By Rebecca Kofod Vinding
Chariman: Anders Juul
Opponent: Ellen Aagaard Nøhr
Opponent: Jovanna Dahlgren
The increased prevalence of overweight children cannot be explained by changes in genetic factors, since the great increase has occurred over a short period of time, the causes must be sought in environmental exposures.
The aim of this thesis is to examine pre and perinatal factors influence on childhood growth in the two birth cohorts Copenhagen Prospective Studies on Asthma in Childhood2000 (COPSAC2000) and COPSAC2010. We have focused on two exposures in this thesis.
Firstly, caesarean section (CS) which has had an increase in prevalence the last decades. Two recent meta-analyses have shown associations between delivery by CS and obesity in the off-spring in both child- and adulthood.
Secondly, we have focused on maternal dietary n-3 long chain polyunsaturated fatty acids (n-3 LCPUFA) during pregnancy, since it is an important determinant of adequate child development and health. In humans, both observational studies on dietary intake of fish as well as randomized trials of fish oil supplementation in pregnancy have shown longer gestation and higher birth weight in children born to women with a high n-3 LCPUFA intake. However, in humans randomized trials with n-3 LCPUFA supplementation in pregnancy and/or lactation have shown ambiguous results regarding anthropometric outcomes later in childhood.
In study I we examined the development of Body Mass Index (BMI) from birth through childhood in children with different delivery mode, to determine if CS were associated with differences in childhood growth and obesity. We collected height/length and weight measurements prospectively from term children until 5 years in COPSAC2010 and 13 years in COPSAC2000, furthermore dual-energy X-ray absorptiometry (DXA) scans were performed at age 3.5 years and 7 years.
We found that children delivered by CS had a higher mean BMI at 6 months compared to those delivered vaginally. However, there were no differences in BMI trajectory between the two groups ages 5 to 13 years, nor cross-sectional at these ages, nor in fat percentages from DXA scans.
In study II we analysed the effect of n-3 LCPUFA supplementation in pregnancy on intrauterine growth, gestational age and birth weight. The study was a double-blinded, RCT. The pregnant women received capsules containing either 2.4 g of n-3 LCPUFA or control daily from pregnancy week 24 until one week after birth.
We found that n-3 LCPUFA compared to control was associated with a longer duration of pregnancy, a higher birth weight and an increased intrauterine growth. We observed no effects on preterm delivery or other pregnancy complications.
In study III we examined the effect of n-3 LCPUFA supplementation in pregnancy on childhood anthropometrics outcomes. The study was nested in the above-mentioned intervention study. We used prospectively collected height/length and weight to examine the development of BMI from birth through 6 years of age. At 6 years we evaluated the cross sectional effect on height, weight, BMI, head and waist measurements. We used data from DXA scans at 3.5 years and 6 years.
We found that the n-3 LCPUFA group had a significantly higher mean z-score BMI from 1 week to 6 years of age compared to the controls, leading to a significantly higher z-score BMI at age 6 years and a larger waist circumference.
From DXA scans, we found a higher total lean soft tissue mass and a higher bone mineral content in the n-3 LCPUFA group. There were not a higher number of children in risk of obesity or with a higher fat percentage at 6 years of age in the n-3 LCPUFA group.
In conclusion: our findings have manifested that these exposures during pregnancy and birth are associated with a changed childhood growth.
We saw that children delivered by CS had a higher BMI at 6 months of age, but this did not track into later childhood.
N-3 LCPUFA supplementation from pregnancy week 24 was associated with prolonged gestation and increased intrauterine growth, leading to a higher birth weight. In addition, it led to an increase in BMI from age 1 year to 6 years. It did not lead to a higher number of obese children or a higher fat percentage at 6 years of age.
This thesis adds knowledge to the field regarding early life exposures and metabolic programming. We find associations between two exposures which have been changing during the last decades and childhood growth, both exposures are still modifiable.