Do Childhood Infections Cause Adult Cardiometabolic Disease?
Do Childhood Infections Cause Adult Cardiometabolic Disease?
An old idea—that infection may increase cardiometabolic risk—has survived well over a century of investigation and intermittent skepticism. Recent epidemiological research increasingly and consistently supports the presence of an association, although there remains a high potential for residual confounding. Ecological population studies could provide powerful support by quantifying differential rates of infection and/or use of antibiotics across countries and relating these to differential inflammation and cardiometabolic outcomes. If upheld, causation of cardiometabolic risk could occur via childhood infection itself, the inflammation that it elicits, and/or antibiotic treatment. The effects are likely to be part of causal pathways that also include traditional risk factors. With rapidly improving "–omics" technology and bioinformatics, mechanistic data should help identify both those at greatest risk and possible interventions. Given the long preclinical period in the development of cardiometabolic diseases, modulation of infectious and inflammatory determinants in childhood may emerge as an important approach to reducing the "epidemic in slow motion" of adult cardiovascular and metabolic diseases.
Conclusions and Future Directions
An old idea—that infection may increase cardiometabolic risk—has survived well over a century of investigation and intermittent skepticism. Recent epidemiological research increasingly and consistently supports the presence of an association, although there remains a high potential for residual confounding. Ecological population studies could provide powerful support by quantifying differential rates of infection and/or use of antibiotics across countries and relating these to differential inflammation and cardiometabolic outcomes. If upheld, causation of cardiometabolic risk could occur via childhood infection itself, the inflammation that it elicits, and/or antibiotic treatment. The effects are likely to be part of causal pathways that also include traditional risk factors. With rapidly improving "–omics" technology and bioinformatics, mechanistic data should help identify both those at greatest risk and possible interventions. Given the long preclinical period in the development of cardiometabolic diseases, modulation of infectious and inflammatory determinants in childhood may emerge as an important approach to reducing the "epidemic in slow motion" of adult cardiovascular and metabolic diseases.
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