Wednesday, September 23, 2015

Discovered: the underlying metabolic problem in ME

@ sciforschenonline:

The Aerobic Energy Production and the Lactic Acid Excretion are both Impeded in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome

Mark Vink, Family Physician/GPwSI, Soerabaja Research Center, The Netherlands

Background: In this study the muscle bioenergetic function in response to exercise in severe ME was explored to see if the underlying metabolic problem in ME, responsible for the severe difficulties with trivial exercise, and the severe loss of muscle power, could be discovered.

Methods: Inorganic phosphate, creatine kinase and lactate were measured in a former Dutch National Field Hockey Champion, who is now a patient bedridden with severe ME, before and 5 minutes after very trivial “exercise”, from which his muscles needed 12 hours to recover.

Results: Inorganic phosphate and creatine kinase were both normal, however, lactate after this trivial exercise was very high, and further testing showed that a second batch of lactic acid was excreted after the same exercise with a 6-fold delay, showing that the lactic acid excretion was impaired and split into two. And this was delayed up to 11- fold by eating closer to the exercise.

Conclusion: This study found that in severe ME, both the oxidative phosphorylation and the lactic acid excretion are impaired, and the combination of these two is responsible for the main characteristic of ME, the abnormally delayed muscle recovery after doing trivial things. The muscle recovery is further delayed by immune changes, including intracellular immune dysfunctions, and by lengthened and accentuated oxidative stress, but also by exercise metabolites, which work on the sensitive receptors in the dorsal root ganglions, which in severe ME are chronically inflamed, and are therefore much more sensitive to these metabolites, which are produced in high quantities in response to trivial exercise, which for ME patients, due to the underlining metabolic problem, is strenuous exercise. And a similar problem is most likely responsible for the abnormally delayed brain recovery after doing trivial things.

This study also shows that the two metabolic problems are the result of an impaired oxygen uptake into the muscle cells or their mitochondria and in combination with the Norwegian Rituximab studies, which suggest that ME is an autoimmune disease, it is suggestive that antibodies are directly or indirectly blocking the oxygen uptake into the muscle cells or their mitochondria.

Monday, September 21, 2015

Characteristics of ME/CFS Responders to Rintatolimod (Ampligen)


Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME): Characteristics of Responders to Rintatolimod

David R Strayer1
Bruce C Stouch2
Staci R Stevens3
Lucinda Bateman4
Charles W Lapp5
Daniel L Peterson6
William A Carter1
William M Mitchell7*

1Hemispherx Biopharma, Inc., Philadelphia, Pennsylvania, United States of America
2BCS Statistical Solutions LLC, Philadelphia, Pennsylvania, United States of America
3Workwell Foundation, Ripon, California, United States of America
4Fatigue Consultation Clinic, Salt Lake City, Utah, United States of America
5Hunter-Hopkins Center, Charlotte, North Carolina, United States of America
6Sierra Internal Medicine Associates, Incline Village, Nevada, United States of America
7Vanderbilt University School of Medicine, Nashville, Tennessee, United States of America

*Corresponding author: William M. Mitchell, Department of Pathology, Microbiology & Immunology, Vanderbilt University, Nashville, TN 37205, USA, Tel: 615-322-3238;

Background: Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is a debilitating disease of unknown pathogenesis consisting of a variety of flu-like symptoms including severe fatigue. Initial analysis of the use of rintatolimod (Poly I: Poly C12U), a selective TLR3 agonist, in a Phase III, double-blind, randomized, placebo-controlled trial of CFS/ME demonstrated statistical significance (p<0.05) in the reduction of fatigue as measured by exercise tolerance (ET) as the primary endpoint using a modified Bruce protocol with reduced physical exertion in patients with severe CFS/ME as defined by a Karnofsky performance score (KPS) of 40-60.

Methods and Findings: In order to better identify responders to rintatolimod, primary and secondary endpoints have been reexamined post hoc as a function of a pre-specified study baseline ET duration >9 minutes. Analysis of improvement in exercise performance at the ≥ 25% and ≥ 50% levels using ET at 40 weeks compared to baseline was performed for the intent-to-treat (ITT) population (n=208) using the pre-specified baseline exercise stratum (baseline ET duration >9 minutes). For this subset of patients (n=126), 33% (n=20), and 12% (n=8) of rintatolimod vs. placebo patients, respectively, improved ET duration by ≥ 25% (p=0.004) while 23% (n=14) compared to 4.5% (n=3) of rintatolimod vs. placebo patients, respectively improved ET duration by ≥ 50% (p=0.003). This corresponds to increases of ≥ 186 and ≥ 373 seconds for patients receiving rintatolimod, respectively, at ≥ 25% and ≥ 50% improvement responses. A frequency distribution analysis of ≥ 25% improvement, <25% change, and ≥ 25% deterioration in ET from baseline at 40 weeks for the baseline >9 minutes cohort showed net improvement to be 18.3% for the rintatolimod cohort vs. 4.6% deterioration for placebo (p=0.015). A continuous responder analysis using 5% increments from ≥ 25% to ≥ 50% provided a robust clinical enhancement in ET effect in the rintatolimod cohorts as compared to placebo. The KPS and Vitality (SF-36 subscale) quality of life secondary endpoints demonstrated similar clinically significant improvements for the rintatolimod cohort as a function of the same ET dichotomization. Rintatolimod was generally well-tolerated in this CFS/ME population.

Conclusions: Using a modified Bruce ET protocol with reduced physical exertion allowed clear identification of patient responders to rintatolimod with severe CFS/ME syndrome. Rintatolimod produced significant enhancement in ET and quality of life indicators in patients able to complete >9 minutes in a modified Bruce ET test. Rintatolimod also reduced deterioration in ET compared to placebo in patients with the poorest initial ET. Exercise endurance >9 minutes in a Bruce protocol modified for patients with CFS/ME provides a method to identify patients most likely to respond to rintatolimod.

Saturday, September 19, 2015

Brain fMRI scan demonstrates that cognitive dysfunction in CFS is due to an energy-inefficient process in the frontal cortex


Less efficient and costly processes of frontal cortex in childhood chronic fatigue syndrome

Kei Mizunoa, b, , , Masaaki Tanakac, Hiroki C. Tanabed, e, Takako Joudoif, Junko Kawatanif, Yoshihito Shigiharac, Akemi Tomodaf, g, Teruhisa Miikef, h, Kyoko Imai-Matsumurai, Norihiro Sadatod, Yasuyoshi Watanabea, c

• Decrease in divided attention was related to fatigue in childhood and adolescence.
• Left frontal cortex of healthy students activated in verbal divided attention task
• Right MFG and ACG were additionally activated in CCFS patients.
CCFS is characterized as an energy-inefficient process in frontal cortex.

The ability to divide one's attention deteriorates in patients with childhood chronic fatigue syndrome (CCFS). We conducted a study using a dual verbal task to assess allocation of attentional resources to two simultaneous activities (picking out vowels and reading for story comprehension) and functional magnetic resonance imaging.

Patients exhibited a much larger area of activation, recruiting additional frontal areas: 1)

The right middle frontal gyrus (MFG), which is included in the dorsolateral prefrontal cortex, of CCFS patients was specifically activated in both the single and dual tasks; this activation level was positively correlated with motivation scores for the tasks and accuracy of story comprehension; and 2) In patients, the dorsal anterior cingulate gyrus (dACC) and left MFG were activated only in the dual task, and activation levels of the dACC and left MFG were positively associated with the motivation and fatigue scores, respectively.

Patients with CCFS exhibited a wider area of activated frontal regions related to attentional resources in order to increase their poorer task performance with massive mental effort. This is likely to be less efficient and costly in terms of energy requirements. It seems to be related to the pathophysiology of patients with CCFS and to cause a vicious cycle of further increases in fatigue.

Thursday, September 17, 2015

Echocardiography objectifies Central nervous system dysfunction responsible for good and bad days in Myalgic Encephalomyelitis  

Original Article, Heart and Vessels, pp 1-7 First online: 15 September 2015:

  Variability of postural orthostatic tachycardia in patients with myalgic encephalomyelitis and orthostatic intolerance
  Kunihisa Miwa 
  Author information
  Department of Internal Medicine, Miwa Naika Clinic, 1-4-3 Shintomicho, Toyama, 930-0002, Japan,

  Central nervous system dysfunction with myalgic encephalomyelitis (ME) has been suggested as the main cause of chronic fatigue syndrome. Fluctuation of the symptom severity and hierarchy is a characteristic feature in ME patients.

  The characteristics of the sympathetic activation may differ between the “good days” and “bad days” in them. Twenty-four ME patients with orthostatic intolerance underwent a conventional 10-min active standing test and echocardiography both on a “good day” and a “bad day”, defined according to the severity of their symptoms.

  The mean heart rate at rest was significantly higher on the “bad days” than on the “good days”. During the standing test on a “bad day”, 5 patients (21 %) failed to maintain an upright posture for 10 min, whereas on a “good day” all the 24 patients maintained it. Postural orthostatic tachycardia (POT) (increase in heart rate ≥30 beats/min) or severe POT (heart rate ≥120 beats/min) was observed on the “bad days” in 10 patients (43 %) who did not suffer from the severe tachycardia on the “good days”, suggesting the exaggerated sympathetic nervous activation.

  In contrast, POT did not occur or severe POT was attenuated on the “bad days” in 5 patients (21 %) who developed POT or severe POT on the “good days”, suggesting the impaired sympathetic activation.

  Echocardiography revealed significantly lower mean values of both the left ventricular end-diastolic diameter and stroke volume index on the “bad days” compared with the “good days”.

  In conclusion, in ME patients with orthostatic intolerance, the exaggerated activation of the sympathetic nervous system while standing appears to switch to the impaired sympathetic activation after the system is loaded with the additional accentuated stimuli associated with the preload reduction.

Wednesday, September 16, 2015

Low Natural killer (NK) cells in CFS is associated with increased symptom severity

@ J Clin Cell Immunol:

Low NK Cell Activity in Chronic Fatigue Syndrome (CFS) and Relationship to Symptom Severity

David Strayer, Victoria Scott and William Carter

1617 JFK Boulevard, Suite 500, Philadelphia, PA 19103, USA

Corresponding Author :David Strayer 1617 JFK Boulevard, Suite 500 Philadelphia, PA 19103, USA Tel: + 215-988-0080 Fax: + 215-988-1739 E-mail:

Received: April 29, 2015 Accepted: July 22, 2015 Published: July 29, 2015

Citation: Strayer D, Scott V, Carter W (2015) Low NK Cell Activity in Chronic Fatigue Syndrome (CFS) and Relationship to Symptom Severity. J Clin Cell Immunol 6:348. doi:10.4172/2155-9899.1000348

Copyright: © 2015 Strayer D, et al. 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 author and source are credited.

Natural killer (NK) cells act as an immune surveillance against invading pathogens and tumors. NK cell cytotoxicity (NKCC) has been reported to be decreased in patients with CFS.

The objective of this review was to conduct an analysis of available publications that reported NKCC data in CFS in order to evaluate any relationships to case definitions used to define CFS and symptom severity.

Of 17 studies that evaluated NKCC in patients with CFS, defined using the CDC 1988 and/or 1994 case definition (CD), 88% (15/17) concluded that NKCC was decreased in CFS patients compared to normal controls.
The NKCC decrease was seen using two established methods, 51Cr release (11/13) and flow cytometry (4/4). The mean percent decrease in NKCC using the CDC 1988 CD (66.3%) was significantly greater than that using the CDC 1994 CD (49.7%) (p<0 data-blogger-escaped-.01="" data-blogger-escaped-br=""> This result is consistent with that of six publications showing a greater decrease in NKCC associated with increased CFS symptom severity based on the lower symptom requirement for the CDC 1994 vs. 1988 CD. In contrast, there was no significant difference in the mean percent decrease in NKCC seen comparing the CDC 1994 CD defined population using the 51Cr release (48.3%) vs. flow cytometry (50.7%) assays (p>0.5).
Finally, seven studies investigating the ability of various agents to augment NKCC in patients with CFS showed increases of NKCC with both in vitro exposure (4/5) and in vivo exposure using randomized trials (2/2).

Low NKCC is commonly seen in CFS and is associated with increase symptom severity.

Wednesday, September 9, 2015

ME made worse by Rituximab ? You might actually have seronegative borreliosis and not ME

Was your ME/CFS made worse by Rituximab? Well you might actually have seronegative borreliosis and not ME/CFS

  CASE 1:
  @ PubMed:

  van Dop WA, Kersten MJ, de Wever B, Hovius JW. BMJ Case Rep. 2013 Feb 14;2013. pii: bcr2012007627. doi: 10.1136/bcr-2012-007627. Seronegative lyme neuroborreliosis in a patient using rituximab.

  A 66-year-old woman presented with severe shooting pains throughout her back and legs, followed by progressive deafness, weight loss and headache. She had a history of marginal zone B-cell lymphoma stage IV-B, for which she was successfully treated with immunochemotherapy and rituximab maintenance therapy.

  A relapse was suspected, but chemotherapy was not administered, since, despite elaborate investigations, malignancy could not be proven.

  Because of a history of tick bites she was tested for antibodies against Borrelia burgdorferi in serum and cerebrospinal fluid (CSF), which were negative.

  However, a B burgdorferi PCR on CSF came back positive. The patient was treated for seronegative Lyme neuroborreliosis with ceftriaxone intravenously and dramatically improved.

  This case presentation demonstrates that, in immunocompromised patients, it is important not to solely rely on antibody testing and to use additional diagnostic tests to avoid missing or delaying the diagnosis.


  CASE 2:
  @ PubMed:

  Harrer T, Geissdörfer W, Schoerner C, Lang E, Helm G., Infection. 2007 Apr;35(2):110-3. Seronegative Lyme neuroborreliosis in a patient on treatment for chronic lymphatic leukemia.

  We report on a patient who developed seronegative Lyme neuroborreliosis complicating chemotherapy for chronic lymphatic leukemia. After the fifth cycle of chemotherapy (FCR: fludarabine, cyclophosphamide, rituximab and prednisone) the 63-year-old patient developed night sweat, arthralgia in elbows, wrists, proximal interphalangeal joints (PIPs) and strong neuropathic pain in both legs, followed by paresthesia and hypesthesia in the feet, arms and face.

  Laboratory analysis revealed an elevated C-reactive protein (CRP), a slight elevation of liver enzymes and decreased IgG levels. Cerebrospinal fluid (CSF) analysis showed a lymphomononuclear pleocytosis and an elevation of protein.

  A broad diagnostic work-up was negative including a negative Borrelia IgG and IgM ELISA.

  The patient did not remember recent tick bites, but after specific questioning he recollected a transient erythema on his leg developing just before the start of the last cycle of chemotherapy.

  As the combination of neuropathic pain and arthralgia, the transient erythema and the lymphomononuclear pleocytosis raised the suspicion of Lyme neuroborreliosis, the patient was treated for 3 weeks with ceftriaxone. On therapy all symptoms resolved and CRP normalized. Retrospective PCR analysis of a CSF sample confirmed the clinical diagnosis by detecting Borrelia garinii DNA.

  This case demonstrates that in immunosuppressed patients borrelial serology may be negative and that additional diagnostic approaches (including tests for direct Borrelia detection) may be needed to demonstrate borrelial infection.

Friday, August 28, 2015

Justin Wilson Children's Fund

The online page for the Wilson Children's Fund is now live. Please click through on the link below for details.

Justin Wilson Children's Fund @

Or purchase stickers & t-shirts with all proceeds going to the Wilson Children's Fund via @ the official Indianapolis Motor Speedway shop

Wednesday, July 29, 2015

Researchers’ discovery may explain difficulty in treating Lyme disease

June 1, 2015 by Greg St. Martin @

North­eastern Uni­ver­sity researchers have found that the bac­terium that causes Lyme dis­ease forms dor­mant per­sister cells, which are known to evade antibi­otics. This sig­nif­i­cant finding, they said, could help explain why it’s so dif­fi­cult to treat the infec­tion in some patients.
It hasn’t been entirely clear why it’s dif­fi­cult to treat the pathogen with antibi­otics since there has been no resis­tance reported for the causative agent of the dis­ease,” explained Uni­ver­sity Dis­tin­guished Pro­fessor Kim Lewis, who led the North­eastern research team.
In other chronic infec­tions, Lewis’ lab has tracked the resis­tance to antibi­otic therapy to the pres­ence of per­sister cells—which are drug-​​tolerant, dor­mant vari­ants of reg­ular cells. These per­sister cells are exactly what they’ve iden­ti­fied here in Bor­relia burgdor­feri, the bac­terium that causes Lyme disease.
The researchers have also reported two approaches—one of them quite promising—to erad­i­cate Lyme dis­ease, as well as poten­tially other nasty infections.
Lewis and his col­leagues pre­sented their find­ings in a paper pub­lished online last week in the journal Antimi­cro­bial Agents and Chemotherapy. He co-​​authored the paper with North­eastern doc­toral stu­dents Bijaya Sharma and Autumn Brown, both PhD’16; recent grad­uate Nicole Matluck, S’15, who received her Bach­elor of Sci­ence in Behav­ioral Neu­ro­science; and Linden T. Hu, a pro­fessor of mol­e­c­ular biology and micro­bi­ology at Tufts University.
The research was sup­ported by grants from the Lyme Research Alliance and the National Insti­tutes of Health.
Lyme dis­ease affects 300,000 people annu­ally in the U.S., according to the Cen­ters for Dis­ease Con­trol and Pre­ven­tion, and is trans­mitted to people via bites from infected black­legged ticks. If caught early, patients treated with antibi­otics usu­ally recover quickly. How­ever, about 10 to 20 per­cent of patients, par­tic­u­larly those diag­nosed later, who have received antibi­otic treat­ment may have per­sis­tent and recur­ring symp­toms including arthritis, muscle pain, fatigue, and neu­ro­log­ical prob­lems. These patients are diag­nosed with Post-​​treatment Lyme Dis­ease Syndrome.
In addi­tion to iden­ti­fying the pres­ence of these per­sister cells, Lewis’ team also pre­sented two methods for wiping out the infection—both of which were suc­cessful in lab tests. One involved an anti-​​cancer agent called Mit­o­mycin C, which com­pletely erad­i­cated all cul­tures of the bac­terium in one fell swoop. How­ever, Lewis stressed that, given Mit­o­mycin C’s tox­i­city, it isn’t a rec­om­mended option for treating Lyme dis­ease, though his team’s find­ings are useful to helping to better under­stand the disease.
The second approach, which Lewis noted is much more prac­tical, involved pulse-​​dosing an antibi­otic to elim­i­nate per­sis­ters. The researchers intro­duced the antibi­otic a first time, which killed the growing cells but not the dor­mant per­sis­ters. But once the antibi­otic washed away, the per­sis­ters woke up, and before they had time to restore their pop­u­la­tion the researchers hit them with the antibi­otic again. Four rounds of antibi­otic treat­ments com­pletely erad­i­cated the per­sis­ters in a test tube.
This is the first time, we think, that pulse-​​dosing has been pub­lished as a method for erad­i­cating the pop­u­la­tion of a pathogen with antibi­otics that don’t kill dor­mant cells,” Lewis said. “The trick to doing this is to allow the dor­mant cells to wake up.”
He added: “This gives you an idea that you could, in prin­ciple, estab­lish a sim­ilar reg­i­ment for treating patients for this and other chronic diseases.”
Lewis is a fac­ulty member in the biology depart­ment and directs Northeastern’s Antimi­cro­bial Dis­covery Center. Over the past decade he has led pio­neering work on this spe­cial­ized class of cells pro­duced by all pathogens known as per­sis­ters. Ear­lier this year, Lewis, biology pro­fessor Slava Epstein, and other col­leagues pub­lished ground­breaking researchin Nature pre­senting a new antibi­otic that kills pathogens without encoun­tering any detectable resistance.
In pre­vious work, Lewis’ lab iden­ti­fied a com­pound called ADEP that causes dor­mant per­sister cells in MRSA to self-​​destruct. This com­pound was among the first options the researchers tried out to combat Lyme dis­ease. But it didn’t work, and nei­ther did com­bi­na­tions of stan­dard antibi­otics used to treat the dis­ease. The team thought it had hit a dead end yet remained vig­i­lant in its quest to iden­tify promising alter­na­tive options.
What we came up with was the pulse-​​dosing reg­imen, which worked beau­ti­fully,” Lewis explained. “I think this could be very useful, espe­cially for antibi­otics for which resis­tance doesn’t rapidly develop.”
Though the researchers iden­ti­fied the pres­ence of these per­sister cells, they also note in their paper that the mech­a­nisms by which the per­sis­ters are able to sur­vive remain unknown. More work in this area will be required, they wrote.

Saturday, July 25, 2015

Gene expression factors differentiate fibromyalgia, ME/CFS, depression and healthy controls from each other

@ PubMed:

  Arthritis Care Res (Hoboken).  2015 Jun 19. doi: 10.1002/acr.22639. [Epub ahead of print]

  Gene expression factor analysis to differentiate pathways linked to fibromyalgia, chronic fatigue syndrome, and depression in a diverse patient sample.

  Iacob E, Light AR, Donaldson GW, Okifuji A, Hughen RW, White AT, Light KC.


  To determine if independent candidate genes can be grouped into meaningful biological factors and if these factors are associated with the diagnosis of chronic fatigue syndrome (CFS) and fibromyalgia (FMS) while controlling for co-morbid depression, sex, and age.

  We included leukocyte mRNA gene expression from a total of 261 individuals including healthy controls (n=61), patients with FMS only (n=15), CFS only (n=33), co-morbid CFS and FMS (n=79), and medication-resistant (n=42) or medication-responsive (n=31) depression. We used Exploratory Factor Analysis (EFA) on 34 candidate genes to determine factor scores and regression analysis to examine if these factors were associated with specific diagnoses.

  EFA resulted in four independent factors with minimal overlap of genes between factors explaining 51% of the variance. We labeled these factors by function as: 1) Purinergic and cellular modulators; 2) Neuronal growth and immune function; 3) Nociception and stress mediators; 4) Energy and mitochondrial function. Regression analysis predicting these biological factors using FMS, CFS, depression severity, age, and sex revealed that greater expression in Factors 1 and 3 was positively associated with CFS and negatively associated with depression severity (QIDS score), but not associated with FMS.

  Expression of candidate genes can be grouped into meaningful clusters, and CFS and depression are associated with the same 2 clusters but in opposite directions when controlling for co-morbid FMS. Given high co-morbid disease and interrelationships between biomarkers, EFA may help determine patient subgroups in this population based on gene expression.


Friday, July 24, 2015

Another clue that ME/CFS might be an autoimmune disease: Increased Risk of ME/CFS for people with allergies

  @ PubMed:

  Medicine (Baltimore). 2015 Jul;94(29):e1211. doi: 10.1097/MD.0000000000001211. Increased Risk of Chronic Fatigue Syndrome Following Atopy: A Population-Based Study.Yang TY1, Kuo HT, Chen HJ, Chen CS, Lin WM, Tsai SY, Kuo CN, Kao CH.

  Author information
  * 1From the Molecular and Genomic Epidemiology Center, China Medical University Hospital, China Medical University, Taichung (T-YY); Division of Nephrology, Department of Internal Medicine, Changhua Christian Hospital, Changhua (T-YY); Department of Developmental and Behavioral Pediatrics, China Medical University Hospital (H-TK); School of Medicine, China Medical University (H-TK); Management Office for Health Data, China Medical University Hospital (H-JC); Department of Public Health, China Medical University; Asia University (H-JC); Division of Chinese Trauma, China Medical University Hospital, China Medical University, Taichung (C-SC); Department of Diagnostic Radiology, Chang Gung Memorial Hospital, Chiayi (W-ML); Chang Gung University, Taoyuan (W-ML); Department of Laboratory Medicine (Clinical Pathology), Mackay Memorial Hospital, Taipei (S-YT); Department of Health Policy and Management, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD (S-YT); Kau-Tang Traditional Medical Hospital (C-NK); Department of Nuclear Medicine and PET Center, China Medical University Hospital (C-HK); and Graduate Institute of Clinical Medical Science and School of Medicine, College of Medicine, China Medical University, Taichung, Taiwan (C-HK).

  Several hypotheses have been proposed to explain the etiopathogenesis of chronic fatigue syndrome (CFS), including immune dysregulation. However, few population-based prospective cohort studies have been conducted on CFS and atopy. We investigated the relationship between atopy and CFS by using a population-based cohort study.

  In this prospective, population-based cohort study of the National Health Insurance Research Database, we identified 42,558 patients with atopy and 170,232 patients without atopy from 2005 to 2007 with follow-up to 2011. The incidence rates and risks for CFS were estimated using Cox proportion hazards regression.

  The overall incidence rate of CFS was higher in the atopy cohort compared with the nonatopy cohort (1.37 versus 0.87 per 1000 person-year), with an adjusted hazard ratio of 1.48 (95% confidence interval 1.30-1.69).

  The risk of CFS in the atopy cohort increased 1.47- to 1.50-fold for each nonexisting comorbidity. Patients with numerous atopic symptoms exhibited a biological gradient of increasing risk for CFS, and the risk changed significantly after adjustment for age, sex, and comorbidities, increasing from 1.46- to 2.59-fold.

  •   We revealed that atopy is associated with CFS, particularly in patients with numerous atopic syndromes. The actual mechanism for CFS development in patients with atopy remains unclear and requires further investigation. We recommend researching the subsequent fatigue symptom in patients with atopy, particularly those with multiple atopic syndromes.

Thursday, July 23, 2015

Research shows graded exercise therapy causes exercise intolerance and makes things worse in ME/CFS

@ PubMed:

  Dyn Med. 2005 Oct 28;4:10. Time course of exercise induced alterations in daily activity in chronic fatigue syndrome. Black CD1, McCully KK.

  Author information  * 1Department of Kinesiology, The University of Georgia, Athens, GA, USA.

In a previous study we demonstrated that while people with CFS had lower daily activity levels than control subjects, they were able to increase daily activity via a daily walking program.

  We reanalyzed our data to determine the time course of activity changes during the walking program. Daily activity assessed via an accelometer worn at the hip was divided into sleep, active, and walking periods. Over the first 4-10 days of walking the subjects with CFS were able to reach the prescribed activity goals each day. After this time, walking and total activity counts decreased.

  Sedentary controls subjects were able to maintain their daily walking and total activity goals throughout the 4 weeks.

  Unlike our previous interpretation of the data, we feel this new analysis suggests that CFS patients may develop exercise intolerance as demonstrated by reduced total activity after 4-10 days.

  The inability to sustain target activity levels, associated with pronounced worsening of symptomology, suggests the subjects with CFS had reached their activity limit.

  FREE PMC article


Wednesday, July 22, 2015

The putative role of viruses, bacteria, and  mold in CFS

@ PubMed:

  Mol Neurobiol. 2015 Jun 17. [Epub ahead of print]

  The Putative Role of Viruses, Bacteria, and Chronic Fungal Biotoxin Exposure in the Genesis of Intractable Fatigue Accompanied by Cognitive and Physical Disability.

  Morris G 1, Berk M 2,3, Walder K 4, Maes M 5,6.



  Patients who present with severe intractable apparently idiopathic fatigue accompanied by profound physical and or cognitive disability present a significant therapeutic challenge.

  The effect of psychological counseling is limited, with significant but very slight improvements in psychometric measures of fatigue and disability but no improvement on scientific measures of physical impairment compared to controls. Similarly, exercise regimes either produce significant, but practically unimportant, benefit or provoke symptom exacerbation.

  Many such patients are afforded the exclusionary, non-specific diagnosis of chronic fatigue syndrome if rudimentary testing fails to discover the cause of their symptoms.

  More sophisticated investigations often reveal the presence of a range of pathogens capable of establishing life-long infections with sophisticated immune evasion strategies, including Parvoviruses, HHV6, variants of Epstein-Barr, Cytomegalovirus, Mycoplasma, and Borrelia burgdorferi.

  Other patients have a history of chronic fungal or other biotoxin exposure. Herein, we explain the epigenetic factors that may render such individuals susceptible to the chronic pathology induced by such agents, how such agents induce pathology, and, indeed, how such pathology can persist and even amplify even when infections have cleared or when biotoxin exposure has ceased.

  The presence of active, reactivated, or even latent Herpes virus could be a potential source of intractable fatigue accompanied by profound physical and or cognitive disability in some patients, and the same may be true of persistent Parvovirus B12 and mycoplasma infection. A history of chronic mold exposure is a feasible explanation for such symptoms, as is the presence of B. burgdorferi. The complex tropism, life cycles, genetic variability, and low titer of many of these pathogens makes their detection in blood a challenge. Examination of lymphoid tissue or CSF in such circumstances may be warranted.

Saturday, July 18, 2015

Frederick Douglass about harmful CBT and GET for ME/CFS: Power concedes nothing without a demand

"Power concedes nothing without a demand. It never did, and it never will. 

  Find out just what people will submit to, and you have found out the exact amount of injustice and wrong which will be imposed upon them; and these will continue until they are resisted with either words or blows, or with both. 

  The limits of tyrants are prescribed by the endurance of those whom they oppress." 

  -- Frederick Douglass, August 4, 1857 

  Born a slave, Frederick Douglass was the most important black American leader of the 19th century.

Thursday, July 16, 2015

Remembering the Outbreak of ME in the Royal Free Hospital on the 13th of July 1955


  Sixty years ago on this very day, July 13th 1955, a resident doctor and a ward sister became ill in the Royal Free Hospital. It was the start of the outbreak of a mysterious disease, which would become known as the Royal Free Disease, one of the most famous and well-documented outbreaks of Myalgic Encephalomyelitis(ME).

  What follows is an excerpt from the book “Myalgic Encephalomyelitis and Postviral Fatigue States – The saga of Royal Free Disease” by Melvin Ramsay.

  On July 13th 1955 a resident doctor and a ward sister on the staff of the Royal Free Hospital were admitted to the wards with an obscure illness.

  By July 25th more than 70 members of the staff were similarly affected and it was plain that there was in the hospital an epidemic of a highly infectious nature producing, among other things, manifestations in the central nervous system. Because of the threat to the health of patients, and because of the large number of nurses involved, the hospital closed on that date and remained closed until October 5th. By that time the epidemic was almost over although sporadic cases appeared up to November 24th.

  Between July 13th and November 24th, 292 members of the medical, nursing, auxiliary medical, ancillary and administrative staff were affected by the illness and of these, 255 were admitted to hospital; 37 nurses were looked after at home or admitted to other hospitals from their home.

  It is remarkable that, although the hospital was full at the time of the epidemic, only 12 patients who were already there developed the disease.


Friday, July 10, 2015

My response to the medically unexplained nonsense from Professor Moss Morris

  Dear Professor Moss Morris,

  as a doctor who has been bedridden for more than a decade with ME/CFS, the result of a major Relapse caused by harmful graded exercise therapy, which breaches the do No Harm principle of the GMC, I'm always amazed that doctors and other medical professionals in this day and age of the computer, where you can read up on all the evidence sitting behind your computer using PubMed, totally ignore all the evidence that what they say is wrong. On the other hand I shouldn't be so surprised as in the first part of your post you write that you are from Kings College and that's where the top dog of Pinocchio psychiatry resides who has been deliberately ignoring clinical evidence for decades that what he says is wrong, to the detriment of people with severely disabling neuro immune diseases.

  In Good Medical Practice, duties of a doctor, the GMC makes it's perfectly perfectly clear that not keeping up to date with the current evidence is unacceptable, unfortunately that is what you and the Pinocchio Psychiatrists are doing when you ignore all the evidence that ME/CFS is a debilitating physical disease and call it a medically unexplained disease instead.

  What is medically unexplained is that people like yourself totally ignore evidence. Or as Dr Shepherd, the honorary medical adviser of the ME Association recently wrote: "Failure to keep up with the research on ME/CFS is 'inexcusable'"

  As professor Hooper wrote a few years ago when does ignoring evidence become serious professional misconduct ? It's clear that the Pinocchio Psychiatrists have crossed that line a long time ago. Please do keep in mind that evidence that something is psychosomatic or all in the mind, because that's basically what you say when you call a disease medically unexplained, does not exist.

  Or to use the words of exercise physiologist professor Keller: "Given what we have learned in the past eight years about this illness, it is intellectually embarrassing to suggest that ME is a psychological illness."

  A Danish study showed a few days ago that the quality of life for people with this disease is the worst when compared with 20 other diseases, including a number of cancers, chronic renal failure, ischaemic heart disease etc. This also makes it perfectly clear that the current "treatments", ie CBT and GET, are at best totally useless.

  It would be "nice" if you change your post in line with all the current evidence that ME/CFS is a debilitating physical disease, and not a psychological or psychiatric disease, as the prestigious American Institute the IOM recently concluded after an extensive review of the literature.

  Instead of ridiculing and belittling us with psychosomatic nonsense it's more than time that we get proper treatment so we get our health and independence back, can come off benefits and go back to work.

  For your information Prof Mella, a Norwegian oncologist and his team recently published their latest study which not only suggests that ME/CFS is an autoimmune disease but also shows that two thirds of responders to the cancer drug Rituximab, are still in remission at the 36-month follow-up.

  So not medically unexplained but a debilitating neuro immune disease. More than time that you and Kings College get up to date with the current evidence instead of ignoring it, which is inexcusable, breaches the GMC guidance and constitutes Bad Medical Practice.

  Kind regards,

  Dr Maik Speedy


  #     Exercise physiologist Prof Keller: "Given what we have learned in the past eight years about this illness, it is intellectually embarrassing to suggest that ME is a psychological illness."

  #     Professor Hooper: When does ignoring evidence by doctors become serious professional misconduct ?

  #     Prof Edward Shorter and the psychic epidemic of ignoring clinical evidence

  #     Evidence that a disease is psychosomatic doesn't exist

  #     Massachusetts Medical Society's NEJM Journal Watch: "There is still no cure, or even any reliably effective treatment, for CFS"

  #     Editorial in Jacobs Journal of Physiotherapy and Exercise: it is essential to protect ME patients against harm by exercise regimes

  #     Rituximab maintenance infusions leads to prolonged disease remission in ME/CFS

  #     Immunological Similarities between Cancer and Chronic Fatigue Syndrome

  #     Danish study finds patients with MEcfs have the lowest health-related quality of life of 21 conditions looked at which means / confirms that CBT and GET are at best totally useless 



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