Evidence for a strong genetic influence on childhood adiposity despite the force of the obesogenic environment

Nutrition Research Newsletter, March, 2008

The dramatic rise in childhood obesity in the past 15 years 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. 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/[m.sup.2]) was largely due to heritable genetic differences. Studies published since 1997 have reached the same conclusion, with heritability estimates in adults ranging from 55% to 85%. 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. 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.

Abdominal obesity has increased even faster than BMI in pediatric populations; this increase has serious health implications, because visceral fat appears to be the primary cause of obesity-related health risks. 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 [for example, truncal skinfold thickness, percentage body fat, and waist circumference (WC)] has been reported in adults, and associations with BMI have implicated both common and unique genetic determinants. No large twin study has examined the heritability of abdominal adiposity in children since the prevalence of that condition began to spiral upward. The researchers of the present study 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.

Twin analyses of BMI and WC was carried out in a UK sample of 5092 twin pairs aged 8 to 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. 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.

These results indicate that adiposity in preadolescent children born since the onset of the obesity epidemic is highly heritable. The heritability of BMI in this sample (77%) is at the higher end of results obtained with large adult samples. Heritability of BMI is also slightly higher than was found in a subsample of the same cohort at age 4 y. This could be due to the use of weight-for-height as the index of adiposity in the earlier analysis, but it is more likely that genetic effects on BMI increase during early childhood, as has been shown for other traits.

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 and is an important contributor to cardiovascular disease and some cancers. The researchers 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.

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