The role of infant nutrition in the global epidemic of non-communicable disease

Abstract

Non-communicable diseases (NCD) and atherosclerotic CVD in particular, are the most important health problems of the 21st century. Already in every world region except Africa, NCD account for greater mortality than communicable, maternal, perinatal and nutritional conditions combined. Although modifiable lifestyle factors in adults are the main determinants, substantial evidence now suggests that factors in early life also have a major role in the development of NCD; commonly referred to as the Developmental Origins of Health and Disease hypothesis. Factors in utero, early postnatal life and throughout childhood, have been shown to affect NCD by influencing risk factors for CVD such as obesity, diabetes, hypertension and dyslipidaemia. Infant nutrition (e.g. breastfeeding rather than bottle feeding) and a slower pattern of infant weight gain have been shown to be particularly protective against later risk of obesity and CVD in both low-and high-income countries. The mechanisms involved are poorly understood, but include epigenetic changes; effects on endocrine systems regulating body weight, food intake and fat deposition; and changes in appetite regulation. As a consequence, strategies to optimise early life nutrition could make a major contribution to stemming the current global epidemic of NCD. This review will consider the role of early life factors in the development of NCD, focusing on the impact of infant nutrition/growth on obesity and CVD. The review will highlight the experimental (randomised) evidence where available, briefly summarise the underlying mechanisms involved and consider the implications for public health.

Long-Term Adverse Effects of Early Growth Acceleration or Catch-Up Growth

“…Since this early report, there has been a huge increase in evidence to support the growth acceleration concept. Faster infant growth (upward centile crossing for weight or length) has been associated with later obesity in 45 of 46 studies (summarized in 6 systematic reviews [9][10][11] ) including an individual-level meta-analysis in 47,661 participants from 10 cohorts [11] . These associations are seen in both high-and lowincome countries, for both weight gain and linear growth, in infants born preterm or at term, in infants with normal or low birth weight for gestation, and in both breast-and formula-fed infants [9][10][11] .…”

“…Importantly, there are now 5 randomized trials that support a causal link between slower infant growth and lower risk of later obesity [9] . These trials found that infants who were fed formulas with higher protein content (and hence had faster weight gain) had a greater risk of later obesity than those who were given lower protein formulas [9,12] .…”

“…These trials found that infants who were fed formulas with higher protein content (and hence had faster weight gain) had a greater risk of later obesity than those who were given lower protein formulas [9,12] . Similar benefits of slower infant weight gain are seen in breast-fed infants.…”

“…In high-income countries, faster post-natal growth in SGA infants appears to increase the later risk of obesity and CVD. For instance, term SGA infants randomly assigned to nutrient-enriched formula that increased weight gain had higher diastolic BP at age 6-8 years and, in 2 trials, 18-38% greater fat mass at age 5-8 years than controls (as reviewed [9] ). Interestingly, differences in childhood fat mass or blood pressure between randomized groups were related to the rate of weight gain in the first 6 months suggesting a "dose-response" association between early growth and later CVD risk [9] .…”

Poor maternal anthropometric status before conception is associated with a deleterious infant growth during the first year of life: a longitudinal preconceptional cohort

“…Different underlying pathophysiological mechanisms, including epigenetic changes, have been proposed to explain the impact of maternal determinants on child and adult health. 7,38,39 Epigenetics has mainly been documented in animals, with the demonstration of changes in body's structure and functions related to epigenetic modifications after fetal undernutrition (either by maternal undernutrition or by fetal growth restriction). 40,41 In humans, epigenetic changes related to maternal nutrition have also been shown in newborns conceived during the hungry vs the harvest season and in offspring of women exposed to the Dutch famine.…”