Background

The prevalence of linear growth stunting in children, defined here as a length-for-age more than 2 standard deviations below NCHS reference data, ranges from 10% to 50% in most developing countries. This is consistent with the 10-15 cm difference in height of the adult populations relative to adults in the industrialized world or in more privileged segments of the population in developing countries.

Linear growth stunting may be present at birth, but is usually a phenomenon that begins mainly between 6 and 18 months of age. Stunting is associated with delays in many functions, for instance mental and motor development, and with increased risk of morbidity and death.

The occurrence of stunting is conditioned by factors which may vary depending on the ecological setting. Although the main cause(s) remain unclear, the following main conditioning factors have been identified in field studies.

1. Genetic factors only account for a small proportion of stunting, as evidenced by the relative lack of growth retardation in privileged groups with the same genetic background, and the reduction in stunting prevalence that occurs when populations move from a poor to a better environment. The Asiatic and Amerindian populations may have a genetically determined lower stature in the order of -0.5 SD, although this remains a point of debate.

2. Altered fetal growth may result from genetic, congenital or environmental (including high altitude and radiation) factors, maternal disease, or nutritional deficits. The effect of maternal malnutrition on infant linear growth in utero may take more than one generation to resolve.

3. Insufficient postnatal nutrient supply will also cause growth stunting. The case for energy deficit alone is weak; most infants who fail to gain in length are adequate in weight-for-length, many of them have access to sufficient food and, if they did not, they would be lacking in other nutrients as well. Recent studies suggest that nutrients present in animal products such as milk may be important for normal linear growth in early life. The potentially relevant nutrients in these products include animal protein, zinc, iron, retinol, riboflavin, vitamin B₁₂ and essential fatty acids among others. The actual growth-limiting deficiencies remain to be identified.

4. Growth stunting can result from an increased prevalence of infection or infestation, either symptomatic or subclinical in nature. The metabolic response to infection, which includes malabsorption and cytokine release, may be in part responsible for growth failure in young children. Presently the evidence indicates that controlling infections and parasitic disease may improve linear growth.

The mechanisms responsible for growth stunting are likely to include the interaction between hormonal responses (growth hormone, insulin, cortisol and others), growth factors (IGFs), their respective binding proteins and cellular receptors at the target site, specific nutrient deficiencies, and cytokine release during infectious disease episodes.

A target organ of particular interest is the growth plate in the epiphysis of long bones, and more research should be directed to understand how it is affected by undernutrition and infection.

The rate of linear growth declines with age, except at puberty, and the effects of stunting under 3 years of age are most significant. However, there is some evidence that stunting can be reversed by nutritional, social or environmental interventions at any time before the growth plate has fused, i.e. before linear growth stops.