Centre for Epidemiology Versus Arthritis, Division of Musculoskeletal and Dermatological Sciences, School of Biological Sciences, Faculty of Biology Medicine and Health, The University of Manchester, Manchester Academic Health Science Centre, Manchester, UK
Medical Research Council Integrative Epidemiology Unit at the University of Bristol, Bristol, UK.
RMD Open. 2022 Aug;8(2). doi: 10.1136/rmdopen-2022-002321.
Using Mendelian randomisation (MR), we examined whether childhood body size affects risk of rheumatoid arthritis (RA), ankylosing spondylitis (AS), psoriatic arthritis (PsA), gout and systemic lupus erythematosus (SLE) after accounting for the effect of adult body size.
Genetic instruments for childhood (age 10 years) and adult body size were derived using data from 453 169 individuals from the UK Biobank study (313 and 580 variants respectively), which have been previously validated using body mass index data from three independent populations. Genome-wide association data comprised 22 350 RA, 9069 AS, 3609 PsA, 13 179 gout and 5201 SLE cases. For each outcome, we conducted univariable MR to estimate the total effects of childhood and adult body size, and multivariable MR to examine the independent effect of childhood body size after accounting for adult body size.
Genetically predicted childhood body size had a total effect on risk of PsA (OR 2.18 per change in body size category; 95% CI 1.43 to 3.31), gout (OR 2.18; 95% CI 1.43 to 3.31) and SLE (OR 2.44; 95% CI 1.14 to 5.22), but not RA (OR 0.95; 95% CI 0.70 to 1.29) or AS (OR 0.96; 95% CI 0.61 to 1.52). After accounting for adult body size, the direct effect of childhood body size was little changed for PsA (OR 1.92; 1.14 to 3.25) and SLE (OR 2.69; 1.24 to 5.87) but was attenuated for gout (OR 1.40; 95% CI 0.94 to 2.09).
Our findings suggest that, for PsA and SLE, the risk conferred from having a larger body size during childhood may not be fully reversable even when a healthy size is achieved in adulthood.
利用孟德尔随机化(MR)方法,我们在考虑成年人体型影响的情况下,研究儿童时期的体型大小是否会影响类风湿关节炎(RA)、强直性脊柱炎(AS)、银屑病关节炎(PsA)、痛风和系统性红斑狼疮(SLE)的发病风险。
使用来自英国生物库研究的 453169 名个体的儿童(10 岁)和成年人体型数据(分别为 313 和 580 个变体)得出儿童和成年人体型的遗传工具,这些数据已经使用来自三个独立人群的体重指数数据进行了验证。全基因组关联数据包括 22350 例 RA、9069 例 AS、3609 例 PsA、13179 例痛风和 5201 例 SLE 病例。对于每种结局,我们进行了单变量 MR 以估计儿童和成年人体型的总效应,并进行了多变量 MR 以在考虑成年人体型后检查儿童体型大小的独立影响。
遗传预测的儿童体型大小对 PsA 的风险有总体影响(体型类别每变化一个单位,OR 为 2.18;95%CI 为 1.43 至 3.31)、痛风(OR 2.18;95%CI 为 1.43 至 3.31)和 SLE(OR 2.44;95%CI 为 1.14 至 5.22),但对 RA(OR 0.95;95%CI 为 0.70 至 1.29)或 AS(OR 0.96;95%CI 为 0.61 至 1.52)没有影响。在考虑成年人体型后,儿童体型大小的直接效应对于 PsA(OR 1.92;1.14 至 3.25)和 SLE(OR 2.69;1.24 至 5.87)变化不大,但对于痛风(OR 1.40;95%CI 0.94 至 2.09)的影响减弱。
我们的研究结果表明,对于 PsA 和 SLE,即使成年后达到健康体型,儿童时期体型较大所带来的风险也可能无法完全逆转。