Hypertension, a progressive and damaging cardiovascular disease characterized by persistent elevation of arterial blood pressure, is the highest death toll worldwide, accounting for roughly 14% of all deaths (1). The World Health Organization reports a yearly rise in the incidence of hypertension, which influences more than 1.3 billion people globally (2), and the age at which it starts tends to be younger. Dietary factors, exceptionally high salt, low potassium diets, and excessive alcohol intake are significant contributors to the development of hypertension (3). To prevent the start and progression of hypertension, a deeper comprehension of the connection between dietary practices and hypertension risk is necessary.

Selenium is a necessary trace element that is a part of selenoproteins, which have a significant physiological function in the body. Selenoproteins contain the most prominent selenium compound, selenocysteine, an antioxidant and redox regulator that protects cells from oxidative stress and free radical damage (4). It is reported that the immune system, oxidative stress, and the inflammatory response are all involved in the initiation and progression of hypertension (5). These factors are also intimately linked to the consequences of hypertension, such as cardiac damage, hemorrhagic stroke, and renal injury (6).

Remarkably, prior epidemiologic research has concentrated chiefly on the value of blood selenium levels rather than emphasizing selenium intake. Therefore, we used data from the National Health and Nutrition Examination Survey (NHANES) from 2003–2018 to explore the association between dietary selenium intake and the prevalence of hypertension.

The study involving 32,928 adults found a significant inverse correlation between dietary selenium intake and hypertension. This suggests that individuals with higher dietary selenium intake may have a lower prevalence of hypertension. Interestingly, this association remained consistent across different demographic groups, including age, gender, BMI, smoking and alcohol use statuses, and diabetes statuses. These findings highlight the potential benefits of increasing dietary selenium intake for reducing the prevalence of hypertension in various populations.

Selenium is a vital micronutrient that is crucial for maintaining human health, particularly in the areas of energy metabolism and gene expression (7). Additionally, selenium performs a range of important functions, such as acting as an antioxidant (8), reducing inflammation (9), regulating the immune system (10), promoting anti-aging effects (11), and potentially inhibiting tumor growth (12). One of the most prevalent and extensively distributed members of the glutathione peroxidase (GPx) class of selenium-dependent enzymes, GPx-1 is responsible for ensuring that cells have the proper amounts of reduced glutathione. Reduced glutathione helps to scavenge dangerous chemicals, such as hydrogen peroxide and lipid hydroperoxides, and prevents them from accumulating within the cell, so protecting the cell from oxidative damage. Selenium deficiency has been associated with various chronic metabolic diseases, including hyperlipidemia, atherosclerosis, hyperglycemia, and hyperphenylalaninemia (13). While micronutrient supplements are becoming increasingly popular for improving health, excessive selenium intake can be harmful. The recommended daily intake for adults is 70μg, with a tolerable upper limit of 400μg. Previous research has indicated a link between dietary selenium intake and various clinical conditions. For instance, high selenium intake has been associated with an increased risk of osteoarthritis (OA), while lower intake (less than 100μg) is not associated with an increased risk of OA (14). It has been found that excessive selenium intake can disrupt the insulin signaling pathway, leading to hyperglycemia and obesity, contributing to systemic inflammation, which is a significant factor in OA and hypertension (15). Furthermore, dietary selenium intake was found to be negatively associated with kidney stones (16), post-stroke depression (17), and stroke risk in adults over the age of 60 (18).

Hypertension is a common cardiovascular disease characterized by a sustained elevation of blood pressure, which can lead to alterations and damage to the structure and function of the heart, brain, kidneys, and fundus. Therefore, the management and prevention of hypertension have become a global public health priority (19). Previous studies have shown mixed results regarding the relationship between blood selenium levels and hypertension. For example, the Kuopio Ischemic Heart Disease Risk Factor Study found a negative correlation between serum selenium and systolic blood pressure (20), while a study of elderly men in rural Finland found no correlation (21). Additionally, a cross-sectional study of 2,638 individuals aged 40 and above in the NHANES revealed a link between high serum selenium concentrations and a higher incidence of hypertension (22), suggesting the need for further research in this area.

Despite being a widespread chronic illness, hypertension’s precise molecular causes are unknown, despite the fact that a number of studies have demonstrated a significant role for inflammation in the onset and progression of the condition (23). The association between inflammatory indicators and hypertension risk was evaluated by investigators. through a meta-analysis of cohort studies. They discovered that elevated levels of hs-CRP and IL-6 were linked to a higher risk of hypertension (24). A more recent study by Mohammad Gholizade et al. found that selenium supplementation reduced CRP and IL-6 plasma concentrations (25). The production of interleukin-6 is strongly correlated with the activation of the nuclear factor κ b (NF - κ b) signaling pathway, which is linked to heightened inflammatory responses. Because selenium controls the expression of the selenoprotein gene, it may prevent NF-kappaB activation. Furthermore, selenium supplementation in chronic inflammation may lessen the inflammatory process by boosting the synthesis of selenium-containing proteins to replenish the liver’s and the blood’s depleted selenium stores, which will stop the generation of CRP (26). It has been demonstrated that arterial stiffness is a significant cause of Isolated systolic hypertension in the elderly (27), increased risk of stroke (28), coronary artery disease, and heart failure that are associated (29). Arterial stiffness is associated with increased angiotensin II activity, increasing NADPH oxidase activity, decreasing NO bioavailability, and increasing reactive oxygen species production (30, 31). Hypertension is commonly distinguished by endothelial dysfunction, a condition predominantly characterized by a diminished bioavailability of NO. Endothelial NO synthase (eNOS) is essential for NO production in endothelial cells; inhibition or dysfunction of eNOS results in NO deprivation, which hinders endothelium-dependent vasodilation and exacerbates the progression of hypertension. On the contrary, selenium increases NO synthesis by stimulating NO synthase (NOS) activity (32). Selenium additionally inhibits NO degradation and preserves NO stability (33). Arterial stiffness primarily arises from vascular remodeling, characterized by alterations in the structure and function of blood vessel walls. These modifications include wall thickening, an elevation in the wall-to-lumen ratio, and a reduction in microarterioles (34). These modifications result in atypical vascular functioning, impacting circulation, oxygenation, and blood provision (35). Furthermore, inflammatory factors, including IL-1, IL-17, and IL-6, are stimulated by AngII signaling (27). Arterial rigidity is associated with inflammation; vascular remodeling is slowed by inhibiting inflammation, and the risk of hypertension is decreased (36).

Our study has strengths, including a focus on dietary selenium intake and its association with hypertension, which is a novel contribution compared to previous research that primarily concentrated on serum selenium levels. Additionally, we rigorously adjusted for confounding variables to enhance the reliability of our findings. Nevertheless, it is crucial to recognize the shortcomings of our study. To begin with, the cross-sectional design constrains our capacity to establish causation, allowing only for the identification of correlations. In addition, the reliance on self-reported dietary information from the NHANES questionnaire introduces potential subjective bias. Moreover, the questionnaire may not accurately capture long-term dietary patterns due to the variability in an individual’s daily diet. Lastly, genetic variation, dietary habits, and socioeconomic factors are also significant contributors to cardiovascular disease susceptibility. Therefore, more research and research is needed on whether the conclusions drawn in this study apply to populations of different ethnicities and regions.

Our findings suggest an independent association between higher dietary selenium intake and reduced hypertension prevalence, warranting further large-scale prospective studies for validation.

The original contributions presented in the study are included in the article/supplementary material. Further inquiries can be directed to the corresponding author.

This study was approved by the National Center for Health Statistics Research Ethics Review Board. The participants provided informed consent to participate in the NHANES survey. The NHANES protocol complies with the U.S. Department of Health and Human Services Policy for the Protection of Human Research Subjects. NCHS IRB/ERC Protocol number: 2011-17. Ethical review and approval were waived for this study as it solely used publicly available data for research and publication.

YW: Writing – original draft. ZY: Writing – original draft, Writing – review & editing.