The Massachusetts ME/CFS & FM Association, a 501(c)3 founded in 1985, exists to meet the needs of patients with ME (Myalgic Encephalomyelitis), CFS (Chronic Fatigue Syndrome) or FM (Fibromyalgia), their families and loved ones. The Massachusetts ME/CFS & FM Association works to educate health-care providers and the general public regarding these severely-disabling physical illnesses. We also support patients and their families and advocate for more effective treatment and research.
- Last Updated: 26 November 2015 26 November 2015
By R. Sanderson
On June 20, 2009, the Connecticut CFIDS & FM Association sponsored a lecture by the internationally renowned Dr. Nancy Klimas. Dr. Klimas is a leading researcher and clinician for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS), Fibromyalgia (FM), as well as Gulf War Illness (GWI). The conference hall at the Crowne Plaza Hotel in Cromwell, CT was filled to capacity with patients and family members, many of whom had traveled a substantial distance to hear her presentation. This year the focus was to provide an "Update on Chronic Fatigue Syndrome and Fibromyalgia—From Research to Management". This summary will provide the highlights on new research developments, new discoveries, and better ways to manage the illnesses.
First and foremost, Dr. Klimas emphasized how important it is to develop well-coordinated clinical and treatment guidelines for ME/CFS. For example, when someone with ME/CFS goes to an emergency room, there are currently no guidelines in place to describe what might be the most beneficial intervention for this patient.
Something as simple as administering a saline IV is not common knowledge, even though this treatment can help to rehydrate, improve low blood volume or orthostatic hypotension, and stabilize a patient in an acute relapse. Klimas also recommends an extra liter of saline before surgery, to keep up blood volume during surgery, as well as after the procedure.
Dr. Klimas reviewed a few basic things such as reminding the audience that the 1994 clinical definition is still being used to diagnose ME/CFS. However, she thinks post-exercise fatigue should be viewed as one of the key symptoms of ME/CFS because this type of fatigue is distinctly unique to this illness.
The degree of debilitation in ME/CFS, according to Klimas, can be compared to the severity of active congestive heart failure. Contrary to earlier data and beliefs (that ME/CFS affects primarily white women), the occurrence of ME/CFS is found to be much higher in individuals of Hispanic and African-American origin and less frequent in those of Asian origin. One major problem remains in that as many as 85% of individuals who have ME/CFS are not diagnosed. People still find it very difficult to find physicians who are knowledgeable enough to recognize, diagnose and treat this illness.
Fibromyalgia (FM), on the other hand, is an illness that presents primarily as widespread pain in all quadrants of the body. In Dr. Klimas' opinion, it is easier to diagnose FM during a physical exam when following the FM diagnostic criteria. Unlike ME/CFS, it does not require the exclusion of so many other conditions in the diagnostic process. Recent FM research promotes a better understanding of the type of chronic pain experienced in FM—which is "centrally mediated". Pain in FM stems from the part of the brain which perceives pain as well as from increased sensory signals along the spinal cord. As a result, FM pain is not viewed as peripheral pain (i.e. pain resulting from injured tissues or chronic inflammation in joints) nor is it mediated by an immune system reaction.
Genomics research has greatly expanded over the past seven years (it is now possible to study 40,000 genes). This research methodology may assist in the recognition of many disease mechanisms. Specific gene patterns have been identified in ME/CFS—88 genes have been associated with ME/CFS and within these genes, there are 7 genomic subtypes.
Dr. Jonathan Kerr's team in London, UK was the first group of researchers to make this discovery in ME/CFS. They were even able to break down these clusters of genes into subtypes based on the number of activated genes and the characteristics and combination of dominant symptoms in each type. The subtypes correlate with the severity of symptoms.
The most severe subtype presents as 8 major symptom groups (i.e. pain, infections, musculoskeletal symptoms, gastrointestinal symptoms, neurological symptoms, neurocognitive symptoms, sleep-related symptoms, and anxiety/depression), while less severely impaired gene subtypes will have fewer symptom groups or will have one or two dominant symptom groups. All subtypes include fatigue.
Dr. Klimas believes this sort of research will provide the biomarkers for diagnosis and will identify better treatments. She has also been working very closely with Gulf War Illness (the troops who became ill after their deployment to the Persian Gulf during 1990-91) in which a number of abnormal gene patterns have also been identified. She mentioned that the incidence of ME/CFS is found to be 16-fold higher in individuals with GWI.
Dr. Klimas spoke about how gene activation does not happen on its own, but is greatly influenced by the state of a person's immune system. A lot also depends on "mediators"—substances or agents that will induce some type of biochemical activity—and the interaction of these mediators. In ME/CFS, various mediators may have triggered the disruption of the homeostasis of internal systems and mechanisms.
These systems would typically function within a range of values/set points, but when a mediator change, such as cytokine oversecretion, is encountered, this can throw the entire balance out of whack. So, what needs to be done in ME/CFS is to find a way to reset the "set points" in patients in order to bring patients back to a healthy (or at least, healthier) state.
Recently there has been an attempt to use mathematical models in ME/CFS research. The work of one scientist whose approach is unique and, Dr. Klimas feels, is most promising is that of Gordon Broderick, PhD, at the University of Alberta's Institute for Biomolecular Design. Dr. Boderick has applied his engineering skills to test and demonstrate the expression of certain gene patterns as well as to "map out" and evaluate the interaction of various systems in ME/CFS—particularly, in how these differ in ME/CFS patients compared to healthy individuals.
These advances in research methods and tools have left Dr. Klimas feeling increasingly more optimistic and excited about how ME/CFS can be evaluated and about how best to determine effective treatment interventions.
Using exercise challenge and then evaluating gene expression patterns or monitoring specific symptoms before, during and after exercise is one of the best ways to capture valuable data about ME/CFS.
Sustained activity will quickly start to demonstrate changes in cytokine secretion and show overactive or underactive immune or neuroendocrine responses, with the results in ME/CFS patients being quite the opposite of those found in healthy individuals (what should be turned on, is turned off, and vice versa).
Taking this a step further, the Pacific Fatigue Lab in Stockton, CA has developed a very effective exercise protocol for ME/CFS by testing patients' ability to produce energy while they are in a crash. This protocol requires that patients undergo a specific exercise routine on two consecutive days. It was discovered that some patients experienced up to a 50% drop in the amount of energy their bodies could produce on the second day.
Other researchers are investigating the roles of neuropeptide Y and CD26 in ME/CFS, especially since these markers are already used to evaluate and measure various biological processes (i.e. those in the cardiac, respiratory, immune, endocrine and nervous systems).
Viral persistence and reactivation continue to plague a segment of the ME/CFS population. For example, Human Herpes virus 6 (HHV-6) has been detected in the spinal fluid in 20% of ME/CFS patients (Peterson D). Epstein-Barr Virus-encoded dUTPase (that refers to deoxyuridine triphosphate nucleotidohydrolase) has been shown to induce immune dysregulation, to upregulate proinflammatory cytokines and in general, is thought to contribute to ME/CFS symptoms (Glaser R). Enterovirus has been detected in 60% of stomach tissue biopsies (Chia JKS) as well as in 13% of muscle biopsies done on CFS/FM patients (Douche-Aourik F). Therefore, these studies confirm the presence of enterovirus and/or human herpes viruses (like EBV, aka HHV-4, and HHV-6) in ME/CFS and FM.
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Notice about names
The Massachusetts ME/CFS & FM Association would like to clarify the use of the various acronyms for Chronic Fatigue Syndrome (CFS), Chronic Fatigue & Immune Dysfunction Syndrome (CFIDS) and Myalgic Encephalomyelitis (ME) on this site. When we generate our own articles on the illness, we will refer to it as ME/CFS, the term now generally used in the United States. When we are reporting on someone else’s report, we will use the term they use. The National Institutes of Health (NIH) and other federal agencies, including the CDC, are currently using ME/CFS.
Massachusetts ME/CFS & FM Association changed its name in July, 2018, to reflect this consensus.