Abstract

Benign  Myalgic  Encephalomyelitis  (ME)  /  Chronic  Fatigue  Syndrome  (CFS) is  a  debilitating  disease  which,  despite  numerous  biological  abnormalities  has remained highly controversial.

Not withstanding  the  medical  pathogenesis  of  ME/CFS,  the  (bio)psychosocial model is adopted by many governmental organizations and medical professionals to legitimize the combination of Cognitive Behavioral Therapy (CBT) and Graded Exercise Therapy (GET) for ME/CFS. Justified by this model CBT and GET aim at eliminating presumed psychogenic and socially induced maintaining factors and reversing deconditioning, respectively.

In this review we invalidate the (bio)psychosocial model for ME/CFS and demonstrate that the success claim for CBT/GET to treat ME/CFS is unjust. CBT/GET is not only hardly more effective than non-interventions or standard medical care, but many patients report that the therapy had affected them adversely, the majority of them even reporting substantial deterioration. Moreover, this review shows that exertion and thus GET most likely have a negative impact on many ME/CFS patients.

Exertion induces post-exertional malaise with a decreased physical performance/aerobic  capacity,  increased  muscoskeletal  pain,  neurocognitive  impairment, “fatigue”, and weakness, and a long lasting “recovery” time. This  can  be  explained  by  findings  that  exertion  may  amplify  pre-existing pathophysiological abnormalities underpinning ME/CFS, such as inflammation, immune dysfunction, oxidative and nitrosative stress, channelopathy, defective stress  response  mechanisms  and  a  hypoactive  hypothalamic-pituitary-adrenal axis.

We conclude that it is unethical to treat patients with ME/CFS with ineffective, non-evidence-based and potentially harmful “rehabilitation therapies”, such as CBT/GET.

A review on cognitive behavorial therapy (CBT) and graded exercise therapy (GET) in myalgic encephalomyelitis (ME) / chronic fatigue syndrome (CFS): CBT/GET is not only ineffective and not evidence-based, but also potentially harmful for many patients with ME/CFS, by Frank NM Twisk and Michael Maes in Neuroendocrinol Lett 2009; 30(3): 284–299