Obesity (1), a chronic metabolic condition, is classified into two types: abdominal obesity and non-abdominal obesity. Abdominal obesity, which is resulted from an excess of buildup of fat caused by the imbalance between the body’s caloric intake and consumption, is the result of the interplay of genetics, environmental variables such as poor food, long-term inactive and insufficient activity, and other factors (2–5). According to a research based on NHANES population, the prevalence of obesity among U.S. adults was 43.4% (6). Obesity is considered a global pandemic, with health hazards affecting practically everyone, particularly abdominal obesity, that is more dangerous than non-abdominal obesity. Obesity (7) also raises the risk of cardiovascular illnesses including atherosclerosis, venous thrombosis, and hypertension, as well as diabetes, cancer, and even all-cause mortality. According to a WHO research in 2018 (8), at least 2.8 million individuals worldwide died of overweight or obesity each year. This is why controlling and managing obesity is critical.

The removal of reactive oxygen species (ROS) that harm an organism is a process known as anti-oxidation. To attain the objective of antioxidation, people can supplement with antioxidants (including vitamins such as vitamins A, C, and E, carotenoids such as α-carotene and β-carotene), or supplement with a suitable quantity of proteins and trace elements such as iron, zinc, selenium, copper, retinol, and so on (9–11). These elements (12–14) are also currently considered to be the nutritional micronutrients associated with obesity. Some studies (14–16) have revealed that obesity development rates are higher in places where micronutrient deficiencies are more frequent, while others have discovered that deficiencies in particular micronutrients may be related to increased aberrant fat deposition in the body. The effect of micronutrients on obesity may occur through changing leptin concentrations in the blood, which control food intake and energy expenditure, leading to changes in adipose tissue mass, and also by regulation of the inflammatory response.

However, considering that the impact of micronutrients is usually dependent on their interaction with one another, their overall effect on the body may differ from that of single antioxidant, and their contribution to the development of obesity may change. Therefore, in this study, the 11 antioxidant micronutrients mentioned above were studied as a whole to investigate their relationship with obesity, and then each antioxidant micronutrient was assessed individually to determine its proportional association with obesity, to examine the relationship between each antioxidant micronutrient and the prevalence of obesity.

After correcting for common confounders, our research of 11 dietary antioxidant micronutrients in a cross-sectional, nationally representative general US population revealed that a combination of 11 antioxidant micronutrients was protective against the prevalence of both obesity and abdominal obesity, i.e., a negative correlation existed between obesity and the combination of 11 antioxidant micronutrients. However, we observed that not all antioxidant micronutrients were reliably protective for those who were both overweight and had excess fat in their abdominal regions. In the WQS model, the weight of each micronutrient showed that practically all antioxidants, except selenium, were negatively related to obesity, notably iron and vitamin C. In our multiple logistic regression study, we found that almost all of the antioxidant micronutrients were independently correlated negatively with obesity, except vitamin E, retinol, and zinc, and that selenium was correlated favorably with obesity. Additionally, the RCS analysis showed that there was a nonlinear relationship between obesity and Retinol, vitamin A, α-carotene, β-carotene, β-cryptoxanthin, vitamin C, Iron, and Cooper, with inflection points at 235.57, 374.81, 58.89, 891.44, 30.70, 43,410.00, 11,240.00, and 990.00 g/day, respectively. While inflection points were found at 7,360.00, 385.34, 55.72, 820.30, 27.86, 42,813.00, 130.69, and 933.00 g/day for vitamin E, vitamin A, α-carotene, β-carotene, β-cryptoxanthin, vitamin C, selenium, and Cooper, respectively, in abdominal obesity.

Factors including as genetics, diet, good physical activity, environment, and socioeconomic status all have a role in the development of obesity which is strongly linked to oxidative stress (19). Current evidence shows that oxidative stress may promote obesity by boosting preadipocyte proliferation, accelerating white adipose tissue (WAT) deposition, and modifying food intake and that obesity can produce systemic oxidative stress by numerous mechanisms, including superoxide generation by NADPH oxidase, oxidative phosphorylation, protein kinase C activation, polyol, and hexosamine pathways, further exacerbating obesity (20). In the meanwhile, dietary antioxidants have gained popularity for their ability to neutralize free radicals in the body. As a result, growing studies are looking at the link between fat storage and antioxidant levels in obese people. Aeberli et al. found in Swedish children that dietary intake of antioxidant vitamins (vitamin E and vitamin C and β-carotene) was significantly associated with leptin levels (p < 0.05), suggesting that low concentrations of antioxidant vitamins may alter the genetic expression of leptin, leading to the development of leptin resistance and increasing the risk of obesity (21, 22). Another cross-sectional investigation revealed that blood levels of vitamin C were substantially correlated with food intake (23). Vitamin C scavenges free radicals and suppresses lipid peroxidation, which leads to increased vitamin C utilization and decreased vitamin C in the blood in obese people as a result of increased body fat and increased systemic oxidative stress (24). Furthermore, research has revealed that vitamin deficits are linked to abdominal fat formation in obese persons. For example, one Indian research (25) discovered a negative relationship between vitamin C and total body fat. A case–control study in Thailand (26) found a negative association between BMI, waist, and hip circumference and serum concentrations of vitamin E and retinol, and another study (27) showed a significant association between vitamin A and insulin resistance in morbidly obese patients which may be due to the fact that high doses of vitamin A may inhibit the formation of mature adipocytes and also indirectly modifies insulin sensitivity by regulating the production of bioactive proteins secreted by adipocytes, including leptin and resistin. Retinol and carotenoids are precursors to vitamin A. According to certain studies, dietary beta-carotene and its blood levels are favorably associated (28). Serum beta-carotene levels were also shown to be lower in obese persons, most likely because carotenoids are primarily distributed between serum and adipose tissue, and because adipose tissue is an essential storage tissue in humans, a greater proportion of carotenoid intake would be absorbed by adipose tissue in individuals with high adiposity than in those with low adiposity (29–31). This also implies that obese people need consume more carotenoids in order to satisfy their antioxidant requirements. Additionally, research has shown that carotenoids (32–34) which has been proven to improve insulin resistance, reduce the size of adipocytes and body fat tissue, lower pro-inflammatory indicators of obesity such as LDL-c and VLDL-c, and raise high-density lipoprotein cholesterol (HDL-c), among other benefits promote prevention. These previous studies are consistent with our partial results that vitamin A, vitamin C, iron, β-cryptoxanthin, and carotenoids are associated with obesity and are negatively correlated and are an independent protective factor.

Interestingly, we discovered that selenium is not an independent protective factor against obesity, but is positively related to it. Selenium is well-known for working as an antioxidant to influence the thyroid, immune system, and reproduction. Some studies have discovered a significant correlation between dietary selenium intake and obesity. Hawkes et al. study’s revealed that those who consumed more selenium gained weight, whereas those in the low-selenium group lost weight (35). Liver cirrhosis and steatosis, which may be caused by obesity, were shown to be positively correlated with increased dietary selenium intake and blood selenium concentrations by Liu. et al. (36). Furthermore, multiple studies have revealed a link between dietary selenium intake and blood selenium levels and an increased risk of type 2 diabetes in diverse groups (37–39). Meanwhile, Excessive selenium exposure has been seen with similar negative consequences in animal experiments, and one possible explanation is that selenoproteins activate the development of insulin resistance. New evidence suggest that selenium toxicity manifests as oxidative stress, blocked biofilm development, and enzyme function suppression when present in excessive amounts. The results match up with what we found.

Zinc’s possible association with obesity remains controversial. Zinc is a vital vitamin that aids in organism development, reproductive tissue repair, and cellular immunity. It has been linked to the degree of obesity in several studies. Zinc deficiency can stimulate fat deposition and raise body weight (37, 38, 40). Similarly to this, the link between zinc status and obesity may be explained by the interaction between zinc metabolism and leptin, since zinc shortage reduces leptin levels in the blood in humans and rat adipocytes while zinc supplementation has the opposite effect (41, 42).Visceral adipose tissue accumulation was induced by long-term zinc supplementation in mice experiments without the involvement of adipogenesis or adipolysis (43). Based on our findings, we found that zinc does not function as a standalone protective factor against obesity and has a modest protective impact against weight gain. It has been suggested that taking zinc supplements may weaken the immune system, lower HDL cholesterol levels, etc., which could lead to copper deficiency or an increase in copper deficiency (44), but researchers still need to figure out the exact mechanism.

Nevertheless, the antioxidant capacity of nutrients can be influenced by other members of the internal antioxidant network, which is another key factor to consider. For instance, vitamin C and vitamin E are known to work together to renew α-tocopherol in membranes and lipoproteins, which is crucial for protecting protein thiol groups from oxidation (45). The change in carotenoids’ (33, 46) prooxidant and antioxidant behavior has also been found to depend on their interaction with vitamin C and vitamin E in biological membranes. Also zinc status can affect vitamin A metabolism, including its absorption, transport, and utilization (47). Both the zinc-dependent conversion of retinol oxidation to the retina by the action of retinol dehydrogenase and the regulatory function of zinc in vitamin A transport mediated by protein synthesis are believed to be involved in this process.

Therefore, the biological effects of antioxidant micronutrients cannot be adequately explained by a single nutrient model. Recently, researchers in the area of nutritional health have begun to shift their attention from looking at the effects of individual nutrients on health to the effects of being exposed to combinations of nutrients. Here, the inverse association found between obesity and 11 different antioxidant combinations is evaluated using WQS regression, with iron and vitamin C accounting for the bulk of the impact.

Despite being the second most common metal on Earth, iron has poor bioavailability in humans because it often forms very insoluble oxides. Obesity is strongly linked to iron deficiency (48–50), and research (51) has found that one of the pathological mechanisms involved in obesity is iron deposition in the cytoplasm of adipocytes, which results in increased iron content in adipose tissue, possibly as a result of a fourfold increase in intracellular iron content in adipocytes and the expression of iron regulatory proteins. Some animal studies (52, 53) have revealed that a high iron diet may lead to elevated leptin levels in the body, whereas iron produces endocrine dysfunction in adipose tissue and decreases adipocyte lipocalin synthesis. This is consistent with our analysis that iron is independently associated with obesity and vice versa. In addition, we found from a threshold effect analysis that iron intake above 11.24 mg/day may contribute to reduced obesity prevalence. Vitamin C (VC, ascorbic acid) has been shown to prevent obesity by the followings (54): (a) regulating lipid accumulation in adipocytes through direct action on differentiation mechanisms or by modulating motor behavior, (b) inhibiting lipolysis and thus reducing the export of fatty acids to the system, (c) inhibiting glucocorticoid production, and (d) directly interfering with adipose cell-macrophage interactions, (e) scavenging of reactive oxygen species, and (f) possible inhibition of the HIF-1a pathway. Our threshold impact study also revealed that consuming more than 43.41 milligrams of vitamin C per day may have contributed to lower obesity rates. Future dietary strategies for the prevention and treatment of obesity might be devised using these results as a reference dosage, but the precise intake for the population still has to be determined by experimental trials.

Our research has various benefits, not the least of which is that we are the first to explore the connection between 11 micronutrients and obesity in a single cohort. For one, to mitigate mistakes and prevent low correlation components from influencing the analysis, we accounted for the age, education, race/ethnicity, socioeconomic situation as well as other possible complicating variables like (BMI, smoking or not, total energy intake, etc.) which may influence the correlation between antioxidant micronutrients and obesity in the RSC model and the WQS regression model. Second, we have confirmed the accuracy of our findings by verifying them using two distinct models.

However, our study has several limitations. Firstly, we were restricted in our ability to draw causal inferences due to the cross-sectional design of the survey. Second, we may have introduced some unintentional bias into our study by limiting ourselves to focusing on the link between micronutrient intake and obesity and not also considering the role of micronutrient supplementation. At the same time, we did not investigate the relationship between circulating levels of antioxidant micronutrients and obesity, which might be a future research topic. Thirdly, our study’s analysis was limited to the NHANES cohort in the United States; the conclusions would have had greater weight if they had been corroborated by data from other nations or areas.

According to our research, the combination of 11 antioxidants is negatively associated with the prevalence of obesity, and iron/vitamin C have the greatest weight in the negative associations between antioxidant complex and obesity, as well as abdominal obesity. Future studies are required to analyze and determine the ideal intake amounts to lower obesity in at-risk individuals, as well as to better understand the interactions and complex of many micronutrients and their combined impact on obesity.

The original contributions presented in the study are included in the article/Supplementary material, further inquiries can be directed to the corresponding authors.

YY and HX designed research, drafted the manuscript, performed statistical analysis, extracted the data, and conducted analyses. YZ, LC, and CT took charge of software operation. LM, YC, and BH revised the manuscript. All authors reviewed, edited, and finalized the final version of the manuscript.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.