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CT38
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==Hypothesis== The primary hypothesis for the use of CT38 is that symptoms arise due to the [[CRFR2 upregulation hypothesis|CRFR2 upregulation]], leading to an oversensitive [[adrenocorticotropic hormone]] (ACTH) response to minor stimulation of the [[hypothalamus]],<ref name="NCT03613129" /> it is also suggested that this will lead to an increase in [[serotonin]] expression.<ref name="HR2018" /> It is proposed that CT38 therapy will stimulate [[CRFR2]], leading to a downregulation of receptor expression and thus normalisation of the response to corticotropin-releasing hormone (CRH) at the end of the therapy. Hypothetically, CT38 may increase symptoms while the peptide is being taken, if this is a key mechanism involved in ME/CFS. In animal models, increased [[CRFR2]] stimulation has been shown to lead to increased sympathetic nervous system activation. However, increased sympathetic nervous system activation is not consistently found in ME/CFS patients, with shifts in some patients to a sympathetic predominance instead explained by a reduction of parasympathetic nervous system activity.<ref name="Nelson2019">{{Cite journal | last = Nelson | first = Maximillian J. | last2 = Bahl | first2 = Jasvir S. | last3 = Buckley | first3 = Jonathan D. | last4 = Thomson | first4 = Rebecca L. | last5 = Davison | first5 = Kade | date = Oct 2019 | title = Evidence of altered cardiac autonomic regulation in myalgic encephalomyelitis/chronic fatigue syndrome: A systematic review and meta-analysis | url = https://journals.lww.com/md-journal/fulltext/2019/10250/Evidence_of_altered_cardiac_autonomic_regulation.36.aspx | journal = Medicine|language=en-US | volume = 98 | issue = 43| page = e17600 |doi=10.1097/MD.0000000000017600|issn=0025-7974|pmc=|pmid=|quote=|access-date=|via=}}</ref> Currently, there is a lack of evidence for the dysregulation of [[CRFR2]] expression in ME/CFS patients but if the trial is successful, this would increase research interest in this area.
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