Association of independent dietary antioxidant intake, and CDAI level with risks of all-cause and cardiovascular-cause death among population with cardiovascular disease | BMC Public Health | Full Text

Apr 09, 2025

BMC Public Health volume 25, Article number: 1327 (2025) Cite this article

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Antioxidants have been investigated for their potential to prevent cardiovascular disease (CVD); however, their association with mortality risk in patients with CVD has not been thoroughly evaluated. The aim of this study was to assess the relationship between individual antioxidants and the composite dietary antioxidant index (CDAI) with the risk of death in patients with CVD.

This study included 1,395 participants with CVD from the National Health and Nutrition Examination Survey (2001–2010). Cox proportional hazards models were employed to estimate the hazard ratios (HRs) and 95% confidence intervals （CIs） for individual antioxidants (including vitamins A, vitamins C, vitamins E, selenium, carotenoids and zinc) and CDAI levels in relation to all-cause mortality and cardiovascular death. Additionally, restricted cubic splines (RCS) were utilized to further investigate potential nonlinear relationships.

Individual antioxidants, including vitamin C and vitamin E, were inversely associated with both all-cause and CVD-cause mortality in patients with CVD. As for CDAI, compared to participants in the first tertile(T1) of CDAI, the fully adjusted HR for all-cause mortality in the third tertile (T3) was 0.62 (95% CI: 0.46, 0.85). For CVD mortality, individuals with T3 of CDAI also exhibited a significantly reduced risk, with an HR of 0. 58 (95% CI: 0. 35,0.97). RCS analysis revealed a linear relationship between CDAI and all-cause mortality, while a non-linear, inverted L-shaped relationship was observed for CVD mortality.

Higher levels of dietary antioxidants are associated with a reduced risk of both all-cause and cardiovascular-cause mortality in patients with CVD. These findings suggest that increasing antioxidant intake may serve as a potential strategy for improving outcomes in this population.

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Cardiovascular disease (CVD) is a kind of fatal diseases affecting human life and health, and has become a major public health problem of global concern. According to the global disease burden 2019, CVD accounted for nearly 18.6 million deaths globally, representing approximately 32% of all annual fatalities [1]. In Europe alone, over 6 million deaths annually are attributed to CVD [2]. The majority of these fatalities are attributed to ischemic heart disease (IHD) and stroke, both of which are closely linked to atherosclerosis [3, 4]. The pathogenesis of atherosclerosis, a hallmark of CVD progression, involves the accumulation of cholesterol and triglycerides within arterial walls, forming lipid-rich plaques that narrow vessel lumina. This process compromises blood flow, precipitating tissue ischemia, hypoxia, and eventual necrosis [5]. Central to this pathological cascade is oxidative stress, a state characterized by an imbalance between reactive oxygen species (ROS) production and the body’s antioxidant defenses [6, 7]. Excess ROS induces the oxidation of low-density lipoprotein, which leads to foam cell aggregation, lipid deposition, and the formation of atherosclerotic plaques. Furthermore, ROS can also stimulate inflammation and endothelial dysfunction, both of which represent essential stages in the progression of atherosclerosis [8]. Given the central role of oxidative stress in CVD pathogenesis, strategies to enhance antioxidant capacity maybe represent promising therapeutic avenues for mitigating disease progression and improving clinical outcomes.

Diet, as a modifiable lifestyle factor, is closely associated with the body’s antioxidant capacity and plays a significant role in the prevention and management of chronic diseases. To more comprehensively assess dietary antioxidant capacity, Wright et al. proposed the Composite Dietary Antioxidant Index (CDAI) [9, 10]. This index takes into account the contribution of various antioxidants to the body’s antioxidant capacity. CDAI has been widely accepted in many other National Health and Nutrition Examination Survey (NHANES) studies to assess the risk associated with disease [10, 11]. In terms of CVD, participants with higher levels of CDAI exhibited a lower risk of developing CHD and stroke [12, 13]. Furthermore, emerging evidence underscores the prognostic significance of CDAI in chronic disease management, including chronic kidney disease(CKD) [14], chronic obstructive pulmonary disease(COPD) [15] dyslipidemia [16], osteoarthritis [17], and hypertension [18]. Higher CDAI levels have been significantly associated with reduced all-cause mortality risk in these populations. However, despite these findings offering initial evidence for the potential role of CDAI in chronic disease management, there is still a lack of in-depth research focusing on patients with CVD. In particular, whether CDAI can provide additional protection to reduce mortality risk in patients already suffering from CVD remains unclear.

The NHANES is a nationally representative health survey that integrates questionnaire responses, clinical examinations, and laboratory data to longitudinally monitor population health trends, provided critical evidence for chronic disease research and public health policymaking. Therefore, the primary purpose of this study was to assess the association of independent dietary antioxidant intake and CDAI levels with the risk of death among patients with CVD by using data from the NHANES.

The NHANES is a nationally representative health survey conducted by the National Center for Health Statistics in the United States. The survey aims to investigate and monitor disease and health trends to providing data support for public health policy development. In this study, we included population samples from 2001 to 2010 year. The following exclusion criteria were applied: (1) age < 20(n = 24611), (2) participants lacking follow-up data(n = 1358), (3) participants with absent dietary information, and implausible energy intake (lower 500 kcal or more than 4000 kcal/d)(n = 2776), (4) participants without CVD (n = 20664), and (5) participants without information concerning conditions such as hypertension, diabetes, and other covariates(n = 1391). Finally, a total of 1,395 participants who met the aforementioned criteria were included in this study (Fig. 1).

Flow chart of sample selection from the NHANES 2001–2010 year

The CVD encompasses conditions such as coronary heart disease (CHD), congestive heart failure, heart attack, stroke, and angina. A diagnosis of CVD is made when an individual meets the criteria for one or more of these conditions. For example, CHD was identified based on the survey question: “Has a doctor or other healthcare professional ever told you that you have CHD?” Individuals who answered “yes” were classified as having CHD [12].

The NHANES employs a rigorous 24-hour dietary recall methodology to collect detailed nutritional data. During standardized interviews, participants systematically report all foods, beverages (including water), and dietary supplements consumed within the preceding 24 h. To accurately record the amount of food intake, interviewers provide participants in estimating the quantity of food using measuring cups, weighing devices, or photographs during the dietary recall process. In alignment with NHANES protocols, two non-consecutive dietary recalls were conducted for each participant, with the average of these measurements used to estimate habitual dietary intake levels.

CDAI incorporates intake of six major antioxidants (including vitamins A, vitamins C, vitamins E, selenium, carotenoids and zinc). The estimation of CDAI levels follows the calculation method proposed by Wright et al. [9]. The intake of each antioxidant was first standardized by dividing the intake of each antioxidant by its corresponding Recommended Dietary Allowance. The normalized values are then weighted and summed. The specific formula is as follows:

Xi represents the daily intake of antioxidant i (i.e. vitamins A, vitamins C, vitamins E, selenium, carotenoid, and zinc); µi represents the mean Xi of the whole cohort for antioxidant i; Si represents the standard deviation for µi.

The mortality information in the NHANES database primarily comes from the National Death Index, as well as individual follow-up and records from state and local governments. Currently, this record is available until December 31, 2019. We defined the survival time as the period from the time of follow-up to the occurrence of the death event.

In order to reduce the interference brought by confounding factors, the following variables were selected for adjustment. Demographic characteristics such as age, gender (male and female), race (Mexican American, White, Black, and other races), and educational level (less than high school, high school, and above high school). Biometric measurements (such as BMI), Other dietary intake(energy, protein, total sugars, dietary fiber, total fat, saturated fatty acids (SFAs), monounsaturated fatty acids (MUFAs), polyunsaturated fatty acids (PUFAs) and sodium), Other chronic diseases, hypertension (yes/no), diabetes (yes/no), and health behaviors including smoking status (never, former, and now), alcohol consumption ( no, mild, moderate, heavy), physical activity(low, moderate, and high intensity physical activity) [19].

Firstly, independent antioxidant intake levels (including vitamins A, C, E; selenium; carotenoids; zinc) and the CDAI were categorized into tertiles (T1: low, T2: moderate, T3: high). Baseline characteristics of the study population were stratified by tertiles of the CDAI. Categorical variables are presented as percentages (%) and compared using chi-square test, and continuous variables are expressed as mean (± standard error (SE)) and analyzed with One-way ANOVA for inter-group comparisons. Cox proportional hazards regression models were used to calculate hazard ratios (HR) and 95% confidence intervals (CI) for independent antioxidants (vitamins A, C, and E, selenium, carotenoids, and zinc) and CDAI levels, assessing their associations with all-cause mortality and CVD-cause mortality in individuals with CVD. Crude model adjusted for age, gender, race, and education. Model 1 additionally adjusted for smoking status, alcohol consumption, physical activity and BMI based on Crude Model. Model 2 additionally adjusted for diabetes, hypertension, energy intake, protein intake, total sugars intake, total fat intake, dietary fiber, dietary supplements based on Model1. Restricted cubic spline (RCS) was applied to evaluate potential non-linear associations between continuous CDAI scores and risk of death. All results were calculated using R (4.2.1) software, when P < 0.05 was considered statistically significant.

The survey-weighted characteristics of the study population, stratified by CDAI level (T1, T2, T3), are summarized in Table 1. The mean age of the population was 62.66 ± 0.48 years, and the sex distribution was 39.7% (n = 521) for females and 60.3% (n = 874) for males. No significant differences were observed in age, BMI, hypertension, diabetes, smoking status, and physical activity among the three groups. When comparing CDAI components between the three groups, individuals with the highest score of CDAI had significantly higher intakes of vitamins A, C, E, carotenoids, and zinc than those with the lowest. A similar pattern was observed in energy and macronutrient intakes, T3 group also having significantly higher intakes of energy, protein, total sugars, dietary fiber, total fat, SFAs, MUFAs, PUFAs, and sodium (P < 0.0001 for all). In addition, we observed a trend of decrease in the proportion of death, as CDAI levels rose. The mortality rate in T1 group was 48.22%, which was significantly higher than that in T3 group (35.38%) (P = 0.006).

During the follow-up period, a total of 682 deaths were observed in the overall population, including 277 deaths due to CVD, with accounting for 40.6% of them. Table 2 displays the association between independent dietary antioxidant intake, and CDAI levels and the risk of all-cause death. In terms of independent dietary antioxidant intake, the T3 of vitamin C (HR = 0.73(95% CI: 0.59,0.91)), vitamin E (HR = 0.68(95% CI: 0.53,0.87)), and carotenoids (HR = 0.78(95% CI: 0.63,0.95)) intakes were negatively associated with all-cause mortality in fully adjusted model. In terms of CDAI level, those individuals in T3 of CDAI also had a decreased risk of all-cause mortality than those in the lower tertiles in all models. Taking the T1 of CDAI as reference, the HRs for all-cause mortality after multivariable adjustment were 0.62(95% CI: 0.46,0.85) for T3 (P for trend < 0.01) in fully adjusted model. The RCS analysis further indicated a negative, linear relationship between CDAI and all-cause mortality (Fig. 2A).

RCS of Association of CDAI level with risks of all-cause and CVD-cause death. (A) all-cause death; (B) CVD-cause death (CDAI = composite dietary antioxidant index, RCS: restricted cubic spline; CVD = cardiovascular disease)

A similar pattern was observed in the risk of cardiovascular-cause death (Table 3). In terms of independent dietary antioxidant intake, only the highest T3 of vitamin E (HR = 0.59(95% CI:0.39,0.89)), Zinc (HR = 0.64(95% CI:0.42,0.96)), and T2 of vitamin C (HR = 0.58(95% CI:0.41,0.84)) intakes were still negatively associated with CVD-cause mortality in fully adjusted model. The T3 of CDAI levels also showed a protective association with CVD-cause mortality across all models. In fully adjusted model, compared with T1 of CDAI, the HRs for CVD-cause mortality was 0.58(95% CI: (0.35,0.97) for T3. The RCS analysis revealed a negative non-linear relationship between CDAI and CVD-cause mortality (Fig. 2B).

To assess the robustness of our findings, we conducted subgroup analyses stratified by key demographic and clinical variables. We further stratified the population by gender, age, race, education level, hypertension, diabetes, alcohol consumption, smoking status, and dietary supplements. The inverse associations between the T3 of CDAI and reduced risks of all-cause mortality and CVD-cause mortality remained consistent across most subgroups (Supplementary Tables 1 and Supplementary Table 2). Additionally, no significant interactions were observed between these stratification variables (all P for interaction > 0.05).

In this study, we investigated the association between intake of independent antioxidants, CDAI levels, and the risk of all-cause and CVD-cause death among patients with CVD. This study has demonstrated that increasing intake of partial antioxidant intake and elevating CDAI levels are linked to a reduced risk of both all-cause and CVD-cause mortality. These findings emphasize the critical preventive role of enhancing the body’s antioxidant capacity in the management of patients with CVD.

Some observational and experimental studies have shown that supplementation of antioxidants can reduce inflammation, oxidative stress levels, improve endothelial dysfunction [20], such as beta-carotene [21], vitamin C [22], vitamin E [23], and selenium [24]. This study revealed that higher intakes of vitamin C, vitamin E, and Zinc were associated with a reduced risk of mortality in patients with CVD. Both vitamins C and E are powerful antioxidants that protect cells from oxidative damage, vitamin C reduces the oxidation of LDL cholesterol by directly trapping free radicals [25], while vitamin E also maintains blood vessel health by protecting lipids from excessive oxidation [26]. Zinc, an essential micronutrient, critically preserves endothelial integrity through its dual roles as an antioxidant and membrane stabilizer, while also modulating NO signaling pathways to support vascular homeostasis [27]. Within the context of daily dietary intake, the consumption levels of these antioxidants are significantly interrelated. Therefore, we introduced the CDAI to assess the combined effects of these dietary antioxidants. Wang, et al. found that high CDAI levels can reduce the risk of all-cause mortality and cardiovascular death in the general population [11]. This finding not only provides strong evidence for the prognostic value of CDAI in the general population, but has also been further validated in patients with chronic diseases [14,15,16,17,18]. Patients with CVD often have multiple medical conditions, such as hypertension, dyslipidemia, and CKD, which not only complicate disease management, but also significantly increase the risk of poor outcomes. Our further analysis of this particular population showed that higher levels of CDAI were consistently associated with a significantly reduced risk of death. This finding not only confirms the protective effect of CDAI in patients with a single disease, but also further reveals its potential protective effect in patients with CVD. The protective effect of CDAI may be closely related to its regulation of inflammation and oxidative stress. Previous study evaluated the association between the CDAI and common inflammatory markers, and found a negative correlation between CDAI levels and the levels of IL-1β and TNF-α [28]. And other study also shown an inverse correlation between CDAI levels and the thickness of the carotid lining in women [29]. Carotid intimal thickness is an early morphological change in atherosclerosis and an early marker of systemic atherosclerosis. Therefore, our findings provide further evidence that the protective effects of an antioxidant-rich diet extend beyond early disease prevention and can also improve outcomes in patients with CVD. This is significant because CVD remain a leading cause of death globally, and diet is an easily modifiable risk factor.

Through subgroup analysis and interaction testing, this study explored the impact of CDAI on the mortality risk across different subgroups, further confirming the robustness and applicability of the research findings. However, we observed that the response to the CDAI effect was weaker among individuals who consumed alcohol or smoked. This phenomenon may be related to the following mechanisms: smoking/alcohol use may interfere with the absorption and metabolism of antioxidants in the body, thereby weakening the protective health effects of dietary intake of antioxidant components [30, 31]. Secondly, smoking, as a potent source of oxidative stress, leads to a significant increase in free radicals. Although CDAI may reduce oxidative stress, in smokers, this protective effect may be overshadowed by the intense oxidative stress induced by smoking, resulting in a diminished effect of CDAI. This finding suggests that alcohol consumption and smoking may interfere with antioxidant mechanisms, affecting the protective role of CDAI in mortality risk. Future research could further investigate the interaction mechanisms between these factors and CDAI, and evaluate whether intervention measures (such as smoking cessation or alcohol limitation) could enhance the health benefits of CDAI in these populations.

The strength of this study is that it is the first to investigate the association between CDAI and the risk of all-cause and cardiovascular-cause mortality in patients with CVD within the U.S. population. Thanks to the high-quality data provided by NHANES, our study has national representativeness. However, this study also has certain limitations. Participants’ dietary habits may be adjusted with changes in health awareness, and the dietary survey data used in the study may not fully represent participants’ long-term dietary consumption patterns. Due to limitations in some of the data, the study was unable to include detailed information on drug use and did not adequately consider specific doses of dietary supplements. Finally, the use of cross-sectional data limits the ability to assess long-term effects or changes in antioxidant intake over time. In the future, clinical trials or intervention studies could provide more direct evidence of the benefits of increasing antioxidant intake on reducing mortality risk.

In conclusion, our study supports the idea that increasing dietary antioxidants, as quantified by the CDAI, may be a promising strategy for reducing the risk of both all-cause mortality and CVD-cause death among patients with CVD. Given the ease of incorporating antioxidant-rich foods into daily diets, this approach could have important public health implications, particularly for individuals at high risk for CVD.

The datasets utilized in this study are publicly available and can be accessed at the National Health and Nutrition Examination Surveys database (https://www.cdc.gov/nchs/nhanes).

Cardiovascular disease

Ischemic heart disease

Reactive oxygen species

Composite dietary antioxidant index

National Health and Nutrition Examination Survey

Chronic kidney disease

Chronic obstructive pulmonary disease

Coronary heart disease

Saturated fatty acids

Monounsaturated fatty acids

Polyunsaturated fatty acids

Body Mass Index

Standard error

Hazard ratios

Confidence intervals

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Gratitude is extended to all participants and investigators involved in the National Health and Nutrition Examination Surveys for their invaluable contributions to the study.

This study was financially supported by the Henan Provincial medical and health service capacity improvement project (peripheral vascular intervention center specialist construction project) (No. p62024006 and ky2023005).

Department of Vascular Surgery, The Fifth Affiliated Hospital of Zhengzhou University, No. 3 Kangfuqian Street, Erqi District, Zhengzhou, Henan, China

Xintao Hu, Zhao Zhao, Qian An, Yang Li & Bing Wang

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(I) Conception and design: Xintao Hu, and Zhao Zhao; (II) Administrative support: Bing Wang; (III) Provision of study materials: Bing Wang; (IV) Collection and assembly of data: Xintao Hu, Zhao Zhao, and Qian An; (V) Data analysis and interpretation: Xintao Hu, and Zhao Zhao; (VI) Manuscript writing: Xintao Hu, and Zhao Zhao; (VII) Final approval of manuscript: All authors.

Correspondence to Bing Wang.

The NHANES study has received informed consent approval from the NCHS Institutional Review Board. Our analysis uses publicly available NHANES data and does not require additional institutional review board review.

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Hu, X., Zhao, Z., An, Q. et al. Association of independent dietary antioxidant intake, and CDAI level with risks of all-cause and cardiovascular-cause death among population with cardiovascular disease. BMC Public Health 25, 1327 (2025). https://doi.org/10.1186/s12889-025-22481-1

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Received: 30 January 2025

Accepted: 25 March 2025

Published: 09 April 2025

DOI: https://doi.org/10.1186/s12889-025-22481-1

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