TGI Friday! | Our weekly round-up of recently published research abstracts | 3 February 2017

February 3, 2017

From Biological Psychiatry, published online 31 August 2016.

Prefrontal Structure Varies as a Function of Pain Symptoms in Chronic Fatigue Syndrome.

van der Schaaf ME(1), De Lange FP(2), Schmits IC(3), Geurts DE(4), Roelofs K(3), van der Meer JW(5), Toni I(3), Knoop H(6).
1) Expert Centre for Chronic Fatigue, Nijmegen; Donders Institute for Brain, Cognition, and Behaviour, Centre for Neuroimaging, Radboud University Nijmegen, Nijmegen. Electronic address:
2) Donders Institute for Brain, Cognition, and Behaviour, Centre for Neuroimaging, Radboud University Nijmegen, Nijmegen.
3) Expert Centre for Chronic Fatigue, Nijmegen.
4) Department of Psychiatry, Radboud University Medical Center, Nijmegen; Donders Institute for Brain, Cognition, and Behaviour, Centre for Neuroimaging, Radboud University Nijmegen, Nijmegen; Adult Personality Disorder Service, South London and Maudsley National Health Service Foundation Trust, London, United Kingdom.
5) Department of Internal Medicine, Nijmegen.
6) Expert Centre for Chronic Fatigue, Nijmegen; Department of Medical Psychology, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands.



Chronic fatigue syndrome (CFS) is characterized by severe fatigue persisting for ≥6 months and leading to considerable impairment in daily functioning. Neuroimaging studies of patients with CFS have revealed alterations in prefrontal brain morphology. However, it remains to be determined whether these alterations are specific for fatigue or whether they relate to other common CFS symptoms (e.g., chronic pain, lower psychomotor speed, and reduced physical activity).


We used magnetic resonance imaging to quantify gray matter volume (GMV) and the N-acetylaspartate and N-acetylaspartylglutamate/creatine ratio (NAA/Cr) in a group of 89 women with CFS. Building on previous reports, we tested whether GMV and NAA/Cr in the dorsolateral prefrontal cortex are associated with fatigue severity, pain, psychomotor speed, and physical activity, while controlling for depressive symptoms. We also considered GMV and NAA/Cr differences between patients with CFS and 26 sex-, age-, and education-matched healthy controls.


The presence of pain symptoms was the main predictor of both GMV and NAA/Cr in the left dorsolateral prefrontal cortex of patients with CFS. More pain was associated with reduced GMVs and NAA/Cr, over and above the effects of fatigue, depressive symptoms, physical activity, and psychomotor speed. In contrast to previous reports and despite a large representative sample, global GMV did not differ between the CFS and healthy control groups.


CFS, as diagnosed by Centers for Disease Control and Prevention criteria, is not a clinical entity reliably associated with reduced GMV. Individual variation in the presence of pain, rather than fatigue, is associated with neuronal alterations in the dorsolateral prefrontal cortex of patients with CFS.

FromBehavioural and Cognitive Psychotherapy, 18 January 2017.

Chronic Fatigue Syndrome: Cognitive, behavioural and emotional processing vulnerability factors

Samantha K. Brooks(1), Trudie Chalder(1), Katharine A. Rimes(2)
1) Department of Psychological Medicine,King's College London, Institute of Psychiatry,Weston Education Centre,Cutcombe Road, London SE5 9RJ.
2) King's College London, Institute of Psychiatry,Psychology and Neuroscience,Department of Psychology,Henry Wellcome Building, De Crespigny Park,London SE5 8AF.



Cognitive-behaviour al models of chronic fatigue syndrome (CFS) suggest that personality factors such as perfectionism and high moral standards may contribute to the development of CFS.


To investigate cognitive, behavioural and emotional processing risk factors for CFS.


CFS patients (n = 67) at a UK specialist clinic completed questionnaires about psychological characteristics both currently and retrospectively (6 months pre-CFS onset). Responses were compared with those of healthy individuals (n=73) who rated their current characteristics. Forty-four relatives retrospectively rated the pre-morbid psychological characteristics of the CFS participants.


CFS patients showed similar levels of current perfectionism to controls, though higher pre-morbid perfectionism. CFS patients showed greater self-sacrificial beliefs and more unhelpful beliefs about experiencing and expressing negative emotions, both currently but more markedly prior to onset. In the 6 months pre-illness onset, CFS patients showed more disruption to their primary goal and greater general stress than controls. Ratings of pre-morbid psychological characteristics by relatives were consistent with patients' self-reports. The extent of overinvestment in one goal was significantly associated with fatigue.


Perfectionism, self-sacrificial tendencies, unhelpful beliefs about emotions, and perceived stress may be present to a greater extent pre-morbidly in CFS patients compared with healthy individuals.

From Psychological Medicine, 23 January 2017 [Epub ahead of print].

Heterogeneity in chronic fatigue syndrome – empirically defined subgroups from the PACE trial.

Williams TE(1), Chalder T(2), Sharpe M(3), White PD(1).
1) Centre for Psychiatry, Wolfson Institute of Preventive Medicine, Barts and the London School of Medicine, Queen Mary University of London, London,UK.
2) Academic Department of Psychological Medicine,King's College London, Weston Education Centre,London,UK.
3) Department of Psychiatry,Psychological Medicine Research, University of Oxford,Oxford,UK.



Chronic fatigue syndrome is likely to be a heterogeneous condition. Previous studies have empirically defined subgroups using combinations of clinical and biological variables. We aimed to explore the heterogeneity of chronic fatigue syndrome.


We used baseline data from the PACE trial, which included 640 participants with chronic fatigue syndrome. Variable reduction, using a combination of clinical knowledge and principal component analyses, produced a final dataset of 26 variables for 541 patients. Latent class analysis was then used to empirically define subgroups.


The most statistically significant and clinically recognizable model comprised five subgroups. The largest, ‘core' subgroup (33% of participants), had relatively low scores across all domains and good self-efficacy. A further three subgroups were defined by: the presence of mood disorders (21%); the presence of features of other functional somatic syndromes (such as fibromyalgia or irritable bowel syndrome) (21%); or by many symptoms – a group which combined features of both of the above (14%). The smallest ‘avoidant-inactive' subgroup was characterized by physical inactivity, belief that symptoms were entirely physical in nature, and fear that they indicated harm (11%). Differences in the severity of fatigue and disability provided some discriminative validation of the subgroups.


In addition to providing further evidence for the heterogeneity of chronic fatigue syndrome, the subgroups identified may aid future research into the important aetiological factors of specific subtypes of chronic fatigue syndrome and the development of more personalized treatment approaches.

From BMC Immunology (open access), 28 January 2017.

Giardia-specific cellular immune responses in post-giardiasis chronic fatigue syndrome

Kurt Hanevik(1,2), Einar Kristoffersen(1,3), Kristine Mørch(1,2), Kristin Paulsen Rye(1), Steinar Sørnes(1), Staffan Svärd(4), Øystein Bruserud(1) and Nina Langeland(1,2).
1) Department of Clinical Science, Lab-building 8.floor, University of Bergen
2) Center for Tropical Infectious Diseases, Haukeland University Hospital
3) Department of immunology and transfusion medicine, Haukeland University Hospital



The role of pathogen specific cellular immune responses against the eliciting pathogen in development of post-infectious chronic fatigue syndrome (PI-CFS) is not known and such studies are difficult to perform. The aim of this study was to evaluate specific anti-Giardia cellular immunity in cases that developed CFS after Giardia infection compared to cases that recovered well. Patients reporting chronic fatigue in a questionnaire study three years after a Giardia outbreak were clinically evaluated five years after the outbreak and grouped according to Fukuda criteria for CFS and idiopathic chronic fatigue. Giardia specific immune responses were evaluated in 39 of these patients by proliferation assay, T cell activation and cytokine release analysis. 20 Giardia exposed non-fatigued individuals and 10 healthy unexposed individuals were recruited as controls.


Patients were clinically classified into CFS (n = 15), idiopathic chronic fatigue (n = 5), fatigue from other causes (n = 9) and recovered from fatigue (n = 10). There were statistically significant antigen specific differences between these Giardia exposed groups and unexposed controls. However, we did not find differences between the Giardia exposed fatigue classification groups with regard to CD4 T cell activation, proliferation or cytokine levels in 6 days cultured PBMCs. Interestingly, sCD40L was increased in patients with PI-CFS and other persons with fatigue after Giardia infection compared to the non-fatigued group, and correlated well with fatigue levels at the time of sampling.


Our data show antigen specific cellular immune responses in the groups previously exposed to Giardia and increased sCD40L in fatigued patients.

2 thoughts on “TGI Friday! | Our weekly round-up of recently published research abstracts | 3 February 2017”

    Williams, Chalder, Sharpe and White.
    Psychological Medicine, 23 January 2017 [Epub ahead of print].
    Someone needs to help these poor suffering people! They clearly have a mass delusion or some other kind of shared mental illness, perpetuating each other. I talk of course about the authors of yet another “PACE Trial data” paper which reaches prejudiced and ignorant conclusions, (much of which is deceitfully disguised in the ‘method’ and ‘result’) on discredited data.
    The way, manner and vocabulary used to define their ‘5 sub groups’ screams preconception, if not prejudice, with an agenda to, (still??!!) classify, investigate and treat ME as a psychosocial dysfunction or psychosomatic illness rather than a physical illness!
    Many will find it upsetting and irritating to read, below, my very sarcastic re-wording of the paper. I beg forgiveness for this, and if you are finding it upsetting, then stop reading it! They are not worth it and they have done far too much damage already. However, if you can read it with a chuckle, it may help you explain, in simple terms, to simple GP’s or simple clinicians, why and how this is just another attempt by a group of ignorant, unscientific people trying to justify something that has already been proven to be fraud and false. The only psychologically, morally and cognitively deficient individuals in the PACE trial were the investigators and authors. Given time, this is going to make a fantastic screen comedy that will embarrass scientists everywhere and be required viewing for budding scientists on “how not to do science”.
    Let me reword the paragraphs under “Methods and “Results”
    “Me Thod (we god it right the first time)”
    We used the initial recruiting screening and questionaire data gleaned from the 640 participants that initially started our discredited and fraudulent PACE trial. We very carefully selected those bits of data that we most wanted to highlight, and perhaps later skew, which, of the possibly 100’s, perhaps1000’s of variable combinations and computations of the recorded individual variables, we chose 26, having to, like last time, exclude a small number of participants (n99, 15.4%) that might not fit the data that we wanted to look at, or fit the data in the way that we wanted them to. Having done all this we had to use several (probably far more than 20!) mathematical models and tricks trying to ‘statistically’ distil the data into showing a difference in CFS sufferers to ‘normals’.

    The best we could come up with is describing CFS sufferers as belonging to one of 5 groups.
    The largest group, which was about one third of sufferers, despite our best efforts to prove otherwise, showed no sign of emotional or psychological distress or dysfunction and was employing positive, self helping cognitive and behavioural mannerisms and traits designed to minimise the effects of any debilitating illness. We should have probably excluded these along with the other 99 at the start, but we were struggling to justify this scientifically.
    A further 3 sub-groups however completely justified our sifting the pre-intervention data from the PACE trial (which was sabotaged by the participants by their not getting better as a group, statistically speaking, and by those who did feel any better only doing so very partially, as anyone without any illness might, with the same interventions.)

    A fifth had symptoms of depression, which if we call a ‘mood disorder’ can help those less insightful, including ourselves, simply interpret as ‘nutters’, after all, there can be nothing depressing about an imaginary illness, can there.
    Another fifth had other imaginary, overvalued and delusional illnesses such as fibromyalgia and irritable bowel syndrome.
    A seventh had both of the above and were nutters with other imaginary illnesses.
    A tenth of those that we filtered into the analysed group actually proved us completely right after all. This group avoided physical activity because they actually believed that it caused them pain. They believed that this imaginary pain indicated that further activity would cause actual physical harm and result in more pain and fatigue. These people were the worst affected by their psychosomatic/ psychosocial/ psychotic illness.

  2. I totally agree with Dr Who.

    Words fail me, there aren’t words in the English langage to describe how I feel on seeing research papers like this one. More PACE trial rehashed!.

    It’s just diabolical that Williams, Chalder, Sharpe, and White are carrying on as if nothing has happened have they no shame! Their total disregard of the exposure of the PACE trial as a fraud and total lack of respect and concern for patients is just beyond belief.

    This has huge implications for the integrity of science, we all rely on science to be be true and not a made up pack of spin. Our science system is truly broken if no one with authority in the world of medicine or in the Media is able or willing to stand up to these researchers and tell it as it is. They have the power to end this charade overnight if they cared to.

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