Literature review for - Flourish Paediatrics

Meulen et al. 2000). Epidemiological studies supporting the hypothesis are now being published from
non-European countries (Fan, Zhang et al. 2010).
The hypothesis has become more complex because it is apparent that, in addition to birthweight, other
dimensions of body shape at birth and subsequent growth from childhood into adulthood must be
considered (Barker 2001). More recently, the status of the placenta at birth has been used as a proxy for
assessment of overall prenatal nutritional status. There is also evidence of a ‘‘U’’ shaped relationship
between placental-to-foetal weight ratio and heart disease (Thornburg, O'Tierney et al. 2010).
The current version of the developmental origins hypothesis describes a relationship between those who
had low birthweight or were thin or short at birth or failed to grow in infancy and later disease. As
adults, children in these categories develop increased rates of coronary heart disease, stroke, type 2
diabetes and hypertension. But as noted the relationship is U-shaped.
Death rates from coronary heart disease increase in those with poor prenatal or infant nutrition followed
by improved postnatal nutrition and a trend towards obesity. The patterns differ for those who later
develop stroke, type 2 diabetes or hypertension (Eriksson, Forsen et al. 2000) and there are slightly
different patterns for each gender. Common to all, however, is a period of reduced early growth during
the period of developmental plasticity followed by a period of accelerated growth (Bruce and Hanson
2010). People who were small at birth are more prone to developing type II diabetes or coronary heart
disease if they become overweight as adults.
Detailed analysis of the Finnish cohort has shown two pathways whereby growth may lead to
subsequent coronary heart disease. In one, thinness at birth is followed by rapid weight gain in
childhood. In the other, failure of infant growth is followed by persisting thinness during childhood.
Both are associated with short stature in childhood (Eriksson, Forsen et al. 2001). Figure 1 illustrates the
combined influences of thinness at birth—a ponderal index of less than 26 (ponderal index =
weight/height 3 )—and subsequent growth rates. For example, a male who is thin at birth but who gains
one standard deviation of body mass index by the age of 6 years has a hazard ratio of 1.2. This compares
with a male born with a normal body shape and who also gains weight but whose subsequent risk of
coronary heart disease remains below average.
449