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Although the exact etiology remains unknown, current evidence points to a significant genetic component in the development and severity of FM which can be associated with a spectrum of diseases, including infections, diabetes, rheumatic diseases, and psychiatric or neurological comorbidities [6]

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GH raises progesterone via several pathways, including: Direct stimulation of human luteal cells Increased cyclic adenosine monophosphate (cAMP) levels Antiapoptotic effects His condition improved promptly following cycle cessation, with his breasts returning to their pre-cycle size