The difficulties of studying whether negative illness beliefs contribute to maintenance of CFS symptoms

Posted on 06/28/2016 by wames

Review abstract:

PURPOSE:

Chronic fatigue syndrome (CFS) is characterized by severe and debilitating fatigue. Studies based on self-report measures suggest negative illness representations, related symptom interpretations, and heightened symptom focusing are maintaining factors of fatigue. This study reviews studies which have investigated these cognitive biases using experimental methods, to (1) review the evidence for information processing biases in CFS; (2) determine the nature of these biases, that is the stages cognitive biases occur and for what type of stimuli; and (3) provide directions for future methodologies in this area.

METHODS:

Studies were included that measured attention and interpretation bias towards negative and illness-related information in people with CFS and in a comparison group of healthy controls. PubMed, Ovid, CINAHL, PsycINFO, Web of Science, and EThOS were searched until December 2014.

RESULTS:

The evidence for cognitive biases was dependent on the methodology employed as well as the type and duration of the stimuli presented.

Modified Stroop studies found weak evidence of an attentional bias in CFS populations, whereas visual-probe studies consistently found an attentional bias in CFS groups for health-threatening information presented for 500 ms or longer. Interpretative bias studies which required elaborative processing, as opposed to a spontaneous response, found an illness-related interpretive bias in the CFS group compared to controls.

CONCLUSIONS:

Some people with CFS have biases in the way they attend to and interpret somatic information. Such cognitive processing biases may maintain illness beliefs and symptoms in people with CFS.

This review highlights methodological issues in experimental design and makes recommendations to aid future research to forge a consistent approach in cognitive processing research.

Statement of contribution

What is already known on this subject? Studies based on self-report measures suggest negative illness representations, related symptom interpretations, and heightened symptom focusing contribute to the maintenance of chronic fatigue. Experimental studies in other clinical populations, such as patients with anxiety, depression, and chronic pain, have identified illness-specific biases in how information is implicitly attended to and interpreted, which has a causal role in these conditions.

What does this study add?

This is the first review of implicit cognitive processes in chronic fatigue syndrome (CFS).
Sustained attention and negative interpretations of somatic information may reinforce negative illness beliefs. Cognitive processes have a role to play in the cognitive behavioural model of CFS.

Attentional and interpretive bias towards illness-related information in chronic fatigue syndrome: A systematic review, by A Hughes, C Hirsch, T Chalder, R Moss-Morris in Br J Health Psychol. 22 June 2016 [Epub ahead of print]

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Activity pacing is associated with better & worse symptoms in long term conditions

Posted on 06/28/2016 by wames

Research abstract:

Background:
Activity pacing has been associated with both improved and worsened symptoms, and its role in reducing disability among patients with long-term conditions has been questioned. However, existing studies have measured pacing according to uni-dimensional subscales, and therefore the empirical evidence for pacing as a multifaceted construct remains unclear. We have developed a 26-item Activity Pacing Questionnaire (APQ-26) for chronic pain/fatigue containing five themes of pacing: activity adjustment, activity consistency, activity progression, activity planning and activity acceptance.

Objective:
To assess the associations between the five APQ-26 pacing themes and symptoms of pain, physical fatigue, depression, avoidance and physical function.

Methods:
Cross-sectional questionnaire design study. Data analysed using multiple regression.

Participants:
257 adult patients with diagnoses of chronic low back pain, chronic widespread pain, fibromyalgia and chronic fatigue syndrome/myalgic encephalomyelitis.

Results:
Hierarchical multiple regression showed that activity adjustment was significantly associated with increased physical fatigue, depression and avoidance, but decreased physical function (all P<=0.030). Activity consistency was associated with decreased pain, physical fatigue, depression and avoidance but increased physical function (all P<=0.003).
Activity planning was associated with reduced physical fatigue (P=0.025) and activity acceptance was associated with increased avoidance (P=0.036).

Conclusion:
Some APQ-26 pacing themes were associated with worse symptoms and others with symptom improvement. Specifically, pacing themes involving adjusting/reducing activities were associated with worse symptoms, whereas pacing themes involving undertaking consistent activities were associated with improved symptoms. Future study will explore the causality of these associations to add clarification regarding the effects of pacing on patients’ symptoms.

Activity pacing is associated with better and worse symptoms for patients with long-term conditions, by Deborah Antcliff, Malcolm Campbell, Steve Woby, Philip Keeley in The Clinical Journal of Pain, 17 June 2016 [Preprint]

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Gastric enterovirus infection: a possible cause of gastroparesis

Posted on 06/27/2016 by wames

Research abstract:

BACKGROUND: Gastroparesis (GP) is a disabling chronic gastroenterologic disorder with high morbidity that severely impacts patients’ quality of life. GP can present acutely after a viral-like gastrointestinal illness resulting in speculation that in some patients, neurologic damage caused by the infection might underlie the pathogenesis of idiopathic gastroparesis (IGP).

AIMS: The aim of this study is to document case reports of Enterovirus (EV) infection as a possible cause of IGP.

METHODS: Eleven patients referred with a diagnosis of GP underwent workup to exclude known causes of GP. Those with a history of flu-like symptoms or gastroenteritis prior to onset of GP symptoms had gastric biopsies taken during upper endoscopy to assess for the presence of gastric mucosal EV infection. Data on presenting symptoms, extra-intestinal symptoms and conditions, prior nutritional support requirements, upper endoscopy findings, and response to therapy were cataloged.

RESULTS: Eleven patients were diagnosed as IGP. Nine had active EV infection on gastric biopsies and were included (7/9 female, mean age 43 years). Eight out of nine received EV treatment with antivirals and/or immune therapies, with a wide degree of variability in treatment regimens. Four out of eight who received EV treatment had symptomatic improvement. One patient had stable symptoms. Three patients are currently undergoing therapy.

CONCLUSIONS: Gastric EV infection was frequently detected (82 %) in patients undergoing investigation for IGP. Antiviral and/or immune therapies against EV seem to be favorable, as most of our patients had resolution of their GP symptoms after treatment. This is the first study to identify EV as a possible infectious etiology of IGP.

Gastric Enterovirus Infection: A Possible Causative Etiology of Gastroparesis. by Barkin JA, Czul F, Barkin JS, Klimas NG, Rey IR, Moshiree B. in Dig Dis Sci. 2016 Jun 25. [Epub ahead of print]

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Indicator of CFS found in gut bacteria

Posted on 06/27/2016 by wames

Cornell Chronicle blog post by Krishna Ramanujan, 24 June 2016: Indicator of chronic fatigue syndrome found in gut bacteria

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.

Due to this lack of information, some people have even suggested the disease may be psychosomatic.

Now, for the first time, Cornell 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 ME/CFS 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 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.”

Ruth Ley, associate professor in the Departments of Molecular Biology and Genetics and Microbiology, is a co-author.

“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 in both Hanson’s and Ley’s labs and first author of the study.

Researchers have evidence that an overactive immune system plays a role in chronic fatigue. Symptoms include fatigue even after sleep, muscle and joint pain, migraines and gastrointestinal distress. One hallmark of the condition is post-exertional malaise, meaning patients may take weeks to recover from minor exertion. To test for ME/CFS, clinicians may give patients a cardio-pulmonary exercise test where they ride a bike until they become fatigued. If the test is repeated the following day,  ME/CFS patients usually cannot reproduce their performance from the first day.

“That’s very typical and specific of people with ME/CFS, because healthy people, or even people who have heart disease, can reproduce the exercise on the second day, but these people cannot,” Giloteaux said.

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.

Co-authors include Julia Goodrich, a doctoral student, and William Walters, a postdoctoral researcher, both in Ley’s lab.

The study was funded by the National Institutes of Health.

Reduced diversity and altered composition of the gut microbiome in individuals with myalgic encephalomyelitis/chronic fatigue syndrome by Ludovic Giloteaux, Julia K. Goodrich, William A. Walters, Susan M. Levine, Ruth E. Ley and Maureen R. Hanson in Microbiome 2016 4:30 [published 23 June 2016]

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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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Can ME/CFS be diagnosed in young children?

Posted on 05/24/2016 by wames

Dr David S Bell, eminent American paediatrician, talks about the difficulty of diagnosing ME/CFS in children. Excerpt from: ME/CFS in children

Diagnosis in Children

For the most part ME/CFS can only be diagnosed in adolescents and older individuals. Children below the age of 8 or 9 do not have the symptom pattern of adolescents past puberty. If the onset of the disease occurs during adolescence, the most common time of onset, the pattern is similar to that of adults. Pediatric criteria have been developed5,6.

Pediatric Symptoms

The onset is usually acute with an illness resembling mononucleosis, but unlike normal mono, it does not resolve in two to three weeks. Instead, the exhaustion, headache, muscle and joint pain, sore throat and lymph node pain become chronic. Exertion, even as seemingly minor as getting on a school bus may trigger a relapse causing the child to have to spend prolonged periods in bed. But not all children describe post-exertional malaise7.  In general, the more severe the symptoms are in the first six months, the less likely to be resolution of the illness over time8. It has been my belief, although never proven in clinical studies, that an adolescent who spent the first three months in bed due to ME/CFS will still be ill at age 35, even though they may have been almost well in the years in between.

Of the many problems here, of course, is that no one has ever studied and published these issues in adolescents. It is impossible to predict at the onset of the disease if a teen has a standard viral infection or the beginning of a severe course of ME/CFS. In general, ME/CFS is a post-infectious phenomenon. The other great problem is that there is no simple laboratory test that can identify the presence or the severity of ME/CFS. Essentially all of the symptoms are subjective, and cannot be measured without subjective bias. It is comparable to the severity of a migraine headache. Normally, when someone says they have a migraine headache, we take their word for it, as it cannot easily be proven. But for ME/CFS, medical providers are reluctant to take the adolescent’s word for the presence of the symptoms.

Instead, providers usually suggest that the symptoms are not that bad, and that some exercise or counseling can remove them. Counseling is useful if an adolescent is coping poorly, and mild exercise can be of use when someone with the illness is improving spontaneously. But too often it precipitates a relapse, which is why the IOM suggested the name Severe Exertion Intolerance Disease4.

There are minor differences between adolescent ME/CFS and the adult ME/CFS. One is that abdominal pain is more common5 while this symptom is not even a part of some adult symptom criteria3. In addition, facial flushing is more common in teens9. I recall once when walking down the street in Lyndonville, I saw a teen with bright red facial flushing. He became ill within one or two days and remained ill for years. I made the mistake once of calling this a rash, but it is not a rash, it is flushing – the same as an adult can have when taking niacin. In some of the early outbreaks, this flushing rash is also mentioned and considered a standard symptom, one that involves the autonomic nervous system, as this part of the nervous system controls the diameter of the blood vessels.

Onset Prior to Puberty

I have seen many children where the parent will state that the child became ill at age 3. What the parent means by this statement is that, in retrospect, they can say that they noticed problems starting at age 3, but not that the whole symptom pattern was present. They may have noticed that their child was sleeping more than usual, or that their child seemed to get sick with viral infections more often than healthy kids. Children at a young age do not understand the concept of tiredness, because this word can only be used in reference to a state of good energy. If someone has never had prolonged ‘good energy’ the word fatigue has no meaning.

However during adolescence the symptom pattern coalesces into that of ME/CFS, so that it becomes possible to say that ‘in retrospect’ the illness began in early childhood. The cognitive symptoms from age 3 to age 12 are indistinguishable from attention deficit disorder, and this is another area that has never been adequately studied.

Read the full article

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Can simple blood tests help to identify ME/CFS

Posted on 05/23/2016 by wames

Health rising forum discussion started by Cort Johnson, 30 April 2016:  Can simple blood tests help to identify Chronic Fatigue Syndrome (ME/CFS)?

How great it would be if a doctor could give a teenager with lingering fatigue after infectious mononucleosis/glandular fever a simple blood test to determine if she had chronic fatigue syndrome (ME/CFS).

She and her parents might not like that result but at least they’d have an answer to their daughters health issues and they could chart their course from there. The doctor, of course, would be quite relieved to have an answer his patients mysterious problems. He or she could study up on how to treat ME/CFS or (hopefully) send her on her way to a doctor who could (instead of a psychiatrist who can’t.)

Significant amounts of stress would be relieved on both ends and both ME/CFS as a disease and the patient would be validated.

That’s what this Renee Taylor/Nancy Klimas group (Broderick, Klimas, Fletcher) and Suzanne Vernon recent study tried to achieve. They tracked almost 300 adolescents diagnosed with infectious mononucleosis in the Chicago area for 24 months and gave the ones who got sick and a handful of the ones who recovered very simple blood, saliva and urine tests.

This study was definitely a gamble; nobody has ever found that standard blood tests tell us anything about chronic fatigue syndrome.

Harvey JM, Broderick G, Bowie A, et al. Tracking post-infectious fatigue in clinic using routine Lab tests. BMC Pediatrics. 2016;16:54 doi:10.1186/s12887-016-0596-8.

Results

There’s nothing like consistency in research. This study underscored and validated what the Dubbo studies found some ten years ago; that if you come down with infectious mononucleosis/glandular fever as an adolescent you, unfortunately, have a pretty good chance of coming with ME/CFS.

At six months 13% of them met the criteria for ME/CFS (CCC criteria tweaked by Jason), at 12 months 7% still did, and two years later 4% (@12 adolescents) were still sick. (Compare that with 11% and 9% at six and 12 months in the Dubbo studies).

It’s not clear if females are more likely to get IM than males but they were definitely hit harder by it. At six months 90% of the ME/CFS adolescents were female; at 12 months 100% were.

Blood, Saliva and Urine Test Results

The results of 59 standard laboratory tests in 13 young women with ME/CFS with those of healthy controls indicated that some differences were found and those differences highlighted the HPA axis and hormones. Unfortunately few of the abnormalities found persisted past one time point.

Reduced levels of glucose and ACTH at six months suggested that the HPA axis was sputtering. ACTH triggers the production of cortisol by the adrenal glands and is produced in response to biological stress.

The authors suggested that a cytokine (Il-6) produced during an infection could be promoting hypoglycemia in these young ME/CFS patients. Older ME/CFS and FM patients will remember that hypoglycemia was all the rage in alternative health circles a couple of decades ago.

Levels of estradiol, the primary sex hormone in women, tanked at 12 and 24 months. Those two findings fit somewhat with Broderick’s past modeling work which highlighted the HPA axis and the hormonal system in ME/CFS.

Broderick’s work suggests that female hormones may play an important role keeping female ME/CFS patients stuck in a suboptimal physiological state. His recent model suggested that women with ME/CFS fall into steady state which includes decreased cortisol, increased estradiol and increased anti-inflammatory activity.

The authors noted that an increase in neutrophils at 24 months could also reflect hormonal changes in ME/CFS women. Plus a close but non-significant tendency towards increased thyroxine levels (T4) at six and twelve months (p<.06/ p<.07) suggested thyroid gland involvement. Ultimately the study suggested that immune changes during infection may be effecting the HPA and HPT axes and female hormones.

Conclusion

This study was probably always something of a crap shoot, but it did underscore possble HPA axis and hormonal problems in ME/CFS. If validated in larger studies and with other disease cohorts it could provide the opportunity for doctors to use simple blood tests to quickly tell who has ME/CFS.

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