BMC Women's Health · 7 authors, 1 centre
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This cross-sectional study of 5,872 US women (NHANES 2013–2020) found that higher serum uric acid (SUA) levels are independently associated with female infertility. Women in the highest SUA quartile (≥5.2 mg/dL) had 59% greater odds of infertility compared to the lowest quartile (≤3.6 mg/dL), with a dose-response relationship observed. The findings suggest that monitoring and managing SUA levels may be a modifiable factor in female reproductive health.
**Background:** Infertility affects approximately 15% of couples worldwide and is recognized as a public health priority by the CDC. Serum uric acid (SUA), a by-product of purine metabolism, can act as both an antioxidant and pro-oxidant, contributing to oxidative stress, inflammation, endothelial dysfunction, and metabolic disorders. Hyperuricemia has been linked to polycystic ovarian syndrome, endometriosis, and adverse pregnancy outcomes, but limited evidence existed connecting SUA levels directly to female infertility. This study aimed to determine whether SUA levels are independently associated with female infertility using a nationally representative US sample.
**Methods:** Data were obtained from four NHANES cycles (2013–2014, 2015–2016, 2017–2018, and 2017–2020). From 44,960 eligible participants, 5,872 women aged 18–49 who completed the reproductive health questionnaire and had SUA measurements were included. Infertility was defined by an affirmative response to: 'Have you ever attempted to become pregnant for at least a year without becoming pregnant?' SUA was measured using a colorimetric method (uricase oxidation). Covariates included demographics (age, race/ethnicity, education, marital status, poverty-to-income ratio [PIR]), lifestyle factors (smoking, drinking), health insurance, BMI, waist circumference, serum creatinine, blood urea nitrogen (BUN), estimated glomerular filtration rate (eGFR), and comorbidities (hypertension, diabetes mellitus, metabolic syndrome [MetS]). Logistic regression models were used with progressive adjustment: Model 1 (unadjusted), Model 2 (demographics + insurance), Model 3 (Model 2 + BUN, Cr, eGFR), and Model 4 (Model 3 + BMI, diabetes, hypertension, MetS). SUA was analyzed as a continuous variable and in quartiles.
**Key Results:** Infertility was present in 649 women (11.1%). Infertile women had higher mean SUA (4.7 vs. 4.5 mg/dL, p<0.001), were older (36.2 vs. 32.9 years, p<0.001), had higher PIR (2.6 vs. 2.3, p<0.001), lower eGFR (108.5 vs. 111.0 mL/min/1.73 m², p<0.001), and higher rates of obesity (55% vs. 40.8%), hyperuricemia (12.8% vs. 9.9%), diabetes (8.8% vs. 4.6%), MetS (12.3% vs. 9.2%), and hypertension (21.6% vs. 15.5%) (all p<0.05). In unadjusted analysis, each 1 mg/dL increase in SUA was associated with 19% higher odds of infertility (OR 1.19; 95% CI: 1.11–1.28). This association remained significant after full adjustment (Model 4: OR 1.16; 95% CI: 1.06–1.27; p=0.001). Quartile analysis showed a dose-response relationship: compared to Q1 (≤3.6 mg/dL), Q3 (4.4–5.1 mg/dL) had aOR 1.38 (95% CI: 1.04–1.82; p=0.024) and Q4 (≥5.2 mg/dL) had aOR 1.59 (95% CI: 1.19–2.13; p=0.002) in the fully adjusted model. Subgroup analyses revealed the association was strongest among women aged 18–35 (OR 1.27; 95% CI: 1.01–1.61), those married or cohabiting (OR 1.18; 95% CI: 1.01–1.38), those below the poverty line (OR 1.23; 95% CI: 1.00–1.51), and those without obesity (OR 1.37; 95% CI: 1.12–1.68).
**Clinical Implications:** This is the first nationally representative US study demonstrating a positive, dose-dependent association between SUA levels and female infertility. The relationship persisted after adjusting for major confounders including age, BMI, diabetes, hypertension, and metabolic syndrome. These findings suggest that SUA may serve as a modifiable biomarker in fertility assessment and management. Potential mechanisms include oxidative stress, inflammation, endothelial dysfunction, and shared pathways with metabolic and reproductive disorders (PCOS, endometriosis). Lifestyle interventions known to lower SUA—such as the DASH diet, Mediterranean diet, weight loss, and physical activity—may simultaneously improve fertility outcomes. However, due to the cross-sectional design, causality cannot be established. Limitations include self-reported infertility (recall bias), exclusion of women who never attempted pregnancy, lack of data on specific gynecologic diagnoses (PCOS, endometriosis, fibroids), and absence of serum lipid covariates. Future prospective studies are needed to confirm these findings and elucidate underlying mechanisms.