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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Dr Zahler Nahle’s outline of ME/CFS research needs

Posted on 07/18/2016 by wames

Solve ME/CFS Initiative blog post: Dr. Zaher Nahle’s Response to the NIH RFI

Solve ME/CFS Initiative submitted a unique and pointed response to the recent NIH request for information (RFI), NOT-NS-16-024, regarding new research strategies for ME/CFS.

On May 24, 2016, the National Institutes for Health (NIH) released the first ever Request for Information (RFI) regarding ME/CFS. The RFI specifically requested submissions to address new research strategies for ME/CFS. From one research organization to another, Solve ME/CFS Initiative (SMCI) used this opportunity to articulate what our vision for an ideal research opportunity from the NIH would look like.

On June 24, 2016, SMCI submitted to the NIH a sample funding opportunity announcement (FOA) addressing the key elements we feel have been absent or underfunded in ME/CFS research. This hypothetical FOA was authored by SMCI’s vice president for research and scientific programs, Dr. Zaher Nahle, and presented utilizing the formatting and language of the NIH itself. The reasoning behind replicating the NIH’s own model was to highlight the dire need for research funding and encourage discussion of the NIH’s responsibility to further ME/CFS studies.

Dr. Nahle’s submission includes discussion on the following topics:

  • Interdisciplinary research and biomarkers
  • Bioenergetics
  • Neuroendocrine systems
  • Immunity and inflammation
  • Epidemiology and diagnosis
  • Physiological interactions
  • Treatment and quality of life
  • Methodological considerations
  • Funding support and timelines

To read SMCI’s full RFI submission, please click here.

[Please note that this is NOT an announcement of (or any part of) an actual FOA. This document was prepared and submitted by Dr. Zaher Nahle, vice president for research and scientific programs at SMCI, using existing material from the NIH website combined with original content and opinions. This document is intended for informational use only and is a fictional FOA.]

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Gut microbes identify 83% of ME/CFS patients

Posted on 07/18/2016 by wames

MEAction blog post by Jaime S, 13 July 2016: New research: gut microbes identify 83% of patients 

Signs of bacterial infection and inflammation

Recently, a team of researchers led by Ludovic Giloteaux of Cornell University measured the levels of several biomarkers in 49 ME/CFS patients and 39 controls, including LPS to measure bacteria in the bloodstream and CD14 and C-reactive protein to measure inflammation.  Researchers also measured the levels of intestinal fatty acid binding protein (I-FABP) to show GI damage.

ME/CFS patients showed significantly higher levels of lipopolysaccharides (LPS) in their blood, which means that they had more gram-negative bacteria than controls. These elevated levels of bacteria then caused the liver to produce LPS-binding protein, which was also elevated above levels found in controls. sCD14 is one of the ways that the body senses invading bacteria.  Levels of this inflammatory marker are high in those experiencing severe bacterial infections.  CD14 levels were also high in ME/CFS patients.

Microbial diversity

Giloteaux found that “ME/CFS samples had a significant overall lower microbial diversity, [which] differed at the phylum and family levels”: ME/CFS patients had especially low levels of Firmicutes in comparison to controls, and higher levels of Proteobacteria.

Proteobacteria include a wide range of pathogens, such as Escherichia, Salmonella, Helicobacter, and Yersinia.  Firmicutes are the largest group of bacteria in the human gut, and include Clostridium, Bacilli, and Ruminococcaceae.  ME/CFS patients were low in Ruminococcaeaea in particular, which has been associated with poor gut health, and low in Bifidobacterium, which is often used as a probiotic.

By using both inflammatory markers and the microbiome ‘blueprint’ of the disease, researchers found they could identify 83% of patients.

Microbiome as biomarker

The coupling of increased inflammatory markers plus dysbiosis led the researchers to conclude that damage to the gut is leading to microbial translocation, or the movement of bacteria from the inside of the gut to the bloodstream.  This in turn could lead to more inflammation and greater immune dysregulation.  While Giloteaux and his team did not claim to have found ‘the answer’ to ME/CFS, they may have identified a series of biomarkers: by using both the inflammatory markers and the microbiome ‘blueprint’, the researchers found they could identify 83% of patients.

More evidence

This is far from the first study to identify microbial dysregulation in ME or CFS patients — it’s not even the first to identify dysregulation in Firmicutes populations in particular.

In 2015, S.K. Shukla and colleagues examined blood and stool samples taken after patients and controls had exerted themselves. They found that both blood and stool sample microbiomes differed in ME/CFS patients (defined using the Fukuda criteria) in the abundance of “several major bacterial phyla”, including Bacilli in blood 48 hours post-exercise and Clostridium XIVa and IV (Firmicutes) in blood samples collected 15 minutes after exercise.  Moreover, the relative abundance of Firmicutes to Bacilli was skewed high in ME/CFS patients.

Other studies have verified dysregulation in the intestinal microbiota in ME/CFS. For example, a study of Norwegian ME patients demonstrated an increase of Firmicutes in patients over controls, including a fifty-fold decrease in Holdemania, and a 20-fold increase in Lactonifactor.

A piece of the puzzle

The gut microbiome plays a crucial role in human health, as 70% of the immune cells of the body live in the gut.  Healthy digestion supplies nutrients, produces beneficial or toxic metabolites and waste products, and destroys – or does not destroy – ingested pathogens.  The gut microbiome can also play a vital role in endocrinology by helping to generate and/or stimulate release of dopamine, norepinephrine, serotonin, nitric oxide, and the inhibitory transmitter aminobutyric acid — the gut bacteria may even directly affect the vagus nerve.

All this means that the gut microbiome could be a central key to unlocking the pathology of ME and CFS.

In the era of the metagenome, efforts to understand chronic disease have forced a shift from reliance on a ‘‘one microbe, one disease’’ model to a focus on how entire populations of microbes can become dysregulated. It is more likely that the structure of entire communities of microbes shift in individuals as they become ill, rather than that one pathogen is to blame.

For a more in-depth review of evidence of microbiome involvement in ME/CFS, see Navaneetharaja et al’s A Role for the Intestinal Microbiota and Virome in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)? in the Journal of Clinical Medicine and check out MEpedia’s page on the microbiome.

[Edit!] If you’re interested in the microbiome’s effect on human health, a new text is coming out in October with a whole chapter devoted to gut dysbiosis and its relation to CNS disturbances. While this author can’t attest to the quality, it does look interesting! The Human Microbiota and Chronic Disease: Dysbiosis as a Cause of Human Pathology by Brian Henderson, Luigi Nibali.

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Six year study of abnormal brain changes in ME/CFS

Posted on 07/18/2016 by wames

ME Australia blog post, by  Sasha Nimmo, 12 July 2016: Six year study of abnormal brain changes in chronic fatigue syndrome patients

An Australian six year study evaluating progressive brain changes associated with chronic fatigue syndrome (Fukuda and Canadian Consensus Criteria definitions) shows patients’ brains deteriorate at an abnormal rate.

The study used optimized voxel based morphometry (VBM), a commonly-used automated tool for studying patterns of brain change in neurological diseases. It shows chronic fatigue syndrome (Fukuda & CCC) is a chronic illness with abnormal connections among brain regions and white matter deficits which continue to deteriorate.

The study, Progressive brain changes in patients with chronic fatigue syndrome: A longitudinal MRI study, was published in the Journal of Magnetic Imaging in April 2016.

The authors are from Griffith University’s National Centre for Neuroimmunology and Emerging Diseases and South Australia’s Lyell McEwin Hospital and Royal Adelaide Hospital. Many of this paper’s authors also published a paper about brain connectivity problems causing signalling problems in March 2016.

The six year study looked at the brains of 15 patients and 10 controls and found white matter decreased over time in the CFS patients. It also says hypoxia, which is a deficiency in the amount of oxygen reaching the tissues, could be causing neurodegeneration.

“The rate-of-change of regional white matter volumes in CFS patients was significantly different from that in controls in the left posterior part of the inferior fronto-occipital fasciculus (IFOF) and/or arcuate fasciculus. In this location, white matter volume relative to global white matter volume decreased with time in the CFS group while in controls it was unchanged.

This study detected continuing shrinkage of white matter in the left IFOF in patients with CFS, but not in controls. This result was consolidated by the pooled inter group comparisons revealing decreased regional white matter volumes in adjacent regions and decreased GM and blood volumes in contralateral regions and by regression analysis showing significant correlations of white matter and grey matter volumes and T2w intensities with CFS symptom scores in those regions.”

The IFOF connects networks of cognitive control, attention, language processing and working memory.

The study may explain symptoms such as impaired concentration, working memory loss, inability to focus vision and poor motor coordination.

This seems to agree with the findings of Boissoneault et al 2005 in the their paper  Abnormal resting state functional connectivity in patients with chronic fatigue syndrome: an arterial spin-labeling fMRI study, which said “results demonstrate altered functional connectivity of several regions associated with cognitive, affective, memory, and higher cognitive function in ME/CFS (Fukuda criteria) patients. Connectivity to memory related brain areas (parahippocampal gyrus) was correlated with clinical fatigue ratings, providing supporting evidence that brain network abnormalities may contribute to ME/CFS pathogenesis”.

BRAIN CROSS SECTIONS

“Chronic functional hypoxia due to dysfunction of the neurovascular unit could also cause neurodegeneration.[34] Of interest, a recent study found seventeen single nucleotide polymorphisms (SNPs) were significantly associated with CFS.[35] Nine of these SNPs were associated with muscarinic acetylcholine receptors and eight with nicotinic ACh receptors (nAChRs). ACh, a neuromodulator in the brain, changes the state of neuronal networks throughout the brain and modifies their response to internal and external inputs. Control of synaptic Ca2+ concentration following nAChR stimulation is a major pathway for ACh to influence neuronal networks.[36] Furthermore, nAChRs are also present in the cerebral vascular endothelium and smooth muscles.[37] Thus, aberrant AChR function may impair cerebrovascular autoregulation and cause chronic functional hypoxia.

This study warrants further investigations to understand the pathomechanism of white matter deficits in the IFOF in CFS.”

The study was funded by the Judith Jane Mason Foundation.
Summary piece. The full paper came out in April.

 

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Canadian perspective on gut research

Posted on 07/15/2016 by wames

The star article, by Lauren Pelley, 4 July 2016: New research unlocking mysteries behind chronic fatigue syndrome,

Study showing biological markers of long-misunderstood condition “one more piece of the puzzle,” researchers say.

’80 per cent of patients still go undiagnosed’

Scott Simpson remembers the exact day his whole world changed.

It was August 9, 2012, and the then 47-year-old medal-winning triathlete woke up with a feeling unlike anything he’d experienced before. It was a deep, inexplicable fatigue and sickness affecting every part of his body, including his thinking and speaking abilities.

The next day, and the day after, Simpson recalls feeling a bit better – enough to compete in another triathlon. But that put him into a much deeper hole.

It felt like the typical exhaustion of competing in a triathlon, coupled with the crippling feelings of influenza and a bad hangover, the west-end Toronto resident says. And it didn’t go away. Simpson had been through a medical crisis before after finding out he was HIV positive more than a decade prior, but this bout of illness was a total mystery, with no link to his HIV status, according to his doctors.

After six weeks of strange symptoms – and no formal diagnosis – Simpson began his own online research.

One condition jumped out: Myalgic encephalomyelitis (ME), also known as chronic fatigue syndrome (CFS), a complex condition characterized by a cluster of symptoms that often overlap with other illnesses. The range of debilitating issues includes pain, unrefreshing sleep, and fatigue that grows worse after exertion, according to medical literature.

“I hit so many of them, especially the cardinal symptom, the post-exertional malaise,” Simpson says, adding he still hasn’t received a formal diagnosis for the frustrating condition that’s left him, four years later, with constant lingering symptoms of pain and fatigue.

ME/CFS has long been a controversial and misunderstood illness, and one that’s often met with stigma both by the general public and the medical community, with no widely-accepted treatment, single diagnostic test, or known cause.

It may affect around 408,000 Canadians, according to self-reported data from Statistics Canada’s 2014 Canadian Community Health Survey, and experts say a large percentage of sufferers aren’t properly diagnosed.

But new research is providing legitimacy to ME/CFS, while shedding light on what’s actually happening inside the bodies of people with the condition.

In a study published June 23 in the journal Microbiome, a team from Cornell University reports finding biological markers of the disease in gut bacteria and inflammatory microbial agents in the blood.

The researchers were also able to correctly diagnose ME/CFS in nearly 83 per cent of subjects just by analyzing stool samples and blood work.

Researcher Maureen Hanson, a professor in Cornell’s department of molecular biology and genetics, says the findings show people with ME/CFS have abnormalities in their gut, much like patients with inflammatory conditions including Crohn’s disease.

The study involved 88 participants – a mix of control subjects and patients with ME/CFS, who were identified by a specialist in New York.

Dr. Harvey Moldofsky, a professor emeritus in the University of Toronto’s department of psychiatry, who spent more than four decades studying the causes and treatments of the illnesses now known as fibromyalgia and ME/CFS and was not involved in the research, says the study has several methodological concerns.

“(The researchers) acknowledge that they really need to study a larger population. OK, fair enough. But there is the question as to who the other people are that they’re going to study,” he says. “What do you mean by normal? How do these people differ in their diet? How do these people differ in terms of their exercise?”

Since the symptoms of ME/CFS often overlap with other conditions, such as fibromyalgia and chronic headaches, Moldofsky says further research also needs to explore these other patient populations sharing similar symptoms.

Still, he says, “this is a beginning,” and it’s one Hanson and her team hopes to build on. Other researchers are conducting similar studies, she says, which could replicate the Cornell results down the road, and her own team plans to keep exploring what’s happening in the gut microbiome of people with ME/CFS.

“There’s lots of biological evidence now indicating this is a biological disease,” she adds. “Our information is one more piece of the puzzle.”

In 2014, a study from Stanford University found abnormalities in the white matter of patients with ME/CFS, while research published the following year by Columbia University researchers showed distinct differences in the immune systems of people with the disease, compared to healthy controls.

Piece by piece, this growing body of research is providing more evidence that ME/CFS is “absolutely a real, physiological illness,” says Dr. Alison Bested, a hematological pathologist who has spent 25 years helping patients with the disease.

“But the whole area of ME/CFS is not being taught in the medical curriculum or the post-grad curriculum,” she adds. “The average doctor in our community is not knowledgeable about ME/CFS, and there’s still a lot of stigmatism – that it’s a belief system, that it’s all in your head.”

Around 80 per cent of patients still go undiagnosed, she says. “It’s shocking to me.”

Simpson, now 50, feels betrayed by the medical system. He said when he was diagnosed with HIV at 33 years of age the treatment he received from physicians was “nothing but positive.” (He is currently on antiretroviral medications and physicians still haven’t linked his ongoing pain and fatigue symptoms to having HIV, he says.)

In contrast, his search for answers to his potential ME/CFS symptoms led to nothing but stigma, such as one internal medicine doctor telling him it was just a “mood disorder.” He’s now advocating for people with the condition as part of a grassroots group called Millions Missing for ME Canada, focused on pushing for more research funding.

“This is basically a crisis situation,” Simpson says. “We are health-care system victims.”

Still, Bested says the medical community has made “tremendous strides” at the research level, which now needs to translate into clinical tools to help patients – including those, like Simpson, who’ve been told the debilitating condition is just make-believe.

“We know it’s a physiological illness,” Bested says.

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