Association between single and multiple dietary vitamin exposure and heart failure risk: a cross-sectional study

Introduction

Heart failure (HF) is a common cardiovascular disease caused by cardiac insufficiency. Its morbidity and mortality are on the rise worldwide (1,2), making it a significant public health concern. HF not only exerts a significant impact on the quality of life (QOL) of patients, but also puts a heavy load on the healthcare system and represents a significant risk to patients’ longevity.

In recent years, nutrients have been widely used to prevent cardiovascular diseases. There have been several studies showing that micronutrients play a key role in the onset and progression of HF, particularly with regard to dietary vitamin intake (3-5). The primary mechanisms through which vitamins prevent cardiovascular disease include anti-inflammatory, antioxidant, improving lipid levels, improving endothelial dysfunction, and decreasing homocysteine and oxidative stress levels (4,5). Numerous studies (6-12) have been conducted on the effect of single dietary vitamins to date. For instance, vitamin K prevents vascular calcification by regulating calcium homeostasis (6); vitamin C, as an antioxidant, helps maintain normal cellular metabolic functions and regenerate other cellular antioxidants, thereby reducing oxidative stress responses in cardiomyocytes (7,8); a previous study (9) has demonstrated that vitamin D deficiency induces endothelial dysfunction and accelerates ventricular remodeling, potentially contributing to the development of HF. Vitamin B deficiency results in adverse effects such as cardiac hypertrophy, reduced cardiac contractility, and arrhythmia (10); in addition, vitamin A has been demonstrated to inhibit the production of pro-inflammatory cytokines. In a related study by Wang et al. (11), the potential association of vitamin A intake with the risk of depression in HF patients was explored. A large-sample study based on the National Health and Nutrition Examination Survey (NHANES) showed that vitamin D deficiency was strongly correlated with cardiovascular disease risk, and maintaining optimal vitamin D levels could reduce such risk (12).

Although many studies (6-12) have examined the potential benefits of a single vitamin on cardiovascular health, real-life dietary patterns often involve the simultaneous intake of multiple vitamins. The combined effects, including synergistic effects and interactions, still require further investigation. Therefore, there is a need to investigate how single and multiple vitamin exposures affect HF risk in order to develop effective prevention strategies and improve patient health management.

This study aimed to utilize data from individuals aged 18 years and older in the NHANES database to comprehensively assess the potential association of single and multiple dietary vitamin exposure with HF risk. The results will provide certain dietary reference opinions and a theoretical basis for the prevention and intervention of HF. We present this article in accordance with the STROBE reporting checklist (available at https://jtd.amegroups.com/article/view/10.21037/jtd-2025-86/rc).

Methods

Study subjects

The data in the current cross-sectional observational study were collected from the NHANES database between 2009 and 2014 (https://wwwn.cdc.gov/nchs/nhanes/default.aspx). The Research Ethics Review Board of the National Centers for Health Statistics approved the study protocol, and written informed consent forms (ICFs) were obtained from all subjects during the recruitment period. This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The following subjects were eligible for this study: (I) subjects aged 18 years or above; (II) subjects with complete information on vitamin intake; (III) subjects with complete information on HF status; and (IV) subjects with complete data on all other covariates. The following subjects were ineligible for this study: (I) pregnant or lactating women; and (II) subjects with missing information on vitamin intake, HF status, and covariates. Finally, 13,025 subjects were enrolled in accordance with the eligibility criteria (Figure 1).

Figure 1 Flow chart for the selection of participants in the study. NHANES, National Health and Nutrition Examination Survey.

Dietary vitamin intake

The dietary data in the NHANES database were derived from the collection and estimation of each subject’s dietary consumption of nutrients, energy, and other food components over the 24 h preceding the interview. The intake of eight dietary vitamins (A, C, D, K, B6, B12, B1 and B2) in this study was calculated as the sum of the daily intake of dietary vitamins and dietary supplements from the 24-hour dietary recall interview conducted on the first day. The data were then divided into two categories in line with the weighted median of the total intake of each dietary vitamin, with the lower quantile category serving as the reference.

Diagnosis of HF

The presence of self-reported HF was confirmed when participants gave a “Yes” answer to the question (MCQ160B) in the questionnaire (MCQ_F): Have you ever received a diagnosis of congestive HF from a physician or other healthcare provider?

Covariates

The covariates considered in this study consisted of age, gender (male or female), body mass index (BMI) (kg/m²), ratio of family income to poverty (PIR), marital status, education level, race, smoking status, drinking status, diabetes mellitus (DM) status, and hypertension status. The race category included Mexican American, non-Hispanic black, non-Hispanic white, and other races. The education level was divided into four levels: less than high school, high school graduate/General Educational Development (GED) or equivalent, some college or associates (AA) degree, and junior college degree and above. The marital status included married/living with a partner, widowed/divorced/separated/unmarried. The PIR category reflected the ratio of family income to poverty, with lower values indicating greater poverty, and it was categorized into three levels: <1, 1–3, and ≥4. The BMI was categorized into three levels: <25 kg/m² (underweight/normal), 25–30 kg/m² (overweight), and >30 kg/m² (obese). A subject was defined as a smoker if he/she smoked at least one hundred cigarettes in his or her lifetime. Similarly, a subject who consumed at least 12 alcoholic beverages per year was defined as an alcoholic drinker. Furthermore, subjects who self-reported a diagnosis of DM or a history of medication, or a laboratory test of fasting blood glucose ≥126 mg/dL, or glycosylated hemoglobin (HbA1c) ≥6.5%, or the oral glucose tolerance test (OGTT) result ≥200 mg/dL were considered diabetic. Hypertension was determined based on the subjects’ self-report.

Statistical analysis

Considering the intricate survey design of the NHANES database, survey weights were utilized in this study throughout the analytical process, with the weighted variables being WTDRD1, SDMVSTRA, and SDMVPSU. To determine the normal distribution of measured data, Kolmogorov-Smirnov test was adopted. Data consistent with the normal distribution were presented as mean ± standard deviation (SD). The weighted independent sample t-test was utilized for intergroup comparison. Data inconsistent with the normal distribution were presented as median (interquartile range). A weighted rank-sum test was applied for intergroup comparison. Count information was expressed as the number of unweighted instances (weighted percentage). A weighted Chi-squared test/Fisher’s exact probability method was employed for intergroup comparison. The association of the consumption of each dietary vitamin with HF risk was assessed using three distinct weighted logistic regression models separately, i.e., Model 1 (no adjustment), Model 2 [adjustment of basic demographic characteristics (age, gender, PIR, marital status, education level, and race)], and Model 3 [adjustment of all covariates (age, gender, BMI, PIR, marital status, race, education level, smoking status, drinking status, DM status, and hypertension status)]. To clarify the dose-response relationship (linear or nonlinear) between eight dietary vitamins intake and HF risk, four nodes were set up at the 5th, 35th, 65th, and 95th percentile of the distribution of vitamins A, C, D, K, B6, B12, B1 and B2. The restricted cubic spline (RCS) analysis was performed based on the fully adjusted model. Furthermore, the correlation coefficients were calculated among the eight dietary vitamins via Pearson correlation analysis. The combined effect of co-exposure to the eight dietary vitamins was assessed via a weighted quantile sum (WQS) model, calculating a WQS index (range [0, 1]) according to the weighted sum of intake of each dietary vitamin. The weight assigned to each vitamin in the WQS index represented the degree of its contribution to the overall effect. Additionally, this study performed subgroup analyses stratified by gender (male and female) and excluded participants with missing data on dietary supplement use in sensitivity analyses, thereby further exploring the potential association between dietary supplements and HF. All statistical analyses in this study were carried out by R version 4.4.1. A statistical significance was considered as a two-sided P value of less than 0.05.

Results

Baseline information

This study utilized data from 13,025 subjects in the NHANES database, collected between 2009 and 2014. Baseline characteristics of subjects are presented in Table 1. Most subjects were non-Hispanic white, and 402 subjects had HF. The median age was 48 (interquartile range, 33–60) years. There were notable discrepancies between the HF and non-HF groups in age, BMI, PIR, education level, race, drinking status, smoking status, and DM status/hypertension status (all P<0.05). In addition, the HF group had lower intakes of vitamin A, vitamin K, vitamin B6, vitamin B1 and vitamin B2 compared to the non-HF group (P<0.05).

Single dietary vitamin exposure and HF

The correlation between single dietary vitamin exposure and HF risk was assessed via the weighted logistic regression model, as illustrated in Table 2. In the three models, high levels of vitamin A [odds ratio (OR): 0.745, 95% confidence interval (CI): 0.570–0.973 for Model 1; OR: 0.707 (95% CI: 0.521–0.958) for Model 2; OR: 0.75 (95% CI: 0.565–0.997) for Model 3; all P<0.05], vitamin K [OR: 0.659 (95% CI: 0.503–0.862) for Model 1; OR: 0.685 (95% CI: 0.516–0.909) for Model 2; OR: 0.702 (95% CI: 0.523–0.942) for Model 3; all P<0.05], vitamin B1 [OR: 0.702 (95% CI: 0.525–0.937) for Model 1; OR: 0.675 (95% CI: 0.493–0.924) for Model 2; OR: 0.680 (95% CI: 0.489–0.946) for Model 3; all P<0.05], vitamin B2 [OR: 0.704 (95% CI: 0.541–0.915) for Model 1; OR: 0.641 (95% CI: 0.474–0.866) for Model 2; OR: 0.673 (95% CI: 0.490–0.925) for Model 3; all P<0.05] were all significantly negatively correlated with HF risk, indicating that this correlation was relatively stable. In Model 1 with no covariates adjusted, the association of vitamins D and B12 with HF risk was not observed, whereas in Model 2 and Model 3 with covariates adjusted, vitamin D [OR: 0.692 (95% CI: 0.519–0.923) for Model 2; OR: 0.715 (95% CI: 0.535–0.955) for Model 3; all P<0.05] and vitamin B12 [OR: 0.670 (95% CI: 0.513–0.875) for Model 2; OR: 0.703 (95% CI: 0.533–0.927) for Model 3; all P<0.05] showed a significant effect on HF, and the HF risk decreased as the consumption of vitamins D and B12 increased. Both Model 1 and Model 2 exhibited an obvious association of vitamin B6 with HF risk [OR: 0.714 (95% CI: 0.536–0.952) for Model 1; OR: 0.695 (95% CI: 0.507–0.952) for Model 2], and this association was not observed (P>0.05) in Model 3. In particular, vitamin C did not show a correlation with HF risk in any of the three models (all P>0.05).

Additionally, the dose-response relationship between vitamins A, C, D, K, B6, B12, B1, B2 and HF risk was assessed by the RCS model with all covariates adjusted, as presented in Figure 2. A linear relationship between vitamins K, B6, B1, B2, and HF was observed in the results (P for nonlinear >0.05, P for overall <0.05), and the HF risk decreased with increasing intake of the above four vitamins.

Figure 2 Associations between eight vitamins and HF were evaluated by RCS. CI, confidence interval; HF, heart failure; OR, odds ratio; RCS, restricted cubic spline.

Multiple dietary vitamin exposure and HF

The Pearson correlation coefficients between the intakes of eight dietary vitamins are presented in Figure 3 (the correlation coefficient r ranged from 0.22 to 0.85), with a notable positive association between vitamins B1 and B2 (r=0.85, all P<0.001). Based on the fully adjusted model, the combined effect of multiple dietary vitamin exposures on HF was estimated by fitting a WQS regression model. The results, as shown in Table 3, demonstrated that the WQS index was markedly negatively correlated with HF (OR: 0.760, 95% CI: 0.643–0.898, P=0.001), and the HF risk was reduced by 24% for every mixed-quartile increase in dietary vitamin intake. In addition, the weighting of each dietary vitamin in the WQS index was calculated in this study, as shown in Figure 4. In the fully adjusted model, vitamin A contributed the most to the WQS index, and the weighting distribution revealed that vitamin A was the most heavily weighted (0.329), followed by vitamin B1 (0.289) and vitamin B12 (0.141); vitamin B2 and vitamin B6 were less heavily weighted (0.014 and 0.001, respectively).

Figure 3 The correlation of the eight vitamins. ***, P<0.001.

Figure 4 The weights of the Weighted Quantile Sum (WQS) index between the mixture of eight vitamins. The dashed red lines represent the cutoff to discriminate which element has a significant weight.

Sensitivity analysis

In the sensitivity analysis, this study further explored whether the association between vitamin intake and HF risk varied by gender within different gender-stratified subgroups. While significant associations between dietary vitamin intake (excluding vitamins C and B1) and HF risk were observed in the female subgroup (all P<0.05), no significant associations were found in the male subgroup. However, interaction analysis revealed no statistically significant interaction between gender and dietary vitamin intake on HF risk (all P for interaction >0.05), as shown in Table S1. This suggests that the significant associations observed in the female subgroup may not be driven by gender itself, and further study is needed to explore the underlying factors.

To assess the robustness of the association between dietary supplement intake and HF, an analysis was conducted excluding participants with missing data on dietary supplement use, resulting in a final sample size of 2,320. In the unadjusted model, higher intake of vitamin B12 supplements was associated with an increased prevalence of HF (OR: 2.175, 95% CI: 1.116, 4.237, P=0.02). However, this association attenuated and became non-significant after adjusting for covariates (Table S2). Across all three weighted logistic regression models, dietary vitamin B1 supplement intake showed a consistently significant inverse association with HF, consistent with our primary findings. No other dietary supplements showed statistically significant associations with HF.

Discussion

Multivitamin supplementation has been demonstrated to decrease the likelihood of cardiovascular disease occurrences (13). In this study, the correlation between single and multiple dietary vitamin exposures and HF risk was examined via weighted logistic regression, RCS analysis, and WQS regression model based on sample data from the NHANES database for three cycles from 2009 to 2014. The weighted logistic regression model with three covariates adjusted showed a significant inverse association of dietary vitamins A, K, B1 and B2 with HF risk. Further RCS analyses revealed a negative dose-response relationship between vitamins K, B6, B1 and B2 and HF. Moreover, the mixture of eight dietary vitamins showed a negative combined effect on HF risk, with vitamin A contributing the most to the correlation between the mixture of eight dietary vitamins and HF.

However, there is some controversy regarding the correlation between vitamin A and cardiovascular disease risk. For example, Vijver et al. (14) observed that a small proportion of HF patients presented with either excessively high or low vitamin A levels, suggesting that elevated vitamin A in HF patients may reflect an increased demand for nutritional antioxidants. Nevertheless, there is currently no evidence to support the efficacy of vitamin A supplementation in HF patients. Another Mendelian randomization study showed that the causality between circulating vitamin A levels and HF was unclear (4). The current study suggested that increased consumption of vitamin A was a protective factor against HF risk. Previous clinical studies confirmed that vitamin A and its derivatives played an important role in many aspects of cardiac metabolic regulation, including adipose tissue biology, hepatic steatosis, and atherosclerosis (15,16). Additionally, vitamin A deficiency contributed to the occurrence of obesity and related diseases, which caused oxidative stress and inflammatory processes that promoted the development of cardiovascular disease (17,18). This study revealed a notable negative linear association of vitamin K with HF risk, i.e., it helped to reduce HF risk. Some studies reported that vitamin K inhibited the progression of vascular calcification through activation of matrix vitronectin, and its inadequate intake might be correlated with an elevated risk of several cardiovascular diseases, such as atherosclerosis (19). Nevertheless, the association of vitamin K consumption with HF has not yet been adequately investigated and confirmed. This study assessed only the results of the recall interview for dietary vitamin intake of subjects within 24 h before the first day, which might have resulted in an overestimation of the impact of vitamin content on HF.

The lack of vitamin D promotes oxidative stress, systemic inflammation, cardiac hypertrophy and myocardial fibrosis, and it is strongly correlated with the presence of cardiovascular diseases such as HF and atrial fibrillation (20-22). This study demonstrated a negative association of high levels of vitamin D intake with HF after controlling all potential confounders, and these results aligned with those previously reported in a study by Pál et al. (23), which showed a U-shaped correlation between vitamin D concentration and cardiovascular health. This might be due to vitamin D’s capacity to maintain the homeostasis of the extracellular matrix of cardiomyocytes and to promote and protect cardiovascular health by modulating immune and inflammatory functions (8). B vitamins play a key role in energy production as cofactors, and their deficiency might lead to reduced energy storage as well as disease development (5,24). A study has indicated that maintaining adequate serum vitamin B1 levels may be effective in preventing adverse outcomes in HF patients (25), and vitamin B6 has been shown to reduce HF risk by inhibiting phenotypic changes in cardiac macrophages (26). The association of vitamins B6 and B12 with HF risk in the current study showed unstable results in models adjusted for different covariates. This might be due to a certain correlation between the two. Further exploration of the potential mechanisms of the correlation is still needed.

Given the diversity of nutrients in daily diet, this study employed WQS regression to explore the overall effect of a mixture of eight dietary vitamins on HF risk. The results demonstrated that the mixture exhibited a notable negative combined effect on HF risk, and specifically, vitamin A played the most important role. Vitamin A is available only through dietary sources and cannot be synthesized by the human body (27), and lifestyle and food consumption affect its concentration in serum, while excessive intake of vitamin A can also lead to serious consequences such as elevated blood calcium levels, increased intracranial pressure, and liver fibrosis (28). Therefore, moderate intake of vitamin A-rich foods in daily life can be effective in preventing HF, such as animal liver, dark-colored vegetables, and fruits, etc., and daily diets should be kept diversified so as to effectively reduce the risk of nutritional deficiencies or excess and to ensure a balanced intake of all types of nutrients (3), thereby promoting overall health.

There are certain limitations in this study. First, a clear causality could not possible to be established between dietary vitamins and HF risk because of the cross-sectional design. Second, the dietary vitamin intake was based on a 24-hour diet recall interview with subjects, which might have introduced recall bias. Finally, the NHANES database is comprised primarily of data from the U.S. population, which may have an impact on the extrapolation of the results. Future studies should further investigate the potential influence of socioeconomic factors, hormone levels, and metabolic differences on the association between dietary vitamin intake and HF, to gain a more complete understanding of their effects on cardiovascular well-being.

Conclusions

In conclusion, the results of this study demonstrated a statistically significant negative association between dietary vitamins A, K, B1 and B2 intake and HF risk. RCS analyses revealed a negative dose-response relationship between vitamin K, B6, B1 and B2 intake and HF. The combined exposure of eight dietary vitamins also showed a negative effect on HF risk, with vitamin A contributing the most to the combined effect.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://jtd.amegroups.com/article/view/10.21037/jtd-2025-86/rc

Peer Review File: Available at https://jtd.amegroups.com/article/view/10.21037/jtd-2025-86/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://jtd.amegroups.com/article/view/10.21037/jtd-2025-86/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All analyses were based on previous published studies, thus no ethical approval and patient consent are required for this research. This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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