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Composite dietary antioxidant index and abdominal aortic calcification: a national cross-sectional study

Nutrition Journal volume 23, Article number: 130 (2024) Cite this article

Abstract

Purpose

The Composite Dietary Antioxidant Index (CDAI) is a novel, inclusive measure for evaluating the antioxidant potential of diets. We aim to explore the link between the CDAI and abdominal aortic calcification (AAC) in U.S. adults aged ≥ 40 years.

Methods

This cross-sectional study collected dietary and AAC data for individuals aged ≥ 40 years from the 2013–2014 National Health and Nutrition Examination Survey (NHANES) database. The CDAI was calculated using six dietary antioxidants. AAC was evaluated using a semi-quantitative scoring system known as AAC-24, with an AAC score greater than 6 as severe AAC (SAAC). To examine the association between CDAI and AAC, including SAAC, liner/logistic regression analyses and smooth curve fitting were applied.

Results

A total of 2,640 participants were included in this study, and significant decreases in AAC score and SAAC prevalence were observed with ascending CDAI levels (P < 0.01). After adjusting for confounding factors, a clear link was established between the CDAI and both AAC score (β = -0.083, 95% CI -0.144–0.022, P = 0.008) and SAAC (OR = 0.883, 95% CI 0.806–0.968, P = 0.008), respectively. Further smooth curve fitting indicated a negative correlation between CDAI and both AAC score and SAAC.

Conclusions

Dietary antioxidant consumption, as quantified by the CDAI, shows an inverse relationship with AAC risk. Additional longitudinal and intervention studies are essential.

Peer Review reports

Introduction

Vascular calcification, characterized by the abnormal accumulation of calcium phosphate crystals within the arterial intima, is identified as a significant risk factor for cardiovascular disease [1]. It is strongly linked to an increased risk of rupture in atherosclerotic plaques, adverse cardiovascular incidents, and all-cause mortality [2]. Physiologically, vascular smooth muscle cells (VSMCs) maintain the tone and elasticity of blood vessels [3]. However, under pathological stimuli such as oxidative stress, aging, uremia, mechanical stress, and inflammation, VSMCs will accept the characteristics of collagen-secreting osteoblasts, leading to vascular calcification [3,4,5].

Abdominal aortic calcification (AAC) appears before coronary artery calcification and is an independent predictor of subclinical and future cardiovascular events, beyond traditional risk factors [6, 7]. Diet-associated cardiometabolic disorders account for around one-fifth of all premature deaths worldwide, presenting a substantial health challenge [8]. Dietary risk factors are known to exert an impact on various vascular-related health issues, including peripheral arterial disease, atrial fibrillation, chronic kidney disease, heart failure and cognitive decline [9]. Consuming dietary antioxidants has been proven to mitigate the adverse health effects associated with oxidative stress and chronic inflammation [10]. Previous studies also indicated that a diet rich in antioxidants is linked to a lower risk of AAC [11]. The Comprehensive Dietary Antioxidant Index (CDAI) is an effective nutritional tool designed to measure the antioxidant quality of a diet [12, 13]. It evaluates the combined effects of six key dietary antioxidants (vitamins A, C, and E, selenium, zinc, and carotenoids), representing a comprehensive profile of dietary antioxidant intake. The CDAI has been proven to have a positive impact on various chronic diseases, including hypertension, diabetes, visceral obesity, chronic kidney disease, and other related conditions [14,15,16,17].

However, it is uncertain whether CDAI could effectively identify those at increased risk of AAC. By analyzing data from the National Health and Nutrition Examination Survey (NHANES) database, this study aims to examine the potential relationship between CDAI and AAC risk through a comprehensive cross-sectional analysis.

Materials and methods

Study population

Data for this study were sourced from the NHANES, a comprehensive survey conducted by the National Center for Health Statistics at the Centers for Disease Control and Prevention. The NHANES employed a rigorously structured, stratified, randomized, multi-stage approach to sampling, ensuring a nationally representative sample. Participants underwent detailed physical exams, completed health and nutrition surveys, and participated in lab tests [18, 19]. The NHANES study protocol received approval from the Ethics Review Board at the National Center for Health Statistics. Written informed consent was obtained from all participants. Detailed methodologies and data are accessible at https://www.cdc.gov/nchs/nhanes/. This analysis compiled NHANES 2013–2014 data, selecting a total of 2,640 qualified participants. Criteria for inclusion were being 40 years or older, not being pregnant, and having complete dietary questionnaire and AAC data.

Exposure and outcome definitions

Dietary and nutrient intakes of participants in the NHANES database were tracked through a 24-hour dietary recall interview, first face-to-face and then via a second recall by telephone within 3 to 10 days. The CDAI was established using food frequency questionnaire (FFQ) data, which identified antioxidant consumption including vitamins A, C, E, zinc, selenium, and carotenoids. Normalization of these antioxidants was achieved by mean subtraction and standard deviation division, with the CDAI representing the total of these normalized values. The calcification severity of abdominal aorta was quantified using the AAC score, derived exclusively from the NHANES 2013–2014 dataset. This score, based on the Kauppila scoring system and measured via dual-energy X-ray absorptiometry (DXA, Densitometer Discovery A, Hologic, Marlborough, MA, USA), varied from 0 to 24, with higher scores indicating greater calcification. An AAC score above 6 was considered as SAAC [20]. Both AAC score and SAAC were analyzed as outcome measures in this study.

Covariate definitions

Our study included some potential covariates including demographic information (age, gender, race), socio-economic status (marital status, annual income, education level), physical activity (vigorous or moderate), smoking status, health conditions (hypertension, diabetes, and cardiovascular disease), body mass index (BMI), glycohemoglobin (HbA1c), triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-c), high-density lipoprotein cholesterol (HDL-c), serum creatinine (Scr), estimated glomerular filtration rate (eGFR), bone metabolism markers (serum calcium, phosphorus, and total 25-hydroxyvitamin D), and total energy intake. Estimation of eGFR was conducted using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation, accounting for age, gender, race, and Scr levels [21]. Diagnosis of diabetes and hypertension was based on individuals’ self-reported health records. The determination of cardiovascular diseases required participants to report history of heart attacks, strokes, heart failure, coronary artery disease, or angina.

Statistical analysis

The statistical approach adhered to the protocols set by the Centers for Disease Control and Prevention, utilizing a complex multistage cluster survey methodology and applying weights from a single cycle. Continuous variables were presented as means with standard errors (SE), while categorical variables were shown as percentages. The comparison of continuous and categorical variables across groups was performed using the weighted Student’s t-test chi-squared test, respectively. The association between CDAI (continuous /categorical) and AAC score, SAAC was analyzed using weighted linear and logistic regression models. Further, subgroup analyses were also conducted. Additionally, the potential nonlinear relationship between CDAI and AAC score, SAAC was explored using weighted smooth curve fitting. All statistical analyses were conducted using Empower software (http://www.empowerstats.com) and R software (http://www.R-project.org), with statistical significance set at a two-sided P value < 0.05.

Results

Baseline characteristics of study population

The study included 2,640 eligible participants. The majority were non-Hispanic whites at 72.77%, followed by non-Hispanic blacks at 9.92%, Mexican Americans at 6.47%, other Hispanics at 4.50%, and other races making up 6.34%. The average age of the participants was 57.64 years, with 46.68% being males (Table 1). The average nutritional intake was recorded as 656.27 mcg of vitamin A, 80.87 mg of vitamin C, 10.05 mg of vitamin E, 9817.17 mcg of carotenoids, 114.36 mcg of selenium, and 10.86 mg of zinc. Based on CDAI levels, participants were divided into three groups. The analysis showed that those in the highest CDAI group were typically younger, mostly male and married, with higher annual household incomes (P < 0.001). They also had a lower prevalence of diabetes, hypertension, and cardiovascular diseases (P < 0.05). Furthermore, these individuals had lower BMI and TC measurements, but higher levels of total 25-hydroxyvitamin D, vitamins A, C, E, selenium, zinc, carotenoids, and total energy intake (P < 0.05). There were also notable differences in racial distribution among the groups. Notably, higher CDAI levels were associated with a lower AAC score and a decreased prevalence of SAAC, with percentages decreasing from 10.39 to 7.97%, and then to 5.26% (P < 0.01).

Table 1 Baseline characteristics of participants grouped by CDAI levels
Full size table

Associations between CDAI and SAAC, AAC score

Our findings show a strong association between higher CDAI levels and a reduced risk of SAAC, which is consistently significant in unadjusted (OR = 0.937, 95% CI 0.903–0.971, P < 0.001), partially adjusted (OR = 0.934, 95% CI 0.896–0.974, P = 0.001), and fully adjusted models (OR = 0.883, 95% CI 0.806–0.968, P = 0.008) (Table 2). Further analysis by splitting CDAI levels into three groups reveals that individuals in the highest group face a significantly decreased risk of SAAC (P = 0.006). Compared to the lowest group, their risk in the fully adjusted model is reduced by 64.8%, with an OR of 0.352 and a 95% CI ranging from 0.167 to 0.741. Additionally, linear regression analysis indicates a significant negative relationship between CDAI and AAC score (β = -0.083, 95% CI -0.144–0.022, P = 0.008) (Table 3). Smooth curve fitting analysis also indicated a negative correlation between CDAI and both AAC score and SAAC (Fig. 1).

Table 2 Results from logistic regression analysis on SAAC
Full size table
Table 3 Results from linear regression analysis on AAC score
Full size table
Fig. 1
figure 1

Results from smooth curve fitting

Full size image

Subgroup analyses

Subgroup analyses were conducted to confirm the consistency of the relationships between CDAI and SAAC across various demographic groups, as shown in Fig. 2. The impact of factors such as age, gender, race, marital status, annual household income, education level, smoking status, BMI, diabetes, hypertension cardiovascular diseases, and eGFR on these relationships was found to be statistically insignificant (P for interaction > 0.05).

Fig. 2
figure 2

Results from subgroup analyses

Full size image

Discussion

To our understanding, this study is the first in-depth examination of the relationship between CDAI levels and the risk of AAC. Our findings indicate a negative correlation between CDAI levels and both AAC score and SAAC, even when accounting for a range of potential confounding factors. This implies that higher CDAI levels might act as a protective element against AAC risk.

Calcification in arterial layers, specifically the intima and media, is driven by an osteogenic activity in VSMCs, resembling osteoblast-like cell formation [22]. The differentiation of VSMCs is majorly influenced by oxidative stress. The accumulation of reactive oxygen species (ROS) following exposure to hydrogen peroxide or oxidized low-density lipoprotein results in elevated Runx2 expression, potentially steering the VSMCs phenotype towards osteoblastic characteristics and initiating calcification in vessels [23, 24]. Oxidative stress also activates inflammatory cells like macrophages, which release inflammatory mediators in the arterial walls, further facilitating calcification [25]. Additionally, oxidative stress may induce the apoptosis or programmed cell death of VSMCs, turning these cells into potential focal points for calcification [26, 27]. It also leads to the degeneration of vascular wall matrix proteins such as collagen and elastin, laying the groundwork for calcium salt deposition [28]. Studies in uremic rats have shown that antioxidants can reduce oxidative stress both in the aorta and systemically, curbing the osteogenic differentiation of VSMCs and the progression of arterial calcification [29].

Vitamin A, a fat-soluble nutrient, plays a critical role in maintaining visual health, supporting the immune system, ensuring skin health, and facilitating cell growth [30]. In a study identifying dietary components associated with abdominal aortic calcification, information on 35 macro and micronutrients was analyzed [30]. Among these, vitamin A was negatively correlated with AAC [30]. Known as ascorbic acid, vitamin C is a naturally occurring, water-soluble substance in food. It plays roles in antioxidation, collagen support, immune system regulation, and diminishing inflammation [31]. Vitamin C acts to lower the production of reactive oxygen species (ROS) like superoxide radicals and hydrogen peroxide by blocking the Jak2/Stat1/IRF1 signaling in endothelial cells [31, 32]. Similarly, vitamin E, another fat-soluble antioxidant, is crucial for preserving cell membrane integrity and safeguarding the body against oxidative stress [33]. Animal experiments have demonstrated that supplementation with vitamin E in the diet provides protection against vascular calcification in rats with uremia induced by a high-fat diet [34]. Selenium and its derivatives, notably selenoproteins that contain selenium in the form of selenocysteine, have been proven to have antioxidant effects [35]. In conditions where oxidative stress is induced by hydrogen peroxide, selenium has been shown to block the process of calcification and differentiation in osteoblastic VSMCs, which lowers the accumulation of calcium in the extracellular matrix by enhancing antioxidant selenoproteins and suppressing the PI3K/AKT and ERK signaling pathways [36,37,38]. Voelkl et al. demonstrated through in vitro and animal studies that zinc supplementation mitigates phosphate-induced arterial calcification [39]. In their experiments with human aortic VSMCs, the application of zinc sulfate was shown to inhibit calcification induced by phosphate and reduce the expression of osteogenic marker mRNA [39]. This effect was attributed to the induction of the zinc-finger protein A20 and the inhibition of NF-κB activation [39]. Carotenoids, fat-soluble pigments found in fruits, vegetables, and seaweed, possess antioxidant capabilities. Previous research also indicated a nonlinear negative association between carotenoid consumption and SAAC [40]. However, as the current U.S. Dietary Guidelines for 2020–2025 highlighted, the significance of adopting comprehensive dietary practices instead of concentrating on specific nutrients, foods, or groups in isolation [41, 42]. The research by Senoner and his team suggests diets that could help reduce ROS related to cardiovascular diseases [43]. They also highlighted the complexity of pinpointing the antioxidant-contributing elements within foods, recommending a varied diet encompassing antioxidants from sources like fruits, vegetables, and fish over single-antioxidant supplements [43]. Research on the CDAI also showed its association with inflammatory indicators such as IL-1β and TNFα, which are implicated in atherosclerosis [12, 44]. Research shows that the CDAI is strongly linked with various adverse health outcomes, highlighting its advantages and usefulness compared to traditional dietary antioxidant indexes in epidemiological research [14, 17, 45, 46].

This study, with its sophisticated sampling weights, depicts the demographic landscape of the United States. Nonetheless, this study also presents certain limitations. First, given the cross-sectional design’s inability to establish causality, there is a crucial need for prospective cohort studies and intervention trials in further investigations. Second, the study did not account for potential confounding factors such as non-alcoholic fatty liver disease and metabolic syndrome, which could result in biased outcomes. Third, the dietary information was based on self-reports, potentially impacting accuracy due to recall bias. Lastly, with the sample derived from the single population, confirming the broader applicability of the results requires further examination.

Conclusion

In a nationally representative study conducted among adults aged ≥ 40 years, a higher overall dietary antioxidant intake, measured by CDAI, is associated with a lower risk of AAC. Additional longitudinal and intervention studies are essential.

Data availability

The datasets generated and/or analyzed during the current study are available in the NHANES database (https://www.cdc.gov/nchs/nhanes/).

References

  1. Bardeesi ASA, Gao J, Zhang K, Yu S, Wei M, Liu P, Huang H. A novel role of cellular interactions in vascular calcification. J Transl Med. 2017;15(1):95. https://doi.org/10.1186/s12967-017-1190-z.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  2. Kendrick J, Chonchol M. The role of phosphorus in the development and progression of vascular calcification. Am J Kidney Dis. 2011;58(5):826–34. https://doi.org/10.1053/j.ajkd.2011.07.020.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  3. Durham AL, Speer MY, Scatena M, Giachelli CM, Shanahan CM. Role of smooth muscle cells in vascular calcification: implications in atherosclerosis and arterial stiffness. Cardiovasc Res. 2018;114(4):590–600. https://doi.org/10.1093/cvr/cvy010.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  4. Leopold JA. (2015) Vascular calcification: Mechanisms of vascular smooth muscle cell calcification. Trends Cardiovasc Med 25(4): 267 – 74. https://doi.org/10.1016/j.tcm.2014.10.021

  5. Pérez-Hernández N, Aptilon-Duque G, Blachman-Braun R, Vargas-Alarcón G, Rodríguez-Cortés AA, Azrad-Daniel S, Posadas-Sánchez R, Rodríguez-Pérez JM. Vascular calcification: current Genetics Underlying this Complex Phenomenon. Chin Med J (Engl). 2017;130(9):1113–21. https://doi.org/10.4103/0366-6999.204931.

    Article  CAS  PubMed  Google Scholar 

  6. Bastos Gonçalves F, Voûte MT, Hoeks SE, Chonchol MB, Boersma EE, Stolker RJ, Verhagen HJ. Calcification of the abdominal aorta as an independent predictor of cardiovascular events: a meta-analysis. Heart. 2012;98(13):988–94. https://doi.org/10.1136/heartjnl-2011-301464.

    Article  PubMed  Google Scholar 

  7. Forbang NI, Michos ED, McClelland RL, Remigio-Baker RA, Allison MA, Sandfort V, Ix JH, Thomas I, Rifkin DE, Criqui MH. Greater volume but not higher density of abdominal aortic calcium is Associated with increased Cardiovascular Disease Risk: MESA (multi-ethnic study of atherosclerosis). Circ Cardiovasc Imaging. 2016;9(11). https://doi.org/10.1161/circimaging.116.005138.

  8. (2018) Global, regional, and national comparative risk assessment of 84 behavioural, environmental and occupational, and metabolic risks or clusters of risks for 195 countries and territories, 1990–2017: a systematic analysis for the global burden of Disease Study 2017. Lancet 392(10159): 1923–94. https://doi.org/10.1016/s0140-6736(18)32225-6

  9. Lim SS, Vos T, Flaxman AD, Danaei G, Shibuya K, Adair-Rohani H, Amann M, Anderson HR, Andrews KG, Aryee M, Atkinson C, Bacchus LJ, Bahalim AN, Balakrishnan K, Balmes J, Barker-Collo S, Baxter A, Bell ML, Blore JD, Blyth F, Bonner C, Borges G, Bourne R, Boussinesq M, Brauer M, Brooks P, Bruce NG, Brunekreef B, Bryan-Hancock C, Bucello C, Buchbinder R, Bull F, Burnett RT, Byers TE, Calabria B, Carapetis J, Carnahan E, Chafe Z, Charlson F, Chen H, Chen JS, Cheng AT, Child JC, Cohen A, Colson KE, Cowie BC, Darby S, Darling S, Davis A, Degenhardt L, Dentener F, Des Jarlais DC, Devries K, Dherani M, Ding EL, Dorsey ER, Driscoll T, Edmond K, Ali SE, Engell RE, Erwin PJ, Fahimi S, Falder G, Farzadfar F, Ferrari A, Finucane MM, Flaxman S, Fowkes FG, Freedman G, Freeman MK, Gakidou E, Ghosh S, Giovannucci E, Gmel G, Graham K, Grainger R, Grant B, Gunnell D, Gutierrez HR, Hall W, Hoek HW, Hogan A, Hosgood HD 3rd, Hoy D, Hu H, Hubbell BJ, Hutchings SJ, Ibeanusi SE, Jacklyn GL, Jasrasaria R, Jonas JB, Kan H, Kanis JA, Kassebaum N, Kawakami N, Khang YH, Khatibzadeh S, Khoo JP, Kok C, Laden F, Lalloo R, Lan Q, Lathlean T, Leasher JL, Leigh J, Li Y, Lin JK, Lipshultz SE, London S, Lozano R, Lu Y, Mak J, Malekzadeh R, Mallinger L, Marcenes W, March L, Marks R, Martin R, McGale P, McGrath J, Mehta S, Mensah GA, Merriman TR, Micha R, Michaud C, Mishra V, Mohd Hanafiah K, Mokdad AA, Morawska L, Mozaffarian D, Murphy T, Naghavi M, Neal B, Nelson PK, Nolla JM, Norman R, Olives C, Omer SB, Orchard J, Osborne R, Ostro B, Page A, Pandey KD, Parry CD, Passmore E, Patra J, Pearce N, Pelizzari PM, Petzold M, Phillips MR, Pope D, Pope CA 3rd, Powles J, Rao M, Razavi H, Rehfuess EA, Rehm JT, Ritz B, Rivara FP, Roberts T, Robinson C, Rodriguez-Portales JA, Romieu I, Room R, Rosenfeld LC, Roy A, Rushton L, Salomon JA, Sampson U, Sanchez-Riera L, Sanman E, Sapkota A, Seedat S, Shi P, Shield K, Shivakoti R, Singh GM, Sleet DA, Smith E, Smith KR, Stapelberg NJ, Steenland K, Stöckl H, Stovner LJ, Straif K, Straney L, Thurston GD, Tran JH, Van Dingenen R, van Donkelaar A, Veerman JL, Vijayakumar L, Weintraub R, Weissman MM, White RA, Whiteford H, Wiersma ST, Wilkinson JD, Williams HC, Williams W, Wilson N, Woolf AD, Yip P, Zielinski JM, Lopez AD, Murray CJ, Ezzati M, AlMazroa MA, Memish ZA. (2012) A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990–2010: a systematic analysis for the Global Burden of Disease Study 2010. Lancet 380(9859): 2224-60. https://doi.org/10.1016/s0140-6736(12)61766-8

  10. Amirkhizi F, Hamedi-Shahraki S, Rahimlou M. Dietary total antioxidant capacity is associated with lower disease severity and inflammatory and oxidative stress biomarkers in patients with knee osteoarthritis. J Health Popul Nutr. 2023;42(1):104. https://doi.org/10.1186/s41043-023-00450-x.

    Article  PubMed  PubMed Central  Google Scholar 

  11. Hu L, Liu Q, Ou Y, Li D, Wu Y, Li H, Zhu Z, Liang M. Dietary lycopene is negatively associated with abdominal aortic calcification in US adults: a cross-sectional study. Ann Med. 2023;55(1):2195205. https://doi.org/10.1080/07853890.2023.2195205.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  12. Wu D, Wang H, Wang W, Qing C, Zhang W, Gao X, Shi Y, Li Y, Zheng Z. Association between composite dietary antioxidant index and handgrip strength in American adults: data from National Health and Nutrition Examination Survey. NHANES; 2023. pp. 2011–4. https://doi.org/10.3389/fnut.2023.1147869. Front Nutr 101147869.

  13. Wright ME, Mayne ST, Stolzenberg-Solomon RZ, Li Z, Pietinen P, Taylor PR, Virtamo J, Albanes D. Development of a comprehensive dietary antioxidant index and application to lung cancer risk in a cohort of male smokers. Am J Epidemiol. 2004;160(1):68–76. https://doi.org/10.1093/aje/kwh173.

    Article  PubMed  Google Scholar 

  14. Wu M, Si J, Liu Y, Kang L, Xu B. Association between composite dietary antioxidant index and hypertension: insights from NHANES. Clin Exp Hypertens. 2023;45(1):2233712. https://doi.org/10.1080/10641963.2023.2233712.

    Article  CAS  PubMed  Google Scholar 

  15. Chen X, Lu H, Chen Y, Sang H, Tang Y, Zhao Y. Composite dietary antioxidant index was negatively associated with the prevalence of diabetes independent of cardiovascular diseases. Diabetol Metab Syndr. 2023;15(1):183. https://doi.org/10.1186/s13098-023-01150-6.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  16. Gu X, Wang X, Wang S, Shen Y, Lu L. Composite dietary antioxidant index is inversely associated with visceral adipose tissue area among U.S. adults: a cross-sectional study. Nutr Res. 2024;12413–20. https://doi.org/10.1016/j.nutres.2024.01.011.

  17. Wang M, Huang ZH, Zhu YH, He P, Fan QL. Association between the composite dietary antioxidant index and chronic kidney disease: evidence from NHANES 2011–2018. Food Funct. 2023;14(20):9279–86. https://doi.org/10.1039/d3fo01157g.

    Article  CAS  PubMed  Google Scholar 

  18. Paulose-Ram R, Graber JE, Woodwell D, Ahluwalia N. The National Health and Nutrition Examination Survey (NHANES), 2021–2022: Adapting Data Collection in a COVID-19 environment. Am J Public Health. 2021;111(12):2149–56. https://doi.org/10.2105/ajph.2021.306517.

    Article  PubMed  PubMed Central  Google Scholar 

  19. Ahluwalia N, Dwyer J, Terry A, Moshfegh A, Johnson C. Update on NHANES Dietary Data: Focus on Collection, Release, Analytical considerations, and uses to inform Public Policy. Adv Nutr. 2016;7(1):121–34. https://doi.org/10.3945/an.115.009258.

    Article  PubMed  PubMed Central  Google Scholar 

  20. Cai Z, Liu Z, Zhang Y, Ma H, Li R, Guo S, Wu S, Guo X. Associations between Life’s essential 8 and abdominal aortic calcification among Middle-aged and Elderly populations. J Am Heart Assoc. 2023;12(24):e031146. https://doi.org/10.1161/jaha.123.031146.

    Article  PubMed  PubMed Central  Google Scholar 

  21. Levey AS, Stevens LA, Schmid CH, Zhang YL, Castro AF 3rd, Feldman HI, Kusek JW, Eggers P, Van Lente F, Greene T, Coresh J. A new equation to estimate glomerular filtration rate. Ann Intern Med. 2009;150(9):604–12. https://doi.org/10.7326/0003-4819-150-9-200905050-00006.

  22. Lian JB, Stein GS. (1995) Development of the osteoblast phenotype: molecular mechanisms mediating osteoblast growth and differentiation. Iowa Orthop J. 1995;15:118-140.

  23. Byon CH, Javed A, Dai Q, Kappes JC, Clemens TL, Darley-Usmar VM, McDonald JM, Chen Y. Oxidative stress induces vascular calcification through modulation of the osteogenic transcription factor Runx2 by AKT signaling. J Biol Chem. 2008;283(22):15319–27. https://doi.org/10.1074/jbc.M800021200.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  24. Farrokhi E, Samani KG, Chaleshtori MH. Oxidized low-density lipoprotein increases bone sialoprotein expression in vascular smooth muscle cells via runt-related transcription factor 2. Am J Med Sci. 2015;349(3):240–3. https://doi.org/10.1097/maj.0000000000000381.

    Article  PubMed  Google Scholar 

  25. Yaker L, Tebani A, Lesueur C, Dias C, Jung V, Bekri S, Guerrera IC, Kamel S, Ausseil J, Boullier A. Extracellular vesicles from LPS-Treated macrophages aggravate smooth muscle cell calcification by propagating inflammation and oxidative stress. Front Cell Dev Biol. 2022;10823450. https://doi.org/10.3389/fcell.2022.823450.

  26. Wang YK, Li SJ, Zhou LL, Li D, Guo LW. GALNT3 protects against vascular calcification by reducing oxidative stress and apoptosis of smooth muscle cells. Eur J Pharmacol. 2023;939175447. https://doi.org/10.1016/j.ejphar.2022.175447.

  27. Grootaert MOJ, Moulis M, Roth L, Martinet W, Vindis C, Bennett MR, De Meyer GRY. Vascular smooth muscle cell death, autophagy and senescence in atherosclerosis. Cardiovasc Res. 2018;114(4):622–34. https://doi.org/10.1093/cvr/cvy007.

    Article  CAS  PubMed  Google Scholar 

  28. Lacolley P, Regnault V, Laurent S. Mechanisms of arterial stiffening: from mechanotransduction to Epigenetics. Arterioscler Thromb Vasc Biol. 2020;40(5):1055–62. https://doi.org/10.1161/atvbaha.119.313129.

    Article  CAS  PubMed  Google Scholar 

  29. Yamada S, Taniguchi M, Tokumoto M, Toyonaga J, Fujisaki K, Suehiro T, Noguchi H, Iida M, Tsuruya K, Kitazono T. The antioxidant tempol ameliorates arterial medial calcification in uremic rats: important role of oxidative stress in the pathogenesis of vascular calcification in chronic kidney disease. J Bone Min Res. 2012;27(2):474–85. https://doi.org/10.1002/jbmr.539.

    Article  CAS  Google Scholar 

  30. Li W, Huang G, Tang N, Lu P, Jiang L, Lv J, Qin Y, Lin Y, Xu F, Lei D. Identification of dietary components in association with abdominal aortic calcification. Food Funct. 2023;14(18):8383–95. https://doi.org/10.1039/d3fo02920d.

    Article  CAS  PubMed  Google Scholar 

  31. Jia J, Zhang J, He Q, Wang M, Liu Q, Wang T, Chen X, Wang W, Xu H. Association between dietary vitamin C and abdominal aortic calcification among the US adults. Nutr J. 2023;22(1):58. https://doi.org/10.1186/s12937-023-00889-y.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  32. Chaghouri P, Maalouf N, Peters SL, Nowak PJ, Peczek K, Zasowska-Nowak A, Nowicki M. Two faces of vitamin C in Hemodialysis patients: relation to oxidative stress and inflammation. Nutrients. 2021;13(3). https://doi.org/10.3390/nu13030791.

  33. Miyazawa T, Burdeos GC, Itaya M, Nakagawa K, Miyazawa T. Vitamin E: Regulatory Redox interactions. IUBMB Life. 2019;71(4):430–41. https://doi.org/10.1002/iub.2008.

    Article  CAS  PubMed  Google Scholar 

  34. Rios R, Raya AI, Pineda C, Rodriguez M, Lopez I, Aguilera-Tejero E. Vitamin E protects against extraskeletal calcification in uremic rats fed high fat diets. BMC Nephrol. 2017;18(1):374. https://doi.org/10.1186/s12882-017-0790-4.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  35. Zhang F, Li X, Wei Y. Selenium and Selenoproteins in Health. Biomolecules. 2023;13(5). https://doi.org/10.3390/biom13050799.

  36. Dong W, Liu X, Ma L, Yang Z, Ma C. Association between dietary selenium intake and severe abdominal aortic calcification in the United States: a cross-sectional study. Food Funct. 2024;15(3):1575–82. https://doi.org/10.1039/d3fo02631k.

    Article  CAS  PubMed  Google Scholar 

  37. Liu H, Li X, Qin F, Huang K. Selenium suppresses oxidative-stress-enhanced vascular smooth muscle cell calcification by inhibiting the activation of the PI3K/AKT and ERK signaling pathways and endoplasmic reticulum stress. J Biol Inorg Chem. 2014;19(3):375–88. https://doi.org/10.1007/s00775-013-1078-1.

    Article  CAS  PubMed  Google Scholar 

  38. Liu H, Lu Q, Huang K. Selenium suppressed hydrogen peroxide-induced vascular smooth muscle cells calcification through inhibiting oxidative stress and ERK activation. J Cell Biochem. 2010;111(6):1556–64. https://doi.org/10.1002/jcb.22887.

    Article  CAS  PubMed  Google Scholar 

  39. Voelkl J, Tuffaha R, Luong TTD, Zickler D, Masyout J, Feger M, Verheyen N, Blaschke F, Kuro OM, Tomaschitz A, Pilz S, Pasch A, Eckardt KU, Scherberich JE, Lang F, Pieske B, Alesutan I. Zinc inhibits phosphate-Induced Vascular calcification through TNFAIP3-Mediated suppression of NF-κB. J Am Soc Nephrol. 2018;29(6):1636–48. https://doi.org/10.1681/asn.2017050492.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  40. Chen W, Li Y, Li M, Li H, Chen C, Lin Y. Association between dietary carotenoid intakes and abdominal aortic calcification in adults: National Health and Nutrition Examination Survey 2013–2014. J Health Popul Nutr. 2024;43(1):20. https://doi.org/10.1186/s41043-024-00511-9.

    Article  PubMed  PubMed Central  Google Scholar 

  41. Zhang J, Lu X, Wu R, Ni H, Xu L, Wu W, Lu C, Feng J, Jin Y. Associations between composite dietary antioxidant index and estimated 10-year atherosclerotic cardiovascular disease risk among U.S. adults. Front Nutr. 2023;101214875. https://doi.org/10.3389/fnut.2023.1214875.

  42. Shams-White MM, Pannucci TE, Lerman JL, Herrick KA, Zimmer M, Meyers Mathieu K, Stoody EE, Reedy J. Healthy eating Index-2020: review and update process to reflect the Dietary guidelines for Americans,2020–2025. J Acad Nutr Diet. 2023;123(9):1280–8. https://doi.org/10.1016/j.jand.2023.05.015.

    Article  PubMed  PubMed Central  Google Scholar 

  43. Senoner T, Dichtl W. (2019) Oxidative Stress in Cardiovascular Diseases: Still a Therapeutic Target? Nutrients 11(9). https://doi.org/10.3390/nu11092090

  44. Luu HN, Wen W, Li H, Dai Q, Yang G, Cai Q, Xiang YB, Gao YT, Zheng W, Shu XO. Are dietary antioxidant intake indices correlated to oxidative stress and inflammatory marker levels? Antioxid Redox Signal. 2015;22(11):951–9. https://doi.org/10.1089/ars.2014.6212.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  45. Liu C, Lai W, Zhao M, Zhang Y, Hu Y. Association between the composite dietary antioxidant index and atherosclerotic Cardiovascular Disease in Postmenopausal women: a cross-sectional study of NHANES Data, 2013–2018. Antioxid (Basel). 2023;12(9). https://doi.org/10.3390/antiox12091740.

  46. Liu J, Tang Y, Peng B, Tian C, Geng B. Bone mineral density is associated with composite dietary antioxidant index among US adults: results from NHANES. Osteoporos Int. 2023;34(12):2101–10. https://doi.org/10.1007/s00198-023-06901-9.

    Article  CAS  PubMed  Google Scholar 

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Acknowledgements

We want to acknowledge all participants of this study and the support provided by the Jiangsu University.

Funding

The study is funded by the Clinical Science and Technology Development Foundation of Jiangsu University (JLY20180109)，the Science and Technology Project of Changzhou Health Commission (WZ202226), and the Young Talent Development Plan of Changzhou Health Commission (CZQM2022029).

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Authors and Affiliations

  1. Department of Endocrinology, Affiliated Kunshan Hospital of Jiangsu University, Kunshan, Jiangsu, 215300, China

    Zhaoxiang Wang & Fengyan Tang

  2. Department of Cardiology, Affiliated Kunshan Hospital of Jiangsu University, Kunshan, Jiangsu, 215300, China

    Bo Zhao

  3. Department of Endocrinology, Affiliated Wujin Hospital of Jiangsu University, Changzhou, Jiangsu, 213017, China

    Han Yan, Xuejing Shao & Qichao Yang

  4. Department of Endocrinology, Wujin Clinical College of Xuzhou Medical University, Changzhou, Jiangsu, 213017, China

    Han Yan, Xuejing Shao & Qichao Yang

Authors
  1. Zhaoxiang Wang
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  2. Fengyan Tang
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  3. Bo Zhao
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  4. Han Yan
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Contributions

Z.W. and Q.Y. wrote the main manuscript text. F.T., B.Z., H.Y., and X.S. prepared figures and tables. All authors reviewed the manuscript.

Corresponding author

Correspondence to Qichao Yang.

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Ethical approval

This study involving human participants were reviewed and approved by the Ethics Review Board of the National Center for Health Statistics.

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The patients/participants provided their written informed consent to participate in this study.

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The authors declare no competing interests.

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Wang, Z., Tang, F., Zhao, B. et al. Composite dietary antioxidant index and abdominal aortic calcification: a national cross-sectional study. Nutr J 23, 130 (2024). https://doi.org/10.1186/s12937-024-01029-w

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Keywords

Nutrition Journal

ISSN: 1475-2891

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