Do Childhood Infections Cause Adult Cardiometabolic Disease?
Do Childhood Infections Cause Adult Cardiometabolic Disease?
Population-level statutory data, available in some settings, allow the use of hospitalization with infection as a proxy marker of infection burden. Although most childhood infections do not result in hospitalization, infection is the commonest reason for childhood admission, and hospitalization is less prone to differences in health-seeking behavior than emergency department or primary care attendances. In Western Australia, where population-based data linkage commenced in 1970, there is a dose–response relationship between infection-related hospitalization in childhood (<18 years) and CVD events in adulthood (>18 years). The association is independent of traditional risk factors that can be identified from population-level data. However, this cohort is relatively young and may represent a more extreme CVD phenotype; as the population born after 1970 ages, it should become apparent whether the findings are more broadly applicable. A similar approach using statutory data from Finland has shown relationships between infection-related hospitalization, particularly in the preschool child, and adult obesity, metabolic syndrome and some adverse cardiovascular intermediate phenotypes. Although infection-related hospitalization per se did not show a significant social gradient, associations with adult cardiometabolic disease were only observed in children raised in families of lower socioeconomic status, suggesting infection may be a mediator on the causal pathway underlying social gradients in cardiometabolic diseases (Liu R, Burgner DP, unpublished data). Similar results linking infection-related hospitalization and adult obesity have been reported in Danish men.
These associations between infection-related hospitalization and cardiometabolic parameters have a number of plausible (and nonexclusive) explanations. The severe infections themselves (and/or the resulting severe acute inflammation) could directly damage blood vessels. Hospitalizations may be a marker for children susceptible to more infection and inflammation overall (most of which does not result in hospitalization) and therefore may also be an indicator of children who may receive more antibiotics earlier in childhood.
Longitudinal Data
Population-level statutory data, available in some settings, allow the use of hospitalization with infection as a proxy marker of infection burden. Although most childhood infections do not result in hospitalization, infection is the commonest reason for childhood admission, and hospitalization is less prone to differences in health-seeking behavior than emergency department or primary care attendances. In Western Australia, where population-based data linkage commenced in 1970, there is a dose–response relationship between infection-related hospitalization in childhood (<18 years) and CVD events in adulthood (>18 years). The association is independent of traditional risk factors that can be identified from population-level data. However, this cohort is relatively young and may represent a more extreme CVD phenotype; as the population born after 1970 ages, it should become apparent whether the findings are more broadly applicable. A similar approach using statutory data from Finland has shown relationships between infection-related hospitalization, particularly in the preschool child, and adult obesity, metabolic syndrome and some adverse cardiovascular intermediate phenotypes. Although infection-related hospitalization per se did not show a significant social gradient, associations with adult cardiometabolic disease were only observed in children raised in families of lower socioeconomic status, suggesting infection may be a mediator on the causal pathway underlying social gradients in cardiometabolic diseases (Liu R, Burgner DP, unpublished data). Similar results linking infection-related hospitalization and adult obesity have been reported in Danish men.
These associations between infection-related hospitalization and cardiometabolic parameters have a number of plausible (and nonexclusive) explanations. The severe infections themselves (and/or the resulting severe acute inflammation) could directly damage blood vessels. Hospitalizations may be a marker for children susceptible to more infection and inflammation overall (most of which does not result in hospitalization) and therefore may also be an indicator of children who may receive more antibiotics earlier in childhood.
