White PD (2010): CFS - Is it 1 discrete syndrome or many? Implications for FSS debate

[Dolphin]

I don't think this is an important paper (quite the opposite) but I made a few comments and thought I'd post them somewhere

(Hasn't reached PubMed yet)

Articles In Press
http://www.jpsychores.com/inpress

Chronic fatigue syndrome: Is it one discrete syndrome or many? Implications for the "one vs. many" functional somatic syndromes debate In Press Corrected Proof,
Available online 18 March 2010 Peter D. White Journal of Psychosomatic Research

DOI: 10.1016/j.jpsychores.2010.01.008

Abstract | Full Text | Full-Text PDF (110 KB)

http://www.jpsychores.com/article/S0022-3999(10)00013-9/abstract

Chronic fatigue syndrome: Is it one discrete syndrome or many? Implications for the "one vs. many" functional somatic syndromes debate

Peter D. White

Received 10 November 2009; received in revised form 12 January 2010; accepted 14 January 2010. published online 18 March 2010.

Corrected Proof

Abstract
There is a current debate as to whether "functional somatic syndromes"

(FSSs) are more similar to or different from each other. While at the same time, there is evidence of heterogeneity within single syndromes. So, it could be that these syndromes are all part of one big process/illness, are discrete in their own right, or that they are heterogeneous collections of different illnesses lumped together by common symptoms but separated by uncommon pathophysiologies. The example of chronic fatigue syndrome (CFS) is instructive. There is evidence to support all three models of understanding.

Three recent large studies have suggested that FSSs are both similar and dissimilar at the same time. The solution to the debate is that we need to both "lump" and "split." We need to study both the similarities between syndromes and their dissimilarities to better understand what we currently call the FSSs.

Keywords: Functional somatic syndromes, Chronic fatigue syndrome, heterogeneity, homogeneity, risk markers

Wolfson Institute of Preventive Health, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK Department of Psychological Medicine, St Bartholomew's Hospital, London, EC1A 7BE, UK. Tel.: +44 207 601 8108; fax: +44 207 601 7097.
PII: S0022-3999(10)00013-9
doi:10.1016/j.jpsychores.2010.01.008
C 2010 Published by Elsevier Inc.

 

[Dolphin]

(Not exciting) Some commentary

I just read the White paper. Not sure if there is a word for a collection of not-exciting studies (or a review of such studies) but if there was, this might be a good example.

All those CDC studies may sound impressive but they used the empiric criteria (means shouldn't count at all as CFS studies in my book) and despite what they said, the "biomarkers" were generally basic blood tests.

The naming of the classes was dodgy e.g. what constitutes obesity. To say that the second study replicated the first is really bending the truth. I posted three comments on the replication study:
http://www.pophealthmetrics.com/content/7/1/17/comments which deal with some of my criticisms.

About the only useful thing I got out of it is some quotes that could be used to show understanding the aetiology and pathophysiology of a condition can be useful (people may remember the MRC Research Strategy said they weren't that important):

"An additional way to better differentiate the heterogeneity within single FSS is to develop an iterative process between a risk marker and its phenotypic expression. An example of this comes from understanding the genetic associations of restless leg syndrome (RLS), in which an association was found with chromosome 12q and the disease expression of RLS, but the association was strongest in those with prominent periodic leg movements [42]. In other words, the genetic association allowed the better differentiation of the associated phenotype. This iterative process may work for any broadly associated risk marker. All these designs require large studies, so pan-European and other international collaborations are the way forward."

Earlier, he also said:

"A second problem is that these attempts to define the heterogeneity of CFS have relied on symptoms and demographic variables alone, excluding associated biological abnormalities, such as down-regulated hypothalamicpituitary- adrenal axis activity [16]. Adding such biomarkers might reveal subphenotypes that are defined by the underlying biological processes, which are called endophenotypes [17]."

The criticism is probably true for some phenotypes:

"Although similar clusters of symptoms are found across studies, no work has looked at the validity of these empirically defined subphenotypes, such as longitudinal studies with risk marker associations. We therefore cannot be sure that these symptom clusters define valid subphenotypes."

e.g. one of them referenced was:

[15] May M, Emond A, Crawley E. Phenotypes of chronic fatigue syndrome in children and young people. Arch Dis Child 2009 [Epub ahead of print] http://www.fetalneonatal.com/content/early/2009/10/19/adc.2009.158162.abstract.

but I didn't have much confidence in the phenotypes when I read it (people's symptoms can change over time - I know mine have - so collections of symptoms at any one time may not give solid subgroups).

Tom

 

[MEKoan]

Forgive me, but, to us it is our very lives... to them it is just slicing off a piece of the pie.

I don't buy the subsets and the divide and conquer strategy.

We know who we are.

 

[MEKoan]

Tom, just want to say, I see you as a brother.

Peace out,
Koan