Introduction

The series of epidemiological studies that set the ball rolling for DOHaD research, by linking data from old obstetric and child health records to adult outcomes, were based in (so-called) developed countries. In brief, they showed that adult cardiovascular disease, type 2 diabetes and the metabolic syndrome were increased in people who were light or thin at birth and during infancy, gained weight or body mass index (BMI) rapidly in childhood, and became overweight or obese adults (Barker 1989, Hales et al. 1991, Barker et al. 1993, Osmond et al. 1993, Forsen et al. 1997, 1999, Eriksson et al. 2001, 2003). The associations with accelerated childhood weight gain and adult obesity were strongest in those who were smallest at birth. These findings led to the ‘fetal origins’ and ‘thrifty phenotype’ hypotheses, which proposed that undernutrition during early development, and a mismatch between undernutrition at this time and later overnutrition and obesity, are crucial factors in the development of these adult diseases (Barker 1989, 1995, Hales and Barker 1992).

The concept that cardiovascular disease and type 2 diabetes, generally considered diseases of affluence, have their origins in transition from poverty and undernutrition offered an explanation for the epidemics of coronary heart disease that swept Europe and the USA in the mid twentieth century (Barker et al. 1989). These appeared first in higher socioeconomic groups (the first to experience transition) and later shifted to the less advantaged (the last to experience improvements in fetal and infant nutrition).