A study by Thomas McDade and colleagues from the Northwestern University, IL, USA, published in the Proceedings of the Royal Society B journal, suggests that lower birth weight babies breastfed less than three months, or not at all, are more likely as young adults to have higher levels of chronic inflammation.
As discussed by the authors – an increasing body of evidence indicates the importance of prenatal and early postnatal environments in influencing physiological function and health over the life course.
Systemic inflammation plays a major pathogenic role in cardiovascular (CV) diseases, insulin resistance, and type 2 diabetes mellitus. C-reactive protein (CRP) is now regarded as a sentinel biomarker of systemic inflammation and has been implicated in the pathogenesis of many chronic diseases. This includes CV diseases, and high systemic levels of this protein are consistently associated with an increased risk for CV illness.
The authors of the Proceedings of the Royal Society B study document large disparities in birth weight and rates of breastfeeding associated with race/ethnicity and education level. We present evidence that lower birth weight and shorter durations of breastfeeding both predict elevated concentrations of CRP in young adulthood, indicating increased risk for cardiovascular and metabolic diseases that are major health burdens in the USA and the UK.
This study is perhaps the first to document an association between birth weight and CRP in sibling comparison models. Overall, birth weights above 2.5 kg, and breastfeeding greater than or equal to three months was significantly associated with lower CRP.
Of note, the study not only linked birth weight and breastfeeding duration to CRP levels in adulthood, but also found striking racial, ethnic and education disparities. Educated mothers were more likely to breastfeed and to give birth to larger babies, as were Whites and Hispanics.
As per an eurekalert press release, Dr. Alan Guttmacher, Director of the Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD, USA, stated that these “results suggest that breast feeding may reduce a major risk factor for heart disease, well into adulthood.”
According to the authors of this study, postnatal feeding decisions may provide additional opportunities for intervention, particularly given the low rates of extended breastfeeding in the USA and the UK.
A 2021 study by Thomas W. McDade and Stephanie M. Koning published in Social Science & Medicine, investigated the extent to which the socioeconomic status (SES) gradient in chronic inflammation in adulthood can be explained by patterns of birth weight and breastfeeding in infancy.
Using data from a large representative sample of young adults in the US (National Longitudinal Study of Adolescent to Adult Health (Add Health)), these investigators document the SES gradient in chronic inflammation, as indicated by concentrations of C-reactive protein (CRP).
The investigators observed substantial inequalities in chronic inflammation in a large, representative cohort of young adults in the US, with lower SES associated with significantly higher concentrations of CRP.
They found that environments early in infancy are important determinants of chronic inflammation in adulthood, and that breastfeeding in particular plays an important role.
Of note, the findings of this study revealed a particularly important role for breastfeeding duration in shaping the SES gradient in CRP.
Interestingly, and as discussed by the authors, the links between low birth weight (LBW), breastfeeding duration and CRP are most likely and largely mediated through their associations with body mass index (BMI), which was positively associated with CRP in both unadjusted and adjusted analyses.
The authors conclude that this study contributes to existing research that has revealed how early-life development and nutrition affect health over the life course by examining more closely how these processes underlie socioeconomic inequities in U.S. adult health.
Cover Image Credit (Right Panel): CRP is predominantly secreted from the liver and adipose tissue(s) in response to inflammatory stress resulting from plaque rupture and subsequent microembolization. High levels of CRP induce endothelial dysfunction, activate platelets, and aggravate stress-induced alterations in cardiac function and morphology (ie, cardiomyocyte apoptosis and hypertrophy, fibrosis, and LV dilatation). NFkB indicates nuclear factor κB; iNOS, inducible nitric oxide synthase; LV, left ventricle; IL-6, interleukin 6. From: C-Reactive Protein – Just a Biomarker of Inflammation or a Pathophysiological Player in Myocardial Function and Morphology? By Rainer Schulz and Gerd Heusch, Hypertension. 2011;57:151–153.