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

Thursday, July 31, 2014
2-3:00pm Eastern (1pm Central/Noon Mountain/11am Pacific)

RSVP to Reserve Your Slot – CLICK HERE

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)

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)

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)

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.

 

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.

 

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. http://www.ncbi.nlm.nih.gov/pubmed/24929332

 

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: http://www.ncbi.nlm.nih.gov/pubmed/24932428

 

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. http://www.ncbi.nlm.nih.gov/pubmed/24791749

 

 

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

Breaking Down the Complexity of ME/CFS – Part 1

July 2, 2014

Clinical Intuition divide and conquer

In 2012 the Solve ME/CFS Initiative organized a meeting at the Banbury Center of Cold Spring Harbor Laboratory, “Decoding Clinical Trials to Improve Treatment of ME/CFS.” We invited many of the investigators that over the years have conducted clinical trials for myalgic encephalomyelitis, Chronic Fatigue Syndrome and related disease areas; Jose Montoya, Øystein Fluge, Katherine Rowe, Carl-Gerhard Gottfries, Nancy Klimas, Peter Rowe, Italo Biaggioni and about 30 others.

Our meeting objective was to understand the science behind the clinical trials – why some worked and others didn’t – and then to take these lessons learned and apply this knowledge to future clinical trials.  It was clear from the many presentations that the complexity of ME/CFS made clinical trials challenging.  Many of the trials were small, few went further than Phase II (there are 4 phases in clinical trials) and none were replicated by other clinical researchers.  It was interesting however, to see that despite the limitations of these clinical trials, there were hints of some beneficial effect to some of the treatments.

This gave Elizabeth Unger MD, PhD, a meeting participant, the idea that we should try to capture this clinical intuition (the sense that doctors have that helps them understand and treat ME/CFS patients.) Dr. Sandra Kweder of the FDA was thinking similarly when she was quoted as saying:

“… But the key is that a lot of the researchers in this to date have been out there on their own. They’re clinicians who are following a series of patients for decades. And no one’s really been able to tap into the kind of information that they have…”

-  ME and CFS Stakeholder Teleconference Participant List, September 13, 2012

We worked with Biovista, one of our 2011 funded investigators, to develop a platform in order to tap into and capture clinical intuition.  Together we developed a web-based survey tool that asked questions focused on three main areas:

  1. Efficacy of drugs currently used in the treatment of ME/CFS symptoms
  2. Alternative treatment options (nutritional supplements, fluids,)
  3. Treatment strategies: How are symptoms interrelated? Which symptoms are more important to treat first?

About 15 ME/CFS expert clinicians participated in the survey.  We are now preparing the results of the survey for publication.  Once published, this will be useful information for ME/CFS patients to bring to their physicians to see how the ME/CFS experts from around the world are managing and treating their patients.

The knowledge that expert ME/CFS clinicians have gained is invaluable to us as we work to break down the complexity of ME/CFS.  By understanding what treatments work and which don’t, we learn about the biology that underpins these treatment responses.  By capturing this information we are expanding our knowledge base and once again putting ME/CFS into the context of other medical and scientific knowledge.  As we strive for a world free of ME/CFS, this is just one of the many ways we are working to accelerate discovery of safe and effective treatments.

_________

Look for Part 2 and Part 3 of this blog series, Breaking Down ME/CFS, coming soon

Dr. Vernon, SMCI Scientific Director, Represents ME/CFS at Life Sciences Meeting

June 18, 2014

DIA2At the beginning of the drug development pipeline are patients. As the scientific director of the Solve ME/CFS Initiative, I understand that I advocate for the patients in many important circles – one of them being the scientific community and drug development circles. In February of this year I applied for a patient advocacy fellowship to the 2014 DIA 50th Annual meeting “Celebrate the Past – Invent the Future”This meeting provides a wonderful opportunity to meet with people from around the world, share knowledge, network, and build new relationships.

The 50th DIA annual meeting is the largest multidisciplinary event that brings together a community of life sciences professionals at all levels and across all disciplines involved in the discovery, development, and life cycle management of medical products all with a common goal to foster innovation that will lead to the development of safe and effective medical products and therapies to patients. DIA has over 18,000 members, connecting people throughout the world that are involved in drug development – from patients to insurance payers. 

After last years ME/CFS FDA workshop, I was particularly excited to apply for this fellowship and have the opportunity to participate in a meeting that was looking toward the future. In March I was notified that I was selected for a full scholarship to represent the Solve ME/CFS Initiative and our community. I see this as an opportunity to tell an important crowd of people about the opportunities available for ME/CFS.   With the publishing of FDA draft guidance for ME/CFS drug development, the timing is fortuitous, allowing me to learn about the successes and challenges others have faced in drug development and developing the regulatory framework for complex and poorly understood chronic disease.

There was a competitive slate of over 40 applicants.  While I am representing the Solve ME/CFS Initiative, there are the 16 other organizations that make up the Class of 2014:

  • Answering TTP Foundation
  • Batten Disease Support and Research Association
  • Connecticut Advocates for Parkinson’s
  • CrossLink Medical Resources
  • Dravet.ca and Dravet.org
  • ECD Global Alliance
  • Foundation for Prader-Willi Research
  • Foundation For Sarcoidosis Research
  • Kennedy’s Disease Association
  • Myotonic Dystrophy Foundation
  • National Foundation for Ectodermal Dysplasias
  • Parent Project Muscular Dystrophy
  • TargetCancer
  • Tarlov Cyst Disease Foundation
  • Tuberous Sclerosis Alliance
  • Tuberous Sclerosis Canada Sclerose Tubereuse

The meeting officially began on Monday, June 16th with a jam-packed program with over 21 tracks and more than 260 educational offerings. You can read the day-one summary HERE and a summary of Day two HERE. In addition to the main program, fellows participated on Sunday, June 15 in a one-day Patient Advocate Pre-Workshop with renown thought leaders designed to:

  • Develop, strengthen, and support patient collaborations with key policy makers, health professionals, industry representatives, and academia
  • Increase the knowledge and understanding of patient groups about key issues central to patient-centered healthcare, biomedical research, and drug development
  • Develop the capacity of patient groups to advocate for change
  • Improve alliances between patient groups and other healthcare stakeholders
  • Stimulate cooperation, promote dialogue, and share best practices

I am very excited to have this opportunity to network, listen and learn from global leaders from industry, regulatory agencies, academia and the other patient advocate fellows.  I am keenly interested in learning how the other patient advocate fellows were able to interest and attract drug developers to work on their diseases.  This will help the Solve ME/CFS Initiative build innovation supply chain making ME/CFS attractive for drug development.  I look forward to sharing with you what I hear and learn as we work together to solve ME/CFS.

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

Research Digest – June 2014: Neuroinflammation in ME/CFS

June 17, 2014

neuroimagin_CFS

Neuroimaging has been used to study the structural, functional and metabolic affects of ME/CFS on the brain in ME/CFS patients for the past 25 years.  To date there are about 50 papers in the peer-reviewed biomedical literature describing these findings.  Even at this time, the neuroimaging findings when examined in the context of the patients symptoms implicated inflammation as the culprit.

The brain was long thought to be immune privileged, which means it is an organ that is relatively free from or only experiences limited inflammation.  We now know that the brain has dynamic two-way communication with the peripheral immune system and that there are immune cells that reside in the brain.  These brain immune cells are called microglia – a specialized immune cell known as a macrophage.  Think of macrophages and microglia as the “Pac Man” of the immune system – gobbling up damaged cells and infectious agents. Microglia are important to keeping the central nervous system environment free from inflammation and in a healthy state.  But too much microglia activity over long periods of time causes inflammation – known as neuroinflammation – and this is detrimental to the brain.

This month we highlight three publications that both directly demonstrate and implicate neuroinflammation in ME/CFS.

 ____________

Dr. Andrew Miller, Emory University and investigators from the Centers for Disease Control and Prevention published the results of a functional neuroimaging study conducted on CFS patients and healthy controls identified from the longitudinal survey of CFS in Georgia.  The investigators focused on the basal ganglia, a region of the brain important for motor activity and fatigue and used a gambling task to activate the basal ganglia.   Compared to healthy controls, CFS patients had reduced basal ganglia activation during the gambling task suggesting possible alterations to dopamine (a nerve signaling molecule) transmission.  The authors cited studies from other diseases including Parkinson’s disease and HIV where inflammation affects the function of the basal ganglia and conclude that since inflammation has been demonstrated in CFS, (peripheral) inflammation may affect basal ganglia function and causing CFS symptoms. While this study only compared CFS patients to healthy controls, it is important to note how other diseases with symptoms similar to CFS are informing these results. http://www.ncbi.nlm.nih.gov/pubmed/24858857

 

In a study that has received widespread media attention and was published in the top nuclear medicine journal worldwide, the team at RIKEN Center for Life Science Technologies led by Professor Yasuyoshi Watanabe used neuroimaging to show widespread neuroinflammation in ME/CFS.  The investigators showed that microglia cells were activated in several regions of the brain in ME/CFS patients compared to healthy controls.  Specific regions of neuroinflammation correlated with ME/CFS symptom severity.  While microglia activation and neuroinflammation is not specific to ME/CFS, it is an important objective indicator that helps further our understanding of ME/CFS pathophysiology. http://www.ncbi.nlm.nih.gov/pubmed/24665088

 

The Solve ME/CFS Initiative funded Dr. Dikoma Shungu, Weill Cornell Medical College to use neuroimaging to examine metabolic differences in the brain.  In the elegant studies conducted by Shungu and his team, brain metabolism in ME/CFS patients was compared to healthy controls and “’disease” controls.  Disease controls are individuals with a disease that presents with similar clinical symptoms as ME/CFS and in Shungu’s studies he used individuals with general anxiety disorder (GAD) and major depressive disorder (MDD) as disease control groups.  Levels of lactate were higher in the ventricular space of the brain (the space that is filled with fluid) in ME/CFS, GAD and MDD compared to controls.  Lactate levels were highest in the ME/CFS and MDD subjects.  Lactate suggests a metabolic defect and the levels of lactate correlated with fatigue severity.  Shungu and his team determined that glutathione, the main antioxidant in the brain, was significantly decreased in ME/CFS and MDD patients.  Increased levels of ventricular lactate and decreased glutathione were significantly associated with function and disability. Shungu describes how these findings support a role of increased oxidative stress in ME/CFS.  http://www.ncbi.nlm.nih.gov/pubmed/22281935

 

 

Guest Blog: Kevin Guibara, Refuting the Status Quo

June 17, 2014
Kevin Guibara nd his father, Albert

Kevin Guibara and his father, Albert

Like many patients, I was a normal athletic college student with my life ahead of me when it was completely ruined by a 1-2 month onset of ME/CFS at the age of 21. Growing up, I was perfectly healthy and I enjoyed baseball and soccer. At UC Santa Barbara, prior to my illness, I also played rugby and surfed.

It took me years to reach a self-diagnosis and even more years to get in front of a doctor who provided real treatment options. I was about 30% functional with brain fog and fatigue as my primary symptoms. Early treatments only seemed to make things worse, to the point where I was primarily limited to my home with a couple short excursions per week. Then, due to lack of activity and the muscular impact of ME/CFS, I ended up causing a significant injury to my back with just minor household movement. I was unable to sleep for 4 days because my nervous system was so activated from lying down or sitting. I was convinced that I had sent my nervous system into free fall and that I would not recover.

Before this injury, I had been in a state of mind that I wanted to protect my body from new treatments and I was paranoid about trying new drugs. But after this injury I cultivated a state of mind in which I believed I could only benefit from venturing into new treatments because the status quo – the state of my health – simply was not acceptable.

I began by taking antibiotics targeted at Lyme Disease. As I improved, I added Valtrex, then Valcyte, which helped; then after about 18 months, I plateaued again and began searching for more solutions. GC-Maf gave me another big kick that allowed me to increase my activity level and improve my post-exertional malaise issue. I have been able to slowly taper off most of the antibiotics. I have more recently achieved a big stamina increase with hormone supplementation. I will consider myself recovered if I can successfully taper from Valcyte, which I will begin at about the time this is printed.

"Helping A Friend" sculpture by Albert Guibara

“Helping A Friend” sculpture by Albert Guibara

It has been a long road, but I believe the puzzle pieces exist for a complete recovery (80-90%), which is where I consider myself to currently function. I returned to finish college at UC Berkeley over the last 18 months. I am currently able to enjoy life and engage in fun activities. In the past month, I climbed to the top of Yosemite Falls, before camping in Yosemite for 3 days and I was able to enjoy 4 days in Honolulu.

I have great faith in the Solve ME/CFS Initiative – their Solve CFS BioBank; cutting edge research that is being funded; the tools being developed to create improved solutions for ME/CFS patients. I also believe that through their hard work, we have made significant progress in raising awareness and increasing access to treatment options. I believe that together we will solve ME/CFS.

 __________

­­­­­

Kevin and his father, artist Albert Guibara, are featured in our spring mailing and the most recent SolveCFS Chronicle. View more of his father’s artwork, at www.Guibara.com

Solve ME/CFS Initiative (SMCI) Position on P2P

June 12, 2014

P2PThe NIH Office of Disease Prevention Pathway to Prevention (P2P) program approved a proposal for a workshop to provide an evidence-based assessment on ME/CFS. We first wrote about the P2P workshop program in April (http://solvecfs.org/pathways-to-prevention-for-mecfs/). Since then we have been working with the advocacy community to stay abreast of the P2P process and assess its impact on ME/CFS.

We applaud the fact that a P2P is focusing on ME/CFS but we have concerns about the evidenced-based literature review. We have reviewed the most recent protocol posted by AHRQ evidence-based assessment center on May 1, 2014 (read it HERE )  and have identified serious flaws with the sample search strategy described in the appendix.

This search and corresponding criteria will bias the evidence base to cognitive behavioral therapy (CBT) and graded exercise therapy (GET) trials – treatment approaches that are not specific to ME/CFS (as noted by AHRQ) – and will not assess any of the important biomarker research that has been conducted and funded (primarily) by NIH over the past 25 years.  This is unacceptable.  The search criteria must be broader and must include terms that reflect the important advances that have been made in biomarker research for ME/CFS. We believe it is not too late to correct this and that many stakeholders would be willing to participate to help make the P2P as effective as possible.

We have written a letter to Paris A. Watson, Senior Advisor, NIH Office of Disease Prevention, Susan E. Maier, Ph.D., Deputy Director, NIH Office of Research on Women’s Health, David M Murray, Ph.D., Associate Director for Prevention, Director of the Office of Disease Prevention, and Francis S. Collins, M.D., Ph.D., NIH Director to address these concerns. You can read our letter to the NIH concerning the P2P HERE.

It is imperative that this P2P workshop address gaps in research because it is plausible that the NIH will use the P2P evidence-based report to inform a new ME/CFS funding opportunity –  the current program announcement expires October 25, 2014 (http://grants.nih.gov/grants/guide/pa-files/PAR-12-032.html).

We have requested that the NIH tell the ME/CFS community whether the P2P will inform a new NIH funding opportunity.  If so, it is critically important that the P2P go forward with an evidence-based review that will result in a compelling funding opportunity that attracts investigators to ME/CFS research.

Dr Suzanne Vernon, the Solve ME/CFS Initiative’s Scientific Director continues to serve on the working group, (made up of content experts in ME/CFS – clinicians, researchers, patients, patient advocates, caregivers and Federal partners). Though the work done they have done to date is limited, she will remain engaged in order to help make this ME/CFS P2P workshop the best it can be.  She is working to bring attention to the flaws in this evidence-based process in the hopes that the P2P will fix it and get it right. We are happy that Dr Vernon is serving in this capacity and able to lend her expertise to the proceedings.

Our understanding is that there will be opportunity to comment and offer feedback on this report; that at the two-day workshop, the P2P panel will hear from the expert speakers and be able to ask clarifying questions in a town-hall-like Q&A that will take place after each session during the meeting.  We will bring you information on how and when to participate as soon as it is available so that together we can do all we can to ensure the resultant recommendations are aimed at improving the robust nature of the research into ME/CFS.

Read our earlier blog post that explained the P2P process HERE

Read more about the Pathway to Prevention workshop program HERE

Read more about the systematic evidence review being performed by AHRQ HERE