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Evidence for a strong genetic influence on childhood adiposity despite the force of the obesogenic environment^1,2,3

¹ From the Department of Epidemiology and Public Health, Health Behaviour Research Centre, University College London, London, United Kingdom (JW and SC), and the Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, King's College London, London, United Kingdom (CMAH and RP)

See corresponding editorial on page 275.

² Supported by a grant from the Biological and Biotechnology Research Council, by Cancer Research UK (to JW), and by the Medical Research Council (to RP).

³ Reprints not available. Address correspondence to J Wardle, Health Behaviour Research Centre, UCL, Gower Street, London WC1E 6BT, United Kingdom. E-mail: j.wardle{at}ucl.ac.uk.

	ABSTRACT

TOP ABSTRACT INTRODUCTION SUBJECTS AND METHODS RESULTS DISCUSSION REFERENCES

 
Background: Body mass index (BMI) has been shown to be highly heritable, but most studies were carried out in cohorts born before the onset of the "obesity epidemic."

Objective: We aimed to quantify genetic and environmental influences on BMI and central adiposity in children growing up during a time of dramatic rises in pediatric obesity.

Design: We carried out twin analyses of BMI and waist circumference (WC) in a UK sample of 5092 twin pairs aged 8–11 y. Quantitative genetic model-fitting was used for the univariate analyses, and bivariate quantitative genetic model-fitting was used for the analysis of covariance between BMI and WC.

Results: Quantitative genetic model-fitting confirmed substantial heritability for BMI and WC (77% for both). Bivariate genetic analyses showed that, although the genetic influence on WC was largely common to BMI (60%), there was also a significant independent genetic effect (40%). For both BMI and WC, there was a very modest shared-environment effect, and the remaining environmental variance was unshared.

Conclusions: Genetic influences on BMI and abdominal adiposity are high in children born since the onset of the pediatric obesity epidemic. Most of the genetic effect on abdominal adiposity is common to BMI, but 40% is attributable to independent genetic influences. Environmental effects are small and are divided approximately equally between shared and nonshared effects. Targeting the family may be vital for obesity prevention in the earliest years, but longer-term weight control will require a combination of individual engagement and society-wide efforts to modify the environment, especially for children at high genetic risk.

Key Words: Heritability • waist circumference • BMI • childhood obesity • twins

	INTRODUCTION

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The dramatic rise in childhood obesity in the past 15 y (1) is clearly due to changes in the environment, because genes have not altered. However, not all children are obese. This difference could be due to inherited genetic differences between children or to differences in their rearing environments. Twin studies provide a unique method for disentangling nature and nurture by taking advantage of the fact that monozygotic twins share all of their genes, whereas dizygotic twins on average share half of their segregating genes (2). If genetic influence is important, monozygotic twins must be more similar than dizygotic twins. Twin studies can also estimate the extent to which the family environment makes family members more similar than would be expected from their genetic relatedness (the shared-environment effect). This is important in the field of childhood obesity because there is considerable interest in the role of the family. Finally, twin studies can go beyond pitting nature against nurture to consider interactions between genes and environment. A novel type of gene-environment interaction is a change in the relative influences of genes and environment after major changes in the environment.

A 1997 review of published adult twin and adoption studies found that variation in body mass index (BMI; in kg/m²) was largely due to heritable genetic differences (3). Studies published since 1997 have reached the same conclusion, with heritability estimates in adults ranging from 55% to 85% (4-7). Twin studies also show that most of the nongenetic effect comes from environmental factors that are unique to each person (nonshared-environment effects) and not from the shared family context; this observation has been confirmed by results from adoption studies (8, 9). Contrary to widespread assumptions about the influence of the family environment, living in the same home in childhood appears to confer little similarity in adult BMI beyond that expected from the degree of genetic resemblance.

One limitation of existing twin studies is that many were carried out in adults, for whom the family home is not a contemporary environment. Shared-environment effects may be stronger in pediatric samples, as has been observed in 2 studies of very young twins (10, 11). Most existing studies were also carried out in cohorts born before the onset of the current "obesity epidemic." Obesogenic environments may either overshadow the observable effect of genetic differences or boost it by providing a permissive substrate for the expression of susceptibility.

Abdominal obesity has increased even faster than BMI in pediatric populations (12-14); this increase has serious health implications, because visceral fat appears to be the primary cause of obesity-related health risks (15, 16). Twin designs make it possible to assess the heritability of abdominal fatness and also to discover whether genetic influences are unique or common to BMI. High heritability of other adiposity phenotypes [eg, truncal skinfold thickness, percentage body fat, and waist circumference (WC)] has been reported in adults (17), and associations with BMI have implicated both common and unique genetic determinants (18). No large twin study has examined the heritability of abdominal adiposity in children since the prevalence of that condition began to spiral upward. We quantified the genetic and environmental influences on BMI and WC and assessed the genetic and environmental overlap between the 2 variables in a population-based sample of 5092 twin pairs born between 1994 and 1996.

	SUBJECTS AND METHODS

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Participants
The sampling frame was the Twins’ Early Development Study (TEDS), a population-based cohort of twins born in the United Kingdom in 1994, 1995, and 1996. The TEDS cohort is reasonably representative of population demographics and is described in more detail elsewhere (19). Zygosity was assessed through a parent questionnaire of physical similarity, which has been shown to be >95% as accurate as DNA testing (20). When zygosity was unclear from the questionnaire, DNA testing was conducted. The results of Koeppen-Schomerus et al (10), described above, were from a subsample of TEDS families when the twins were 4 y old.

Procedures
For the present study, carried out in 2005, parents were invited to weigh and measure their children. They were sent a tape measure for WC and height and were instructed to take the waist measurement directly over the skin at a point 4 cm above the navel (bellybutton) while the child was relaxed and after a slight exhalation (21). Weights, heights, and waists were also measured by researchers visiting the homes in a subsample of 228 children within a year of the parents’ return of the questionnaire (mean: 5 mo). Correlations between researcher-measured and parent-measured heights, weights, and waists were 0.90, 0.83, and 0.92, respectively. On average, the measures taken by researchers showed children to be 1.7 cm taller and 2.6 kg heavier than the parental measurements found, and those values gave a BMI that was 0.9 higher. WCs measured by the researchers were on average 0.78 cm larger than parental measures. These differences were probably the result of a time lag between the 2 measures.

BMI and WC SD scores (SDSs) were calculated by using the EXCEL GROWTH MACRO software (version 2.12; Microsoft Corp, Redmond, WA) for the 1990 British growth reference curves, which have a mean of 0 and an SD of 1 at each age (22, 23). Overweight and obese status was determined by using the International Obesity Task Force criteria, which identify BMI values for each age associated with predicted BMIs of 25 and 30 at age 18 y (24).

The request for information on weights and heights was sent to 8978 families who were active participants in TEDS at the time of data collection; of this group, 5543 (62%) returned completed questionnaires. The remaining 3234 families were not currently active, and only 359 of them returned completed questionnaires. Thus, the total sample comprised 5902 families. Excluded from the analyses were families in which either twin had a specific medical condition or was an extreme outlier for perinatal problems (eg, very low birth weight) or for whom zygosity information was unavailable. Criteria for raw data cleaning were based on the ranges of measured heights and weights from the Health Survey for England 2003 (Internet: www.archive2.official-documents.co.uk/document/deps/doh/survey03/hse03.htm). Children with height <1.10 m or with weight <13 kg or >84 kg were excluded. When BMI was calculated from the cleaned data, we also excluded children with a BMI < 12. After exclusions, complete BMI and WC data were available for 5092 pairs of twins: 1813 monozygotic (845 M, 968 F) and 3279 dizygotic (818 M, 840 F; n = 1621 opposite-sex) pairs.

Each child's parents provided written informed consent. The study was approved by the ethics committees of King's College London and University College London.

Statistical analysis
The twin method depends on comparing the phenotypic similarity of genetically identical (monozygotic) and fraternal (dizygotic) twin pairs. Differences in within-pair correlations between monozygotic and dizygotic twin pairs give an estimate of the contribution of inherited genetic differences to phenotypic variation; the remaining variation is attributed to environmental differences. To the extent that within-pair correlations are higher than would be predicted from the heritability of the trait, shared-environment effects are implicated. The remaining environmental variance is therefore a nonshared-environment effect plus errors of measurement.

Quantitative genetic model fitting is standard in twin studies; it has been described elsewhere (25). Observable variation is decomposed into dominant and additive genetic components and shared and nonshared environmental components. Removal of each component in turn and testing of the deterioration in the fit of the model relative to the full model allows the identification of the best-fitting and most parsimonious model. We used MX software for structural equation modeling (26) to test the fit of the models to the data and to obtain CIs for estimates of genetic and environmental effects (25, 27). A sex-limitation model was used that examined quantitative differences in variables estimates between boys and girls and qualitative differences in parameter between same-sex and opposite-sex twin pairs (26). For the analysis of covariance between BMI and WC, standard bivariate quantitative genetic model–fitting techniques were used to decompose the phenotypic covariance into genetic and environmental components of covariance (25).

	RESULTS

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The mean age of the twins at the time of measurement was 9.9 y (range: 8.3–11.6 y). Mean heights, weights, BMI, and WC and the respective SDs, which showed the comparison with the 1990 norms, are given in Table 1. Heights were 0.22 SDSs higher and weights 0.14 SDSs higher than 1990 norms, but BMI was close to the 1990 levels (0.02 SDSs). WCs were substantially higher than 1990 norms (0.80 SDSs), and more so in girls (0.87 SDSs) than boys (0.74 SDSs). Overweight and obesity rates (Internal Obesity Task Force criteria) were similar in boys and girls: 11% of the subjects were overweight, and an additional 3% were obese (Table 1). Twins from dizybotic pairs were significantly taller than those from monozygotic pairs, but the difference was very small (0.58 cm; t = 3.40, P = 0.001). Dizygotic twins had significantly higher BMIs (difference = 0.15; t = 2.46, P = 0.014) and WCs (difference = 0.40, t = 2.72, P = 0.007) than did monozygotic twins.

Table 2

Table 3

Figure 1

View larger version (12K): [in this window] [in a new window]   FIGURE 1.. Estimates of genetic and environmental correlations between BMI and waist circumference. The 95% CIs for the variable estimates from the correlated-factors model-fitting solution are rG = 0.77 (0.75, 0.79); rC = 0.76 (0.64, 0.85); rE = 0.69 (0.66, 0.71). The A, C, and E estimates are similar to those from the univariate model-fitting (Table 3), but they are not identical because the bivariate analysis includes the variance of BMI and waist circumference as well as the covariance between them.

	DISCUSSION

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The results in the present study are broadly comparable to findings from earlier cohorts of young adults, which indicates that the balance of genetic and environmental effects is much the same as that before the external environment became so obesogenic. Therefore, although contemporary environments have made today's children fatter than were children 20 y ago, the primary explanation for variations within the population, then and now, is genetic differences between individual children.

This is the first study to assess the heritability of WC in children, an increasingly important issue in the light of evidence that fat in the visceral region is the major cause of metabolic syndrome (30) and is an important contributor to cardiovascular disease (31) and some cancers (32). We found that WC was as heritable as BMI, with comparable contributions of shared- and nonshared- environment effects. The results of the bivariate analysis indicated that 60% of the heritability of WC was common to BMI, but 40% was due to different genetic factors. The etiologic significance of visceral fat stores, as compared with other fat stores, may therefore be related to different underlying genetic factors.

BMI tends to be lower and obesity tends to be less prevalent in twins than in singletons (11, 33), a difference that may be related to the intrauterine environment or to the effect of growing up as a twin. Heights, weights, and the prevalence of obesity also were lower in the present sample than in 10-y-olds in the Health Survey for England (2003), but it was interesting that WCs in the present sample were as high as those in the surveyed 10-y-olds. However, there is no evidence that these effects differ significantly between monozygotic and dizygotic twins, and therefore the validity of the twin design and of any conclusions related to genetic and environmental effects should be secure.

Probably the most controversial finding from twin studies is the relatively low shared-environment effect, a finding that has been observed for behavioral traits. Discussions about the obesity epidemic almost invariably ascribe a key role to the family, but, in the present study, as in other twin and adoption studies, siblings from the same family were only slightly more similar in adiposity than would be expected from their genetic similarity, and the shared-environment effect was estimated at just over 10%. The fact that siblings’ experience of being served similar food, being given the same options for television viewing and active outdoor play, seeing the same behaviors modeled by parents, and going to the same school does not make siblings more similar is a challenge for etiologic models that highlight the home environment as the root cause of obesity. This finding will, however, come as no surprise to parents, who are well aware that their children come in different shapes and sizes despite having a similar upbringing. What is important is this finding means that "blaming" parents is wrong. Findings from twin studies were influential in persuading clinicians that the "schizophrenogenic" mother was a myth. Results from the present study highlight the fact that excessive weight gain in a child is unlikely to be the fault of the parents and is more likely to be due to the child's genetic susceptibility to the obesogenic features of the modern environment.

Does the fact that the shared-environment effects were comparatively small have implications for the potential effect of interventions that target the home? It certainly counsels caution against assumptions that, if all parents followed current child-feeding recommendations, the obesity problem would be solved. But etiologic processes do not always have simple indications for interventions. Strongly genetic conditions—notably, phenylketonuria—have proved to be entirely treatable by environmental interventions, eg, a phenylalanine-free diet in the case of phenylketonuria. It is therefore possible that aspects of family life could be modified enough to achieve a protective environment for children who are vulnerable to obesity. It is also worth remembering that control over 10% of the variance in an important health risk factor is not insignificant. Population-attributable risks for many of the risk factors for coronary heart disease are <10%, yet recommendations for behavior change are a central part of prevention and management (34). Nevertheless, these results signify that achieving major shifts in population weights—as proposed in recent public health targets—will require at least as much emphasis on creating healthier external environments and teaching vulnerable persons to adopt life-long prudent habits as on encouraging parents to modify home settings.

The present study had limitations. The twin method makes several assumptions, such as that monozygotic and dizygotic twins have similar environments. These assumptions have been discussed in detail elsewhere (25, 35, 36) To the extent that the environments (uterine or familial) of monozygotic twin pairs are more similar than those of dizygotic pairs, heritability estimates from twin studies will be inflated. However, existing evidence suggests that this effect is likely to be small and that it would not materially change the conclusion that phenotypic variation in adiposity is significantly determined by heritable genetic differences between persons. There is also the potential for bias in volunteer samples, despite a population-based sampling frame, although this potential is common to all epidemiologic studies that depend on voluntary participation. If the participation bias is unrelated to the trait, it may not matter, but overweight families may be reluctant to participate in a study requiring weight reports. However, so long as the volunteer bias is the same in families with monozygotic and dizygotic twins, the twin comparisons remain valid. In common with many large-scale anthropometric studies, the present study used parental reports of the height, weight, and WC of the children. However, we gave careful guidance on how to take the measurements and showed high correlations between parental reports and all 3 measures in a subsample of families visited at home, which provides confidence in the results.

Quantitative genetic studies indicate how much of the variation in weight is due to genetic differences between persons, but they neither identify the genes nor address their mechanisms. It appears increasingly likely that weight variation is due to large numbers of genes, each exerting small effects, because no major genes for common obesity have been identified (37). Part of the genetic effect may well be due to variations in appetite and satiety and not just to the biology of fat storage (38). A quantitative, behavioral, genetic model helps makes sense of the paradox that obesity is both predominantly environmental (as in the rapid secular increases) and predominantly genetic (as in quantitative genetic studies). In such a model, the epidemic of obesity is attributed squarely to changes in the environment, whereas individual differences are attributed to genetic differences between individual persons.

	ACKNOWLEDGMENTS

 
The authors’ responsibilities were as follows—JW and RP: the study concept; SC: the design and analysis; CH: the model fitting; JW: the drafting of the manuscript; and all authors: contributions to the writing of the manuscript. None of the authors had a personal or financial conflict of interest.

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This Article Abstract Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Citation Map Services Related articles in AJCN Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Wardle, J. Articles by Plomin, R. Search for Related Content PubMed PubMed Citation Articles by Wardle, J. Articles by Plomin, R. Agricola Articles by Wardle, J. Articles by Plomin, R.