There are also possible adverse effects of poor childhood nutrition14 that, if conclusively proven, would have an enormous impact on the developing countries, which still have a substantial fraction of the population that was underweight at birth.

Ref: Barker DJP, Martyn CN, Osmond C, et al. Growth in utero and serum cholesterol concentrations in adult life. Br. Med J. 1993; 307: 1524–7
 

The possibility of such programming, or as yet unascertained genetic factors, may underlie the enhanced susceptibility of some ethnic groups (e.g. South Asian migrants) to CHD15. This excess risk may be explained by gene–environment interactions or fetal programming in these groups, but public health action must focus on the environmental changes that trigger the expression of susceptibility

Ref: Enas EA, Mehta J. Malignant coronary artery disease in young Asian Indians. Thoughts on pathogenesis, prevention and therapy. Clin. Cardiol. 1995; 18: 131–5.

Such genetic environmental interactions may need to be clarified in the varied ethnocultural populations of the developing countries so that the relevant environmental interventions could be preferentially promoted for CVD prevention.