Symposium: Causes and Etiology of Stunting

Introduction1
Edward A. Frongillo, Jr.
Division of Nutritional Sciences, Cornell University, Ithaca, NY 14853 6301
micronutrients and toxic factors); 2) infection (injury to gastrointestinal mucosa, systemic effects and immunostimulation); and 3) mother-infant interaction (maternal nutrition
and stores at birth, and behavioral interactions). The workshop group suggested that a priority for further research should
be intervention studies that enable the differentiation among
possible causal factors. The 1998 Experimental Biology symposium was timely because a number of important intervention studies have examined multiple causes of stunting during
the five years that have passed since the 1993 workshop. The
symposium was also timely because of some relatively recent
observations that affect how we think about the causes and
etiology of stunting.
Much of our thinking about why and how stunting occurs
is depicted in the classic model of the nutrition and infection
cycle (Tompkins and Watson 1989). As an explanation for
how malnutrition and disease result in excess mortality of
children, this so-called vicious cycle model has been supplanted by the synergism model (Scrimshaw et al. 1968) that
has now been demonstrated epidemiologically (Pelletier et al.
1993 and 1995). Furthermore, it is not clear how much the
nutrition and infection cycle helps us understand why and how
stunting occurs.
At the individual level, an episodic model has been demonstrated to explain daily patterns of linear growth (Lampl et
al. 1992). Growth observed daily shows periods of stasis (i.e.,
no growth) punctuated by daily saltations of growth. This
research suggests that stunting must result from a decreased
frequency of growth events, a decreased amplitude of growth
when an event occurs, or both. We do not know why and how
these might happen and which is more important.
The postnatal time most susceptible to poor linear growth
is after 3 6 mo and up to 24 36 mo (SCN 1997). Why poor
conditions have less effect after this time is not understood. A
common explanation is that poor conditions affect growth
when velocity is greater, but this is not very satisfying, especially in light of Lampl9s observations about episodic growth.
Stunting is a cumulative process that can begin in utero and
continue to ;3 y after birth. Low birth weight is an important
indicator of fetal/intrauterine nutrition and a strong predictor
of subsequent growth and well-being. Recent data from de
Onis et al. (1997) have shown that, in the least developed
countries, ;23% of infants are born with low birth weight
compared with ;7% in developed countries. The primary
reason for these high rates of low birth weight is intrauterine
growth retardation. We do not know how much prenatal
stunting contributes to the postnatal stunting we observe, and
therefore how much attention relative to causes of stunting
should be focused prenatally. Furthermore, because maternal

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This symposium considered why and how stunting of children occurs. As described in the comprehensive examination
made by WHO of the use and interpretation of anthropometry
(1995), stunting (i.e., short stature due to poor living environments) is one of the two most important indices of child
well-being in use throughout the world. The assessment of
stunting is integral to public health, clinical and research
workers in many fields concerned with the well-being of children and with the biology of growth and development.
In developing countries, ;40% of children ,5 y of age are
stunted [de Onis and Blossner 1997, WHO Subcommittee on
Nutrition (SCN) 1997]. This means that .200 million young
children are stunted. The timing of stunting is reasonably
understood in that most stunting occurs before the age of 3 y,
and stunted children usually become stunted adults. The consequences of becoming and remaining stunted are increased
risk of morbidity, mortality, delays in motor and mental development, and decreased work capacity (SCN 1997, Waterlow and Schurch 1994).
The causes and etiology of stunting are much less understood than are its timing and consequences. In particular,
there is little understanding of why and how stunting occurs
extensively in environments that are poor, but not desperately
so, and in environments that seem to be improving. In a
population, an individual child can become stunted or not. In
addition, some populations are much more stunted than others
(WHO 1995). This means that an understanding of why and
how children become stunted is needed at both the individual
and ecological levels.
The objectives of this symposium were as follows: 1) review
and synthesize our understanding about why and how young
children become stunted, emphasizing new knowledge gained
since 1993; 2) consider the implications of this understanding
for efforts to improve child well-being; and 3) highlight new
ideas about the causes and etiology of stunting that especially
warrant further investigation in the next few years.
An important foundation for this symposium was a workshop held in London in January 1993 to examine what was
then known about the causes and mechanisms of linear growth
retardation (Waterlow and Schurch 1994). From that workshop emerged the view that the causes and etiology of stunting
include the following: 1) nutrition (energy, macronutrients,

1
Presented at the symposium Causes and Etiology of Stunting as part of
Experimental Biology 98, April 18 22, 1998, San Francisco, CA. The symposium
was sponsored by the American Society for Nutritional Sciences and the Society
for International Nutrition Research. Published as a supplement to The Journal of
Nutrition. Guest editor for the symposium publication was Edward A. Frongillo,
Jr., Cornell University, Ithaca, NY.

0022-3166/99 $3.00 1999 American Society for Nutritional Sciences. J. Nutr. 129: 529S530S, 1999.

529S

530S

SUPPLEMENT

child interactions relate to growth failure. Ramakrishnan,

Martorell, Schroeder and Flores present evidence on why and
how stunting persists across generations.
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size, nutrition, and other factors are important determinants of

prenatal size, why and how stunting occurs is potentially
explainable at least in part by conditions that affected the
previous generation.
Recently, there has been substantial attention paid to the
role of feeding mode on growth patterns of infants. For example, the WHO Working Group on Infant Growth (1994 and
1995) has shown that the pattern of growth for breast-fed and
formula-fed infants differs substantially. Subsequent research
has shown that the pattern of growth is not sensitive to the
duration of breast-feeding (Cohen et al. 1994, Frongillo 1996).
Why these patterns are different and what this might tell us
about why and how stunting occurs is not understood.
It has long been recognized that deficits in macronutrients
cause stunting, but there has been increasing attention paid to
the role of micronutrients. We must determine for which
micronutrients do deficits limit growth and whether stunting is
due primarily to deficits in single nutrients or in multiple
nutrients simultaneously.
The United Nations Children9s Fund, through its wellknown conceptual model and more recent Care Initiative
(Engle et al. 1997a) has helped bring to our attention the role
of maternal and child care in child nutrition. Understanding
the ways in which care affects why and how stunting occurs is
limited (Engle et al. 1997b).
The UNs Coordinating Subcommittee on Nutrition has
just published its Third Report on the World Nutrition Situation. The prevalence of stunting and recent rates of progress
differ substantially across regions (SCN 1997). We can explain
about three quarters of the variability among countries in the
prevalence of stunting by social, human development and
economic factors (Frongillo et al. 1997). But we know less
about why and how some countries improve and others do not
(Gillespie et al. 1996).
WHO has proposed that the goal for reducing stunting
should be that the prevalence of stunting in any country
should be ,20% by the year 2020. Only about one quarter of
developing countries meet that target now, and if past trends
continue, only about one half would meet that target in the
year 2020 (SCN 1997). It is important to identify what are the
most important actions to be taken to make better progress,
and what research be done to assist with these decisions.
The papers presented in this symposium aimed to address
many of these issues. Answering why and how stunting occurs
requires fundamental understanding of how bones elongate to
produce linear growth. This understanding has been lacking,
but Wilsman, the first presenter at the symposium, provides
some clues concerning the nature of this process (see: Farnum
and Wilsman 1998, Wilsman et al. 1998). The paper by
Rosado for this symposium presents evidence that stunting is
associated with marginal deficiencies of several micronutrients
simultaneously. Stephensen discusses current thinking about
how infection may play a causal role in stunting. Black and
Krishnakumar examine how factors such as child temperament, maternal depression, and responsiveness of maternal-