What is the clinical evidence from this study?

Study design: Systematic Review. Population: Body mass index (BMI) heritability (n=183493). Intervention: Childhood age vs. Adulthood. Primary outcome: Difference in BMI heritability (MD 0.07, 95% CI 0.03-0.11, p=0.001).

January 1, 2012Open Access

Variability in the Heritability of Body Mass Index: A Systematic Review and Meta-Regression

CECathy E. ElksAstraZeneca (United Kingdom)MHMarcel den HoedUppsala University JZJing Hua ZhaoHarbin Medical University

Key Result

Genetic factors have a greater influence on body mass index during childhood than adulthood, with heritability estimates being 0.07 higher in children compared to adults.

Study Design

Type

Systematic Review (n=183,493)

Structured PICO

Population

183,493 participants from 88 twin studies and 27 family studies included in a systematic review and meta-regression to assess the heritability of body mass index.

Outcome

Estimates of BMI heritability and factors explaining heterogeneity

Study design factors and age explain nearly half of the heterogeneity in BMI heritability estimates reported in twin studies, with genetic contributions appearing greater during childhood.

Main Result

Mean Difference: 0.07 (95% CI 0.03–0.11)

p-value: p=0.001

Limitations

Lack of longitudinal information and reliance on the mean or mid-point of age used in meta-regression analyses
Inability to distinguish effects of demographic and methodological factors from other correlated study characteristics
Family study design does not permit the differentiation of familial similarity arising from genetics as opposed to shared environmental conditions
Models used to calculate heritability are often based on the unlikely assumption that there is no synergistic interaction between genes

Abstract

Evidence for a major role of genetic factors in the determination of body mass index (BMI) comes from studies of related individuals. Despite consistent evidence for a heritable component of BMI, estimates of BMI heritability vary widely between studies and the reasons for this remain unclear. While some variation is natural due to differences between populations and settings, study design factors may also explain some of the heterogeneity. We performed a systematic review that identified 88 independent estimates of BMI heritability from twin studies (total 140,525 twins) and 27 estimates from family studies (42,968 family members). BMI heritability estimates from twin studies ranged from 0.47 to 0.90 (5th/50th/95th centiles: 0.58/0.75/0.87) and were generally higher than those from family studies (range: 0.24-0.81; 5th/50th/95th centiles: 0.25/0.46/0.68). Meta-regression of the results from twin studies showed that BMI heritability estimates were 0.07 (P = 0.001) higher in children than in adults; estimates increased with mean age among childhood studies (+0.012/year, P = 0.002), but decreased with mean age in adult studies (-0.002/year, P = 0.002). Heritability estimates derived from AE twin models (which assume no contribution of shared environment) were 0.12 higher than those from ACE models (P < 0.001), whilst lower estimates were associated with self reported versus DNA-based determination of zygosity (-0.04, P = 0.02), and with self reported versus measured BMI (-0.05, P = 0.03). Although the observed differences in heritability according to aspects of study design are relatively small, together, the above factors explained 47% of the heterogeneity in estimates of BMI heritability from twin studies. In summary, while some variation in BMI heritability is expected due to population-level differences, study design factors explained nearly half the heterogeneity reported in twin studies. The genetic contribution to BMI appears to vary with age and may have a greater influence during childhood than adult life.

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