosis of exclusion, meaning a process of elimination. A physician must first discern whether a patient has any other overlapping conditions that present in a similar way as ME/CFS, to either eliminate it as a possibility or understand that it is only one piece of the medical puzzle, because the patient has more than one medical condition (which is often the case.)

  • Chronic infection with Epstein Barr virus, hepatitis C virus or human immunodeficiency virus has a similar clinical profile to ME/CFS.
  • Endocrine diseases like diabetes and thyroid disease share symptoms and features with ME/CFS.
  • Autoimmune diseases like Sjögren’s syndrome, PANDAS and celiac disease present with many of the symptoms experienced by ME/CFS patients.

As we gather data about the symptoms and genetics of ME/CFS, we can increase our knowledge by putting them in the context of these other “medically explained” diseases.  When we take this more holistic view, we can begin to explain what is going on in ME/CFS.

One way that research deals with this type of complexity is to break it down so that the most similar people are being studied.  The code of our genes can be used to group people that are similar.  The genetic similarities can relate to any number of body functions including things like metabolism, immune function or endocrine function and even the types of symptoms that patients experience.  Once this complexity is broken down, people with a complex disease like ME/CFS can be grouped based on a more specific genetic profile.  Genetic information is helpful to delineate the complexity of ME/CFS and it may also be useful for helping us understand the disease process.

Pharmaceutical companies understand that breaking down this complexity and facilitating studies with the most consistent groups is important to showing maximum efficacy. A study done by the Tufts Center for the Study of Drug Development in 2010 indicated that 100% of pharmaceutical companies surveyed were using genetic technologies to target specific groups of patients and understand how patients will react to specific treatments.

The SolveCFS BioBank is an important part of this research progress. We simplify the process for investigators by creating a ‘bank’ of research-ready patients and healthy controls where important data that helps group similar patients together has already been collected. As we expand the efficacy and efficiency of the SolveCFS BioBank and Registry, we continue to enhance systems that allow us to use patient data to break down the complexity of ME/CFS and move discovery forward at a more rapid pace. When you participate in our BioBank, just having your name on the roster while you wait to be called to offer a sample, makes you a critical component in our efforts to solve ME/CFS.


Learn more about our Solve CFS BioBank in this earlier 4 part blog series:

Part 1:  An Important Tool in Accelerating the Discovery of Effective Treatments

Part 2:  Breaking Down Barriers to ME/CFS Support

Part 3:  Breaking Down Barriers Through BioMarker Discovery

Part 4:  Calling YOU to Participate in Gathering a Breadth and Depth of Data