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Am J Clin Nutr 89: 551-557, 2009. First published December 23, 2008; doi:10.3945/ajcn.2008.26759
 American Journal of Clinical Nutrition, doi:10.3945/ajcn.2008.26759
Vol. 89, No. 2, 551-557, February 2009
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© 2009 American Society for Clinical Nutrition

ORIGINAL RESEARCH COMMUNICATION

Intergenerational influences on childhood body mass index: the effect of parental body mass index trajectories

Leah Li1,2,3,4, Catherine Law1,2,3,4, Rossella Lo Conte1,2,3,4 and Chris Power1,2,3,4

1 From the Center for Pediatric Epidemiology & Biostatistics, UCL Institute of Child Health, London, United Kingdom.

2 The views expressed herein are those of the authors and not necessarily those of the Department of Health. Information about the wider program of the Public Health Research Consortium is available from www.york.ac.uk/phrc.

3 The study was undertaken by the Institute of Child Health as part of the Public Health Research Consortium, which was supported by the Department of Health Policy Research Programme. The GOSH/UCL Institute of Child Health was supported in part by the Department of Health's NIHR Biomedical Research Centre. The Centre for Paediatric Epidemiology and Biostatistics was supported in part by the Medical Research Council in its capacity as the MRC Centre of Epidemiology for Child Health.

4 Address reprint requests and correspondence to L Li, CPEB, UCL Institute of Child Health, 30 Guilford Street, London WC1N 1EH, United Kingdom. E-mail: l.li{at}ich.ucl.ac.uk.


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Background: Parental obesity in adulthood is a strong determinant of offspring obesity. Whether parental body mass index (BMI; in kg/m2) at earlier life stages is associated with offspring BMI is unknown.

Objective: The main objective was to assess whether recent BMI of parents in adulthood and their recent BMI gain are more strongly associated with offspring BMI than are BMI or changes in parental BMI in childhood.

Design: Two generations in the 1958 British birth cohort were studied, including cohort members (parents' generation) with BMI at 7, 11, 16, 23, and 33 y (n = 16,794) and a one-third sample of their offspring selected in 1991 aged 4–18 y (n = 2908). We applied multilevel models to allow for within-family correlations.

Results: Childhood BMI increased on average by 0.25–1.10 between the 2 generations, depending on sex and age group, and overweight/obesity increased from 10% to 16%. Parents' BMI in childhood and adulthood independently influenced offspring BMI, but no significant difference in the strength of influence was observed. For example, adjusted increase in BMI for offspring aged 4–8 y was equivalent to 0.37 and 0.23 for a 1-SD increase in maternal BMI at 7 and 33 y, respectively. Similar patterns were observed for risk of overweight/obesity and for paternal BMI at most ages.

Conclusions: Excessive BMI gains of parents during childhood and adulthood were associated with a higher BMI and risk of obesity in the offspring. Reductions in the incidence of child obesity in the current population may reduce obesity in future generations.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Parental obesity is arguably the strongest determinant of offspring obesity, with measures of offspring fatness increasing linearly with increasing level of parental fatness (1–3). Correlation coefficients between the body mass index (BMI) of parents and their offspring at various ages have been reported to be 0.15–0.25 in a large British study (1). Identification of genetic variants related to obesity (4) suggests that parent-offspring BMI associations are due in part to genetic influences (5). On the other hand, rapid increases in obesity worldwide in recent decades (6, 7) are likely attributable to changes in environmental factors (1, 2, 5, 8, 9). It is possible that parent-offspring associations could be due to shared environment, such as socioeconomic position, diet, physical activity levels, and other lifestyle factors (10–13). Whether the intergenerational association largely reflects genetic influences and the extent to which environmental influences are involved is not well understood.

Existing evidence for intergenerational links to obesity is primarily based on the BMI of parents in adulthood (3, 5). Few studies have considered parental BMI at earlier life stages, although some studies suggest that this is an important factor to consider (14), whereas others argue that obesity may be programmed before birth (15–17). One approach to improving the understanding of the intergenerational association is to compare the strength of the effect of parental BMI at different life stages on offspring BMI. If the intergenerational BMI association is partly due to shared environmental factors, we would expect the association with offspring BMI to be stronger for parental BMI in adulthood than for their BMI earlier in life. If the association is mainly due to genetic influences, then we would expect the associations for parents at earlier life stages to be as strong as those for current BMI.

In the present study, we used 2 generations of the 1958 British birth cohort to assess whether parental BMI during childhood has a long-term effect on the BMI of their offspring. Specifically, our aim was to establish 1) the magnitude of the increase in BMI between 2 generations and 2) whether recent BMI of parents in adulthood and their recent BMI gain are more strongly associated with offspring BMI than are changes in parental BMI that had occurred in childhood. For each aim, we examined associations for overweight and obesity as well as for the distribution of BMI.


   SUBJECTS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Study samples
The 1958 British birth cohort includes all children born in England, Scotland, and Wales in one week of March 1958. Approximately 17,000 live births were followed at ages 7, 11, 16, 23, 33, 42, and 45 y (18). Immigrants born in the relevant week were included in the target sample at ages 7, 11, and 16 y. In 1991, when 11,407 cohort members were interviewed, a random sample of one-third of those who had become parents (about two-thirds of the remaining cohort members) was selected for a study of their children (19). Information was collected from {approx}4300 offspring, of whom those aged ≥4 y (3076 offspring from 2027 cohort families) were eligible for height and weight measurements (20). Thus, offspring were clustered within families. The sample of respondents in the 33-y survey was generally representative of the original birth sample in most respects, although individuals who were most disadvantaged tended to be slightly underrepresented (19). We used information collected from cohort members at several ages to 33 y. For offspring, data were collected at one time point only (in 1991); therefore, the age of the offspring varied.

Anthropometric measurements
The height and weight of cohort members were measured by trained medical personnel using standard protocols at ages 7, 11, 16, and 33 y and were self-reported at 23 y. There was no information on the height and weight of the cohort member's partner, who was the other parent of the offspring. Height and weight of the offspring aged ≥4 y were measured to the nearest 1 cm and 0.1 kg, respectively, with the use of portable measuring equipment. BMI was derived as weight/height2 (kg/m2) at each age for cohort members and at one age for offspring. Childhood overweight and obesity for cohort members (n = 13,294 at 7 y and 12,498 at 11 y) and for their biological offspring (n = 2908 offspring aged ≥4 y with a plausible BMI measure) were derived by using age- and sex-specific international standards from the International Obesity Task Force (21) corresponding to BMI cutoffs at age 18 y for overweight (BMI > 25) and obesity (BMI > 30), as used by the World Health Organization (22).

Statistical analysis
Mean BMI and prevalence of overweight and obesity were calculated for cohort members at ages 7, 11, 16, 23, and 33 y and for offspring for each separate age from 4 to 18 y. To assess increases in childhood overweight/obesity between generations, we compared BMI of cohort members at ages 7 and 11 y with BMI in offspring combined into 2 age groups (4–8 and 9–18 y). Because of differences in the ages of the 2 generations, the comparisons were based on external BMI SD scores (z scores), derived by using an external reference population—the 1990 British growth reference sample:

Formula
where M is the median, S = SD/M is the CV, and L is the Box-Cox transform power at specific age and sex of the reference sample (23). Exact age at measurement was used to derive the BMI (external) z scores. Implausible BMI values, ie, external z scores outside of the range –6 to 6 (n = 26), were excluded from the analyses because the probability of a measure lying outside of this range is almost zero.

BMI is correlated within families (ie, between siblings and also between offspring and parents); therefore, to compare BMIs across generations, it was necessary to account for the family structure of the population. Thus, the mean BMI z score for each generation was estimated by using 2-level linear models (24), with families being level-2 units and individuals (cohort member or offspring) being level-1 units (20). Because cohort members and the offspring were the same level units, the difference in mean BMI z scores between the 2 generations can be directly tested (cohort members at 7 and 11 y compared with offspring 4–8 and >9 y, respectively). The correlation coefficients between siblings and between offspring and parents at each age from childhood to adulthood were estimated from these models. The prevalence of overweight and obesity was estimated by using 2-level logistic models.

An analysis of parent-offspring associations was conducted in 3 stages; the dependent variable was the BMI (external) z score for the offspring. However, because there was no external reference for parental adult BMI (ie, at 23 and 33 y), for the independent variables we derived internally standardized BMI scores for parents at all ages so that the effect of parental BMI at different ages in childhood and adulthood could be compared. An internal BMI z score, derived as the difference between the individual's BMI and the mean BMI, divided by the SD of the BMI for the sample at each age and sex, was used for parents at all ages. Thus, a 1-unit increase in parental BMI (internal) z score corresponds to a 1-SD increase in BMI at a given age and sex, eg, an increase of 1.6 for the father when he was age 7 y (Table 1 and Table 2).


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  		TABLE 1. BMIs and the distribution of overweight/obesity in female cohort members and their offspring, by age1

 

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  		TABLE 2. BMIs and the distribution of overweight/obesity in the male cohort members and offspring, by age1

 
The analyses proceeded in 3 stages. First, we examined the simple associations of offspring BMI (external z score) with BMI of the parent at each age (internal z score), separately, using 2-level linear models, with families being level-2 units and offspring being level-1 units (model 1). Thus, the models accounted for the correlations between siblings. Second, to assess whether any association of parental BMI in early life was independent of later BMI, the simple associations (including only one childhood BMI in the models) were adjusted for parental BMI (internal z score) at 33 y (model 2). The strength of the associations with parental BMI at one age in childhood (7 y) and current BMI (33 y) were compared by using contrast tests. Third, the associations between offspring BMI and change in BMI of the parent between successive ages in childhood or in adulthood were examined by conditioning on the prior BMI (internal z score) of the parent (model 3). For example, the regression model for the association between parental change in BMI at ages 7–11 y and offspring BMI was as follows:

Formula
where offspring BMI is the external BMI z score for offspring, and BMI7 and BMI11 are internal BMI z scores at 7 and 11 y, respectively, for cohort members. The coefficient for BMI11 (c) can be interpreted as the estimated change in offspring BMI associated with parental gain in BMI between ages 7 and 11 y, expressed as per unit increase in z score at 11 y, given the BMI at 7 y.

These 3 stages of analyses (models 1–3) were repeated for the binary outcome (overweight/obesity) by using 2-level logistic models. Because of the study design, the age of the parent at childbirth was inversely correlated with the age of their offspring (r = –1). We therefore included age of the child as a covariate in all models to reduce possible confounding effects of parental age. The effect of parental BMI was examined separately for the father and mother (ie, male and female cohort members). In all models, offspring were analyzed in 2 age groups. The analyses were first performed separately for boys and girls, and the associations for mother/son and mother/daughter and for father/son and father/daughter were similar. Thus, we present results for boys and girls combined with adjustment for sex.

The parents (754 male and 1273 female cohort members) included in this study had given birth to children before age 30 y. To establish whether these parents were representative of the cohort study, we compared the adult BMI of the parents with the BMI of all participants from the original birth study. The 2 samples had a similar mean BMI at age 33 y: 25.8 compared with 25.7 in males and 24.9 compared with 24.7 in females.

Descriptive analyses were performed by using SPSS for Windows (version 14.0; SPSS Inc, Chicago, IL). The intergenerational comparisons and relations were assessed by using MLwiN (version 2.10; University of Bristol, Bristol, United Kingdom).


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
The mean age of the parents at childbirth was 24.3 y (range: 15–29 y). Although the age of the offspring ranged from 4 to 18 y, their average age was 8.7 y; 84% were 11 y of age or younger (Tables 1 and 2).

The analysis of the 2 generations confirmed that BMI was clustered within families. The correlation coefficient of offspring from the same family was 0.36 and that between offspring and their parents was weaker, but significant (r = 0.14–0.22 with the father and 0.18–0.20 with the mother at different ages from childhood to adulthood) (data not shown).

Trend in BMI across 2 generations
On average, the offspring were more overweight than were the cohort members (Tables 1 and 2). The increase in mean BMI (external) z score from cohort members at age 7 y to offspring at ages 4–8 y (average: 6.4 y) was 0.17 for boys and 0.26 for girls, equivalent to an increase of 0.25 and 0.46 from the median BMI for 7-y-old boys and girls, respectively. The increase was greater between cohort members at age 11 y and offspring at ages 9–18 y (average: 11.7 y)—0.21 for boys and 0.46 for girls, equivalent to 0.42 and 1.10 from the median BMI for 11-y-old boys and girls, respectively. As expected, the prevalence of overweight and obesity also increased significantly across the 2 generations (Tables 1 and 2).

Associations between parental BMI throughout the life course and offspring BMI
Parental BMI at all ages, from childhood to adulthood, had a strong positive association with the BMI of their offspring (Table 3). Associations with maternal BMI were evident at age 7 y and remained throughout life to adulthood. For every 1-unit increase in maternal BMI z score (internal) at 33 y (an SD of 4.9), the BMI of the offspring increased by a z score (external) of 0.24 (model 1; Table 3), which is equivalent to an increase of 0.35 kg/m2 for a 7-y-old boy; and the risk of being overweight or obese also increased significantly (model 1; Table 4). Maternal BMI in childhood (age: 7–16 y) was significantly associated with offspring BMI, independently of maternal adult BMI; for a 1-SD increase in maternal BMI at 7 y (1.9), the BMI of the offspring aged 4–8 y and ≥9 y increased by a z score (external) of 0.25 and 0.20 respectively, after adjustment for maternal BMI at 33 y (model 2; Table 3), equivalent to increases in BMI of 0.36 and 0.40 for a 7- and 11-y-old boy, respectively. Similar patterns were observed for paternal BMI, although for the overweight/obesity status of their offspring aged ≥9 y, associations with paternal BMI at ages 7, 11, and 33 y were not significant (model 2; Table 4). Parental childhood and adult BMI were independently associated with offspring BMI, at most but not at all ages (model 2; Table 3), and there was no significant differences in the strength of their associations (data not shown).


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  		TABLE 3. Change in offspring BMI (external) z scores for a 1-SD increase in maternal and paternal BMI (internal) z scores at different life stages1

 

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  		TABLE 4. Odds ratios and 95% CIs for overweight/obesity of offspring for a 1-SD increase in maternal and paternal BMI at different life stages1

 
In general, large gains in BMI during particular life periods of the parents were associated with an increase in the BMI of the offspring (Table 3). For maternal BMI, excessive gains throughout childhood (7–16 y) and recently in adulthood (23–33 y) were significantly associated with offspring BMI; a 1-SD increase between ages 11 and 16 y was associated with an increase in offspring BMI z score of 0.23 (external) (model 3; Table 3), and risk of being overweight or obese (model 3; Table 4). Similarly, excessive gains in paternal BMI in early childhood (7–11 y) and adulthood (16–33 y) were associated with higher BMI and an increased risk of offspring being overweight or obese, although evidence of an association with recent BMI gain (23–33 y) was weak (Tables 3 and 4).


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
This study had several important findings. First, childhood BMI increased between the 2 generations—the 1958 cohort and their offspring—by between 0.25 and 1.10, depending on sex and age group. Correspondingly, the prevalence of overweight and obesity has risen from {approx}10% of the cohort at ages 7 and 11 y in 1965–1969 to {approx}16% of the offspring in 1991. Second, increased parental BMI and a high BMI gain in childhood and adulthood were associated with a higher BMI and an increased risk of overweight/obesity in the offspring. Third, these associations with offspring BMI were observed for parental BMI and BMI gain in both childhood and adulthood; notably, the associations for parental BMI in childhood were independent of parental current adult BMI. Furthermore, the effect of parental BMI in childhood on offspring BMI was as strong as that in adulthood.

To our knowledge, this was the first study to examine the long-term effect of childhood BMI and changes in BMI during different periods of the life course on BMI in the next generation. The increase in childhood obesity between cohort members and their offspring suggests that environmental changes may underlie the generational trends in BMI. The circumstances in which the 2 generations were growing up are likely to have been in marked contrast. Britain has passed from an era of postwar hardship, experienced by mothers of the cohort and cohort members in their early life, to one of relative affluence and economic security experienced by the cohort members as they grew up and by their offspring (25, 26). Dietary patterns have changed over this period, with an increase in fast foods and ready-to-eat meals, which are generally high in fat and energy dense (27, 28).

The availability of repeated measures of BMI across the life course of the 1958 birth cohort and a single BMI measure for their offspring provided a unique opportunity to explore these intergenerational associations. The multigenerational design of this study enabled us to explore trends in BMI and BMI transitions across generations within families, and the application of multilevel models allowed the within-family correlations of BMI to be taken into account. However, we were unable to examine the joint influence of maternal and paternal BMI because BMI measures were available for only one parent—the cohort member. The offspring sample was selected at a particular age of one parent (cohort member age: 33 y). As a result, the age of the child and the age of the parent at childbirth (difference between 33 y and the age of the child) were inversely correlated. Consequently, the offspring were all born to a parent younger than 30 y, and their mothers were therefore younger on average (24.4 y) than the general population (ie, 27.0 y in 1986) (29). The offspring sample resembled the general population with respect to birth weight, social class, and height (23, 30), yet they were heavier than the reference sample (by 0.18 and 0.20 external z scores in boys and girls, respectively). In our study, although maternal age was not associated with higher offspring BMI, young parenthood is associated with higher parental BMI in adulthood. Thus, the intergenerational relations in BMI may be affected by maternal age, but we are unable to fully adjust for this or assess it further.

Many previous studies have established that parental adiposity in adulthood is positively associated with the adiposity of the offspring (1, 3). Our study also showed that high parental BMI in adulthood is associated with increased offspring BMI. Furthermore, we showed that this association is independent of the parents' BMI in early life. It is possible that this association between parental BMI in adulthood and offspring BMI is largely attributable to their shared environment, because many risk factors for obesity—such as social environment, lifestyle, dietary intake, and activity patterns—often co-occur within families (10–12). For example, children living with obese parents have been found to have a greater preference for fatty foods, to have a lower preference for vegetables, and to be less active than children of nonobese parents (31).

Importantly, however, our study suggests that intergenerational BMI associations are also influenced by parental BMI at earlier life stages. Parental BMI and BMI gain in early life were independently associated with BMI and the risk of obesity in their biological children. The strength of the association for childhood BMI was as strong as that for adult BMI. Excessive weight gain of the parent during childhood was associated with an increased risk and earlier development of obesity in the offspring. This finding may reflect genetic influences or early establishment of lifestyle patterns, which are maintained into adult life and transmitted to offspring, or both of these influences may be operating. The genetic influence on BMI is supported by adoption and twin studies (3, 5, 32, 33), which have shown that correlations in BMI between adopted children and their biological parents are higher than the correlations with their adoptive parents (32, 34) and, more recently, genetic variants have been identified (4). Our finding of an independent effect of parental childhood BMI on offspring BMI is also consistent with the hypothesis that obesity is in part programmed before birth (15–17). Although there is some evidence that patterns of eating, physical activity, or other lifestyle factors established during the early life of the parents may persist over time (35), in this cohort the correlation between level of physical activity at ages 11 and 33 y was weak (36).

To conclude, our study showed a substantial increase in the prevalence of overweight/obesity across 2 generations. The effect of parental BMI in early life and also in adulthood on obesity in the next generation suggests that genetic as well as shared environmental factors influence child obesity. Given this finding and that today's children have a higher BMI than their parents did at the same age, it is possible that children in contemporary society will in turn have offspring who will have an increased risk of obesity, which strengthens the trend of increased obesity in children. It is therefore important to understand how the transmission of obesity within families underlies the development of the emerging obesity epidemic.


   ACKNOWLEDGMENTS
 
The authors' responsibilities were as follows—LL, CL, and CP: designed the study and wrote the manuscript; LL: devised and conducted most of the statistical analysis; and RLC: conducted the preliminary analysis. None of the authors or the funders of this study had a conflict of interest.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

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Received for publication July 28, 2008. Accepted for publication November 19, 2008.




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