Journal of IiMER June 2024 better prognosis. However, the latter study relies on limited data and is contradicted by a more recent and larger study [14]. Cognitive treatment plays a limited role in ME/CFS as pointed out in the NICE-guidelines [2]. In lumping patients with a diagnosis of ME/CFS in to one non-specific group of patients with fatigue clearly demonstrates the authors’ limited clinical and scientific experience in ME/CFS and the fact that several of the manifestations of this disease may be alleviated by targeted treatment [15-17]. The authors state that the approach often recommended by the public narrative of inactivity, isolation, and sensory deprivation, risks worsening symptoms and associated disability. Firstly, such a statement discloses the authors’ lack of clinical experience with the range of severity and phenotypes in ME/CFS requiring modifications in the therapeutic approach. Secondly, it is an unsubstantiated claim (no references) and for the potential risks, the authors refer to a meta-analysis on bed rest as a primary treatment in conditions such as acute low back pain, preeclampsia, and myocardial infarction [15] and to an unpublished study on long-term sensory deprivation related to space flights [16]. Sensory deprivation is not a choice but a necessity in ME/CFS-patients due to the general increased sensitivity of the nervous system to afferent input secondary to neuroinflammation. Symptoms of neuroinflammation are essential in the diagnosis of ME/CFS and different imaging techniques have shown neuroinflammation to be present in several studies [17,18] and that neuroinflammation is a common denominator in ME/CFS and longCOVID19. In the “Oslo Declaration’s” justification for a new perspective, the authors refer to chronic pain, fibromyalgia, and post COVID syndrome for support, but recent advances do not support their narrative. The “Oslo Declaration” is flawed, and the dismissal of biological evidence as non-specific associations is bewildering, with the authors seeking to replace it with a biopsychosocial model entirely based on associations. A recent study in fibromyalgia has demonstrated that patient autoantibodies mediate the sensory, motor, and anatomical symptoms and signs that patients present with [20]. Similarly, studies have revealed pathophysiological mechanisms including immune cell dysregulation and altered cortisol levels in post COVID patients [21]. The authors claim “After 40 years of research into CFS/ME … neither a specific biological defect or pathology, nor a specific biomarker, has been identified”. It is estimated that at least 10,000 scientific papers have been published on ME/CFS and several distinct biological changes have been discovered resulting in targeted interventions and thorough descriptions of the pathobiology of ME/CFS [22, 23]. In opposition to the vast amount of biopathological evidence, the authors refer to a publication where the initial part of the summary reads: “The basic assumption underlying the model presented here is that the brain makes sense of the internal state of the body by being sensitive to statistical regularities in its own neural activity” [24]. The publication title seems to state the validity of this concept by “Taking the inferential leap” perhaps not knowing that inferring denotes either a conclusion based on known facts or the act of passing from statistical sample data to generalization. The authors fail to provide any of these. Invest in ME Research Page 22 of 32
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