# Association Between Ketogenic Diet and Overactive Bladder: The Mediating Roles of Dietary Inflammatory Index and Weight‐Adjusted Waist Index

**Authors:** Xuefeng Jin, Tong Zhang, Hao Li, Jie Wang, Shiquan Xu, Jingping Ge, Zizhi Li, Xiangrui Kong, Junlin Chen, Xuejiao Wen, Wenhui Tong, Xiaoyan Liu, Hangxu Li

PMC · DOI: 10.1002/fsn3.71587 · Food Science & Nutrition · 2026-02-24

## TL;DR

A higher ketogenic diet was linked to fewer cases of overactive bladder, possibly due to reduced inflammation and belly fat.

## Contribution

This study identifies the mediating roles of dietary inflammation and central adiposity in the relationship between ketogenic diets and overactive bladder.

## Key findings

- Each unit increase in DKR was associated with 43% lower odds of OAB.
- DII and WWI mediated 8.29% and 6.57% of the DKR-OAB association, respectively.
- Higher DKR was linked to lower OAB prevalence in U.S. adults.

## Abstract

Overactive bladder (OAB) is characterized by urinary urgency, often accompanied by increased frequency and nocturia, and is associated with impaired quality of life and substantial healthcare burden. Although ketogenic dietary patterns have been linked to weight reduction, decreased systemic inflammation, and improved metabolic profiles, their relationship with OAB remains unclear. This study aimed to examine the association between the dietary ketogenic ratio (DKR) and OAB, and to explore the potential mediating roles of the Weight‐adjusted‐waist index (WWI) and the Dietary Inflammatory Index (DII). Data were derived from 23,763 participants in the 2009–2018 National Health and Nutrition Examination Survey (NHANES), including 4991 individuals reporting OAB. Dietary intake was assessed using two 24‐h dietary recalls. DKR, DII, and WWI were calculated using validated approaches. Multivariable logistic regression, subgroup analyses, and smoothed curve fitting were performed to evaluate the association between DKR and OAB, and mediation analyses were conducted to assess indirect effects. Each unit increase in DII was associated with 11% higher odds of OAB (OR = 1.11, 95% CI: 1.06–1.16), whereas each unit increase in DKR was associated with 43% lower odds of OAB (OR = 0.57, 95% CI: 0.42–0.77). Compared with the lowest quartile, participants in the highest quartile of DKR had a significantly lower prevalence of OAB. Mediation analyses suggested that DII and WWI accounted for 8.29% and 6.57% of the association between DKR and OAB, respectively. Higher DKR was associated with a lower prevalence of OAB, and this relationship was partially mediated by dietary inflammatory potential and central adiposity. These findings highlight the potential relevance of dietary patterns in OAB prevention and warrant further prospective investigation.

Higher dietary ketogenic ratio was associated with lower prevalence of overactive bladder, partially mediated by dietary inflammation and central adiposity in U.S. adults (NHANES 2009–2018).

## Linked entities

- **Diseases:** overactive bladder (MONDO:0006624)

## Full-text entities

- **Genes:** IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, LEP (leptin) [NCBI Gene 3952] {aka LEPD, OB, OBS}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}
- **Diseases:** epilepsy (MESH:D004827), DKR (MESH:D000740), atherogenic (MESH:D050197), hypertension (MESH:D006973), gastrointestinal discomfort (MESH:D005767), LUTS (MESH:D059411), acute myocardial infarction (MESH:D009203), cardiovascular disease (MESH:D002318), IR (MESH:D007333), urinary tract infection (MESH:D014552), weight loss (MESH:D015431), hypercholesterolemic (MESH:D006938), hypercholesterolemia (MESH:D006937), adiposity (MESH:D018205), WWI (MESH:D000275), depression (MESH:D003866), coronary artery disease (MESH:D003324), nutritional ketosis (MESH:D007662), UUI (MESH:D014549), hyperlipidemia (MESH:D006949), Hyperglycemia (MESH:D006943), metabolic syndrome (MESH:D024821), Dietary Inflammatory (MESH:D007249), Diabetes (MESH:D003920), cancer (MESH:D009369), urothelial irritation (MESH:D014526), Overactive Bladder (MESH:D053201), Obesity (MESH:D009765), Overweight (MESH:D050177), Urinary dysfunction (MESH:D001745), Ischemia (MESH:D007511), fat (MESH:D004620), hypoxia (MESH:D000860), nocturia (MESH:D053158)
- **Chemicals:** LDL-C (-), carbohydrate (MESH:D002241), acetoacetate (MESH:C016635), lipid (MESH:D008055), alcohol (MESH:D000438), Short-chain fatty acids (MESH:D005232), glucose (MESH:D005947), beta-hydroxybutyrate (MESH:D020155), adenosine (MESH:D000241), sugar (MESH:D000073893), prostaglandin (MESH:D011453), triglycerides (MESH:D014280), ketone (MESH:D007659), phospholipid (MESH:D010743), cholesterol (MESH:D002784), ketone bodies (MESH:D007657)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12930284/full.md

## References

85 references — full list in the complete paper: https://tomesphere.com/paper/PMC12930284/full.md

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Source: https://tomesphere.com/paper/PMC12930284