Assessing reduction in activity levels in ME/CFS

Posted on 07/22/2016 by wames

Research abstract:

Background: Myalgic encephalomyelitis and chronic fatigue syndrome have case definitions with varying criteria, but almost all criteria require an individual to have a substantial reduction in activity level.

Unfortunately, a consensus has not been reached regarding what constitutes substantial reductions.

One measure that has been used to measure substantial reduction is the Medical Outcomes Study Short-Form-36 Health Survey (SF-36). [1]

Purpose: The current study examined the relationship between the SF-36, a measure of current functioning, and a self-report measure of the percent reduction in hours spent on activities.

Results: Findings indicated that select subscales of the SF-36 accurately measure significant reductions in functioning.

Further, this measure significantly differentiates patients from controls.

Conclusion: Determining what constitutes a significant reduction in activity is difficult because it is subjective to the individual.

However, certain subscales of the SF-36 could provide a uniform way to accurately measure and define substantial reductions in functioning.

Assessing current functioning as a measure of significant reduction in activity level, by Taylor Thorpe, Stephanie McManimen, Kristen Gleason, Jamie Stoothoff, Julia L. Newton, Elin Bolle Strand & Leonard A. Jason in Fatigue: Biomedicine, Health & Behavior [Published online: 19 Jul 2016]

 

 

 

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Dietetic and nutrition case study CFS/ME

Posted on 07/22/2016 by wames

Case study summary:

This chapter discusses the case of a 25 years old woman, Melissa, who was diagnosed with moderate chronic fatigue syndrome/myalgic encephalopathy (CFS/ME).

Melissa’s symptoms include headaches, eye pain, muscle and joint pain, poor sleep and concentration, sensitivity to light, palpitations and dizzy spells. Melissa was experiencing stomach pain, nausea and diarrhoea and as a result eliminated lactose and gluten from her diet, resulting in an improvement in the stomach pain and diarrhoea but not the nausea.

Melissa has been referred due to poor nutritional intake, reduced appetite and recent weight loss of 4 kg. The referral also states Melissa takes a combination of vitamins in large doses including magnesium and coenzyme Q10.

Melissa is prescribed a low dose of amitriptyline. The questions raised in this chapter include queries regarding the nutrition and dietetic diagnosis, special diets for CFS/ME, aim and objectives of the dietary intervention, and diagnosis of coeliac disease.

Chronic fatigue syndrome/myalgic encephalopathy, by Caroline Foster and Jennifer McIntosh in Dietetic and Nutrition Case Studies March 5, 2016

 

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Is CFS/ME autoimmune & inflammatory?

Posted on 07/22/2016 by wames

VeryWell blog post, by Adrienne Dellwo [Reviewed by a board-certified physician], 8 July 2016: Is Chronic Fatigue Syndrome Autoimmune & Inflammatory?

What We Know About It
You still hear that chronic fatigue syndrome (ME/CFS) is a “mystery illness,” but the nature and mechanisms of the disease are beginning to take shape, thanks to the ongoing efforts of researchers. Over the years, especially recent ones, we’ve learned a huge amount. Some of that knowledge points to roles that inflammation and autoimmunity may play in this illness.

To understand the research, it helps to know a little about the processes themselves.

Inflammation: Helpful & Harmful

We all know that inflammation is involved in many illnesses and injuries, and it’s rare to find a house that doesn’t contain at least one anti-inflammatory drug. We ice and elevate our injuries, to keep them from getting too inflamed.

However, it might surprise you to learn that inflammation is part of a healthy response to problems in the body. When your system detects a problem—whether it be an invading virus or bacteria, or tissues damaged from injury—it triggers an inflammatory response.

What happens is that blood vessels dilate to get more blood to the area, and extra protein is pumped into that blood. White blood cells move from the blood vessels into the problem area and kill or clean up anything that shouldn’t be there. Then the tissue can begin to heal.

So when you bash your shin or twist an ankle, a little swelling is a good thing. It means the healing process is at work.

On the other hand, when inflammation becomes chronic due to ongoing damage or a misfiring immune system, then you’ve got a problem.

An example of ongoing damage can be something like back pain from an injury that’s aggravated by poor posture, or repeated damage due to disease. A misfiring immune system can mean autoimmunity.

Autoimmunity: The System Misfires

In autoimmunity, the body is suffering from friendly fire. The immune system has gone haywire and now identifies a part of your body as a foreign invader. It then triggers the inflammatory process and sends in specialized cells to destroy the target and begin the healing process.

Only now, the healing process creates more of whatever body part your immune system doesn’t like, so the process continues indefinitely.

It’s important to note that not all immune-system dysfunction is autoimmune.

ME/CFS: What Do We Know?

Researchers have long believed ME/CFS involved chronic inflammation. Studies reveal several biomarkers of inflammation and a sustained immune response in the blood of ME/CFS patients. Some researchers now consider ME/CFS to be a neuroimmune or neuroendocrineimmune disease.

However, we’re still learning about the specific role of inflammation in the condition. Recent research paints a growing picture of autoimmunity as well. And when autoimmunity is involved, a major question is: what is its target?

Possible Causes of Inflammation

Much of the ME/CFS research community takes inflammation as a given. In the alternative name myalgic encephalitis (ME), which has been adopted by some researchers, encephalitis means inflammation of the brain and spinal cord.

Some researchers point to possible inflammatory triggers that don’t involve autoimmunity.

A 2012 study attempting to separate chronic fatigue, chronic fatigue syndrome, and myalgic encephalitis into different categories found that ME patients had higher levels of the pro-inflammatory cytokines interleukin-1 and tumor necrosis factor alpha as well as neopterin, which is an indicator of pro-inflammatory immune activity.

More recently, studies have shown that inflammatory markers can accurately distinguish the condition from depression or sickness behaviors.

A study published in Metabolic Brain Disease is just one of a growing body considering oxidative and nitrosative stress (O&NS) coupled with low antioxidant levels a possible mechanism of ME/CFS, saying these factors could point to an immuno-inflammatory pathology. (Learn more about this theory: Oxidative Stress & the Pall Protocol.)

Other researchers have suggested that certain pathogens may, in predisposed people, trigger a chronic immune activation, which would create chronic inflammation and a cascade of problems. One of the main suspects in this scenario is the Epstein-Barr virus, which causes mononucleosis (“the kissing disease.”)

A 2013 study investigated markers of retrovirus activity in the gut based on the theory that, through the brain-gut connection, a gut infection may lead to inflammation of the brain. Researchers did find some evidence, but this was a small, preliminary study and a lot of work remains to be done in this area.

The Case for Autoimmunity

Some researchers have found evidence suggesting ME/CFS is, at least in part, an autoimmune disease. A few different targets of a misfiring immune system have been suggested.

In a 2013 study examining the possible relationship of O&NS and autoimmunity, researchers said that the presence of pro-inflammatory cytokines and several other known dysfunctions associated with ME/CFS may predispose you to autoimmunity. That means autoimmune activity may be a consequence of the condition rather than a cause of it. These researchers suspect that constant viral infections may lead to a couple of theoretical processes that may induce autoimmunity: bystander activation and molecular mimicry.

In molecular mimicry, the immune system fights an infectious agent and then begins to confuse it with a similar cell in the body and therefore begins attacking it. Essentially, because both cells look like a duck, the immune system labels them both ducks, when in fact one is a goose, and the goose belongs in that ecosystem.

In bystander activation, the body is attacked by a virus, the immune system responds by activating specialized cells, and, for some reason, that activation mistakenly triggers a different type of specialized cell—an autoimmune cell—that begins attacking the body’s tissues.

In the same study, researchers also list several other methods by which ME/CFS may trigger autoimmunity, including dysfunction of mitochondria, which provide energy to your cells, and cellular damage caused by O&NS that cause your immune system to misidentify them.

A different 2013 study involving many of the same researchers puts forth the possibility of an autoimmune reaction to 5-HT, also known as serotonin. As a hormone and neurotransmitter, serotonin performs several crucial roles in both the gut and the brain. Serotonin dysregulation has long been believed to be involved in ME/CFS.

Researchers say that just over 60 percent of the participants with ME/CFS tested positive for autoimmune activity against 5-HT—more than 10 times the rate of the control group, and quadruple the rate of those with long-lasting fatigue that didn’t meet the criteria for ME/CFS.

Could Several Answers Be Right?

In the end, it could be that different cases of ME/CFS have different causes of inflammation, and that some cases are autoimmune while others are not. Remember that ME/CFS can be significantly different from one person to another. It may be that several different subgroups, and perhaps even different diseases, are currently lumped into one basket.

Scientists are still working to sort it all out. Meanwhile, you need to find ways to manage your condition. It’s important that you work with your doctor to determine the nature of your specific case of ME/CFS and how best to treat it.

Sources:
Agliari E, et al. Journal of biological dynamics. 2012;6(2):740-62. Can persistent Epstein-Barr virus infection induce chronic fatigue syndrome as a Pavlov reflex of the immune response?
Arnett SV, Clark IA. Journal of Affective Disorders. 2012 Dec 10;141(2-3):130-42. Inflammatory fatigue and sickness behaviour -lessons for the diagnosis and management of chronic fatigue syndrome.

De Meirleir KL, et al. In Vivo. 2013 Mar-Apr;27(2):177-87. Plasmacytoid dendritic cells in the duodenum of individuals diagnosed with myalgic encephalomyelitis are uniquely immunoreactive to antibodies to human endogenous retroviral proteins.

Fujinami RS, et al. Clinical microbiology reviews. 2006 Jan;19(1):80-94. Molecular mimicry, bystander activation, or viral persistence: infections and autoimmune disease.

Maes M, Ringel K, et al. Journal of affective disorders. 2013 Sep 5;150(2):223-30. In myalgic encephalomyelitis/chronic fatigue syndrome, increased autoimmune activity against 5-HT is associated with immuno-inflammatory pathways and bacterial translocation.

Maes M, Twisk FN, Johnson C. Psychiatry research. 2012 Dec 30;200(2-3):754-60. Myalgic Encephalomyelitis (ME), Chronic Fatigue Syndrome (CFS), and Chronic Fatigue (CF) are distinguished accurately: results of supervised learning techniques applied on clinical and inflammatory data.

Maes M, Twisk FN, Ringel K. Psychotherapy and psychosomatics. 2012;81(5):286-95. Inflammatory and cell-mediated immune biomarkers in myalgic encephalomyelitis/ chronic fatigue syndrome and depression: inflammatory markers are higher in myalgic encephalomyelitis/chronic fatigue syndrome than in depression.

Morris G, Anderson G, et al. BMC medicine. 2013 Mar 8;11:64. A narrative review on the similarities and dissimilarities between myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and sickness behavior.

Morris G, Berk M, et al. Molecular neurobiology. 2013 Sep 26. [Epub ahead of print] The ermerging role of autoimmunity in myalgic encephalomyelitis/chronic fatigue syndrome (me/cfs).

Morris G, Maes M. Metabolic brain disease. 2012 Jun 21. A neuro-immune model of Myalgic Encephalomyelitis/Chronic fatigue syndrome.

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Investigating unexplained fatigue in general practice with a particular focus on CFS/ME

Posted on 07/21/2016 by wames

Review abstract:

Unexplained fatigue is not infrequent in the community. It presents a number of challenges to the primary care physician and particularly if the clinical examination and routine investigations are normal. However, while fatigue is a feature of many common illnesses, it is the main problem in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME).

This is a poorly understood condition that is accompanied by several additional symptoms which suggest a subtle multisystem dysfunction. Not infrequently it is complicated by sleep disturbance and alterations in attention, memory and mood.

Specialised services for the diagnosis and management of CFS/ME are markedly deficient in the UK and indeed in virtually all countries around the world. However, unexplained fatigue and CFS/ME may be confidently diagnosed on the basis of specific clinical criteria combined with the normality of routine blood tests. The latter include those that assess inflammation, autoimmunity, endocrine dysfunction and gluten sensitivity. Early diagnosis and intervention in general practice will do much to reduce patient anxiety, encourage improvement and prevent expensive unnecessary investigations.

There is presently an on-going debate as to the precise criteria that best confirms CFS/ME to the exclusion of other medical and psychiatric/psychological causes of chronic fatigue. There is also some disagreement as to best means of investigating and managing this very challenging condition. Uncertainty here can contribute to patient stress which in some individuals can perpetuate and aggravate symptoms. A simple clinical scoring system and a short list of routine investigations should help discriminate CFS/ME from other causes of continued fatigue.

Investigating unexplained fatigue in general practice with a particular focus on CFS/ME, by Amolak S Bansal in BMC Family Practice 2016 17:81 [Published: 19 July 2016]

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Can the MIND diet reduce brain fog due to CFS & FM?

Posted on 07/21/2016 by wames

ProHealth blog post, by Dr Richard Podell, 23 June 2016: Can the “MIND Diet” Reduce “Brain Fog” Due to Chronic Fatigue Syndrome and Fibromyalgia?

The short answer is we don’t know, because research on “brainfog” has been extremely limited–to say the least. (For specifics, see research by Anthony Ocon.)

Therefore, I hope our readers will be encouraged to learn that a relatively simple diet change is probably effective for reducing or delaying another currently “untreatable” form of brain fog-that due to Alzheimer’s Disease.

Diet fads versus Diet Science

For many decades we’ve faced an army of dietary fads. Each has claimed the ability to improve health. But, almost all claims are based mainly on anecdotes. Scientific studies have largely been absent. Fortunately, that’s changing.

Mediterranean Diet

The best research has focused on the “Mediterranean Diet” as a preventive treatment for heart disease and stroke. For this study, researchers recruited more than 7,000 Spanish men and women who were at high risk for heart disease or stroke. Each person was assigned to follow either the “Mediterranean Diet” plan (high in unsaturated fats such as olive oil and/or nuts, high in fruits, vegetables and whole grains, but low in saturated fat) or the “control” diet (the standard low fat diet such as the American Heart Association might advise).

The results showed that the Mediterranean Diet:

  • Had 30% fewer heart attacks and strokes compared to those on a low fat diet.
  • Is practical. People were able to follow it for more than 5 years.
  • Can help significantly within only 5 years.
  • These researches continued the study and applied neuro cognitive testing to 522 persons from within the main study. After six years, results further showed that the group on the Mediterranean Diet scored significantly higher in the cognitive testing compared to those in the low fat diet even after adjusting for risk factors.

Findings

The Mediterranean Diet, not only prevents heart attacks and stroke, but also helps maintain cognitive skills leading to the possibility of delaying or preventing the onset of Alzheimer’s dementia. But, since baseline cognitive scores were not measured, a true controlled study was still needed.

In 2015, Valls-Pedret and the Mediterranean Diet study group reported the results of a small controlled study that used 447 60+ year old Spanish volunteers who followed either a Mediterranean-style Diet or a low-fat diet. After 4.1 years, the results showed:

  • The Mediterranean Diet can reduce cognitive decline
  • Cognitive test and memory scores were higher for the Mediterranean Diet group compared to the low fat diet group
  • Further work on diet and Alzheimer’s comes from Martha Morris, Ph.D. and her research team at Chicago’s Rush University Medical Center. Dr. Morris’ team may be the world’s leading experts on the effects of nutrition on cognitive decline due to aging. She modified the Mediterranean diet to take into account other research on dementia and named it the MIND Diet. This was used in a study of 923 Chicago men and women, age 58 to 98. Each person did not have Alzheimer’s at the start of the study and their current eating pattern was scored against the key principles of the MIND Diet.

After 4.5 years, the following was found:

  • 144 of 923 (16%) were diagnosed with Alzheimer’s
  • Participants whose MIND Diet compliance scores were initially in the top third were only 47% as likely to develop Alzheimer’s compared to those in the bottom third
  • Those in the middle third did better than those in the lowest third, but not as well as those in the upper third
  • The Mediterranean Diet pattern also predicted a low Alzheimer’s rate but not quite as well as did high scores for the MIND Diet
  • A separate paper by Dr. Morris’s group reported the difference in cognitive skills between the top third on the MIND Diet and those in the bottom third were equivalent to the top third being “7.5 years younger in age” compared to the bottom third”-although chronologically in fact their average age was the same.

Take Home Thoughts

Evidence is increasing that the Mediterranean Diet, not only prevents heart attacks and stroke, but likely also helps maintain cognitive skills. We are not certain if the Mediterranean Diet would also help patients with brain fog due to ME/CFS or FM but we can probably reject as outdated the long-held “cliché it must be a “placebo effect” when people report that symptoms improve after a change in diet.

The strength of the MIND DIET study was that the statistical analysis was controlled for life style behaviors, illnesses and genetic risks for Alzheimer’s. However, researchers did not actively assign subjects to each diet. They simply scored how closely each subject’s self-chosen diet compared to the MIND Diet ideal. So, we can’t be sure whether high adherence to the MIND Diet caused the lower rate of Alzheimer’s or whether other factors might have been at work.

So, which diet should one follow if we have brain fog due to Fibromyalgia (FMS) or Chronic Fatigue Syndrome (CFS)? At this time, we have no easy answer. Ideally, someone would fund a study where patients with CFS or Fibromyalgia would take a cognitive test, then go on either the MIND Diet (or Mediterranean Diet) or their usual way of eating. (Readers who have major wealth, might consider this project!) Aside from this, people who adopt the MIND Diet or the Mediterranean on their own, can report their experience to their doctors to our blog and/or to a widely read health support website such as Prohealth.com.

For those interested in the Mediterranean Diet, consider a book by Nick Nigro and Bay Ewald, Living the Mediterranean Diet: Proven Principles and Modern Recipes for Staying Healthy. See links for a brief summary of the MIND Diet and a more detailed summary in pdf format.

For either diet, plan on a minimum 3 to 6 month trial before judging it’s effects.
We welcome comments from any patient or doctor who has useful information to share about diets in this context.

Dr. Richard Podell Richard Podell, M.D., MPH, is a graduate of Harvard Medical School and the Harvard School of Public Health. He has been treating patients with ME-CFS and Fibromyalgia for more than 20 years. A clinical professor at New Jersey’s Robert Wood Johnson Medical School, Dr. Podell see patients at his Summit, NJ and Somerset, NJ offices. His website is DrPodell.org

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Narratives of partners of people affected by CFS/ME

Posted on 07/20/2016 by wames

Research abstract:

Background and Aims:
Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME) remains a poorly understood condition, shrouded in uncertainty and dispute.

Research suggests this context to have a profound bearing on those touched by the condition, impacting significantly on their experience and the narratives constructed thereof. However, no studies examining the narratives of partners of individuals affected by CFS/ME appear to have been carried out to date. Based upon this gap in the literature, this study sought to hear the narratives of partners of adults living with CFS/ME, giving particular consideration to the ways in which these narratives were told to an outsider, and how the outsider may have influenced the narrative.

Methodology:
This study drew on a qualitative approach. A purposive sample of six partners of adults affected by CFS/ME (4 men and 2 women) was recruited. Individual interviews were conducted that were audio-recorded and transcribed. Narrative analysis was used to analyse the transcripts, focusing principally on how participants narrated their accounts, as well as on the content of narratives and the narrative and discursive features that shaped the telling of the accounts.

Analysis and Findings:
Multiple readings of the narratives identified two areas of collective focus within participants’ accounts – ‘stories from then’ and ‘stories from now’. Some similarities in how ‘stories from now’ were told were seen to emerge down gender lines. Notably participants’ storytelling could be seen to represent a form of response to wider narratives that purvey around CFS/ME, with participants’ being observed to construct particular meanings around CFS/ME, as well as particular ‘identities’ of themselves, their partner, their relationship and ‘others’ who had played a key role in their story of living with the condition.

The findings are discussed in terms of their potential bearing for clinical practice and future research endeavours. In addition, the strengths and the limitations of the research are considered.

Narratives of partners of individuals affected by Chronic Fatigue Syndrome/Myalgic Encephalomyelitis, by Rebecca Mary Ramsden. University of Herefordshire Doctor of Clinical Psychology thesis, 18 May 2016 [Full thesis]

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CFS flare-ups caused by straining muscles and nerves

Posted on 07/20/2016 by wames

University of Birmingham press release, by Alicia Rohan, 18 July 2016: 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 HealthDepartment 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.

The study was funded by a grant from the Solve ME/CFS Initiative.

Neuromuscular Strain Increases Symptom Intensity in Chronic Fatigue Syndrome
Peter C. Rowe, Kevin R. Fontaine, Megan Lauver, Samantha E. Jasion, Colleen L. Marden, Malini Moni, Carol B. Thompson, Richard L. Violand in PLOSone 11(7) [Published: July 18, 2016]

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Reduced cardiac volumes in ME/CFS

Posted on 07/19/2016 by wames

ME Research UK article: Reduced cardiac volumes in chronic fatigue syndrome associate with plasma volume but not length of disease: a cohort study

Over the years, a number of reports in the scientific literature have pointed to the presence of abnormalities of heart (cardiac) function in ME/CFS. For example, a study in 2006 found that ME/CFS patients had relatively short QT intervals (measures of the heart’s electrical cycle) compared with healthy people (read more). Also, in 2009, Japanese researchers reported cardiac dysfunction with low cardiac output in some oriental patients (read more), and another investigation found that cardiac function was diminished (read more).

Alongside these reports, ME Research UK-funded investigations by Prof Julia Newton, Dr Kieren Hollingsworth and colleagues at Newcastle University have also throw up some intriguing findings concerning the function of the heart in ME/CFS. For example, they have shown that ‘bioenergetic abnormalities’ could be found both in heart muscle and in the muscles of the skeleton, with a correlation between the two suggesting the existence of linked underlying mechanisms (read more).

In the same investigation, they found that the hearts of the ME/CFS patients had to work harder during prolonged standing than in healthy people. The research group has also looked at the function of the heart using cardiac MRI tagging to identify defects that are not yet clinically apparent. One of their main findings has been a dramatic increase in ‘residual torsion’ in patients compared with controls.

This is a measure of the efficiency of the release of torsion and strain during the relaxation phase of the heartbeat, and ME/CFS patients had 200% more residual torsion than healthy people, indicating that their heart muscle was taking longer to relax. Also, the left ventricular mass (the thickness of the heart wall at the ventricle) was reduced compared with controls; and cardiac output (the output of blood by the heart per minute) was lower (read more).

The Newcastle researchers have been continuing their investigations, and their latest report has just been published in the journal Open Heart (read more). It describes work to confirm these previous findings in a larger group of new patients and controls, and extend them to include cardiac output and blood volume.

In the experiments, cardiac magnetic resonance examinations were performed in 47 patients with ME/CFS who had been ill for 14 years on average and 47 case-matched controls, and blood volume measurements in 41 CFS and 10 controls. Patients with a diagnosis of depression were specifically excluded from the study so that depression could be ruled out as a potential, if unlikely, cause of the abnormalities.

The results were fascinating. Compared with healthy controls, stroke volume (the amount of blood pumped by the left ventricle in one contraction) was 23% lower in the ME/CFS patients; end-diastolic volumes were 25% lower; end-systolic volumes were 29% lower; and end-diastolic wall masses were 26% lower (all p<0.0001). In essence, these findings confirm, in a larger and different group of patients, the reductions in cardiac volume observed previously in ME/CFS patients in Newcastle.

The total volume of blood (plasma and red cells) was 4% lower in the ME/CFS group compared with controls, though this difference was not statistically significant. In 63% of the patients, however, the volume of red blood cells was below 95% of the expected levels for healthy people. Also, there were strong positive correlations between blood volume measurements and cardiac end-diastolic wall mass, and a weak relationship between plasma volume and fatigue severity. Importantly, the length of illness was not related to any cardiac magnetic resonance or volume measurements, suggesting that deconditioning (which would be greater the longer a person was ill) was unlikely to be the cause of these abnormalities.

SV-influences

Stroke volume and its influences (Anatomy & Physiology, Connexions Web site. http://cnx.org)

The finding that red cell volume was low is intriguing, and it may be that blood volume plays at least a part in the symptoms experienced by ME/CFS patients. One intriguing possibility alluded to by the researchers is that the abnormalities detected in this study, particularly the reduction in end-diastolic blood volume,  may be due to problems with venous compliance (see diagram above), as nearly two-thirds of the blood in the systemic circulation is stored in the venous system and compliance is controlled by the autonomic nervous system which is also affected in ME/CFS. In fact, low total blood volume has been proposed as part of the disease process in subgroups of ME/CFS patients before. One investigation in 2002 found a 9% lower blood volume in ME/CFS patients than in controls (read more). A further study in 2009 showed that the reductions in cardiac output and end-diastolic volume in ME/CFS could be entirely accounted for by a reduction in the total blood volume (read more), and an accompanying editorial pointed out that the results did not imply heart disease, but rather pointed to “circulatory impairment” (read more).

Overall, these findings using state-of-the art MRI confirm the presence of cardiac abnormalities in people with ME/CFS. It remains unknown, however, whether these are caused by ME/CFS and its consequences per se or whether, for instance, a (pre-existing) reduced cardiac volume may make people more vulnerable to the development of the illness. As regards low blood volume, there is anecdotal evidence that the symptoms of ME/CFS improve in some patients after treatment with intravenous fluid (although the procedure is not without drawbacks and risks), and the team in Newcastle intend to explore interventions to restore fluid volume in ME/CFS patients in further studies.

Authors

Newton JL, Finkelmeyer A, Petrides G, Frith J, Hodgson T, Maclachlan L, MacGowan G and Blamire AM

Institution

Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne Hospitals NHS; Newcastle Magnetic Resonance Centre, Newcastle upon Tyne, UK

Published abstract

Objectives

To explore potential mechanisms that underpin the cardiac abnormalities seen in chronic fatigue syndrome (CFS) using non-invasive cardiac impedance, red cell mass and plasma volume measurements.

Methods

Cardiac MR (MR) examinations were performed using 3 T Philips Intera Achieva scanner (Best, NL) in participants with CFS (Fukuda; n=47) and matched case-by-case controls. Total volume (TV), red cell volume (RCV) and plasma volume (PV) measurements were performed (41 CFS and 10 controls) using the indicator dilution technique using simultaneous 51-chromium labelling of red blood cells and 125-iodine labelling of serum albumin.

Results

The CFS group length of history (mean±SD) was 14±10 years. Patients with CFS had significantly reduced end-systolic and end-diastolic volumes together with reduced end-diastolic wall masses (all p<0.0001). Mean±SD RCV was 1565±443 mL with 26/41 (63%) having values below 95% of expected. PV was 2659±529 mL with 13/41 (32%) <95% expected. There were strong positive correlations between TV, RCV and PV and cardiac end-diastolic wall mass (all p<0.0001; r2=0.5). Increasing fatigue severity correlated negatively with lower PV (p=0.04; r2=0.2). There were no relationships between any MR or volume measurements and length of history, suggesting that deconditioning was unlikely to be the cause of these abnormalities.

Conclusions

This study confirms an association between reduced cardiac volumes and blood volume in CFS. Lack of relationship between length of disease, cardiac and plasma volumes suggests findings are not secondary to deconditioning. The relationship between plasma volume and severity of fatigue symptoms suggests a potential therapeutic target in CFS.

Publication

Newton et al, Open Heart 2016; 3(1): doi:10.1136

Funding

Medical Research Council, ME Research UK

 

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Is FM a danger to ME/CFS?

Posted on 07/19/2016 by wames

Health rising blog post by Cort Johnson, 5 June: Is Fibromyalgia a danger to Chronic Fatigue Syndrome (ME/CFS)?

Extract:
Sharing similar symptoms with a much larger disease could be problematic if the two diseases are not precisely differentiated. Not only is fibromyalgia much more prevalent than ME/CFS (10 million people vs 1 million in the U.S), but the FDA approved drugs for it and the commercials featuring those drugs means that virtually everyone has heard of fibromyalgia.

Because doctors are much more familiar with FM than ME/CFS they are more likely, if given the chance, to diagnose a patient with FM. The ACR 2010 criteria gives doctors that chance.

The broad diagnostic criteria for FM could, conceivably, create a long term challenge to the viability of ME/CFS. If ME/CFS patients keep getting thrown into the FM basket the support for the ME/CFS community could weaken over time.)

In fact, Natelson believes that the less restrictive diagnostic criteria for FM (which has no exclusionary conditions) may be partly responsible for the greatly increased prevalence of FM relative to ME/CFS.

Read more

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The role of infectious and stress-related onsets in ME & CFS

Posted on 07/19/2016 by wames

Research abstract:

This study examined how the mode of onset for myalgic encephalomyelitis and chronic fatigue syndrome (ME and CFS) impacts patients’ presenting symptomatology. Specifically, this study investigated the differences between the most commonly reported ME and CFS onsets: infectious, stress-related, and a combined infectious and stress-related onset (referred to as ‘combined onset’).

Three patient samples were combined and utilized. All participants met Fukuda et al. 1994) criteria and self-reported their illness onset. Analyses showed the infectious group reported the most impairment for general health functioning-which relates to the susceptibility of getting or feeling sick-in comparison to the stress-related group.

Meanwhile, both the stress-related and combined groups reported more impairment for mental health functioning than the infectious group. Lastly, the infectious and combined groups reported worse autonomic and immune symptomatology than the stress group.

These findings illustrate that the mode of onset for ME and CFS could play a factor in a patient’s prognosis. An infectious onset might lead to worse physical and somatic symptoms, while a stress onset might lead to worse psychological functioning.

These findings are consistent with prior research. Future research should continue investigating the differences amongst patients based on illness onset, as well as other factors (e.g., psychiatric co-morbidity).

The role of infectious and stress-related onsets in Myalgic Encephalomyelitis and Chronic Fatigue Syndrome symptomatology and functioning by Andrew R. Devendorf, Abigail A. Brown, Leonard A. Jason in DePaul Discoveries Vol 5, no.1, article 6, July 15, 2016

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