Huhmar et al. (2025)
- Authors: Helena M. Huhmar, Lauri S. Soinne, Bo Christer Bertilson, Per Hamid Ghatan, Björn A. Bragée, Olli J. Polo
- Institutes: ME Center, Bragée Clinics, Stockholm, Sweden, Neurology, University of Helsinki, Helsinki, Finland, Department of Neurobiology, Care Sciences and Society, Karolinska Institute, Stockholm, Sweden
- Publisher: Endocrine Practice
- Link: DOI
Summary
This study identifies a significant and measurable hormonal deficiency in the majority of ME/CFS patients that explains common symptoms such as extreme thirst and orthostatic intolerance. By demonstrating that vasopressin levels remain inappropriately low even when patients are dehydrated, the research provides evidence of a ‘central’ dysregulation in the brain’s fluid control centers. These findings offer a biological marker for the disease and point toward potential new avenues for managing blood volume issues in patients.
What was researched?
The study investigated the regulation of water homeostasis and the secretion of the antidiuretic hormone vasopressin in patients diagnosed with ME/CFS.
Why was it researched?
Researchers sought to understand the biological basis for common ME/CFS symptoms like excessive thirst (polydipsia), frequent urination (polyuria), and low blood volume, which suggest a disruption in fluid balance.
How was it researched?
An observational study was conducted with 111 ME/CFS patients who underwent 10 hours of fluid deprivation. Following this, researchers measured plasma and urine osmolality as well as plasma vasopressin levels, while also performing brain MRIs to rule out structural pituitary or hypothalamic damage.
What has been found?
Vasopressin levels were below the limit of detection in 82% of the patients despite high blood osmolality, which normally triggers hormone release. This physiological state mimics idiopathic central diabetes insipidus, where the brain fails to signal the kidneys to conserve water.
Discussion
The lack of structural abnormalities on brain MRIs suggests that the low vasopressin levels are a functional down-regulation rather than a result of physical injury to the hypothalamus or pituitary gland. This chronic deficiency likely contributes to the persistent hypovolemia and cardiovascular instability seen in ME/CFS.
Conclusion & Future Work
The findings indicate that impaired vasopressin secretion is a fundamental and measurable part of the disease mechanism in ME/CFS. This hormonal failure underlies several criterial symptoms, including orthostatic intolerance.