Low Vasopressin in Myalgic Encephalomyelitise/Chronic Fatigue Syndrome.
Huhmar, Helena M, Soinne, Lauri S, Bertilson, Bo Christer et al. · Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists · 2025 · DOI
Quick Summary
This study found that most people with ME/CFS have abnormally low levels of vasopressin, a hormone that helps your body control water balance and blood volume. The researchers measured this hormone and fluid markers in over 100 ME/CFS patients and discovered that 82% had vasopressin levels below the detectable range. This may help explain why many ME/CFS patients experience excessive thirst, frequent urination, and dizziness when standing up.
Why It Matters
This study provides a potential biochemical explanation for several hallmark ME/CFS symptoms, particularly orthostatic intolerance and polyuria-polydipsia, which are poorly understood. Identifying vasopressin dysregulation as a measurable disease mechanism could lead to better diagnostic approaches and targeted interventions for managing these debilitating symptoms.
Observed Findings
82.0% (91 of 111) of ME/CFS patients had vasopressin levels below the detection limit (<1.6 pg/mL)
57.3% (71 of 124) of patients showed abnormally high plasma osmolality (>292 mOsm/kg)
66.1% (82 of 124) of patients had abnormally low urine osmolality (<750 mOsm/kg)
9.9% (11 of 111) showed vasopressin levels appropriate for their osmolality level
No structural abnormalities in hypothalamus or pituitary were detected on brain MRI
Inferred Conclusions
Chronic down-regulation of vasopressin is a measurable feature of ME/CFS disease mechanisms
Vasopressin dysregulation mimics central diabetes insipidus and may contribute to orthostatic intolerance and water homeostasis symptoms
Absence of structural brain pathology suggests functional rather than anatomical endocrine dysfunction
This dysregulation represents a potential objective biomarker for ME/CFS
Remaining Questions
Is vasopressin dysregulation a primary disease mechanism or a secondary consequence of ME/CFS pathology?
Do vasopressin levels fluctuate with disease severity, activity level, or symptom flares?
What This Study Does Not Prove
This study does not prove that low vasopressin causes ME/CFS or that treating vasopressin levels will improve symptoms—it demonstrates an association in a cross-sectional snapshot. The study cannot establish whether vasopressin dysregulation is a primary driver of disease or a secondary consequence of ME/CFS pathology. Long-term follow-up and intervention studies would be needed to clarify causality and clinical utility.