BACKGROUND Few studies have examined the independent and combined relationships of body mass index (BMI) peak and rebound with adiposity, insulin resistance and metabolic risk later in life. We used data from Project Viva, a well-characterized birth cohort from Boston with repeated measures of BMI, to help fill this gap. METHODS Among 1681 children with BMI data from birth to mid childhood, we fitted individual BMI trajectories using mixed-effects models with natural cubic splines and estimated age, and magnitude of BMI, at peak (in infancy) and rebound (in early childhood). We obtained cardiometabolic measures of the children in early adolescence (median 12.9 years) and analysed their associations with the BMI parameters. RESULTS After adjusting for potential confounders, age and magnitude at infancy BMI peak were associated with greater adolescent adiposity, and earlier adiposity rebound was strongly associated with greater adiposity, insulin resistance and metabolic risk score independently of BMI peak. Children with a normal timing of BMI peak plus early rebound had an adverse cardiometabolic profile, characterized by higher fat mass index {β 2.2 kg/m2 [95% confidence interval (CI) 1.6, 2.9]}, trunk fat mass index [1.1 kg/m2 (0.8, 1.5)], insulin resistance [0.2 units (0.04, 0.4)] and metabolic risk score [0.4 units (0.2, 0.5)] compared with children with a normal BMI peak and a normal rebound pattern. Children without a BMI peak (no decline in BMI after the rise in infancy) also had adverse adolescent metabolic profiles. CONCLUSIONS Early age at BMI rebound is a strong risk factor for cardiometabolic risk, independent of BMI peak. Children with a normal peak-early rebound pattern, or without any BMI decline following infancy, are at greatest risk of adverse cardiometabolic profile in adolescence. Routine monitoring of BMI may help to identify children who are at greatest risk of developing an adverse cardiometabolic profile in later life and who may be targeted for preventive interventions.

中文翻译：

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生命早期的体重指数里程碑模式和青春期早期的心脏代谢风险。

背景 很少有研究探讨体重指数 (BMI) 峰值和反弹与肥胖、胰岛素抵抗和晚年代谢风险之间的独立和综合关系。我们使用 Viva 项目的数据来帮助填补这一空白，该项目是来自波士顿的一个特征明确的出生队列，重复测量 BMI。方法 在 1681 名拥有从出生到童年中期 BMI 数据的儿童中，我们使用具有自然三次样条的混合效应模型和估计年龄以及峰值（婴儿期）和反弹（幼儿期）的 BMI 大小来拟合个体 BMI 轨迹。我们获得了青春期早期（中位 12.9 岁）儿童的心脏代谢指标，并分析了它们与 BMI 参数的关联。结果调整潜在的混杂因素后，婴儿期 BMI 峰值的年龄和幅度与青少年肥胖程度较高相关，早期肥胖反弹与肥胖程度、胰岛素抵抗和代谢风险评分密切相关，与 BMI 峰值无关。BMI 峰值时间正常且早期反弹的儿童具有不良的心脏代谢特征，其特征是较高的脂肪质量指数 {β 2.2 kg/m2 [95% 置信区间 (CI) 1.6, 2.9]}、躯干脂肪质量指数 [1.1 kg] /m2 (0.8, 1.5)]、胰岛素抵抗 [0.2 单位 (0.04, 0.4)] 和代谢风险评分 [0.4 单位 (0.2, 0.5)] 与具有正常 BMI 峰值和正常反弹模式的儿童相比。没有 BMI 峰值的儿童（婴儿期 BMI 上升后没有下降）也有不良的青少年代谢特征。结论 BMI 反弹的早期年龄是心脏代谢风险的一个重要危险因素，与 BMI 峰值无关。具有正常峰值早期反弹模式或婴儿期后体重指数没有任何下降的儿童，在青春期出现不良心脏代谢特征的风险最大。BMI 的常规监测可能有助于识别在以后的生活中最有可能出现不良心脏代谢特征的儿童，以及哪些儿童可能成为预防性干预的目标。