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Universal malnutrition?

By Sridhar Srikantiah

All children in India display a slower growth rate, but we look only at those that have ‘fallen’ below the cut-off and call the rest ‘normal’. Surely poverty and hunger cannot be the only cause of this near-universal malnutrition? Is malnutrition caused by not feeding our children enough dal, milk, eggs, meat and vegetables, in addition to cereals, in the first two years? Does that explain why cereal-based ICDS food supplements are ineffective in reducing malnutrition? 

‘Malnutrition’ is a much-defined term even within the limited context of India. It stands for the numbers that determine national shame, as in India being home to more malnourished children than any other nation in the world. It connotes a range of nutrient deficiencies -- such as iron, Vitamin A, iodine or zinc -- which are known to be widely prevalent in India and in most developing economies. It describes and explains why South Asian adults are so much shorter than Scandinavians, for instance. It also includes the complex of excessive food intake and genetic predisposition that contributes to a disproportionate incidence of diabetes and coronary heart disease in the subcontinent. But for the purposes of this essay, ‘malnutrition’ means the phenomenon of children not growing quite as well as expected and becoming vulnerable to high death rates as infants and under-5s, or ending up as stunted adults.

One of the first instincts in tackling malnourished children is the ‘find them and fix them’ approach: design a programme that efficiently and accurately identifies the 50% of all children who are malnourished, and then proceed to make good the gap in nourishment. Programmes like the Integrated Child Development Services (ICDS) appear to have been conceived on the basis of this principle: weigh children monthly, identify those not growing well, and offer the most severely malnourished double the amount of food supplements that ‘normal’ children are provided. In addition, for good measure, identify children who fall sick and send them to the doctor for treatment. Ask almost any ICDS official and you are likely to be told that malnutrition is all a matter of poverty, and that the ICDS is supplying the food that children from poor families need.

This is not quite the truth. There are many fatal flaws in this logic, some of which are widely spoken of, others not. To understand these, it would help to begin with understanding how malnutrition is measured.

Measuring and classifying poor growth

Children grow. In the womb, the foetus begins as a tiny mass of cells, develops all its limbs and organs by about 10 weeks after conception, but at this stage weighs very little. Its growth in length accelerates over the next three months, and slows down a little after the sixth month. The foetus nearly triples in weight in the last three months by the time the baby is born at 40 weeks. At birth, a ‘normal’ baby is well-proportioned -- the body weight being in proportion to the length. After birth, the baby continues to grow but at a progressively slower rate, in both length and weight accretion until the age of about two, by which time both height and weight gains have slowed to a minimal, steady pace. The adolescent growth spurt begins any time after the age of eight, when both height and weight increase. Adult height is largely determined by the sum of length or height accretions during the two spurts: the first between the second trimester of pregnancy until about two years of age, and the second at adolescence.

Indians are short or ‘stunted’ because something gets messed up during one or both height spurts. Weight can, in principle, be gained or lost (unlike height) at any time, and is indeed largely a function of height: the tendency is to have weight that is appropriate for height. If one is too heavy for one’s height, one is obese; if too light, one is thin or ‘wasted’. While good height is a function of long-standing wellness and adequate nourishment, wasting is often a function of relatively recent illness -- when weight was lost due to the illness. When we say someone is stunted or wasted (or obese), we are comparing the height to the expected height for that age, and weight to the expected weight for the height. The ‘expected’ heights and weights come from reference standards which are now accepted as globally applicable: we know now that given the right environment, Indian children would grow as well as any other children in the world. This fact is no longer seriously disputed.

The standardisation of norms and terms allows us to compare the prevalence of malnutrition across countries. Figures, such as from the National Family Health Survey (NFHS), tell us that about half our children under three years of age are stunted and about a fifth wasted. These categories are based on statistically determined cut-offs. For instance, a boy is expected to be about 77 cm long at 12 months, on average, and the distribution of heights around the average is such that most boys fall within 72 and 82 cm at this age -- these are the cut-offs or limits of ‘normal’; a 12-month-old boy with a length of less than 72 cm is therefore considered stunted. One instinctively assumes that if half the children are stunted, the rest must be normal. In reality, even children above the cut-off are not necessarily growing to their potential. If they had all been growing normally, one would have expected about half of them to fall somewhere between the average and the upper limit of normal; a cursory analysis of most data sets such as the NFHS tells us that by the age of two almost no single child in most communities, rural or urban, falls above the ‘average’. What we are witnessing is a wholesale slowdown in the growth rate of all children -- almost no one is growing normally -- but we are trained to look only at those that have ‘fallen’ below the cut-off and happily call the rest ‘normal’.  Seen thus, malnutrition in India is close to 100%.

So, what causes malnutrition?

That effectively pulls several rugs from under our feet: we are no longer justified in the ‘find them and fix them’ approach when it comes to stunting -- there is no need to seek what is universal. A moment’s reflection tells us that poverty alone cannot explain a lot of malnutrition, nor can hunger: neither is as universal as poor growth is in India. One must rather ask, what is it that makes all our children grow inadequately? Is there a universal ‘cause’ that afflicts all of us?

From what we understand today, there are not one, but two and perhaps three such ‘causes’. The earliest operative cause is what has been called the ‘intergenerational factor’: at the core, there appears to be a complex metabolic regulation where the past experience of a hostile environment (insufficient nutrients, too many infections) or its consequence (smaller achieved body size, particularly of the mother) makes the child’s body grow to a smaller than full size -- an adaptation in anticipation of a sustained hostile environment, tending to conserve losses and minimise maintenance costs. This complex hypothesis is still being fleshed out with empirical evidence. The second ‘cause’ is the nearly universal poor feeding of children in the first two years: neither breastfeeding nor complementary feeding (what the child must get in addition to breastfeeding once breastfeeds become insufficient for the infant’s needs by about six months of age) is optimal -- complementary feeding practices being particularly poor. The third ‘cause’ is the high frequency of common infections (such as diarrhoea and fevers) during this age, significantly interrupting growth.

Plenty of empirical evidence exists to show that the latter two causes apply to a large proportion of children. We also observe that malnutrition prevalence peaks around the age of two, by which time the child learns to demand food and feed herself, and by which time the child has passed the age of peak vulnerability to repeated infections.

Where does poverty fit into this? It undoubtedly heightens the risk of malnutrition in many ways: more infections, less access to healthcare and health information, poor variety and quality of food, less time for childcare, diffidence and demoralisation. In most contexts, however, it is not hunger: adults in families with malnourished children (even if we consider only those below the cut-off) eat five to 10 times as much as an under-2-year-old needs to eat, and even desperate families are not generally given to selectively starving children. In better-off families, children are fed equally poorly. Poor feeding is a societal norm, and its effect on growth is not visible because poor growth in children is also a societal ‘norm’ -- everyone feeds the same small amounts, no child grows much better than others. If, in this scenario, all families were to substantially increase the amount of home-available foods they feed their children, one would predict that children in better-off homes would begin to grow visibly better -- because they have access to a variety of foods and thus a variety of nutrients. That is where poverty kicks in: not in terms of how much cereal is available at home, but how much dal, milk, eggs, meat, vegetables are available. That ICDS food supplements are largely cereal-based, and that they are rarely consumed by children under 2, explains why the ‘main’ intervention of the ICDS is singularly ineffective in moving malnutrition rates down. This also explains why the provisions of the new Food Security Act are likely to leave malnutrition rates unscathed, even if well-implemented.

Some red herrings

A number of other potential causes of malnutrition -- and interventions stemming from these -- have been considered in literature and merit attention, even if only to acknowledge that they are not likely to be of immediate consequence in combating malnutrition.

A commonly discussed hypothesis is whether cultural vegetarianism in India leads to poor growth in children. The fact is that the majority of families in most states in India are culturally not vegetarian. However, among non-vegetarians, the frequency of consumption of meat is very low, at least partly because many of them cannot afford more meat. In addition, even where foods from animal sources are available at home, cultural proscriptions appear to severely limit consumption by children -- the proportion of children under 2 who actually consumed milk, fish, poultry or meat is much lower than the proportion of families that consumed these items. This is found in secondary analyses of large surveys (1, 2). Poverty and such cultural feeding norms appear to be responsible for poor intake of foods from animal sources more often than cultural vegetarianism.

To what extent can the lack of food quality be compensated by micronutrient supplements or food fortification? Despite extensive research, there is thus far no evidence of a viable micronutrient intervention that can, of itself, alter rates of stunting. Zinc is the most promising micronutrient in this regard, but has not yet been unequivocally recommended for regular supplementation, from lack of consistent evidence. It is now well-accepted that iodine, iron, Vitamin A and zinc deficiencies are not amenable to dietary interventions alone -- they require fortification or supplementation. Potentially, food supplements fortified with micronutrients could address specific deficiencies, provided there is a way to cut through the diversity of food sources and deliver fortified food to families in need. Micronutrient interventions have proven effective in correcting nutritional anaemia, for instance, which is a nutritional deficiency of considerable importance, but not in reducing stunting or wasting (3).

Even after decades of research on prenatal interventions to impact low birth weight, there is little concrete evidence that such interventions have a demonstrably large effect on either low birth weight or longer-term nutritional status. Considerable interest persists, however, in interventions that can partly or wholly overcome the intergenerational factor. Such an effect would presumably add to the effect of other direct interventions, such as interventions to improve feeding practices, nutrient availability and sanitation.

Would interventions to address wasting be more fruitful? After all, recent weight loss is the easiest to regain, and as mentioned earlier, the cause of wasting is often an acute illness, which is treatable. While finding and fixing wasting does work in individual cases, it is unlikely to make a serious dent on overall malnutrition rates. For one, wasting rates are much lower than stunting rates. Secondly, very few children are purely wasted -- most of them are stunted to a degree as well. Short-term feeding interventions, which are the standard of care for the wasted (in addition to the management of any infections), could raise wasted children to a non-wasted state, but will not substantially affect concurrent stunting, and therefore will only marginally affect malnutrition rates. Interventions for severe acute malnutrition (SAM), which is the same as severe wasting, are in the same genre: not more than 5% of children in most states are severely wasted, and while nutritional rehabilitation would save lives, rates of malnutrition would remain largely untouched. Nonetheless, the health and ICDS programmes should be addressing SAM as a routine, since a lot of malnutrition-related mortality comes from wasted children.

What about interventions that can influence growth during the adolescent growth spurt? There is probably some truth in the belief that adolescence is not too late to intervene and prevent further loss of growth opportunity. Wholesome food, with micronutrient supplements, should be the best bet. However, obviously, child malnutrition rates will not be affected by such interventions for adolescents, except as a hypothesised intergenerational effect: when better-fed adolescents become adult parents, their children are likely to start with a smaller handicap than they themselves did as children.  

Focused, direct interventions and patience

Interventions that might bring about a measurable change in rates of stunting would thus necessarily address the more proximal causes that we understand well: tackle feeding practices, food quality, infections -- addressing all children, not targeting ‘malnourished’ children only. The Lancet estimates (4) that such ‘direct’ interventions could reduce stunting rates by about 30%, given near-universal coverage of all children using effective interventions. The challenge currently is not so much about what happens to the rest of malnutrition, as whether we will ever get our act together to deliver even these relatively simple, direct interventions to all our children. On the face of it, none of these direct interventions are by themselves extraordinarily difficult to implement -- what is lacking is focused effort, and an acknowledgement that hunger and malnutrition (as we measure it) are largely unrelated and require very different approaches to eliminate. And that both are worth eliminating.

For the rest of malnutrition to disappear, however, we will probably need to wait a long time, as each successive generation experiences a more growth-friendly environment, and this triggers less inhibited growth during intrauterine life and early childhood for the next generation. At least we will need to wait for a deepened understanding of the mechanisms that impair growth during intrauterine life and during early infancy, and hope that new, effective interventions emerge from these explorations. But if we are unable to deliver interventions that we have understood well for decades to the people who need them, is it rational to believe that some future magic bullet will perchance find its mark?

(Dr Sridhar Srikantiah is a public health consultant supporting a number of national programmes, including the ICDS, malaria and kala-azar. He received his MD in paediatrics from the Medical College at MS University, Baroda. He has worked with community health organisations and NGOs to initiate alternative, comprehensive and effective approaches to healthcare. He is currently Technical Director, Integrated Family Health Initiative, a project of CARE-India in Bihar)


1 CARE-India. ‘Changing Infant and Child Feeding Behaviours’. InWomen and Child Health at Scale. Working Paper Series 4. 2008. Available from
2 Patel, Archana et al. ‘Determinants of Inappropriate Complementary Feeding Practices in Young Children in India: Secondary Analysis of National Family Health Survey 2005-2006’. In Complementary Feeding Practices in South Asia: Analyses by the South Asia Infant Feeding Research Network (SAIFRN), Maternal and Child Nutrition, Volume 8, Supplement 1, January 2012. Pp 28-44. Available from
3 WHO. ‘Guideline: Use of Multiple Micronutrient Powders for Home Fortification of Foods Consumed by Infants and Children 6-23 Months of Age’. 2011. Available from
4 Bhutta, Z A, Ahmad, T, Black, R E et al, for the Maternal and Child Undernutrition Study Group. ‘What Works? Interventions for Maternal and Child Undernutrition and Survival’. The Lancet,February 2, 2008. 417-40

Infochange News & Features, July 2012