Wei Jiajun, Yao Xinyu, Guo Jingxuan, Guo Ying, Wang Yong, Wu Jinyu, Kong Hongyue, Qiu Fengyu, Zhang Yu, Liu Yizhou, Su Jiawen, Nie Jisheng, Yang Jin
MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, NHC Key Laboratory of Pneumoconiosis, Department of Occupational Health, School of Public Health, Shanxi Medical University, Shanxi Key Laboratory of Environmental Health Impairment and Prevention, Xinjiannan Road 56, Taiyuan 030001, Shanxi Province, China.
MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, NHC Key Laboratory of Pneumoconiosis, Department of Occupational Health, School of Public Health, Shanxi Medical University, Shanxi Key Laboratory of Environmental Health Impairment and Prevention, Xinjiannan Road 56, Taiyuan 030001, Shanxi Province, China.
J Affect Disord. 2025 Jun 15;379:304-312. doi: 10.1016/j.jad.2025.03.066. Epub 2025 Mar 13.
The effect of basal metabolic rate (BMR) on depression was unclear. This study investigated the potential role of BMR in the association of polycyclic aromatic hydrocarbons (PAHs) exposure and depression.
The study based on the National Health and Nutrition Examination Survey (NHANES). BMR was calculated using both the revised Harris-Benedict equation (BMR1) and the Mifflin-St Jeor equation (BMR2). Generalized linear and logistic regression models were applied to examine the associations between PAH metabolites, BMR, and depression. Weighted Quantile Sum (WQS) regression and Bayesian Kernel Machine Regression (BKMR) were utilized to analyze the combined effects of multiple PAH metabolites. Mediation analysis was conducted to explore the role of BMR.
The study included 8323 participants. A 100 kcal/day increase in BMR1 and BMR2, the depression risk increased by 5 % (95%CI: 1.00, 1.10) and 7 % (95%CI: 1.02, 1.13), respectively. WQS model indicated that mixed PAH metabolites were negatively associated with BMR1 (β: -0.06, P = 0.020) and BMR2 (β: -0.06, P = 0.014). BKMR models showed that when all PAH metabolites were at P compared to P, BMR1 and BMR2 decreased by 20.54 and 20.31 units, respectively, while the depression risk increased by 0.23 units (95 % CI: 0.07, 0.38). Mediation analyses suggested that BMR exerted a competitive mediation effect in the association between 1-NAP, 2-FLU, 1-PHE, 1-PYR, and depression.
PAH exposure led to a reduction in BMR and contributed to depression at high levels of exposure. An increase in BMR mitigated the impact of PAH exposure on depression.
基础代谢率（BMR）对抑郁症的影响尚不清楚。本研究调查了基础代谢率在多环芳烃（PAHs）暴露与抑郁症关联中的潜在作用。
该研究基于美国国家健康与营养检查调查（NHANES）。使用修订的哈里斯-本尼迪克特方程（BMR1）和米夫林-圣乔尔方程（BMR2）计算基础代谢率。应用广义线性和逻辑回归模型来检验PAH代谢物、基础代谢率和抑郁症之间的关联。采用加权分位数和（WQS）回归以及贝叶斯核机器回归（BKMR）来分析多种PAH代谢物的联合效应。进行中介分析以探究基础代谢率的作用。
该研究纳入了8323名参与者。BMR1和BMR2每增加100千卡/天，抑郁症风险分别增加5%（95%CI：1.00，1.10）和7%（95%CI：1.02，1.13）。WQS模型表明，混合PAH代谢物与BMR1（β：-0.06，P = 0.020）和BMR2（β：-0.06，P = 0.014）呈负相关。BKMR模型显示，当所有PAH代谢物处于P水平与P水平相比时，BMR1和BMR2分别下降20.54和20.31个单位，而抑郁症风险增加0.23个单位（95%CI：0.07，0.38）。中介分析表明，基础代谢率在1-萘酚、2-氟萘、1-菲、1-芘与抑郁症的关联中发挥竞争性中介作用。
PAH暴露导致基础代谢率降低，并在高暴露水平时促使抑郁症的发生。基础代谢率的增加减轻了PAH暴露对抑郁症的影响。
