Ananda Roshan A, Solomon Bethlehem, Ray Kausik K
School of Public Health, Imperial College London, London, UK.
Department of General Medicine, Box Hill Hospital, Melbourne, Victoria, Australia.
Diabetes Obes Metab. 2025 Feb;27(2):899-910. doi: 10.1111/dom.16090. Epub 2024 Nov 25.
There is conflicting evidence regarding whether excess adiposity without metabolic abnormalities reflects a truly benign phenotype. This study evaluated the independent and joint associations of the presence of excess adiposity and metabolic abnormalities on arterial stiffness.
Participants in UK Biobank with body mass index (BMI) and arterial stiffness index (ASI) recorded between 2006 and 2010, free from cardiovascular diseases and not underweight (BMI <18.5 kg/m) were included. The primary outcome was severity of ASI analysed using multivariate-adjusted linear regression.
Of 162 590 participants, 42.5% were overweight and 24.4% were obese. Within the normal BMI strata, 50.7% had ≥1 metabolic abnormality. Compared to individuals with normal BMI and no metabolic abnormality (reference group), increased BMI or metabolic abnormalities were similarly associated with higher ASI: normal BMI with metabolic abnormalities (adjusted β-coefficient and 95% CI, 0.35; 0.30-0.40); overweight without metabolic abnormalities (0.32; 0.26-0.37). Individuals with obesity and no metabolic abnormality had higher ASI (0.65; 0.57-0.74) but was lower than individuals with overweight and metabolic abnormalities (0.80; 0.75-0.84). Individuals with obesity and metabolic abnormalities had the highest ASI (1.07; 1.02-1.12) among all six metabolic combinations, p < 0.001 for each versus reference group. Sensitivity analysis suggested higher ASI with increasing number of metabolic abnormalities within BMI categories and higher ASI in the presence of abdominal obesity within metabolic categories.
Excess adiposity and metabolic abnormalities are independently associated with increased arterial stiffness to a similar degree, suggesting that metabolically healthy individuals with overweight and obesity are not benign groups. This reinforces the need to prevent excess adiposity and consider primary prevention strategies even before metabolic abnormalities emerge.
关于无代谢异常的超重肥胖是否反映真正的良性表型，证据存在冲突。本研究评估了超重肥胖的存在与代谢异常对动脉僵硬度的独立及联合关联。
纳入英国生物银行中2006年至2010年间记录了体重指数（BMI）和动脉僵硬度指数（ASI）、无心血管疾病且非体重过低（BMI<18.5kg/m）的参与者。主要结局是使用多变量调整线性回归分析的ASI严重程度。
在162590名参与者中，42.5%超重，24.4%肥胖。在正常BMI分层中，50.7%有≥1种代谢异常。与BMI正常且无代谢异常的个体（参照组）相比，BMI升高或代谢异常与更高的ASI同样相关：BMI正常但有代谢异常（调整后的β系数和95%CI，0.35；0.30 - 0.40）；超重但无代谢异常（0.32；0.26 - 0.37）。肥胖但无代谢异常的个体有更高的ASI（0.65；0.57 - 0.74），但低于超重且有代谢异常的个体（0.80；0.75 - 0.84）。肥胖且有代谢异常的个体在所有六种代谢组合中ASI最高（1.07；1.02 - 1.12），每种与参照组相比p<0.001。敏感性分析表明，BMI类别内随着代谢异常数量增加ASI升高，代谢类别内存在腹型肥胖时ASI升高。
超重肥胖和代谢异常与动脉僵硬度增加独立相关，程度相似，这表明超重和肥胖的代谢健康个体并非良性群体。这强化了预防超重肥胖以及甚至在代谢异常出现之前就考虑一级预防策略的必要性。
