Background Childhood obesity increases the risk of obesity inadulthood, but how parental obesity affects the chances of achild's becoming an obese adult is unknown. We investigatedthe risk of obesity in young adulthood associated with bothobesity in childhood and obesity in one or both parents.
Methods Height and weight measurements were abstracted fromthe records of 854 subjects born at a health maintenance organizationin Washington State between 1965 and 1971. Their parents' medicalrecords were also reviewed. Childhood obesity was defined asa body-mass index at or above the 85th percentile for age andsex, and obesity in adulthood as a mean body-mass index at orabove 27.8 for men and 27.3 for women.
Results In young adulthood (defined as 21 to 29 years of age),135 subjects (16 percent) were obese. Among those who were obeseduring childhood, the chance of obesity in adulthood rangedfrom 8 percent for 1- or 2-year-olds without obese parents to79 percent for 10-to-14-year-olds with at least one obese parent.After adjustment for parental obesity, the odds ratios for obesityin adulthood associated with childhood obesity ranged from 1.3(95 percent confidence interval, 0.6 to 3.0) for obesity at1 or 2 years of age to 17.5 (7.7 to 39.5) for obesity at 15to 17 years of age. After adjustment for the child's obesitystatus, the odds ratios for obesity in adulthood associatedwith having one obese parent ranged from 2.2 (95 percent confidenceinterval, 1.1 to 4.3) at 15 to 17 years of age to 3.2 (1.8 to5.7) at 1 or 2 years of age.
Conclusions Obese children under three years of age withoutobese parents are at low risk for obesity in adulthood, butamong older children, obesity is an increasingly important predictorof adult obesity, regardless of whether the parents are obese.Parental obesity more than doubles the risk of adult obesityamong both obese and nonobese children under 10 years of age.
The prevalence of obesity has increased in both children andadults.1,2 The medical illnesses associated with obesity3 usuallyoccur in adulthood, but adults rarely achieve sustained weightloss.4 Therefore, prevention of obesity in childhood and effectivetreatment of overweight children are essential. Although severalstudies have tracked fatness from childhood to adulthood,5,6,7,8,9,10,11only one study contained data on subjects' height and weightthroughout childhood.11 Whether parental obesity alters theprobability that a child will become an obese adult is not known.
The purpose of this study was to determine the probability ofobesity in young adulthood in relation to the presence or absenceof obesity at various times throughout childhood and the presenceor absence of obesity in the child's parents. We hypothesizedthat the probability that a child would become an obese adultdepends on the presence of both childhood and parental obesityand that the effects of these two factors on the risk of obesityin adulthood differ according to the age of the child.
Methods
In this retrospective cohort study, we abstracted height andweight measurements from the outpatient medical records of acohort of young adults and their parents who were long-termmembers of Group Health Cooperative of Puget Sound, a staff-modelhealth maintenance organization established in 1947 in WashingtonState.
Selection of Subjects
Using computerized enrollment and outpatient-visit data bases,we identified all 1333 members who were born at the cooperativein 1965 through 1970 and who had at least one outpatient visiteach after the age of 21 years. The majority of the subjectshad received health care at the cooperative all their lives,and most outpatient visits were for routine health care andminor illnesses. The medical records of eight subjects couldnot be located or were partially missing. Among the remaining1325 subjects, 854 (64 percent) met the following criteria forinclusion in the study cohort: at least one weight measurementat the age of 21 years or older, at least one height measurementat the age of 18 years or older for men and at the age of 16years or older for women, no chronic condition that might affectstature or weight (e.g., cancer or inflammatory bowel disease),and birth at a gestational age of 36 weeks or more. The parentsof all 854 subjects were Group Health Cooperative members. Twopairs of parents each had three adult children in the cohort,and 56 pairs of parents each had two. Thus, 118 subjects (14percent) had at least one sibling each in the cohort. Amongthe 794 pairs of parents, we located records for 747 mothers(94 percent) and 699 fathers (88 percent).
Outcome Measures
All height and weight measurements recorded before January 1,1994, were abstracted unless these measurements were from avisit to the emergency department or the subject was pregnant.For each subject, we calculated the average body-mass index(the weight in kilograms divided by the square of the heightin meters) between 21 and 29 years of age. Adult obesity wasdefined as an average body-mass index >27.8 for men and >27.3for women.12
Obesity in Childhood
We also defined childhood obesity in terms of the body-massindex, because it is the best and most widely used surrogatemeasure of adiposity among indexes derived from height and weightmeasurements.13,14 The body-mass index in children is correlatedwith direct measures of adiposity,15 blood pressure,16 and serumconcentrations of lipids17 and insulin.18 Although there isno established cutoff point for childhood obesity,19 we classifiedsubjects with a body-mass index at or above the 85th percentilefor age and sex as obese and those with a body-mass index ator above the 95th percentile as very obese. We used as referencestandards the 85th and 95th percentiles for body-mass indexin the combined data of the First and Second National Healthand Nutrition Examination Surveys.20
We defined five consecutive age intervals from 1 to 18 yearsof age (Table 1). The first interval, for example, includedall measurements between the first and third birthdays. Foreach subject, all body-mass-index values (calculated from heightand weight recorded on the same date) were standardized forage and sex by conversion to a z score. The z score was calculatedas follows: (body-mass index - mean)/standard deviation; themean and standard deviation for the body-mass index were fromthe chosen reference population of the same age and sex as thesubject.20 Means and standard deviations for the body-mass indexat specific ages (e.g., 3.2 years) were found by linear interpolationbetween the discrete ages (e.g., 3 years and 4 years) givenin the reference data. We calculated the average z score forthe body-mass index for each subject during each interval bythe method described below. We classified a subject as obeseduring an interval if the average z score for the body-massindex was >1.036 and as very obese if the average was >1.645.These z scores correspond to the 85th and 95th percentiles,respectively, of a normal distribution.
Table 1. Availability of Data on Body-Mass Index (BMI) and the Prevalence of Obesity in 854 Subjects at Various Ages, Their Mothers, and Their Fathers.
Parental Obesity
If a parent's record contained an adult height, then that heightwas used to calculate the body-mass index for all recorded parentalweights. The parent's body-mass index was then estimated onthe five dates when the subject reached the midpoint in eachof the five age intervals. For the age interval one throughtwo years, for example, we estimated each parent's body-massindex on the date of the subject's second birthday. To estimatethe body-mass index, we used linear interpolation between valuescalculated for the parent before and after that date. Parentalobesity was defined as a body-mass index >27.8 for fathersand >27.3 for mothers.
Statistical Analysis
We computed a weighted average of the body-mass-index valuesfor each subject during each childhood age interval and in adulthood(at 21 through 29 years of age). The weighting was based onthe time between the available values. Values closely spacedin time received less weight than widely spaced values, so thatthe average would not be unduly influenced by the values clusteredclose together in time. The formula used for the average wasas follows:
when the ages at which body-mass indexes were measured wereti, . . . tK and where t0 and tK+1 denoted the end points ofthe time interval.
For each age interval, associations between obesity in youngadulthood and both childhood and parental obesity were tabulatedand analyzed by logistic-regression analysis. Regression parametersfor these models were estimated with the generalized-estimating-equationmethod of Liang and Zeger,21 which incorporates adjustmentsfor correlations between data from siblings.
Results
Ninety-four percent of the 854 subjects were non-Hispanic whites,64 percent were female, and 93 percent were born to marriedmothers. More women than men met the inclusion criteria forthe study, because in young adulthood women are more likelyto use health care services.22 At the time of the subjects'births, the mean ages of their mothers and fathers were 29 and32 years, respectively.
The 854 subjects had a median of nine body-mass-index valuesfrom 1 through 17 years of age; the last value was at a meanage of 24.5 years. The prevalence of adult obesity in the cohort(16 percent) (Table 1) was near the current value for the prevalenceof obesity in 20-to-29-year-old non-Hispanic white subjectsin the United States (18 percent).1 The prevalence of obesityin the parents increased with age and reached 30 percent whentheir children were 15 to 17 years of age; this figure is nearthe current prevalence of obesity in older U.S. adults.1
The probability of being obese as a young adult increased withthe age of the obese child and was higher at all ages for thegroup of very obese children (Table 2). After six years of age,the probability of obesity in adulthood exceeded 50 percentfor obese children, as compared with about 10 percent for nonobesechildren. Obesity at one or two years of age was not associatedwith an increased risk of adult obesity. Overall, there wereno significant differences between the sexes in the risk ofadult obesity associated with childhood obesity (data not shown).The risk of adult obesity was significantly greater if eitherthe mother or the father was obese (Table 2). There were nosignificant differences in these risk estimates between boysand girls (data not shown). Although the odds ratios for obesityassociated with maternal obesity were slightly higher than wasthe case for paternal obesity, the differences between theserisk estimates were not statistically significant for any ageinterval.
Table 2. Odds Ratios for Obesity in Young Adulthood According to the Child's Age and the Obesity Status of the Child and the Parents.
Subjects were included in Table 3 and Table 4 only if data onobesity were also available for their parents. There was nosignificant difference in the rates of obesity in adulthoodbetween subjects with and those without data on parental obesity.At every age interval, both obese and nonobese children wereat greater risk for obesity as adults if at least one parentwas obese. The effect of parental obesity on the risk of obesityin adulthood was most pronounced among obese and nonobese childrenunder 10 years of age. For example, among nonobese one- andtwo-year-olds, those with at least one obese parent had a greaterchance of being obese as adults than those without an obeseparent (28 percent vs. 10 percent), and among obese three-to-five-year-olds,the chance of adult obesity increased from 24 percent if neitherparent was obese to 62 percent if at least one parent was obese(Table 3). Very obese children with at least one obese parenthad the highest risk of adult obesity.
Table 4. Odds Ratios for Obesity in Young Adulthood According to Subjects' Obesity Status in Childhood and Their Parents' Obesity Status, from Multivariate Logistic-Regression Models.
Before three years of age, the primary predictor of obesityin adulthood was the parents' obesity status; the child's obesitystatus was not an indicator of the risk of adult obesity (Table 4).For children three through nine years of age, the child'sand the parents' obesity status were both important predictors,but as the child aged, the child's obesity status became themore important predictor. Especially before six years of age,obesity in both parents substantially increased the odds ofthe child's becoming an obese adult.
Among children who were obese in any age interval, neither theage of onset nor the duration of obesity increased the riskof adult obesity after adjustment for parental obesity and forwhether or not the child was very obese (data not shown).
Discussion
Advancing knowledge about the molecular mechanisms and geneticsof obesity23 supports the results of observational studies thathave revealed an inherited susceptibility to obesity.24,25 Althoughthe parents' body-mass indexes are a readily available markerfor the susceptibility to obesity, the probability that a childwill become an obese adult if at least one parent is obese hasnot previously been estimated. We found that parental obesitysignificantly alters the risk of obesity in adulthood for bothobese and nonobese children, especially those under 10 yearsof age. Obesity in one or both parents probably influences therisk of obesity in their offspring because of shared genes orenvironmental factors within families.
Direct comparison of our results with those of other studies5,6,7,8,9,10,11is difficult because of differences in the birth years of thecohorts, the ages at which examinations were performed, themethods used for the measurement of adiposity, the definitionsof obesity, and the reference populations used to adjust measurementsfor age and sex.26 Because our height and weight measurementswere obtained from clinical records, they lack the precisionthat could be obtained in a prospective study. However, anyerrors in these measurements are likely to have been random.
We caution against interventions to treat overweight childrenunder three years of age who do not have obese parents. Physiciansshould avoid labeling these children as being at risk for laterobesity, because few of them will become obese adults. In contrast,any one- or two-year-old who has an obese parent, especiallyany who has two obese parents, appears to be susceptible toobesity in young adulthood. One- and two-year-olds with an obeseparent may benefit most from efforts to prevent obesity, butit remains unclear what factors in the environments of thesechildren contribute to the expression of obesity. These factors,once identified, may present reasonable targets for preventiontrials.
Obese three-through-nine-year-olds with obese parents may beideal candidates for treatment because the parents still havethe opportunity to influence their children's activity and dietpositively.27 However, because many obese children, if leftuntreated, will not become obese adults, treatment trials shouldbe designed to consider the benefits and risks, both physicaland psychological, of any interventions. Between 10 and 17 yearsof age, parental obesity has a much more limited effect on achild's risk of future obesity. Decisions to treat overweightchildren after they reach 10 years of age can be made primarilyon the basis of the child's obesity status.
This study demonstrates the importance of parental obesity inpredicting children's risk of obesity in adulthood. Severalstudies now indicate that obesity in young adult life is associatedwith increased morbidity28,29 and mortality.30,31 Furthermore,excessive weight during adolescence predicts a number of adverseeffects on health later in life, including increased mortalityamong men.32
Supported by a Generalist Physician Faculty Scholars Award fromthe Robert Wood Johnson Foundation (to Dr. Whitaker) and bya grant (P30-DK46200) from the National Institutes of Health(to Dr. Dietz).
We are indebted to Thomas N. Robinson, M.D., M.P.H., for inspiringthis project and for his ongoing advice; to Evan Charney, M.D.,Marian O. Hodges, M.D., M.P.H., and Heidi J. Kalkwarf, Ph.D.,for their careful review of the manuscript; to Edward H. Wagner,M.D., M.P.H., for facilitating our research at the Center forHealth Studies at Group Health Cooperative of Puget Sound inSeattle; to Mr. Richard L. Furman for detailed abstraction ofall the medical records for this study; and to Ms. Vicki Livengoodfor her assistance in the preparation of the manuscript.
Source Information
From the Department of Pediatrics, Children's Hospital Medical Center and the University of Cincinnati College of Medicine, Cincinnati (R.C.W.); the Department of Pediatrics, University of Washington School of Medicine, Seattle (J.A.W.); the Biostatistics Program, Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle (M.S.P., K.D.S.); and the New England Medical Center, Boston (W.H.D.). Presented in part at the 5th National Program Meeting of the Robert Wood Johnson Foundation Generalist Physician Faculty Scholars Program, San Antonio, Texas, December 11, 1996, and at the 37th Annual Meeting of the Ambulatory Pediatric Association, Washington, D.C., May 3, 1997.
Address reprint requests to Dr. Whitaker at the Division of General and Community Pediatrics, Children's Hospital Medical Center, CH-1 South, 3333 Burnet Ave., Cincinnati, OH 45229-3039.
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Kipping, R. R, Jago, R., Lawlor, D. A
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