Is chronic fatigue syndrome a connective tissue disorder? A cross-sectional study in adolescents, 2005, Van de Putte et al.

Abstract
Objectives: To investigate whether constitutional laxity of the connective tissues is more frequently present in adolescents with chronic fatigue syndrome (CFS) than in healthy controls. Increased joint hypermobility in patients with CFS has been previously described, as has lower blood pressure in fatigued individuals, which raises the question of whether constitutional laxity is a possible biological predisposing factor for CFS.

Design: Cross-sectional study.

Participants: Thirty-two adolescents with CFS (according to the criteria of the Centers for Disease Control and Prevention) referred to a tertiary hospital and 167 healthy controls.

Methods: The 32 adolescents with CFS were examined extensively regarding collagen-related parameters: joint mobility, blood pressure, arterial stiffness and arterial wall thickness, skin extensibility, and degradation products of collagen metabolism. Possible confounding factors (age, gender, height, weight, physical activity, muscle strength, diet, alcohol consumption, and cigarette smoking) were also measured. The results were compared with findings in 167 healthy adolescents who underwent the same examinations.

Results: Joint mobility, Beighton score, and collagen biochemistry, all indicators of connective tissue abnormality, were equal for both groups. Systolic blood pressure, however, was remarkably lower in patients with CFS (117.3 vs. 129.7 mm Hg; adjusted difference: -13.5 mm Hg; 95% confidence interval [CI]: -19.1, -7.0). Skin extensibility was higher in adolescents with CFS (mean z score: 0.5 vs. 0.1 SD; adjusted difference: 0.3 SD; 95% CI: 0.1, 0.5). Arterial stiffness, expressed as common carotid distension, was lower in adolescents with CFS, indicating stiffer arteries (670 vs 820 mum; adjusted difference: -110 mum; 95% CI: -220, -10). All analyses were adjusted for age, gender, body mass index, and physical activity. Additionally, arterial stiffness was adjusted for lumen diameter and pulse pressure.

Conclusions: These findings do not consistently point in the same direction of an abnormality in connective tissue. Patients with CFS did have lower blood pressure and more extensible skin but lacked the most important parameter indicating constitutional laxity, ie, joint hypermobility. Moreover, the collagen metabolism measured by crosslinks and hydroxyproline in urine, mainly reflecting bone resorption, was not different. The unexpected finding of stiffer arteries in patients with CFS warrants additional investigation.

Link: Is Chronic Fatigue Syndrome a Connective Tissue Disorder? A Cross-Sectional Study in Adolescents | Pediatrics | American Academy of Pediatrics (aap.org)

 

An old study from 2005, but they measured a couple of interesting thing regarding the EDS connection, which was not supported. They also tried to control for various factors such as physical activity.

 

I'm not remotely bendy but lots of my MEep friends are. I suspect it is a distinct phenotype. You could envisage either a potentially different causation or that the connective tissue issue makes them more at risk of infections.

 

What was the CDC diagnostic criteria for CFS back in 2005? I also have issues with the limitations of the Beighton Score in that it excludes obvious hypermobility in so many other joints, which means you can have extreme hypermobility but not meet the criteria because you don't have a couple of the ones specified.

 

But lots of people are bendy anyway. Anything from 20-40 of young women can score as 'hyper mobile'. So yes lots - regardless of having ME/CFS. There seems to be no more evidence that it is a 'distinct phenotype' than having ME/CFS and brown eyes to be honest.

 

The Beighton score was never shown to be a useful marker of anything. It was just made up.
But if hypermobility is nothing to do with anything much, except for those with shoulder dislocations or knock knees then the whole thing is a waste of time anyway.

 

Yes although zero of my healthy friends are in my n=1 sample, so it is a very marked split. I'm very much the odd one out.
It would be good to see some robust science answering this as part of the phenotype question either way at some point though . As it could be a confounding factor if not pertinent.