Monday, May 25, 2015

IBS can be quickly diagnosed with new blood test

by James McIntosh, Medical News Today, 20 May 2015:
Until now, irritable bowel syndrome (IBS) has only been diagnosed after a long and drawn out process of ruling out other conditions, often involving invasive procedures such as colonoscopies and sigmoidoscopies.
Dr. Mark Pimentel, a gastroenterologist at Cedars-Sinai in Los Angeles, CA, created the tests. He explains that as there have been no definitive tests for IBS, patients have frequently had to go from doctor to doctor, repeating tests before they have been able to get a diagnosis they are confident with.
"Having an early diagnosis means patients can avoid years of invasive tests and visits to specialists that often leave them with more questions than answers," he explains. "With these new blood tests, many patients will now be able to proceed right to therapy for their condition."
Around 10% of the global population is estimated to have IBS, with around 10-15% of the US population affected. The condition is characterized by a variety of symptoms that includes abdominal pain, bloating and bouts of diarrhea and constipation that can cause stress and fatigue.
"Imagine a patient who wakes up in the morning and doesn't know when they're going to have a bowel movement, if it's going to be diarrhea or constipation," says Dr. Pimentel. "Are they going to be at a restaurant with friends? Are they going to be in a meeting? I mean, it's very traumatic because it's unpredictable in terms of the function."
The tests, developed by Dr. Pimentel over the course of 8 years, identify when IBS has developed by recognizing the presence of specific antibodies - anti-Cdtb and anti-vinculin - that react to toxins associated with food poisoning. These toxins, produced by bacteria such as salmonella, damage nerves that are vital to healthy gut functioning.

Tests detect biomarkers with greater than 90% accuracy

To validate the accuracy of the blood tests, Dr. Pimentel and colleagues analyzed nearly 3,000 people aged 18-65, comparing participants with IBS with people with inflammatory bowel disease, celiac disease or no gastrointestinal disease at all.
The researchers found that the blood tests identified anti-Cdtb and anti-vinculin antibodies successfully with greater than 90% accuracy. These antibodies were elevated in participants with IBS compared with participants that did not have IBS.
As a result, the researchers state that these biomarkers may be especially helpful in distinguishing IBS from inflammatory bowel disease in the workup of chronic diarrhea.
The authors acknowledge that the new tests are limited by a lower specificity for identifying IBS compared with celiac disease, though they suggest this problem is easily solved by testing for celiac disease antibodies alongside the IBS tests.
The study is published in PLOS ONE, and Dr. Pimentel presented the findings at Digestive Disease Week 2015 in Washington, DC.
"For the 40 million Americans who have irritable bowel syndrome, they now have a test that says 'You have IBS, it's real, it's an organic disease, it's not a psychological disorder,' and they can go straight to therapy, or at least get an answer," says Dr. Pimentel.
In November, Medical News Today reported on new guidelines published by the American Gastroenterological Association for IBS. The aim of the document is to make it easier for patients and their doctors to select the correct drugs for their particular symptoms.

Sunday, May 24, 2015

Once again a study demonstrating physical abnormalities in ME/CFS decides to ignore their own findings

By Ruth R Miller1 , W Darlene Reid2 , Andre Mattman3 , Cristiane Yamabayashi4 , Theodore Steiner5 , Shoshana Parker6 , Jennifer Gardy7 , Patrick Tang and David M Patrick, Published online: 20 May 2015:


This submaximal exercise testing protocol revealed attenuated changes in oxygenated and deoxygenated hemoglobin, which may be attributable to poor exercise tolerance and rapid fatigue seen in ME/CFS compounded by decreased fitness. Because of the variable responses among participants, it does not provide a clear distinction between cases with ME/CFS and healthy controls and is therefore not a useful diagnostic marker. However, testing did reveal a disproportionate level of perceived exertion and lower force production in cases with ME/CFS, and in two cases, adverse responses to low levels of exercise. The repetitive handgrip protocol may be useful to screen individuals for adverse responses and other conditions, including mitochondrial disease. It may also be useful for stratifying ME/CFS sufferers to determine appropriate levels of exercise prescription.

There are a number of issues with this study. I'm just going to mention a few.

Obviously the first one is "This submaximal exercise testing protocol revealed attenuated changes in oxygenated and deoxygenated hemoglobin, which may be attributable to poor exercise tolerance and rapid fatigue seen in ME/CFS compounded by decreased fitness."
So you find abnormalities which you don't want to find and and then you just come up with some nonsense to say they're not important. Typical Pinocchio doctoring.

If you look at the average BMI of the healthy controls and patients then there is a massive difference.
In patients it's on average 25.1 and in healthy controls 20.8. Simply put, I'm 175 cm. If my BMI was 25.1, my weight would be 76.9 kg and if my BMI was 20.8 it would be 63.7 kg. And that's a difference of 13.2 kilo which is 17.2 percent and that's a massive difference. And you cannot use healthy controls who are very slim and compare those with patients that are not.

If you look at the following sentence, "All cases and no healthy controls fit both the Canadian case definition and the CDC Fukuda definition of ME/CFS" it actually means that healthy controls can actually have ME/CFS as defined by Fukuda or defined by CCC but not by both. Which means that the healthy controls might not be healthy controls at all and they might actually have ME/CFS.

The researchers selected 25 ME patients and 25 healthy controls but they only analysed 16 of both. In the patient group they explained why they couldn't use 6 of the 25, which means that 3 were unaccounted and in the healthy controls 5 were accounted and 4 unaccounted. And in a small group that's a large percentage which is unaccounted. That should not happen but that is something which happens a lot in denial doctoring as Frank Twisk has shown repeatedly when he analysed studies by Nijmegen etc

There is one other interesting thing I would like to mention. "The CCD study pre-screened 102 people and excluded 52:24 with another diagnosis (e.g., sleep apnea, hypothyroidism, etc.), three who did not meet the case definitions, 11 that declined to participate, and 14 eligible patients that could not be matched to a control."

So 102 patient had a diagnosis of ME/CFS and after checking with the CCC criteria, in 24 of them, which is 23.5 %, the diagnosis was wrong. Which shows once again that doctors are not very good at diagnosing ME/CFS.

So once again a study demonstrating physical abnormalities in ME/CFS decides to ignore their own findings because it doesn't fit with their own ideas about ME/CFS for which they do not have any proof and they use psychoblahblah to do as if these physical abnormalities are not important. Whereas these abnormalities are actually "pretty diagnostic of impaired oxidative phosphorylation which is presumably where the "fear " of excercise comes from. Many patients with syndromic mitochondrial diseases fear excercise because their symtoms can worsen dramatically during or following the activity." As GJ rightly wrote on Facebook.

Their conclusion should have been something like: this clearly shows physical abnormalities related to exercise pointing towards mitochondrial problems in patients with ME/CFS which might aid doctors in diagnosing this condition

Tuesday, May 19, 2015

Fibromyalgia now considered a lifelong central nervous system disorder

News-Medical.Net -Published on May 18, 2015:

  Fibromyalgia is the second most common rheumatic disorder behind osteoarthritis and, though still widely misunderstood, is now considered to be a lifelong central nervous system disorder, which is responsible for amplified pain that shoots through the body in those who suffer from it.

  Daniel Clauw, M.D., professor of anesthesiology, University of Michigan, analyzed the neurological basis for fibromyalgia in a plenary session address today at the American Pain Society Annual Scientific Meeting.

  "Fibromyalgia can be thought of both as a discreet disease and also as a final common pathway of pain centralization and chronification. Most people with this condition have lifelong histories of chronic pain throughout their bodies," said Clauw. "The condition can be hard to diagnose if one isn't familiar with classic symptoms because there isn't a single cause and no outward signs."

  Clauw explained that fibromyalgia pain comes more from the brain and spinal cord than from areas of the body in which someone may experience peripheral pain. The condition is believed to be associated with disturbances in how the brain processes pain and other sensory information. He said physicians should suspect fibromyalgia in patients with multifocal (mostly musculoskeletal) pain that is not fully explained by injury or inflammation.

  "Because pain pathways throughout the body are amplified in fibromyalgia patients, pain can occur anywhere, so chronic headaches, visceral pain and sensory hyper-responsiveness are common in people with this painful condition," said Clauw.

  More @ News-Medical.Net

Sunday, May 17, 2015

One of the reasons why patients with a very disabling neuro immune disease are still being subjected to torture by doctors and other medical professionals

Yesterday someone posted her own personal story about ME on Facebook which she started with: "Question for my M.E. friends: 

  Does this ring true?"  

  So I simply answered that question as a Doctor and a patient who has been bedridden with severe ME for more than a decade, thanks to harmful graded exercise, who is spending his days in darkened rooms and is always in pain amongst other things. But that doesn't mean I feel ill as I stated in my response, as there is a clear difference between being ill, feeling ill and being disabled.

  What I find staggering, and I see it time and again with people with mild or moderate ME, and especially people who say they have ME when it is very clear they don't, is that when they disagree, and you don't have to agree with me, that they can't have a civilized, normal discussion and as they do not have any arguments to counter what I or others are saying, they start becoming very personal and abusive, just like someone did on this thread towards me.

  And if ME patients, or so called ME patients behave like this, and they do it time and again, as you can see for example almost daily on Facebook, then it's no wonder that many very good, intelligent and dedicated researchers and doctors are not interested in ME as they think it is a mental health problem, as they are not aware that this is actually a very disabling neuro immune disease and therefore we are still stuck in the dark ages of Pinocchio psychiatry, being subjected to torture, also known as graded exercise therapy, by doctors and other medical professionals.

Thursday, May 14, 2015

Griffith University: genetic changes in important receptors associated with immunological and cellular function in ME/CFS

@, 11 may 2015:

Researchers shed new light on cause of Chronic Fatigue Syndrome

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

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

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

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

"These are primitive genes that are involved in many cellular signals in the brain, gut, cardiovascular and immune systems, as well as in the mediation of pain."
These research findings coincide with International Neuroimmune Awareness week commencing Monday 11 May.

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

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

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

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

Monday, May 11, 2015

STAGGERING: the ridiculous mumbo jumbo by Van der Meer still being paraded as science in Britain's leading medical journal

Stephen A Hawkins, 08 May 2015:

Re: The long wait for a breakthrough in chronic fatigue syndrome

I am generally quite impressed with BMJ output, but I find it hard to believe that there are still people in this country that are so wilfully ignorant of the real nature of ME and the dreadful predicament those who suffer it are in.

This editorial is so misinformed that I could not do justice to a full rebuttal without filling the whole magazine, so I will just say why your blinkered adherence to the doctrine of exercise for everything is utterly absurd to anyone who really has ME.

ME 'research' very rarely includes anyone who is seriously affected. Recommendations coming from something like PACE are as relevant as cancer drug trials that only included people who had no tumours.

The most ludicrous irony of the whole dogma is that I, in common with many sufferers, i'm sure, ONLY WENT TO THE DOCTOR IN THE FIRST PLACE BECAUSE I COULDN'T EXERCISE!

For my persistence in wanting to get better i was merely branded a hypochondriac, and, eventually, just left at home to rot in bed.

The ignorance of the medical profession as exemplified in your piece, has destroyed my life, and made me spend most of the last 30y both having to fight a serious illness, and be treated worse than a criminal by most of society at the same time.

In the US, the medical authorities seem to, at last, be coming to their senses, and are trying to address this illness seriously. In light of this, it is quite staggering to read the ridiculous and easily falsifiable mumbo jumbo still being paraded as science in Britain's leading medical journal.

Competing interests: No competing interests

08 May 2015
Stephen A Hawkins

Sunday, May 10, 2015

Voices from the Shadows, free on Vimeo until 9th June

  "Voices from the Shadows" - a I hour film - can be watched free on Vimeo for the next month - until 9th June - by using the promo code VOICES.

  After registering with Vimeo with an email address and password (no card details needed), enter the promo code VOICES This allows you to access the video for a week. 

  Please re-post and publicise, but include the warning that this film is NOT SUITABLE FOR CHILDREN AND YOUNG PEOPLE WITH ME and similar illnesses, because they would find it very distressing. This film was made during 2009-11.

  ‘Voices from the Shadows’ shows the brave and sometimes heartrending stories of five ME patients and their carers, along with input from Dr Nigel Speight, Prof Leonard Jason ...

Saturday, May 9, 2015

post-Ebola syndrome: time to call the BMJ, CDC and the pinocchio psychiatrists to deny the existence of this syndrome ..

By DENISE GRADY,, MAY 7, 2015 :

  Dr. Crozier, 44, ruefully calls himself a poster child for “post-Ebola syndrome”: Besides eye trouble, he has had debilitating joint and muscle pain, deep fatigue and hearing loss. Similar problems are being reported in West Africa, but it is not clear how common, severe or persistent they are.

  more @

Thursday, May 7, 2015

In silico analysis in ME/CFS: exercise worsens the situation considerably

@ pubmed:
 2015 Jul;202:21-31. doi: 10.1016/j.bpc.2015.03.009. Epub 2015 Apr 4.

In silico analysis of exercise intolerance in myalgic encephalomyelitis/chronic fatigue syndrome.


Post-exertional malaise is commonly observed in patients with myalgic encephalomyelitis/chronic fatigue syndrome, but its mechanism is not yet well understood. A reduced capacity for mitochondrial ATP synthesis is associated with the pathogenesis of CFS and is suspected to be a major contribution to exercise intolerance in CFS patients. To demonstrate the connection between a reduced mitochondrial capacity and exercise intolerance, we present a model which simulates metabolite dynamics in skeletal muscles during exercise and recovery. CFS simulations exhibit critically low levels of ATP, where an increased rate of cell death would be expected. To stabilize the energy supply at low ATP concentrations the total adenine nucleotide pool is reduced substantially causing a prolonged recovery time even without consideration of other factors, such as immunological dysregulations and oxidative stress. Repeated exercises worsen this situation considerably. Furthermore, CFS simulations exhibited an increased acidosis and lactate accumulation consistent with experimental observations.
Copyright © 2015 Elsevier B.V. All rights reserved.


ATP synthesis; Chronic fatigue syndrome; Exercise intolerance; Exercise recovery; Myalgic encephalomyelitis; Post-exertional malaise
[PubMed - in process]

Monday, May 4, 2015

Brain MRI in CFS: severity-dependent upregulation of prefrontal myelination

Evidence in CFS for severity-dependent upregulation of prefrontal myelination that is independent of anxiety and depression. 

  @ PubMed:

  NMR Biomed. 2015 Mar;28(3):404-13. doi: 10.1002/nbm.3261.

  Barnden LR, Crouch B, Kwiatek R, Burnet R, Del Fante P

  Abstract White matter (WM) involvement in chronic fatigue syndrome (CFS) was assessed using voxel-based regressions of brain MRI against CFS severity scores and CFS duration in 25 subjects with CFS and 25 normal controls (NCs). As well as voxel-based morphometry, a novel voxel-based quantitative analysis of T1 - and T2 -weighted spin-echo (T1w and T2w) MRI signal level was performed. Severity scores included the Bell CFS disability scale and scores based on the 10 most common CFS symptoms.

  Hospital Anxiety and Depression Scale (HADS) depression and anxiety scores were included as nuisance covariates. By relaxing the threshold for cluster formation, we showed that the T1w signal is elevated with increasing CFS severity in the ventrolateral thalamus, internal capsule and prefrontal WM.

  Earlier reports of WM volume losses and neuroinflammation in the midbrain, together with the upregulated prefrontal myelination suggested here, are consistent with the midbrain changes being associated with impaired nerve conduction which stimulates a plastic response on the cortical side of the thalamic relay in the same circuits. The T2w signal versus CFS duration and comparison of T2w signal in the CFS group with the NC group revealed changes in the right middle temporal lobe WM, where impaired communication can affect cognitive function.

  Adjustment for depression markedly strengthened cluster statistics and increased cluster size in both T1w severity regressions, but adjustment for anxiety less so.

  Thus, depression and anxiety are statistical confounders here, meaning that they contribute variance to the T1w signal in prefrontal WM but this does not correlate with the co-located variance from CFS severity. MRI regressions with depression itself only detected associations with WM volume, also located in prefrontal WM. We propose that impaired reciprocal brain-body and brain-brain communication through the midbrain provokes peripheral and central responses which contribute to CFS symptoms.

  Although anxiety, depression and CFS may share biological features, the present evidence indicates that CFS is a distinct disorder.

Saturday, May 2, 2015

Inability of myalgic encephalomyelitis/chronic fatigue syndrome patients to reproduce VO2peak indicates functional impairment‏


Inability of myalgic encephalomyelitis/chronic fatigue syndrome patients to reproduce VO2peak indicates functional impairment

Betsy A Keller1*John Luke Pryor2 and Ludovic Giloteaux3

1Department of Exercise & Sport Sciences, Ithaca College, School of Health Sciences & Human Performance, 318 Center for Health Sciences, Ithaca, NY 14850, USA
2Department of Kinesiology, University of Connecticut, Neag School of Education, 2095 Hillside Rd, Unit 1110, Storrs, CT 06269-1110, USA
3Department of Molecular Biology and Genetics, Cornell University, College of Agriculture and Life Sciences, 321 Biotechnology Building, Ithaca, NY 14853, USA
For all author emails, please log on.

Journal of Translational Medicine 2014, 12:104  doi:10.1186/1479-5876-12-104
The electronic version of this article is the complete one and can be found online at:

Received:7 February 2014
Accepted:11 April 2014
Published:23 April 2014
© 2014 Keller et al.; licensee BioMed Central Ltd. 
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated.



Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a multi-system illness characterized, in part, by increased fatigue following minimal exertion, cognitive impairment, poor recovery to physical and other stressors, in addition to other symptoms. Unlike healthy subjects and other diseased populations who reproduce objective physiological measures during repeat cardiopulmonary exercise tests (CPETs), ME/CFS patients have been reported to fail to reproduce results in a second CPET performed one day after an initial CPET. If confirmed, a disparity between a first and second CPET could serve to identify individuals with ME/CFS, would be able to document their extent of disability, and could also provide a physiological basis for prescribing physical activity as well as a metric of functional impairment.


22 subjects diagnosed with ME/CFS completed two repeat CPETs separated by 24 h. Measures of oxygen consumption (VO2), heart rate (HR), minute ventilation (Ve), workload (Work), and respiratory exchange ratio (RER) were made at maximal (peak) and ventilatory threshold (VT) intensities. Data were analyzed using ANOVA and Wilcoxon’s Signed-Rank Test (for RER).


ME/CFS patients showed significant decreases from CPET1 to CPET2 in VO2peak (13.8%), HRpeak (9 bpm), Ve peak (14.7%), and Work@peak (12.5%). Decreases in VT measures included VO2@VT (15.8%), Ve@VT (7.4%), and Work@VT (21.3%). Peak RER was high (≥1.1) and did not differ between tests, indicating maximum effort by participants during both CPETs. If data from only a single CPET test is used, a standard classification of functional impairment based on VO2peak or VO2@VT results in over-estimation of functional ability for 50% of ME/CFS participants in this study.


ME/CFS participants were unable to reproduce most physiological measures at both maximal and ventilatory threshold intensities during a CPET performed 24 hours after a prior maximal exercise test. Our work confirms that repeated CPETs warrant consideration as a clinical indicator for diagnosing ME/CFS. Furthermore, if based on only one CPET, functional impairment classification will be mis-identified in many ME/CFS participants.


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