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Inflammaging mediates testosterone declines in men while maintaining high testosterone increases mortality risk.

Jacob E Aronoff1, Benjamin C Trumble1

  • 1Center for Evolution and Medicine, School of Human Evolution and Social Change, Institute of Human Origins, Arizona State University, Tempe, AZ, USA.

Biorxiv : the Preprint Server for Biology
|June 12, 2026
PubMed
Summary
This summary is machine-generated.

Chronic inflammation (inflammaging) and declining testosterone levels in aging men are linked by an energetic trade-off. Inflammaging drives testosterone loss, potentially increasing mortality risk with testosterone therapy.

Keywords:
GDF-15UK Biobankaginginflammaginginflammationtestosterone

Related Experiment Videos

Area of Science:

  • Gerontology
  • Endocrinology
  • Immunology

Background:

  • Aging is associated with declining testosterone levels and increased chronic inflammation (inflammaging).
  • A theoretical model suggests an energetic trade-off links these processes, where accumulated damage activates costly inflammation, suppressing energy-intensive testosterone production for cellular repair.

Purpose of the Study:

  • To investigate the relationship between inflammaging markers and age-related testosterone decline.
  • To explore the role of GDF-15 and IL-6 in mediating testosterone changes.
  • To examine the association between testosterone levels, inflammation, and mortality risk.

Main Methods:

  • Analysis of data from the UK Biobank (n = 18,347, mean age 57).
  • Measured testosterone levels and markers of inflammaging, including IL-6 and GDF-15.
  • Statistical mediation analysis to assess the role of inflammaging markers in testosterone decline.
  • Follow-up analysis of mortality risk in relation to testosterone and inflammation levels.

Main Results:

  • Markers of inflammaging, specifically IL-6 and GDF-15, were found to mediate age-related declines in testosterone.
  • GDF-15 emerged as the strongest predictor and mediator of testosterone reduction.
  • Individuals with high testosterone relative to their inflammation status exhibited increased mortality risk, suggesting a maintenance-reproduction trade-off.

Conclusions:

  • Energetic trade-offs are crucial for understanding testosterone decline in later life.
  • Reducing cellular damage may mitigate inflammaging and its hormonal consequences.
  • Exogenous testosterone therapy in the presence of chronic inflammation warrants caution due to potential increased mortality risk.