Epidemiological association between metabolic health obesity phenotype and chronic low back pain: a cross-sectional analysis based on the NHANES database

doi:10.12307/2026.268

Abstract

Abstract: BACKGROUND: Currently, whether and how the metabolically healthy obesity phenotype influences the risk and pathological progression of chronic low back pain compared to metabolically unhealthy obese individuals remain unclear. Research is urgently needed to clarify their association and potential mechanisms.
OBJECTIVE: To investigate the epidemiological association between the metabolically healthy obesity phenotype and chronic low back pain.
METHODS: Using data from the US National Health and Nutrition Examination Survey (NHANES) 1999-2004 and 2009-2010 (n=4 956), this retrospective cross-sectional study defined obesity status based on body mass index and waist circumference according to World Health Organization criteria. Metabolic phenotypes were stratified using core metabolic syndrome indicators (such as fasting blood glucose, lipid profile, and blood pressure), establishing classifications for metabolically healthy and unhealthy obesity. The adjusted multivariable logistic regression models and restricted cubic splines were constructed to systematically evaluate the nonlinear dose-response relationship between metabolically healthy obesity phenotypes and chronic low back pain risk. An adjusted multivariable model was established to stratify chronic low back pain risk. Model robustness was validated through subgroup analysis, threshold effect analysis, and multiple sensitivity analysis frameworks.
RESULTS AND CONCLUSION: (1) Metabolically unhealthy obesity significantly increased the risk of chronic low back pain (body mass index standard: OR (95% CI): 1.44 (1.11, 1.85), P = 0.007 0; waist circumference standard: OR (95% CI): 1.57 (1.25, 1.97), P = 0.000 3), smoking (OR (95% CI): 1.44 (1.24, 1.67), P < 0.000 1), arthritis (OR (95% CI): 2.44 (2.06, 2.88), P < 0.000 1), and other comorbidities significantly amplified the risk effect of metabolically healthy obesity on chronic low back pain. Body mass index ≥ 39.73 kg/m2 and waist circumference ≥ 125 cm served as risk thresholds for chronic low back pain in metabolically unhealthy individuals. Low education level and income, and widowed/divorced or separated status increased the risk of chronic low back pain. A linear relationship existed between body mass index and chronic low back pain in the total population and among metabolically unhealthy participants (P < 0.05). Among metabolically healthy participants, the dose-response relationship between body mass index and chronic low back pain exhibited an approximately linear relationship (P > 0.05). An approximately linear dose-response relationship was observed for chronic low back pain across the total population, metabolically healthy participants, and metabolically unhealthy participants (P > 0.05). (2) Cross-sectional analysis based on NHANES data revealed a significant positive independent association between metabolically unhealthy obesity and chronic low back pain. The association between metabolically healthy obesity and chronic low back pain was weak and not statistically significant, indicating that metabolic health status is an important confounding factor influencing the occurrence of chronic low back pain in obese populations. The association model between metabolically healthy obesity and chronic low back pain established through international research provides a critical theoretical reference for exploring racial heterogeneity and localized mechanisms (e.g., Asia-specific metabolic thresholds) in similar conditions among the Chinese population. The findings suggest that it is urgent to address low back pain risks among metabolically healthy obese populations, promote optimized clinical classification intervention strategies (e.g., avoiding excessive weight loss), and proactively prevent the public health burden of obesity-related musculoskeletal diseases in the Chinese population.

Key words: metabolically healthy obesity phenotype, chronic low back pain, China National Health and Nutrition Examination Survey, insulin resistance, social determinants

CLC Number:

Ye Shicheng, Liu Yuxin, Zeng Xuan, Sui Lili, Liu Jiao, Chen Yuting, Qu Chongzheng. Epidemiological association between metabolic health obesity phenotype and chronic low back pain: a cross-sectional analysis based on the NHANES database[J]. Chinese Journal of Tissue Engineering Research, 2026, 30(35): 9365-9374.

Figures/Tables 6

2.1 研究人群的描述研究参与者在代谢健康-肥胖表型中的特征见表1(n=4 956)。慢性腰痛的总体患病率为40.7%(n=2 019)，女性患病率更高(男性vs.女性：46.7% vs. 53.3%)，代谢健康表型在总人群中占比约为16.6%。基于体质量指数/腰围双维度的表型分层分析显示：①代谢健康亚组中，正常体质量及超重组的慢性腰痛患病率显著低于代谢不健康组(体质指数标准：代谢健康正常体质量组8.6% vs.代谢不健康正常体质量组18.2%；代谢健康超重组4.4% vs.代谢不健康超重组32.1%；P=0.002 6；腰围标准：代谢健康正常体质量组7.1% vs.代谢不健康正常体质量组13.2%；代谢健康超重组3.9% vs. 代谢不健康超重组15.7%；P=0.009 9)；②肥胖表型(代谢健康肥胖/代谢不健康肥胖)在慢性腰痛组呈显著聚集趋势(体质指数标准：代谢健康肥胖组1.9% vs. 代谢不健康肥胖组34.8%；腰围标准：代谢健康肥胖组3.9% vs. 代谢不健康肥胖组56.2%)。多维度风险分析揭示，在社会梯度效应(低教育水平、低收入、吸烟状态)、婚姻解组效应(丧偶/离异或分居)、代谢负荷累积效应(胰岛素浓度)及心脑血管疾病(心脏病、脑卒中)中慢性腰痛风险显著(P < 0.05)。在临床共病中，糖尿病、关节炎、高血压展现出强关联(所有P < 0.001)。组间均衡性检验表明，非慢性腰痛组与慢性腰痛组在基础人口学特征(年龄、性别、种族)、核心代谢参数(空腹血糖、高密度脂蛋白胆固醇、甘油三酯、收缩压/舒张压)及恶性肿瘤患病率方面比较差异均无显著性意义(P > 0.05)，证实研究结果的独立性和稳健性。 2.2 代谢健康肥胖表型与慢性腰痛的相关性根据Logistic回归分析的结果，在代谢不健康型肥胖群体中患有慢性腰痛的风险更大，体质指数标准：OR(95%CI)=1.44 (1.11，1.85)，P=0.007 0；腰围标准：OR(95%CI)=1.57 (1.25，1.97)，P=0.000 3。此外，在婚姻状态[OR(95%CI)=1.63 (1.30，2.03)，P=0.000 1]、贫富收入比[OR(95%CI)=0.89 (0.84，0.94)，P=0.000 1]、体质量[OR(95%CI)=1.01 (1.00，1.01)，P=0.000 3]、体质量指数[OR(95%CI)=1.03 (1.02，1.04)，P < 0.000 1]、胰岛素[OR(95%CI)=1.01(1.00，1.02)，P=0.038 1]、吸烟[OR(95%CI)=1.44 (1.24，1.67)，P < 0.000 1]、骨质疏松[OR(95%CI)=1.65 (1.18，2.30)，P=0.004 9]、糖尿病[OR(95%CI)=1.56 (1.26，1.92)，P=0.000 1]、关节炎[OR(95%CI)=2.44 (2.06，2.88)，P < 0.000 1]、冠心病[OR(95%CI)=1.38 (1.02，1.88)，P=0.042 9]、脑卒中[OR(95%CI)=1.65 (1.06，2.58)，P=0.030 6]、高血压[OR(95%CI)=1.34 (1.14，1.56)，P=0.000 7]等方面更能体现出与慢性腰痛的强关联性，见表2。 2.3 体质量指数和腰围与慢性腰痛的独立关联建立了3个二元Logistic回归模型，以探讨体质量指数和腰围对慢性腰痛的潜在影响，结果表明，体质量指数和腰围与未调整模型、模型1、模型2中的慢性腰痛呈正相关，与受控协变量关系不大，见表3。在未调整模型中，体质量指数或腰围增加一个单位，患有慢性腰痛的概率增加[体质量指数：OR(95%CI)=1.03(1.02，1.04)，P < 0.000 1；腰围：OR(95%CI)=1.01(1.01，1.02)，P < 0.000 1]。体质量指数或腰围每增加一个单位，模型1中[体质量指数：OR(95%CI)= 1.03(1.02，1.04)，P < 0.000 1；腰围：OR(95%CI)=1.02(1.01，1.02)，P < 0.000 1]和模型2[体质量指数：OR(95%CI)=1.04(1.03，1.05)，P < 0.000 1；腰围：OR(95%CI)=1.02(1.01，1.02)，P < 0.000 1]中患有慢性腰痛的概率也增加。将体质量指数和腰围转换为分类变量(体质量指数分为3组：“正常”“超重”和“肥胖”；腰围也分为3组：“正常”“中心性超重”和“中心性肥胖”)。校正模型2的协变量后，根据体质量指数标准的肥胖与发生慢性腰痛的可能性增加相关[OR(95%CI)=1.55(1.33，1.81)，P < 0.000 1]，根据腰围标准的中心性肥胖也与发生慢性腰痛的概率增加相关[OR(95%CI)=1.47(1.25，1.74)，P < 0.000 1]。 2.4 代谢健康肥胖表型与慢性腰痛的关系按代谢健康和肥胖(体质量指数类别和腰围类别)交叉分类的慢性腰痛风险，见表4。在调整模型2协变量后，代谢健康型肥胖患者发生慢性腰痛的概率相对高于代谢健康型正常体质量患者[体质量指数标准：OR(95%CI)=1.74 (1.06，2.85)，P=0.0292；腰围标准：OR(95%CI)=1.53 (1.01，2.31)，P=0.0423]。此外，代谢不健康型肥胖参与者发生慢性腰痛的可能性显著高于代谢不健康型正常体质量个体[体质指数标准：OR(95%CI)=1.49(1.25，1.77)，P < 0.000 1；腰围标准：OR(95%CI)=1.38(1.14，1.66)，P=0.000 8]。在代谢健康和不健康的参与者中，体质量指数每增加一个单位都会增加发生慢性腰痛的概率[代谢健康：OR(95%CI)=1.04(1.00，1.08)，P=0.039 3；代谢不健康：OR(95%CI)=1.03 (1.02，1.05)，P < 0.000 1]。在代谢不健康的参与者中，腰围每增加一个单位发生慢性腰痛的概率也增加[OR(95%CI)=1.02(1.01，1.02)，P < 0.000 1]。而在代谢健康参与者中腰围和发生慢性腰痛的概率关系不显著(P=0.249 5)。 2.5 亚组分析结果亚组分析结果见表5。未检测到代谢健康肥胖表型在性别、吸烟状况、肿瘤状态和关节炎状态方面发生慢性腰痛概率的显著交互作用(P > 0.05)。 2.6 敏感性分析结果在敏感性分析中，当在模型2的基础上额外调整婚姻状态、教育水平、关节炎状态、胰岛素浓度和胰岛素抵抗指数时，代谢健康肥胖表型和慢性腰痛之间的关联基本不变，见表6。 2.7 限制性立方样条图此次研究利用限制性立方样条来模拟和建模总人群、代谢健康和代谢不健康参与者中体质量指数/腰围与慢性腰痛的关系，见图2所示。在总人群和代谢不健康参与者中，体质量指数和慢性腰痛之间的剂量-反应关系存在线性关系(P < 0.05)，表明体质量指数和慢性腰痛之间存在正相关。在代谢健康参与者中，体质量指数和慢性腰痛之间的剂量-反应关系存在近似线性关系(P > 0.05)；在总人群、代谢健康和代谢不健康参与者中，腰围和慢性腰痛之间的剂量-反应关系存在近似线性关系(P > 0.05)。 2.8 阈值效应分析结果根据体质量指数标准类别，在总人群参与者中，当体质量指数< 39.75 kg/m2时，每增加1单位发生慢性腰痛的概率增加3%[OR(95%CI)=1.03(1.02，1.04)，P < 0.000 1]；当体质量指数≥39.75 kg/m2时，每增加1单位发生慢性腰痛的概率升至9%[OR(95%CI)=1.09(1.03，1.14)，P=0.001]。在代谢健康参与者中，体质量指数与慢性腰痛的整体关联较弱[OR(95%CI)=1.04(1.00，1.08)，P=0.039 3]。在代谢不健康参与者中，与总人群结果几乎保持一致，当体质量指数≥39.73 kg/m2时发生慢性腰痛的概率显著增加9%(OR=1.09，P=0.001 1)，见表7。根据腰围标准类别，在总人群参与者和代谢不健康人群中，腰围每增加1 cm发生慢性腰痛概率均增加2%[OR(95%CI)=1.02(1.01，1.02)，P < 0.000 1]，而在代谢健康人群中二者无显著关联(OR=1.01，P=0.249 5)。如表7所示。"

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