The Response of Child Nutrition to Changes in Income:

Linking Biology with Economics*

Harold Alderman
y
y
World Bank 1818 H St., Washington, DC 20433, USA. e-mail: halderman@worldbank.org
Abstract
It is regularly pointed out that despite impressive economic growth India has the largest
number of malnourished children in the world. It also has the largest number of people with
diabetes despite moderate levels of obesity. These two observations may in fact be linked;
poverty breeds malnutrition in children and chronic diseases in adults. This article reviews
evidence on the critical role of early nutrition both for long-term health and also for reducing
the intergenerational transmission of poverty. (JEL codes: I12, I14, O15)
Keywords: nutrition, child development
1 Introduction
There is likely little doubt on the validity of either the proposition that
income growth reduces malnutrition or that reducing malnutrition
promotes income growth. How much emphasis is placed on the latter,
however, depends, in part, on the expectations on the magnitude of the
former. In particular, if there is a sharp gradient of nutritional status as
one moves away from poverty then a different set of programs might be
prioritized than ifas evidence in Haddad et al. (2003) impliesincome
growth even when evenly distributed over a population has a relatively
modest, albeit significantly positive, impact on undernutrition rates.
Because it is comparatively easy to derive quasi-reduced form estimates
of the association of child malnutrition and current household income this
relationship can be used to both guide development priorities as well as
address pragmatic operational questions such as how much transfer is
needed to effect a meaningful change in health-seeking behavior
(Fernald et al. 2008). This article therefore begins with a discussion of
two observations on the relation of income and income growth to nutri-
tional status. One observation is on the magnitude of the association of
income and nutrition and the other focuses on evidence on the timing of
income. The next section explores new evidence on how these economic
paths may relate to aspects of physical growth again choosing to highlight
two particular features: (i) the timing of critical periods of growth and (ii)
some recent studies that potentially have a bearing on why obesity and
* Paper prepared for CESifo workshop on Malnutrition in South Asia Venice International
University, San Servolo, Venice 2021 July 2011.
The Author 2012. Published by Oxford University Press
on behalf of Ifo Institute, Munich. All rights reserved.
For permissions, please email: journals.permissions@oup.com 256
CESifo Economic Studies, Vol. 58, 2/2012, 256273 doi:10.1093/cesifo/ifs012
Advance Access publication 2 May 2012

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malnutrition are often observed in the same households, never mind the
same communities. The final section links these themes.
2 Some observation on the path from income growth to child
growth
A. The global evidence that income growth is not a sufficient condition for
the rapid reduction of malnutrition
On average, country-level rates of undernutritiondefined as low weights
for agedecline at roughly 50% of the rate that gross national products
(GNP) per capita increase. This cross country evidence differs little from
results generally derived from household surveys at the individual level
(Haddad et al. 2003). Likewise, anemiadefined as hemoglobin levels
below 10.9 g/dldeclines at roughly 25% of the rate of income growth
(Alderman and Linnemayr 2009).
The majority of studies reporting such evidences are based on
cross-sectional surveys and, as always, there are challenges to the causal
interpretation of these associations. However, since anthropometric
surveys are increasingly available, one main issue for deriving such esti-
mates at the individual level for any population or subpopulation strati-
fied by classifications such as gender or age is the source of expenditure or
income data. Many data sets with information on anthropometric meas-
urements or on anemia such as Demographic and Health Surveys [DHS]
lack income or expenditure information. Filmer and Pritchett (2001) have,
however, shown that asset indices can be conveniently used to map the
relationship of economic status and nutrition. This techniquenow
widely employedalso addresses the fact that a graphic or regressional
analysis of the association of an outcome with one that is measured with
substantial error (as are expenditures and income) is biased towards zero
in proportion to the measurement error. The construction of an asset
index sweeps out most measurement error and thus reduces this bias
appreciably.
Alternatively, a measure of income or expenditures that is predicted
from assets also has this appreciable advantage over directly reported
income. This treatment for errors in variables is closely related to the
use of instrumental variables to address the simultaneity or endogenity
of income, although the issue of exclusion restrictions does not necessarily
arise when considering errors in variable bias. In any case, the mismeas-
urement of income or expenditures is plausibly the dominant issue relative
to the lagged endogeneity of assets. That is, the former is known to be
appreciable while the latter is unknown. While very young children do not
directly contribute to asset accumulation, other possible sources of bias
CESifo Economic Studies, 58, 2/2012 257
Response of Child Nutrition to Changes in Income
may reflect either the impact of a childs illness on parents ability to
acquire assets or the correlation of unobserved preferences for savings
over current consumption and health seeking behavior.
1
An asset index provides only an ordinal proxy for income or wealth.
Often the index is reported in quintiles as illustrated in Table 1 or similar
aggregations. Such tables confirm that malnutrition rates are high even
among those who are not poor. For example, using the data in Table 1,
where all households in the lowest two quintiles by wealth in Pakistan to
have the characteristics of the middle quintile, poverty in the country
would be virtually eliminated, yet over 38% of the entire population of
children would still be malnourished.
Such an association of malnutrition and asset rankings can be used to
derive an approximation of income elasticities if the ranking of assets can be
associated with the average income of each quintile using alternative data.
Similarly, it is straightforward to construct average elasticities of income
Table 1 Nutrition and poverty: prevalence of child underweight by wealth
quintiles
Region Country Lowest 2nd 3rd 4th Highest
South Asia
Bangladesh 59 53 45 43 30
India 61 54 49 39 26
Pakistan 54 47 43 37 26
Africa
Benin 29 30 23 20 10
Burkina Faso 42 40 41 39 22
Ethiopia 49 51 51 45 37
Mozambique 31 28 26 19 9
Rwanda 27 30 28 24 14
Tanzania 25 26 22 20 12
Uganda 27 26 25 19 12
Source: Gwatkin et al., Country Reports on HNP and Poverty: Socio-economic Differences
in Health, Nutrition and Population, April 2007.
Note: Data for children <5 years. Below 2SD.
1
Testing the degree to which unobservable preferences might bias an income response in
this context would require creativity. The standard approach to instrumental variables or
the implementation of a randomized control trial might provide some insights but these
are also subject to the question of whether the local response represents the use of tran-
sitory or permanent income. Theoretically, one would expect more investment off the
former. However, as food is both a consumption good as well as a key input into child
nutrition, the expected relative magnitudes are hard to bracket.
258 CESifo Economic Studies, 58, 2/2012
H. Alderman
growth at an aggregate level. For example, in the 1990s, India experienced a
growth rate in GDP per capita of 5.3% whereas malnutrition declined by
1.5% (World Bank 2006). The implied average elasticity of 0.28 is lower
than the rule of thumb of 0.5 mentioned above and lower than that of
China (0.67) or Bangladesh (0.73) over the same period.
Indeed, results from India on the prospects of addressing malnutrition
primarily through income growth are generally discouraging. For exam-
ple, Subramanyam et al. (2011) find that state-level economic growth in
India offers little or no explanation for reductions in malnutrition between
1992 and 2006. Since this analysis of three rounds of the National Family
Health Survey also includes family wealth among the covariates and since
there were strong gradients of the risk of underweight with poverty as well
as maternal and paternal education in this data, the result hints at the role
of state infrastructure and execution of its programs rather than private
resources. This does not completely remove the puzzle of the relatively low
response to growth, but it does help locate it.
Still, for many purposes a cardinal estimate of the impact of income
growth is required at a more disaggregated level. Even in the absence of
direct survey data on income or expenditures it is nevertheless often pos-
sible to map expenditures to the same assets that are commonly used to
construct an asset index using data from an income and expenditure
survey and then use these parameters to predict expenditures within a
DHS or similar survey that has information on assets. Such an approach
was used within the context of a randomized longitudinal trial of a com-
munity nutrition program in rural Uganda. This estimate found that while
income growth will have a positive and statistically significant impact on
undernutrition, a 5% rate of per capita income growthsubstantially
larger than the average for the decade that preceded the studywould
take 33 years to reduce underweight rates by half (Alderman 2007).
As mentioned, such indications of the magnitude of improvements given
income growth can be useful in policy projections. Such a starting point
may, however, not fully guide the design of cash transfers support programs
since there is some evidence that the source of income matters, either
through labeling effects (Kooreman 2000; Paxson and Schady 2010) or
through gender control. Ideally, to understand the path from income to
nutrition one would like to complement a reduced form approach with a
nutrition production function to gain insights on the contribution of key
inputs in overall health as well as assess how income and prices affect the
demand for these inputs. While health production functions are likely to be
more stable than reduced form estimates (Rosenzweig and Schultz 1988),
the difficulty in finding suitable identifying restrictions for input demand
remains an obstacle to their application. Randomized controlled trials have
served to derive the impact of selective inputs, particularly micronutrients,
CESifo Economic Studies, 58, 2/2012 259
Response of Child Nutrition to Changes in Income
but as is increasingly recognized it is still the exception that the heterogen-
eity of response within a population is addressed in such studies.
Additionally, the issue of substitution and complementarity of inputs is
generally not assessed in randomized trials.
B. Timing of income seems to matter
The evidence discussed above, being based on instrumented expenditures
or income and thus indirectly on assets, should reflect a measure of
permanent income. Why then, is the evidence that short-term shocks to
income have long-term consequences on nutritional outcomes so perva-
sive? In one example from this body of evidence, Alderman et al. (2006)
found that children who were 2 years old during a period of drought and
civil unrest in Zimbabwe were more malnourished than their siblings.
Moreover, this shock has a long reach; when this cohort was tracked
over two decades, the malnourished children were found to be both
shorter and had fewer grades completed than other children.
Shocks need not even be of a magnitude commonly deemed droughts to
have an impact on child nutrition. Maccini and Yang (2009) look at rain-
fall in Indonesia and find girls born in years of low rainfall achieved
smaller adult heights and also have less schooling than those born in
years with normal rainfall. The study notes that the impact of a shortfall
of rain in a year immediately prior to birth does not have a similar mea-
sureable impact on nutrition. Recent research using the Indian National
Family and Health Survey and an international database of natural dis-
asters is in keeping with this result (Datar et al. 2011). This study finds that
small to moderate disasters reduce child growth as well as lead to
increased morbidity, with the impact being greater for girls. The study
also found that children who were post weaning were most vulnerable.
The timing of nutritional shocks is not only found when comparing
across years. Birth outcomes reflect intra-year patterns as well. Lokshin
and Radyakin (2012) find that Indian children born in the monsoon
months have lower anthropometric scores than children born in the
post-monsoon period. This holds for both girls and boys and the results
vary little between the ordinary least squares estimates and the family
fixed effects estimates (on a much smaller sample).
2
Wealth and education
mitigate these seasonal patterns without eliminating them, whereas rainfall
at the time of a childs birth has little impact. Lokshin and Radyakin,
however, cannot determine at what age this pattern kicks in, although it is
clearly prior to the age of 3 years.
2
As Alderman et al. (2011) point out, selective survival is unlikely to influence anthropo-
metric patterns at the level of mortality in South Asia.
260 CESifo Economic Studies, 58, 2/2012
H. Alderman
Studies of the timings of nutritional insults, however, seldom distinguish
the impact of prices from that of liquidity. Changes in relative prices,
whether for food or for child care, can plausibly account for a share of
either seasonal or inter-year weather-related patterns of malnutrition. But
food prices cannot be the entire story since similar patterns of increased
mortality in light of financial shocks have been regularly noted. For exam-
ple, Baird et al. (2011) confirmed that macroeconomic shocks, defined as
deviation from trends in 59 developing countries were associated with
increased infant mortality particularly for girls. However, shocks that
occurred during gestation did not seem to affect mortality. These results
are in keeping with those for India based on family fixed effects estima-
tions (Bhalotra 2010). Again, this study finds that income shocks increase
mortality, particularly of girls. It also notes that shocks in utero have a
smaller (marginally significant) impact relative to those in the neonatal
period while post-neonatal shocks do not affect mortality. When
rainfallthe impact of which is presumed to be additional to any
income effect and thus may be considered a proxy for disease environ-
mentwas included the aggregate shock decreased but not substantially.
Health care expenditures andgiven the measured increased labor of
mothers in times of distresschild care were found to decrease in times
of aggregate income shocks. Finally, Bhalotra finds that the aggregate
shocks affect children of uneducated and younger mothers more than
they affect others.
In the absence of evidence on massive selection bias, it is reasonable to
assume that nutrition results move in a similar manner as these income
and mortality patterns particularly if they are driven by health seeking
and child care. Note, however, that these results are observed after any
government, non-governmental organization, or family responses to the
crises. Even if a public safety net cannot gear up expenditures and cannot
refine its targeting rapidly enough to address an aggregate shock, it is a
bit of a puzzle why families are unable to buffer their expenditures using
their own and community resources. This is especially true for seasonal
patterns; Paxson (1993) notes that seasonality in Thailand is mainly an
issue of prices and not total expenditures. Indeed, while the phenomenon
of seasonality of consumption is widespread, it is hard to explain in
terms of intertemporal utility theory. Even income fluctuations between
years are often protected by household savings and other measures to
self insure or to co-insure within a community. However, repeated or
presumablylong-term shocks may have different impact (Alderman
1996). As there are clear mechanisms to transfer income, but few to
transfer time available for child care, it remains important to determine
the manner by which these income shocks transmit to the health of
children.
CESifo Economic Studies, 58, 2/2012 261
Response of Child Nutrition to Changes in Income
3 Two features of child growth particularly relevant for
economic inquiry
A. Timing matters from a biological standpoint
The literature on human development often refers to critical and sensitive
periods after which it is either impossible or at least difficult (and expen-
sive) to offset a lost opportunity for physical and cognitive development.
Given the obvious importance of understanding the timing of interven-
tions, the temporal sensitivity of undernutrition risks has been the focus of
a range of studies. Alderman et al. (2006), for example, identify impacts on
the assumption that children under 2 years are more vulnerable than
slightly older ones. Likewise, Maccini and Yang (2009) interpret their
results as implying the weather shocks they study have an effect during
the critical period of weaning rather than the prenatal period. The limited
period of vulnerability is consistent with extensive epidemiological
evidence that shows most growth faltering occurs in the first 18 months
of life (Victora et al. 2010).
3
This reflects both the risk of diarrheal disease,
especially for children who are not exclusively breastfed until 6 months, as
well as the overall deceleration of growth in infancy. Based on the lower
bound of the average change across the 5th, 50th, and 95th percentiles in
the new growth curves published by World Health Organization, a child
can be expected to grow 24 cm in year 1 and only 12 cm in year 2 and less
in its third year.
Similar critical periods of vulnerability to nutritional shocks are
observed in pregnancy. For example, one of the earliest finding of the
Dutch Famine study was that women in their third trimester of pregnancy
during the relatively brief period of severe food shortages in the winter of
1944/5 were at increased risk of low birth weight babies (Stein et al. 1975).
This risk was not noted for women who conceived later and, thus, who
entered the third trimester after the famine was relieved.
Turning such observations around, clinical and epidemiological studies
have pinpointed optimal times for intervention. For example, folate
supplementation is most likely to prevent birth defects if available
prior to conception and iodine status is also more important in early
pregnancy than after the child is born. In a study in the Gambia, Ceesay
et al. (1997) provided supplements to women in the 20 weeks prior to
expected delivery and found a six percentage points reduction in the
prevalence of low birth weight. Notably, the mean birth weight among
the intervention group increased by a larger amount in the nutritionally
poor hungry season.
3
This does not rule out catch up growth, for example, during adolescence. With increase
availability of longitudinal data this is an area of promising research.
262 CESifo Economic Studies, 58, 2/2012
H. Alderman
The timing of pregnancy itself is important for the outcome of preg-
nancy in another sense as well. Birth weight is lower and mortality risk
higher when a pregnancy occurs prior to age 18a time when a woman is
still growingalthough the relative contributions to birth outcomes of
young women of biology, knowledge and practices for health, and
family wealth are hard to assess due to the endogeneity of reproductive
choices. But one critical period for pregnancy outcomes occurs long before
conception; the evidence on the role of maternal nutrition on the next
generation is quite strong. For example, using 109 DHS data sets from
54 countries, Ozatlin et al. (2010) found a negative association of risk of
child mortality and maternal height in 52 countries, with 46 of these
statistically significant. This was found for all regions including Europe
(although the risk was somewhat less in Africa) and was robust when
household wealth rankings were taken into consideration. Thus, while
the association was not driven by differences in current wealth or
income it does reflect the wealth of the mothers natal family.
This indicator of the inter-generational transmission of healthand,
given other evidence, the transmission of povertyis fairly general; mater-
nal stature is almost always a significant determinant of child anthropom-
etry, even when other wealth and education variables are included in the
estimates (Black et al. 2008).
4
This pattern, often obtained in cross section,
but a similar finding has also been shown in results of a randomized trial
in Guatemala conducted between 1969 and 1977 (the participants of which
are still being tracked). This research found that the children of women
who received nutritional supplements in childhood had higher birth
weights as well as better anthropometric indicators of nutritional status
(Behrman et al. 2009). The precise pathway of this generational impact
could not be elucidated as the benefits of this intervention also included
higher education of the mothers who were supplemented when they were
children although a physiological contribution is consistent with the wider
literature.
This particular study did not find any influence of next generations
nutrition from the participation of the father in the intervention as a
child. Often, but not universally, paternal stature also has a smaller coef-
ficient in cross-sectional estimates (Alderman 1990). Assuming that errors
in variables are not driving this (as it might if paternity was regularly
misassigned), it implies that phenotype influences the childs health in
4
The reference cited here is part of a series of articles that review the state of the art for
nutrition. The reader who wants an introduction to the consensus views in the field (to the
degree that any discipline remains in consensus) might begin with this series. See also,
Victora et al. (2008) and Bhutta et al. (2008).
CESifo Economic Studies, 58, 2/2012 263
Response of Child Nutrition to Changes in Income
addition to genotype. As height represents the choices and conditions that
prevailed when the mother was herself a child, this is a strong indication of
the transmission of one generations wealth (among other factors) to the
health of the next.
The timing for the impact of an intervention is shown in a few published
studies. Community nutrition programs that stress changes in care giving
and health seeking behavior but which do not provide macro-nutrient
supplementation or income support generally find the initial impacts
only among the youngest children in the treatment group (Linnemayr
and Alderman 2011, Alderman 2007). This is in keeping with the import-
ance of exclusive breast feeding and diarrheal disease prevention in the
first months of a childs life.
The provision of supplementary foods for weaning age children have
been shown to make a difference, but, again, it is important to fine tune
the age of the child for whom these supplements are provided. An analysis
of the Guatemala trial discussed above, found that the youngest children
were prone to increased diarrhea when receiving supplements but from age
6 to 36 months the supplements contributed to increased growth but at a
decreasing rate. After 36 months no impact was observed (Schroeder et al.
1995). As discussed in the next section, there is also a concern that as a
child ages past 2 years, addressing malnutrition with the same approaches
that have an impact at the start of weaning, such as with macronutrient
supplements, may not merely be ineffective, the approach may increase the
risk of chronic illness when the child is an adult.
B. The double burden of malnutrition and chronic disease
Research over the past decade has been able to narrow down the under-
standing of the periods of nutritional sensitivity and, in doing so, have
been able to make headway on understanding the biological pathways. In
doing so, recent research leads to the conclusion that separating the con-
cept of malnutrition into under- and over-nutrition is, to a fair degree, a
false dichotomy. For example, given the short duration of the Dutch
Famine and the rapid return to relative food abundance, this event has
facilitated a nuanced assessment of critical periods for pregnancy. As men-
tioned, birth weight was mainly influenced by deprivation in the third
trimester. However, that measure provides only a limited perspective on
development, while birth weight is a commonly used indicator for birth
outcomes it is only one of many aspects of fetal growth linked to
long-term health. As the children born during and immediately after the
famine enter into their middle age, it is apparent that they have increased
risk of chronic disease and some mental illnesses. For example, glucose
metabolism is impaired in adults who were in utero at any time during the
264 CESifo Economic Studies, 58, 2/2012
H. Alderman
famine. However, only those adults whose mothers were in their first
trimester were found to be at increased risk of obesity and heart disease
as well as breast cancer.
5
Recently it was noted that while no cognitive
impairment was found when the cohort were young adults as they age they
are showing loss of attention and cognitive ability at a greater rate than
the general population. Individuals whose mothers were deprived in their
first trimester show the greatest decline of ability (de Rooij et al. 2010).
Although the study of the Dutch Famine is the most comprehensive of
its genre, similar finding have been noted from the disastrous Chinese
Great Leap and in follow up from the Biafra famine of 19671970. In
the latter example, Hult et al. (2010) report increased risk of diabetes and
hypertension among children with fetal exposure to the famine compared
to the cohorts immediately preceding and immediately following the
famine.
While famines are extreme events, the patterns uncovered by studying
these temporally circumscribed events are also found in other analyses.
Moreover, although the findings are explained in terms of a biological
model that transcends political boundaries and, indeed, is not specific to
our species, there is a particular South Asian nuance to the assembled
data. For example, a longitudinal study of a cohort of births in South
Delhi followed up to age 32 found that those children who were thinner in
infancy (with a body mass index [BMI] less than 15) had an accelerated
increase of BMI until adulthood. Although none were classified as obese
by age 12, those with the greatest increase in BMI by this age had impaired
glucose tolerance of diabetes by the age of 32 (Bhargava et al. 2005).
Similar results have been reported using a panel in Pune (Yajnik 2009).
While there is not a standard definition for rapid weight gain, the findings
in the Delhi and Pune studies are in parallel with a systematic global
review that found a similar association of early rapid growth in infancy
and early childhood and subsequent obesity in 13 of the 16 studies
reviewed (Monteiro and Victora 2005).
Despite this global patterns there appear to be characteristics of the
population in India that lead to unique risk factors for chronic disease.
Moreover, the transition from a resource poor environment to one that is
less constrained may aggravate these risks. India has not only the largest
number of malnourished children in the world, but it also has the largest
number of people with diabetes (Ramachandran and Snehalatha 2010).
These two statistics may very well have a common origin. While the Indian
population does not have a high rate of obesity relative to the rest of the
5
Personal correspondence with T. J. Roseboom based on a presentation in Santiago Chile
November, 2009, cited with permission.
CESifo Economic Studies, 58, 2/2012 265
Response of Child Nutrition to Changes in Income
world, or even other Asian countries, there is a tendency to accumulate
adipose tissue around the waist. This pattern is associated with elevated
risk of chronic disease. Thus, Indians have been referred to as thin but fat
(Yajnik 2009). Another risk factor for diabetes largely specific to India is
low maternal intake of vitamin B-12 coupled with high folate. Finally, in
another dimension of intergenerational transmission of health, maternal
hyperglycemia, or diabetes poses an elevated risk of diabetes for the next
generation.
It is largely beyond this article to assess the contribution of these studies
to rapidly accumulating evidence on chronic disease. But before returning
to some semblance of economics, it is useful to allude to the larger picture
that is emerging from such epidemiological results. A seminal paper by
David Barker and Clive Osmond (1986) in which they traced adult illness
in England and Wales to birth weight records has led to a hypothesis of
the etiology of diseases termed the fetal origin hypothesis and a body of
research (as well as a professional association and journal) on the
development origins of health and disease. Gluckman et al. (2009) have
placed this in the context of human evolution; contemporary humans
inhabit an environment very different than that in which they evolved
leading to a mismatch of their biological programming and the conditions
in which they live.
The so-called Barker hypothesis remains controversial, though stronger
than when originally proposed. The original epidemiological results
showed an association. However, it is difficult, if not impossible, to
design an experiment that can provide a direct casual interpretation for
humans within the constraints of research ethics and the practicality of
observing outcomes that take a generation to manifest.
6
Nevertheless, a
causal interpretation is strengthened when there is an underlying structural
biological model. Since Barkers and Osmonds original observations in a
range of laboratory studies using animals has explored this biology
(Harding et al. 2011), bolstering, if not necessarily proving, the causal
interpretation.
One manner in which this plays out is illustrated with adaption to stress
in the womb. The signal derived from limited nutrients in utero leads to an
adaptation in which the child or adult is particularly efficient at conserving
resources. However, when that individual is subsequently confronted with
a resource-rich environment, this maladapted response, or mismatch,
contributes to overnutrition and increased risk of chronic diseases. This
6
While there are a few randomized nutrition interventions in pregnancy that are being
tracked as the children mature (Fall 2009), even in these rare cases the assignment has
occurred after the women knew they were pregnant, while laboratory studies of animals
indicate that preconception nutrition is critical.
266 CESifo Economic Studies, 58, 2/2012
H. Alderman
is occasionally referred to as a manifestation of a thrifty gene, but this is
less genetic than epigenetic. This latter concept refers to a developmental
plasticity that is not directly driven by genes, but rather a process by which
parts of the genes or gene-associated proteins are activated usually, but
not exclusively, through methylation. Thus, genes are not altered, but their
expression is.
7
Gluckman and Forrester (personal communication) have used the
concept of fetal plasticity to gain insights on the question of why some
children manifest undernutrition in the form of marasmus and others with
kwashiorkor. The former emaciation is less likely to be fatal than the
mixture of edema and protein breakdown that occurs in the latter.
Gluckman and Forresters sample of Jamaican survivors of both forms
of malnutrition proved to be quite different. Whereas children who were
diagnosed as marasmic were often born at low weights the other group
was not. The former group also had a tendency to consume more food
when given the opportunity. These results can be interpreted as a result of
fetal nutritional stress that led to low birth weight and an adaption to
consume resources efficiently consistent with the higher survival reported
for marasmus relative to kwashiorkor. But, if the child should survive and
live in an environment replete with resources this risk response is
mismatched with their current conditions, increasing risks of obesity.
4 Bringing it all home
The expanding understanding of biological plasticity and of the link of
undernutrition and subsequent health risk adds a when to the question of
what inputs are most critical. It poses some tricky questions for the timing
of interventions since the maxim, do no harm, is challenged when the
timing of interventions is considered. In the Indian context, recent
research indicates that given the possible negative interaction of micronu-
trients such as vitamin B-12 and folate mentioned above, both of which
are individually shown to be important, new guidelines may be needed.
More generally, program design must consider the risk that addressing
malnutrition in infants and young children may increase illnesses later in
7
Insights from epigenetics do not require interpretation in terms of evolutionary adapt-
ability although Gluckman et al. (2009) offer a range of plausible hypotheses that tie in
the concept of mismatch. To illustrate, evolutionary theory poses a tradeoff between
fecundity and longevity. Under stress plants and animals may increase fitness by shifting
resources into early reproduction rather than growth. This may help explain the plasticity
of menarche. For example, Indian girls, presumably from a low resource environment,
adopted in Sweden, reached puberty earlier than Swedish girls and much earlier than girls
in India.
CESifo Economic Studies, 58, 2/2012 267
Response of Child Nutrition to Changes in Income
life. Similarly, this understanding provides a perspective to assist in antici-
pating the public health challenges that emerge in South Asia as it tran-
sitions from a low income environment.
Gluckman et al. (2009) poses basic and applied research questions
that come out of the understanding of developmental plasticity including
some questions such as what level of risk in later life disease is acceptable
and what are the social costs of less than optimal development and what
are the benefitcost ratios of early interventions. These are difficult ques-
tions and need to be addressed in an interdisciplinary manner but it is
likely that economists have a comparative advantage in approaching
them.
Almond and Currie (2011) have recently taken up the challenge, pla-
cing the fetal origins hypothesis through an economists lens.
8
While they
are in part correct that economics has much to offer, many of the con-
tributions they illustrate come more from econometrics than from eco-
nomics, that is, from techniques and data useful for identifying causal
factors in free living populations more than behavioral choices under
constraints.
They do, however, present a general and useful model in which adult
human capital is produced from inputs in both the prenatal and postnatal
periods with the relative contribution reflected in the parameter .
Health AI

prenatal
1 I

postnatal

1=

This framework has been applied to early child development to explain

success in schooling and in wage earnings. It has the advantage of illus-
trating the potential for inputs in one period to complement the invest-
ments in another. Similarly, this model provides a tool for understanding
the manner by which a short-term income shock affects outcomes among
siblings. It also helps frame some key questions. Economists rightfully ask
the manner in which preferences for intra-household equity affect how
much will be invested in a child in a subsequent period. This has direct
applicability to postnatal investment in nutrition and child stimulation.
They also can give a perspective on how much investment may be needed
to reduce the impact of a bad draw in either period from having serious
consequences for the prospects of the next generation.
In modeling the production of health, conventionally one looks for the
demand for inputs given prices and preferences or uses a reduced form. In
either case, endowments are generally taken as endogenous. The fetal
8
The disciplines may not be as distinct as they first appear. Both economics and evolu-
tionary biology are about resource scarcity; both tribes consider Malthus among their
ancestors.
268 CESifo Economic Studies, 58, 2/2012
H. Alderman
origin hypothesis and the recognition of epigenetics move the question
back, at least to pregnancy and perhaps to the preconception period.
Practically speaking, the implies an increased focus on adolescent health
and, as Almond and Currie put it, a the need for a greater understanding
of what is the cost of an ounce of prevention relative to a pound of cure
(properly discounted, of course).
Gluckman et al. (2009) also argued that the issue of plasticity implies
that the focus on birth weight may miss major indicators that point to later
health risks. Expanding on this theme, as progress is made on reducing
child mortality, emphasis on anthropometric indicators may be too narrow
a guide to health programs. First, while the Millennium Development
Goal indicator of weight for age has the advantage of relative ease in
monitoring, rapid weight gain after infancy may have attendant risks.
Moreover, once the period of greatest risk for child mortality is passed,
neither weight nor height is the direct measure of what is most important
for public policy. As implied in Almond and Currie (2010, 2011), the
outcome of interest in the inter-period model in equation 1 is human
capital more broadly defined than physical growth alone.
More than the implication of maternal height or hyperglycemia for the
intergenerational transmission of poverty, one is concerned about a wider
range of cognitive and non-cognitive measures to address inequality. As
Naudeau et al. (2011) point out, there is a sharp wealth gradient in these
measures in which the gap between children from poorer households and
wealthier households widens over the same time period that is the period
of focus for most nutrition interventions. As the human capital model gets
more nuanced in terms of time indexed inputs, the range of indicators of
development should be correspondingly more nuanced as well.
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