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Environment and Obesity in the National Children's Study Author(s): Leonardo Trasande, Chris Cronk, Maureen Durkin, Marianne Weiss, Dale A. Schoeller, Elizabeth A. Gall, Jeanne B. Hewitt, Aaron L. Carrel, Philip J. Landrigan and Matthew W. Gillman Reviewed work(s): Source: Environmental Health Perspectives, Vol. 117, No. 2 (Feb., 2009), pp. 159-166 Published by: Brogan & Partners Stable URL: http://www.jstor.org/stable/25434919 . Accessed: 23/10/2012 02:26
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Review
Environment
" Department New York,

and Obesity

in the National

Children's

Study
Elizabeth A. Gall,4

Leonardo Trasande,1'2 Chris Cronk,3 Maureen Durkin,4 Marianne Weiss,5 Aaron L. Carrel,8 Philip J. Landrigan,1'2 and Matthew Jeanne B. Hewitt/

Dale A. Schoeller,6 W. Gillman9

of Community and Preventive and department of Pediatrics, Mount Sinai School of Medicine, New York, Medicine, of Wisconsin and Children's of Wisconsin, of USA; 3Medical Milwaukee, Wisconsin, USA; department College Hospital Health Sciences, of Wisconsin, of Nursing, Madison, Wisconsin, USA; Milwaukee, University Population University, 5College Marquette in Nutritional of Wisconsin, and Wisconsin, USA; interdepartmental Sciences, Madison, Wisconsin, USA; 7Marine Program University Freshwater Biom?dical of Wisconsin-Milwaukee, Sciences of Pediatrics, Center, Milwaukee, Wisconsin, USA; department University of Wisconsin, of Ambulatory Prevention Care and Prevention, Madison, Wisconsin, USA; 9Obesity University Program, Department School and Harvard Health Care, Boston, Harvard Medical USA Massachusetts, Pilgrim

OBJECTIVE: In this review we describe (NCS), a 21-year prospective study of factors in the development environmental Data SOURCES and EXTRACTION:We in the NCS that relate to environmental to test each hypothesis. Data SYNTHESIS:

the approach taken by the National Children's Study to the role of 100,000 American children, understanding of obesity. review the literature with of obesity regard and describe to the two core hypotheses strategies that will be used

to sugary soft drinks resulted the prevalence of overweight

in a decline children

in from

20.8% in the 2004-2005 school year to 20.4% in 2005-2006 (Anonymous 2007).

Access ence activity Direct through to safe play patterns also influ spaces may and thus reduce risk

origins

it is clear that obesity in an individual results from an imbalance Although between energy intake and expenditure, control of the obesity epidemic will require understanding of factors in the modern built environment and chemical that may have the capacity to exposures is the largest prospective The NCS birth energy intake and expenditure. disrupt the link between in the United to seek information on cohort study ever undertaken States that is explicidy designed causes of the environmental p?diatrie disease. its embrace of the life-course approach to

of obesity (Ewing et al. 2003; Frumkin et al

2004). ple, to children (for exam marketing television ads during child-focused of encourages consumption content influence foods and is a (Gortmaker

programming) and high-sugar high-fat environmental negative windows Unique for many identified Stressors tion and such

the NCS will be epidemiology, of obesity from preconception through late adolescence, including factors to individual to the social, built, and natural environ inheritance behaviors ranging from genetic ment and chemical exposures. It will have sufficient statistical power to examine interactions among sec these multiple and gene-obesity interactions. A major influences, including gene-environment ondary benefit will derive from A, built the banking of specimens endocrine Health for future analysis. Key WORDS: bisphenol obesity, ehp.l phthalates, 1839 available environment, activity. Environ Children's diet, National disruptors, Study, 117:159-166 doi:10.1289/ (2009). Perspect 2008]

CONCLUSIONS: Through able to study the origins

et al. 1996; Lobstein and Dibb 2005).

of vulnerability have been of the environmental expo nutritional result

sures linked to obesity (Ong et al. 2007). Fetal

as maternal can smoking depriva in intrauterine

growth restriction (IUGR) and thereby influ

ence to axis hypothalamic-pituitary programming increase future risk of obesity and diabe with

physical via http://dx.doi.org/

[Online

12 September

tes (Meaney and Seckl 2004). Infants born to

women at are diabetes insulin-dependent risk of obesity, and milder, diet-con higher trolled gestational diabetes also increase may et al. 2004; Dabelea et al. 2000). is an pregnancy of

Obesity

positive sity in American past 30 years

is the consequence energy balance. The children (Ogden

of a chronic prevalence has trebled

net

Study (NCS) will employ to develop under

of the causes of obesity, standing especially to environmental with factors. regard

of obe in the and

et al. 2006;

Strauss

risk (Bo Maternal independent

Pollack 2001; Troiano et al. 1995). In 2003 2006, 31.9% of 2- to 19-year-olds had a body mass index (BMI) > 85th percentile for age and
sex (Ogden obesity of heart disease et al. 2008). future portends This in great increase increases in incidence

Background
Behavioral tion and change treatment to the preven of childhood Yet obesity. is critical

smoking during risk factor for the development

childhood obesity (Bergmann et al. 2003; Oken

been ity et al. 2008). Excess gestational weight with associated increased child at 3 years of age in at least one gain has adipos

interventions on modifying

that focus solely against obesity to increase individual behavior and/or reduce caloric

prospective

et al. 2007), (Bibbins-Domingo diabetes and possi stroke, (Lee et al. 2007), cancer et al. 2008) and is there bly (Bjorge to in fore projected the first decline produce U.S. since the Great life expectancy Depression et al. 2005). The recent explosive (Olshansky increase in of obesity reflects a com prevalence in individual a) changes plex interplay among behaviors; lifestyle, b) changes and the built in community environment; synthetic structure, and c) pos

energy success

expenditure in

intake in individual children have had limited

sustaining to weight loss or prevent its

ing obesity (Summerbell et al. 2005). A suc

cessful approach must comorbidities and obesity reducing also embrace understand factors

ing of community-level social, built, and natural environmental child's diet, et al. a influences physical 1991; Ong of

the including environments. These interact genetic with makeup, An that exam took influ in a

to L. Trasande, Department Address correspondence of Community and Preventive Medicine, Mount Sinai School of Medicine, L. Levy One Gustave 10029 USA. Place, Box 1043, New York, NY Fax: (212) 996-0407. (212) 241-8029. Telephone: E-mail: leo.trasande@mssm.edu The authors are investigators in the Queens, New York, and Waukesha County, Wisconsin, Vanguard Centers and the Coordinating Center of the National Children's Study. This project has been funded in whole or in part with federal funds from the National Institute of Child Health and Human Development, National of Health, under contracts Institutes NICHD HHSN275200503411C/N01-HD-5-3411. The content of this publication does not necessar of ily reflect the views or policies of the Department Health and Human of Services, nor does mention trade names, commercial products, or organizations imply endorsement by the U.S. Government. The authors declare they have no competing financial interests. Received 21 June 2008; accepted 11 September 2008.

activity,

sibly exposures such as endocrine have the capacity

to certain

chemicals,

and metabolism
Moll ple of careful ences multipronged

(Meaney and Seckl 2004;

et al. 2007). approach environmental

that may (EDs), disruptors to disrupt energy balance.

Control

of the obesity

epidemic will
factors under multi

each of these require understanding and the interplay them. This among will of guide development standing evidence-based for pronged strategies control. The goal of that this review the approaches the National

cognizance is the success obesity

of the state of Arkansas among school-age

reducing

prevalence

children. A thoughtful redesign of the school

environment, options, education to school dietary changes of universal implementation physical and reduction of access programs, with

obesity is to describe Children's

Environmental

Health

Perspectives

volume

1171 number 21 February 2009

159

Trasande

et

al.

cohort

(Oken

may

crine-disrupting enhance

pregnancy during in childhood the risk for obesity

et al. 2007). chemicals

Exposure

to endo

persistence States and 2000; 2005; et al.

into adulthood in other

both

in the United et al. et al. et al. et al. et al.

epidemiology (Ben-Shlomo and Kuh 2002),

an approach adult disease (or even fetal) that embraces can have its the concept that in early life origins Barker and Osmond

Demerath

(Newbold et al. 2007). Rapid weight gain dur ing the first year of life (Reilly et al. 2005) and
fewer hours of et al. 2008) sleep during further enhance (Taveras infancy the risk for the

(Berkey et al. 2004; Freedman et al. 2006; Guo Gordon-Larsen 1991; Nader and et al. 2006; Nelson

countries

2002; Lake et al. 1997; Lauer et al. 1997;Moll 2006; Parsons 2001; Siervogel et al. 2000;
Strauss Knight several have 1999; Thompson

(1986) promulgated for an association and adult

exposures. to account this concept between low birth weight in Britain isch?mie heart disease The

development of childhood obesity.

Although contributed individual-level development previous greatly factors of obesity to cohort studies have many to the and its identifying that contribute in children

and Wales.

2007), findings from those previous longitudi

nal studies have studies limitations: not on fully capitalized to chronic disease Previous the

increasingly to understanding

has been adopted concept in the approach epidemiologic chronic conditions (Lynch

life-course

approach

and Smith 2005) including obesity (Gillman 2004; James et al. 2006; Novak et al. 2006)
and conditions neurodegenerative (Landrigan et al. 2005). The of the life-course application to relation approach temporal identifying risk factors for childhood among ships and 1. their interaction studies have is depicted documented in

Hierarchical Macro

axis Social, built, natural environment

Laws, regulations, Cultural norms (e.g., body image) Area deprivation (e.g., poverty) hazards Psychological (e.g., crime)

policies

(e.g., farm subsidies) Built environments (e.g., connectivity, walkability) Local food environment (e.g., presence of fast food) Commercial messaging (e.g., TV ads to kids)

obesity Figure unique mental causation

Multiple windows hazards

to environ of vulnerability to the that may contribute of chronic conditions such as obe to date

sity (National Research Council 1993; Oken

et al. 2008), at yet few studies have col

lected the scope of data depicted in this figure

multiple points in the life span.

Health behaviors Pre- and perinatal factors Energy in (diet) Energy out (physical activity) Weight gain Health outcomes

Although
Environmental have collected sures to Time axis these

the Centers
Health data on

for Children's
Prevention

and Disease

expo women and young children, pregnant on research centers have rarely focused

environmental

Mood Micro Metabolism Genes

HPA
Appetite

status as an outcome child weight (Wolff et al. is relevant in 2008a). This weakness especially new from animal studies, light of knowledge Chemical factors (e.g., phthalates, which chem suggest that endocrine-disrupting to icals may modulate intake response dietary et al. Enan and Velasquez 2002; (Bhathena 1996), (Rubin the hypothalamic-pituitary disrupt et al. 2001), increase and possibly some studies have and collected been axis risk

BPA)

BPA, bisphenol A; HPA, hypothalamic Figure 1. A life-course approach to childhood obesity. Abbreviations: pituitary axis. The life span is depicted horizontally, while factors are depicted at various levels hierarchi factors in the lower part of the figure to the community-level factors in the cally, from the individual-level (2006). upper part. Adapted from Glass and McAtee

for childhood obesity (Newbold et al. 2007).

Although data on identify participants have that genetic able to risk for

obesity, lected the data Preconception H Infancy Early childhood ?y / Later childhood* that

polymorphisms not they have on

increase

are necessary interactions of genetic diet

col simultaneously environmental exposures to examine the carefully and environmental

CH C

factors with Recent

develops than the school-age years (Kim et al. 2006). Earlier cohort studies that were first initiated

and physical activity. studies also that obesity suggest as a chronic condition much earlier

it

when

1st

2nd

3rd

6
Months

12

5 7 9

12

16

20

in the years was rela preschool are to data tively infrequent unlikely provide on exposures in life that are essential early obesity

Trimester

Years Ultrasound assessment

to identify prenatal and early childhood risk

factors Many for obesity. in their cohorts were limited previous to risk factors for obesity capacity identify a that may be unique among Hispanics, for which especially cohorts included obesity rapidly are limited is prevalence et al. (Freedman in that numbers

Initial visit

Birth visit

visit | Home/clinical (H/C)

% Denotes telephone follow-up * Timeline of telephone/mail questionnaires still in development

population increasing

of visits, NCS. Stars denote ultrasound assessment, while Figure 2. Schedule | on the timeline represents assessments and asterisk denotes home/clinical (denoted by H/C). Circles denote telephone follow-ups, of the timeline for telephone and mail questionnaires that are still under development. components

2006; Strauss and Pollack 2001).

Previous have not sufficient they of

160

volume

1171 number 21 February 2009

Environmental

Health

Perspectives

Studying obesity

in the National Children's

Study

children tors

to draw

contrasts

between

risk fac

2007) and theDanish National Birth Cohort

(Olsen et al. 2001), the environmental in American and will provide factors important that contrib

specific (Nelson et al. 2006). Past studies have been rate assessment and other of

to rural and urban

environments

Landrigan assistance for Health a

2004; from

et al. 2006). With Trasande Center the staff of the National at the Centers for Disease

insights into the etiology of childhood obe

unable to allow to accu parks sity, ute to obesity to be different, are children likely the pool of genetic poly risk may be much that modify that of European children.

Statistics

Control and Prevention, NCS

staff developed

the role of access that

activity

among cohort

places children

encourage physical in urban areas living before the

(Kipkeetal.2007).
Many occurred studies were begun

morphisms from different

to clustered approach sampling multistage a live births of 100,000 enroll rep sample resentative of all American children (Strauss who are enrolled of visit in the 13 data before at early in a minimum at least one during 18 months

tripling of childhood
(Kroke 1995; Wisemandle

obesity prevalence
et al. trend effect

Progress
In response and obesity ditions, Children's

of the NCS
to increases a number in the of prevalence con of other chronic the

et al. 2004). Families study will participate collection conception; birth; at 6, encounters: two

et al. 2006; Troiano et al. 2000)?a

times

12, and

pregnancy; of age in

policy for the only effective means changes in obesity preva further increases preventing et al. 2005). To assess lence (Summerbell may be the impact of these more level factors, new cohorts factors exist are needed. studies from other countries, Study such recent community in which these risk

to the collective attributed increasingly of community-level factors for which

the U.S. Health

Congress, through Act of 2000, authorized

the National
Human a national tal influences

Institute of Child Health

(NICHD) study of environmen

and

childhood; at 3, 5, 7, 9, and 12 years of age in childhood; and at 16 and 20 years of age in adolescence (Figure 2). Figure 2 depicts the
timeline and Tables planned age for of visits across 1 and 2 describe the complete study, the measurements through 3 years of

Development longitudinal (including and

"to conduct

biological,

psychosocial)

physical, on

chemical, children's

Although as the Avon

health and development" (Children's Health Act 2000). The design of the NCS has been
described elsewhere extensively et al. 2006; 2003; Landrigan through pregnancy. (Branum Trasande et al. and

for preconception seven Vanguard Enrollment of women will the

locations. (pilot) occur in 105 pri

Longitudinal

of Parents

and Children (Moll et al. 1991; Ong et al.

Table 1. NCS proposed measurements

units or, in the case (counties mary sampling of more of areas, clusters sparsely populated in and began 2009. counties) January

from preconception

Pregnancy Preconception First trimester month month First trimester follow-up First trimester ultrasound 16-17 weeks Second trimester (22-24 weeks)

Third
trimester (28-32 weeks)

Third
trimester follow-up 36 weeks

Initial First Second Fourth

Measurement Location/type Body composition Initial follow-up month

Home Mail

Phone Phone Phone

weeks) (<14 weeks) (<14 Home Mail

Clinic

Phone

Clinic

Clinic Mail back Phone

Length/height Weight
Head circumference Arm circumference Waist circumference Hip circumference Leg length

M, F

M M M

M, F M, F M, F M, F Ma M, F

M M M M M M

M M M M M M

Skinfolds
Ultrasound Blood pressure Bioimpedance analysis Diet Community-based food collection Food frequency questionnaire Self-completion diary Activity measures Activity questionnaire TV viewing Time outdoors Activity diary Biological specimens Vaginal swabs Blood Urine (self-collected) Saliva (self-collected) Hair

M,N

M M

M M

M M

M M, F M, F M M, F

M M M

blood Cord
Umbilical cord and placenta Meconium Breast milk Socioeconomic/environmental Mother/father education/ data M, F M M M M M M M M M M M M M M

SES/housing
Medical provider visit log Medical record/chart abstraction

Abbreviations: F, data from father; M, data from mother; N, neighborhood level data; SES, socioeconomic status. "Data to be abstracted from clinical ultrasound ifavailable; otherwise ultrasound to be performed on mother in clinic setting as part of NCS.

Environmental

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Perspectives

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161

Trasande

et

al.

The mission federal guide scientific government to disease rigor

of

is to provide the robust scientifically and to assure prevention, the study has always been the NCS a with The topical working groups

obesity insulin

and

lower

risk of

insulin

resistance

and

studies geographic

have

focused areas and and/or

upon

circumscribed

fiber; and whole grains, high glyc?mie index,

resistance, these and obesity. its In this

socioeconomically

Table 3 also presents how the NCS will

address gaps new through

advantaged communities access economic documented

hypothesis-driven.

convened by the NCS Advisory Committee

initial core hypotheses developed in consultation with thousands and from for the study, of scientists

review, we highlight how the study will pro

vide to the important two core chemical hypotheses and built knowledge that with link regard in factors with

design.

ethnically homogeneous et al. 2007). Decreased (Papas to in low socio healthy eating choices status has been neighborhoods least two studies (Galvez et al. 2006). Morland Factors in at and topography have been

groups representatives community A current and professional list organizations. of hypotheses with scientific ratio supporting nales that were accepted and refined by the Committee from NICHD, for Disease the U.S. Control [com the Health

environments

et al. 2008; such as climate taken into

childhood obesity.

Interagency Coordinating of senior scientists posed National Sciences, Institute the Centers and

Obesity-Related of the NCS

Impact

Hypotheses

infrequently (Timperio et al. 2006). The effect of after-school and summer on obe programs adult-organized is unknown. resistance In the sity and insulin absence urban of such areas may home directly are and programs, instruct from parents living their children school to where watching games in to

account

of Environmental

on risk environment of neighborhood envi resistance. Built and insulin of obesity ronment such as mixed features land use, increased proximity to recreational as safety traffic activities (e.g., low

and Prevention,

Environmental

go activities vision

indoor tele in the

Protection Agency (EPA)] is available on the NCS website (NCS 2008). Childhood obesity is a lead focus of the NCS and is addressed in 6 of 30 core hypoth
eses. Table that remain the gaps of 3 presents knowledge with respect to four of these core from obesity and insulin resistance obesity IUGR; rates of

largely

limited computer

as well green space, rates and crime perceived and bicyclists) pedestrian and ated in cross-sectional

have

for safety been associ increased

playing security of the home. A systematic review the built identified environment

studies

with

and

physical activity (Cervero and Duncan 2003; Ellaway et al. 2005; Li et al. 2005) and lower
risk of obesity have among adults (Ewing of et al.

inconsistencies environment

of previous studies of childhood obesity in measurements across studies and

of

the built

hypotheses:

cross-sectional vious rarely ity studies, studied

impaired maternal glucose metabolism; resistance and insulin associated with breast-feeding associated with lower

2006; Frank et al. 2004; Lopez 2004). Few

studies examined on younger of age. the impact children, the built and those environment

as deficits major designs that these and noted both diet

of pre studies

(Papas

et al. 2007).

activ and physical of its focus Because

Table 2. NCS proposed

measurements

from birth through 3 years Neonate

Childhood 6-month 12-month

6 months follow-up 9 months 12 months follow-up

Birth Predischarge
Delivery Location/type Body composition visit 3 months

18
months

36 24 30
months months months

Hospital Hospital

Phone

Home Mail back

Phone

Home

Mail back Phone

Phone

Phone

Clinic
C C C C C C C C C C

Length/height Weight
Head circumference Arm circumference Waist circumference Hip circumference Leg length

Skinfolds
Ultrasound Blood pressure Bioimpedance analysis C.N

Diet
Community-based food collection Food frequency questionnaire Self-completion diary Activity measures Activity questionnaire TV viewing Time outdoors Activity diary Biological specimens Vaginal swabs C.N C C C C C C

Blood
Urine (self-collected) Saliva (self-collected) Hair

M,C M M, F C M

blood Cord
Umbilical cord and placenta Meconium Breast milk data Socioeconomic/environmental Mother/father education/SES/housing Medical provider visit log Medical record/chart abstraction

M M M.C

M, F M

M M

F M

M M

M M

F M

M M

M M

M, F C C

Abbreviations: C, data from child; F, data from father; M, data from mother; N, neighborhood

level data; SES, socioeconomic

status.

162

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Environmental

Health

Perspectives

Studying obesity

in the National Children's

Study

characterization community (Landrigan et al. 2006), the NCS will allow more careful of neighbor identification of those features and diet, that affect physical hoods activity to availabil such as proximity spaces, play

on

undergoing for Children's Disease

examination

in at least one Center Health and

Conclusion
The NCS tunities childhood elimination care on presents previously for the identification obesity, through and for unrealized oppor of risk factors for their subsequent Just as the information disease that advice of fatty will

Environmental

(Wolff et al. 2008). are used in a variety Phthalates of per such as shampoos and sonal care products Prevention

prevention.

ity of healthy food stores, and neighborhood

walkability. The NCS to explore represents the role of a major opportunity of the

in the synthesis

of polyvinyl
Phthalates in animal

chloride
have been studies

Framingham Heart Study provided health

novel providers with hitherto risk factors for cardiovascular them to offer

2008). (Sathyanarayana documented consistently

neighborhood in a child's

spaces near be especially protective the early school years,

periods to safe Access development. play a child's home, for example, may

aspects specific at different environment

to have antiandrogenic
Fisher ies have 2004; Parks begun in humans and to assess

effects (Bell 1982;

stud effects

enabled to limit

evidence-based the intake

et al. 2000). Cohort for potential

foods,

smoking, and control

reduce

against obesity during but less so during ado on lescence. The design of the NCS capitalizes the life-course and allows for separate approach on the analyses of the impact of certain factors or increase in adipos Simultaneous periods. socioeconomic and genetic data of diet and physical activity

levels have

suggest than of exposure effects in animals. severe in

at lower susceptibility to those documented It is hypothesized that

suggest vent obesity of

hypertension, interventions that can be used by communities, policy

the NCS

to pre makers,

and child health providers. A major strength

American of the study is that it will be representative for exam It is anticipated, children. > 20,000 in the cohort will children ple, that examination of unique be Hispanic, permitting a risk factors that has been among subgroup affected by the epidemic. disproportionately in this review The hypotheses presented a small cover of the findings percentage only

the most exposures Decreases males urinary (Swan monoester

effects may be associated with life. and early postnatal prenatal in distance infant among anogenital been associated levels and with elevated pregnancy during breast milk levels of been associated

of obesity development certain time ity within collection as well of as measures

have

phthalate et al. 2005), phthalates

have

(Tables 1 and 2) will permit careful distinction

of the role of certain during Chemical the on each window environmental risk factors of vulnerability. and environmental agents The of EDs system. impact first identified observed

with higher serum hormone binding globulin

levels terone and luteinizing ratios (Main hormone et al. 2006). to free testos Diminished

likely to emerge from theNCS. The coreNCS

hypotheses are is and as the study dynamic, new will emerge and implemented, questions to the result in modifications study protocol. be clearly may or other studies, body of answered or become the through outdated

endocrine humans was

sperm motility has been identified among exposed men (Duty et al. 2003; Hauser 2006;
et al. 2006), and low-molecular have been associated with phthalates weight increased birth weight and longer duration of Hauser in at least one birth cohort (Wolff gestation et al. 2008b). few studies have ana Although on of phthalate exposure lyzed the impact increased adiposity in children, has analysis of the

by Herbst cases of clear eight in young cell adenocarcinoma of the vagina women to in utero who had been exposed a (DES), diethylstilbestrol estrogen synthetic women to pregnant in the 1950s, prescribed to prevent and 1970s 1960s, miscarriage to DES Prenatal has (Bern 1992). exposure and Bern, who been found subsequently to induce obesity chemi

Others NCS

of knowledge the adjusts For some areas of inquiry inquiry. nascent is in where the science stages, relatively to be the major benefits from the study gained nature. from derive its hypothesis-generating direction

as the whole

1999-2002 National Health

Examination in urinary increased static model resistance Lack

and Nutrition
increases

The NCS will provide a major opportunity

to confirm in other sequences links identified putative genetic the study of genetic studies through of children their and families

in an animal model
Identification

(Newbold et al. 2007).

of endocrine-disrupting available so few for many have

Survey levels among men with phthalate waist circumference and homeo assessment, a measure of on et al. 2007). information

identified

cals has been limited by the lack of toxicity

testing data chemicals in

insulin

widespread use (U.S. EPA 1998).

Because for other their chemicals been tested and the possibility exists that toxicity, chemicals somatic besides DES influence (Bhathena obesity et al. 2001). One and Velasquez endo potential A (BPA), resin in

(Stahlhut of accurate

the

level

to EDs has been of past exposures the principal limitation of most stud previous ies of the human of EDs. impacts potential timing limitation will be directly addressed of the NCS. In design to chemicals will in breast milk, by the

et al. 2008). As new EDs putative (Landrigan are identified, of biospecimens subsamples can stored at the NCS Specimen Repository to test for associations in be rapidly analyzed a cohort that represents the large-scale popula tion of U.S. children. can demonstrate study by itself iden causality. The NCS will for which be may tify risk factors causality on the basis of consistency, suggested strength, and plausi temporality, biological gradient, interventions trials, such as randomized con Of course, no observational

and growth 2002; Rubin

This

chemical, bisphenol crine-disrupting is used to manufacture polycarbonate the coatings of food and (Brotons 1995). and other EDs children Prevention Exposure is widespread for Disease (Centers beverage to BPA,

the prospective NCS, exposures sured

be mea

containers phthalates, in American and

and in during pregnancy, the perinatal before the appearance of period health effects. The large sample size will facili tate of possible links between investigation exposures low-prevalence endocrine-disruptor and health outcomes, and state-of-the-art lab oratory further effects assessment of chemical will exposures to discern ability

bility. Findings from the NCS will prompt

further trolled initiatives and other interventions, policy or refute the role that will confirm

Control

and animal studies increas 2005), at cur the potential for toxicity ingly suggest rent levels of exposure (Vom Saal and Hughes induces fibroblast (Masuno found that differentiation into

of identified risk factors in the development of

and its associated comorbidities. obesity The life-course approach underlying the duration behavioral, and and the

2005). In vitro studies have found that BPA

cytes have et al. 2002). Animal BPA affects glucose secretion levels in adipo studies trans

the study's sharpen to EDs. The of exposures large sample size will also permit study of genetic polymor and gene-environment interactions, phisms which may unearth to EDs. can individual As new differences EDs are identi from the in

design of the NCS may very well

delineating ronmental, women

lead to

port in fat cells (Sakurai et al. 2004). BPA

also disrupts Langerhans Magdalena the possibility for glucagon cells at nanomolar et al. 2005). that BPA intact (Alonso raise studies a

impact of envi on social exposures

susceptibility fied, specimens NCS

risk for obesity. No

from

study will have followed

be withdrawn

These could

be a risk factor question

to their content for repository analyze to assess whether biomarkers these appropriate EDs may in the be risk factors development

the development

of obesity,

of obesity (Landrigan et al. 2003).

and subsequently preconception at such followed their children inter frequent vals early in childhood and then ado through lescence and young adulthood. The NCS will collect an array of biospecimens, dietary and

Environmental

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Trasande

et

al.

activity data, physical environmental factors for all proposed whereas other limited complete data data data cohorts

and

social

and

chemical children points, more

and Monteilh
instruments dietary intake, instruments

1997; Teufel
commonly although have

1997) and other

used to measure alternatives

measure of adiposity (Pietrobelli et al. 1998),

been and dual-absorption has X-ray absorptiometry with correlated cardiovascular strongly

on all 100,000 collection have time time collected

promising not proven

have been developed for populations inwhich

past reliable et al. 2000). The vagaries of collect (Yaroch on activity by ques ing information physical are well tionnaire documented (Kohl et al. 2000), and accelerometry are ing techniques increasingly their precision and application Janz et al. 2002). BMI but other measur in et al. perfect

disease

at each

point sample.

or collected

on a smaller

A major challenge of the NCS will be

to overcome in the difficulties measuring and anthropometry diet, activity, physical in children that have bedeviled past studies.

et al. in children factors (Lindsay and skinfold 2001). analysis Bioimpedance are to measure thickness used increasingly et al. 1996; Kettaneh et al. (Gutin adiposity These will challenges the opportunity that the obesity the best be easily dis is ripe for contri research community questionnaires and not

2005).
missed, butions to ensure and

promising (Ekelund is not a

Limitations of reliability and validity do exist

with food-frequency questionnaires of the National (Coates Children's

from

2001;

Table 3. Core hypotheses

Study

relating to obesity. Breast-feeding associated with lower rates of obesity and lower risk of insulin resistance Inthe absence of proven alternatives, breast-feeding could serve as a lead component of obesity prevention in the United States. Because breast-feeding initiation, exclusivity, and continuation vary greatly by race and ethnic group, breast-feeding could also be a major causative factor for existing andwidening disparities inprevalence of childhood obesity and its comorbidities, and targeted interventions among populations where breast-feeding is less frequent

Hypothesis domain Relevance

Obesity and insulin resistance from impairedmaternal glucose metabolism Ifgestational diabetes (or excessive gestational weight gain) is conclusively demonstrated to increase risk of childhood obesity/insulin resistance, then prevention of overweight among women of childbearing age may be especially useful in the prevention of childhood obesity.

Obesity and insulin resistance associated with intrauterine growth restriction If IUGRis identified as a preventable cause of obesity, then could form a prevention of IUGR major component of obesity prevention inthe United States.

Fiber,whole grains, high glyc?mie index and obesity, insulin resistance The role of glyc?mie content in modulating response to an energy load is of tremendous interest in the policy community. Soft drink consumption by children is on the rise, and easy access in some schools is cited as a possible exacerbating factor to the obesity epidemic. The most recent USDA Dietary Guidelines now encourages three ounces/day whole grain intake, but this amount of intakemay not be sufficient to reduce risk.

Gaps instate of knowledge

Most studies have had small sizes, and have not completely differentiated severe, insulin dependent and mild diet-controlled gestational diabetes. Follow-up has typically been limited to the offspring preschool years, thus precluding documentation of longer term effects on child body composition and metabolic status.

Most studies of IUGR and adult insulin resistance are based on historical data, and limited to information about size at birth and adult outcomes, with no information available about different periods during prenatal development. Results have been contradictory because of differing definitions of key dependent and independent variables, use of different measurements, and limitation on the period of follow up.Many apparent confounders for this phenomenon (e.g., levels of such hormones as cortisol and insulin-like growth factors) are likelyembedded in the same causal frameworkwith IUGR that underlies the fetal origins of later life phenomena. Few studies have serially measured fetal size and growth using ultrasound. The National Children's Study design will measure maternal nutritional status and fetal Stressors at different periods during prenatal development; fetal growth measured with serial ultrasounds; fetal body composition; size and body composition at birth and throughout childhood, adolescence and early adulthood; dietary intake of mother during pregnancy and the offspring postnatally; and key hormonal levels in the mother and child. Information about family factors (e.g., sibling birth size, body composition of other family members, maternal history of birth size) will better control confounding.

would be urgently indicated. Ifbreast-feeding is protective for childhood obesity, it is unclear whether this is due to constituents of breast milk, metabolic programming, regulation/control of intake by mother and/or infant, or aspects of family lifestyle/home environment that are different for breast- and formula-fed infants.Measurement of family-level confounders appears to be extremely important, and has been lacking in previous studies of breast-feeding and obesity. Studies do suggest that breast-feeding may only proffer protection from future risk of obesity incertain subpopulations.

Studies of the role of glyc?mie index to date have been limited to small samples, and because the duration of follow-up has typically been brief, the applicability of these findings to broad populations of children has been limited. The contribution of sugary snacks and drinks to current prevalence is unknown, and studies to date have not had the statistical power to isolate for confounding with caloric intake, genetics, physical activity among other factors, or to examine the possibility of specific windows of vulnerability with regard to high glyc?mie content. Few studies have assessed the impact of whole grains on risk of obesity and insulin resistance inyounger children.

Unique capacity of the National Children's Study

A cohort of 100,000 is adequate for assessment of main effects for exposures at least as prevalent as maternal gestational diabetes, and outcomes at least as prevalent as adolescent type 2 diabetes. It is certainly not too large, as power becomes marginal formain effects within sex and race/ethnicity-specific strata, when exposures are as uncommon as gestational diabetes, even for relatively common outcomes such as obesity, for odds ratios < 1.5.

Prospective report of breast-feeding, and use of a metric that incorporates duration of breast-feeding with the percentage of intake derived from breast milk will settle existing debates about the protective benefit offered by breast-feeding. Collection of genetic data will provide an opportunity to identifywhether genetic or other factors influence the relationship between breast-feeding and obesity/insulin resistance among whites and nonwhites. The NCS will follow a largemultiethnic population and have the power to assess the influence of cultural factors on breast-feeding and formula supplementation.

The National Children's Study offers strong statistical power to examine the role of factors in the dietary environment of children, and is the first large cohort study with the potential to use the knowledge produced by the Human Genome Project to examine the role of genetic vulnerability in modifying the risk posed by factors such as glyc?mie index.

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Studying obesity

in the National Children's

Study

measurement efficient and

approaches cost-effective

are utilized way. At this

in an time, even The study mea

the protocol has been finalized only for the

locations, (pilot) Vanguard locations for those only through also offers major NCS opportunities the validity surement and reliability seven and birth. to

of alterative

approaches in collaboration with studies may use

through

These

studies adjunct centers. study existing the full or a subsample

the caveat that pro of the study cohort, with not new data collection impose undue posed or on burden additional study participants on the burden financial additional study.

The NCS will also trigger ancillary and

studies follow-up eration of obesity the next and provide researchers opportunities gen to

apply for funding (Lyman et al. 2005). The NCS will make public use, deidentified data
sets available vacy in accordance with federal pri regulations. Previous cohort plowed and allow

Bibbins-Domingo K, Coxson P, Pletcher MJ, Lightwood J, Goldman L 2007. Adolescent overweight and future adult coronary heart disease. New EnglJMed 357(23):2371-2379. Bjerge T, Engeland A, Tverdal A, Smith GD. 2008. Body mass index inadolescence in relation to cause-specific mortal ity:a follow-up of 230,000 Norwegian adolescents. Am J Epidemiol 168:30-37. Bo S, Menato G, Gallo ML, Bardelli C, Lezo A, Signorile A, et al. 2004.Mild gestational hyperglycemia, the metabolic syndrome and adverse neonatal outcomes. Acta Obstet Gynecol Scand 83(4):335-340. Branum AM, Coliman GW, Correa A, Keim SA, Kessel W, Kimmel CA, et al. 2003. The National Children's Study of environmental effects on child health and development. EnvironHealth Perspect 111:642-646. Brotons J. 1995. Xenoestrogens released from lacquer coatings infood cans. EnvironHealth Perspect 103:608-612. Centers for Disease Control and Prevention. 2005. Third National Report on Human Exposure to Environmental Chemicals. Atlanta, GA:Centers for Disease Control and Prevention. Cervero R, Duncan M. 2003.Walking, bicycling, and urban landscapes: evidence from the San Francisco Bay Area. Am J Public Health 93(9):1478-1483. Children's HealthAct of 2000. 2000. Public Law 106-310. Coates RJ,Monteilh CP. 1997.Assessments of food-frequency questionnaires inminority populations. Am J Clin Nutr 65(suppl4):1108S-1115S. Dabelea D, Hanson RL, Lindsay RS, Pettitt DJ, Imperatore G, GabirMM, et al. 2000. Intrauterineexposure to diabetes conveys risks for type 2 diabetes and obesity: a study of discordant sibships. Diabetes 49(12):2208-2211. Demerath EW, Li J, Sun SS, Chumlea WC, Remsberg KE, Czerwinski SA, et al. 2004. Fifty-year trends in serial in girls: the Fels body mass index during adolescence LongitudinalStudy.Am J ClinNutr 80(2):441-446. Duty SM, Silva MJ, Barr DB, Brock JW, Ryan L, Chen Z, et al. 2003. Phthalate exposure and human semen parameters. Epidemiology 14(3):269-277. Ekelund ULF, Sj?str?m M, Yngve A, Poortvliet E, Nilsson A, Froberg K, et al. 2001. Physical activity assessed by activ itymonitor and doubly labeledwater in children.Med Sei Sports Exerc33(2):275-281. Ellaway A, Macintyre S, Bonnefoy X. 2005. Graffiti, greenery, and obesity in adults: secondary analysis of European cross sectional survey. BMJ 331(7517):611-612. Enan E, Lasley B, Stewart D, Overstreet J, Vandevoort CA. modu 1996.2, 3, 7, 8-Tetrachlorodibenzo-p-dioxin (TCDD) lates function of human luteinizing granulosa cells via cAMP signaling and early reduction of glucose transport ingactivity. Reprod Toxicol 10(3):191-198. Ewing R, Brownson RC,Berrigan D. 2006. Relationship between urban sprawl and weight of United States youth. Am J PrevMed 31(6):464-474. Ewing R, Schmid T, KillingsworthR,ZlotA, Raudenbush S. 2003. Relationship between urban sprawl and physical activity, obesity, and morbidity.Am J Health Promot 18(1):47-57. Fisher JS. 2004. Environmentalanti-androgens and male repro ductive health: focus on phthalates and testicular dysgen esis syndrome. Reproduction 127(3):305?315. FrankLD, Andresen MA, Schmid TL. 2004. Obesity relationships with community design, physical activity, and time spent in cars. Am J PrevMed 27(2):87-96. Freedman DS, Khan LK,Serdula MK, DietzWH, Srinivasan SR, Berenson GS. 2005. The relation of childhood BMI to adult adiposity: the Bogalusa Heart Study. Pediatrics 115(1):22-27. Freedman DS, Khan LK,Serdula MK, Ogden CL, Dietz WH. 2006. Racial and ethnic differences in secular trends for childhood BMI,weight, and height. Obesity (SilverSpring) 14(2):301-308. FrumkinH, Frank L, Jackson R. 2004. Urban Sprawl and Public Health: Designing, Planning, and Building for Healthy Communities. Washington, DC:lsland Press. Galvez MP, Morland K, Raines C, Kobil J, Siskind J, Godbold J, et al. 2008. Race and food store availability inan inner-city neighbourhood. Public Health Nutr 11(6):624-631. GillmanMW. 2004. A life course approach to overweight and A obesity. In: Life Course Approach to Chronic Diseases Epidemiology (Kuh D, Ben-Shlomo Y, eds). Oxford, UK:0xfordUniversity Press. Glass TA,McAtee MJ. 2006. Behavioral science at the cross roads inpublic health: extending horizons, envisioning the future.Soc Sei Med 62(7):1650-1671.

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studies

of cardiovascular to identify major to close in on obe

risk have risk factors solutions

the terrain the NCS

to the epidemic However, sity. they have that these relationships dependent, temporally tudinal cohort study tal period great essential.

of childhood also are

demonstrated and complex a large longi in the prena thus offers us epidemic

making beginning The NCS

in the obesity hope combating children. America's among

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