Introduction

Type 2 diabetes (T2D) is a chronic condition characterized by insulin resistance and elevated blood glucose levels. As of 2021, approximately 537 million adults worldwide have diabetes, with more than 90% of these cases being T2D—a figure projected to rise to 643 million by 2030 [1]. In 2021, T2D accounted for an age-standardized mortality rate of 18.5 per 100,000 individuals [2] and, in 2019, a disability-adjusted life years rate of 801.5 per 100,000 individuals [2]. T2D leads to severe complications, including cardiovascular diseases, kidney damage, and neuropathy [3]. Major contributing factors include obesity, physical inactivity, and unhealthy dietary habits [4].

There is growing interest in the role of oxidative stress and inflammation in chronic conditions such as atherosclerosis, obesity, and T2D [5]. An imbalance between prooxidants and antioxidants, resulting in oxidative stress, is a key pathogenic mechanism that increases diabetes risk [6]. Hyperglycemia promotes glucose autoxidation, non-enzymatic glycation, and impairs monocyte function, all of which lead to increased free radical production [7]. In addition, reduced levels of antioxidants exacerbate oxidative stress [8], resulting in lipid and DNA damage as observed in patients with diabetes [9].

A healthy diet rich in antioxidants and anti-inflammatory compounds may reduce the risk of chronic diseases, including cardiovascular disease, diabetes, and certain cancers [10]. Dietary intake has been linked to modulation of oxidative stress [11,12], and energy restriction has been suggested to lower levels of oxidative stress intermediaries [13]. Consumption of antioxidants is proposed as a protective strategy to mitigate oxidative damage [14], and evidence indicates that dietary antioxidants reduce T2D risk by inhibiting peroxidation chain reactions [15]. Moreover, consuming fruits and vegetables is associated with reduced incidence and mortality from various chronic diseases [16,17]. One hypothesis suggests that the collective impact of antioxidants—such as vitamins C and E, carotenoids, flavonoids, and proanthocyanidins—protects cells against free radical-induced oxidative damage [18].

Recent research indicates that higher total plasma antioxidant capacity is correlated with the intake of antioxidant-rich fruits and vegetables [19,20]. Because individual antioxidant concentrations do not fully capture the overall antioxidant potential of whole foods, the concept of dietary total antioxidant capacity (DTAC) was introduced [21]. DTAC functions as a valuable indicator of the overall antioxidant status of a diet [22,23].

Over recent decades, researchers have developed various methods to assess the total antioxidant capacity (TAC) of complex materials like foods. These assays include ferric reducing-antioxidant power (FRAP), which measures the reduction of Fe³⁺ to Fe²⁺; total radical-trapping antioxidant parameter (TRAP), which monitors protection during a controlled peroxidation reaction; Trolox equivalent antioxidant capacity (TEAC), which compares the ability of antioxidants to quench the ABTS¹⁺ radical with that of Trolox; and oxygen radical absorbance capacity (ORAC), which evaluates the complete reaction of antioxidants with biologically relevant free radicals [24,25].

In recent years, substantial research has focused on the relationship between DTAC and T2D risk [26,27]. Although a recent systematic review examined the relationship between DTAC and cardiometabolic risk factors in diverse populations, no review has comprehensively summarized the evidence linking DTAC to T2D risk and related biomarkers such as fasting blood glucose (FBG), hemoglobin A1C (HbA1C), insulin levels, and homeostatic model assessment for insulin resistance (HOMA-IR).

Materials and Methods

We adhered to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines to ensure a transparent and systematic report [28].

Search Strategy

We conducted a systematic literature search in PubMed, Scopus, ScienceDirect, and Google Scholar up to July 2024 without imposing any date restrictions. Our search strategy used specific keywords relevant to the research question: “Dietary antioxidant capacity OR Dietary antioxidant index OR Dietary antioxidant intake OR Dietary total antioxidant” in title, abstract, and keywords, combined with “Diabetes OR Glycemic indices OR Metabolic indices OR insulin resistance OR insulin OR HOMA-IR OR glucose OR sugar” in title, abstract, and keywords. Only English-language original articles were included. Details of the search strategy are provided in Table S1. Reference lists of the included studies were also reviewed to identify additional relevant articles.

The research question was: “Is there an association between DTAC and T2D risk and levels of glycemic biomarkers?” Table 1 outlines the population, exposure, comparator, outcome (PECO) approach for this review, with individuals with diabetes or at risk defined as the population, low DTAC as the exposure, high DTAC as the comparator, and diabetes risk and glycemic biomarkers (FBG, HbA1C, insulin, and HOMA-IR) as the outcomes.

Eligibility Criteria

We included original articles published in English that evaluated the association between DTAC and either the risk of developing diabetes or glycemic biomarkers (including FBG, HbA1C, insulin, and HOMA-IR). Studies were excluded if they focused on a single dietary antioxidant (e.g., vitamin E or carotenoids) in relation to T2D, the effects of antioxidant supplementation on diabetes biomarkers, the impact of specific active constituents with antioxidant activity from special foods on diabetes management, interactions between DTAC and specific genotypes (e.g., the caveolin-1 gene variant, rs 3807992) on diabetes biomarkers, or the combined effect of DTAC with other factors on diabetes or glycemic biomarkers. Animal studies, theses, dissertations, conference abstracts, editorials, reviews, and posters were also excluded.

Selection of Studies

Extracted studies were transferred to an EndNote file, and duplicate articles were removed. Two independent researchers screened the remaining articles based on their titles and abstracts to identify potentially eligible studies. Full texts of the selected articles were then reviewed independently to assess eligibility and extract relevant data. Any disagreements regarding study eligibility were resolved through discussion until consensus was reached.

Data Extraction

The following information was collected: first author and year of publication, study country and design, participant demographics (including age and sex), physical condition, follow-up duration, dietary assessment method, DTAC evaluation method, covariates, and outcome measures reported as correlation indicators (odds/hazard ratios, confidence intervals, p-values, if available). Only results from fully adjusted models were considered.

In studies that employed multiple statistical approaches to assess the association between DTAC and T2D risk, priority was given to findings from regression analyses. When analyses were conducted separately by sex and an association was observed in only 1 sex, only the relevant sex-specific findings were documented.

Ethics Approval

The ethics committee of Tabriz University of Medical Sciences, Tabriz, Iran, registered and approved the protocol of this study (IR.TBZMED.REC.1401.824).

Results

Selection of Studies

Initially, 314 studies were retrieved (Figure 1). After removing duplicates, 143 studies remained. A review of titles and abstracts identified 43 publications relevant to the study’s scope. Following critical appraisal, 11 studies were excluded because 1 was irrelevant, 1 was unavailable, 1 was a duplicate of an already included study, 1 was a letter, 5 investigated the interaction of DTAC with other factors regarding T2D, and 2 focused on single dietary antioxidants. Ultimately, 32 studies were included in the review (comprising 8 cohort studies, 20 cross-sectional studies, and 4 case-control studies) (Figure 1).

Characteristics of the Included Studies

As shown in Table 2, the included investigations [26,27,29–58] were conducted across diverse global regions. The studies were published between 2010 and 2024, with the majority (n=26) published after 2015. In the cohort studies, follow-up durations ranged from 3 to 37 years, although 4 studies had excessively long follow-up periods. Most studies (23 of 32) used food frequency questionnaires (FFQs) to assess dietary intake. DTAC was measured using various methods, including FRAP (21 studies), ORAC (9 studies), TRAP (5 studies), TEAC (5 studies), a composite dietary antioxidant index (3 studies), and other methods (2 studies). Different cut-off points were employed to categorize DTAC values. Twenty-one studies focused on subjects with diabetes or prediabetes, and most studies (n=23) adjusted for potential covariates in their analyses.

Relationship between DTAC and Risk of Developing Prediabetes and Diabetes

Among the 19 studies assessing the association between DTAC and diabetes risk [27,29–46], 15 reported a lower risk of diabetes in individuals with higher DTAC values [30,31,33–35,37–46]. In contrast, 4 studies found no significant association [27,29,32,36]. All 4 studies that evaluated the link between DTAC and prediabetes risk reported lower risk in individuals with higher DTAC values [27,40,47,48].

Relationship between DTAC and Glycemic Biomarkers

As shown in Table 2, out of 15 studies that evaluated the association between DTAC and FBG [26,27,29,31,43,48-57], 9 reported lower FBG levels in individuals with higher DTAC values [27,29,43,48,51–54,57]. Six studies investigated the association between DTAC and HbA1C [27,31,49,50,55,56], with only 1 study reporting lower HbA1C levels in those with higher DTAC values [27]. Furthermore, 6 studies assessed the relationship between DTAC and insulin levels [50–55], and 5 of these found that higher DTAC values were associated with lower insulin levels [50–53,55]. Among the 9 studies evaluating DTAC and HOMA-IR [32,40,50–55,58], 8 reported lower HOMA-IR values in subjects with higher DTAC values [32,40,50–53,55,58].

Discussion

A healthy and diverse diet can enhance overall health outcomes and well-being [59,60]. Antioxidants play a critical role in maintaining health by neutralizing free radicals—highly reactive molecules that can damage cells and genetic material. These free radicals arise from metabolism, exercise, and environmental exposures such as air pollution and sunlight [61]. Evidence indicates that a diet rich in antioxidants, particularly from fruits, vegetables, and legumes, reduces the risk of chronic diseases related to oxidative stress. Epidemiological studies and meta-analyses of prospective observational studies have consistently linked higher intakes of antioxidant-rich foods with reduced risks of cardiovascular diseases, cancer, and all-cause mortality [62,63]. Thus, incorporating antioxidant-rich foods into one’s diet may improve overall health and well-being [64,65].

In the present study, we reviewed both interventional and observational investigations to provide an overview of the relationship between an antioxidant-rich diet and the risk of developing diabetes or altered glycemic biomarkers. Our systematic review provides robust evidence that high DTAC is associated with decreased diabetes risk as well as improved levels of FBG, insulin, and HOMA-IR.

Oxidative stress is central to the pathophysiology of diabetes [66]. Excess production of reactive free radicals, often triggered by hyperglycemia, leads to oxidative stress, which further exacerbates diabetes and its complications [66,67]. In diabetes, oxidative stress interacts with cellular biomolecules—including proteins and lipids—resulting in harmful effects such as lipid peroxidation, which compromises cellular structure and function [68]. Genetic studies related to oxidative stress have revealed potential causal links with diabetes and microvascular complications [69]. Elevated lipid peroxidation coupled with reduced antioxidant activity has been observed in patients with diabetes [70]. Although classic antioxidants like vitamin E have not demonstrated clinical benefits in large-scale trials, a more comprehensive strategy that both prevents reactive species generation and scavenges free radicals appears promising [67]. Moreover, synergistic low-dose antioxidant blends have shown potential in reducing lipid peroxidation and restoring redox homeostasis [71]. Understanding the interplay among dietary antioxidants, lipid peroxidation, and hyperglycemia is essential for managing diabetes and its associated complications.

Oxidative stress also contributes significantly to the development of insulin resistance. Research has shown that systemic oxidative stress is correlated with insulin resistance. For instance, data from the Framingham Offspring Study revealed that individuals with higher levels of oxidative stress (measured by urinary 8-epi-prostaglandin F2α) had an increased prevalence of insulin resistance, even after adjusting for body mass index [72]. A similar positive association between oxidative stress markers and HOMA-IR has been reported in young adults [73]. Oxidative stress may impair insulin signaling by damaging cellular components such as proteins, lipids, and DNA, leading to reduced glucose uptake [74]. Additionally, the activation of inflammatory pathways further exacerbates insulin resistance [75]. Antioxidants help counteract this process by reducing inflammation; for example, Luu et al. [76] reported an inverse association between dietary antioxidant intake and inflammatory biomarkers in a study of 3,853 women, while Beharka et al. [77] demonstrated that prolonged dietary antioxidant supplementation reduced the production of specific inflammatory mediators in mouse macrophages.

Elevated oxidative stress can also impair insulin secretion. In both type 1 and type 2 diabetes, chronic hyperglycemia contributes to complications in target organs. High glucose levels trigger the production of reactive oxygen (ROS) and reactive nitrogen species, which damage DNA, proteins, and lipids, and activate stress-sensitive pathways such as nuclear factor kappa B (NF-κB) and p38 mitogen-activated protein kinase [78]. In T2D, elevated glucose and free fatty acid levels further activate these pathways, contributing to both insulin resistance and impaired insulin secretion [78]. Studies have reported increased oxidative and endoplasmic reticulum stress in pancreatic β-cells under hyperglycemic conditions, adversely affecting insulin production [79]. Furthermore, oxidative stress compromises insulin sensitivity and contributes to insulin resistance by impairing glucose uptake into cells [66]. Accumulating evidence indicates that oxidative stress plays a central role in β-cell dysfunction and insulin secretory failure in T2D [80,81].

Dietary bioactive compounds, including antioxidants, play a crucial role in protecting pancreatic β-cells from oxidative stress, which is a key factor in the development and progression of diabetes [82,83]. Dietary antioxidants may protect β-cells by inhibiting NF-κB activity [84] and by activating nuclear factor erythroid-derived factor 2-related factor 2 (Nrf2), a transcription factor that upregulates antioxidant and cytoprotective genes [85]. NF-κB is a transcription factor that regulates the expression of genes involved in inflammation and immune responses. The activation of NF-κB increases the production of pro-inflammatory cytokines, which can damage β-cells [86]. Meanwhile, Nrf2 is a transcription factor that regulates the expression of antioxidant and cytoprotective genes. Nrf2 activation upregulates antioxidant enzymes and proteins, which help to neutralize ROS and reduce oxidative stress [87]. Studies have shown that polyphenols and other dietary antioxidants can inhibit NF-κB activation and reduce oxidative stress [88] and activate the Nrf2 pathway [89], thereby protecting β-cells from oxidative damage and improving their function.

Dietary antioxidants also help maintain serum antioxidant levels and mitigate oxidative stress, which is essential for overall health [90]. Vahid et al. [91] reported that higher dietary antioxidant intake was associated with increased serum TAC. Similarly, Jewell et al. [92] found that an antioxidant blend—including vitamin E, vitamin C, and β-carotene—increased cellular protection and improved antioxidant status in dogs and cats. Avila-Escalante et al. [11] demonstrated that a high-antioxidant diet enhances plasma antioxidant capacity and reduces oxidative stress markers in individuals with various chronic diseases. Therefore, incorporating antioxidant-rich foods into the diet is crucial for maintaining overall health and preventing chronic diseases.

In summary, as illustrated in Figure 2, consumption of antioxidant-rich foods enhances circulating antioxidant levels and mitigates oxidative stress. This effect contributes to reduced insulin resistance, improved insulin secretion and sensitivity, and ultimately lower blood glucose levels, thereby decreasing the risk of T2D and its associated complications.

Strengths of the Study

The included investigations were conducted in diverse regions worldwide, enhancing the generalizability of the findings. The recent publication dates of most studies indicate that the topic is current. The presence of several prospective cohort studies with substantial sample sizes strengthens the statistical power of the results. Additionally, most studies accounted for potential confounders in their analyses of the DTAC–diabetes risk relationship, underscoring the independent role of DTAC.

Limitations of the Study

Several studies did not adequately consider covariates in their statistical analyses, and diverse statistical methods were employed across investigations. Furthermore, different techniques were used to calculate DTAC, and varying cut-off points were applied when categorizing DTAC values, which may have influenced the findings. The heterogeneity among the included studies—in terms of study populations, measured outcomes, and methodologies (including statistical analyses and DTAC evaluation methods)—precluded the performance of a meta-analysis and limited the ability to draw definitive conclusions.

Conclusion

The majority of existing evidence indicates that high adherence to an antioxidant-rich diet may reduce diabetes risk and improve glycemic biomarkers, including FBG, insulin, and HOMA-IR.

Implications of the Findings

The findings of this study have significant public health implications, particularly in managing T2D. They provide valuable insights for developing dietary recommendations aimed at preventing chronic diseases. Improved blood glucose parameters can lead to better glycemic control, reducing the risk of diabetes-related complications such as cardiovascular disease, neuropathy, and nephropathy. Enhanced glycemic control further contributes to overall metabolic health and quality of life for individuals with or at risk for T2D.

HIGHLIGHTS

• Oxidative stress contributes to the pathophysiology of diabetes.

• An antioxidant-rich diet intake may reduce diabetes risk.

• An antioxidant-rich diet intake may improve glycemic biomarkers, including fasting blood glucose, insulin, and homeostatic model assessment for insulin resistance.

Supplementary Material

Article information

Ethics Approval

The ethics committee of Tabriz University of Medical Sciences, Tabriz, Iran, registered and approved the protocol of this study (IR.TBZMED.REC.1401.824).

Conflicts of Interest

The authors have no conflicts of interest to declare.

Funding

This study was financially supported by Tabriz University of Medical Sciences (Project No: 70938).

Availability of Data

All study-related data are included in the publication or provided as supplementary information.

Figure 1.

Flow diagram of the study. DTAC, dietary total antioxidant capacity.

Figure 2.

Potential mechanistic pathways for the association between dietary total antioxidant capacity and the diabetes risk and its related glycemic biomarkers.

NrF2, nuclear factor erythroid-derived factor 2-related factor 2; NF-κB, nuclear factor kappa B; IRSP, insulin receptor signaling pathway.

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