The present invention relates to methods for reversing maladaptations involving the corticotropin-releasing factor receptor subtype 2 (CRFR2). It is postulated that in functional somatic syndrome (FSS), a group of diseases with overlapping symptoms, including systemic exertion intolerance disease (SEID, also known as chronic fatigue syndrome or myalgic encephalomyelitis), and several others, this receptor is up-regulated and relocated to the neuronal membranes of key regions of the brain including the raphe nuclei, the limbic system and the cortex. This configuration leads to a dysfunctional stress response. According to one embodiment of the invention, a method for reversing CRFR2 maladaptations includes the sustained stimulation of the receptor over a period of time to bring about a persistent receptor endocytosis, resulting in measurable symptom improvement.