TGI Friday!| Our weekly round-up of recently published research abstracts | 29 July 2016

From the Journal of Psychosomatic Research, published online 19 July 2016.

Enhanced psychological flexibility and improved quality of life in chronic fatigue syndrome/myalgic encephalomyelitis

Sarah Densham(1), Deborah Williams(2), Anne Johnson(2), Julie M. Turner-Cobb(1)
1) Department of Psychology, University of Bath, Claverton Down, Bath, UK
2) The Royal National Hospital for Rheumatic Diseases, Royal United Hospitals Bath, NHS Foundation Trust, Bath, UK


* Interdisciplinary group treatment may improve quality of life in CFS/ME.

* Psychological Flexibility (PF) has applied utility in the treatment of CFS/ME.

* Changes in PF activity/occupational engagement suggest greatest benefit in CFS/ME.



Psychological Flexibility (PF) is a relatively new concept in physical health. It can be defined as an overarching process of being able to accept the presence of wanted/unwanted experiences, choosing whether to change or persist in behaviour in response to those experiences. Associations between processes of PF and quality of life (QoL) have been found in long-term health conditions such as chronic pain, PF has not yet been applied to Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME).


Changes in PF, fatigue severity and QoL were examined in one hundred and sixty-five patients with CFS/ME engaged in a six-week outpatient interdisciplinary group treatment programme. Participants were assessed using a series of self-report measures at the start of the start (T1) and end of a six-week programme (T2) and at six months follow up (T3).


Significant changes in PF and QoL were observed from pre-treatment (T1) to post treatment follow-up (T2 and T3); changes in fatigue severity were observed from T1 to T3 only. Controlling for fatigue severity, changes in the PF dimension of activity/occupational engagement were associated with improvement in QoL at six month follow up (T3) but not at six weeks post programme (T2).


Findings indicate an interdisciplinary group treatment approach for people with CFS/ME may be associated with improved QoL, processes of PF and fatigue severity, supporting a link between PF and long term health conditions. Results highlight links between PF and patient QoL in CFS/ME and the value of interdisciplinary treatment approaches in this patient population.

From the Journal of Cardiology, 28 January 2016.

Down-regulation of renin–aldosterone and antidiuretic hormone systems in patients with myalgic encephalomyelitis/chronic fatigue syndrome

Kunihisa Miwa
Miwa Naika Clinic, Toyama, Japan



Central nervous system dysfunction associated with myalgic encephalomyelitis (ME) has been postulated as the cause of chronic fatigue syndrome (CFS). A small heart or reduced left ventricular volume with reduced cardiac output has been reported to be common in patients with ME. The main circulatory blood volume regulators may be down-regulated.


Plasma levels of the neurohumoral factors that regulate circulatory blood volume were determined in 18 patients with ME and 15 healthy subjects (Controls).


The echocardiographic examination revealed that the mean values for the left ventricular end-diastolic diameters, stroke volume index, and cardiac index as well as the mean blood pressure were all significantly smaller in the ME group than in the Controls. The mean plasma renin activity (1.6 ± 1.0 ng/ml/h vs. 2.5 ± 1.5 ng/ml/h, p = 0.06) was considerably lower in the ME group than in the Controls. Both the mean plasma aldosterone (104 ± 37 pg/ml vs. 157 ± 67 pg/ml, p = 0.004) and antidiuretic hormone (ADH) (2.2 ± 1.0 pg/ml vs. 3.3 ± 1.5 pg/ml, p = 0.02) concentrations were significantly lower in the ME group than in the Controls. Desmopressin (120 μg), a synthetic version of arginine vasopressin, was orally administered for five successive days to 10 patients with ME. In five patients (50%), the symptoms of orthostatic intolerance during a 10 min active standing test were ameliorated in association with a significant increase in urinary osmotic pressure and decrease in heart rate. Furthermore, in five patients (50%), the performance status scores for the activities of daily living were improved.


Both the renin–aldosterone and ADH systems were down-regulated despite the existence of reduction in cardiac preload and output in patients with ME. Desmopressin improved symptoms in half of the patients.

From the Journal of Psychosomatic Research, 16 July 2016.

A UK-based review of recommendations regarding the management of chronic fatigue syndrome

Miriam Mallet(1), Eleanor King(1), Peter D. White(2)
1) Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK
2) Wolfson Institute of Preventive Medicine, Barts and the London School of medicine and Dentistry, Queen Mary University of London, London, UK


* There were marked discrepancies between patient and professional sources’ views on treatment recommendations

* Patient organisations preferentially recommended medicines, pacing and complementary treatments

* Medical organisations recommended rehabilitation therapies



Chronic fatigue syndrome (CFS) is a controversial illness, with apparent disagreements between medical authorities and patient support organisations regarding safe and effective treatments. The aim of this study was to measure the extent of different views regarding treatments, comparing patient support organisations and medical authorities in the UK.


Two independent raters analysed two groups of resources: UK patient support websites and both medical websites and textbooks. A 5-point Likert scale was developed with the question ‘With what strength does the source recommend these treatments?’ The various treatments were divided into the following four groups: complementary and alternative medicine (CAM), pharmacological, rehabilitative, and pacing therapies.


There were significant differences between the scores for patient support organisations and medical sources for all 4 treatment groups. The results for supporting CAM were 74% (patient group) vs 16% (medical source) (p < 0.001), 71% vs 42% for pharmacological (p = 0.01), 28% vs 94% for rehabilitative (p < 0.001) and 91% vs 50% for pacing treatments (p = 0.001). CONCLUSIONS There were substantially different treatment recommendations between patient support organisations and medical sources. Since expectations can determine response to treatment, these different views may reduce the engagement in and effectiveness of rehabilitative therapies recommended by national guidelines and supported by systematic reviews.

The Pharmacogenomics Journal, 26 July 2016.

Genetic variation in catechol-O-methyltransferase modifies effects of clonidine treatment in chronic fatigue syndrome

K T Hall, J Kossowsky, T F Oberlander, T J Kaptchuk, J P Saul, V B Wyller, E Fagermoen, D Sulheim, J Gjerstad, A Winger and K J Mukamal


Clonidine, an α2-adrenergic receptor agonist, decreases circulating norepinephrine and epinephrine, attenuating sympathetic activity. Although catechol-O-methyltransferase (COMT) metabolizes catecholamines, main effectors of sympathetic function, COMT genetic variation effects on clonidine treatment are unknown.

Chronic fatigue syndrome (CFS) is hypothesized to result in part from dysregulated sympathetic function. A candidate gene analysis of COMT rs4680 effects on clinical outcomes in the Norwegian Study of Chronic Fatigue Syndrome in Adolescents: Pathophysiology and Intervention Trial (NorCAPITAL), a randomized double-blinded clonidine versus placebo trial, was conducted (N=104).

Patients homozygous for rs4680 high-activity allele randomized to clonidine took 2500 fewer steps compared with placebo (Pinteraction=0.04). There were no differences between clonidine and placebo among patients with COMT low-activity alleles.

Similar gene–drug interactions were observed for sleep (Pinteraction=0.003) and quality of life (Pinteraction=0.018).

Detrimental effects of clonidine in the subset of CFS patients homozygous for COMT high-activity allele warrant investigation of potential clonidine–COMT interaction effects in other conditions.


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