Development of a recumbent isometric yoga program for patients with severe chronic fatigue syndrome/myalgic encephalomyelitis: A pilot study to assess feasibility and efficacy

Abstract:

BACKGROUND: Our previous randomized controlled trial demonstrated that isometric yoga in a sitting position reduces fatigue in patients with chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME). However, some patients experience difficulties sitting or practicing isometric yoga in a sitting position for long periods. To date, therapeutic interventions for patients with severe symptoms have not been established. Therefore, we developed a recumbent isometric yoga program, which takes approximately 20 min to complete, designed to reduce fatigue in patients with severe CFS/ME. The aim of this pilot study was to assess the feasibility, safety, and usefulness of this program.

METHODS: This pilot study included 12 adult patients with CFS/ME. Six patients were reluctant to practice isometric yoga in a sitting position because of the severity of their fatigue (group 1). The remaining six patients had previously practiced isometric yoga in a sitting position (group 2). For 3 months, the patients of both groups practiced recumbent isometric yoga every 2 to 4 weeks with a yoga instructor and at home on other days if they could. The short-term effects of isometric yoga on fatigue were assessed using the Profile of Mood Status (POMS) questionnaire immediately before and after their final session with the yoga instructor. The long-term effects of isometric yoga on fatigue were assessed using the Chalder Fatigue Scale (FS) questionnaire before and after the intervention period. Adverse events, satisfaction with the program, and preference of yoga position (sitting or recumbent) were also recorded.

RESULTS: All subjects completed the intervention. In both groups, the POMS fatigue score was significantly decreased after practicing the 20-min yoga program and the Chalder FS score was decreased significantly after the 3-month intervention period. There were no serious adverse events. All subjects in group 2 preferred the recumbent isometric yoga program over a sitting yoga program.

CONCLUSIONS: This study suggests that recumbent isometric yoga is a feasible and acceptable treatment for patients with CFS/ME, even for patients who experience difficulty practicing isometric yoga in the sitting position.

 

Source: Oka T, Wakita H, Kimura K. Development of a recumbent isometric yoga program for patients with severe chronic fatigue syndrome/myalgic encephalomyelitis: A pilot study to assess feasibility and efficacy. Biopsychosoc Med. 2017 Mar 3;11:5. doi: 10.1186/s13030-017-0090-z. ECollection 2017. https://www.ncbi.nlm.nih.gov/pubmed/28270860

 

Issues in Estimating Rates of Pediatric Chronic Fatigue Syndrome and Myalgic Encephalomyelitis in a Community-based Sample

Abstract:

There is a need to examine the prevalence of pediatric chronic fatigue syndrome (CFS) and Myalgic Encephalomyelitis (ME) in the general community, as well as the relative frequency of CFS and ME among various groups (e.g., different age groups, genders, racial/ethnic groups, and socioeconomic strata) and to compare these individuals with community controls.

In the present study, we describe an ongoing NIH-funded study, which uses a multiple-stage design, beginning with a brief screening for CFS- and ME-like symptomatology, followed by a more rigorous medical and psychiatric diagnostic evaluation to determine the prevalence of pediatric CFS and ME status in the general community. We provide two case studies showing the types of data we are collecting, and how the data are being used to inform diagnostic decisions.

 

Source: Jason LA, Katz BZ, Mears C, Jantke R, Brown A, Sunnquist M, O’Connor K. Issues in Estimating Rates of Pediatric Chronic Fatigue Syndrome and Myalgic Encephalomyelitis in a Community-based Sample. Avicenna J Neuropsychophysiol. 2015 Nov;2(4). pii: e37281. doi: 10.17795/ajnpp-37281. Epub 2015 Nov 21. https://www.ncbi.nlm.nih.gov/pubmed/28261672

 

The Neuroinflammatory Etiopathology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)

Abstract:

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a debilitating multi-systemic chronic illness of unknown etiology, classified as a neurological disorder by the World Health Organization (WHO). The symptomatology of the condition appears to emanate from a variety of sources of chronic neurological disturbance and associated distortions, and chronicity, in noxious sensory signaling and neuroimmune activation. This article incorporates a summary review and discussion of biomedical research considered relevant to this essential conception perspective. It is intended to provide stakeholders with a concise, integrated outline disease model in order to help demystify this major public health problem. The primary etiopathological factors presented are:

(A) Postural/biomechanical pain signaling, affecting adverse neuroexcitation, in the context of compression, constriction, strain, or damage of vertebral-regional bone and neuromuscular tissues;

(B) Immune mediated inflammatory sequelae, in the context of prolonged immunotropic neurotrophic infection-with lymphotropic/gliotropic/glio-toxic varieties implicated in particular;

(C) A combination of factors A and B. Sustained glial activation under such conditions is associated with oxidative and nitrosative stress, neuroinflammation, and neural sensitivity. These processes collectively enhance the potential for multi-systemic disarray involving endocrine pathway aberration, immune and mitochondrial dysfunction, and neurodegeneration, and tend toward still more intractable synergistic neuro-glial dysfunction (gliopathy), autoimmunity, and central neuronal sensitization.

 

Source: Glassford JA. The Neuroinflammatory Etiopathology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). Front Physiol. 2017 Feb 17;8:88. doi: 10.3389/fphys.2017.00088. eCollection 2017. http://journal.frontiersin.org/article/10.3389/fphys.2017.00088/full (Full article)

 

Clinical criteria versus a possible research case definition in chronic fatigue syndrome/myalgic encephalomyelitis

Abstract:

Background: The Institute of Medicine (IOM) recently developed clinical criteria for what had been known as chronic fatigue syndrome. Given the broad nature of the clinical IOM criteria, there is a need for a research definition that would select a more homogenous and impaired group of patients than the IOM clinical criteria. At the present time, it is unclear what will serve as the research definition.

Purpose: The current study focused on a research definition which selected homebound individuals who met the four IOM criteria, excluding medical and psychiatric co-morbidities.

Methods: Our research criteria were compared to those participants meeting the IOM criteria. Those not meeting either of these criteria sets were placed in a separate group defined by six or more months of fatigue. Data analyzed were from the DePaul Symptom Questionnaire and the 36-item Short-Form Health Survey (SF-36). Due to unequal sample sizes and variances, Welch’s F tests and Games-Howell post-hoc tests were conducted.

Results: Using a large database of over 1000 patients from several countries, we found that those meeting a more restrictive research definition were even more impaired and more symptomatic than those meeting criteria for the other two groups.

Conclusion: Deciding on a particular research case definition would allow researchers to select more comparable patient samples across settings, and this would represent one of the most significant methodologic advances for this field of study.

 

Source: Leonard A. Jason, Stephanie McManimen, Madison Sunnquist, Julia L. Newton & Elin Bolle Strand. Clinical criteria versus a possible research case definition in chronic fatigue syndrome/myalgic encephalomyelitis. Fatigue: Biomedicine, Health & Behavior. Published online: 06 Mar 2017

 

Characteristic chemical signature for chronic fatigue syndrome identified

Chronic fatigue syndrome (CFS) is a mysterious and maddening condition, with no cure or known cause. But researchers at the University of California San Diego School of Medicine, using a variety of techniques to identify and assess targeted metabolites in blood plasma, have identified a characteristic chemical signature for the debilitating ailment and an unexpected underlying biology: It is similar to the state of dauer, and other hypometabolic syndromes like caloric restriction, diapause and hibernation.

Dauer is the German word for persistence or long-lived. It is a type of stasis in the development in some invertebrates that is prompted by harsh environmental conditions. The findings are published online in the August 29 issue of PNAS.

“CFS is a very challenging disease,” said first author Robert K. Naviaux, MD, PhD, professor of medicine, pediatrics and pathology and director of the Mitochondrial and Metabolic Disease Center at UC San Diego School of Medicine. “It affects multiple systems of the body. Symptoms vary and are common to many other diseases. There is no diagnostic laboratory test. Patients may spend tens of thousands of dollars and years trying to get a correct diagnosis.”

As many as 2.5 million Americans are believed to have CFS. It most often afflicts women in their 30s to 50s, though both genders and all ages can be affected. The primary symptom is severe fatigue lasting at least six months, with corollary symptoms ranging from muscle pain and headaches to sleep and memory problems.

Naviaux and colleagues studied 84 subjects: 45 men and women who met the diagnostic criteria for CFS and 39 matched controls. The researchers targeted 612 metabolites (substances produced by the processes of metabolism) from 63 biochemical pathways in blood plasma. They found that individuals with CFS showed abnormalities in 20 metabolic pathways. Eighty percent of the diagnostic metabolites measured were decreased, consistent with hypometabolic syndrome or reduced metabolism. The diagnostic accuracy rate exceeded 90 percent.

“Despite the heterogeneity of CFS, the diversity of factors that lead to this condition, our findings show that the cellular metabolic response is the same in patients,” said Naviaux. “And interestingly, it’s chemically similar to the dauer state you see in some organisms, which kicks in when environmental stresses trigger a slow-down in metabolism to permit survival under conditions that might otherwise cause cell death. In CFS, this slow-down comes at the cost of long-term pain and disability.”

Naviaux said the findings show that CFS possesses an objectively identifiable chemical signature in both men and women and that targeted metabolomics, which provide direct small molecule information, can provide actionable treatment information. Only 25 percent of the metabolite disturbances found in each person were needed for the diagnosis of CFS. Roughly 75 percent of abnormalities were unique to each individual, which Naviaux said is useful in guiding personalized treatment.

“This work opens a fresh path to both understanding the biology of CFS and, more importantly to patients, a robust, rational way to develop new therapeutics for a disease sorely in need of them.”

The study authors noted additional research using larger groups of participants from diverse geographical areas is needed to validate both the universality and specificity of the findings.

 

Journal Reference: Robert K. Naviaux, Jane C. Naviaux, Kefeng Li, A. Taylor Bright, William A. Alaynick, Lin Wang, Asha Baxter, Neil Nathan, Wayne Anderson, Eric Gordon. Metabolic features of chronic fatigue syndrome. Proceedings of the National Academy of Sciences, 2016; 201607571 DOI: 10.1073/pnas.1607571113

 

Source: University of California – San Diego. “Characteristic chemical signature for chronic fatigue syndrome identified: Discovery, along with revealed underlying biology, could lead to faster, more accurate diagnoses and more effective, personalized therapies.” ScienceDaily. ScienceDaily, 29 August 2016. https://www.sciencedaily.com/releases/2016/08/160829163253.htm

 

Chronic fatigue syndrome is in your gut, not your head

Physicians have been mystified by chronic fatigue syndrome, a condition where normal exertion leads to debilitating fatigue that isn’t alleviated by rest. There are no known triggers, and diagnosis requires lengthy tests administered by an expert.

Now, for the first time, Cornell University researchers report they have identified biological markers of the disease in gut bacteria and inflammatory microbial agents in the blood.

In a study published June 23 in the journal Microbiome, the team describes how they correctly diagnosed myalgic encephalomyeletis/chronic fatigue syndrome (ME/CFS) in 83 percent of patients through stool samples and blood work, offering a noninvasive diagnosis and a step toward understanding the cause of the disease.

“Our work demonstrates that the gut bacterial microbiome in chronic fatigue syndrome patients isn’t normal, perhaps leading to gastrointestinal and inflammatory symptoms in victims of the disease,” said Maureen Hanson, the Liberty Hyde Bailey Professor in the Department of Molecular Biology and Genetics at Cornell and the paper’s senior author. “Furthermore, our detection of a biological abnormality provides further evidence against the ridiculous concept that the disease is psychological in origin.”

“In the future, we could see this technique as a complement to other noninvasive diagnoses, but if we have a better idea of what is going on with these gut microbes and patients, maybe clinicians could consider changing diets, using prebiotics such as dietary fibers or probiotics to help treat the disease,” said Ludovic Giloteaux, a postdoctoral researcher and first author of the study.

In the study, Ithaca campus researchers collaborated with Dr. Susan Levine, an ME/CFS specialist in New York City, who recruited 48 people diagnosed with ME/CFS and 39 healthy controls to provide stool and blood samples.

The researchers sequenced regions of microbial DNA from the stool samples to identify different types of bacteria. Overall, the diversity of types of bacteria was greatly reduced and there were fewer bacterial species known to be anti-inflammatory in ME/CFS patients compared with healthy people, an observation also seen in people with Crohn’s disease and ulcerative colitis.

At the same time, the researchers discovered specific markers of inflammation in the blood, likely due to a leaky gut from intestinal problems that allow bacteria to enter the blood, Giloteaux said.

Bacteria in the blood will trigger an immune response, which could worsen symptoms.

The researchers have no evidence to distinguish whether the altered gut microbiome is a cause or a whether it is a consequence of disease, Giloteaux added.

In the future, the research team will look for evidence of viruses and fungi in the gut, to see whether one of these or an association of these along with bacteria may be causing or contributing to the illness.

 

Journal Reference: Ludovic Giloteaux, Julia K. Goodrich, William A. Walters, Susan M. Levine, Ruth E. Ley, Maureen R. Hanson. Reduced diversity and altered composition of the gut microbiome in individuals with myalgic encephalomyelitis/chronic fatigue syndrome. Microbiome, 2016; 4 (1) DOI: 10.1186/s40168-016-0171-4

 

Source: Cornell University. “Chronic fatigue syndrome is in your gut, not your head.” ScienceDaily. ScienceDaily, 27 June 2016. https://www.sciencedaily.com/releases/2016/06/160627160939.htm

 

Chronic fatigue syndrome flare-ups caused by straining muscles and nerves

A recent study conducted by researchers at the University of Alabama at Birmingham and Johns Hopkins University School of Medicine published in PLOS ONE shows that symptoms of chronic fatigue syndrome, a complex and disabling multisystem disorder, can be provoked by imposing a mild to moderate strain to the muscles and nerves.

Eighty individuals, 60 with CFS and 20 without CFS, reported their levels of fatigue, body pain, lightheadedness, concentration difficulties and headache every five minutes while undergoing 15 minutes of either a passive supine straight leg raise — the raising and holding up of one of an individual’s legs while they lie on their back on an exam table — or a sham leg raise that did not cause strain.

Participants were contacted 24 hours later and again reported their symptoms. Compared to those with CFS who underwent the sham leg raise, individuals with CFS who underwent the passive leg raise that actually strained their muscles and nerves reported significantly increased body pain and concentration difficulties during the procedure. After 24 hours, these same individuals who underwent the true strain also reported greater symptom intensity for lightheadedness and the overall combined score for symptoms. The individuals with CFS who underwent the true strain also reported more symptoms during, and 24 hours after, the true strain compared to individuals without CFS.

“These findings have practical implications for understanding why exercise and the activities of daily living might be capable of provoking CFS symptoms,” said Kevin Fontaine, Ph.D., professor and chair of the UAB School of Public Health Department of Health Behavior and a co-author of the paper. “If simply holding up the leg of someone with CFS to a degree that produces a mild to moderate strain is capable of provoking their symptoms, prolonged or excessive muscle strain beyond the usual range of motion that occurs during daily activities might also produce symptom flares.”

As Peter Rowe, M.D., lead author and director of Johns Hopkins Children’s Center Chronic Fatigue Clinic, noted in the article, “The lengthwise strain applied to the nerves and muscles of the lower limb is capable of increasing symptom intensity in individuals with CFS for up to 24 hours, indicating that increased mechanical sensitivity may be a contributor to the provocation of symptoms in this disorder.”

Rowe and Fontaine, and their physical therapist collaborator Rick Violand, intend to extend this work to further understand the effects that strains to the muscles and nerves have on CFS, as well as whether specific physical therapy methods could be used to improve neuromuscular function to reduce symptoms.

Journal Reference: Peter C. Rowe, Kevin R. Fontaine, Megan Lauver, Samantha E. Jasion, Colleen L. Marden, Malini Moni, Carol B. Thompson, Richard L. Violand. Neuromuscular Strain Increases Symptom Intensity in Chronic Fatigue Syndrome. PLOS ONE, 2016; 11 (7): e0159386 DOI: 10.1371/journal.pone.0159386

 

Source: University of Alabama at Birmingham. “Chronic fatigue syndrome flare-ups caused by straining muscles and nerves.” ScienceDaily. ScienceDaily, 18 July 2016. https://www.sciencedaily.com/releases/2016/07/160718194125.htm

 

Further clues in the fight against chronic fatigue syndrome

New findings regarding the pathology of Chronic Fatigue Syndrome (CFS) are bringing Griffith University researchers closer to identifying the cause of this disabling illness.

This is the news from a team at the National Centre for Neuroimmunology and Emerging Diseases at the Menzies Health Institute Queensland.

Professors Marshall-Gradisnik and Don Staines and their research team have identified significant impairments in cellular function of people with CFS.

CFS — sometimes known as ME (myalgic encephalomyelitis) — is a complex illness characterized by impaired memory and concentration, metabolic, cardiac, gut and immune dysfunction and debilitating muscle pain and fatigue on exertion (also known as neuroimmune exhaustion).

It is estimated that the prevalence rate of CFS/ME worldwide is between 1 and 2 per cent.

“While the patho-mechanism of CFS/ME is unknown, these recent findings by NCNED researchers provide further evidence for the pathology of this illness,” says Professor Sonya Marshall-Gradisnik, who speaks as we approach International CFS Awareness Day on Thursday May 12.

Published in the Journal of Translational Medicine, the results report significant differences in intracellular signalling of cells with CFS patients.

“In this group, we see that dysfunctional signalling may contribute to impaired cell activity. These findings are consistent with our previous findings and align with the presentation of symptoms in patients,” says Professor Staines.

The current research findings build upon recent discoveries including novel identification of key genetic changes in cells of the immune system.

The NCNED — internationally recognised for research into CFS/ME — will present a seminar on current research findings on this disease on International CFS/ME Awareness Day, Thursday May 12 at Griffith University, Gold Coast Campus, commencing 1pm, location G17, Lecture theatre 3.

Griffith University will also be illuminating the Griffith Health Centre in blue to further help raise awareness for CFS/ME.

Journal Reference: Teilah Kathryn Huth, Donald Staines, Sonya Marshall-Gradisnik. ERK1/2, MEK1/2 and p38 downstream signalling molecules impaired in CD56dimCD16 and CD56brightCD16dim/− natural killer cells in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis patients. Journal of Translational Medicine, 2016; 14 (1) DOI: 10.1186/s12967-016-0859-z

 

Source: Griffith University. “Further clues in the fight against chronic fatigue syndrome.” ScienceDaily. ScienceDaily, 10 May 2016. https://www.sciencedaily.com/releases/2016/05/160510093906.htm

 

Chronic fatigue syndrome: Inherited virus can cause cognitive dysfunction and fatigue

Many experts believe that chronic fatigue syndrome (CFS) has several root causes including some viruses. Now, lead scientists Shara Pantry, Maria Medveczky and Peter Medveczky of the University of South Florida’s Morsani College of Medicine, along with the help of several collaborating scientists and clinicians, have published an article in the Journal of Medical Virology suggesting that a common virus, Human Herpesvirus 6 (HHV-6), is the possible cause of some CFS cases.

Over 95 percent of the population is infected with HHV-6 by age 3, but in those with normal immune systems the virus remains inactive. HHV-6 causes fever and rash (or roseola) in infants during early childhood, and is spread by saliva. In immunocompromised patients, it can reactivate to cause neurological dysfunction, encephalitis, pneumonia and organ failure.

“The good news reported in our study is that antiviral drugs improve the severe neurological symptoms, including chronic pain and long-term fatigue, suffered by a certain group of patients with CFS,” said Medveczky, who is a professor of molecular medicine at USF Health and the study’s principal investigator. “An estimated 15,000 to 20,000 patients with this CFS-like disease in the United States alone may ultimately benefit from the application of this research including antiviral drug therapy.”

The link between HHV-6 infection and CFS is quite complex. After the first encounter, or “primary infection,” all nine known human herpesviruses become silent, or “latent,” but may reactivate and cause diseases upon immunosuppression or during aging. A previous study from the Medveczky laboratory showed that HHV-6 is unique among human herpesviruses; during latency, its DNA integrates into the structures at the end of chromosomes known as telomeres.

Furthermore, this integrated HHV-6 genome can be inherited from parent to child, a condition commonly referred to as “chromosomally integrated HHV-6,” or CIHHV-6. By contrast, the “latent” genome of all other human herpesviruses converts to a circular form in the nucleus of the cell, not integrated into the chromosomes, and not inheritable by future generations.

Most studies suggest that around 0.8 percent of the U.S. and U.K. population is CIHHV6 positive, thus carrying a copy of HHV-6 in each cell. While most CIHHV-6 individuals appear healthy, they may be less able to defend themselves against other strains of HHV-6 that they might encounter. Medveczky reports that some of these individuals suffer from a CFS-like illness. In a cohort of CFS patients with serious neurological symptoms, the researchers found that the prevalence of CIHHV-6 was over 2 percent, or more than twice the level found in the general public. In light of this finding, the authors of the study suggest naming this sub-category of CFS “Inherited Human Herpesvirus 6 Syndrome,” or IHS.

Medveczky’s team discovered that untreated CIHHV-6 patients with CFS showed signs that the HHV-6 virus was actively replicating: determined by the presence of HHV-6 messenger RNA (mRNA), a substance produced only when the virus is active. The team followed these patients during treatment, and discovered that the HHV-6 mRNA disappeared by the sixth week of antiviral therapy with valganciclovir, a drug used to treat closely related cytomegalovirus (HHV-5). Of note, the group also found that short-term treatment regimens, even up to three weeks, had little or no impact on the HHV-6 mRNA level.

The investigators assumed that the integrated virus had become reactivated in these patients; however, to their surprise, they found that these IHS patients were infected by a second unrelated strain of HHV-6.

The USF-led study was supported by the HHV-6 Foundation and the National Institutes of Health.

Further studies are needed to confirm that immune dysregulation, along with subsequent chronic persistence of the HHV-6 virus, is the root cause of the IHS patients’ clinical symptoms, the researchers report.

Journal Reference: Shara N. Pantry, Maria M. Medveczky, Jesse H. Arbuckle, Janos Luka, Jose G. Montoya, Jianhong Hu, Rolf Renne, Daniel Peterson, Joshua C. Pritchett, Dharam V. Ablashi, Peter G. Medveczky. Persistent human herpesvirus-6 infection in patients with an inherited form of the virus. Journal of Medical Virology, 2013; DOI:10.1002/jmv.23685

 

Source: University of South Florida (USF Health). “Chronic fatigue syndrome: Inherited virus can cause cognitive dysfunction and fatigue.” ScienceDaily. ScienceDaily, 26 July 2013. https://www.sciencedaily.com/releases/2013/07/130726092427.htm

 

New light shed on cause of chronic fatigue syndrome

New research findings may shed new light on the potential cause of Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME).

Researchers from Griffith University’s National Centre for Neuroimmunology and Emerging Diseases (NCNED) — part of the new Menzies Health Institute Queensland — have uncovered significant factors contributing to the pathology of this illness.

The results reveal genetic changes in important receptors associated with immunological and cellular function and contribute to the development of this complex illness.

“These findings have been achieved through a team effort involving researchers, patients, funding bodies, clinicians and the support of Griffith University and the Queensland Government,” say chief investigators Professor Sonya Marshall-Gradisnik and Professor Donald Staines.

Co-researcher and consultant immunologist Professor Pete Smith said that important signalling mechanisms are disrupted as a result of these genetic changes involving the detection and response to threats.

“These are primitive genes that are involved in many cellular signals in the brain, gut, cardiovascular and immune systems, as well as in the mediation of pain.”

These research findings coincide with International Neuroimmune Awareness week commencing Monday 11 May.

The Griffith Health Centre on the university’s Gold Coast campus is being lit up each evening from 10 -12 May to raise awareness of neurological conditions such as CFS/ME as well as other conditions such as Fibromyalgia and Gulf War Syndrome.

“The lighting up of the Griffith Health Centre signifies Griffith’s commitment to the CFS patient community and our team approach to this research,” says Pro-Vice Chancellor (Health) Professor Allan Cripps.

CFS/ME is a highly debilitating disorder characterized by profound fatigue, muscle and joint pain, cerebral symptoms of impaired memory and concentration, impaired cardiovascular function, gut disorder and sensory dysfunction such as noise intolerance and balance disturbance. Many cases can continue for months or years. It is believed to affect around 250,000 Australians.

The research findings are to be presented at an international conference in London later this month.

Journal Reference: Sonya Marshall-Gradisnik, Donald Staines, Pete Smith, Bernd Nilius, Ekua Brenu, Sandra Ramos. Examination of Single Nucleotide Polymorphisms (SNPs) in Transient Receptor Potential (TRP) Ion Channels in Chronic Fatigue Syndrome Patients. Immunology and Immunogenetics Insights, 2015; 1 DOI: 10.4137/III.S25147

 

Source: Griffith University. “New light shed on cause of chronic fatigue syndrome.” ScienceDaily. ScienceDaily, 11 May 2015. https://www.sciencedaily.com/releases/2015/05/150511172755.htm