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Inflammatie in ME/CVS

sterker dan in depressie,

beide aandoeningen

gaan gepaard met







Uit een studie van dr. Michael Maes, Karl Ringel en ondergetekende blijkt dat

interleukin-1 (IL-1α en ) en tumor necrosis factor-α (TNF-α), markers voor inflammatie,

in ME/CVS in veel sterkere mate aanwezig zijn dan dan in depressie met fysieke klachten en

ME/CVS ťn "depressie" beide gepaard gaan met (cellulaire) immuunactivatie (neopterine).


In depressie die vergezeld gaat met lichamelijke klachten is er een nauw verband tussen inflammatie aan de ene kant en immuunactivatie aan de andere kant, in ME/CVS niet.


Het feit dat ME/CVS en depressie met fysieke klachten immunologisch deels overlappen, verklaart wellicht waarom ME/CVS soms gepaard gaat met "inflammatoire depressie".


Ook bij de diagnose depressie zou immunologisch onderzoek moeten plaatsvinden,

omdat depressie een vergaarbakdiagnose is en lichamelijke oorzaken kan hebben.






Inflammatory and cell-mediated immune biomarkers

in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome and depression:

inflammatory markers are higher in

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome than in depression

Psychother Psychosom 2012;81(5):286-295. doi: 10.1159/000336803.

Michael Maes a, Frank N.M. Twisk b, Karl Ringel c

  1. Maes Clinics, TRIA, Bangkok, Thailand;
  2. ME-de-patiŽnten Foundation, Limmen, The Netherlands;
  3. Immunologische Laboratorien, Aachen, Germany







Depression is an inflammatory disorder

while many authors declare

myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS)

to be a functional disorder.


The aim of the present study

is to compare inflammatory and cell-mediated immune (CMI) responses

between depression and ME/CFS.





We measured

two proinflammatory cytokines (PICs) in plasma,

interleukin-1 (IL-1) and tumor necrosis factor-α (TNF-α),

with enzyme-linked immunosorbent assays, and

serum neopterin with a radioimmunoassay

in controls, ME/CFS and depressive patients.





Plasma PICs were significantly higher in ME/CFS than in depression and

higher in both patient groups than in controls.


Increased PIC levels in depression were attributable to

the presence of fatigue and physio-somatic symptoms.


Serum neopterin did not differ significantly between depression and ME/CFS

but was higher in both patient groups than in controls.


The significant positive correlations between neopterin and either IL-1 or TNF-α

were significantly greater in depression than in ME/CFS.





Since PICs cause depression-like behaviors and fatigue/malaise,

we suggest that

inflammation may play a role in the pathophysiology of ME/CFS and depression.


Increased neopterin also seems to contribute to the pathophysiology of both disorders.


This study has detected a shared 'pathway phenotype',

i.e. disorders in inflammatory and CMI pathways,

which underpins both ME/CFS and depression and,

therefore, may explain the co-occurrence of both disorders.


ME/CFS and depression are discriminated from each other

by increased PICs in ME/CFS and

differences in the immune cell communication networks.