School of Sport Exercise and Health Sciences, Loughborough University, Loughborough, United Kingdom.
UCL Great Ormond Street Institute of Child Health, London, United Kingdom.
PLoS Med. 2020 Dec 8;17(12):e1003387. doi: 10.1371/journal.pmed.1003387. eCollection 2020 Dec.
Individuals with obesity do not represent a homogeneous group in terms of cardiometabolic risk. Using 3 nationally representative British birth cohorts, we investigated whether the duration of obesity was related to heterogeneity in cardiometabolic risk.
We used harmonised body mass index (BMI) and cardiometabolic disease risk factor data from 20,746 participants (49.1% male and 97.2% white British) enrolled in 3 British birth cohort studies: the 1946 National Survey of Health and Development (NSHD), the 1958 National Child Development Study (NCDS), and the 1970 British Cohort Study (BCS70). Within each cohort, individual life course BMI trajectories were created between 10 and 40 years of age, and from these, age of obesity onset, duration spent obese (range 0 to 30 years), and cumulative obesity severity were derived. Obesity duration was examined in relation to a number of cardiometabolic disease risk factors collected in mid-adulthood: systolic (SBP) and diastolic blood pressure (DBP), high-density-lipoprotein cholesterol (HDL-C), and glycated haemoglobin (HbA1c). A greater obesity duration was associated with worse values for all cardiometabolic disease risk factors. The strongest association with obesity duration was for HbA1c: HbA1c levels in those with obesity for <5 years were relatively higher by 5% (95% CI: 4, 6), compared with never obese, increasing to 20% (95% CI: 17, 23) higher in those with obesity for 20 to 30 years. When adjustment was made for obesity severity, the association with obesity duration was largely attenuated for SBP, DBP, and HDL-C. For HbA1c, however, the association with obesity duration persisted, independent of obesity severity. Due to pooling of 3 cohorts and thus the availability of only a limited number harmonised variables across cohorts, our models included adjustment for only a small number of potential confounding variables, meaning there is a possibility of residual confounding.
Given that the obesity epidemic is characterised by a much earlier onset of obesity and consequently a greater lifetime exposure, our findings suggest that health policy recommendations aimed at preventing early obesity onset, and therefore reducing lifetime exposure, may help reduce the risk of diabetes, independently of obesity severity. However, to test the robustness of our observed associations, triangulation of evidence from different epidemiological approaches (e.g., mendelian randomization and negative control studies) should be obtained.
就心血管代谢风险而言,肥胖个体并不能代表一个同质群体。我们利用三个具有全国代表性的英国出生队列研究,调查肥胖持续时间与心血管代谢风险的异质性之间是否存在关联。
我们使用了来自三个英国出生队列研究的 20746 名参与者(49.1%为男性,97.2%为白种英国人)的经协调的体重指数(BMI)和心血管代谢疾病风险因素数据:1946 年全国健康与发展调查(NSHD)、1958 年全国儿童发展研究(NCDS)和 1970 年英国队列研究(BCS70)。在每个队列中,在 10 至 40 岁之间创建了个体生命历程 BMI 轨迹,并从中得出肥胖的起始年龄、肥胖持续时间(范围为 0 至 30 年)和累积肥胖严重程度。检查了肥胖持续时间与成年中期收集的多项心血管代谢疾病风险因素之间的关系:收缩压(SBP)和舒张压(DBP)、高密度脂蛋白胆固醇(HDL-C)和糖化血红蛋白(HbA1c)。肥胖持续时间与所有心血管代谢疾病风险因素的不良值均呈正相关。与肥胖持续时间的关联最强的是 HbA1c:与从未肥胖者相比,肥胖持续时间<5 年的 HbA1c 水平相对高 5%(95%CI:4,6),而肥胖持续时间为 20 至 30 年的 HbA1c 水平高 20%(95%CI:17,23)。当调整肥胖严重程度时,SBP、DBP 和 HDL-C 的肥胖持续时间的关联大大减弱。但是,对于 HbA1c,与肥胖持续时间的关联仍然存在,与肥胖严重程度无关。由于三个队列的合并,并且各队列之间仅有有限数量的经协调变量,因此我们的模型仅调整了少数几个潜在混杂变量,这意味着可能存在残余混杂。
鉴于肥胖流行的特点是肥胖的发病年龄更早,因此一生中暴露的时间更长,我们的研究结果表明,旨在预防早期肥胖发病从而减少终生暴露的健康政策建议,可能有助于降低糖尿病的风险,而与肥胖严重程度无关。但是,为了验证我们观察到的关联的稳健性,应该从不同的流行病学方法(例如孟德尔随机化和阴性对照研究)获得证据的三角验证。