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Department of International Health, The Rollins School of Public Health of Emory University, Atlanta, GA 30322
2To whom correspondence and reprint requests should be addressed at The Rollins School of Public Health of Emory University, Department of International Health, 1518 Clifton Road, N.E. Atlanta, GA 30322. E-mail: rmart77{at}sph.emory.edu.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONOBSERVATIONAL STUDIESEXPERIMENTAL AND...BREASTFEEDING AND LATER OBESITY...REFERENCES |
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KEY WORDS: • obesity • birthweight • stunting • breastfeeding • gestational diabetes • programming
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONOBSERVATIONAL STUDIESEXPERIMENTAL AND...BREASTFEEDING AND LATER OBESITY...REFERENCES |
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The present review is narrowly focused on whether nutrition in early
life predisposes individuals to be fatter later in life. Three distinct
hypotheses about nutrition in early life have been considered in the
literature: 1) overnutrition increases the risk of later
fatness; 2) at the other extreme, undernutrition is also
associated with increased risk of fatness; and 3) optimal
nutrition during infancy, represented by breastfeeding, is protective
of future obesity (Fig. 1
). Several mechanisms were proposed that may account for programming of
adiposity including the following: disruptions in organ function,
leading to alterations in insulin secretion and sensitivity; increases
in the number and/or size of fat cells or alterations in adipose tissue
function; and disturbances in the regulation of appetite caused by
central nervous system dysfunction (Whitaker and Dietz 1998
).
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OBSERVATIONAL STUDIES |
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TOPABSTRACTINTRODUCTIONOBSERVATIONAL STUDIESEXPERIMENTAL AND...BREASTFEEDING AND LATER OBESITY...REFERENCES |
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The most common approach used to test whether fetal nutrition influences adult fatness relates two reasonable but imperfect indicators of these aspects, birthweight and adult BMI [estimated as weight in kg divided by height in meters squared (wt/ht2)]. These studies have been used to test hypotheses regarding both under- and overnutrition and are best discussed together. Most of the available literature of this type is from developed nations.
The relationship between birthweight and adult BMI was observed to be J-shaped in a few studies, with slightly greater adult BMIs among subjects born small and much greater adult BMIs among subjects born large in comparison to the BMIs of subjects who were of average size at birth. More commonly, studies fail to find the inflection in the curve at the lower end of the distribution, reporting only that larger newborns have greater BMIs as adults.
Among the studies finding a J-shaped relationship is the Nurses’
Health Study I (Fig. 2
). This investigation is notable for its large sample size, 71,100, and
for the age of its subjects at the time of the assessment as adults,
56 y on average (Curhan et al. 1996a
). A limitation
is that both birthweight and BMI were obtained from questionnaires
completed and returned by the subjects, although a substudy found that
reported birthweights matched official birth records reasonably well.
Over 18,000 cases had missing data for birthweight but the
characteristics of this group were similar to those of the middle
birthweight category (7.1–8.5 lbs). Adjustment for several known risk
factors of obesity did not appreciably change the results. A second
study, Nurses’ Health Study II, replicated the findings among women
36.5 y in average age at the time of the assessment (Curhan et al. 1996a
)
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). BMI values were 27.3, 26.0, 27.1, 27.1, 27.6 and
28.3, respectively, for birthweight categories 
5.5, 5.6–6.5,
6.6–7.5, 7.6–8.5, 8.6–9.5 and > 9.5 lbs. BMI values were not
adjusted for age or for potential confounders.
Many more studies fail to find that low birthweights are associated
with greater BMIs while finding that high birthweights are
(Whitaker and Dietz 1998
). The Health Professional
Follow-up Study examined the relationship between BMI and
birthweight among 38,668 U.S. men at around 60 y of age
(Curham et al. 1996b
). Five categories of birthweight
were used: <5.5, 5.5–6.9, 7.0–8.4, 8.5–9.9 and 
10 lbs. Mean
BMI values were 25.9, 25.8, 26.0, 26.6 and 27.0, respectively. Some
15,822 subjects had missing birthweight; other than being older, their
characteristics were similar to those of the middle birthweight group
(7.0–8.4 lbs). The age-adjusted odds ratios for being in the
highest vs. lowest BMI quintile varied as follows for each of the
birthweight categories listed above: 0.82, 0.75, 1.00, 1.50 and 2.08,
respectively (P < 0.05 for all comparisons to the
reference category).
A study conducted in Israel used measured rather than reported
birthweights and BMIs (Seidman et al. 1991
). These data
were obtained from hospital records and draft board army records at age
17 y, respectively. The study population was 33,413 subjects born
between 1964 and 1971 in Jerusalem at three major obstetric wards; as
participants of a previous study their birthweights had been recorded
at birth. Subsequently, birth records were matched to draft board
records of physical examinations. Odds ratios for being severely
overweight (BMI > 27.8 kg/m2), adjusted for
confounding, are shown in Figure 3
by category of birthweight and for males and females. Relative to those
born with weights between 3000 and 3499 g, those of lower
birthweight did not tend to be more prone to overweight; in contrast,
those with heavier birthweights were at increased risk of severe
overweight (odds ratios were elevated for all three higher birthweight
categories). There was an apparent heightened response among females of
large birthweight (>5000 g). The authors stressed that the
predictive power of the association was poor; they found that most
overweight adults had normal birthweights, as others also previously
reported (Serdula et al. 1993
, Whitaker et al. 1997
).
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). We are particularly
interested in IUGR rather than prematurity because the former condition
explains most of the low birth weight prevalence in developing
countries (Villar and Belizan 1982
). In this study BMI
at age 17 y did not differ between IUGR and non-IUGR subjects
in either males or females. A similar study from Sweden
(Lagerström et al. 1994
) also suggests that BMIs
recorded by the army at age 18 were not greater in males born with IUGR
compared to those who were not (we estimated BMIs from mean heights and
weights for each group). These two studies need to be interpreted with
caution because average and large birthweight cases were combined into
one group and contrasted with the IUGR group. Given the known
association between high birthweight and elevated BMI, use of this
comparison group may have obscured differences between the IUGR and the
average birthweight groups. Finally, a study of 169 males and 162
females in rural Guatemala (Martorell et al. 1998
),
where the birthweight distribution is shifted to the left such that
large newborns are rare, showed that IUGR had an impact on height but
not on fatness by late adolescence (Table 1
). Relative to subjects born full-term but of average weight
(2500–3000 g), those born with IUGR (<2500 g, full-term) were shorter
but had similar percentage body fat (% Fat) and waist-to-hip ratio
(WHR). A strength of this study is that it used % Fat rather than BMI.
Percentage fat was predicted from anthropometric variables using
equations based on hydrostatic weighings of Guatemalan subjects of
similar age and body composition as those the sample studied
(Conlisk et al. 1992
).
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).
Each additional kilogram of birthweight resulted in an increase in %
Fat of 1.27 (95% CI: 0.12 to 2.44). These analyses were based on
linear regression, which increases statistical power, and controlled
for confounding; sample sizes were also larger (372 women vs. 162
females) than the earlier study by Martorell et al.
(1998
). These differences may explain why a relationship
between birthweight and % Fat was found in the later study. Postnatal growth and adult percentage body fat
In Guatemala being stunted at age 3 y (height for age
z-score < -2) was associated with a lower BMI and a
reduced % Fat in men but not in women (Schroeder et al. 1999
). In analyses that included birthweight group as well as
the change in height for age z-score from 15 d to
3 y of age, IUGR and postnatal growth failure were both
independently related to reduced % Fat in late adolescence
(Martorell et al. 1998
). In Guatemala therefore, both
prenatal and postnatal growth failure were associated with reduced, not
increased, % Fat. Finally, the study by Schroeder et al.
(1999
) is unique in considering the modifying effects of
migration to urban areas and of changes in socioeconomic status between
childhood and adulthood. Migration, but not socioeconomic status, was
associated with increased WHR in women who were stunted as children,
after adjustment for % Fat.
Early growth and abdominal fatness in adults
Abdominal fatness, as measured by the WHR, increases the risk of
cardiovascular disease and diabetes independent of BMI (Law et al. 1992
). For this reason, researchers have focused on
relationships of birth and infant size to both overall fatness as well
as its distribution.
Much of the literature on the relationship between birthweight, or
postnatal growth, and adult abdominal fatness includes adult BMI or %
Fat in the equation (Lucas et al. 1999
). Various
rationales are given; one stated purpose is to test whether the risk of
central adiposity is enhanced among those with poor early growth and
increased adiposity as adults.
Few analyses have been published that do not control for adult BMI. In
work from the Barker group, neither birthweight nor weight at 1 y
of age was related to the WHR prior to adjusting for adult BMI
(Fall et al. 1995
, Law et al. 1992
). Data
from Guatemala showed that birthweight was not related to the WHR among
adolescents (Martorell et al. 1998
). Also in Guatemala,
height for age at 3 y was inversely related to WHR in females but
not in males (Fig. 4A
), although the regression coefficients were nearly
identical in both groups (Schroeder et al. 1995
).
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). A study of English men found that,
after adjusting for current BMI, birthweight became significantly and
negatively related to WHR (Law et al. 1992
). In
Guatemala birthweight and the ponderal index at birth were both
negatively related to the WHR after adjusting for % Fat or for BMI
(Schroeder et al. 1999
). Finally, also in Guatemala,
adjustment for BMI at follow-up strengthened considerably the
negative relationship between categories of stunting at 3 y of age
and WHR at follow-up (Fig. 4A, B
).
Law and colleagues (1992
) interpreted their
BMI-adjusted results as follows: "The tendency to store fat
abdominally ... may be a persisting response to adverse conditions
and growth failure in fetal life and infancy" (p. 184). But, as Lucas
et al. (1999
) previously argued, this interpretation is
problematic. They state "when size in early life is related to later
health outcomes only after adjustment for current size, it is probably
the change in size between these points (postnatal centile crossing)
rather than fetal biology that is implicated" (p. 245). Even when
birth size is directly related to adult outcome, Lucas et al.
(1999
) caution that studies should explore whether this
is partly or wholly explained by postnatal rather than prenatal
factors.
It may be that people who are born small in early life, but whose food
intake is subsequently increased and their growth consequently
accelerated, are more at risk than those who remain small. This may be
the essential element of the "early origins" hypothesis. However,
to test this notion, several questions would need to be answered: Is
becoming obese later in life only, or most, deleterious in people who
were growth retarded at birth? Could the change in size be important
for future health in its own right? Is the change in size from a low
birthweight more serious in terms of outcome than an equivalent change
from a higher birthweight? Lucas and colleagues (1999
)
propose that all investigations seeking to uncover fetal programming
effects should test four models: 1) early model: regression
relating early size to later outcome; 2) combined model:
regression relating early size to later outcome, controlling for late
size; 3) interaction model: regression testing the
interaction of early and later size (i.e., combined model plus
interaction term); and 4) late model: regression relating
later size to later outcome. No investigation to date, including our
own, has reported on all these models.
Gestational diabetes and adiposity
As reviewed by Strauss (1997
) and Whitaker and
Dietz (1998
), gestational diabetes leads to
overnutrition in the fetus. The fetus of a diabetic mother is exposed
to relatively high concentrations of glucose, amino acids and fatty
acids. Fetal hyperglycemia, in turn, leads to hyperinsulinemia and
increased growth of fat, lean body and glycogen stores; consequently,
babies of diabetic mothers are larger at birth. In fact, the consistent
relationship between large birthweights and subsequent obesity may be
explained in part by maternal gestational diabetes. Surprisingly,
infants of diabetic mothers become similar in weight for length to
infants born to nondiabetic mothers at ages 1–5 y and it is not until
5 y of age or later, near the period of the adiposity rebound,
that they again become heavier for their lengths. It is at this point
that the risk of obesity in children of diabetic mothers begins to be
significantly increased compared to those born to nondiabetic mothers.
Diabetic mothers also tend to be heavier and the effects of gestational diabetes on birthweight could reflect the influence of maternal obesity, which like diabetes also increases the availability of fuel substrates to the fetus. Moreover, inherited genes for obesity could explain the relationship between maternal obesity, large infant birth size and subsequent obesity in the children. That is, mothers with a genetic propensity for large size have children much like them because of shared genes. Research shows that the risk of subsequent obesity in newborns of diabetic mothers is independent of maternal fatness and this suggests that the metabolic intrauterine experience associated with diabetes is the cause of the propensity for fatness.
One can also ask whether birthweight influences the future risk of
gestational diabetes. Studies among Pima Indians indicate that the
probability of gestational diabetes is influenced by a host of
conditions occurring early in the life of the mother (Pettit and Knowler 1998
). Exposure to gestational diabetes enhances risk,
whereas being breastfed lowers the risk that girls will one day
experience gestational diabetes while pregnant. On the other hand, the
relationship between women’s birthweights and their future risk of
gestational diabetes is U-shaped: lower as well as larger newborns are
more likely one day to experience gestational diabetes compared to
average newborns.
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EXPERIMENTAL AND QUASIEXPERIMENTAL STUDIES |
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TOPABSTRACTINTRODUCTIONOBSERVATIONAL STUDIESEXPERIMENTAL AND...BREASTFEEDING AND LATER OBESITY...REFERENCES |
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Acute famine ravished the western part of Holland during the last
6 mo of World War II. Energy intakes during pregnancy in affected areas
may have been reduced from about 1400 to < 800 calories per day.
This provided an opportunity to examine the effects of acute famine on
many outcomes. In one study records of about 300,000 19-y-old men
collected at the time of induction into the army were used to relate
obesity to famine exposure (Ravelli et al. 1976
).
Because the specific timing of the famine and its geographical reach
was well known, investigators could define birth cohorts with varying
exposures to famine during pregnancy and select concurrent controls
from nonexposed areas (Fig. 5
). Obesity was defined as a weight-for-height value equal to or
> 120% of the reference. Two differences were found between
famine-exposed and unexposed subjects. Those exposed to the famine
during the last trimester of pregnancy or during early infancy had
lower levels of obesity than did controls. However, subjects exposed
during the first two trimesters of pregnancy had higher levels of
obesity than did controls.
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). The sample
(n = 741) included men and women born at term in
Amsterdam before, during and after the famine. Birthweights were
obtained from hospital records and the investigators measured
anthropometry. In men, in contrast to the earlier study, exposure to
famine at any time during pregnancy was unrelated to any measure of
fatness (BMI, waist circumference, WHR). Among women, BMI was increased
by 7.4% (95% CI: 0.7%, 14.5%) compared to that of nonexposed women
but only for women exposed in their first trimester of intrauterine
life. The waist circumference was 5.7% (95% CI: 1.1, 10.3) greater,
whereas the increase of 2.2% (95% CI: -3.1, 7.8) in the waist-to-hip
ratio did not reach statistical significance.
The recent Dutch famine follow-up study also examined the
relationship between birthweight and adult body size and composition
(Ravelli et al. 1999
). Birthweight was strongly related
to attained height; the difference in adult height between upper
(>3750 g) and lower (<2750 g) categories of birthweight was
6.7 cm in men and 6.2 cm in women. On the other hand, as found in the
categorical analyses in Guatemala (Table 1)
, birthweight was unrelated
to BMI, waist circumference or WHR.
The INCAP supplementation trial
We have been involved in a follow up study of a nutrition
intervention carried out from 1969 to 1977 in four Guatemalan villages
(Martorell et al. 1995
). Two villages were randomized to
receive a high energy and protein supplement called Atole, while two
villages received a low energy, no protein beverage called Fresco.
Exposure to Atole in comparison to Fresco resulted in faster linear
growth and larger head circumferences during the first 3 y of
life, but was unrelated to all measures of fatness, including weight
for height and skinfold thicknesses (Martorell et al. 1982
). A follow-up study during adolescence and young
adulthood found that effects on height persisted in both sexes,
although they were attenuated somewhat in men (Rivera et al. 1995
). As in childhood, no effects of Atole could be detected
on any measure of fatness, including % Fat, BMI and WHR (Rivera et al. 1995
, Schroeder et al. 1999
).
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BREASTFEEDING AND LATER OBESITY STUDIES |
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TOPABSTRACTINTRODUCTIONOBSERVATIONAL STUDIESEXPERIMENTAL AND...BREASTFEEDING AND LATER OBESITY...REFERENCES |
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, Kramer 1981
). Two recurring
problems with this literature are small sample sizes and poor control
for confounding. For these reasons, two large, well-conducted
studies are emphasized here. One of the best studies is a
case-control study conducted in two samples of Canadian subjects 12
to 18 y old: 639 Canadian patients attending an adolescent clinic
and 533 students enrolled in a high school (Kramer 1981
). This carefully designed and executed study included
blind ascertainment of the feeding history of subjects and careful
control for confounding. The feeding history was obtained through
telephone interviews of mothers. Subjects were classified as either
obese, overweight or nonobese based on measurements of height, weight,
and triceps and subscapular skinfolds. Results were adjusted for age,
sex, race, ethnicity, birth order, socioeconomic status and family
history of obesity. The results were suggestive of a protective effect
of breastfeeding against subsequent obesity in both study samples. The
risk of obesity associated with not being breastfed was two- to
fourfold greater than that associated with being breastfed. This
protective effect was associated with the duration of breastfeeding.
The authors cautioned that the protective effect was of low magnitude
in comparison to the influence on obesity of genetic, racial,
socioeconomic and behavioral factors.
A second large study was recently conducted in Bavaria, southern
Germany, among 5- to 6-y-old children. The occasion of the obligatory
health examination before school entry provided the opportunity to ask
parents in two rural regions to fill out a questionnaire and this
information was linked to the results of the examination. Respondents
(n = 9357) were 77% of the target sample and differed
from nonrespondents in terms of some health care behaviors but not in
terms of overweight and obesity in their children. Parents were asked
whether the child was ever breastfed and then to recall the duration of
"exclusive" breastfeeding in terms of four categories: 2 mo or
less, 3 to 5 mo, 6 to 12 mo, or > 12 mo. Among children ever
breastfed (56.3% of all cases), the percentage distribution by each of
the duration categories was 40.2, 39.6, 16.6 and 2.3, respectively. If
the meaning of exclusive breastfeeding referred to breast milk to the
exclusion of all other foods, rates of exclusive breastfeeding were
extremely high compared to other settings. Overweight was defined as
greater than the 90th percentile and obesity as greater than the 97th
percentile of the distribution of all Bavarian school children that
year. Potentially confounding factors subjected to analyses included
family socioeconomic status, parental education, household structure,
smoking during pregnancy, born low birthweight, early feeding habits
and current diet of the children. Breastfeeding, higher parental
education and low birthweight were protective of obesity. The
prevalence of obesity in children who had never been breastfed was
4.5% compared to 2.8% in breastfed children. A dose response was
found among children who had been breastfed; the prevalence of
obesity was 3.8, 2.3, 1.7 and 0.8%, respectively, for the four
categories of exclusive breastfeeding listed above. The findings
could not be explained by confounding, as indicated by the
comparison of adjusted and nonadjusted odds ratios of the
dose-dependent impact of breastfeeding on being overweight or obese
(Table 2
).
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The subject matter of this review was the relationship between nutrition in early life and risk of fatness later in life. Three hypotheses tested in previous studies guided the presentation: 1) that early undernutrition increases the risk of later fatness, 2) that overnutrition increases risk as well and 3) that breast-feeding protects against the risk of obesity.
Undernutrition increases risk
The evidence linking undernutrition to future risk of fatness is limited and contradictory. The expression of risk of obesity and related conditions may be detectable only among subjects who move across the plane of nutrition from scarcity early in life to abundance or even excess in adulthood. Few studies have considered this possibility in simply relating size in early life to fatness in adulthood. Studies of migrants, from rural to urban areas in developing countries or from poor to rich nations, offer possibilities for study. Another approach would be to take into account changes in conditions of early childhood and adult households.
A few studies find that low birthweight is associated with greater
fatness at follow-up in comparison to subjects of average birth
size. The indicators of fatness used have included BMI, % Fat and the
WHR. The populations in which the hypothesized relationship was found
cannot be easily distinguished from those where this was not the case.
For example, both Nurses’ Health Studies (Curhan et al. 1996a
) but not the Health Professional Follow-up Study
(Curhan et al. 1996b
) found that lower birthweights
increased the risk of obesity in adulthood. The former were studies of
women and the latter of men but the populations and methods were
otherwise similar. Although a study among English women (Fall et al. 1995
) found that risk of obesity increased among those of
low birthweight, a similar study among Dutch women did not
(Ravelli et al. 1999
). Studies in Israel (Paz et al. 1993
) and Guatemala (Martorell et al. 1998
)
did not find a relationship between small birth size and increased
fatness in adulthood. Other evidence failed to find that postnatal
undernutrition leads to fatness later. Growth retardation in height at
3 y of age in Guatemala was associated with reduced rather than
increased % Fat, but only in men (Schroeder et al. 1999
). A nutrition intervention that improved rates of
postnatal growth in Guatemala was associated with taller adult stature
but was unrelated to measures of fatness (Rivera et al. 1995
).
Several studies found that the relationship between birthweight or
postnatal growth and the WHR in adulthood became negative after
controlling for adult BMI. This tendency to store fat abdominally once
BMI has been allowed for has been interpreted as an outcome of prenatal
undernutrition. However, additional analyses would need to be carried
out to properly interpret this finding (Lucas et al. 1999
). It could be, for example, that it is the change in body
size between birth and some age later that accounts for the
relationship.
The results of the two Dutch famine studies are somewhat contradictory.
The first follow-up study of the Dutch famine, which was among men
17 y of age, found that exposure to famine during the last
trimester of pregnancy was associated with decreased risk of obesity,
whereas exposure during the first two trimesters of pregnancy was
associated with increased risk of obesity. The second follow-up was
among men and women of around 50 y of age and was much smaller in
sample size and consisted of adults in Amsterdam only rather than in
all of the famine area (Ravelli et al. 1999
). Exposure
to famine during the last trimester of pregnancy, which was associated
with much decreased birthweights (Stein et al. 1995
),
was unrelated to increased fatness in both men and women and, thus, did
not replicate the findings of the earlier study. Among women, exposure
in the first trimester of pregnancy only was associated with increased
risk of fatness, whereas the earlier follow-up found that exposure
during the first two trimesters produced the same effect in young men.
Therefore, the most consistent finding across the two follow-up
studies is that early exposure during pregnancy to acute famine, which
was associated with larger birthweights (Stein et al. 1995
), may increase the risk of future fatness. This idea has
not been tested with data from developing countries and deserves the
attention of researchers, although the potential for conducting such
studies may be limited.
The evidence that low birthweight and postnatal growth retardation are
risk factors for increased fatness later in life is inconsistent.
Obesity appears to be rising in developing countries (Martorell et al. 2000
) but there is no evidence that undernutrition is an
important factor in causing these trends, as has been claimed
(James et al. 2000
). On the other hand, low birthweight
is a predictor of other symptomatology, including hypertension,
diabetes, lipid levels and cardiovascular disease (Curhan et al. 1996a
, 1996b
, Pettitt and Knowler 1998
, Lucas et al. 1999
). These relationships
were observed without considering changes in conditions between early
life and adulthood. Clearly, obesity is less sensitive as an outcome of
early undernutrition than other metabolic disorders.
Overnutrition increases risk
The evidence linking higher birthweights, particularly
birthweights above 10 lbs, to increased fatness in adulthood is fairly
consistent in studies from developed countries. Of the studies
reviewed, only the follow-up of the Dutch famine at 50 y
failed to find that high birthweights were related to greater BMI and
other measures of increased adiposity (Ravelli et al. 1999
). On the other hand, early exposure during pregnancy to
famine was associated with larger birthweights (Stein et al. 1995
) and increased risk of future fatness (Ravelli et al. 1999
). Some of the relationship between large birthweights
and later fatness may reflect gestational diabetes (Whitaker and Dietz 1998
).
Whether the prenatal environment is a critical period for the
development of excess adiposity has been called into question. One
alternative hypothesis is that birthweight "tracks" into adulthood
because of genetic factors; for example, heavier newborns may become
heavier adults simply because of the steady influence of genotypes that
lead to fatness (Allison et al. 1999
). To test whether
the tracking that occurs in anthropometry is independent of genotype,
intrapair differences in the birthweights of 699 monozygotic twins were
correlated to intrapair differences in anthropometry collected in these
subjects as adults (Allison et al. 1999
). Associations
uncovered in this manner cannot be the result of genetics and have to
be ascribed to environmental influences. The correlation of intrapair
differences in birthweight with those in height was 0.316 (P
< 0.0005), with weight 0.136 (P < 0.0005) and
with BMI 0.026 (P = 0.331). This was interpreted by the
authors as suggesting that the intrauterine environment has an enduring
effect on height but not on adiposity.
Gestational diabetes appears to have clear and long-term effects
that suggest an effect of prenatal programming on later fatness. There
is much supporting evidence for this, including that chemically induced
diabetes in pregnant rats produced heavier newborn rats
(Whitaker and Dietz 1998
). The fact that children born
to diabetic mothers "thin out" during the preschool period and
begin to put on weight during the early phase of the obesity rebound
suggest that complex mechanisms are involved (Strauss 1997
).
Birthweight distributions in developing countries are shifted to the
left such that large newborns are rare. It is unlikely therefore that
the relationship between birthweights and later adiposity should be as
in developed countries. In Guatemala we found that the relationship was
positive but weak and only evident in analyses expressing birthweight
as a continuous variable (Schroeder et al. 1999
). More
studies from developing countries are needed.
Breastfeeding
This literature is contradictory in part because many studies are
based on small sample sizes and lack adequate control for confounding.
The two landmark studies, published in 1981 and 1999, are in agreement
that breast-feeding has a protective effect on childhood obesity
(Kramer 1981
, Von Kries et al. 1999
). In
both these studies, the findings were robust and could not be accounted
for by confounding. Breastfed infants are fatter than formula-fed
infants in the first months of life (Garza and de Onis 1999
). This is probably achieved by increases in fat cell size
rather than cell number (Pi-Sunyer 1999
). In the latter
half of infancy breastfed babies thin out in comparison to nonbreastfed
infants (Garza and de Onis 1999
). It is not clear what
makes them lose the weight and what makes them remain thinner at later
ages. Future investigations should explore whether breastfeeding is
related to the timing of the adiposity rebound. Also, investigations
are needed from developing countries to assess whether the protective
effect of breastfeeding is as found in Canada and Germany. Finally,
studies are needed to address whether the protective effect of
breastfeeding on obesity persists into adulthood.
Poor nutrition in early life has not been shown to predispose to fatness later in life. Therefore, claims that poor nutrition may be fueling an epidemic of obesity in developing countries would seem unfounded. On the other hand, it appears that intrauterine overnutrition and breastfeeding have an enduring influence on subsequent adiposity. These two nutritional influences, the former associated with greater risk of later fatness and the latter protective of it, appear to be important causes of childhood obesity but of modest importance relative to known causes of obesity among adults (i.e., excessive caloric intakes and sedentarism) for the simple reason that most obese adults were not obese as children.
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FOOTNOTES |
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REFERENCES |
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TOPABSTRACTINTRODUCTIONOBSERVATIONAL STUDIESEXPERIMENTAL AND...BREASTFEEDING AND LATER OBESITY...REFERENCES |
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1. Allison D. B., Paultre F., Heymsfield S. B., Pi-Sunyer F. X. Is the intra-uterine period really a critical period for the development of adiposity?. Int. J. Obes. 1999;19:397-402
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