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Related Experiment Videos

Inflammation underlying cardiovascular mortality is a late consequence of evolutionary programming.

Anita H J Van Den Biggelaar1, Anton J M De Craen, Jacobijn Gussekloo

  • 1Department of General Internal Medicine, Section Gerontology and Geriatrics, Leiden University Medical Center, C2-R, Albinusdreef 2, P.O. Box 9600, 2300 RC Leiden, The Netherlands. Biggelaar@lumc.nl

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|April 16, 2004
PubMed
Summary

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Cardiovascular disease mortality in older women is linked to inflammation. Higher tumor necrosis factor-alpha (TNF-alpha) increased risk, while interleukin-10 (IL-10) was protective, suggesting an evolutionary basis for inflammation.

Area of Science:

  • Immunology
  • Gerontology
  • Evolutionary Medicine

Background:

  • Cardiovascular disease (CVD) mortality is increasing with life expectancy.
  • Inflammation is increasingly recognized as a key factor in CVD development.
  • This study explores the hypothesis that CVD in old age results from evolutionary programming for early-life inflammation.

Purpose of the Study:

  • To investigate the association between pro-inflammatory (TNF-alpha) and anti-inflammatory (IL-10) cytokine production and cardiovascular mortality in elderly women.
  • To examine the role of a specific IL-10 gene variant in cardiovascular mortality risk.
  • To explore the relationship between reproductive success as a proxy for evolutionary programming and inflammatory markers.

Main Methods:

  • Prospective study of 311 women aged 85 years.

Related Experiment Videos

  • Measurement of tumor necrosis factor-alpha (TNF-alpha) and interleukin-10 (IL-10) production in lipopolysaccharide-stimulated whole blood samples.
  • Analysis of genetic variants in the IL-10 gene promoter.
  • Assessment of reproductive success as a measure of evolutionary programming.

    • Main Results:

    • Elevated TNF-alpha levels were a risk factor for cardiovascular mortality (RR=1.56).
    • Higher IL-10 levels showed a protective effect (RR=0.58).
    • An IL-10 gene variant linked to lower IL-10 production increased cardiovascular mortality risk 2.8-fold.
    • Reproductive success was inversely associated with TNF-alpha and positively with IL-10 production.

    Conclusions:

    • Cardiovascular mortality in old age may be a delayed consequence of evolutionary programming favoring pro-inflammatory responses for early-life survival.
    • Inflammatory cytokine balance, influenced by genetics and evolutionary pressures, plays a critical role in late-life cardiovascular health.