The Journal of Nutrition

Infant Feeding and the Development of Obesity: What Does the Science Tell Us?

Impact of Infant Feeding Practices on

Childhood Obesity1,2
Nancy F. Butte*

USDA/ARS Children’s Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, Texas 77030

Abstract
Childhood obesity is a complex disease influenced by genetic and environmental factors and their interactions. The current
surge in childhood obesity in the United States is attributable to an interaction between a genetic predisposition toward
obesity and a permissive environment. Several recent systematic reviews and meta-analyses have been published on the
association between breast-feeding and childhood obesity. In these analyses, adjustment for confounding factors
attenuated or nullified the protective effect of breast-feeding on later obesity. The Viva La Familia Study was designed to
identify genetic and environmental factors affecting obesity and its comorbidities in 1030 Hispanic children from 319

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families. Odds ratios for potential risk factors associated with childhood overweight were computed using binary logistic
regression for panel data. Early infant-feeding practices were not significant. Salient independent risk factors for childhood
obesity in this cohort of Hispanic children were age, birth weight, maternal obesity, paternal obesity, number of children in
the family, and the percentage of awake time spent in sedentary activity. Breast-feeding may have a small protective
effect against childhood obesity, although residual confounding may exist. Human milk is exquisitely fitted for optimal
infant growth and development and may uniquely modulate neuroendocrine and immunologic pathways involved in the
regulation of body weight. Nevertheless, other genetic and environmental determinants such as socioeconomic status,
parental obesity, smoking, birth weight, and rapid infancy weight gain far supersede infant-feeding practices as risk factors
for childhood obesity. J. Nutr. 139: 412S–416S, 2009.

Introduction
Childhood obesity is a complex disease influenced by genetic and
environmental factors and their interactions. The current surge
in childhood obesity in the United States is attributable to an
interaction between a genetic predisposition toward obesity and
a permissive environment. Epidemiological studies have identi-
fied several risk factors for childhood obesity, each with its own
genetic and environmental determinants. In this article, the
potential effect of early infant feeding on later childhood obesity
is evaluated in conjunction with other predictors of childhood
obesity.
1
Published as a supplement to The Journal of Nutrition. Presented at the
conference ‘‘Infant Feeding and the Development of Obesity: What Does the
Science Tell Us?’’ held in San Diego, CA, April 9, 2008. The conference was
sponsored by The International Formula Council (IFC), Atlanta, GA. The contents
are the sole responsibility of the authors. The articles comprising this supple-
ment were developed independently, and the conclusions drawn do not
represent the official views of IFC. The mention of trade names, commercial
products, or organizations does not imply endorsement by IFC. The Supplement
Coordinator was Heather Gorby, Life Sciences Research Office, Bethesda, MD.
Supplement Coordinator disclosure: H. Gorby is an employee of Life Sciences
Research Office and received compensation for services performed as
Supplement Coordinator. There are no other pending financial interests.
2 3
Author disclosures: N. Butte, no conflicts of interest.
* To whom correspondence should be addressed. E-mail: nbutte@bcm.edu.
Effect of infant feeding practices on childhood obesity
Several systematic reviews and meta-analyses have recently been
published on the relation between early infant feeding and later
development of obesity in childhood, adolescence, and early
adulthood (1–5). Inconsistency exists across studies because of
variation in study design and subjects, statistical power, defini-
tions of infant feeding and obesity, extent of adjustment for
potentially confounding factors, and age of outcome assessment.
A systematic review of published studies on early infant
feeding and later obesity was performed by Owen et al. (1). The
meta-analysis included 28 studies (298,900 subjects). Breast-
feeding was associated with a reduced risk of obesity compared
with formula feeding. The unadjusted odds ratio (OR)3 was 0.87
(95% CI: 0.85, 0.89). In 6 studies, adjustment for potential
confounders, parental obesity, maternal smoking, and social
class, changed the associated risk from 0.86 (95% CI: 0.81, 0.91)
to 0.93 (95% CI: 0.88, 0.99). Low maternal social class and
maternal obesity are both associated with formula feeding and a
greater risk for obesity among offspring. Adjustment for
confounders in the 6 studies markedly attenuated the relation-
ship between breast-feeding and later obesity.
Owen et al. (2) also conducted a meta-analysis on the effect
of breast-feeding on mean BMI later in life to establish whether
Abbreviations used: AOR, adjusted odds ratio; FFM, fat-free mass; FM, fat
mass; OR, odds ratio; SES, socioeconomic status.

412S 0022-3166/08 $8.00 ª 2009 American Society for Nutrition.

First published online December 23, 2008; doi:10.3945/jn.108.097014.
breast-feeding reduces adiposity. Thirty-six studies (355,301
subjects) were identified. Breast-feeding was associated with
slightly lower BMI than formula feeding (20.04; 95% CI:
20.05, 20.02). Adjustment for socioeconomic status (SES),
maternal BMI, and maternal smoking in 11 studies abolished the
effect of breast-feeding on mean BMI (20.10, 95% CI: 20.14,
20.06 to 20.01, 95% CI: 20.05, 0.03). In 3 studies, prolonged
breast-feeding had a slightly greater protective effect on BMI,
but the protective effect was eliminated once data were adjusted
for SES, maternal BMI, and maternal smoking in 2 studies.
Breast-feeding may be associated with lower prevalence of
obesity but not related to mean BMI.
The effect of breast-feeding duration on the risk of obesity was
explored in a comprehensive meta-analysis of 17 studies by Harder
et al. (3). Duration of breast-feeding was negatively associated
with the risk of overweight; the crude OR was 0.94 (95% CI: 0.89,
0.98). The OR decreased with the duration of breast-feeding from
0.81 at 1–3 mo, 0.76 at 4–6 mo, 0.67 at 7–9 mo, and 0.68 at .9
mo. The authors argue that it is unlikely that exposure-confounder
association would exaggerate the dose-response gradient. How-
ever, confounding factors such as the extent of maternal obesity or
familial diet and physical activity practices may covary in a graded
response with the duration of breast-feeding (6).
Quigley (4) suggested that the meta-analysis performed by
Harder et al. (3) may have been inappropriate because of the
significant heterogeneity among the included studies. Studies
included a wide age range (,1 mo to 33 y), variable definitions of
overweight, breast-feeding and the comparison non-breast-fed
category, and a lack of adjustment for potential confounding
factors. Quigley (4) repeated the meta-analysis on the duration of
breast-feeding and risk of overweight, adjusting for confounding
factors where possible. In 5 studies that used the definition of
overweight as BMI percentile $95 or 97, the crude OR was 0.95
(95% CI: 0.92, 0.98). Adjustment for confounders weakened the
OR to adjusted odds ratio (AOR) ¼ 0.97 (95% CI: 0.94, 0.99). In
4 studies that used the definition of overweight as BMI percentile
$90, the crude OR was 0.94 (95% CI: 0.89, 1.01). Adjustment
for confounders weakened the OR to 0.97 (95% CI: 0.93, 1.02).
Although the duration of breast-feeding seems to be associated
with a reduction in childhood obesity, it is unclear if this is
because of residual confounding; for instance, only 3 studies
adjusted for maternal BMI.
In a systematic review using a priori selection criteria of eligible
studies, Arenz et al. (5) identified 9 studies including 69,000
participants to investigate the relationship between breast-feeding
and childhood obesity. Inclusion criteria were obesity defined by
BMI $90, 95, or 97 kg/m2, age at follow-up assessment 5–18 y,
presentation of a risk estimate, and adjustment of at least 3
relevant confounding factors. The crude OR for breast-feeding
and obesity was 0.67 (95% CI: 0.62, 0.73). The AOR was 0.78
(95% CI: 0.71, 0.85). In a meta-analysis, birth weight, maternal
overweight, maternal smoking, and SES contributed up to 0.14 to
the difference between AOR and crude OR. A dose-dependent
effect of breast-feeding duration on the prevalence of obesity was
reported in 4 of the studies. Although results were adjusted for at
least 3 confounding variables, residual confounding is still
possible. Further adjustment for other relevant factors might
reduce the effect, but the protective effect would not likely be
reduced to zero. Breast-feeding appears to have a small but
consistent protective effect against obesity in children.
Other early life determinants of childhood obesity
In addition to infant feeding practices, epidemiological studies
have identified several other risk factors for childhood obesity. In
the Avon Longitudinal Study of Parents and Children, early-life
risk factors for childhood obesity at age 7 were explored (7).
Paternal obesity (AOR ¼ 2.54; 95% CI: 1.72, 3.75), maternal
obesity (AOR ¼ 4.25, 95% CI: 2.86, 6.32), very early adiposity
rebound (AOR ¼ 15.0, 95% CI: 5.32, 42.3), . 8 h/d TV at age 3
(AOR ¼ 1.55, 95% CI: 1.13, 2.12), catch-up growth (AOR ¼
2.60, 95% CI: 1.09, 6.16), weight at 8 mo (AOR ¼ 3.13, 95%
CI: 1.43, 6.85), weight gain in y 1 of life (AOR ¼ 1.06, 95% CI:
1.02, 1.10), birth weight (AOR ¼ 1.05, 95% CI: 1.03, 1.07),
and short sleep duration (AOR ¼ 1.45, 95% CI: 1.10, 1.89)
were associated with increased risk of childhood obesity. Sex,
breast-feeding, age of introduction of solids, and dietary
patterns were not significant predictors.
Socioeconomic status. The effect of SES on childhood obesity
varies across populations. In Westernized countries and societies
in transition, obesity is usually more prevalent in areas of social
deprivation and poverty (8). In the United States, the relation-
ship between SES and overweight is weaker and less consistent
(9). In the NHANES III data, overweight prevalence among
Mexican-American and black children and adolescents was not
related to family income; however, an inverse relation was seen
for white adolescents. In general, $13 y parental education was
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associated with the lowest prevalence of childhood overweight.
Parental obesity. Parental obesity is a strong predictor of
childhood obesity, reflecting both environmental and genetic
contributions. Numerous studies have documented the positive
influence of maternal and paternal obesity on the risk of obesity in
the offspring (10–13). Early-onset obesity (,10 y) has been
associated with an increased relative risk of 2.14 (95% CI not
reported) for obesity in first-degree relatives, suggesting higher
genetic loading and familial aggregation (14). The genetic
contribution to the epidemic of childhood obesity may also
involve an increase in assortative mating (15). If this is occurring,
children born to 2 obese parents would have a substantial chance
of inheriting susceptibility gene variants from both parents and of
developing severe obesity.
Maternal smoking. Maternal smoking during pregnancy has
been identified as a positive predictor of childhood obesity despite
the well-recognized adverse effect of maternal smoking on birth
weight (16). Smoking leads to intrauterine growth retardation
and a substantial reduction in birth weight. In a cohort of Swedish
men born 1973–1985, maternal BMI (AOR ¼ 1.23, 95% CI:
1.16, 1.30) and smoking (AOR ¼ 1.71, 95% CI: 1.21, 2.43) were
the strongest predictors of overweight at age 18 y. A modifying
effect of maternal smoking on the association between birth
weight and later overweight was seen. Birth weight was positively
associated with later obesity only in offspring born to mothers
who were nonsmokers (AOR ¼ 1.46, 1.18, 1.81).
Birth weight. Early life experiences can impact later childhood
obesity. A large number of epidemiological studies have dem-
onstrated a positive relationship between birth weight and BMI
attained in childhood and adulthood (17,18). Low birth weight
seems to be associated with later risk for central obesity, which
also confers increased risk for cardiovascular disease (19), type 2
diabetes (20), and the metabolic syndrome in young adults (21).
Rapid infancy weight gain. A systematic review of 18 studies
examined the relationship between infant weight or BMI and
rapid infancy weight gain on later obesity (22). The OR for
infant weight or BMI and obesity at age’s 3–35 y ranged from
Risk factors for childhood obesity 413S
1.50–9.38. The OR for rapid growth and later obesity ranged
from 1.17–5.70. There was no convincing evidence that expo-
sure at a particular time during infancy was more critical than
others. Infants defined as obese, at the upper end of distribution
for weight or BMI, or who grew rapidly during infancy, were
more likely to develop obesity or to remain obese later on.
In the National Collaborative Perinatal Project, the crude OR
for weight gain during the first 4 mo of life (per 100 g per mo) on
overweight status at age 7 y was 1.29 (95% CI: 1.25, 1.33) (23).
Adjusted for confounding factors of sex, race, first-born status,
birth weight, weight at age 1 y, maternal BMI, and maternal
education, the AOR was 1.17 (95% CI: 1.11–1.24). In an
alternative model, risk of overweight also was associated with
weight gain between 4 and 12 mo (OR ¼ 1.60, 95% CI: 1.48,
1.73). Initiation of breast-feeding was not significantly associ-
ated with overweight status at age 7 y.
The association between rapid infancy weight gain and later
obesity appears to be independent of birth weight. No significant
interaction between birth weight and rapid infancy weight gain
on risk for later obesity was detected (24). Full-term infants who
experience catch-up growth after intrauterine growth retarda-
tion are not protected against an increased risk of later obesity.
the risk of being obese is increased when relatives are also obese.
Formalized quantitative genetic analyses of measures of obesity-
related phenotypes have consistently found significant heritabil-
ities, suggesting that there is an additive or oligogenic component
to obesity. Estimates of the heritability of BMI generally range
from 20% to 60% (25). Based on data from .25,000 twin pairs
and 50,000 biological and adoptive family members, the
weighted mean heritabilities for BMI were 0.74 for monozygotic
twins, 0.32 for dizygotic twins, 0.25 for siblings and 0.19 for
parent-offspring pairs (26).
Viva La Familia Study: Early life determinants of
childhood obesity
The Viva La Familia Study was designed to identify genetic and
environmental factors affecting obesity and its comorbidities in
1030 Hispanic children from 319 families enrolled between
November 2000 and August 2004 in Houston, Texas (27). Family
eligibility included an overweight child between ages 4 and 19 y.
Here we compute OR for potential risk factors associated with
childhood overweight. Binary logistic regression for panel data
were used to examine the effect of putative risk factors on
childhood obesity (STATA, v 10; STATA Corp, College Station,
TX) (Table 1). To account for correlated data within families,

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Genetics. Classical genetic studies on twins, siblings, nuclear family identification number was used as a cluster variable.
families, and in extended pedigrees have repeatedly shown that Childhood overweight was defined according to the Centers for

TABLE 1 Early life risk factors for childhood obesity evaluated in the Viva La Familia cohort of
Hispanic children and adolescents

Risk factors OR 95% CI P-value AOR 95% CI P-value

Child characteristics
Age, y 1.046 1.004 1.09 0.03 0.923 0.854 0.998 0.04
Gender 0.704 0.524 0.946 0.02
Tanner stage 1.058 0.934 1.199 0.37
Child order 0.854 0.75 0.974 0.02
Birth weight, kg 1.826 1.278 2.613 0.001 1.538 1.097 2.157 0.01
Family characteristics
Children in family, n 0.778 0.679 0.891 0.001 0.781 0.639 0.953 0.02
Household income 0.949 0.861 1.046 0.29
Maternal education, y 0.994 0.92 1.074 0.87
Paternal education, y 0.894 0.83 0.964 0.003
Maternal obesity ($30 kg/m2) 1.843 1.348 2.520 0.001 1.613 1.029 2.531 0.04
Paternal obesity ($30 kg/m2) 1.666 1.235 2.248 0.001 1.461 1.0 1.220 0.05
Early infant feeding
Exclusive breastfeeding (yes/no) 1.09 0.799 1.498 0.58
Partial breastfeeding (yes/no) 1.037 0.768 1.402 0.81
Breastfeeding duration, mo 0.995 0.964 1.028 0.76
Age introduction of solid food, mo 0.986 0.935 1.04 0.6
Diet intake
Total energy intake, kJ/d 1.0004 1.0001 1.0006 0.003
Diet fat, % energy 1.021 0.996 1.046 0.11
Diet carbohydrate, % energy 0.977 0.957 0.998 0.03
Diet protein, % energy 1.038 0.988 1.092 0.14
Dinner test meal, kJ 1.004 1.003 1.005 0.001
Eating in absence of hunger, kJ 1.001 1.0006 1.002 0.001
Physical activity
TV, h/wk 1.116 1.014 1.228 0.02
Sleep time, min 0.998 0.996 1.0009 0.23
Total counts, counts/d 0.996 0.994 0.999 0.006
Awake sedentary time, % 1.037 1.023 1.05 0.001 1.051 1.028 1.074 0.001
Awake light time, % 0.946 0.929 0.964 0.001
Awake moderate time, % 0.974 0.948 1 0.06
Awake vigorous time, % 0.841 0.629 1.124 0.24

414S Supplement
Disease Control as percentile for BMI $95 and was coded 0 ¼
nonoverweight, 1 ¼ overweight. Risk factors were evaluated
individually and then simultaneously to identify statistically
independent risk factors for overweight.
Family characteristics. A high degree of obesity was present in
these families (27). The majority of the parents were either
overweight (34%) or obese (57%). Mean BMI of the fathers and
mothers was 30.8 6 0.2 and 33.5 6 0.2, respectively. OR for
obesity increased significantly if the mother (OR ¼ 1.84; P ¼
0.001) or father (OR ¼ 1.67; P ¼ 0.001) was obese. Risk
decreased with increasing years of paternal education. Risk for
obesity increased with the number of children in the family.
Child characteristics. Birth weight was higher in overweight
than nonoverweight children (3.56 6 0.03 vs. 3.42 6 0.03 kg),
controlling for gestational age (28). Birth weights exceeded 4.0 kg
in 17.7% of the children. Birth weight, controlled for gestational
age, was a significant predictor of current BMI Z-score (adj r2 ¼
0.14; P ¼ 0.004), height Z-score (adj r2 ¼ 0.44; P ¼ 0.001), but
not percentage fat mass (FM) (28). Risk of childhood obesity
increased significantly with birth weight (P ¼ 0.001).
Childhood obesity was shown to be heritable in this cohort of
children (28). The heritabilities of body weight, BMI, and FM
were 0.36, 0.39, and 0.33, respectively (27). Birth weight was
highly heritable (h2 ¼ 0.92), controlling for gestational age,
gestation diabetes, mother’s age in pregnancy, birth order, father
and mother’s education level, family income, and gender.
Bivariate genetic analyses between birth weight and later
body size and composition were performed (28). Positive genetic
correlations between birth weight and childhood height (r ¼
0.56), weight (r ¼ 0.36), fat-free mass (FFM) (r ¼ 0.59), and
FM (r ¼ 0.37) suggest shared genetic determinants of birth
weight and later body size. Bivariate linkage analyses of birth
weight mapped to a region on chromosome 10q22, providing
further evidence of shared genetic influences on birth weight,
childhood body weight, hip circumference, and FM in Hispanic
children.
Infant feeding practices. With respect to infant feeding
practices, the predominant milk source was human milk only in
34% of cases for a median duration of 8.2 6 0.4 mo (27). Mixed
feeding of human milk and formula was reported in 24% of cases.
Formula only was used in 42% of cases for a median duration of
10.4 6 0.2 mo. Solid foods were introduced at a mean of 5.1 6
0.1 mo for all cases. Neither exclusive nor partial breast-feeding
was associated with the risk of childhood obesity. Nor was the age
of introduction to solid foods related to the risk of obesity.
Childhood diet intake. Adjusted for FFM and FM, total energy
intake assessed by 2 24-h diet recalls (29) was positively
associated with the risk of childhood obesity (P ¼ 0.003).
Carbohydrate, as a percentage of energy intake, was inversely
related to the risk (P ¼ 0.03). In a laboratory-based test of eating
behavior (30), ad libitum energy intake at dinner and amount of
energy consumed in the absence of hunger were associated with
increased obesity risk (P ¼ 0.001).
Childhood physical activity. Physical activity, as reflected by
total accelerometry counts (31), was protective against obesity
risk. Television viewing (h/wk) was related to increased risk of
obesity. OR for obesity increased with the percentage of awake
time spent in sedentary activity and decreased with the time
spent in light activity.
Multiple logistic regression identified independent risk fac-
tors for childhood obesity in this cohort of Hispanic children
(Table 1). AOR were significant for age, birth weight, maternal
obesity, paternal obesity, number of children in the family, and
the percentage of awake time spent in sedentary activity.
SUMMARY
Epidemiological studies have identified several risk factors for
childhood obesity, including infant-feeding practices. Breast-
feeding appears to have a small but consistent protective effect
against childhood obesity. Residual confounding may exist, but
then again, human milk is exquisitely suited for optimal infant
growth and development and uniquely may modulate neuroen-
docrine and immunologic pathways involved in the regulation of
body weight. Nevertheless, other genetic and environmental
determinants such as SES, parental obesity, parental smoking,
birth weight, and rapid infancy weight gain far supersede infant-
feeding practices as risk factors for childhood obesity.
QUESTION AND ANSWER SESSION
[Q1]: If part of the relationship of maternal obesity to child
obesity is mediated by less breast-feeding, then you are over-
controlling by putting maternal obesity in the model. I think that
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all investigation in this field needs to carefully consider the
possible mechanisms and adjust or construct their models
accordingly. If part of the reason for higher rate of overweight
in non-breast-fed children has to do with gaining more energy by
bottle, just because it is easier and there is less opportunity for self-
regulation by the baby, then the only category where that would
be ruled out would be exclusive breast-feeding.
[Dr. Butte]: If there is a mechanism for the protective effect of
breast-feeding, it is unlikely that it will be discovered through
epidemiological or observational studies because of confound-
ing. For instance, if breast-feeding is having an effect on later
rates of weight gain, you need to carefully assess complementary
feeding and what was happening during and beyond that period.
Our study provided a cross-sectional view of what was going on
during childhood, but I certainly do not know what was going
on in the interim. I leave open the possibility that human milk
may have a unique programming effect on neuroendocrine or
immunological pathways during intrauterine development and
during that first year of life, when the brain is developing, but
I do not think we are going to get those answers from the
epidemiological studies.
[Q2]: I was wondering if you had stratified your results by sex
and saw differences between males and females, especially
because males and females metabolize LDL and triglycerides
differently.
[Dr. Butte]: No, we did not stratify for sex, but we always
control for sex in our models.
[Q3]: The issue of noise is a matter of noise to signal; every
measurement has some noise in it; and if the signal is large enough
you pick the signal up despite the noise. So, for instance, a 91%
signal, which is what we saw for yes-or-no recall of breast-
feeding, is an enormously good signal; you need very little to pick
that up. The critical factor is the sample size; the bigger the sample
size, the less the noise plays a role, and with an infinite sample size,
noise plays no role whatsoever. In studies that are negative, it is
very important to look at that noise-to-signal ratio because you
will conclude that something is not there when in fact it is just
noise.
[Dr. Butte]: The quality of the epidemiological studies in this
area has improved greatly, both in sample size and in the
assessment of confounding factors. There seems to be a small
Risk factors for childhood obesity 415S
consistent protective effect of breast-feeding on later obesity,
even though we cannot rule out the possibility of confounding.
What I was trying to get across is that there are other, stronger
predictors of childhood obesity that should be considered in
evaluating the potential effect of the early infant feeding factors
on later childhood obesity in research studies and public policy.
Other articles in this symposium include references (32–34).
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