Early life determinants of overweight and obesity: a review of systematic reviews.
Lorenzo Monasta1, G. David Batty2, Adriano Cattaneo3, Vittoria Lutje4, Luca Ronfani1, Frank J.
van Lenthe5, Johannes Brug6
1
Epidemiology and Biostatistics Unit, Institute for Maternal and Child Health IRCCS Burlo
Garofolo, Via dell’Istria 65/1, Trieste, Italy.
2
Medical Research Council Social and Public Health Sciences Unit, University of Glasgow, UK;
The Centre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, UK.
3
Health Services Research, Epidemiology and International Health Unit, Institute for Maternal and
Child Health IRCCS Burlo Garofolo, Via dell’Istria 65/1, Trieste, Italy.
4
International Health Research Group, Liverpool School of Tropical Medicine, UK.
5
Department of Public Health, Erasmus Medical Centre, Rotterdam, the Netherlands.
6
EMGO Institute for Health and Care Research, VU University Medical Centre, Amsterdam, the
Netherlands.
Key words: obesity; determinants; children; review.
Running head: Early life determinants of obesity
Acknowledgments
The project this paper is part of is being carried out with financial support from the Commission of
the European Communities, SP5A-CT-2006-044128 “Health-promotion through Obesity
Prevention across Europe (HOPE): an integrated analysis to support European health policy”. The
study does not necessarily reflect the Commission’s views and in no way anticipates the
Commission’s future policy in this area.
Authors’ contribution

Lorenzo Monasta gathered all published and unpublished papers, carried out the analysis,
including the AMSTAR score, and contributed to writing the different drafts of the paper.

David Batty carried out the analysis, including the AMSTAR score, and contributed to
writing the different drafts of the paper.

Adriano Cattaneo was in charge of the overall project and wrote the different drafts of the
paper, including the final version.

Vittoria Lutje designed the search strategies and searched the databases.

Luca Ronfani contributed to the analysis of results and to the evaluation and discussion of the
AMSTAR scores.

Frank van Lenthe designed and coordinated the HOPE project, and critically reviewed drafts
of the paper.

Johannes Brug designed and originated the HOPE project, and critically reviewed drafts of
the paper.
Correspondence: Lorenzo Monasta, Epidemiology and Biostatistics Unit, Institute for Maternal and
Child Health IRCCS Burlo Garofolo, Via dell’Istria 65/1, 34137 Trieste, Italy, Phone +39 040 3785
520, Fax +39 040 3785 260, E-mail monasta@burlo.trieste.it
All authors declare that they have no conflict of interests.
2
Abstract
Objective: To review the evidence for early life (from conception to five years of age) determinants
of obesity.
Design: Review of published systematic reviews.
Data sources: Medline, Embase, Web of Science, Cochrane Library, CINAHL, PsycINFO.
Review methods: Identification of 22 eligible reviews from a database of 12,021 independent
publications. Quality of selected reviews assessed using the AMSTAR score. Articles published
after the reviews used to confirm results.
Results: No review classified as high quality, 11 as moderate and 11 as low. Factors associated with
later overweight and obesity: maternal diabetes, maternal smoking, rapid infant growth, no or short
breastfeeding, obesity in infancy, short sleep duration, <30 minutes of daily physical activity,
consumption of sugar-sweetened beverages. Other factors were identified as potentially relevant,
though the size of their effect is difficult to estimate. Maternal smoking, breastfeeding, infant size
and growth, short sleep duration and television viewing are supported by better quality reviews.
Conclusions: It is difficult to establish a causal association between possible determinants and
obesity, and the relative importance of each determinant. Future research should focus on early life
interventions to confirm the role of protective and risk factors and to tackle the high burden obesity
represents for present and future generations.
3
Introduction
Concern is growing about the escalating prevalence of overweight and obesity in children and
adolescents worldwide. In Europe, for instance, an estimated 20% are overweight with one third of
these being considered obese.1 Prevalence has been rapidly increasing for more than a decade, in
parallel with changes in dietary and physical activity patterns, with an unequal distribution across
socioeconomic groups.2,3 Childhood obesity has well documented, serious adverse psychological,
social and health consequences in childhood and later in life, especially as far as cardiovascular
disease,4 metabolic syndrome, and associated mortality, are concerned.5,6 Other, more subtle,
negative sequelae have been described, with overweight adolescents reporting lower likelihood of
marriage and educational attainment and income as adults,7,8 presumably as a result of
discrimination in their professional and social lives.
To address an epidemic, it is crucial to monitor prevalence and trends, to review its determinants,
and to identify effective strategies and interventions.9 Given the suggestion that foetal life, infancy
and early childhood may be a particularly sensitive period for predicting obesity later on,10 a work
package within the Health promotion through Obesity Prevention across Europe (HOPE) project
(http://www.hopeproject.eu/) focussed on children under five years of age. Having completed an
analysis of current prevalence and trends,11 the objective of this paper is to review, describe and
discuss the evidence for early life (from conception to five years of age) determinants of overweight
and obesity. It is hoped that this review, in conjunction with a parallel review on potentially
effective interventions, will contribute to the development and implementation of policies and
strategies aiming at controlling the obesity epidemic in countries of the European Union (EU).
Methods
Scope of the review and theoretical underpinnings
4
Although ultimately the result of an imbalance between energy intake and expenditure, overweight
and obesity are associated with a complex set of upstream determinants. These may act during
foetal life, infancy and childhood, and may be influenced by genetic and other biological factors, as
well as micro- and macro-environment factors, that have been classified into four categories:
physical, economical, political and sociocultural.12 Each possible determinant may have, in turn,
more distal determinants, located in multiple layers and belonging to different categories. To find
our way into this maze and to construct a model that would facilitate a more detailed search to be
applied to different electronic databases, we conducted, in January 2008, a scoping search for
factors related to overweight and obesity in children under five years of age using PubMed. We
retrieved in this way 1,371 articles; of these, 244 were reviews. A quick analysis of the abstracts of
about 100 articles and reviews allowed to construct a simplified conceptual model that we used for
our systematic search. We also noticed that systematic reviews on a specific determinant or group
of determinants were already available. This led to the decision to carry out a review of existing
published systematic reviews. This approach is becoming increasingly common to summarise the
extensive scientific knowledge on widely explored research topics,13-15 and has already been used
for the association between infant feeding and obesity.16 Systematic reviews were included if they
studied determinants of overweight and/or obesity acting on children from conception to five years
of age.
Systematic search and selection criteria
Given that the inclusion of a term for ‘review’ or ‘systematic review’ may lead to the unreliable
identification of the target item, we selected systematic reviews once the main, wide-ranging search
had been completed. The electronic search took place in April 2008; a range of databases was used:
Medline (from its inception in January 1966), Embase (from 1980); Web of Science (Social
Sciences Citation index/Science Citation Index, from 1970); the Cochrane Library (Issue 2 2008) –
including the Cochrane Central Register of Controlled Trials (CENTRAL) and the Database of
5
Abstracts of Reviews of Effects (DARE); CINAHL (Cumulative Index to Nursing & Allied Health
Literature; from 1982); and PsycINFO (from 1887). The Medline search strategy reported in Table
1, adapted and amended as necessary for the remaining databases, was used to retrieve 21,436 hits.
Citations were catalogued and managed, including removal of duplicates, with Reference Manager.
The final database consisted of 12,021 independent publications from which 589 reviews were
retrieved by screening titles and abstracts; of these, 17 were systematic reviews of early life
determinants of overweight and obesity. In parallel, by searching titles, abstracts and keywords with
the terms “systematic review” or “meta-analysis”, 18 additional systematic reviews were identified.
After duplicate removal and including 4 systematic reviews retrieved from personal files,
bibliographies of selected papers and consultation with experts, we reached a total of 23 systematic
reviews (Figure 1). One of these was excluded because no anthropometric measures nor prevalence
of overweight or obesity were used as outcome.17 We therefore based our final analysis on 22
systematic reviews (Table 2).
Data extraction and analysis
Data were extracted from hard copies of the systematic reviews and the quality of all retrieved
reviews was independently evaluated by two authors (LM, GDB) using the Assessment of Multiple
Systematic Reviews (AMSTAR) protocol.18-20 This is an 11-item tool that measures the review’s
design, its search strategy, the inclusion and exclusion criteria, the quality assessment of included
studies, the methods used to combine the findings, the likelihood of publication bias, and the
statements of conflict of interest. The maximum score is 11, scores of 0-4 indicating low quality, 58 moderate quality, and 9-11 high quality. If the total scores of the independent evaluation differed
by one or two points, the average was calculated. If the differences were wider, a third author (LR)
carried out an additional independent evaluation. The differences were discussed and agreement
was reached on the final score. We did not attempt to pool the results from systematic reviews
together: comparison groups were different and, more importantly, the variables, their definitions,
6
and adjustment methods differed across reviews. Some of the included reviews, however, presented
the results of a meta-analysis, as indicated in the last column of Table 2, and in such cases, pooled
estimates were extracted.
Further search for updates
Having completed the review of reviews, we systematically searched the database of 12,021
independent publications for articles published after the date of the most recent systematic review
for each possible determinant or group of determinants. In this way, we retrieved 317 papers. Only
58 of these papers had overweight and obesity outcomes, and focussed on early life determinants.
These 58 papers reported the results of 33 longitudinal studies, two randomised controlled trials,
two case-control studies, one twin study, two narrative reviews and 18 cross-sectional studies; these
were included only if the sample size was larger than 200. Of the 58 papers, 14 were on genetic and
11 on biological factors, 13 on breastfeeding and other maternal factors, 7 on family, 8 on
neighbourhood and community, and 14 on society factors. All were read in full and their results
were used to update those of the review of systematic reviews. Discussion and conclusions,
however, will be based on systematic reviews, newer studies were used only to confirm or explain
the results of the systematic reviews, or to suggest new hypotheses.
Results
All the 22 reviews but one21 were published between 2004 and 2008. Apart from a World Health
Organization (WHO) report,22 a technology assessment report,23 and an entirely dedicated journal
supplement,24 all the reviews were published as articles in 13 peer reviewed journals. All papers
were published in English except for one in Portuguese,25 a language three of the authors can read.
Among the 22 corresponding authors, ten were from the USA, four from the UK, three from
Germany, two from Brazil and one each from Australia, Greece, and WHO. Not all the systematic
7
reviews report the origin and setting of the included studies. When they do, the original studies were
mostly conducted in North America and Western Europe. Australasia is present with one or two
studies in at least half of the reviews. Five reviews report data from developing countries and five
more from China and Japan. Based on the AMSTAR score, 11 reviews were classified as low and
11 as moderate quality; none as high quality; the average score was 4.9. Three of the four reviews
with the highest scores (7 and 8) focused on the role of breastfeeding, while three of the four with
the lowest scores (below 4) centred on socioeconomic aspects. Nine reviews dealt with the relation
between mother and child, in particular with breastfeeding, and with maternal conditions or
behaviours during pregnancy; six explored family related risk and protective factors, three infant
size and growth, three society related issues, two neighbourhood environmental factors, and one
inherited traits. The 58 papers used to update the results of the systematic reviews were carried out
in North America (29), Western Europe (19), Australasia (4), China (3), Latin America (2) and
Belarus (1).
Genetics
The systematic review by Parsons and colleagues (1999) on childhood predictors of adult obesity
summarized the findings of studies that had examined the inheritance of this phenotype.26 The
authors concluded, on page S5, that “parent obesity is an important factor in predicting adult obesity
of offspring, and that offspring of obese parents who themselves are fatter in childhood may be at
particular risk.” A significant association was found in three out of three longitudinal studies and in
all other types of studies (family and sibling, twin and adoption studies). More recent studies,
published between 1999 and 2008, confirmed a significant heritability component of several
anthropometric indexes including parental height, weight, body mass index (BMI) and percent body
fat.27-34 Maternal birthweight has also been shown to be significantly associated with offspring
birthweight.35,36 However, the size of this genetic contribution to childhood obesity has not been
thoroughly investigated. Maes and collaborators, in their review of twin, adoption and family
8
studies, estimated that 20% to 90% of the variation in BMI may be explained by genetic factors.37
More recently, Farooqi estimated the heritability of BMI at around 40% to 70%.38
Maternal factors
In a systematic review by Huang and colleagues, four out of six studies found a higher prevalence
of overweight or obesity (four different definitions) associated with pregestational and gestational
diabetes. However, only the highest quality study showed an adjusted significant association (OR
1.4; 95%CI 1.0-1.9). Regarding the association between prenatal exposure to maternal smoking and
childhood overweight and obesity, all eight included studies reported significant results with OR
ranging from 1.52 to 2.22.39 According to the authors, these factors, as well as maternal
malnutrition early in pregnancy,40 may act through programming of structural and functional
abnormalities of various endocrine systems. A similar estimate of the size of the association
between maternal smoking and childhood obesity, unaffected by adjustment for confounding and
with evidence of a dose-response relationship, was found in a systematic review of 14 studies by
Oken et al (pooled adjusted OR 1.50; 95%CI 1.36-1.65).41 Seven of the 14 studies were also
included in Huang’s review.
Birth weight, infant size and growth
A systematic review by Martins and Carvalho found a positive association between birth weight and
obesity in infancy and childhood in most of the 20 studies reviewed,42 an observation that accords
with studies conducted subsequently in different countries on children followed up through infancy
and childhood.43-50 The strength of this association tended to diminish following control for a
greater range of covariates, but, in general, remained significant at conventional levels. However,
the authors emphasize the existence of inconsistencies in the relation between birthweight and
childhood obesity which might be explained by the lack of consideration of other factors in the
childhood obesity risk framework. As an example from newer studies, infants who have been
9
growth restrained in utero, as indexed by their lower birth weight, tend to gain weight, or “catch
up”, more rapidly during the early postnatal period, which leads to increased central fat deposition
and greater insulin resistance.51,52 More recent evidence also suggests that the effect of maternal
nutrition on foetal growth can be programmed during the periconceptional period, thus contributing
to an intergenerational cycle of overweight and obesity.53
A systematic review by Baird and colleagues assessed the association between infant size or growth
and subsequent overweight or obesity in 24 studies meeting their inclusion criteria (22 cohort and
two case-control studies).54 Of these, 18 assessed the association between infant size and
subsequent overweight or obesity, most showing that infants defined as obese or at the highest end
of the distribution for weight or BMI were at increased risk of obesity, with Odds Ratios (OR) or
Risk Ratios (RR) between 1.35 and 9.38, a finding confirmed in subsequent studies.55,56 The 18
studies, however, used a wide variety of definitions of overweight and obesity. Ten of the 24 studies
assessed the association between infant growth and subsequent overweight or obesity, and most
showed that infants who grew more rapidly were at increased risk at ages ranging from 4.5 to 20
years (OR or RR from 1.06 to 5.70). The associations were consistent at different ages and for
people born over a period from 1927 to 1994. Another systematic review, by Monteiro and Victora,
included 16 studies;57 13 of these reported on early rapid growth and found significant associations
with later overweight or adiposity (five of these studies were included also in the systematic review
by Baird; no OR or RR reported). There was wide variability in the indicators used for defining
rapid growth as well as overweight or obesity. The age range in which weight or adiposity were
measured ranged from 3 to 70 years. The most frequent definition for rapid growth was a z-score
change greater than 0.67 in weight-for-age between two different ages in childhood. In a narrative
review not included in our review, Ong and collaborators identified 21 studies with data on the
association between rapid weight gain up to two years of age and subsequent risk of obesity.58 All
these studies, and other studies published afterwards,59-68 showed that rapid weight gain is
consistently associated with increased risk of obesity, but the predictive ability of different weight
10
gain cut-offs needs to be tested.
Infant feeding
Seven systematic reviews, six of which were classified as of moderate quality using the AMSTAR
score, examined the association between infant feeding and obesity later in life. Arenz and
colleagues reviewed nine studies meeting their inclusion criteria, with over 69,000 participants.69
They found that breastfeeding had an inverse association with childhood obesity (pooled adjusted
OR 0.78; 95%CI 0.71-0.85). Four studies in the review reported an inverse dose-response effect of
breastfeeding duration on the risk of obesity. Similar results have been found in studies conducted
subsequent to this review,70-74 while other studies found no association between breastfeeding and
obesity later in life until adulthood.75-78 Owen and collaborators examined the association between
breastfeeding and BMI throughout life.79 Despite a significant difference in the mean BMI for
breastfed compared with formula fed infants (lower BMI for breastfed infants: -0.04; 95%CI -0.05,
-0.02), the adjustment for possible confounders (socioeconomic status, maternal smoking during
pregnancy, maternal BMI) in 11 studies removed the effect. A similar reduction of the association
between breastfeeding and obesity after controlling for confounders was reported also by other
researchers.80,81 In a subsequent review, Owen and collaborators compiled 28 studies providing OR
estimates on a total of almost 299,000 subjects.82 Breastfeeding appeared to be associated with
reduced risk of obesity if compared with formula feeding (pooled OR 0.87; 95%CI 0.85-0.89).
Adjustment for three major potential confounders (parental obesity, maternal smoking and social
class) was reported in six studies and the OR, even if closer to one, remained statistically significant
(pooled adjusted OR 0.93; 95%CI 0.88-0.99). Harder and colleagues reviewed the literature using
exclusively formula-fed subjects as the referent.83 The duration of breastfeeding was inversely
associated with the risk of overweight (regression coefficient 0.94, 95%CI 0.89-0.98) and the
results were confirmed using categorical analysis (<1 month of breastfeeding: OR 1.00; 95%CI
0.65-1.55; 1–3 months: OR 0.81; 95%CI 0.74-0.88; 4–6 months: OR 0.76; 95%CI 0.67-0.86; 7–9
11
months: OR 0.67; 95%CI 0.55-0.82; >9 months: OR 0.68; 95%CI 0.50-0.91). In their systematic
review on maternal and infant health outcomes of breastfeeding,84 Ip and colleagues analysed three
already cited reviews,83,85,86 emphasizing how sensitivity analyses carried out by Arenz and Owen
showed a continuous reduction of the effect of breastfeeding on overweight and obesity when more
factors were accounted for in the analysis. They also underlined how exclusive breastfeeding was
not considered in most of the included studies. Horta and collaborators, in a systematic review
published by the WHO,22 obtained 39 estimates of the effect of breastfeeding on the prevalence of
overweight and obesity. In a random-effect model, breastfed individuals were less likely to be
overweight and/or obese, with a pooled OR of 0.78 (95%CI 0.72-0.84). Control for confounding,
age at assessment, year of birth, and study design did not modify the effect of breastfeeding.
Finally, in their systematic review, Plagemann and Harder found that breastfeeding is associated
with decreased risk of overweight, decreased blood cholesterol and blood pressure, and a reduced
risk of developing type 2 diabetes later in a child’s life.87 All the studies included in these
systematic reviews on the association between breastfeeding and obesity, however, were
observational. The only randomised trial that looked at the effect of an intervention on
breastfeeding rates and duration, and subsequently at the effects of breastfeeding on obesity, did not
report a lower prevalence of adiposity (measured as BMI and waist or hip circumference) among
children in the intervention group compared to the control group.88 Randomization, however, was
applied to clusters, as opposed to individuals, and looking at the effect of breastfeeding on obesity
was not among the primary objectives of the study.89
Sleep duration
Two reviews explored the association between sleep duration and weight gain. The first one found
that short sleep duration at age 3-4 years is independently associated with weight gain and
overweight or obesity at later ages (7 and 10 years).90 The authors, however, stated that major
limitations in study design, mainly related to the definition of normal sleep duration and to the
12
possibility of reverse causality, preclude definitive conclusions. The second review summarised the
findings of 17 observational studies and found that children with shorter sleep duration had a 58%
(pooled OR 1.58; 95%CI 1.26-1.98) higher risk for overweight or obesity, and children with
shortest sleep duration had an even higher risk (pooled OR 1.92; 95%CI 1.15-3.20) when compared
with children having the longest sleep duration.91 For each hour increase in sleep, the pooled OR for
overweight or obesity was 0.91 (95%CI 0.84-1.00). A significant inverse linear dose-response effect
could be found only in young children (<10 years-old) or for combined overweight and obesity, but
not for children as a whole group. There was also a significant gender difference, boys having a
stronger inverse association than girls (OR 2.50 vs. 1.24). Studies published after these reviews
support their conclusions: in the US Project Viva, for instance, infants who slept for less that 12
hours per day during infancy experienced a greater prevalence of overweight by age 3 years.92
Family
Considering that children exposed to intimate partner violence may be at increased risk for adverse
mental and behavioural health sequelae, a systematic review analysed the results of 22 studies and
found no evidence that abuse on mothers had an association with general health, use of health
services, breastfeeding, or weight gain in their children.93 More recently, a series of studies have
related obesity in adulthood to early life experience of abuse and/or ill-treatment.94-96 In another
study, 3-year old children experiencing subtle neglect, defined as a failure by the parent to engage
in behaviours that supported their offspring’s development, such as inadequate supervision, had a
higher prevalence of obesity than their non-neglected peers.97 Two other systematic reviews
examined the association of obesity with family social factors. In the first, by Parsons and
colleagues, which accords with more recent work,98,99 six out of nine studies found a lower risk of
fatness associated with higher socioeconomic status in childhood as determined by parental
occupation, education, family income, or a combination of these three factors.100 The influence of
other social factors, such as family size, number of parents at home, and child-care, however, had
13
not been well researched. In the second, limited to the USA, a higher prevalence of overweight and
obesity was found in American native Indians, Mexican Americans and non-Hispanic Blacks, in
lower socioeconomic status groups, and in children living in rural working class, exurban and
mixed-ethnicity urban areas.101 An extensive narrative review had previously found a strong direct
association between socioeconomic status and obesity among men, women, and children in
developing but not in developed countries.102 In a related field, data are emerging regarding the role
of food insecurity or insufficiency, even in high income countries, in the aetiology of childhood
obesity. Defined as episodes of a family running short of food due to inadequate money,
paradoxically, its occurrence appears to be associated with an increased risk of overweight among
Canadian children under five years of age,103 perhaps because of overconsumption of mass
manufactured, high energy foods which are lower in cost that healthier alternatives. It is plausible
that such an association could be explained by residual confounding due to socioeconomic status.
Physical activity and sedentary behaviour
A systematic review by Marshall and colleagues looked at television viewing and video/computer
games and found a statistically significant association with body fatness among children and youth
and a negative association with physical acitivity.104 These associations were small in magnitude
but remained virtually unchanged after correcting for common sources of bias, suggesting mediabased inactivity to be implicated in the increased prevalence of overweight and obesity. The
association between inactivity due to television viewing and childhood obesity is robust and
confirmed by other studies,105-112 including a non-systematic review113 and an intervention study.114
However, a perennial problem in interpreting many of these studies is their cross-sectional design
which raises the issue of reverse causality: while it is of course possible that the sedentary nature of
television viewing is a predictor of weight gain, it is likely that obesity in its own right may be
related to television viewing because sports or active play are more prohibitive for the obese child.
After the publication of this review, a longitudinal study on 871 New Zealand children followed up
14
to age 7 years found that sedentary activity time was a predictor of overweight and obesity.115 An
association between a “snacking and sedentary” lifestyle was positively associated with overweight
in children 3 to 6 years of age also in France; in addition, a “varied food and physically active”
pattern was inversely correlated with overweight in older children 7 to 11 years of age.116,117 A
study that tracked activity and sedentary behaviour in Iowa between 1998 and 2004 in 379 children
aged 5.6 years on average at baseline, found that children maintaining a high degree of vigorous
activity and low levels of television viewing were less likely than peers to be in the upper quartile
for adiposity – measured with whole body, dual energy x-ray absorptiometry – at follow-up, and
were less likely to gain adiposity during the study period.118,119 In another longitudinal study,
children in the highest tertile of average daily activity, monitored with electronic accelerometers
from age 4 to 11 years, had consistently smaller gains in BMI and other measures of adiposity.120
Using data from the USA, a paper reported a significant association between increasing levels of
physical activity and lower risk of overweight and obesity in 3 to 4 years old children followed for
three years.121 In the same country, less than 30 minutes of physical activity or active play per day
was associated with an increased risk of overweight and obesity (OR 1.80; 95%CI 1.10-2.94) in 316
children 2 to 4 years of age.122
Society and built environment
A systematic review explored the relationship between built environment and obesity in children 3
to 18 years of age.123 In the 20 studies analysed – three with data on pre-school children – it found
no difference in the average distance to a play space by BMI status, and no association between
proximity to playgrounds and fast-food restaurants and risk of overweight. Lower prices for fruits
and vegetables predicted lower gains in BMI over a 3-year period. Social models of consumption
may affect eating, drinking and sedentary behaviours. A systematic review selected 30 publications
(15 cross-sectional, 10 prospective, and 5 experimental studies) to relate the consumption of sugarsweetened beverages with weight gain in children 1.5 to 19 years.124 It found a positive association
15
between greater intakes of sugar-sweetened beverages and weight gain and obesity in both children
and adults. Later studies provide mixed support for these conclusions: while beverages with added
sugar125 and those that are naturally sugar-rich but otherwise unsweetened (e.g., fruit juice)126
appear to increase the risk of developing obesity or promote weight gain in pre-school children,
other data show null effects.127,128 Another systematic review explored the association between
childhood obesity and food advertising on Australian television and found that childhood obesity
rates had tripled since 1985, mirrored by increases in consumption of energy-dense foods and
advertising of these foods on children’s television programmes.129 Finally, a systematic review
examined the distribution of obesity by geographical location, income, age and sex in the
Mediterranean region during the last decade.130 The review covered nine countries in Europe, five
in the Middle East and three in Africa. In a meta-analysis of 102 articles, it showed that the
prevalence of obesity was not significantly different by sex nor by levels of income. The results
applied to both children (≤18 years) and adult populations. Among children living in Europe,
however, the prevalence of obesity was higher than among children living in the Middle East.
Discussion
The results of this review of systematic reviews indicate that breastfeeding may be a protective
factor for later overweight and obesity, while obesity in infancy, rapid infant growth, maternal
diabetes, maternal smoking, short sleep duration, less than 30 minutes of daily physical activity, and
consumption of sugar-sweetened beverages may be considered as risk factors. Parental obesity,
restricted or excessive intra-uterine growth, small or large size at birth, television viewing, food
insecurity and low socioeconomic status can also be included among risk factors, although it is
difficult to estimate the size of their effect. Among all these possible determinants, maternal
smoking, breastfeeding, infant size and growth, short sleep duration and television viewing,
including video and computer games, are those supported by better quality systematic reviews.
16
It is also difficult to disentangle the complex web of associations and of reciprocal influence of all
these factors, tentatively represented in Figure 2. Maternal overweight, for example, can have
metabolic consequences, through nutrition in pregnancy, on the development of the foetus, on birth
weight and on infant growth in the breastfed child. Moreover, for an obese mother, the decision to
breastfeed can have psychological and physiological implications, and obese mothers are known to
breastfeed less.131 Maternal overweight may have a bearing on childhood obesity also through
diabetes and genetic factors. Finally, maternal obesity is associated with lower socioeconomic status
and education, which in turn acts indirectly on childhood obesity through a series of other factors,
including not only those related to the child’s diet but also physical activity. Maternal smoking is
another example of the different pathways that lead to childhood obesity through direct effects on
maternal and foetal nutrition during pregnancy, through its association with less breastfeeding,132
and through its indirect links with socioeconomic status and education. It is also an example of the
multiple effects an intervention may have. The decision to quit or not smoking during pregnancy
can have an impact on the development of the foetus, but also on breastfeeding, on infant growth
and, through socioeconomic status, on other important factors (e.g. more money available to buy
healthier foods), let alone other health outcomes.
Another difficulty is the interpretation of an independent role of breastmilk on patterns of child
growth as separated from the socio-cultural effect of the decision to breastfeed.133 Behavioural,
hormonal and nutritional mechanisms seem to play a role in explaining the inverse association
between breastfeeding and childhood overweight and obesity. Lower protein intake, lower plasmainsulin concentrations, and bioactive factors in breastmilk could have a protective effect against fat
deposition in breastfed infants. However, factors related to the socio-economic circumstances of the
mother might be influencing, at least to some extent, both her decisions regarding breastfeeding and
the child nutritional status. The authors of the systematic reviews on breastfeeding and obesity tend
17
to consider that even if the association is not strong, breastfeeding appears to consistently affect
child weight and reduce the risk of obesity. Others note how, according to the growth acceleration
hypothesis, faster postnatal growth induced by formula, as compared to breastmilk, programs the
major components of the metabolic syndrome, including obesity.134
Breastfeeding is not the only possible determinant for which it is difficult to establish a causal
association with obesity. It is difficult to identify the mechanisms that lead to obesity also for other
possible determinants, such as short sleep duration or lower socioeconomic status, either because
these mechanisms are biologically unclear or because there are too many possible mediators
between determinants and outcome. Moreover, none of the studies and reviews conducted so far has
been able to include in a multivariate model, that would anyway result very complex, all the factors
potentially contributing to obesity. Finally, even if a determinant or group of determinants were
confirmed as causally associated with obesity, we would still have to identify those associated with
the increase in the rates of obesity.
The large number of possible determinants means also that for each of them the association may be
weak. i.e. the risk in exposed people may be not much higher than the risk in non exposed.
However, even acting on a small attributable risk may have a large effect on the outcome if the risk
factor is highly prevalent in a population, like the low rate of exclusive breastfeeding is, for
example, in many European countries.135 Also, some possible determinants may be more important
than others for the simple reason that it may be easier to implement an effective intervention. For
example, it may be easier to increase the prevalence and duration of exclusive breastfeeding that to
reduce the incidence of large or small birthweight, or it may be easier to act on parental physical
activity levels than on television viewing by children even though the former is less directly
associated with childhood obesity than the latter. Finally, the impact of an intervention on a
potential determinant may have different effects in different populations owing to the relative
18
weight of that determinant within the complex web of other determinants in different settings.
As far as strengths and weaknesses for the 22 systematic reviews are concerned, we can mention:
lack of clear research question, lack of independent searches and assessment of studies to be
included, lack of thorough search in all possible databases, little exploration of grey literature,
studies not always tabulated, and use of definitions, reference populations and cut-offs for
overweight and obesity that are not standardised. In addition, almost all the individual studies
included in the systematic reviews are observational and suffer from the problem of potential
confounding. This is particularly well illustrated for breastfeeding or smoking, where the
characteristics of mothers who smoke or elect to breastfeed (and those of the offspring born to
them) differ consistently and markedly from those that do not; similar problems with confounding
were described for different outcomes.136 Statistical adjustment can be made to identify independent
effects but does not completely eliminate the problem, in particular when data are not available for
all potential confounders, especially those associated with socioeconomic status. A multiple
regression approach, therefore, can still result in residual confounding that can only be removed
with a randomised controlled trial design. This, however, is not applicable for many of the potential
determinants of obesity.
To conclude, we think that we have put together most of the knowledge currently available on
potential early life determinants of overweight and obesity. There is no doubt that this knowledge
needs to be extended, in particular with respect to more distal determinants, to reach firmer
conclusions about the relative weight of each determinant and its direct or indirect causal
association with the outcome. We think, however, that researchers, and their funding agencies,
should focus on interventions aimed at these determinants, firstly because intervention studies have
a higher chance of confirming the real effects of potential determinants, but ultimately because a
delay in the study and implementation of effective interventions is not justified given the damage
19
overweight and obesity are already causing to present and future generations.
20
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systematic review. Am J Clin Nutr 2006;84:274-88.
125. Dubois L, Farmer A, Girard M, Peterson K. Regular sugar-sweetened beverage consumption
between meals increases risk of overweight among preschool-aged children. J Am Diet Assoc
2007;107:924-34.
126. Faith MS, Dennison BA, Edmunds LS, Stratton HH. Fruit juice intake predicts increased
adiposity gain in children from low-income families: weight status-by-environment
interaction. Pediatrics 2006;118:2066-75.
127. O'Connor TM, Yang SJ, Nicklas TA. Beverage intake among preschool children and its effect
on weight status. Pediatrics 2006;118:e1010-e1018.
128. Welsh JA, Cogswell ME, Rogers S, Rockett H, Mei Z, Grummer-Strawn LM. Overweight
among low-income preschool children associated with the consumption of sweet drinks:
Missouri, 1999-2002. Pediatrics 2005;115:e223-e229.
129. Carter OB. The weighty issue of Australian television food advertising and childhood obesity.
Health Promot J Austr 2006;17:5-11.
130. Papandreou C, Mourad TA, Jildeh C, Abdeen Z, Philalithis A, Tzanakis N. Obesity in
Mediterranean region (1997-2007): a systematic review. Obes Rev 2008;9:389-99.
131. Amir LH, Donath S. A systematic review of maternal obesity and breastfeeding intention,
initiation and duration. BMC Pregnancy Childbirth 2007;7:9.
132. Amir LH. Maternal smoking and reduced duration of breastfeeding: a review of possible
mechanisms. Early Hum Dev 2001;64:45-67.
133. Schack-Nielsen L, Michaelsen KF. Advances in our understanding of the biology of human
milk and its effects on the offspring. J Nutr 2007;137:503S-10S.
134. Singhal A. Does breastfeeding protect from growth acceleration and later obesity? Nestle Nutr
Workshop Ser Pediatr Program 2007;60:15-25.
135. Cattaneo A, Burmaz T, Arendt M, Nilsson I, Mikiel-Kostyra K, Kondrate I, Communal MJ,
Massart C, Chapin E, Fallon M. Protection, promotion and support of breast-feeding in
Europe: progress from 2002 to 2007. Public Health Nutr 2009;1-9.
136. Batty GD, Der G, Deary IJ. Effect of maternal smoking during pregnancy on offspring's
cognitive ability: empirical evidence for complete confounding in the US national longitudinal
survey of youth. Pediatrics 2006;118:943-50.
137. Arenz S, Ruckerl R, Koletzko B, Von Kries R. Breast-feeding and childhood obesity--a
systematic review. Int J Obes Relat Metab Disord 2004;28:1247-56.
138. Bair-Merritt MH, Blackstone M, Feudtner C. Physical health outcomes of childhood exposure
to intimate partner violence: a systematic review. Pediatrics 2006;117:e278-e290.
139. Baird J, Fisher D, Lucas P, Kleijnen J, Roberts H, Law C. Being big or growing fast:
systematic review of size and growth in infancy and later obesity. BMJ 2005;331:929.
140. Carter OB. The weighty issue of Australian television food advertising and childhood obesity.
Health Promot J Austr 2006;17:5-11.
141. Chen X, Beydoun MA, Wang Y. Is sleep duration associated with childhood obesity? A
systematic review and meta-analysis. Obesity 2008;16:265-74.
142. Huang JS, Lee TA, Lu MC. Prenatal programming of childhood overweight and obesity.
Matern Child Health J 2007;11:461-73.
143. Ip S, Chung M, Raman G, Chew P, Magula N, DeVine D, Trikalinos T, Lau J. Breastfeeding
and maternal and infant health outcomes in developed countries. Evid Rep Technol Assess
(Full Rep ) 2007;1-186.
144. Malik VS, Schulze MB, Hu FB. Intake of sugar-sweetened beverages and weight gain: a
systematic review. Am J Clin Nutr 2006;84:274-88.
145. Martins EB, Carvalho MS. [Birth weight and overweight in childhood: a systematic review].
Cad Saude Publica 2006;22:2281-300.
27
146. Monteiro PO, Victora CG. Rapid growth in infancy and childhood and obesity in later life--a
systematic review. Obes Rev 2005;6:143-54.
147. Oken E, Levitan EB, Gillman MW. Maternal smoking during pregnancy and child
overweight: systematic review and meta-analysis. Int J Obes 2008;32:201-10.
148. Owen CG, Martin RM, Whincup PH, Smith GD, Cook DG. Effect of infant feeding on the
risk of obesity across the life course: a quantitative review of published evidence. Pediatrics
2005;115:1367-77.
149. Owen CG, Martin RM, Whincup PH, Davey-Smith G, Gillman MW, Cook DG. The effect of
breastfeeding on mean body mass index throughout life: a quantitative review of published
and unpublished observational evidence. Am J Clin Nutr 2005;82:1298-307.
150. Papandreou C, Mourad TA, Jildeh C, Abdeen Z, Philalithis A, Tzanakis N. Obesity in
Mediterranean region (1997-2007): a systematic review. Obes Rev 2008;9:389-99.
151. Parsons TJ, Power C, Logan S, Summerbell CD. Childhood predictors of adult obesity: a
systematic review. Int J Obes Relat Metab Disord 1999;23 Suppl 8:S1-107.
152. Patel SR, Hu FB. Short sleep duration and weight gain: a systematic review. Obesity
2008;16:643-53.
28
Titles and legends of figures
Figure 1. Flow of citations for the identification of systematic reviews on determinants of
overweight and obesity in children.
Figure 2. The complex web of potential determinants of overweight and obesity in children.
29
Table 1. Search strategy in Medline.
1.
(Obesity/epidemiology"[Mesh] OR "Obesity/ethnology"[Mesh] OR
"Obesity/etiology"[Mesh] OR "Obesity/genetics"[Mesh] OR "Obesity/prevention and
control"[Mesh] OR "Obesity/statistics and numerical data"[Mesh] OR
"Obesity/therapy"[Mesh])
2.
Weight gain [Mesh]
3.
Obesity OR obese OR obesogenic ti, ab
4.
“Weight gain” OR overweight OR “over weight” OR “weight change” ti, ab
5.
(BMI OR “body mass index”) AND (gain OR change OR increase*) ti, ab
6.
1 OR 2 OR 3 OR 4 OR 5
7.
child OR children OR child* OR infant* OR pediatr* OR pre-school OR preschool
8.
6 AND 7
9.
“Epidemiological factors” [Mesh]
10.
“Risk Factors” [Mesh]
11.
(("Breast Feeding"[Mesh] OR "Smoking"[Mesh]) OR "Birth Weight"[Mesh]) OR ("Fetal
Development"[Mesh] OR "Embryonic and Fetal Development"[Mesh])
12.
Smoking AND (pregnan* OR gestation*) ti, ab
13.
nutrition ti, ab
14.
Television/statistics and numerical data [Mesh]
15.
physical AND (activ* OR inactiv*) ti, ab
16.
(maternal OR parental) AND (nutr* OR obes*) ti, ab
17.
Randomized controlled trial* ti, ab, pt
18.
CASE-CONTROL STUDIES [Mesh]
19.
COHORT STUDIES [Mesh]
20.
review pt
21.
9 OR 10 OR 11 OR 12 OR 13 OR 14 OR 15 OR 16 OR 17 OR 18 OR 19 OR 20
22.
8 AND 21
30
Table 2. Included systematic reviews and their characteristics.
Citation
(year)
[Amstar score]
Arenz137
(2004)
[8]
Databases searched
(years)
[number of studies]
MedLine 1966–2003
Embase 1988-2003
Cochrane 2003 Issue 2
Google [9]
MedLine 1966-2001
PsycInfo 1887-2000
CINAHL 1982-2000
Sociological Abstracts
1952-2000 [22]
MedLine 1966-2005
Embase 1980-2005 [24]
Exposures
Outcomes
Age range
Summary of results
[MA] if a meta-analysis was carried out
breastfeeding,
exclusivity, duration
2 to 26 years
for follow-up
intimate partner
violence (IPV)
different
measures of
overweight and
obesity
weight,
anthropometry
Breastfeeding has a small but consistent protective effect against
obesity (adjusted OR 0.78; 95%CI 0.71-0.85). A dose-dependent
effect of breastfeeding duration was demonstrated in 4/8 studies.
[MA]
No clear association between IPV and weight gain.
infant size, infant
growth
obesity after
infancy
3 months to 2
years for
exposure
2 to 70 years
for outcome
Carter140
(2006)
[1.5]
MedLine
ScienceDirect
Google [not specified]
food advertising
childhood
obesity
Not clearly
stated
Chen141
(2008)
[5.5]
MedLine 1980-2007 [17]
sleep duration (different
according to age group:
<5, 5-10, ≥10)
childhood
overweight and
obesity (BMI)
0 to 18 years
for exposure
and outcome
Harder83
(2005)
[7]
MedLine 1966-2003
CINAHL 1982-2003
Serfile 2002-2003
Embase 1989-2003 [17]
MedLine 1966-2006
[33]
breastfeeding duration
overweight and
obesity later in
life (6 months to
33 years)
overweight and
obesity later in
6 months to 33
years for
outcome
Bair-Merritt138
(2006)
[5.5]
Baird139
(2005)
[5.5]
Horta22
(2007)
breastfeeding,
exclusivity, duration
0 to 6 years for
exposure and
outcome
1 to 66 years of
age for
Four of six studies found that infants who had been obese were
more likely to be obese at 5-7 years of age (OR ranging from 1.35
to 9.38). Four of five studies found a significant association
between larger size in infancy and obesity at 9-18 years (from a
RR of 1.35 to an OR of 3.00). Seven of ten studies found that more
rapid growth in infancy was significantly associated with obesity at
ages ranging from 4.5 to 20 years (ORs 1.17 to 5.70). Associations
appeared to be independent of age at obesity assessment and epoch
of data collection (pre and post World War II).
No evidence that children up to six years of age understand the
persuasive intent of advertising. Thus not possible to establish a
relation between food advertising and obesogenic behaviours at
last up to the age of six.
Children with shorter sleep duration have higher risk of overweight
or obesity if compared with children having longer sleep duration
(pooled OR 1.58; 95%CI 1.26-1.98). A significant linear doseresponse relationship was only found in <10 years-old but not for
all children. There was a gender difference: inverse association
stronger in boys than girls (OR=2.50 vs. 1.24). [MA]
Duration of breastfeeding inversely associated with the risk of
overweight: 4% decrease in risk per one month (OR 0.96; 95%CI
0.94-0.98). Definitions of overweight and age had no influence.
[MA]
In a random-effects model including 39 estimates of the potential
effect of breastfeeding, breastfed individuals were less likely to be
31
[6.5]
life
outcome
Huang142
(2007)
[4]
MedLine 1975-2005
MDConsult 1975-2005
[6 maternal diabetes]
[1 maternal malnutrition]
[8 maternal smoking]
maternal diabetes,
smoking and
malnutrition
childhood
overweight and
obesity
5 to 21 years
for outcome
Ip143
(2007)
[6]
MedLine 1966-2005
CINAHL 1982-2005
Cochrane Nov 2005
[3 systematic reviews
included in this Table]
breastfeeding,
exclusivity, duration
childhood
overweight and
obesity
0 to 33 years
for outcome
(see the three
systematic
reviews cited)
Malik144
(2006)
[4.5]
MedLine 1966-2005 [30]
sugar-sweetened
beverages (SSB)
childhood
overweight and
obesity
1.5 to 19 years
for exposure
and outcome
Marshall104
(2004)
[5.5]
PsycInfo 1985-2002
SportDiscus 1985-2002
MedLine 1985-2002
Ingenta 1985-2002 [30]
media use and
video/computer games
use
body fatness
(BMI, skinfold,
other) and
physical activity
3 to 18 years
for exposure
and outcome
Martins145
(2006)
[4]
1st step:
MedLine 1993-2003
Adolec 1993-2003
LILACS 1993-2003
2nd step
MedLine 1993-2004 [20]
MedLine 1966-2004 [16]
birth weight
overweight and
obesity
0 to 7 years for
outcome
rapid growth in infancy
overweight and
obesity (3 to 70
0 to 18 years
for exposure
Monteiro146
(2005)
considered as overweight and/or obese, with a pooled OR of 0.78
(95%CI 0.72–0.84). Control for confounding, age at assessment,
year of birth, and study design did not modify the effect of
breastfeeding.
Higher prevalence of childhood overweight and obesity among
offspring of diabetic mothers (4/6 studies). One significant
adjusted OR (1.4; 95%CI 1.0-1.19) and one significant unadjusted
OR (3.7; 95%CI 1.1-12.6) only for large for gestational age
infants. The only study on maternal malnutrition reported an
association between malnutrition in early, not late, gestation and
childhood obesity (OR 1.9; 95%CI 1.5-2.4). All eight studies of
prenatal exposure to maternal smoking showed significantly
increased odds of childhood overweight and obesity (OR range:
1.5 to 2.0).
Reports on three reviews included in this table (Arenz, Owen,
Harder). The magnitude of the effect of breastfeeding on later
obesity is reduced when more factors are adjusted for in the
analyses. The observed association between breastfeeding and a
reduced risk of obesity could also reflect selective reporting and
publication bias.
One of four cross-sectional studies including children under five
show a significant association between obese subjects and
consumption of SSB (p<0.05). One of two prospective studies
including under fives report an association between SSB and
overweight only in children at risk of overweight or overweight at
startup (after 1 year OR 1.8; 95%CI 1.1-2.8 for children at risk,
OR 1.8; 95%CI 1.1-2.9 for overweight children).
Based on data from 52 independent samples, the mean sampleweighted correlation (Pearson r) between television viewing and
body fatness is 0.066 (95%CI 0.056–0.078; total N=44,707). The
mean sample-weighted correlation between video/computer game
use and body fatness, based on 6 studies, is not significant (r
0.070; 95%CI –0.048 to 0.188; total N=1722). [MA]
Positive association between birth weight and obesity in infancy
and childhood found in 14/20 studies. Negative association found
in 3/20. Increasing attenuation of significant associations apparent
as more variables added to multivariable models.
Thirteen of 15 studies report a significant association between
early rapid growth and later overweight or adiposity.
32
[4.5]
years)
3 to 70 years
for outcome
3 to 33 years
for outcome
Oken147
(2008)
[7]
MedLine 1966-2006
[14; 84,563 subjects]
maternal prenatal
smoking (mainly yes vs.
no in different periods
during pregnancy)
child and adult
overweight
Owen148
(2005)
[8]
MedLine 1966-2003
Embase 1980-2003
[61; 28 with OR, 298,900
subjects]
initial infant feeding
(formula vs.
breastfeeding)
obesity in
childhood and
adulthood
0 to 33 years
for outcome
(meta-analysis)
0 to 53 years
for outcome
(all articles)
Owen149
(2005)
[6.5]
MedLine 1966-2003
Embase 1980-2003
[36; 355,301subjects]
infant feeding
(breastfeeding vs.
formula feeding)
obesity
1 to 64 years
for outcome
Papandreou150
(2008)
[2.5]
MedLine 1997-2007
[102]
overweight and
obesity
0 to 18 years
for exposures
and outcome
Papas123
(2007)
[4.5]
MedLine 1966-2007
PsycInfo 1966-2007
Web of Science 19662007 [20; 3 with data on
preschool children]
sex, geographic area,
level of income (Gross
National Income per
capita)
physical and social
elements of the built
environment
obesity (BMI)
3 to 18 years
for exposures
and outcome
(in three
studies)
Parsons151
(1999)
[4]
MedLine 1966-98
EMBASE 1980-98
CAB Abstracts 1973-98
PSYCLIT 1996-98
Sport Discus 1975-98
[8 genetics; 31
socioeconomic status; 20
inheritance,
socioeconomic status,
intra-uterine growth,
physical activity, dietary
factors including
breastfeeding
obesity later in
life and
adulthood
0 to 18 years
for exposures,
outcomes at
least one year
later
Children whose mothers smoked during pregnancy experienced
higher risk for overweight (pooled adjusted OR 1.50; 95%CI 1.361.65) at ages 3-33 years, compared with children whose mothers
did not smoke during pregnancy. Controlling for covariates had
modest impact on these effects. [MA]
Breastfeeding associated with a reduced risk of obesity, compared
with formula feeding (OR 0.87; 95%CI 0.85-0.89). Association
stronger in small scale studies. In six studies that adjusted for
potentially important confounding factors (parental obesity,
maternal smoking, and socioeconomic status), the association was
reduced markedly but not abolished after combined adjustment:
OR from 0.86 (95%CI 0.81-0.91) to 0.93 (95%CI 0.88-0.99).
[MA]
Breastfeeding associated with a slightly lower mean BMI than
formula feeding (-0.04; 95%CI -0.05 to -0.02). Mean difference in
BMI larger in smaller studies. Adjustment for socioeconomic
status, maternal smoking in pregnancy, and maternal BMI in 11
studies abolished the effect. [MA]
Adults more obese than children in all Mediterranean countries. In
high and middle levels of income, adults more obese than children.
Prevalence of obesity higher among European children than among
Asians. European adults more obese than European children. [MA]
Most articles (17/20) reported a statistically significant positive
association between some aspect of the built environment and
obesity. However, in the three studies on children, two showed no
difference in BMI according to average distance to a play space.
One showed no association between neighbourhood crime and
proximity to fast-food restaurants with risk of overweight. One
reported that lower prices for fruits and vegetables predicted lower
gains in BMI over the 3-year period but no association with
density of grocery stores, fast-food and full-service restaurants,
and convenience stores and full-service restaurants.
Offspring of obese parent(s) were consistently at increased risk of
fatness. A strong consistent relationship is observed between low
socioeconomic status in early life and increased fatness in
adulthood. Clear relationship was found for increased fatness with
higher birth weight, less consistent when potential confounding
factors are included in the analysis. There was almost no evidence
for an influence of activity in infancy on later fatness, and
33
Patel152
(2008)
[4]
Plagemann87
(2005)
[3]
Wang101
(2007)
[0]
intra-uterine growth; 21
maturation; 19 physical
activity; 17+12 dietary
factors; 13 behaviour and
psychology]
MedLine 1966–2007
[36; 13 with data on
children 3-18 y]
MedLine 1966-2003
Embase 1980-2003
[23 for overweight and
obesity outcome]
MedLine 1990–2006
[80; 20 for meta-analysis]
inconsistent but suggestive evidence for a protective effect of
activity in childhood on later fatness. Studies investigating diet in
childhood were limited and inconclusive.
sleep duration
overweight and
obesity
breastfeeding,
exclusively formula-fed
subjects as reference
overweight and
obesity,
metabolic
syndrome (blood
pressure and
cholesterol
level), type 2
diabetes in
childhood
child overweight
and obesity
gender, age, ethnicity,
and socioeconomic
status
3 to18 years
for exposure
and outcome
not specified
Short sleep duration independently associated with weight gain,
particularly in children (all 13 studies, 11 cross-sectional and two
longitudinal).
Breastfeeding is associated with a decreased risk of overweight
and obesity in children later in life (23 studies, pooled OR 0.75;
95%CI 0.71–0.79). [MA]
2 to 9 years for
exogenous
exposures and
outcome
Higher prevalence of overweight and obesity in American native
Indians, Mexican Americans and non-Hispanic Blacks, in lower
socioeconomic groups, and in children living in rural working
class, exurban and mixed-ethnicity urban areas.
34