Research project to evaluate daily activity patterns and heart rate

Posted on 06/25/2016 by wames

Newswise Stony Brook University blog post, by …, 23 June 2016: Getting to the Heart of Chronic Fatigue Syndrome

Stony Brook researcher receives $1.5 million NIH grant to evaluate daily activity patterns and heart rate of those who suffer from this debilitating illness

By better understanding daily activity levels and heart rate patterns of those who suffer from Chronic Fatigue Syndrome (CFS), scientists hope to discover more about this complex illness condition. Fred Friedberg, PhD, Associate Professor of Psychiatry at Stony Brook University School of Medicine, has received a four-year $1.5 million grant from the National Institutes of Health to take this research approach to determine if heart rate fluctuations in combination with certain daily activity patterns can be used to predict or prevent relapse in people with CFS.

According to Dr. Friedberg, also the President of the International Association for Chronic Fatigue Syndrome/Myalgic Encephalomyelitis, CFS affects some one million people in the United State and millions worldwide. This condition is characterized by a state of chronic fatigue and other debilitating symptoms, such as post-exertional collapse and cognitive difficulties. These symptoms and related impairments persist for more than six months and have no clearly identified cause.

This study will involve patients self-reporting their symptoms and activities on a weekly online diary over a period of six months. Data will also be recorded from mobile heart devices and activity monitors that the patients wear at home. Over the six month study period, patients will regularly send this objective data back to the Stony Brook laboratory where the information will be downloaded and analyzed for patterns related to CFS symptoms, activities, and impairments. The participants will then be interviewed by a psychiatric nurse via phone about other potentially important illness factors including major life events they have experienced over the study period, their physical and social functioning, and changes in their illness status – i.e., improved or worsened.

“What is promising is that we have proposed an illness model to potentially identify the factors that lead to relapse or improvement,”  said Dr. Friedberg. “If a predictor of relapse is discovered, such as heart rate variability in conjunction with certain activity patterns, we may be able to prevent or reduce relapse by adjusting such activity patterns in advance. This could potentially be the first biomarker of illness worsening or improvement in this illness.”

Dr. Friedberg expects that the data collected from the study will be used to generate a new, potentially more effective self-management program that ultimately helps patients avoid relapses and feel and function better.

About Stony Brook University
Part of the State University of New York system, Stony Brook University encompasses 200 buildings on 1,450 acres. Since welcoming its first incoming class in 1957, the University has grown tremendously, now with more than 25,000 students and 2,500 faculty.
Its membership in the prestigious Association of American Universities
(AAU) places Stony Brook among the top 62 research institutions in North America. U.S. News & World Report ranks Stony Brook among the top 100 universities in the nation and top 40 public universities, and Kiplinger names it one of the 35 best values in public colleges. One of four University Center campuses in the SUNY system, Stony Brook co-manages Brookhaven National Laboratory, putting it in an elite group of universities that run federal research and development laboratories. A global ranking by U.S. News & World Report places Stony Brook in the top 1 percent of institutions worldwide. It is one of only 10 universities nationwide recognized by the National Science Foundation for combining research with undergraduate education. As the largest single-site employer on Long Island, Stony Brook is a driving force of the regional economy, with an annual economic impact of $4.65 billion, generating nearly 60,000 jobs, and accounts for nearly 4 percent of all economic activity in Nassau and Suffolk counties, and roughly 7.5 percent of total jobs in Suffolk County.

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CFS following low-level radiation exposure

Posted on 06/24/2016 by wames

2 articles about the effects of low-level radiation are on the National CFIDS Foundation website at

Health of Liquidators (Clean-up Workers) 20 Years after the Chernobyl explosion

Chronic Fatigue Syndrome is one of the most important consequences of radioecological disaster resulting in an interaction of different hazardous environmental factors. CFS can be considered as an environmentally induced predisposition and vestige of forthcoming neurodegeneration that included cognitive impairment.  Increased incidence of CFS has been seen in exposed populations in Chernobyl, Hiroshima and Nagasaki.

Health Effects of Chernobyl and Fukushima: 30 and 5 years down the line

The article was commissioned by Greenpeace of Belgium.

A prospective study of personnel working on transformation of the Chernobyl NPP Object “Shelter” into an ecologically safe system showed that exposure to radiological (0–56.7 mSv, М±SD:19.9±13.0 mSv dose) and industrial risk factors may lead to the onset of cognitive CFS characterized by a dysfunction of cortical-limbic system mainly in the dominant (left) hemisphere with an important involvement of hippocampus. page 45

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PACE trial cost-effectiveness conclusions faulty

Posted on 06/24/2016 by wames

Health rising blog post, by Cort Johnson, 31 May 2016: Another Ball Drops in PACE Controversy: Cost-effectiveness Conclusions Faulty – Plus Update

Some past efforts to clear up the controversies around the now notorious PACE trials have requested that the authors release the raw data to researchers to be re-analyzed. Not so this time. In the latest ball to drop for the PACE studies, MEAction reported that five researchers including Ron Davis, two biostatisticians and an epidemiologist requested that the PLOS One Journal simply delete a finding they assert the papers own figures indicate is incorrect.

The paper in question is “Adaptive Pacing, Cognitive Behaviour Therapy, Graded Exercise, and Specialist Medical Care for Chronic Fatigue Syndrome: A Cost-Effectiveness Analysis.”

The finding is not a minor one. It asserts that the authors conclusion that the CBT/GET protocols used in the study were, from a societal perspective, cost/effective was incorrect. One of the main goals of the PACE Trial, was to demonstrate to the UK government and other funding bodies that they would get the most bang from their buck with ME/CFS by employing CBT/GET.

The PACE trial protocols called for sensitivity analyses that examined cost-effectiveness from a several scenario’s including CBT/GET’s ability to reduce the amount of home care provided by professional home care providers or by family members either paid a minimum wage or no wages.

The paper report that the societal benefits outweighed the costs of CBT/GET under any of these scenario’s was inaccurate. CBT/GET was only determined to be cost-effective from a societal perspective if the authors treated family caregivers as if they being paid as if they were home care providers. Under the other scenario’s it was not. It was another case of the authors stretching their findings beyond the breaking point.

As with other instances patient advocates played a major role in getting the word out about PACE trial problems.

Simon McGrath,Tom Kindlon and other ME/CFS advocates took the authors to task regarding a number of their conclusions. Using figures from one of the CBT/GET centers used in the trial Kindlon demonstrated that the PACE authors underestimated the cost of GET treatments by as much as 300% (if I’m reading it correctly). At that cost of treatment the CBT/GET doesn’t begin to pay for the advantages it provides.

The Davis paper simply asks that the paper be changed to reflect what Davis and other believe the authors have already admitted; that only if you treat the value of family members time as if they were paid home care providers, do the conclusions make any sense.

PACE Controversy Update

The Lancet Study – Over ten studies have emanated from the PACE trial thus far. The first was published in The Lancet; one of the oldest and most prestigious medical journals in the world. In Nov. 2015 Ron Davis, Lenny Jason, Vincent Racaniello and others posted a open letter to Lancet asking that independent analyses of the PACE trial be redone using outside researchers.

We therefore urge The Lancet to seek an independent re-analysis of the individual-level PACE trial data, with appropriate sensitivity analyses, from highly respected reviewers with extensive expertise in statistics and study design. The reviewers should be from outside the U.K. and outside the domains of psychiatry and psychological medicine. They should also be completely independent of, and have no conflicts of interests involving, the PACE investigators and the funders of the trial.

Horton replied that he was traveling and would get to the issue. Three months later after Horton had still not replied another letter went out with three dozen more signatories. It’s now six months later and Horton has still not replied.

The PLOS Study – The complaints began soon after the present paper was published in 2012. In Dec. 2015 PLOS stated that it expected the study authors to share the study data, and that they were doing their own internal investigation using outside experts to help them evaluate the issues.

In March, 2016 PLOS stated they had determined which data they believed should be shared and had requested the authors share it.

University – Jennie Spotila reported that the University sponsoring the study refused, citing the privacy needs of the participants and “prejudice to the programme”, to provide the raw study data (was it not anonymized?) to Vincent Racaniello and others. An appeal has been filed.

Conclusion

The PACE trial authors and the journals publishing their studies appear to be engaged in a waiting game in hopes the controversy will simply disappear over time. Until that happens they are ignoring requests or simply ignoring major issues.

David Tuller has tried and failed to have substantive, or in most cases, any conversations with the PACE trial authors. He and others have also contacted the journals the papers were been published in. When they do go on record – which is rare – Tuller reports they are evasive and provide misleading answers.

An investigative reporter of long standing Tuller has seen a lot, but even he seems taken aback by the unwillingness of the PACE authors or their publishers to address the legitimate issues that have been raised.

They appeared to excel at avoiding hard questions, ignoring inconvenient facts, and misstating key details. I was surprised and perplexed that smart journal editors, public health officials, reporters and others accepted their replies without pointing out glaring methodological problems—such as the bizarre fact that the study’s outcome thresholds for improvement on its primary measures indicated worse health status than the entry criteria required to demonstrate serious disability.

Jenny Spotila reported that Racaniello has little faith in the journals doing the right thing:

“I think they are going to ignore, obfuscate, and give their usual responses until we are all dead. I don’t have hope that the PACE authors, or Lancet, will respond in any meaningful way until there is more of an outcry.” Vincent Racaniello

The battle is not over by an means, however. The key to getting Lancet and the other publishers to act is simply getting more researchers to join in the fray and keeping the pressure on.

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Circulatory Impairment in ME

Posted on 06/23/2016 by wames

ME Advocacy Blog post extract, 14 June 2016: Circulatory Impairment in Myalgic Encephalomyelitis: A Preliminary Thesis, by Maryann Spurgin, Ph.D.

Here is my proposal:
For many years, I have followed and collated research on Myalgic Encephalomyelitis (ME), in particular on the circulatory impairment of which Dr. A. Melvin Ramsay spoke and of which there are many recently discovered facets. Despite lack of research on circulatory impairment in ME in the 1950’s, Dr. A. Melvin Ramsay astutely observed it clinically as one of the three essential components of ME, noting pale, cold skin as a sign.

Sixty years later, the research behind these observations is now extensive, although some of that research was published under the name “CFS”; yet it applies to patients with ME or those with ME who are misdiagnosed with “CFS,” itself a govt construct that, as noted above, has impeded consistent findings. My view is that “CFS” is a government construct.

There are people with everything from MS to fibromyalgia to depression to ME who are diagnosed with “CFS.” So there are not two separate diseases, ME and “CFS”; rather, those diagnosed with “CFS” have something else in need of diagnosis, whether ME or another disease. Much of the research on ME was done under the name “CFS.”

I have spent 22 years studying circulatory impairment in ME by reading published research on its many facets, beginning over 20 years ago with Dr. L.O. Simpson’s work on impaired capillary blood flow [1], the haematological/ hemorheological flow problems that impede delivery of oxygen and nutrients to organs and tissues and impede removal of lactic acid, toxins and metabolic waste due to poorly deformable Red Blood Cells.

Much later, in the 1990’s, Dr. David Bell’s and the late Dr. David Streeten’s joint work on low blood volume (hypovolemia) in ME was published [2, 3]. Dr. Streeten was a world-renowned endocrinologist whose area of specialization was blood pressure and orthostatic disorders.

The third aspect of circulatory impairment is cardiac:

The late Dr. A. Martin Lerner pioneered it, with his hypothesis that the disease is a viral cardiomyopathy. He found on biopsies virally infected cardiac myocytes in the disease, published in the 1990’s [4-6]. He argued that the disease is at its root a viral cardiomyopathy.

Importantly, there was also NIH grant-funded research by Drs Benjamin Natelson and Arnold Peckerman on abnormal impedance cardiography and other cardiac abnormalities in ME patients [7]. These important studies influenced researcher/clinician Dr. Paul Cheney, who found and illuminated problems with cardiac diastolic dysfunction in the disease (diastolic problems not caused by volume depletion but by a pathology in the heart itself), following his own experience with heart failure and his subsequent heart transplant.

This extensive body of research shows that, without identifying the root cause of ME, disorders of microcirculation and macrocirculation are well established pathophysiological findings [8-11], and that combined circulation problems can conspire to create havoc in the heart and other organs of the body.

I have thought a lot about circulatory problems over many years, and how these impairments come together to create the intolerable symptomatology of ME that could lead someone to be so impaired as to not be able to swallow, and could lead the Institute of Medicine to declare that organ failure, even death, can occur from the slightest exertion and/or sensory overload.

This happens, I believe, when one or more or all of the following three conditions hold:

  1. Metabolic demand exceeds the capacity for cardiac output. Studies have shown that if the level of exertion or metabolic demand on the heart exceeds the capacity of the heart to pump blood by even 1%, the organism dies. Rest and limiting demands on a heart whose output is reduced by disease is crucial to survival.
  2. An impaired RBC/capillary delivery system is present (My own theory is that this impairment may be a defense mechanism to slow metabolic demand in order to protect the heart); And…
  3. When low blood volume is present.

One of these impairments alone could cause havoc, but the three of these pathophysiologies together could lead to extreme multisystem involvement and death. In a patient who is already volume depleted, poor diastolic filling from still another, cardiac problem could be doubly dangerous, yet this is exactly what Dr. Cheney has found.

Although this research does not hypothesize a cause, and circulation problems are likely the result of some underlying (likely viral) cause, this particular aspect of the pathophysiology, I believe, is crucial to a biological understanding of ME, and to explaining why ME patients relapse and can die from exertion. Mitochondrial problems that are not primary mitochondrial disease but are an epiphenomenon of the (unknown) cause or causes likely also play a role, especially in cardiac and brain dysfunction (see the home page of my website that discusses mitochondrial epiphenomena and the references I provided on the site).

 

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A new approach for investigating mitochondrial DNA in ME

Posted on 06/23/2016 by wames

Research abstract:

In mitochondrial research, many investigators have examined the association between mitochondrial DNA (mtDNA) variants in rare as well as common complex diseases. Previous studies at the CHM (NWU) detected three known pathogenic mtDNA variants (m.7497G>A, m.9185T>C and m.10197G>A) at low allele frequencies in a number of patients diagnosed with myalgic encephalomyelitis (ME).

Since no diagnostic examinations or conclusive treatments currently exist for ME, an association between ME and known pathogenic variants, or a cumulative effect of rare non-synonymous variants (pathogenicity score) on ME, could provide valuable insights into understanding the causes of ME.

Literature shows contradicting data regarding the role of mitochondrial dysfunction in ME, and while uncommon mtDNA deletions have been reported, the three known pathogenic mtDNA variants introduced here have not previously been observed in ME patients (but were later identified as sequencing artefacts in the duration of this study), nor has the combined effect of numerous rare non-synonymous variants on the mitochondrial bioenergetics of ME patients been assessed.

To do this, cytoplasmic hybrid (cybrid) cells were developed by fusing ρ0 (mtDNA-depleted) cells with healthy control and ME patient‟s blood platelets (containing solely mtDNA). These cybrid cells were used for mitochondrial bioenergetic analyses, using a Seahorse XFe96 analyser, and for determination of the relative mtDNA copy number (RMCN), using real-time PCR.

In addition, conditions for analysing selected cell lines (including the cybrids) using the Seahorse XFe96 analyser were optimized. While no apparent bioenergetic irregularities were observed in ME patient cybrids compared to healthy controls, an increased pathogenicity score appeared to be associated with a decrease in ATP production and a decreased electron transport system (ETS) capacity in ME patients.

This new approach for investigating mtDNA variants and a common complex disease may provide new insights into the diagnostic and causative factors of ME.

Evaluating the involvement of mtDNA variants in patients diagnosed with myalgic encephalomyelitis, by Hayley Christy Van Dyk. MSc Dissertation, North-West University (South Africa), May 2016 [Published 8 June 2016]

 

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Complementary & alternative healthcare use by participants in PACE trial

Posted on 06/22/2016 by wames

Research abstract:

Background:
Chronic Fatigue Syndrome (CFS) is characterised by persistent fatigue, disability and a range of other symptoms. The PACE trial was randomised to compare four non-pharmacological treatments for patients with CFS in secondary care clinics. The aims of this sub study were to describe the use of complementary and alternative medicine (CAM) in the trial sample and to test whether CAM use correlated with an improved outcome.

Method
CAM use was recorded at baseline and 52 weeks. Logistic and multiple regression models explored relationships between CAM use and both patient characteristics and trial outcomes.

Results:
At baseline, 450/640 (70%) of participants used any sort of CAM; 199/640 (31%) participants were seeing a CAM practitioner and 410/640 (64%) were taking a CAM medication. At 52 weeks, those using any CAM fell to 379/589 (64%). Independent predictors of CAM use at baseline were female gender, local ME group membership, prior duration of CFS and treatment preference. At 52 weeks, the associated variables were being female, local ME group membership, and not being randomised to the preferred
trial arm. There were no significant associations between any CAM use and fatigue at either baseline or 52 weeks. CAM use at baseline was associated with a mean (CI) difference of 4.10 (1.28, 6.91; p=0.024) increased SF36 physical function score at 52 weeks, which did not reach the threshold for a clinically important difference.

Conclusion
CAM use is common in patients with CFS. It was not associated with any clinically important trial outcomes.

Complementary and alternative healthcare use by participants in the PACE trial of treatments for chronic fatigue syndrome, by G. Lewith, B. Stuart, T. Chalder,  C. McDermott, P.D. White in Journal of Psychosomatic Research Vol 87, pp 37-42 [Available online 10 June 2016]

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More in-depth mitochondrial testing in ME/CFS proposed

Posted on 06/22/2016 by wames

Blog post by Cort Johnson in Health Rising forum, 20 June 2016: Researchers Call For More In-depth Mitochondrial Testing in Chronic Fatigue Syndrome (ME/CFS)

More Extensive Mitochondrial Testing Proposed

A letter to the editor of the BioMed Central Journal urged more in depth mitochondrial testing than has been done be done in ME/CFS. The letter referred to a study done by an ME/CFS researcher, Maureen Hanson, and funded by the Chronic Fatigue Initiative.

The CFI is very interested in the mitochondria and it is funding more research by Dr. Hanson – so they made an honest effort to find something. They did find something, but the results were not particularly encouraging.

Results

No ME/CFS subject exhibited known disease-causing mtDNA mutations. Extent of heteroplasmy was low in all subjects. Although no association between mtDNA SNPs and ME/CFS vs. healthy status was observed, haplogroups J, U and H as well as eight SNPs in ME/CFS cases were significantly associated with individual symptoms, symptom clusters, or symptom severity.

Conclusions

Analysis of mitochondrial genomes in ME/CFS cases indicates that individuals of a certain haplogroup or carrying specific SNPs are more likely to exhibit certain neurological, inflammatory, and/or gastrointestinal symptoms. No increase in susceptibility to ME/CFS of individuals carrying particular mitochondrial genomes or SNPs was observed.

The two researcher researchers proposed that study into the mitochondria in ME/CFS be deepened. They proposed

  • that nuclear DNA (nDNA) be studied (as well as mtDNA)
  • that parts of the mitochondria other than the respiratory chain such as betaoxidation, hem synthesis, calcium handling, coenzyme-Q metabolism, or the urea cycle be examined
  • that analyses be done on other than blood lymphocytes
  • that immune-histological and biochemical examinations of muscle biopsies be done. In fact, they said these types of investigations “were essential not to miss dysfunction of the respiratory chain or other mitochondrial pathways.

The mitochondria are known to be very complex. In fact, one of the problems facing the field apparently is just how complex they are and this letter reflected that.

Mitochondria Affected – But Not the Problem?

Maureen Hanson is at work on another mitochrondrial study and we should know more soon from Ron Davis and Robert Naviaux when their paper gets published. Their findings, by the way, do not necessarily suggest that the mitochondria are broken. My understanding is that it’s more likely that the mitochondria are fine, but that something in the blood is turning them off in ME/CFS patients. (The same may apply with NK cells).

Absent some genetic abnormality it’s been hard for me to understand how the mitochondria across the body get damaged unless by something in the blood. The good news is that given the dearth of drug options for mitochondrial problems a problem in the blood seems like a far, far easier problem to deal with than an issue in the mitochondria themselves.

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CBT for CFS: differences in outcomes in the UK & Netherlands

Posted on 06/21/2016 by wames

Research abstract:

Objective:
Cognitive behaviour therapy (CBT) reduces fatigue and disability in chronic fatigue syndrome (CFS). However, outcomes vary between studies, possibly because of differences in patient characteristics, treatment protocols, diagnostic criteria and outcome measures. The objective was to compare outcomes after CBT in tertiary treatment centres in the  Netherlands (NL) and the United Kingdom (UK), using different treatment protocols but identical outcome measures, while controlling for differences in patient characteristics and diagnostic criteria.

Methods:
Consecutively referred CFS patients who received CBT were included (NL: n=293, UK: n=163). Uncontrolled effect sizes for improvement in fatigue (Chalder Fatigue Questionnaire), physical functioning (SF-36 physical functioning subscale) and social functioning (Work and Social Adjustment Scale) were compared. Multiple regression analysis was used to examine whether patient differences explained outcome differences between centres.

Results:
Effect sizes differed between centres for fatigue (Cohen’s D NL=1.74, 95% CI=1.52-1.95; UK=0.99, CI=0.73-1.25), physical functioning (NL=0.99, CI=0.81-1.18; UK=0.33, CI=0.08-0.58) and social functioning (NL=1.47, CI=1.26-1.69; UK=0.61, CI=0.35-0.86). Patients in the UK had worse physical functioning at baseline and there were minor demographic differences. These could not explain differences in centre outcome.

Conclusion:
Effectiveness of CBT differed between treatment centres. Differences in treatment protocols may explain this and should be investigated to help further improve outcomes.

Cognitive behaviour therapy for chronic fatigue syndrome: Differences in treatment outcome between a tertiary treatment centre in the United Kingdom and the Netherlands, by M. Worm-Smeitink, S. Nikolaus, K. Goldsmith, J. Wiborg, S. Ali, H. Knoop, T. Chalder in Journal of Psychosomatic Research, August 2016 Vol 87, pp 43–49 [June 11, 2016 Preprint]

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The psychological impact of dependency in adults with CFS/ME

Posted on 06/21/2016 by wames

Research abstract:

Chronic fatigue syndrome/myalgic encephalomyelitis can limit functional capacity, producing various degrees of disability and psychological distress.

Semi-structured interviews explored the experiences of adults with chronic fatigue syndrome/myalgic encephalomyelitis being physically dependent on other people for help in daily life, and whether physical dependency affects their psychological well-being.

Thematic analysis generated six themes: loss of independence and self-identity, an invisible illness, anxieties of today and the future, catch-22, internalised anger, and acceptance of the condition.

The findings provide insight into the psychological impact of dependency. Implications for intervention include better education relating to chronic fatigue syndrome/myalgic encephalomyelitis for family members, carers, and friends; ways to communicate their needs to others who may not understand chronic fatigue syndrome/myalgic encephalomyelitis; and awareness that acceptance of the condition could improve psychological well-being.

The psychological impact of dependency in adults with chronic fatigue syndrome/myalgic encephalomyelitis: A qualitative exploration, by AM Williams, G Christopher, E Jenkinson in J Health Psychol. 2016 Apr 19. pii [Epub ahead of print]

Comment by ME Research UK: This is a valuable piece of qualitative research that throws light on the impact of physical dependency on others, an aspect of the daily experience of ME/CFS patients that is rarely discussed or addressed in the scientific literature. Read more

 

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Altered neuroendocrine control in adolescent CFS

Posted on 06/20/2016 by wames

Research abstract:

BACKGROUND:

Chronic fatigue syndrome (CFS) is a common and disabling disorder, and a major threat against adolescent health. The pathophysiology is unknown, but alteration of neuroendocrine control systems might be a central element, resulting in attenuation of the hypothalamus–pituitary–adrenalin (HPA) axis and enhancement of the sympathetic/adrenal medulla (SAM) system. This study explored differences in neuroendocrine control mechanisms between adolescent CFS patients and healthy controls, and whether characteristics of the control mechanisms are associated with important clinical variables within the CFS group.

METHODS

CFS patients 12–18 years of age were recruited nation-wide to a single referral center as part of the NorCAPITAL project. A broad case definition of CFS was applied. A comparable group of healthy controls were recruited from local schools. A total of nine hormones were assayed and subjected to network analyses using the ARACNE algorithm. Symptoms were charted by a questionnaire, and daily physical activity was recorded by an accelerometer.

RESULTS

A total of 120 CFS patients and 68 healthy controls were included. CFS patients had significantly higher levels of plasma norepinephrine, plasma epinephrine and plasma FT4, and significantly lower levels of urine cortisol/creatinine ratio. Subgrouping according to other case definitions as well as adjusting for confounding factors did not alter the results. Multivariate linear regression models as well as network analyses revealed different interrelations between hormones of the HPA axis, the SAM system, and the thyroid system in CFS patients and healthy controls. Also, single hormone degree centrality was associated with clinical markers within the CFS group.

CONCLUSION

This study reveals different interrelation between hormones of the HPA axis, the SAM system, and the thyroid system in CFS patients and healthy controls, and an association between hormone control characteristics and important clinical variables in the CFS group. These results add to the growing insight of CFS disease mechanisms.

Trial registration Clinical Trials NCT01040429

Altered neuroendocrine control and association to clinical symptoms in adolescent chronic fatigue syndrome: a cross-sectional study, by Vegard Bruun Wyller, Valieria Vitelli, Dag Sulheim, Even Fagermoen, Anette Winger, Kristin Godang and Jens Bollerslev in Journal of Translational Medicine, 5 May 2016 (open access).

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