# Association of composite dietary antioxidant index with incidence and mortality of aortic aneurysm and dissection: insights from the UK Biobank

**Authors:** Shengwei Lai, Handai Qin, Minghao Liu, Zhiwei Lai, Shuaifei Ji, Dan Rong, Wei Guo

PMC · DOI: 10.3389/fnut.2026.1713690 · Frontiers in Nutrition · 2026-02-13

## TL;DR

Higher dietary antioxidant intake is linked to lower risk and mortality from aortic aneurysm and dissection, according to a study of over 170,000 people.

## Contribution

This study is the first to show a link between the composite dietary antioxidant index and aortic aneurysm and dissection outcomes.

## Key findings

- Higher CDAI scores were associated with a 7% lower risk of developing aortic aneurysm and dissection.
- Participants with the highest CDAI had a 17% lower risk of mortality from aortic aneurysm and dissection.
- Metabolic indicators like uric acid and CRP partially explained the protective effect of dietary antioxidants.

## Abstract

The composite dietary antioxidant index (CDAI) is a scoring system designed to assess overall dietary antioxidant capacity and has been associated with a reduced risk of cardiovascular diseases. However, its specific impact on aortic aneurysm and dissection (AA/AD) remains unclear. This study aimed to investigate the associations of CDAI with both the incidence and mortality of AA/AD.

In this UK Biobank-based study, univariate and multivariate logistic regression models were used to assess the association between CDAI and the incidence of AA/AD, the association of CDAI with mortality was evaluated using Cox proportional hazards models. We employed restricted cubic spline (RCS) analyses to examine potential linear or non-linear relationships between the key nutrient components of the CDAI and the outcomes. Furthermore, mediation analysis was performed to assess the potential mediating effects of selected metabolic indicators.

A total of 172,450 participants were included in this study, of whom 1,486 developed AA/AD. Univariate logistic regression analysis revealed a significant inverse association between CDAI and the incidence of AA/AD (OR = 0.93, 95% CI: 0.88–0.99, p = 0.024). A significantly lower risk of AA/AD mortality was observed in participants within the highest quartile of CDAI compared to those in the lowest quartile (HR = 0.83, 95% CI: 0.71–0.96, p = 0.018), based on the Cox regression analysis. RCS analysis indicated a linear relationship between CDAI and the mortality of AA/AD (P for overall < 0.001; P for nonlinear > 0.05). Furthermore, mediation analysis suggested that uric acid, neutrophil-to-lymphocyte ratio (NLR), C-reactive protein (CRP), and high-density lipoprotein cholesterol (HDL-C) mediated the association between CDAI and AA/AD incidence.

This study supports the pathogenic role of oxidative stress and inflammation in AA/AD, demonstrating that a higher CDAI is associated with lower incidence and mortality of AA/AD in a UK-based adult population. These findings provide new insights, suggesting that dietary antioxidant intervention could serve as a potential preventive strategy against these conditions.

## Full-text entities

- **Genes:** IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, AGT (angiotensinogen) [NCBI Gene 183] {aka ANHU, SERPINA8, hFLT1}, CDAN1 (codanin 1) [NCBI Gene 146059] {aka CDA1, CDAI, CDAN1A, DLT, PRO1295}, ALDH2 (aldehyde dehydrogenase 2 family member) [NCBI Gene 217] {aka ALDH-E2, ALDHI, ALDM}, PRDX5 (peroxiredoxin 5) [NCBI Gene 25824] {aka ACR1, AOEB166, B166, HEL-S-55, PLP, PMP20}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, IL10 (interleukin 10) [NCBI Gene 3586] {aka CSIF, GVHDS, IL-10, IL10A, TGIF}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, SOD2 (superoxide dismutase 2) [NCBI Gene 6648] {aka GC1, GClnc1, IPO-B, IPOB, MNSOD, MVCD6}
- **Diseases:** death (MESH:D003643), hypertension (MESH:D006973), AA (MESH:C566236), AAA (MESH:D017544), vascular endothelial injury (MESH:D057772), dilation of the aorta (MESH:D002311), cardiovascular conditions (MESH:D002318), Cardiovascular-kidney-metabolic syndrome (MESH:D007674), hypertriglyceridemia (MESH:D015228), coronary heart disease (MESH:D003327), liver disease (MESH:D008107), inflammation (MESH:D007249), TAA (MESH:D017545), aortic diseases (MESH:D001018), hyperlipidemia (MESH:D006949), NLR (MESH:D015467), Aortic aneurysm (MESH:D001014), aortic rupture (MESH:D001019), aneurysm (MESH:D000783), lung cancer (MESH:D008175), aortic syndromes (MESH:D000094683), AD (MESH:D000544), cancer (MESH:D009369), AA/AD (MESH:D000784), rupture (MESH:D012421), diabetes (MESH:D003920), overweight (MESH:D050177), obese (MESH:D009765)
- **Chemicals:** TG (MESH:D013866), O2- (MESH:D013481), AA (-), H2O2 (MESH:D006861), Selenium (MESH:D012643), peroxides (MESH:D010545), lipid (MESH:D008055), beta-carotene (MESH:D019207), -OH (MESH:C031356), ROS (MESH:D017382), alcohol (MESH:D000438), sugar (MESH:D000073893), Zinc (MESH:D015032), triglycerides (MESH:D014280), polyacrylamide (MESH:C016679), Vitamin E (MESH:D014810), uric acid (MESH:D014527), dehydroascorbic acid (MESH:D003683), vitamin A (MESH:D014801), Vitamin C (MESH:D001205)
- **Species:** Homo sapiens (human, species) [taxon 9606], Mus musculus (house mouse, species) [taxon 10090]

## Full text

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## Figures

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## References

32 references — full list in the complete paper: https://tomesphere.com/paper/PMC12945778/full.md

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Source: https://tomesphere.com/paper/PMC12945778