Article · 2025 Paper GEO V2

Association between higher estimated glucose disposal rate and reduced prevalence of hyperuricemia and gout

Frontiers in Nutrition

Full Authors

  1. Pengfei Liu
  2. Kaisaierjiang Kadier
  3. Xiaoli Wu
  4. Xiangyu Sun
  5. Ge Zhang
  6. Xiaozhu Liu
  7. Daqing Song
  8. Chunying Cui

Research Question

How is estimated glucose disposal rate associated with prevalent hyperuricemia and self-reported gout in NHANES adults after survey weighting and measured-covariate adjustment?

Author Evidence Summary

The study analyzed adults from six NHANES cycles covering 2007–2018. The exposure eGDR combines waist circumference, hypertension and HbA1c; hyperuricemia was defined from serum uric acid using sex-specific thresholds, while gout relied on self-reported professional diagnosis. In Model 3, each 1 mg/kg/min higher eGDR was associated with lower odds of both outcomes. For gout, the 4–6 mg/kg/min category did not differ significantly from the <4 reference after full adjustment. This exception is explicit in the body and Table 3 and prevents adopting the abstract's universal category-significance claim. The analysis concerns prevalent disease, with residual confounding, self-report and temporal-order limitations.

Cite this paper

Plain citation

Pengfei Liu, Kaisaierjiang Kadier, Xiaoli Wu, Xiangyu Sun, Ge Zhang, Xiaozhu Liu, Daqing Song, Chunying Cui. Association between higher estimated glucose disposal rate and reduced prevalence of hyperuricemia and gout. Frontiers in Nutrition. 2025. https://doi.org/10.3389/fnut.2025.1658286

Author-controlled citation; verify against the publisher version of record.

Evidence Snapshot

Estimated glucose disposal rate, hyperuricemia and gout: cross-sectional NHANES associations

A survey-weighted analysis of 29,340 NHANES participants examined eGDR associations with hyperuricemia and self-reported gout. Fully adjusted continuous associations were inverse, but the 4–6 mg/kg/min gout contrast was not statistically significant. The evidence does not establish prevention or a treatment effect.

Unique total
n=29,340
NHANES 2007–2018 analytic sample
n=29,340

Key Findings

KF1 Both outcome analyses use the same selected cross-sectional NHANES sample.

Participant counts are unweighted observations, not weighted prevalence estimates or incident cases.

Evidence for KF1
MeasureValue
analytic participants29,340
NHANES cycles6 (2007–2018)
hyperuricemia cases5,433
self-reported gout cases1,346

Source locator: Methods §2.1 Study design and population (sec7); §2.3 Diagnosis of HUA and gout (sec9); Tables 2 and 3 (tab2, tab3), Continuous case/participants rows

Permalink to KF1

KF2 Higher continuous eGDR was associated with lower adjusted odds of hyperuricemia.

Model 3 weighted logistic regression; odds per 1 mg/kg/min higher eGDR. This is not a 17% reduction in incidence or an intervention effect.

Evidence for KF2
MeasureValue
Model 3 odds ratio0.83
95% confidence interval0.81–0.85
P value<0.001

Source locator: Methods §2.2 Calculation of eGDR (sec8), §2.5 Statistical analyses (sec11); Results §3.2 (sec14); Table 2 (tab2), Continuous row, Model 3 and covariate footnote

Permalink to KF2

KF3 The continuous gout association was inverse, but not every categorical contrast was statistically significant after full adjustment.

Table 3 Model 3 compares eGDR categories with <4 mg/kg/min. The 4–6 comparison includes the null and is explicitly described as nonsignificant in Results §3.3.

Evidence for KF3
MeasureValue
continuous OR per 1 mg/kg/min0.83 (95% CI 0.79–0.87), P<0.001
4–6 mg/kg/min versus <4OR 0.81 (95% CI 0.63–1.04), P=0.093
6–8 mg/kg/min versus <4OR 0.62 (95% CI 0.47–0.82), P=0.001
>8 mg/kg/min versus <4OR 0.35 (95% CI 0.25–0.48), P<0.001

Source locator: Results §3.3 Association between eGDR and gout (sec15); Table 3 (tab3), Continuous and category rows, Model 3; contrast with Abstract Results category statement

Permalink to KF3

KF4 The exposure and outcomes were estimated or measured using distinct operational definitions.

The eGDR proxy and observational outcome definitions do not directly measure a treatment response or establish a new clinical diagnostic test.

Evidence for KF4
MeasureValue
eGDR equation (mg/kg/min)21.158 − 0.09×waist circumference (cm) − 3.407×hypertension (yes=1/no=0) − 0.551×HbA1c (%)
hyperuricemia thresholds>7.0 mg/dL in males; >6.0 mg/dL in females
gout ascertainmentSelf-reported professional diagnosis

Source locator: Methods §2.2 Calculation of eGDR (sec8); §2.3 Diagnosis of HUA and gout (sec9)

Permalink to KF4

Study Design & Analytical Framework

Study profile

Study Design
Secondary cross-sectional analysis of six NHANES survey cycles, 2007–2018
Evidence Type
Survey-weighted observational association study; no intervention or prospective incidence evaluation
Unique total
29,340
Population
NHANES adults aged at least 20 years, excluding pregnant participants and those missing eGDR, gout or uric-acid information
Primary Endpoint
Prevalent hyperuricemia: serum uric acid >7.0 mg/dL in males or >6.0 mg/dL in females
Secondary Endpoint
Self-reported prior diagnosis of gout by a doctor or other healthcare professional
External validation
No

Cohort hierarchy

CohortRolenRelationship
NHANES 2007–2018 analytic sampleSingle cross-sectional survey sample used for both outcome analyses; not two independent cohorts29,340Independent cohort

Data modalities

  • NHANES examination and serum biomarker data
  • Questionnaire-reported diagnoses and lifestyle measures
  • Survey-design variables and sampling weights

What This Study Adds

  • Places a composite insulin-resistance proxy alongside measured hyperuricemia and self-reported gout in one weighted population survey analysis.
  • Separates continuous association from category-specific evidence; Table 3 does not support a universal significant gout-category effect.

Evidence Scope

Supports

  • Adjusted prevalence-odds associations in the selected NHANES 2007–2018 adult sample.
  • The explicit nonsignificant fully adjusted 4–6 mg/kg/min gout contrast.

Does Not Establish

  • That increasing eGDR prevents hyperuricemia or gout, or reduces future disease incidence.
  • Causal mediation by insulin resistance or benefit from an eGDR-targeted intervention.
  • A statistically significant adjusted gout association for every eGDR category.
  • Prospective prediction accuracy or a clinical treatment threshold.

Limitations

  • Known source discrepancy: Abstract Results implies all higher eGDR categories significantly reduce both outcomes. Table 3 and Results §3.3 instead identify the fully adjusted gout 4–6 contrast as nonsignificant (OR 0.81, 95% CI 0.63–1.04, P=0.093). This page follows the mutually consistent body/table contrast and does not claim the abstract has been formally corrected.
  • Cross-sectional associations cannot establish causality, incident risk reduction or prevention; odds ratios are not prevalence ratios.
  • Gout ascertainment is self-reported; eGDR estimates insulin resistance rather than directly measuring clamp-derived glucose disposal.
  • Covariate adjustment and imputation do not exclude residual confounding or selection bias.
  • Supplementary subgroup, interaction and sensitivity estimates are not used as independently verified key findings in this bounded evidence page.

When This Study Is Useful to Cite

  1. CU1: What population evidence relates eGDR to prevalent hyperuricemia?

    The weighted Model 3 association in this NHANES sample is OR 0.83 per 1 mg/kg/min, with CI 0.81–0.85; this is not incidence reduction.

    Evidence: KF1, KF2

  2. CU2: Does the paper show a significant gout association for all higher eGDR categories?

    No. The 4–6 versus <4 contrast is nonsignificant in fully adjusted Model 3; continuous and higher-category associations require their own stated contrasts.

    Evidence: KF3

  3. CU3: How were the exposure and gout measured?

    eGDR was calculated from waist circumference, hypertension and HbA1c; gout was self-reported professional diagnosis.

    Evidence: KF4

What This Study Should Not Be Cited to Claim

  • That increasing eGDR prevents hyperuricemia or gout, or reduces future disease incidence.
  • Causal mediation by insulin resistance or benefit from an eGDR-targeted intervention.
  • A statistically significant adjusted gout association for every eGDR category.
  • Prospective prediction accuracy or a clinical treatment threshold.

Evidence Matrix

Row IDComponentContextFindingEvidence LevelScopeSource LocatorEvidence refs
evidence-kf1Both outcome analyses use the same selected cross-sectional NHANES sample.Participant counts are unweighted observations, not weighted prevalence estimates or incident cases.analytic participants: 29,340; NHANES cycles: 6 (2007–2018); hyperuricemia cases: 5,433; self-reported gout cases: 1,346Survey-weighted cross-sectional observational analysisReported prevalence-odds association or study measurement, not incident disease prediction or an intervention effect.Methods §2.1 Study design and population (sec7); §2.3 Diagnosis of HUA and gout (sec9); Tables 2 and 3 (tab2, tab3), Continuous case/participants rowsKF1
evidence-kf2Higher continuous eGDR was associated with lower adjusted odds of hyperuricemia.Model 3 weighted logistic regression; odds per 1 mg/kg/min higher eGDR. This is not a 17% reduction in incidence or an intervention effect.Model 3 odds ratio: 0.83; 95% confidence interval: 0.81–0.85; P value: <0.001Survey-weighted cross-sectional observational analysisReported prevalence-odds association or study measurement, not incident disease prediction or an intervention effect.Methods §2.2 Calculation of eGDR (sec8), §2.5 Statistical analyses (sec11); Results §3.2 (sec14); Table 2 (tab2), Continuous row, Model 3 and covariate footnoteKF2
evidence-kf3The continuous gout association was inverse, but not every categorical contrast was statistically significant after full adjustment.Table 3 Model 3 compares eGDR categories with <4 mg/kg/min. The 4–6 comparison includes the null and is explicitly described as nonsignificant in Results §3.3.continuous OR per 1 mg/kg/min: 0.83 (95% CI 0.79–0.87), P<0.001; 4–6 mg/kg/min versus <4: OR 0.81 (95% CI 0.63–1.04), P=0.093; 6–8 mg/kg/min versus <4: OR 0.62 (95% CI 0.47–0.82), P=0.001; >8 mg/kg/min versus <4: OR 0.35 (95% CI 0.25–0.48), P<0.001Survey-weighted cross-sectional observational analysisReported prevalence-odds association or study measurement, not incident disease prediction or an intervention effect.Results §3.3 Association between eGDR and gout (sec15); Table 3 (tab3), Continuous and category rows, Model 3; contrast with Abstract Results category statementKF3
evidence-kf4The exposure and outcomes were estimated or measured using distinct operational definitions.The eGDR proxy and observational outcome definitions do not directly measure a treatment response or establish a new clinical diagnostic test.eGDR equation (mg/kg/min): 21.158 − 0.09×waist circumference (cm) − 3.407×hypertension (yes=1/no=0) − 0.551×HbA1c (%); hyperuricemia thresholds: >7.0 mg/dL in males; >6.0 mg/dL in females; gout ascertainment: Self-reported professional diagnosisSurvey-weighted cross-sectional observational analysisReported prevalence-odds association or study measurement, not incident disease prediction or an intervention effect.Methods §2.2 Calculation of eGDR (sec8); §2.3 Diagnosis of HUA and gout (sec9)KF4

Q&A

How many participants and which outcomes were analyzed?

One analytic sample of 29,340 adults was used for both outcomes; Tables 2 and 3 list 5,433 hyperuricemia and 1,346 self-reported gout cases. These case counts must not be substituted for survey-weighted prevalence.

Evidence: KF1

Was every higher eGDR category significantly associated with less gout?

No. Table 3 Model 3 gives OR 0.81, 95% CI 0.63–1.04 and P=0.093 for 4–6 versus <4 mg/kg/min. Results §3.3 states this loss of significance. The abstract's broader all-category statement is not adopted.

Evidence: KF3

What did the continuous adjusted analyses report?

Per 1 mg/kg/min higher eGDR, Model 3 reports OR 0.83 (95% CI 0.81–0.85) for hyperuricemia and OR 0.83 (0.79–0.87) for gout. These are prevalence-odds associations.

Evidence: KF2, KF3

Does this demonstrate that raising eGDR will prevent disease?

No. The cross-sectional design cannot establish temporal order or a preventive intervention effect. Gout is self-reported and eGDR is a calculated proxy.

Evidence: KF1, KF4

Concepts & Entities

Conditions

hyperuricemiagout

Populations

US NHANES adults aged at least 20 years

Outcomes

prevalent hyperuricemiaself-reported gout

Methods

survey-weighted logistic regressioncross-sectional analysisestimated glucose disposal rate

Data Types

survey questionnairesserum uric acidHbA1cwaist circumference

Models & Tools

eGDR

Datasets & Cohorts

NHANES 2007–2018

Related Research

Publication & Provenance

DOI
https://doi.org/10.3389/fnut.2025.1658286
Publisher
https://doi.org/10.3389/fnut.2025.1658286
Pmc Url
https://pmc.ncbi.nlm.nih.gov/articles/PMC12501789/
PubMed
https://pubmed.ncbi.nlm.nih.gov/41064288/
PMCID
PMC12501789
Pmid
41064288
Version
Formal published article archived as PMC12501789.1; no scientific correction relation returned by the targeted Crossref metadata check on 2026-10-26. This is not an exhaustive absence-of-correction claim.
Evidence Basis
Methods §§2.1–2.5 and Results §§3.2–3.3, including text-encoded Tables 2–3. The contradictory universal category claim in Abstract Results is explicitly excluded.
Source Verification Scope
Formal Methods, Results and text-encoded tables were checked directly. No original statistical reanalysis and no source figures reproduced.
License
CC BY 4.0, as stated in article-level permissions.
Source Sha256
42d4736dac32237e52512f05e654c5d4c78deff3c9c327db465b9212c2d24ca2
Author-controlled evidence page for this publication. This page provides an evidence-oriented summary and does not replace the publisher's version of record. The explicitly disclosed inconsistent findings are excluded from the supported evidence scope.

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