This study shows that dietary zinc intake is strongly associated with SBP in obese Korean women. Dietary zinc intake was negatively correlated with SBP after adjusting for energy intake, and multivariate regression analysis revealed an inverse association between dietary zinc and SBP after adjusting for body weight, energy intake and sodium intake. These results suggest that zinc deficiency is an independent risk factor of an elevated blood pressure in obese Korean women.
The findings of previous studies agree with our results. Tomat et al. [9
] reported that moderate zinc restriction (9 mg/kg) for 60 days increased arterial blood pressure on day 30 and resulted in lower urinary excretion levels of nitrates and nitrites in three-week-old weaned male rats. Sato et al. [24
] showed that spontaneously hypertensive (SH) rats fed zinc deficient diet (6.5 µg Zn/day) for 2 weeks exhibited a progressive increase in systolic blood pressure, whereas SH rats fed a standard diet (0.26 g Zn/day) did not. On the other hand, some have reported that zinc deficiency does not change blood pressure in rats or in human [11
]. Taittonen et al. [13
] found that dietary zinc was not associated with blood pressure in healthy children in a 6-year follow up study, and Sato et al. [11
] found that a zinc deficient diet for 4 weeks did not influence systolic or diastolic blood pressure in normotensive rats. However, these studies used different subjects and study conditions, and thus, direct comparisons are not possible. Nevertheless, conflicting results regarding the association between zinc status and blood pressure might be due to duration of diet treatment, the degree of zinc deficiency, the period of life involved (pregnancy, fetal life, weaning, childhood, adulthood), the presence of hypertension, and the environment.
The mechanism underlying the association between zinc status and blood pressure remains unclear. However, zinc deficiency may be associated with an impaired vascular nitric oxide (NO) system due to reduced NOS activity and an increase in oxidative stress caused by superoxide. NO is an important regulator of blood flow and blood pressure in mammals, because of its vasodilatory effects. Thus, it is likely that systemic NO impairment, due to an increase in the action of superoxide, could explain increased blood pressures levels. Zinc deficiency reduces NOS activity because NOS contains zinc, and reduced NOS activity in artery walls could cause endothelial dysfunction and reduce endothelium-mediated vasodilation, and thus, contribute to the development of hypertension [25
]. Furthermore, many enzymes that are involved in the regulation of arterial blood pressure, such as angiotensin-converting enzyme and neutral endopeptidases, contain zinc [28
]. In addition, zinc deficiency reduces the activity of superoxide scavengers, such as, Cu/Zn SOD. Sato et al. [24
] showed that the administration of NOS inhibitor increased arterial pressure, and that conversely, the administration of superoxide scavenger (Cu/Zn SOD) decreased arterial pressure in genetically hypertensive rats. Therefore, adequate zinc intake seems to be necessary to maintain endothelial cell integrity and normal blood pressure, because this zinc has antioxidant effects and membrane-stabilizing properties [4
In the present study, we failed to find any significant association between serum zinc levels and blood pressure in obese women, which may have been due to zinc homeostasis. Serum zinc concentrations are maintained within a narrow range even when dietary zinc levels fluctuate [21
]. In a 6-year follow up study, it was found that serum zinc levels were not correlated with blood pressure either during the year of measurement or during subsequent years in 3,596 healthy children [13
], which concurs with our results. Thus, reported differences regarding relationships between markers of zinc status and blood pressure support a hypothesis of modified zinc homeostasis and of borderline zinc deficiency in tissues. Another possibility is that the women in the present study had normal blood pressures even though they are obese. This might cause no relationship between serum zinc concentration and blood pressure in obese women. Bergomi et al. [10
] found no relationship between serum zinc levels and blood pressures in normotensive adults, but did find that serum zinc levels were inversely correlated with blood pressures in hypertensive subjects.
This study is limited by its cross-sectional design, which prevented the identification of a causal relationship between dietary zinc intake and the risk of an elevated blood pressure. Despite this limitation, the study involved the collection of various lifestyle factors, dietary data, and anthropometric and blood pressure measurements by trained staff using standardized protocols. Furthermore, this study is the first to examine the relationship between zinc status and blood pressure in an obese population by multivariate analysis adjusted for potential confounding factors, such as body weight, energy intake and sodium intake.
In conclusion, dietary zinc was found to be inversely associated with SBP in obese Korean women after adjusting for body weight, energy intake and sodium intake, which suggests that zinc deficiency is an independent risk factor of elevated blood pressure in this subpopulation. We recommend that large-scale clinical trials and longitudinal studies be undertaken to investigate the possibility of a causal relationship between zinc status and blood pressure in different populations.