[Genes and intra-uterine growth retardation]

Genetic analysis of growth from birth to adulthood shows the existence of a strong genetic component in the variance of size at particular milestones in the growth process, such as height at take-off, at peak velocity and at adulthood. While it is well known that postnatal growth is strongly genetically determined, the importance of genes in normal variations of prenatal growth is less known. Genetic analysis of prenatal growth in human is not an easy problem and weighing the genetic and non-genetic component in intra-uterine growth retardation an almost impossible task. It is now well known that adults who had a low birthweight or who were thin at birth, with a low ponderal index, tend to be insulin resistant and have an increased risk of developing non-insulin-dependent diabetes mellitus later in life. According to the thrifty genotype hypothesis, genes predisposing to type 2 diabetes mellitus are very likely to have been survival genes for our ancestors, helping them to store energy during long periods of starvation. Both epidemiological surveys of adults born after prenatal exposure to exposure to famine and biochemical investigations of insulin resistance in low birthweight children show that the association between a low birthweight and an increased risk of developing type 2 diabetes mellitus later in life has a genetic basis. While low birthweight infants have a decreased survival probability in infancy, having a small baby may have been a selective advantage during long periods of starvation. This could explain why the same genetic variants cause low birthweight phenotype and insulin resistance predisposing to non-insulin-dependent diabetes.