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Assessing causality in the association between child adiposity and physical activity levels: a Mendelian
Rebecca C Richmond1, George Davey Smith1, Andy R Ness2
1MRC Integrative Epidemiology Unit, School of Social and Community Medicine, University of Bristol, Bristol, United Kingdom.
Insights
Childhood adiposity causally reduces physical activity levels. This Mendelian randomization study found higher body mass index (BMI) in children leads to less total and moderate-to-vigorous activity, and more sedentary time.
Area of Science:
- Pediatrics
- Genetics
- Public Health
Background:
- Cross-sectional studies indicate a link between physical activity and childhood adiposity.
- The potential for reverse causation, where adiposity influences activity, requires further investigation.
Purpose of the Study:
- To investigate whether childhood adiposity causally impacts physical activity levels.
- Utilizing genetic variants associated with adiposity to estimate causal effects.
Main Methods:
- Employed Mendelian randomization with a weighted allelic score using 32 genetic correlates of BMI as an instrumental variable.
- Analyzed data from 4,296 children aged 11 years from the Avon Longitudinal Study of Parents and Children.
- Objectively measured physical activity levels, body mass index (BMI), and genotypic data were collected.
Main Results:
- A one standard deviation increase in BMI was causally associated with reduced total physical activity (p=0.04) and moderate-to-vigorous activity (p=0.04).
- Increased adiposity also led to a significant increase in sedentary time (p=0.03).
- Observational analyses showed similar trends, with no strong evidence of divergence between observational and causal estimates.
Conclusions:
- Findings suggest that increased childhood adiposity is a causal factor in reducing physical activity.
- Supports targeting body mass index (BMI) to enhance childhood activity levels.
- Acknowledges the possibility of bidirectional causation between physical activity and adiposity.
Background:
Cross-sectional studies have shown that objectively measured physical activity is associated with childhood adiposity, and a strong inverse dose-response association with body mass index (BMI) has been found. However, few studies have explored the extent to which this association reflects reverse causation. We aimed to determine whether childhood adiposity causally influences levels of physical activity using genetic variants reliably associated with adiposity to estimate causal effects.
Methods And Findings:
The Avon Longitudinal Study of Parents and Children collected data on objectively assessed activity levels of 4,296 children at age 11 y with recorded BMI and genotypic data. We used 32 established genetic correlates of BMI combined in a weighted allelic score as an instrumental variable for adiposity to estimate the causal effect of adiposity on activity. In observational analysis, a 3.3 kg/m² (one standard deviation) higher BMI was associated with 22.3 (95% CI, 17.0, 27.6) movement counts/min less total physical activity (p = 1.6×10⁻¹⁶), 2.6 (2.1, 3.1) min/d less moderate-to-vigorous-intensity activity (p = 3.7×10⁻²⁹), and 3.5 (1.5, 5.5) min/d more sedentary time (p = 5.0×10⁻⁴). In Mendelian randomization analyses, the same difference in BMI was associated with 32.4 (0.9, 63.9) movement counts/min less total physical activity (p = 0.04) (∼5.3% of the mean counts/minute), 2.8 (0.1, 5.5) min/d less moderate-to-vigorous-intensity activity (p = 0.04), and 13.2 (1.3, 25.2) min/d more sedentary time (p = 0.03). There was no strong evidence for a difference between variable estimates from observational estimates. Similar results were obtained using fat mass index. Low power and poor instrumentation of activity limited causal analysis of the influence of physical activity on BMI.
Conclusions:
Our results suggest that increased adiposity causes a reduction in physical activity in children and support research into the targeting of BMI in efforts to increase childhood activity levels. Importantly, this does not exclude lower physical activity also leading to increased adiposity, i.e., bidirectional causation.
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