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Te Hauora Me Te Oranga O Te Māori (māori Health And Wellbeing)
Te Whaikaha Me Te Māori (māori And Disability)
Monge's Disease At 100 Years: Revisiting The Origins And Endocrine Mechanisms Of Chronic Mountain Sickness.

Home
Research Domains
Indigenous Studies
Te Hauora Me Te Oranga O Te Māori (māori Health And Wellbeing)
Te Whaikaha Me Te Māori (māori And Disability)
Monge's Disease At 100 Years: Revisiting The Origins And Endocrine Mechanisms Of Chronic Mountain Sickness.

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Monge's disease at 100 years: Revisiting the origins and endocrine mechanisms of chronic mountain sickness.

Gustavo F Gonzales¹

¹Faculty of Health Sciences, Universidad San Ignacio de Loyola, Lima, Peru.

Science Progress

|October 21, 2025

View abstract on PubMed

Summary

This summary is machine-generated.

Chronic mountain sickness (CMS) involves excessive red blood cell production and cognitive issues at high altitudes. Sex hormones, particularly testosterone, play a key role alongside hypoxia in its development and severity.

Keywords:

GATA-1 SENP1 Testosterone chronic mountain sickness

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Area of Science:

Physiology
Endocrinology
Altitude Medicine

Background:

Chronic mountain sickness (CMS) is a condition affecting high-altitude dwellers, characterized by excessive erythrocytosis (EE) and neurocognitive deficits.
Historically attributed to hypoxia-driven erythropoietin (EPO) stimulation, modern research reveals a more complex etiology.
Carlos Monge Medrano first described CMS in 1925, a condition now recognized globally.

Purpose of the Study:

To review the historical contributions of Carlos Monge Medrano to understanding CMS.
To integrate modern research findings, particularly the role of sex hormones, into the understanding of CMS.
To highlight current challenges in CMS diagnosis and management.

Main Methods:

Narrative review of existing literature on Chronic Mountain Sickness.

Analysis of recent molecular biology and endocrinology research.

Revisiting Carlos Monge Medrano's original observations in the context of current scientific understanding.

Main Results:

Sex hormones, especially testosterone, significantly modulate erythropoiesis in CMS, influencing hemoglobin and hematocrit levels.
Elevated testosterone or high testosterone-to-estradiol ratios are linked to increased EE and severity, particularly in men.
The hypoxia-testosterone-EPO axis, involving regulators like SENP1 and GATA1, is crucial for disease susceptibility.
Androgenic signaling exacerbates sleep and cognitive issues, while estrogenic modulation may offer protection.

Conclusions:

CMS is a multifactorial disorder influenced by hypoxia, sex hormones, genetic factors, and environmental stressors.
Understanding the interplay of hormones and hypoxia offers potential therapeutic and preventive strategies for CMS.
Despite advancements, CMS remains underdiagnosed and under-treated in many high-altitude regions, particularly in South America.