MRC Integrative Epidemiology Unit, School of Social and Community Medicine, University of Bristol, Bristol, United Kingdom.
Department of Oral and Dental Science, University of Bristol, Bristol, United Kingdom.
PLoS Med. 2014 Mar 18;11(3):e1001618. doi: 10.1371/journal.pmed.1001618. eCollection 2014 Mar.
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.
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.
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.
横断面研究表明，客观测量的身体活动与儿童肥胖有关，并且发现与体重指数（BMI）呈很强的反比剂量反应关系。然而，很少有研究探讨这种关联在多大程度上反映了反向因果关系。我们旨在使用与肥胖相关的可靠遗传变异来确定儿童肥胖是否会导致身体活动水平发生因果变化。
阿冯纵向研究的父母和孩子收集了 4296 名 11 岁儿童的身体活动水平的客观评估数据，这些儿童有记录的 BMI 和基因型数据。我们使用 32 种已建立的 BMI 遗传相关因素，结合加权等位基因评分作为肥胖的工具变量，来估计肥胖对活动的因果效应。在观察性分析中，BMI 每增加 3.3 公斤/平方米（一个标准差），总身体活动减少 22.3（95%CI，17.0，27.6）计数/分钟（p=1.6×10⁻¹⁶），中等到剧烈强度活动减少 2.6（2.1，3.1）分钟/天（p=3.7×10⁻²⁹），久坐时间增加 3.5（1.5，5.5）分钟/天（p=5.0×10⁻⁴）。在 Mendelian 随机化分析中，BMI 的相同差异与总身体活动减少 32.4（0.9，63.9）计数/分钟有关（p=0.04）（约占每分钟计数的 5.3%），中等到剧烈强度活动减少 2.8（0.1，5.5）分钟/天（p=0.04），久坐时间增加 13.2（1.3，25.2）分钟/天（p=0.03）。没有强有力的证据表明观察性估计值和变量估计值之间存在差异。使用脂肪质量指数也得到了类似的结果。活动的低功效和仪器的不完善限制了身体活动对 BMI 的影响的因果分析。
我们的结果表明，肥胖程度增加会导致儿童身体活动减少，并支持针对 BMI 的研究，以努力提高儿童的身体活动水平。重要的是，这并不排除较低的身体活动也会导致肥胖，即双向因果关系。
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