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Objective: Prior research suggests a connection between obesity assessed by body mass index (BMI) and lung function, such that classifying as overweight/obese indicated by BMI is associated with poor lung function (Huang et al., 2021; Köchli et al., 2019). Further, work with adults has suggested that this association may be at least partially explained by genetic influences (Thomsen et al., 2008). The current study aimed to examine 1) longitudinal phenotypic associations between weight-related health (BMI, body fat percentage, waist circumference) and lung function, and 2) the extent to which genetic and environmental influences explain associations between weight-related health and lung function across childhood.
Methods: Participants included 980 twin children (51.2% female; 59.4% non-Hispanic White, 28.2% Hispanic; 30.8% identical, 37.8% same-sex fraternal, 31.4% opposite-sex fraternal) and their caregivers from the longitudinal Arizona Twin Project (Lemery-Chalfant et al., 2019). Twins were assessed annually at eight years (M=8.42 SD=0.68) nine years (M=9.71, SD=0.93) and ten years (M=10.88, SD=1.15). Height, weight, waist circumference, BMI, body fat percentage, and lung function were reliably assessed by trained staff in the home at each wave. For lung function, three maneuvers were completed with digital peak flow meters that yielded estimates of FEV1 and PEF with the highest values retained. Child sex and age were regressed out from all variables prior to twin analyses.
Results: Phenotypic correlations (Table 1) displayed that health parameters were longitudinally stable. In most cases, weight-related health was correlated with lung function both concurrently and longitudinally. The heritability of the weight-related health parameters remained relatively stable across the three years: BMI (.56-.86; with shared environmental influences emerging at age nine), waist circumference (.84-.87), body fat percentage (.88-.92). The heritability of lung function varied for FEV1, with the nine- and ten-year assessments exhibiting higher heritability (.63-.77) and greater shared environmental influences (.54) at eight years. PEF heritability estimates remained stable (.62-.69). Bivariate models were fit across weight and lung assessments. For body fat percentage at nine years and FEV1 at ten years as an example, the AE-A-AE model fit best (Δ-2LL=3.31, Δdf=4, p=.51), suggesting that body fat percentage was associated with FEV1 solely for additive genetic reasons. The same pattern of findings was evident when examining associations between nine-year waist circumference and BMI with ten-year FEV1. For body fat percentage at nine years and PEF at ten years, the AE-A-AE model also fit best (Δ-2LL=0.27, Δdf=4, p=.99), with this model also best representing associations between nine-year waist circumference and BMI with ten-year PEF.
Conclusions: As expected, weight-related health was positively associated with lung function in late childhood. The longitudinal associations between weight-related health and later lung function were driven by common genetic influences. Findings suggest that across childhood, it is unlikely that weight-related health is causing changes in lung function (or the reverse), but that a third, genetically-influenced variable such as physiological dysregulation is impacting both health factors. Continued work is needed to disentangle the complex mechanisms underlying associations between weight-related health and lung function across the lifespan to best inform prevention and intervention efforts.