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.

 

Wanted: Patient Participation in Quality of ME/CFS Medical Care Survey

January 23, 2015

checkboxThe Chronic Fatigue Syndrome Advisory Committee’s Centers of Excellence Working Group invites the participation of all ME/CFS patients, 18 years of age and older, worldwide, but particularly within the United States, to participate in an online survey the purpose of which is to determine the ease of patient access to ME/CFS Specialists and to assess the quality of medical care received by individuals with ME/CFS from all of their healthcare providers. While it is of primary importance to establish the quality of care received by patients on a country-by-country basis, the intent of this survey is to establish the need for improved care within the United States based upon the quality of their care when compared to that of other illnesses within the United States, and based upon the comparison of their care to that received elsewhere in the world. The more robust the patient participation in this survey, the more significant the data and the more convincing the results drawn from it will be. We are hoping to obtain a minimum of 1,000 respondents in the United States. If you know ME/CFS patients, please encourage their participation. The results of this survey will inform us of the magnitude of need for ME/CFS Centers of Excellence, the services they should provide, and where they should be located.

This online survey is anonymous. Participant identity will not be revealed. Patients will be asked about their experiences with: access to ME/CFS specialists, barriers to access to ME/CFS specialists, the quality of care they have received from ME/CFS specialists, and the quality of care they have received from healthcare providers who are not ME/CFS specialists.

Patients will be asked to provide information, anonymously, about their current living circumstances (such as age, gender, and employment status), their ME/CFS diagnosis, ability to perform tasks of daily living, and illness onset characteristics. Patients will be provided with an opportunity to describe their medical care in their own words.

SMCI is pleased to share this information in order to garner as wide a response as possible.

To access the survey please follow the link:
https://redcap.is.depaul.edu/surveys/?s=wGI2stCALK

Download a PDF of this information and share the information with others: MECFS_Patient_Quality_of_Medical_Care_Survey

Public Release of the IOM ME/CFS Study February 10

January 23, 2015

The Institute of Medicine’s Committee on the Diagnostic Criteria for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome will hold a public release event for its consensus report on February 10th, 2015 from 11:00 am-12:00 pm EST at the Keck Center of the National Academies in Washington, D.C.  (500 Fifth Street NW, Washington, DC).

IOM_Meeting
Interested individuals will be able to attend the public release event in person or virtually via webcast. Persons who plan on attending the meeting in person are requested to register in advance prior to February 5, 2015. Registration for persons attending the meeting in person will be open until seating capacity of the conference room is reached. All participants may participate via webcast. A link for the webcast will be available on the public release webpage shortly before the event begins at 11:00 a.m. on February 10, 2015.

The public will be able to submit questions online, and a PowerPoint will be available at that time.

A PDF of the report will be available for free download on the event webpage beginning at 11 AM.
For more details of the event please visit the public release webpage

http://www.iom.edu/Activities/Disease/DiagnosisMyalgicEncephalomyelitisChronicFatigueSyndrome/2015-FEB-10.aspx

 

We first brought you news of the IOM Committee’s charge in October of 2013 and have posted information about it to our blog routinely in the months since (Access all our posts on the IOM HERE). The process has been highly scrutinized and widely debated, but SMCI has remained cautiously optimistic as the committee has held public meetings and worked privately. After 16 months of watching and waiting, the committee’s report is to be released a month earlier than originally expected. (View the committee roster HERE.)

We will bring you news of the report’s details soon after its release. If you have not already, sign up to follow this blog and receive an email notification the day a post is published, you can do so today by entering your email on the “Blog Update Sign Up” on the top right of this page.

 

Research Digest – January 2015: High Interest in ME/CFS Shown in Journal Rankings

January 23, 2015

Patients often describe the relapsing of their disease symptoms following physical or mental activity as a “crash” or “hitting the wall”.  The biomedical field describes this characteristic and hallmark feature of ME/CFS as post-exertional malaise (PEM) – a term that grossly understates the debility that comes with this disease-defining symptom.

Deciphering PEM is a critically important area of research for ME/CFS; you can’t begin to fix a problem like post-exertional malaise until you can understand its underlying cause. If research can help our understanding of PEM we will move closer to mitigating its effects.

Despite the lack of gravity and specificity a term like “post exertional malaise” signifies, research into what PEM is and how to measure it has been some of the most important research conducted on ME/CFS. It has also been among the most popular. The Journal of Translational Medicine ranks its most highly accessed articles in three categories: “Top Cited Articles of 2014”, “Top Downloaded Articles of 2014” and the “Top Social Articles of 2014”. In this month’s Research Digest we take a look at some of the most highly accessed and shared studies, both of which dealt with PEM.

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First in downloads and 3rd in social shares was research conducted by Betsy Keller at Ithaca College titled, “Inability of myalgic encephalomyelitis/chronic fatigue syndrome patients to reproduce VO2peak indicates functional impairment.”  Keller used a 2-day cardiopulmonary exercise test (CPET) to show that physiological values in ME/CFS patients worsened on the second CPET, a phenomena unique to ME/CFS patients.

We featured Keller’s work in our May 2014 Research Digest
http://solvecfs.org/research-digest-may-2014-post-exertional-malaise/

You can also access it directly via the Journal of Translational Medicine here:
http://www.translational-medicine.com/content/12/1/104

 

The Dutch Vermeulen team’s article titled, “Decreased oxygen extraction during cardiopulmonary exercise test in patients with chronic fatigue syndrome” ranked second in the Journal of Translation Medicine among “Top Social Articles.”  They used CPET to show that oxygen extraction – or the ability of oxygen to be removed from the blood and used by tissues to support metabolism – was significantly lower in ME/CFS patients and could be a causal explanation for exercise intolerance in ME/CFS patients.

You can access the full text of this paper via The Journal of Translational Medicine here:
http://www.translational-medicine.com/content/12/1/20

 

It is interesting – and exciting – that papers on ME/CFS ranked so high in their review of 2014 downloads and social shares. The Solve ME/CFS Initiative funded some of the first PEM and CPET studies and continues to fund top research to understand and objectively measure PEM (http://solvecfs.org/deciphering-post-exertional-malaise/). We are certain that by doing so, we will be able to solve ME/CFS.

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The Solve ME/CFS Initiative is taking strategic steps to speed up progress. Despite our modest budget, SMCI was the first organization to fund research into epidemiology, viral causes, immunology, neuroimaging, exercise physiology and the autonomic nervous system. big-donate-modifiedThis is made possible through the support of our donors. The investments made by those suffering with ME/CFS and their loved ones have fueled the Solve ME/CFS Initiative’s work. With your support, we are paving the road to objective diagnosis, treatment and a cure.

Guest Blog: Armin Alaedini, PhD – The Search for Food Sensitivity Biomarkers in ME/CFS

January 17, 2015

Often those with ME/CFS experience gastrointestinal symptoms. Biomarkers of these symptoms could help to identify subtypes in ME/CFS. Dr. Armin Alaedini is using samples from the SolveCFS BioBank™ to study the gastrointestinal immune response in patients with ME/CFS. In the following blog post he discusses celiac disease, an autoimmune disorder with a wide range of symptoms, some of which resemble those seen in ME/CFS.

The Search for Food Sensitivity Biomarkers in ME/CFS
alaediniby Armin Alaedini, PhD
Assistant Professor of Medical Sciences, Department of Medicine, Celiac Disease Center, and Institute of Human Nutrition
Columbia University Medical Center

 

Celiac disease, also known as gluten-sensitive enteropathy, is an autoimmune disorder that affects about 1% of the population in the United States. It is triggered by the ingestion of gluten in genetically susceptible individuals. The term “gluten” refers to the major storage proteins of wheat (and related cereals, such as rye and barley), which represent about 75% of the total protein content of the grain and are responsible for the elastic and cohesive nature of dough. In individuals with the genetic predisposition for celiac disease, the immune system in the gut mounts a reaction in response to the ingested gluten, which leads to inflammation and damage to the intestinal villi (the finger-like projections involved in absorption of nutrients). In addition to intestinal symptoms, such as abdominal pain and diarrhea, celiac disease is associated with various extra-intestinal complications, including bone and skin disease, anemia, endocrine disorders, and neurologic deficits.

Fatigue is commonly seen in patients with untreated celiac disease. It is believed to result partly from the malabsorption of nutrients in the gut. Caused by the intestinal damage, the malabsorption may lead to deficiencies in vitamin B12, iron, copper, zinc, and carnitine, among others, which can produce fatigue, weakness, and lethargy in patients. In addition, the immune response in celiac disease is associated with significant changes in the levels of a number of cytokines and other inflammatory molecules. These abnormalities can contribute to physical and mental fatigue, as well as changes in cognitive functioning.

A definitive diagnosis of celiac disease requires blood tests and intestinal biopsy, as well as a positive response to gluten-free diet. Celiac disease is usually suspected in a patient either because of the presence of associated characteristic symptoms, and/or due to being in an at-risk group, including celiac disease-associated conditions and the first- and second-degree relatives of celiac disease patients. The IgA anti-tTG (tissue transglutaminase) antibody (or the related anti-endomysial antibody) is currently the most sensitive and specific biomarker for celiac disease.   A positive blood test result for IgA anti-tTG/endomysial antibody is followed by an intestinal biopsy to assess the presence of the characteristic inflammation and damage to the villi. Positive identification of these abnormalities leads to a presumptive diagnosis of celiac disease, which should be followed by institution of a gluten-free diet. A diagnosis of celiac disease is made after improvement in response to diet (towards resolution of either the symptoms or the damage to villi) has occurred.

Treatment for celiac disease involves the strict exclusion of gluten and related proteins from diet, whereby foods containing wheat, rye, and barley are avoided.  While these cereals and any derivatives should be eliminated from food, they can be substituted by other grains, such as rice, corn, quinoa, amaranth, sorghum, and buckwheat, which are found to be safe. Oats are generally considered to be well-tolerated by the majority of patients, although some commercial preparations have been reported to contain contamination from gluten-containing cereals. The United States Food and Drug Administration (FDA) has issued a ruling that defines the term “gluten-free” in the labeling of foods as meaning that “the food either is inherently gluten free; or does not contain an ingredient that is: 1) a gluten-containing grain (e.g., spelt wheat); 2) derived from a gluten-containing grain that has not been processed to remove gluten (e.g., wheat flour); or 3) derived from a gluten-containing grain that has been processed to remove gluten (e.g., wheat starch), if the use of that ingredient results in the presence of 20 parts per million (ppm) or more gluten in the food. Also, any unavoidable presence of gluten in the food must be less than 20 ppm”. Improvement in intestinal symptoms is generally seen within days to weeks after the start of a gluten-free diet, while full intestinal recovery usually takes longer, often years in adults.  Anti-tTG/endomysial antibody levels will start going down with the elimination of gluten-containing foods from diet, and usually normalize after 6-12 months of strict gluten avoidance.   Substantial improvement in celiac disease-associated fatigue and lethargy have also been reported to occur after the institution of a gluten-free diet, though precise data on this are lacking, and individual responses can vary. In some instances, vitamin or mineral deficiencies are identified and remedied with supplementation. Although a gluten-free diet is currently the only effective treatment for celiac disease, a number of novel non-dietary therapies are now in the developmental stage. These therapies may offer additional choices for treatment of celiac disease and its associated symptoms in the future.

Some individuals experience a range of symptoms in response to ingestion of gluten-containing foods, despite testing negative for the characteristic intestinal lesion or antibodies associated with celiac disease.  The terms “non-celiac gluten sensitivity” or “non-celiac wheat sensitivity” have been used to refer to this condition, although a role for gluten or other wheat proteins as the trigger for the condition has not yet been demonstrated. Gastrointestinal problems, headache, cognitive difficulties, and fatigue are among the symptoms reported by affected individuals. As our understanding of the condition is currently very limited, further research is necessary to delineate its mechanism and identify biomarkers for the diagnosis of patients.

Dr. Alaedini is preparing the results of his research on the SolveCFS BioBank™ samples for publications. We will share those results with you here when available.

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Dr. Armin Alaedini is Assistant Professor of Medical Sciences in the Department of Medicine at Columbia University.  His team’s research is aimed at understanding the link between immunologic response to foreign antigens and the development of immune-mediated disease processes, including those affecting the gut and the nervous system.  Areas of research in his laboratory include investigation of immune mechanisms in celiac disease, autism, schizophrenia, and Lyme disease.  Dr. Alaedini is currently a recipient of grants from the National Institutes of Health, the Department of Defense, and the Stanley Medical Research Institute.

 

 

The P2P Report – CFSAC Drafts Substantive, Expert Response

January 15, 2015

P2P_titleOn December 9 & 10, 2014, the NIH Office of Disease Prevention held its Pathway to Prevention Workshop for “Advancing the Research on Myalgic Encephalomyelitis/Chronic Fatigue Syndrome”. Upon the conclusion of the workshop, the panel prepared their Draft Report and recommendations. It was posted to the workshop website on Thursday, December 18, 2014 and is open for comments until Friday, January 16, 2015, at midnight.

The P2P Draft Report has been met with some enthusiasm, as it officially addresses many things the patient community has known for years…

“ME/CFS is an unmet public health need with an economic burden estimated to be greater than $1 billion. ME/CFS results in major disability for a large proportion of the people affected. Limited knowledge and research funding creates an additional burden for patients and health care providers. Unfortunately, ME/CFS is an area where the research and medical community has frustrated its constituents, by failing to assess and treat the disease and by allowing patients to be stigmatized.”

“ME/CFS exists…” and “ME/CFS has a physical, psychological, social, and economic impact at the individual, family, and societal level. Patients are typically underserved, and clinicians have a poor understanding of ME/CFS.”

“…this is not a psychological disease in etiology.”

The report goes on to point out the lack of diagnostic criteria and the harm that creates; the problems with small enrollment numbers in studies; too much focus on fatigue with too little focus on other important symptoms, like post-exertional malaise; the need to include a wider diversity of patients in research; the need for collaborative, multicenter studies; the need for more rigorous studies, therapeutic targets, translational efforts, and more.

Though this report ratifies what so many in the ME/CFS community have known for years, it lacks “teeth”; the recommendations are broad and there is no direct funding associated with them. The charge now is upon the scientific community to increase its rigor and the NIH to significantly increase funding to support it.

The Chronic Fatigue Syndrome Advisory Committee (CFSAC) convened a working group to craft a response to the P2P draft report in the hopes of strengthening it by providing expert feedback. Skillfully led by CFSAC member Donna Pearson, and dedicating countless hours over the holidays, the working group – comprised of advocates, researchers and ME/CFS experts – judiciously reviewed the P2P draft report and created a thorough, detailed, and thoughtful response. As an active (non-voting) member of the CFSAC, Carol Head, SMCI president and CEO, participated in that work. On Tuesday, January 13, 2015, the CFSAC held a special-called meeting to finalize and approve their official response to the P2P draft report.

 The CFSAC call was recorded and will be posted HERE 

The official CFSAC comments on the P2P report are expected to be posted by Friday, January 16th HERE as well.

http://www.hhs.gov/advcomcfs/meetings/index.html

In the meantime, an unofficial draft version can be found on the blog, Occupy CFS  HERE

SMCI is endorsing the CFSAC response in its official response to the P2P draft report. Our hope is that the work done through the P2P and the soon-to-be-released Institute of Medicine (IOM) recommendations will serve as an actionable wake-up call. And we hope that these efforts, along with the voices of patients, advocates, and groups like SMCI, will move us to significantly increased funding, more rigorous science and dramatic steps forward for all affected by ME/CFS. 

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Any stakeholder is invited to offer their feedback on the draft report. Access it HERE

https://prevention.nih.gov/docs/programs/mecfs/ODP-MECFS-DraftReport.pdf

Please reference the corresponding line number of the report. And, as there are two slightly different versions of the report in circulation, please utilize the version in this link and note “I am referring to the report with 389 line numbers” so that feedback can be correctly attributed to the proper line number.

Submit your comments no later than midnight on Friday, January 16, via:

Email - prevention@mail.nih.gov
Or
Postal mail
Office of Disease Prevention
National Institutes of Health
ATTN: Paris A. Watson
6100 Executive Boulevard, Suite 2B03
Bethesda, MD 20892

If you were unable to participate in/watch the P2P meeting, and want to access that information now, you can access the video archive HERE.
https://prevention.nih.gov/programs-events/pathways-to-prevention/workshops/me-cfs/workshop-resources#archivedvideocast

On day 2, our own Dr. Suzanne Vernon spoke to the panel about the importance of the patient perspective and their voice in research in a session they titled “What Outcomes Represent Improvement, Recovery, Prevention, Benefits or Harm?” You can advance to her presentation at time code 3:46:00

P2P Draft Report Set to be Published, 30 days for Feedback

December 18, 2014

P2P_title On December 9 & 10, 2014, the NIH Office of Disease Prevention held its Pathway to Prevention Workshop for “Advancing the Research on Myalgic Encephalomyelitis/Chronic Fatigue Syndrome”. If you were unable to participate in the meeting or watch the live stream, you can access the video archive HERE.

https://prevention.nih.gov/programs-events/pathways-to-prevention/workshops/me-cfs/workshop-resources#archivedvideocast  P2P_screenshot2

On day 2, our own Dr. Suzanne Vernon spoke to the panel about the importance of the patient perspective and their voice in research in a session they titled  “What Outcomes Represent Improvement, Recovery, Prevention, Benefits or Harm?” You can advance to her presentation at time code 3:46:00

Upon the conclusion of the workshop, the panel began writing their report and recommendations. The draft report will be posted on the workshop website on Thursday, December 18, 2014. Comments will be accepted through Friday, January 16, 2015. 

The Solve ME/CFS Initiative will work with members of its Research Advisory Council and other advisers to issue a response to the report. Many other individual advocates and organizations will be doing the same, including members of the federal CFS Advisory Committee (CFSAC), upon which we play an active role.

The Solve ME/CFS Initiative will publish its reaction and response to the draft report on this blog as soon as it is available. Any stakeholder is also invited to offer their response to the draft report. Please reference the corresponding line number of the report, and submit your comments via:

Email - prevention@mail.nih.gov
Or
Postal mail
Office of Disease Prevention
National Institutes of Health
ATTN: Paris A. Watson
6100 Executive Boulevard, Suite 2B03
Bethesda, MD 20892

 

Read our earlier blog posts about the P2P HERE

$500,000 grant awarded to the Solve ME/CFS Initiative to further epigenetic research

December 15, 2014

We are thrilled to announce that the Solve ME/CFS Initiative (SMCI) has received a one-year, $500,000 Catalyst Research Program Award through the Dr. Ralph & Marian Falk Medical Research Trust. This competitive funding opportunity was designed to support research that leads directly to the development of treatments and cures for diseases for which there are no effective treatments or cures today.

SMCI will partner with Drs. Lucinda Bateman founder and director of the Fatigue Consultation Clinic and Patrick O. McGowan of the University of Toronto to expand the epigenetic study of myalgic encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) originally funded by SMCI in 2012. “Epigenetics is really a funnel by which the outside environment interacts with the genome,” explains Patrick O. McGowan, PhD, assistant professor at the University of Toronto and co-investigator on this project. This, in turn, influences how cells work (or don’t work). In research originally funded by SMCI, McGowan found evidence of distinct epigenetic profiles in immune and other physiologically relevant genes in a selected group of female ME/CFS patients.  This award from the Falk Medical Research Trust will allow the team to expand on these original findings and partner with ME/CFS clinical expert Dr. Lucinda Bateman.  Bateman will be the lead clinical investigator to expand enrollment of study participants to include male ME/CFS patients and more female patients. This new study will be substantially expanded to include 300 patients and healthy controls.

The Solve ME/CFS Initiative is targeting its work in order to one day understand ME/CFS at an unprecedented molecular level to guide research and development of new diagnostic tests and better treatments. SMCI will do this through funding and organizing rigorous, expansive, early research to deliver results that lead to the development of new diagnostics, therapies and cures. This grant will allow SMCI to accelerate its work, yet there is still much to be done. The support and participation of many patients, caregivers and loved ones has provided the funds for SMCI’s work thus far and remains critical to the path forward.

 

The Solve ME/CFS Initiative is a 501(3) non-profit organization, whose mission is to make ME/CFS understood, diagnosable and treatable.  Founded in 1987, SMCI is the longest standing organization serving ME/CFS patients by advancing rigorous research.

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Research Digest – December 2014: 10 Important Advances in ME/CFS

December 12, 2014

By Suzanne D. Vernon, Ph.D., Scientific Director, Solve ME/CFS Initiative top10
Dr. Anthony Komaroff, Simcox-Clifford-Higby Professor of Medicine, Harvard Medical School, Senior Physician, Brigham & Women’s Hospital, Boston MA

 

In this year-end blog post and December Research Digest, Dr. Vernon and Dr. Komaroff summarize what they regard as the most important recent advances in our field. They are not listed in any specific order. If noted, SMCI played a role in the discovery.

SMCI-Supported1. There is ample evidence that ME/CFS is a heterogeneous illness. As is true with many illnesses, not every person with the illness has all of the same features.   Now we are able to delineate ME/CFS subtypes using tools that measure phenotype (the ensemble of a patient’s observable and measureable signs and symptoms) and genotype (the inherited genetic code and gene expression). By objectively identifying subtypes, researchers are able to study groups of patients that are similar: this increases the likelihood of identifying biomarkers and of targeting treatment.

 

SMCI-Supported2. Many studies now have demonstrated that people with ME/CFS suffer from oxidative stress.  Oxidative stress occurs when the damaging effects of reactive oxygen species (free radicals) are not taken care of by antioxidant defense mechanisms. In other words, oxidative stress occurs when too many free radicals are produced, or not enough antioxidants are produced, or both.  Prolonged oxidative stress can damage cells and the structures inside cells that affect energy production and cell signaling.  Evidence for oxidative stress in ME/CFS has been found in the brain, as reflected by increased levels of lactate.  Oxidative stress more generally throughout the body is reflected by increased lipid peroxidation—which is caused when free radicals attack the lipids in cell membranes.  Oxidative stress is not specific to ME/CFS but it does help us understand the biological processes that are going awry.

 

3. Scientists at RIKEN, Japan’s renowned research institution have shown that the ME/CFS brain is inflamed.  They used a particular kind of brain imaging to show that immune system cells in the brain were highly activated (inflammation) in people with ME/CFS, compared to healthy individuals.  They further showed that the greater the inflammation, the greater a person’s symptoms.  The inflammation was a chronic, continuing state.  Investigators from other countries including the U.S. are now collaborating with the Japanese team to develop possible diagnostic markers and effective treatments.

 

SMCI-Supported4. Central sensitization is state in which the pain-sensing mechanism in the central nervous system gets “stuck” in a highly reactive state.  When this happens, a simple bump or light pressure causes greater and more widespread pain than it otherwise would.  Central sensitization has been best demonstrated in people with fibromyalgia, an illness similar in many respects to ME/CFS.  New research on restrictions in range of motion in ME/CFS patients indicates that central sensitization may also explain the fatigue, brain fog and post-exertion malaise. 

 

SMCI-Supported5.  The immune system is built to attack “foreign” things (like germs) and substances (like plant pollen).  In autoimmune diseases, instead of attacking something foreign, the immune system attacks healthy cells and organs.  Since women experience higher rates of many autoimmune diseases, and since women appear to develop ME/CFS more often than men,  autoimmunity has been suspected as a possible cause of ME/CFS.  A clinical trial of rituximab, a drug that destroys B cells (these are the antibody producing cells of our immune system), showed benefit in a number of ME/CFS patients.   This result has suggested that autoimmunity may be present in at least a subset of ME/CFS patients.  There are also several studies that show elevated antibodies to various “self” proteins in ME/CFS patients.   Understanding the role of autoimmunity in ME/CFS will help identify biomarkers and target treatments.

 

6. Patient-centered outcomes research seeks to determine if a treatment is leading to an improved outcome: reduced symptoms and suffering.  One problem with outcomes research has been that the “outcomes” that doctors measure do not always reflect the outcomes that are important to patients.  For example, during a 2012 FDA patient-focused drug development teleconference, an ME/CFS patient told the audience that she knew she was doing better when she could stand in the kitchen and make a salad.  Another problem with outcomes research until recent years has been that it was very difficult for patients to report, and therefore for doctors to study, how well the patient was doing every day. Now web-based, smart phone or personal device tracking and monitoring technology is making it possible for patients to participate in patient-centered outcomes research from anywhere including the comfort of their home.

 

7. Risk factors are behaviors or conditions that raise the risk of developing a particular disease.  Identifying risk factors can help us understand how to control and prevent disease.  Smoking is a classic example of a factor that increases your risk of lung cancer. Epidemiological research has suggested a few risk factors for developing ME/CFS such as a history of viral infection. Research has shown that ME/CFS patients have a 2-fold increased instance of high allostatic load, a quantitative index of hormones, inflammatory and cardiovascular measures of the body’s physiological balance. It is not yet clear if the high allostatic load caused the ME/CFS or the ME/CFS caused the high allostatic load, but additional research may show that allostatic load can be used to screen patients to assess ME/CFS risk.

 

8. Abnormalities in the white matter of the brain (white matter contains the nerve bundles) have been found in ME/CFS patients using a variety of magnetic resonance imaging (MRI) scanning techniques. The abnormalities have been found throughout the brain (likely due to the heterogeneous nature of ME/CFS).  A team at Stanford University found that a specific area of white matter on the right side of the brain was altered, adding to the increasing evidence that the neurocircuitry is affected in ME/CFS patients.

 

SMCI-Supported9. Abnormalities of the autonomic nervous system have been found by numerous independent researchers. These include a failure of the body to maintain blood pressure after a person stands up, abnormal responses of the heart rate to standing and unusual pooling of blood in the veins of the legs. These heart rate abnormalities persist during sleep along with abnormal levels of hormones known to regulate the cardiovascular system.  This is further evidence of a physiological imbalance in ME/CFS patients.

 

10.  Although many viruses and other infectious agents are completely eliminated by the immune system after an infection, other viruses can remain “latent” in the body for a long time—even for the rest of a person’s life.  There’s evidence of more frequent latent active infection with various herpesviruses and enteroviruses. The herpesviruses include Epstein Barr, HHV-6 and cytomegalovirus. Other infectious agents, like bacterium that cause Lyme disease, Ross River virus and Q fever, can also trigger CFS.  Whether these chronic infections cause the symptoms of ME/CFS remains unclear.

__________

The road to real discovery and life-changing progress is long, arduous, costly. The Solve ME/CFS Initiative is taking strategic steps to shorten the road and speed up progress. Despite our modest budget, SMCI has made great strides and was the first organization to fund research into epidemiology, viral causes, immunology, neuroimaging, exercise physiology and the autonomic nervous system.

big-donate-modifiedAll of this research work is only possible because of the support of the many who fund it. The investments made by those suffering with ME/CFS and their loved ones have fueled the Solve ME/CFS Initiative’s work. With that support, we have become one of the largest and most successful private funders of ME/CFS research… paving the road to objective diagnosis, treatment and a cure.

 

Funding Research to Inform the Path Forward, part 2

December 10, 2014

The Solve ME/CFS Initiative (SMCI) began funding research into myalgic encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) as soon as it was founded in 1987. But the first competitive funding opportunity occurred in 2008. In part 1 of this blog post we reviewed the advances made through this competitive funding cycle.

Read it HERERIWW.2

In this second part of the series, we share the progress being made through our second competitive funding opportunity, which occurred in 2011. That year, SMCI solicited research proposals that would bridge the gap between bench discoveries and clinical implementation by funding research aimed at discovery and replication of diagnostic and treatment biomarkers and exploring new drug targets and treatments for ME/CFS. Knowledge acquired would be used to attract pharmaceutical and biotech study as well as augment the evidence base for clinical practice and health policy. That year, we funded 5 investigators, bringing 2 additional new researchers into the field of ME/CFS. Through the virtual structure of the Research Institute Without Walls, every investigator now has a means to archive all of their results in a central place called RedCap – the Research Electronic Data Capture system.

This innovative, collaborative approach, along with Dr. Vernon’s knack for recruiting leaders into the field, has allowed SMCI to begin to change the paradigm while bringing important discoveries to light.

 

2011 Funded Investigators Progress Report
Six grants were awarded totaling $470,487 to investigators in the US and Canada.  To date this funding has led to more than $1.6 million in additional funding for our grantees.

The Solve ME/CFS Initiative awarded Biovista, a small biotech company, to find new uses for approved drugs – a process known as drug repurposing.  Spyros Deftereos, MD, PhD, vice president for drug discovery, was excited to research ME/CFS because of the neurological impairment and neurology-related mechanisms, an area Biovista specializes in. They used their proprietary software to explore the biomedical literature, pharmaceutical databases and the SolveCFS BioBank for all of the symptoms of ME/CFS then matched these with underlying mechanisms of these symptoms and drugs known to target these mechanisms. In less than a year, Biovista identified two drugs that, when used in combination, could potentially target fatigue and pain – two major ME/CFS symptoms. A proof of concept clinical trial needs to be conducted to determine the efficacy of this drug combination in ME/CFS. Biovista is currently seeking partners and raising funds to conduct this trial.

Dane B. Cook, PhD is associate professor of Kinesiology at University of Wisconsin, Madison.  SMCI provided funding to Cook to study the relationships between the post-exertion crash, gene expression and brain function in ME/CFS patients and controls. Post-exertion malaise (PEM) can be induced by physical and mental exertion and has been described by patients as a “crash” because of the relapse that occurs within 24 hours. This “crash” presents in a worsening of all symptoms affecting thinking and memory, heart function, and sleep for days or even weeks. Despite being a cardinal feature of ME/CFS, no single research group had ever evaluated the effects of mental and/or physical stress on PEM in a comprehensive manner. Cook’s team is using both an exercise challenge and mathematical mental challenge to define PEM. He has completed testing on most of the ME/CFS patients and all the healthy controls and is deep into analyzing this amazing dataset. He has teamed up with Alan Light and Gordon Broderick for an integrated, systems biology approach to defining PEM.  Because of the work he was able to do under our award, Cook recently received a $750,000 award from the Department of Veterans Affairs to conduct the same study in Gulf War Veterans. (Go to https://www.youtube.com/watch?v=k7OLt6J4ySk&feature=youtu.be to watch Dane Cook’s webinar in which he presents his research results.)

Patrick O. McGowan, PhD, is an assistant professor of neuroscience and epigenetics at the University of Toronto. McGowan’s award allowed him and his team to study epigenetics – a first of its kind study for ME/CFS. Epigenetics refers to patterns of change in gene expression—not the gene itself—that occur in response to such things as nutrition, infection and physical and mental trauma, not genetic factors. These outside influences trigger a process called methylation that affects gene function but doesn’t change the underlying DNA structure. McGowan and his team used the SolveCFS BioBank for this innovative study; they’ve already published results in PLOS One, an open-access high-impact journal and are preparing the next set of results for publication. SMCI has provided McGowan with additional funding because his research shows promise for delineating ME/CFS subtypes and identifying biomarkers. Further, because of the results achieved through our seed funding, McGowan has received $845,000 from the Department of Defense to establish an animal model to further study how these epigenetic changes effect the immune and endocrine response. (Go to https://www.youtube.com/watch?v=QjrBP7MFVPY&feature=youtu.be  to watch Patrick McGowan’s webinar in which he presents his research results.)

Peter C. Rowe, MD is the Sunshine Natural Wellbeing Foundation Professor of Chronic Fatigue and Related Disorders at Johns Hopkins University School of Medicine. Rowe was the first to describe the connection between orthostatic intolerance and ME/CFS. The Solve ME/CFS Initiative has funded Rowe to determine if neuromuscular strain increases the cardinal symptoms, contributes to post-exertional malaise and increases central sensitization. Central sensitization is the process of the brain and nervous system becoming more sensitive and reactive. In Fibromyalgia for example, central sensitization helps explain why light pressure is felt as intense and widespread pain. So far Rowe’s research indicates that ME/CFS patients have more body areas with impaired range of motion and are more likely to have abnormal responses like increased heart rate variability to simple physical examination maneuvers. He’s published these results and is now analyzing how central sensitization might help explain post-exertion malaise.  (Go to http://www.youtube.com/watch?v=YnCcEoFSgvc&feature=youtu.be to watch Peter Rowe’s webinar in which he presents his research results.)

 

In part one of this series we discussed the 2008 funding cycle and the progress being made through those researchers. Read it HERE

On December 16th we will be holding a free webinar where we distill this information a bit more and answer your questions about this research progress and what it means to you. Register for that webinar today HERE.

https://attendee.gotowebinar.com/register/119787780;jsessionid=abc276q-OYylr4Ky6axOu

 

The road to real discovery and life-changing progress is a long, arduous and costly. The Solve ME/CFS Initiative is taking strategic steps to shorten the road and speed up progress. Despite our modest budget, SMCI has made great strides and was the first organization to fund research into epidemiology, viral causes, immunology, neuroimaging, exercise physiology and the autonomic nervous system.

big-donate-modifiedAll of this research work is only possible because of the support of the many who fund it. The investments made by those suffering with ME/CFS and their loved ones have fueled the Solve ME/CFS Initiative’s work. With that support, we have become one of the largest and most successful private funders of ME/CFS research… paving the road to objective diagnosis, treatment and a cure.

Funding Research to Inform the Path Forward, part 1

December 9, 2014

The Solve ME/CFS Initiative (SMCI) began funding research into myalgic encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) as soon as it was founded in 1987. But the first competitive funding opportunity occurred in 2008. That funding cycle solicited research proposals that would advance the discovery of biomarkers and methods for early detection, objective diagnosis and effective treatment of ME/CFS, and included a rigorous review process. That year, SMCI awarded 6 grants, engaging 3 researchers who were new to the field of ME/CFS research. All agreed to use similar measures, share data and collaborate with one another – breaking down the silos researchers typically work in.

RIWW.2In 2010, SMCI launched our Research Institute Without Walls, offering a stronger ‘virtual’ infrastructure to support collaboration and data-capture. This was also the year SMCI launched the SolveCFS BioBank™ – an important resource for researchers, lowering barriers, reducing costs and attracting new investigators into the field.

2011 brought our second competitive funding opportunity. SMCI solicited research proposals that would bridge the gap between bench discoveries and clinical implementation by funding research aimed at discovery and replication of diagnostic and treatment biomarkers and exploring new drug targets and treatments for ME/CFS. Knowledge acquired would be used to attract pharmaceutical and biotech study as well as augment the evidence base for clinical practice and health policy. That year, we funded 5 investigators, bringing 2 additional new researchers into the field of ME/CFS. Through the virtual structure of the Research Institute Without Walls, every investigator now has a means to archive all of their results in a central place called RedCap – the Research Electronic Data Capture system.

This innovative, collaborative approach, along with Dr Vernon’s knack for recruiting leaders into the field, has allowed SMCI to begin to change the paradigm while bringing important discoveries to light. In this two part blog series we explore our funded research projects in more depth.

 

2008 Funded Investigators Progress Report

Six awards totaling $647,940 were made to investigators in the US and Canada.  Our 2008 grant funding led to more than $7 million in follow-on funding from federal agencies for several of the investigators listed below. In other words, we provided important seed money.

Eric Aslakson, MS and Bud Mishra PhD, Professor of Computer Science & Mathematics New York University are accustomed to dealing with massive amounts of data.  Their 2008 award was to create a relational database of the 20 million abstracts in PubMed to begin to translate publicly available biomedical knowledge to further our understanding of ME/CFS. The Solve ME/CFS Initiative is now contracting with Eric’s company, Poiema, LLC, to utilize large scale natural language processing techniques to analyze hundreds of thousands of ME/CFS-related full text journal articles and all 20 million PubMed abstracts to categorize and explore biological relationships detailed in text and open source biological datasets.  When complete, the system will allow querying of complex biological causal relationships to elucidate ME/CFS etiology and potential treatment methods.

Gordon Broderick PhD, professor at NOVA Southeastern University and Ben Katz, MD professor of pediatrics at Northwestern University Feinberg School of Medicine teamed up to identify predictive markers of post-infection fatigue. Their 2008 award from the Solve ME/CFS Initiative was used to study samples that Katz had collected from an NIH-funded study. Broderick applied his computational skills to create a model of how the molecules worked and communicated with each other. (He spent years as a chemical engineer before Dr. Vernon recruited him into the field of ME/CFS research.) The Broderick team showed that five specific cytokines might be useful in diagnosing ME/CFS that occurs as a result of infection. Our 2008 award to Broderick has helped him receive funding from the Department of Defense to extend these findings in both ME/CFS and Gulf War Illness. He is also co-investigator on grants made by the National Institutes of Health to Mary Ann Fletcher and Nancy Klimas.

Alan R. Light PhD and Kathleen C. Light PhD are both research professors at the University of Utah.  The Light team generated intriguing preliminary data of receptors on blood cells that detect metabolites that could be biomarkers for fatigue and pain. SMCI awarded the Lights a grant to increase the sample size and test the markers in other diseases. Subjects in their study provided blood samples before and several times after riding a stationary bicycle to induce fatigue and the post-exertion crash. The Lights confirmed that the metabolite detection sensory gene expression increased following exercise in ME/CFS patients but not in the other disease groups or in healthy controls. They have received more than $2 million from the National Institutes of Health to learn more about these sensory receptors and how they can be used as biomarkers for ME/CFS. Even more important, the Light team continues to collaborate with our funded investigator Dane Cook to examine these biomarkers in Cook’s study.

Marvin Medow PhD, Associate Director of the Center for Hypotension at NY Medical College and Julian Stewart MD, PhD, Director of the Center for Hypotension at NY Medical College received an award from SMCI in 2008 to investigate how blood flow and orthostatic intolerance affect the flow of blood to the brain in ME/CFS patients. Medow and his team have been one of the most prolific scientific teams we’ve funded, publishing more than 10 papers in the biomedical literature. These results describe altered blood flow to the brain and how this altered flow affects ME/CFS symptoms, particularly brain fog. SMCI funded Medow again in 2011 to study how various treatments could be used to increase the blood flow to the brain. The Medow team has just published a paper showing that phenylephrine (a drug that increases blood pressure) improved blood flow to the brain when ME/CFS patients were on a tilt table and this improved blood flow correlated with improved cognitive testing.

Dikoma Shungu PhD, Professor of Physics in Radiology at Weill Cornell Medical College and Sanjay Mathew MD now Associate Professor of Psychiatry at Baylor College of Medicine were awarded seed funding by SMCI to use a powerful imaging technology known as proton magnetic resonance spectroscopic imaging to measure brain metabolism and oxidative stress in ME/CFS compared to other diseases and healthy controls. They published several papers and showed conclusively that there was oxidative stress (increased levels of reactive oxygen species) in the brain of ME/CFS patients. Shungu and his team went on to receive more than $1.4 million from the National Institutes of Health to continue studying the role of oxidative stress in ME/CFS and how it may be treated.

Sanjay Shukla PhD and Steve Yale MD of Marshfield Medical Research Foundation in Marshfield Wisconsin received a grant from SMCI to determine whether the gut microbiome was affecting post-exertion relapse. Shukla and Yale teamed up with Dane Cook at University of Wisconsin to conduct the exercise challenge testing and the Light team in Utah to test the blood biomarkers (described above). ME/CFS patients and controls provided blood and stool samples before and after the exercise challenge and reported their symptoms before and after the exercise challenge to determine the extent of their post-exertion relapse. The Shukla team identified another gene that was expressed in ME/CFS patients that correlated with their post-exertion symptoms. They also found increased microbe DNA in the blood (that likely came from the gut microbes) in both patients and healthy people following exercise. These results are being prepared for publication and put an interesting new twist on possible causes of the cardinal feature of ME/CFS – post-exertion crash.

In part two of this series we discuss the 2011 funding cycle and the progress being made through those researchers.

On December 16th we will be holding a free webinar where we distill this information a bit more and answer your questions about this research progress and what it means to you. Register for that webinar today HERE.

https://attendee.gotowebinar.com/register/119787780;jsessionid=abc276q-OYylr4Ky6axOu

For the many of our readers who have donated to our organization, you can take pride in having supported this important work to advance ME/CFS understanding.