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A Father Responds: Riding Hard for ME/CFS Research

Everyone’s Nightmare

It was a nightmarish situation.  Struck down by ME/CFS at the age of eight after a series of staph/herpes infections and infectious mononucleosis, the Spearing’s formerly healthy and energetic daughter, Stephanie, was soon confined to her bed.

Then it got worse. Much worse.  As Stephanie’s illness progressed, severe sensory problems left her unable to tolerate bright light, sounds, smells and touch. Migratory nerve and abdominal pain left her in severe pain much of the time. Dysautonomia and muscle weakness left her unable to walk. Food sensitivities  and gut problems left her unable to tolerate many foods and her weight dropped precipitously.  The UK health authorities were – surprise, surprise –  no help at all. They didn’t even attempt to be polite in their denials.

Improvement

stephanie spearing

Stephanie has improved tremendously but is still far from being able to lead a normal life

It was a tragic story that could have easily lead to an even more tragic ending but Stephanie’s move out of the  damp UK into the colder but drier climate and more ME friendly health system in Canada helped  Rest and more rest, dietary changes, probiotics and immune supplements produced progress.

Seven years later Stephanie is still weak but she no longer experiences the severe sensory problems and pain she once did. She’s not in school but no longer needs her wheelchair and is able to go on walks. Stephanie’s reduced suffering is a great relief to her parents but they want their entire daughter back.

Riding for ME/CFS Research

They want real relief. They want mounds of research. They want their daughter well and they don’t want anyone else to go through what Stephanie and they went through. The awful nights. The walking on tiptoes in order not to cause their daughter – huddled in her bed upstairs – pain from too much noise.  The ugly comments from the medical authorities.

Everyone is affected by these severe illnesses. Some give up in the face of the opposition but Peter Spearing  has just gotten more determined.  In three days in his Ride For ME/CFS Research Peter is riding 100 kilometers in Tour de l’Île de Montréal cycling event  to raise funds for the Simmaron Research Foundation. He’s going to ride full out – as hard as he can.

Ride For ME/CFS research

The Institute’s collaborative efforts with top researchers and Dr. Peterson’s years of experience drew the Spearmans to the Simmaron Research Institute

When asked why they choose the Simmaron Research Institute Stephanie’s mother Suzy emphasized Dr. Peterson’s years of experience, and the close ties the Institute has forged with important research efforts across the globe.  One of the first articles they read about ME/CFS, she noted, involved Dr. Peterson’s efforts in the Incline Village outbreak over thirty years ago.

Created in 2012, the Simmaron Research Institute is dedicated to scientifically redefining how ME/CFS is studied and treated. It’s dedicated to giving people like Stephanie options. To breaking up the ignorance that is causing so many people to be cruelly treated. To producing an environment in which ME/CFS is given the resources that other chronic illnesses are.

The Institute is currently participating in and/or funding work on

  • The gut microbiome
  • Tick, mosquito borne and other pathogens
  • Determining subsets and defining ME/CFS
  • Epidemiology including the long term effects of ME/CFS
  • A genomic analysis of immune cell functioning
  • The cause of the natural killer cell dysfunction
  • The extent of severe T-cell abnormalities found
  • Autoimmunity, non-Hodgkin’s lymphoma and cancer prevalence
  • Ampligen’s effectiveness in treating ME/CFS
  • Spearheading efforts to make immune tests a standard part of diagnostic protocols
  • Collaborating with Columbia University to train future doctors how to treat ME/CFS
Simmaron Research Foundation

The Simmaron Research Institute is dedicated to scientifically redefining ME/CFS

Peter, Suzanne and Stephanie request that you support Peter’s efforts to bolster ME/CFS research by donating to the Simmaron Research Institute here.  Everyone, young and old, deserves a shot at a normal, healthy life.  (Please reference Stephanie Spearing in the dedication box provided).

Simmaron Scientist Awarded NIH Grant Probing Cause of Immune Holes in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis

August 31, 2014

NIH Grant to Study Genetics of Immune Response in ME/CFS

Simmaron Research Foundation’s Scientific Director, Isabel Barao PhD, has been awarded the IDeA Clinical and Translational Research Pilot Grant (CTR-IN) from the National Institutes of Health (NIH) to examine ways ME/CFS patients’ genetic heritage may contribute to immune dysfunction and their inability to fight off viruses. Dr. Peterson will select the patients, collect their blood and provide their clinical information. The laboratory work will be performed at University of Nevada School of Medicine (UNSOM), Department of Microbiology and Immunology, where Dr. Barao is academically affiliated.

DNA

This study will probe genetic holes in natural killer cells

The $75,000 grant is small, but it is an important sign of Simmaron’s ability to advance new investigators involved in immunological research on ME/CFS at the NIH. The CTR-IN grant is supported by the National Institute of General Medical Sciences. The 1-year grant supports 20% of Dr. Barao’s pay and supplies for laboratory work.

Dr. Barao has also submitted an R21 grant proposal to the NIH in collaboration with the National Cancer Institute (NCI), Dr. Peterson and UNSOM.

ME/CFS is believed to be a multi-factorial disorder caused by a combination of one’s genetic makeup, an environmental trigger such as a pathogen, and other factors. It’s believed that 20-40% of the reason people came down with ME/CFS lies in their genes.

Take away that genetic component and maybe that infection that never went away passes on through like every other cold did. Maybe that bout of fatigue that stayed and got worse resolves with rest this time. It may take one factor to tip the system into the situation we call ME/CFS. That factor could lie in our genes.

First Line of Immune Defense Down

This grant will help determine if altered FcRs (e.g. CD16) on natural killer (NK) cells have made it more difficult for ME/CFS patients t0 fight off viruses.  NK cells are the cells our immune system uses to hold the invader at bay while cytotoxic T-cells and B-cells gear up to wipe out the invader.

We know that poorly functioning NK cells could be allowing pathogens to get entrenched more deeply into ME/CFS patients’ systems, perhaps even into immunologically privileged parts of our nervous system that the big guns of our immune system have trouble getting to.

Second Line of Immune Defense Down As Well?

pathogens

Could ME/CFS genetics be giving pathogens the upper hand in ME/CFS?

It turns out, though, that natural killer cells not only play a vital role in the first lines of our immune defense – they also play an important role in fighting off chronic infections. This study suggests NK cell problems in ME/CFS may also be allowing chronic viral infections to persist.

During an infection, B-cells start pumping out IgG antibodies that attach to and stop pathogens from infecting our cells. Once IgG antibodies have attached to a pathogen, NK cells are able to recognize, attack and kill cells infected with pathogens through FcRs, using a process called ‘antibody-dependent cell-mediated cytotoxicity’ (ADCC).

Studies have shown that individuals with genetic alterations (polymorphisms) of the genes associated with that ADCC response have an increased risk of cancer and autoimmune disorders. Genetic impairment of the ADCC response could also make it more difficult to clear herpes viral infections, which are of such interest in ME/CFS.

A Talk With Isabel Barao Ph.D

Dr. Barao is Adjunct Assistant Professor at UNR’s Department of Microbiology and Immunology and Scientific Director of Simmaron Research.

How did you get involved in ME/CFS research?

In 2009, the Whittemore Peterson Institute (WPI) invited me to be their scientific consultant and to find out why NK cells are dysfunctional in CFS. I conducted immunological studies at the WPI until September of 2010.

What has your research into ME/CFS told you about this disease thus far?

Isabel Barao Ph.D

Isabel Barao Ph.D

I believe that variations in particular genes that affect the functioning of the immune system increase the risk of CFS.

You recently presented a paper at the 1st Annual Mountain West CTR-IN meeting suggesting that ME/CFS patients may have higher than normal levels of “hybrid” immune cells. Can you tell us what those immune cells are and what effects they might have?

The ‘hybrid’ lymphocytes are NKT-like cells that are increased in the blood of some of Dr. Peterson’s CFS patients and that may have unique properties in CFS patients.

We are characterizing these immune cells further.

You’re also engaged in a Simmaron Research Foundation study examining genetic changes in a range of immune cells in ME/CFS. Most ME/CFS research has focused on natural killer cells but you’re also really interested in other immune cells. Why?

Because NK cells communicate with B cells, T cells, macrophages, etc. and if the communication between them is defective, immune deregulations involving all these cells can occur and lead to disease. 

What comes next and what are the treatment implications if the study is positive?

Our expectations are that FcRs polymorphisms define CFS and its severity and predict those patients who may benefit from ADCC-based therapies.

Read more about Isabel’s work at Simmaron Research Foundation Study Targeting Roots of Immune System Breakdown in Chronic Fatigue Syndrome (ME/CFS)

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Simmaron Foundation’s Immunology Workshop: the Forefront of Diagnosing and Treating ME/CFS

Simmaron’s Immunology Workshop on ME/CFS, Part I

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Immunologists came to the Simmaron Foundation’s Immunology Workshop to decide if immune tests should be standard practice in ME/CFS diagnosis and treatment

Immunologists came to the Simmaron Foundation’s Immunology Workshop to decide if immune tests should be standard practice in ME/CFS diagnosis and treatment.

Simmaron Research Foundation is focused on redefining ME/CFS scientifically. They produced the Immunology Workshop at the 2014 IACFS/ME Conference in order to get a consensus from immunologists and practitioners on whether immune testing should help guide diagnosis and treatment in Chronic Fatigue Syndrome (ME/CFS). Immunologists were invited to give presentations and then queried regarding whether immune tests should be incorporated into diagnostic protocols for this disorder.  Dr. Unger, the head of the CDC’s CFS program, was invited to attend.

Overviews of  some of the presentations make up Pt I of the Immunology Workshop Overview.

(I used my notes from the Workshop to build the foundation for this blog and then expanded on many of the subjects presented; i.e. the blog reflects my interpretation of the presentations and what they mean; it may not in places reflect the presenters viewpoints.)

Troy Querec, Ph.D, CDC – Natural Killer Cell Testing 

The CDC ignored natural killer (NK) cell functioning in ME/CFS for many years, but they appear to be convinced now that it’s a key problem.

Natural killer cells are called ‘natural killers’ because they don’t need to be activated to kill cells that don’t have the right MHC markers on them. They are also the only immune cells that can recognize infected cells without antibodies and MHC markers being present.

medical tests

The NK cell function test that reveals how effective NK cells are at killing invaders is laborious, expensive and, according to an NSU presentation at the IACFS/ME conference, not suited to most labs.  (This isn’t the first immune test relevant to ME/CFS that has not been readily available. Most of the tests associated with the RNase L enzyme are still available only at one lab in country.)

Recognizing the need for your average doctor to have access to a less expensive test of NK cell functionality, the CDC is working on one. (They’re not the first. The Klimas/Fletcher group in Miami was reportedly working on one several years ago.)

They’re focusing on measuring how effective the receptors found on the surface of NK cells are at turning the cells on. Receptor deficiency could play a role in the poor NK cell functioning found in ME/CFS. To that end they’re developing CD 107 antibodies that attach to the receptors.

Because shipping has also been shown to reduce NK cell viability, they’re also proposing ways to optimize NK cell viability during the shipping process. This involves keeping cells in their natural habitat – the whole blood – and isolating PMBC’s first. They propose a pilot study to determine ways to optimize viability of NK cells during shipping.

Finding an easier and more effective way to measure NK cell functionality would go a long way to establishing NK cell dysfunction as a biomarker for ME/CFS.

Dr. Constance Knox – B-cells and Chronic  Fatigue Syndrome

“Lots of vacuums in this field” 

After noting how little we know about the role B-cells play in ME/CFS, Dr. Knox echoed Mady Hornig’s statements that there are “lots of vacuums in this field” and then went onto a short overview.

A cornerstone of our immune defense, B-cells directly ‘attack’ pathogens and trigger other parts of the immune system to respond.

B_cell_activation

B-cells could be a major contributor to ME/CFS but the role they play is largely a mystery

First, they are activated by antigens (proteins associated with pathogens) brought to them by macrophages and dendritic cells – two innate immune cells. B-cells then produce hordes of pathogen specific antibodies that search for the pathogen outside the cell and attach to it in order to prevent it from attacking our cells. They also take that antigen and present it to killer T-cell’s which then mount a pathogen specific defense which gets at pathogens located inside the cell.

Two recent findings have overturned medical dogma concerning B-cells.

Naturally Occurring Antibodies: At one time it was thought B-cells only produced antibodies that were directed at specific invaders, but it’s now clear that naturally occurring antibodies – which are not directed at specific pathogens – are present as well. These antibodies are derived from unusual sugar residues synthesized in the gut – an interesting finding given the emphasis both Dr. Hornig and Dr. Lipkin place on the gut in ME/CFS.

Regulatory B-Cells – Cells regulating the powerful T-cell response (T-regulatory cells) received most of the attention until regulatory B-cells were discovered. Regulatory B-cells make up only 0.5% of total B-cells but are powerful regulators of immune activation and inflammation. They induce two important anti-inflammatory cytokines (IL-10, TGF-beta), which dampen the inflammation produced by the innate immune system.

b-cell signaling

Problems with B-cell signaling would pose problems for other parts of the immune system.

IL-10 restores Th1/Th2 balance (a problem in ME/CFS) and inhibits inflammatory cascades while TGF-B wipes out some types of T-cells, dampens the activity of cytotoxic T-cells, and takes other actions to reduce inflammation. These cells often get upregulated in states of chronic inflammation and elevated levels of both have been found in ME/CFS.  (They suggest the immune systems of ME/CFS patients are attempting to reign in inflammation.)

Research  is need to determine if either cell plays a role in ME/CFS, but several ongoing studies may give us clues regarding the role B-cells play. Rituxian (Rituximab) – an monoclonal antibody directed against mature or activated B-cells – reduces B-cell numbers. (A successful result in Rituximab trial could indicate B-cells in ME/CFS are triggering an autoimmune response or could implicate EBV infection.)

A 2011 study documenting increased rates of lymphoma in ME/CFS patients suggests more problems with B-cell regulation may  be present in a subset of  patients.

David Baewer, M.D., Ph.D – Serology and HHV-6 Infections

Most humans carry latent herpesviruses in their cells that do little harm. Once activated, though, in people with poorly functioning immune systems such as transplant patients, these seemingly innocuous viruses can cause enormous damage. With their immune systems intentionally knee-capped in order to avoid an immune attack on their transplanted organ, they are ripe for herpesvirus activation. Several antivirals under development that could assist some people with ME/CFS come from research devoted to preventing herpesvirus activation in transplant patients.

herpesvirus

Some researchers believe herpesvirus activation is common in ME/CFS -but that the typical virus tests are not up to the job.

Dr. Baewer proposed that the same  general processes causing herpesvirus reactivation in transplant victims is occurring in ME/CFS. Standard testing for herpesviruses, however, is unable to distinguish the kind of active herpesvirus infections he believes are present in ME/CFS.

He noted that primary active infections – which occur when the body is first introduced to a pathogen – are often diagnosed via a high IgM response.

The kind of herpesvirus infection suspected in ME/CFS, however, (and the kind that mostly occurs in adults) involves reactivation from a latent infection. Because these kinds of infections rarely generate a robust IgM response, Dr. Baewer asserted IgM readings in adults have little clinical value.

Viral DNA with PCR isn’t effective either because it only tells us if the virus is present and it is present in 95-100% of population.

Viral mRNA using reverse transcriptase PCR, on the other hand, shows whether the virus replicating or not.  This type of testing tells which genes in herpesvirus genome are present in the blood – and identifying which genes show up is the key to determining whether the virus is actively replicating or not.

Herpesviruses need to be able to attack and establish themselves in B-cells, ward off the immune system’s efforts to find them and then replicate when the time is right. They are complex viruses with big genomes that have genes associated with maintaining latency, with altering the immune response and with building new viruses. Viral mRNA using reverse transcriptase PCR can identify which stage the virus is  in.

gene

Tests can reveal which stage of its lifecycle EBV is in. Unfortunately, those tests are rarely done in ME/CFS patients

If there is evidence of genes associated with latency, but nothing is present, the virus is simply maintaining latent state. If genes produced later in its life cycle are found, the virus is active but not replicating. If genes devoted to building the outer membrane of the herpesvirus are present – you have an active, replicating virus on your hands.

(The fact that Epstein-Barr virus can hijack the nuclear machinery in B-cells and go through its early, medium and late cycles without ever replicating suggests it can cause much mischief simply sitting in B-cells.  We know that in order to maintain latency, EBV affects how B-cells, a critical part of the immune machinery, function.  We know EBV increases the lifespan of B-cells and that it prompts them to replicate. Some researchers believe EBV’s effects on B-cells underlie all autoimmune processes in the body. )

The smoldering herpesvirus infection hypothesis in ME/CFS produced by Dr. Lerner and researchers at Ohio State University proposes EBV is perturbing immune cells and causing immune cell dysfunction without causing cell death, while producing only very low levels of viral transcription.

Because herpesvirus serology tests will not pick up this type of infection, however, it will never be picked up by standard serology tests.

(to be continued…)___________________

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The Immunology Workshop – Redefining how ME/CFS is diagnosed and treated

Simmaron’s Immunology Workshop Participants

  • Daniel Peterson, M.D. Sierra Internal Medicine, Incline Village, NV
  • Nancy Klimas, M.D. Ph.D Nova South Eastern University, Miami, FL
  • Paula Waziry, Ph.D Nova South Eastern University, Miami, FL
  • Sonya Marshall, Ph.D Griffith University Gold Coast Australia
  • Sharni Hardcastle, Ph.D Griffith University Gold Coast Australia
  • Konstance Knox, Ph.D., Founder, CEO, Coppe Healthcare Solutions
  • David Baewer, M.D. Ph.DMedical Director, Coppe Healthcare Solutions
  • Isabel Barao, Ph.D., Research Assistant Professor, University of Nevada, Reno, Simmaron Research Scientific Director
  • Gunnar Gottschalk, B.S., Simmaron Research, Incline Village, NV
  • Troy Querec, Ph.D., Associate Service Fellow, Centers for Disease Control and Prevention, Atlanta, GA
  • Dennis Mangan, Ph.D., Former Chair, Trans-NIH ME/CFS Research Working Group, Office of Research on Women’s Health, U.S. National Institutes of Health
  • Mary Ann Fletcher, Ph.D., University of Miami Miller School of Medicine Professor of Medicine, Microbiology/Immunology and Psychology
  • Elizabeth Unger, M.D. Ph.D., Chief, Chronic Viral Disease Branch, Division of High-Consequence Pathogens and Pathology, National Center for Emerging and Zoonotic Infectious Diseases. Centers for Disease Control and Prevention, Atlanta, GA

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 


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Simmaron Research Foundation Study Targeting Roots of Immune System Breakdown in Chronic Fatigue Syndrome (ME/CFS)

June 13, 2014

Simmaron Research’s  new immune study builds on exciting research that is changing how we think about ME/CFS.

Twenty years ago  the internationally known virus hunter, Dr. Ian Lipkin of Columbia University, didn’t find Borna Virus in people with ME/CFS, but he never forgot the immune dysfunction he found.  Twenty years later he found more immune dysfunction in another study.

Isabel Barao, PhD, Simmaron Research Scientific Director

Isabel Barao, PhD, the Simmaron Research Foundations Scientific Director believes a genetic predisposition to immune problems could underlie ME/CFS

He doesn’t know why it’s there but he does believe that all ME/CFS cases – no matter what pathogen or other factor has triggered them –  devolve to a ‘common pathway’. The fact that pathogens of all types – from Epstein-Barr Virus, to SARS, to Giardia – can trigger ME/CFS suggests a core immune deficiency lies at the heart of the illness.

Every genetic study suggests an inherited susceptibility to Chronic Fatigue Syndrome is present. Dr. Mady Hornig of the Center for Infection and Immunity at Columbia University believes that a genetic predisposition in combination with an environmental trigger (such as an infection) occurring at just the right (wrong) time is probably key to coming down with ME/CFS.

For thirty or forty years you might be able to easily slough off this bug or that pathogen, but at some point for some reason the stars aligned; you were depleted in just the right way, the pathogen hit and with your immune system genetically predisposed to crack under the pressure – it did – and your entire system faltered.

gene strand

Simmaron is looking for the genetic roots of an immune system breakdown

Simmaron Research’s next pilot study is looking for that immune crack in the dike – the genetic underpinnings of the system collapse that occurred. Led by Simmaron’s Scientific Director, Isabel Barao, PhD, in collaboration with researchers at the National Cancer Institute and University of Nevada Reno, it will determine if your NK and B-cells and macrophages are genetically predisposed to respond poorly to a virus, toxin, or cancer cell.

Dr. Barao is studying whether people with ME/CFS have polymorphisms – unusual gene formations – that make their key immune cells less likely to respond well to viruses and other threats. That immune ‘hole’ many people have talked about with regards to ME/CFS could start here. We all know about the rampant NK cell problems in ME/CFS, but this study could help explain the B-cell problems recently uncovered in a German research study – and perhaps even shed light on why Rituximab may be working in some patients.

It’s the initial part of a projected three-part study that could end with drugs for ME/CFS. Once genetic alterations have been found, they’ll be correlated with immune findings. If that holds up, it’ll  be time to look for drugs to fix the problem, two of which are currently in clinical trials.

We-Have-Ideas

Support the Simmaron Research Foundation as it redefines how ME/CFS is understood and treated

Think about it. The high heritability rates in ME/CFS indicate genetic problems exist somewhere. Where better to look than the immune system?

This study is a no-brainer to me. It’s relatively cheap – it has a quick six-month turnaround – and the data it produces will lay the foundation for an NIH grant on topics they’ve  shown they’re willing to fund.

Help us redefine ME/CFS.  Support breakthrough science on immune deficiencies at Simmaron.

Simmaron Research | Give | Donate | Scientifically Redefining ME/CFS

A Talk with Dennis Mangan, New Member of Simmaron’s Scientific Advisory Board

 Communication was central to all of our activities

My first memory of Dennis Mangan came at the end of a long day at a Federal Advisory Meeting for ME/CFS (CFSAC).  As the meeting broke up, Dennis strode over, pulled up a chair and motioned for everyone to gather around.  He asked what we thought needed to happen.  For the next hour  or so he sat and quietly, listening to stories of distress, frustration and hope.  Never had anyone from the National Institutes of Health attempted to get so close to the patient community. Changes, I thought, were surely in the wind.

Dennis-Mangan pci

Dennis Mangan created the State of the Knowledge Conference, created a Listserv, re-vitalized the CFS Working Group, changed the name and communicated, communicated, communicated during his time working on ME/CFS at the NIH

After that he started to act. He redid the NIH website, and they became the first federal agency to call chronic fatigue syndrome ‘ME/CFS’.  He started a Listserv to be in better communication; he enlarged and revitalized  the NIH Working Group  (they had their first meeting in a year). Soon we had State of the Knowledge Workshop – put together in collaboration with patients.   Throughout, Dennis was open and in communication, and the ME/CFS community embraced him.  It was like day and night at the NIH.

Dennis Mangan ended his career at the NIH as the head of the CFS Working Group at the NIH. You could argue that everything in his career lead him there, and that his experiences there have continue to inform his current activities.

With a Ph.D. in biology (dissertation – “Mannose sensitive interaction of Escherichia coli with human peripheral leukocytes in vitro“), Dennis did hard-core immune research for 15 years, before moving to the National Institute of Dental and Craniofacial Resarch (NIDCR) at the National Institutes of Health (NIH).

As director of the  Infectious Disease Program NIDCR Dennis engaged in numerous activities including identifying key research areas, designing major trans-NIH efforts on mucosal immunity, biofilms and the microbiome, leading the Human Microbiome Project, liasing with professional groups, developing funding opportunities, etc. A member of  Information Technology Advisory Committee, Dennis produced the first Listserv to provide infectious disease researchers with up to date  funding opportunities.

At the Office on Research on Women’s Health (ORWH) in 2009 Dennis developed strategic plans, identified opportunities for growth, etc., and chaired the NIH Working group on ME/CFS.   His commitment to open and effective communication was put to the test with a frustrated and often suspicious ME/CFS community that ended up embracing him.

Family issues prompted Dennis’s retirement, but he promised to stay engaged with the ME/CFS community, and he has. Now, as he joins the Scientific Advisory Board of the Simmaron Research Foundation, I asked him about the federal government and his work with Simmaron and the ME/CFS community.

Interview

“I never left” 

When you retired in late 2011 you promised to stay engaged with the Chronic Fatigue Syndrome community and you have. Since then  you’ve chaired a session at the FDA Workshop for ME/CFS, become an Advisory Board Member for the Stanford Chronic Fatigue Research Group, a Board Member for the IACFS/ME, and now the Simmaron Research Foundation.  That’s a lot of stuff. Am I missing anything?

That pretty much covers it.  In addition, since 2011, I took a variety of communication classes so that I might help scientists talk about their work with the public they serve and the people who support their research.  Public interactions, of course, have direct application to increasing the awareness of CFS and related disorders.

I give workshops in which the researchers learn to be more conversational, boil down complex data, explain their research briefly (elevator pitches), and talk about research in the form of stories instead of cold facts.  Improved communication will, I hope, help science become more transparent to everyone, including news media, legislators, funding agencies, administrators, donors, students, patients, family and friends.

I’m not sure helping out the sometimes surly ME/CFS community would fit into many people’s retirement plans.   You could surely have found easier subjects to be engaged with, yet you’ve committed a good chunk of energy to supporting this community.  Why? What has made you come back?

figures collaborating

Dennis Mangan’s forte has been bridging the gap between patient and researcher and bringing people together to work on disease.

I never left.  Helping connect the research scientists with the public has been my career for 30+ years.  There is much excitement and promise in what is happening in science right now (e.g., genomics, high throughput technologies, regenerative medicine, the microbiome, systems biology) and I see opportunities for that science to have direct impact on our understanding and treatment of CFS.  When I retired from civil service as an advisor to the NIH, I continued to talk with patients as well as researchers.  By learning more about how to communicate science to the public, I found a way to contribute to the progress in the CFS field.

You’re a past researcher, you’ve checked out the research on ME/CFS as well as disorders allied with it. Is there anything that really pops out for you? That says to you – this is what ME/CFS is all about?

Like many others, I am impressed with the findings related to disorders of the neuro-immune system and infectious diseases studies.  They seem to point to an abnormal response of the body to microbes (viruses or bacteria) that might ultimately serve as both biomarkers of disease and targets for treatment.   The similarity of some CFS features with other diseases suggests there might be common pathways.

My NIH colleagues and I strived for transparency in order to increase awareness for CFS at all levels of NIH leadership

You were the NIH representative and Chair of the ME/CFS working group at the NIH from 2010 to 2011 – a short time! – but you made a big impact. You enlarged the NIH Working Group on ME/CFS, created a Listserv, changed the name to ME/CFS, remade the NIH website, and communicated, communicated, communicated.  It seemed to me that you really had a vision that you wanted to accomplish and a big part of that involved communication. Can you speak about that?

NIH State of Knowledge cover pic

The State of the Knowledge Workshop on Chronic Fatigue Syndrome was the first ME/CFS focused Workshop sponsored by the DHHS in almost 10 years.

Communication was central to all of our activities.  My NIH colleagues and I strived for transparency in order to increase awareness for CFS at all levels of NIH leadership, among researchers and within the patient/advocate communities.  We all wanted to advance the science of CFS and to translate basic laboratory research into clinical practice.

As experienced program directors at NIH, we knew that exchange of ideas and scientific debate moves research fields forward.  To that end, in cooperation with leadership at the Office of Research on Women’s Health and the Office of the Director, the Working Group designed a unique State of the Knowledge workshop on CFS in April 2011.

The intent was to bring together basic and clinical researchers from many disciplines to share their knowledge and help point to where future research was headed.  It truly was a workshop.  The meeting generated great discussions and some collaboration.  It also emphasized the need for access to common data that spawned the goal of a shared database of clinical information.

The database, which we referred to as the CASA (i.e., home) project, is currently under construction.  Simmaron Research, with its wealth of clinical data, is a participating contributor.

Simmaron’s openness to working with other researchers makes them a great partner in studying and treating CFS.

Why did you chose the Simmaron Research Foundation to work with?

The CFS groups that I work with have common features.  They all have a passion to solve the mysteries of CFS using the best scientific principles.  They all value collaborative and cross-disciplinary research.  Simmaron incorporates these values in all their work.   The group has limited resources but leverages what they have with other laboratories.  In particular some of their biospecimens reach back almost 30 years and when shared with others can have spectacular impact on medical discovery.

SR Facebook logo new

Mangan cited Simmaron’s professionalism and willingness to creatively collaborate with other groups as two reasons for joining their board.

Although a small organization, Simmaron offers extensive clinical expertise and biospecimens for medical research.  Moreover, their clinics are designed to capture important information about CFS patients that could lead to better diagnosis and treatment.  I greatly admire their creative administrative structure, and the connection with a non-profit umbrella organization that maximizes resources and reduces operating expenses.

Simmaron’s openness to working with other researchers makes them a great partner in studying and treating CFS.  Simmaron is also committed to developing the next generation of CFS clinical researchers and has established an advanced training fellowship program for physicians.  Moreover, Simmaron has helped increase public awareness for CFS in many public sectors.

 

To my knowledge, never before has CFS taken such a front stage position within the Department.

Dr. Wanda Jones told me earlier this year that significant shifts in the federal governments attitude towards chronic fatigue syndrome (ME/CFS) have occurred, but that we, for the most part, don’t see them, in part because of the ongoing budget situation. Is that your experience? Did you see shifts in how ME/CFS was viewed when you were there?

Wanda Jones was a terrific resource and a friend to me.  She worked tirelessly to connect the various DHHS agencies’ efforts to address the needs CFS patients and researchers.  She was always down to earth, direct and honest with me, and did not pander to anyone.  I used her passion as a building block for my efforts at the NIH.  We all wanted more funding for CFS research and to encourage more scientists from multiple disciplines to enter the field.

My guess is that the changes I saw happening at the NIH are also happening at the DHHS now.  Deputy Secretary Howard Koh and Nancy Lee, Director of the Office of Women’s Health, are keeping CFS on the “radar screen” at the DHHS.  Sometimes even within the government we don’t know what is happening at all the agencies.  Koh is working to increase transparency within the DHHS  (e.g., when I was there he hosted monthly teleconference calls among the heads of key agencies involved in CFS.)   To my knowledge, never before has CFS taken such a front stage position within the Department.

People with ME/CFS look at NIH funding and they, honestly, want to scream. They feel abandoned and angry at the little support the federal government gives to this disorder. It’s not as if we’re alone, though.  Fibromyalgia, IBS, interstitial cystitus and other ‘allied disorders’ also get funding that is out of sync with their prevalence and the degree of suffering they cause.  These are all complex disorders that primarily affect woman and cause a lot suffering but don’t usually cause death.  Why do you think these types of disorders receive low amounts of funding relative  to other chronic illnesses?

I know…I received a few of those screams directly…but they did not land on deaf ears!  We might be one experiment or observation away from a breakthrough in CFS and every experiment is important.  The key to scientific credibility is to have validated biomarkers and targets for treatment.

This is why the XMRV story went viral: we finally had a target.  As a result, funding for CFS spiked in 2009 and several grants were awarded to study aspects of XMRV.  If we could reduce the scientific complexity of CFS (e.g., by having good biomarkers and targets for treatment), I suspect that more researchers would want to invest a career in studying it.  Such knowledge breeds an intellectual feeding-frenzy for research, new researchers and more funded grants.

 The NIH never moves as fast as I would like.

microbiome project

Dennis Mangan played a key role in launching the Human Microbiome Project to study the microbial populations present in humans. If Dr. Ian Lipkin is correct, the the gut microbiome may play a crucial role in ME/CFS.

If there’s one thing you’d like people with ME/CFS to know about federal government and its approach to chronic illness what would it be?

Patience and persistence is necessary.  The NIH never moves as fast as I would like.  For example, in the late 1990s, I recommended NIH support more projects on high-throughput sequencing of microbes in order to advance our understanding of both pathogens and the microbes that normally colonize our healthy bodies.  NIH leadership, many of my colleagues and some researchers were reluctant to support such projects, labeling them as fishing expeditions in which massive amounts of data would overwhelm existing computer technology, and waste funds and resources.

It took me six years working with likeminded colleagues at the NIH and other agencies to finally see the Human Microbiome Project (HMP) get funded ($173+ million to date).   Today, the HMP project is generating new technologies (e.g., faster computing software and hardware), new hypotheses of diseases and conditions (e.g., a better understanding of how gut microbes are involved in allergies and obesity), and a new generation of infectious disease researchers (e.g., Ian Lipkin.)

What could the chronic fatigue syndrome patient community be doing better to get its needs satisfied?

I have found the patient communities to be thoroughly engaged and eager to learn more about the pathophysiology of CFS.  Past history makes it hard for some patients and advocates to have hope for government support for their illness.   “Hardliner” skeptics are eager to create conspiracy theories for everything.

However, many patients and I understand the value of scientific principles and debate.  We saw science work with XMRV.  Yet, while the debate was ongoing, theories of the government hiding data abounded as scientists worked on replicating experiments and getting the truth out about XMRV.

What patients might not realize is that researchers also need hope and encouragement to move forward.  I encourage all of us to offer researchers a few kind words of support and to inspire them to keep working on the illness.

Besides more funding, what could the federal government be doing better to satisfy the needs of the ME/CFS community?

Resources for scientific discovery come in various forms.  My colleagues on the Trans-NIH ME/CFS Research Working Group understand this very well.  Although funding is always at the top of our list, we recognize other ways to support CFS research.  This includes support for research conferences; increasing awareness of the illness in the government, the medical communities and general public; support for training and career development; and public-private ventures to leverage limited financial resources.

The reasons for the Institute of Medicine and NIH evaluation of case definitions still puzzle me

Diagnosis

Dennis Mangan hopes the IOM projects are laying the ground for larger future initiatives

How important would having a federally recognized clinical or research definition be? Would that open doors that are now closed?

I think clinical and research definitions are extremely important for the future of the study and recognition of CFS.  Having a diagnosis take months, and needing to exclude so many other diseases and conditions, stifles understanding of the etiology and pathogenesis of CFS.  The current definitions could greatly be aided by a biomarker, and, with more research, these are gaining validation.

The reasons for the Institute of Medicine and NIH evaluation of case definitions still puzzle me.  However, I do know that the government as a basis for larger initiatives sometimes uses such evaluation reports.  I remain hopeful that the DHHS has such initiatives awaiting the outcome of these reports.

Gunnar Gottschalk Talks About CDC Collaboration

August 20, 2013

Watch as Simmaron Research Coordinator Gunnar Gottschalk describes our collaboration in the CDC clinical assessment study. Thank you Deborah Waroff and Llewellyn King at ME/CFS Alert for continuing to follow our research progress.

Recordings from Simmaron’s Roundtable: Scientifically Redefining ME/CFS

Simmaron’s Pre-FDA Workshop Roundtable: Scientifically Redefining ME/CFS, April 25, 2013

Simmaron Scientific Advisor Dr. Daniel Peterson hosted a roundtable discussion in the hours before the FDA’s Drug Development Workshop. He is joined by Dr. Nancy Klimas, Dr. Derek Enlander, Dr. Charles Lapp and Simmaron Researcher Gunnar Gottschalk to discuss state of the art diagnosis and clinical excellence in ME/CFS.

Read Cort Johnson’s Blog, Physicians Roundtable I: Diagnostics

Each of the recordings below is about 30 minutes long (the first is just a recording of the date).

Listen in on the field’s top experts at your own pace!

Scientifically Redefining ME/CFS Recording 1 – Date stamp (1 minute)

 

Scientifically Redefining ME/CFS Recording 2

 

Content:  Dr. Peterson opens the roundtable, discusses improvements in diagnostics and identifies immunological abnormalities that can be tested. He continues with a discussion of Natural Killer Cells and biological measures for treatment and improvement.

 

 Scientifically Redefining ME/CFS Recording 3

 
Content:  Dr. Klimas and Dr. Enlander discuss approaches to diagnosis and evaluation of ME/CFS patients.

 

Scientifically Redefining ME/CFS Recording 4

 

Content:  Drs. Peterson, Klimas, Enlander and Lapp begin an interactive discussion about the needs and approaches to clinical assessment.


 

Scientifically Redefining ME/CFS Recording 5

 

Content:  Drs Peterson, Klimas, Enlander and Lapp discusses biomarkers, treatments, outcome measures and misdiagnoses.

 

 

Scientifically Redefining ME/CFS Recording 6

 

Content:  Simmaron Research Coordinator Gunnar Gottschalk gives Cidofovir results presented at Paris HHV6/7 International Conference

 

 

Scientifically Redefining ME/CFS Recording 7

 

Content: Dr. Peterson and Mr. Gottschalk discuss Simmaron’s research activities for the last two years.

Patient Bob Miller Skydives to Raise Funds for Simmaron!

Taking Fundraising for ME/CFS Research to New Heights!

ME/CFS Patient Robert Miller and Research Coordinator Gunnar Gottschalk PARACHUTE from 13,000 feet to raise funds for Simmaron Research!  Simmaron has 2 new studies to help Scientifically Redefine ME/CFS, so Bob and Gunnar took to the skies on ME/CFS Awareness Day to inspire patients to invest in our science. Every amount helps!

Geronimo!!  Here goes Bob…

As Cort Johnson wrote before Bob jumped:

“Bob Miller can’t dance…he can’t run…he can’t even play baseball for ME/CFS – he’s not strong enough for that but he can fall, and May 12th, ME/CFS International Day, he’s going to fall a long way, very quickly, to raise money for ME/CFS research.”
Read more: Bob Miller Skydiving for ME/CFS Research on May 12th, International ME/CFS Day

Gunnar Gottschalk SkyDives to Raise Funds for Simmaron!

Taking Fundraising for ME/CFS Research to New Heights!

ME/CFS Patient Robert Miller and Research Coordinator Gunnar Gottschalk PARACHUTE from 13,000 feet to raise funds for Simmaron Research!  Simmaron has 2 new studies to help Scientifically Redefine ME/CFS, so Bob and Gunnar took to the skies to inspire patients to invest in our science.

Watch them jump, and help support our science. Every amount helps!

Geronimo!!  Here goes Gunnar…

FDA Drug Development Workshop Real Time Tweets

Below are Simmaron Research’s real time tweets from the FDA Drug Development Workshop on April 25th and April 26th last week. They are notes from most of the workshop sessions. While tweets usually have the most recent on top we have swapped this so the tweets here are in chronological order so you can follow the conversation from the beginning. If you are interested in more updates from Simmaron’s Twitter page you can follow us here @RedefiningMECFS.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Join our conversation on Twitter follow us here @RedefiningMECFS.