Determinants of Growth, Adiposity and Bone Mass in Early Life

Abstract

Environmental influences during fetal life and early infancy have been suggested to influence body composition throughout the life-course. Especially poor fetal nutrition and fetal growth restriction have been designated important risk factors for gaining high fat mass or low bone mass during later life. As body composition tends to track from childhood into adulthood, the fight against widespread overweight and osteoporosis should focus on prevention from early life onwards. This thesis aimed to assess the impact of maternal diet, more specific fish and milk consumption during pregnancy on fetal growth; define the strongest early maternal, paternal, fetal and infant risk factors of preschool overweight, study the influence of maternal smoking on childhood body composition and explore the associations of maternal diet as well as fetal and infant growth patterns with childhood bone mass. To address these aims the studies included in this thesis were conducted within the Generation R Study, a population-based prospective cohort study from fetal life onwards.

The findings of this thesis indicate maternal fish consumption is not associated with fetal growth characteristics. Maternal shell fish consumption even showed a negative association with birth weight. Contrary, maternal milk consumption was associated with increased fetal growth leading to a higher weight and head circumference at birth. Drinking more than one glass of milk daily increased fetal growth from the third trimester of pregnancy onwards. The protein fraction from milk, rather than the fat or carbohydrate fraction seemed to drive the association. These findings suggest that maternal milk consumption during pregnancy influences fetal growth patterns, whereas fish consumption may play a lesser role. Furthermore, results of this thesis show that parental anthropometrics, household income, fetal and infant growth, and infant diet were most strongly predicted preschool overweight. Also, 6-year-old girls, but not boys, born from mothers who continued smoking throughout pregnancy were found to have higher BMI, total fat mass, android/gynoid fat ratios, subcutaneous abdominal fat mass, and preperitoneal abdominal fat mass than girls of mothers who did not smoke. Remarkably, paternal smoking showed a similar association.

Hence, these findings indicate that fetal and infant nutrition, as well as subsequent growth patterns may play an important role in the risk of developing overweight. The increased adiposity and adverse fat mass distribution found in girls exposed to smoking during pregnancy is more likely explained by familial factors related to smoking behavior than by intrauterine mechanisms. Both fetal growth and infant growth were found to independently contribute to childhood bone mass. Growth in the first year of life appeared to have the largest impact on bone mineral accrual. After the first year, the impact of height and weight growth slowly decreased every year. Furthermore, if present, catch-up growth in the first two postnatal years compensated for the consequences fetal growth restriction had on childhood bone mass. Also, maternal nutrient intakes during pregnancy are associated with childhood bone measures. Maternal phosphorus intake and homocysteine concentrations most-strongly predicted absolute bone mineral accrual in childhood, whereas maternal protein intake and vitamin B-12 concentrations were the strongest predictors of actual bone mineral density. Maternal smoking appeared to be positively associated with childhood bone measures. However, this association was fully explained by increased body weight. Paternal and household smoking were not associated with childhood bone health. Taken together, these results show maternal diet during pregnancy as well as fetal and infant growth patterns may influence childhood bone health. Yet, maternal smoking does not seem to a play a role.

In conclusion, the findings of this thesis suggest maternal dietary factors during pregnancy influence fetal growth, while maternal diet and nutritional status, as well as subsequent fetal and infant growth patterns may influence childhood adiposity and bone mass. Shared familial factors related to maternal smoking, rather than maternal smoking itself, seemed to adversely affect childhood adiposity. Prevention of future overweight and osteoporosis should therefore start from early pregnancy onwards.