Size at Birth, Postnatal Growth and Risk of Obesity

Abstract

Epidemiological studies over the last 15 years have shown that size at birth, early postnatal catch-up growth and excess childhood weight gain are associated with an increased risk of adult cardiovascular disease and type 2 diabetes. At the same time, rising rates of obesity and overweight in children, even at pre-school ages, have shifted efforts towards the identification of very early factors that predict risk of subsequent obesity, which may allow early targeted interventions. Overall, higher birth weight is positively associated with subsequent greater body mass index in childhood and later life; however, the relationship is complex. Higher birth weight is associated with greater subsequent lean mass, rather than fat mass. In contrast, lower birth weight is associated with a subsequent higher ratio of fat mass to lean mass, and greater central fat and insulin resistance. This paradoxical effect of lower birth weight is at least partly explained by the observation that infants who have been growth restrained in utero tend to gain weight more rapidly, or ‘catch up’, during the early postnatal period, which leads to increased central fat deposition. There is still debate as to whether there are critical early periods for obesity: does excess weight gain during infancy, childhood or even very early neonatal life have a greater impact on long-term fat deposition and insulin resistance? Early identification of childhood obesity risk will be aided by identification of maternal and fetal genes that regulate fetal nutrition and growth, and postnatal genes that regulate appetite, energy expenditure and the partitioning of energy intake into fat or lean tissue growth.

The effect of birthweight upon insulin resistance and associated cardiovascular risk factors in adolescence is not explained by fetal growth velocity in the third trimester as measured by repeated ultrasound fetometry

“…IUGR was associated with higher total cholesterol:HDL-cholesterol ratio compared with not-IUGR (B= 11%; 95% CI 1. [8][9][10][11][12][13][14][15][16][17][18][19][20]. Other non-significant trends for lipid profile (raised triacylglycerol, LDL-cholesterol and total cholesterol) were seen for IUGR (Fig.…”

“…Small size at birth indicates some period(s) of slow fetal growth, and thus poor intrauterine growth conditions have been suggested to be the cause of the observed impact upon later health. However, there also seems to be an interaction between birthweight (BW) and weight gain during infancy and childhood in determining later health [7][8][9][10]. Identification of particularly critical periods of fetal life, as well as of individuals at particular risk of later disease, could be crucial for prevention.…”

Epigenetic changes in early life and future risk of obesity

“…Small babies who undergo early catch-up growth that is characterized by a greater accumulation of fat mass relative to lean body mass have an increased risk of becoming obese in later life compared with those born at higher birth weights. [18][19][20] Early catch-up growth in infants born pre-term, who also have a reduced fat mass at birth, and who were fed formula milk also show increased risk of cardio-metabolic disease in later life, 21,22 including obesity. 23 A number of studies have also shown a greater incidence of obesity in adults who were formula fed as opposed to breast fed during infancy, 23,24 although not all studies found this.…”

Weight and weight gain during early infancy predict childhood obesity: a case-cohort study

“…30 Others have, however, reported that birth weight was inversely associated with central obesity after adjustment for BMI. 31 Further, neither secular changes in the distribution of birth weight, nor secular changes in the association between birth weight and later risk of obesity can explain the increase in the prevalence of obesity among Danish children. 30 Adjustment for sex, preterm birth, parental socioeconomic status, and concurrent breastfeeding did not change the results.…”