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Division of Nutritional Sciences, Cornell University, Ithaca, NY 14853–6301
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INTRODUCTION |
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 TOP INTRODUCTION REFERENCES |
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In developing countries, ~40% of children <5 y of age are stunted
[de Onis and Blössner 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 Schürch 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 Schürch 1994
). From that workshop emerged the view that the causes and etiology
of stunting include the following: 1) nutrition (energy,
macronutrients, 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 Lampl's 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 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 Children's Fund, through its well-known 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 UN's 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-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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FOOTNOTES |
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REFERENCES |
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TOPINTRODUCTIONREFERENCES |
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1. Cohen R. J., Brown K. H., Canahuati J., Landa Rivera L., Dewey K. G.. Effects of age of introduction of complementary foods on infant breast milk intake, total energy intake, and growtha randomised intervention study in Honduras. Lancet 1994;344:288-293.[Medline]
2. de Onis, M. & Blössner, M. (1997) World Health Organization Global Database on Child Growth and Malnutrition. WHO/NUT/97.4. Programme of Nutrition, WHO, Geneva, Switzerland. .
3. de Onis M., Blössner M., Villar J.. Levels and patterns of intrauterine growth retardation in developing countries. Eur. J. Clin. Nutr. 1997;52(suppl. 1):):5-15.
4. Engle P., Lhotská L., Armstrong H.. The Care InitiativeAssessment, Analysis and Action to Improve Care for Nutrition 1997 United Nations Children's Fund, Nutrition Section New York.. .
5. Engle P., Menon P., Haddad L.. Care and NutritionConcepts and Measurement 1997 International Food Policy Research Institute Washington, DC.. .
6. Farnum C., Wilsman N. J.. Growth plate cellular function. Buckwalter J. Ehrlich M. Sandell L. Trippel S. eds. Skeletal Growth and DevelopmentClinical Issues and Basic Science Advances 1998:203-223 American Academy of Orthopedic Surgeons .
7. Frongillo, E. A., Jr. (1996) The Effects of Timing and Type of Complementary Foods on Post-Natal Growth. Report submitted to the Nutrition Unit, Division of Food and Nutrition, World Health Organization. Division of Nutritional Sciences, Cornell University, Ithaca, New York..
8.
Frongillo E. A., Jr, de Onis M., Hanson K.M.P.. Socioeconomic and demographic factors are associated with worldwide patterns of stunting and wasting. J Nutr 1997;127:2302-2309.
9. Gillespie, S., Mason, J. & Martorell, R. (1996) How Nutrition Improves. ACC/SCN State-of-the-Art Series, Nutrition Policy Discussion Paper # 15. United Nations Administrative Committee on Coordination/Sub-Committe on Nutrition, Geneva, Switzerland. .
10. Jonsson U.. Towards an improved strategy for nutrition surveillance. Food Nutr. Bull. 1995;16:102-111.
11.
Lampl M., Veldhuis J. D., Johnson M. L.. Saltation and statisa model of human growth. Science (Washington, DC) 1992;258:801-803.
12.
Pelletier D. L., Frongillo E. A., Jr, Habicht J. P.. Epidemiologic evidence for a potentiating effect of malnutrition on child mortality. Am. J. Public Health 1993;83:1130-1133.
13. Pelletier D. L., Frongillo E. A. Jr, Schroeder D. G., Habicht J. P.. The effects of malnutrition on child mortality in developing countries. Bull. WHO 1995;73:443-448.[Medline]
14. Scrimshaw, N. S., Taylor, C. E. & Gordon, J. E. (1968) Interaction of Nutrition and Infection. Monograph series 57. World Health Organization, Geneva, Switzerland. .
15. SCN (1997) Stunting and young child development. In: Third Report on the World Nutrition Situation. United Nations Administrative Committee on Coordination/Sub-Committe on Nutrition, Geneva, Switzerland..
16. Tomkins A., Watson F.. Malnutrition and InfectionA Review 1989 United Nations Administrative Committee on Coordination/Sub-Committe on Nutrition Geneva, Switzerland.. .
17. Waterlow J. C., Schürch B.. Causes and Mechanisms of Linear Growth RetardationProceedings of an I/D/E/C/G Workshop held in London, January 15–18. Eur. J. Clin. Nutr. 1994;48:S1-S216.
18. Wilsman, N. J., Farnum, C. E., Leiferman, E. M. & Lampl, M. (1998) Consideration of growth plate biology in the context of growth by saltations and stasis. In: Saltation Stasis and Human Growth (Lampl, M., ed.). Smith-Gordon, London (in press)..
19. World Health Organization (1995) Physical Status: The Use and Interpretation of Anthropometry. Report of a WHO Expert Committee. Technical Report Series no. 854. WHO, Geneva, Switzerland. .
20. World Health Organization Working Group on Infant Growth (1994) An Evaluation of Infant Growth. Doc WHO/NUT/94.8. WHO, Geneva, Switzerland. .
21. . World Health Organization Working Group on Infant Growth. An evaluation of infant growththe use and interpretation of anthropometry in infants. WHO Bull 1995;73:165-174.
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