# The impact of dietary inflammation index on benign prostatic hyperplasia: insights from patient data and animal models

## TL;DR

This study shows that pro-inflammatory diets may cause benign prostatic hyperplasia through systemic and local inflammation, while anti-inflammatory diets may help prevent it.

## Contribution

The study provides causal evidence linking dietary inflammation to BPH using population data, genetic analysis, and animal experiments.

## Key findings

- Higher dietary inflammation index scores were associated with increased BPH risk in human data.
- Anti-inflammatory diets reduced prostate inflammation and preserved glandular structure in rats.
- Genetic analysis confirmed a causal link between anti-inflammatory diets and lower BPH risk.

## Abstract

Benign prostatic hyperplasia (BPH) is a common chronic condition among elderly males, typically manifesting as lower urinary tract symptoms (LUTS), including increased urinary frequency, urgency, nocturia, urinary stream splitting, and dysuria. Previous reports have indicated a potential association between dietary habits and BPH; however, the specific causal relationship between dietary factors and prostatic hyperplasia remains unclear. Therefore, this study aimed to investigate the potential causal relationship between the dietary inflammation index (DII) and BPH through a cross-sectional cohort analysis, two-sample Mendelian randomization (TS-MR), and complementary animal experiments.

DII and BPH were defined using data from the National Health and Nutrition Examination Survey (NHANES), and their association was investigated. We then used TS-MR to screen nine dietary preferences and evaluate their causal effects on BPH risk. To validate these findings, we conducted external dietary interventions on rats according to three dietary patterns (baseline diet group, pro-inflammatory diet group, and anti-inflammatory diet group) to modulate dietary preferences, and assessed prostatic hyperplasia as well as systemic and local inflammation in the rats using H&E, Masson, and IHC staining, and ELISA assays.

Higher DII scores were significantly associated with increased BPH risk (fully adjusted OR = 1.07, 95% CI: 1.03–1.12, P < 0.001), with a primarily linear dose–response relationship. MR analysis revealed that genetically predicted anti-inflammatory diet was inversely associated with BPH risk (OR = 0.80, 95% CI: 0.66–0.98, P = 0.034), providing genetic evidence of causality. In vivo, rats on a pro-inflammatory diet exhibited a significantly elevated prostate index, pronounced epithelial hyperplasia, and increased collagen deposition, along with higher serum levels of IL-6, TNF-α, and IL-1β. Conversely, anti-inflammatory diets mitigated these effects, preserving normal glandular architecture and reducing inflammatory marker expression. Collectively, these findings demonstrate that pro-inflammatory dietary patterns promote benign prostatic enlargement and inflammation both systemically and locally.

Our integrated population-based, genetic, and experimental evidence supports a causal role of dietary inflammatory load in the development of BPH. Chronic consumption of pro-inflammatory diets may promote BPH through sustained systemic and prostate-specific inflammation, while anti-inflammatory dietary patterns may confer protective effects. These findings highlight the potential of dietary modulation as a preventive and therapeutic strategy for BPH management.