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Testosterone, SHBG and differential white blood cell count in middle-aged and older men

Judith S Brand1, Yvonne T van der Schouw, Mitch Dowsett

  • 1Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, 3508 GA Utrecht, The Netherlands. J.S.M.Brand-3@umcutrecht.nl

Maturitas
|January 7, 2012
PubMed

Insights

Higher levels of testosterone and sex hormone-binding globulin (SHBG) are linked to lower white blood cell (WBC) counts in men. This suggests a connection between hormonal status and reduced inflammation, a factor in cardiovascular disease risk.

Area of Science:

  • Endocrinology
  • Immunology
  • Cardiovascular Disease Research

Background:

  • Low-grade chronic inflammation is increasingly recognized as a contributor to cardiovascular disease (CVD) pathogenesis.
  • Testosterone and sex hormone-binding globulin (SHBG) may influence CVD risk through inflammatory pathways.

Purpose of the Study:

  • To investigate the associations between endogenous testosterone, SHBG, and white blood cell (WBC) counts in men.
  • To explore the potential link between hormonal status and subclinical inflammation relevant to CVD.

Main Methods:

  • Cross-sectional study of 2418 men aged 40-78 years from the EPIC-Norfolk cohort.
  • Data collected on sex hormones (total testosterone (TT), SHBG, free testosterone (FT)) and WBC counts.
  • Linear regression models used to assess associations between sex hormones and WBC counts.

Main Results:

  • Higher SHBG and TT levels were significantly associated with lower total WBC counts.
  • The inverse association was primarily driven by a reduction in granulocyte count.
  • No significant associations were found between free testosterone (FT) and WBC counts.

Conclusions:

  • Endogenous TT and SHBG levels show an inverse relationship with total WBC and granulocyte counts in middle-aged and older men.
  • These findings support a potential link between hormonal status and low-grade inflammation.
  • Further research is needed to elucidate the underlying mechanisms and causal directionality.
Abstract

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