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However, there was no significant association between plasma zinc and first total stroke (<104.0 versus ≥104.0 μg/dL [median]; multivariate-adjusted odds ratio, 0.93; 95% CI, 0.69–1.25) and first ischemic stroke (<103.3 versus ≥103.3 μg/dL [median]; multivariate-adjusted odds ratio, 1.16; 95% CI, 0.83–1.61; Table 2).
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Read More »In this sample of hypertensive patients, we found a significant, inverse association between plasma zinc and first hemorrhagic stroke. Compared with participants with baseline plasma zinc <106.9 μg/dL (median), a significantly lower risk of first hemorrhagic stroke was found in those with plasma zinc ≥106.9 μg/dL (multivariate-adjusted odds ratio, 0.45; 95% CI, 0.21–0.94). Furthermore, the inverse plasma zinc-first hemorrhagic stroke association was significantly stronger in participants with body mass index ≥25.0 kg/m 2 or plasma copper <100.1 μg/dL at baseline ( P interaction <0.05 for both variables). However, there was no significant association between plasma zinc and first ischemic stroke (<103.3 versus ≥103.3 μg/dL [median]; multivariate-adjusted odds ratio, 1.16; 95% CI, 0.83–1.61). The study population was drawn from the CSPPT (China Stroke Primary Prevention Trial), using a nested case-control design, including 599 first stroke cases and 599 matched controls. We aimed to examine the relation of baseline plasma zinc with the risk of first stroke and investigate any possible effect modifiers in hypertensive patients. Zinc is the second most abundant essential mineral in the body, and it supports a wide range of biochemical functions.1 According to previous studies, zinc deficiency has been associated with damage to the immune, central nervous, and reproductive systems, as well as causing cardiovascular diseases.1 However, most previous studies that investigated the association between blood zinc and the risk of stroke were cross-sectional2 or case-control3–6 in design, and the reported findings have been inconsistent. Prospective studies concerning the association between plasma zinc and the risk of stroke are limited, particularly in hypertensive populations. To address these significant gaps in knowledge outlined above, the current study aimed to examine the relationship of baseline plasma zinc with the risk of first stroke (overall and subtypes) among hypertensive patients in a nested, case-control design, using data from the CSPPT (China Stroke Primary Prevention Trial, n=20 702).7
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Read More »The current study demonstrated an inverse association between plasma zinc and the risk of first hemorrhagic stroke in hypertensive patients; this association was even stronger among those with higher BMI or lower plasma copper levels. Zhao et al10 have investigated the detrimental impact of the excess of zinc following ischemia in experimental brain ischemia. Our study, however, only included participants without major cardiovascular diseases. Moreover, the zinc levels found in our study population may not be high enough to promote cerebral mitochondrial reactive oxygen species production in brain tissue. Therefore, we did not find a significant association between plasma zinc and the risk of ischemic stroke in the present study. Consistently, a recent case-control study3 including 1277 ischemic stroke patients and 1277 control subjects also showed no significant correlation between plasma zinc and risk of ischemic stroke in a Chinese population. The association and the underlying mechanisms between plasma zinc and ischemic stroke needs further investigation in more studies. The exact mechanism underlying the plasma zinc-first hemorrhagic stroke association, especially in populations with higher BMI or lower plasma copper levels, remains unclear. Hemorrhagic stroke is mainly because of rupture and pathological changes of small vessels. Obesity is a recognized risk factor for stroke because of its capacity to impair mitochondrial function and cause systemic inflammation.11 There is a high prevalence rate of obesity in hypertensive patients in China.12 Zinc plays a part in the regulation of cytokine expression and has anti-inflammatory and antioxidant effects, protecting vascular cells from free radical and inflammatory injury.13 Therefore, we speculate that high zinc levels may reduce the inflammatory and oxidative damage associated with obesity, and therefore have a greater effect on hemorrhagic stroke risk. Shellfish and meats are the major dietary sources of zinc, whereas organ meats (liver), seafood, and nuts are the major dietary sources of copper.14 In our study, the stronger inverse zinc-hemorrhagic stroke relationship was also found in those with lower plasma copper levels. It has been hypothesized that copper ions catalyze the production of OH from H 2 O 2 . Zinc may compete with copper for binding to the cell membrane, thus decreasing the production of OH.15 In this way, increased zinc levels and decreased copper levels might jointly reduce any oxidative damage and the related hemorrhagic stroke risk. Our findings, if further confirmed, may inform clinical and nutritional research on hemorrhagic stroke, by considering zinc as a potentially modifiable risk factor, especially for individuals who are obese or with high plasma copper levels. However, more studies are needed to confirm our findings and to further investigate the underlying mechanisms. There are several potential limitations to our study. First, the current study was a post hoc analysis of the CSPPT. Any residual confounding effects cannot be fully accounted for. Furthermore, the relatively small sample size may cause types I and II statistical errors. However, adjusting for the covariates strengthened the relationship, the results of which may possibly indicate that the observed zinc-hemorrhagic stroke relationship may not be a product of incomplete adjustment for potential confounding variables. Second, our current study used the data from the CSPPT, in which all of the study participants had hypertension and used an enalapril-based antihypertensive treatment. As such, the generalizability of our results to populations without hypertension and without the use of enalapril remains to be determined. Third, only data on plasma zinc concentrations at baseline were available. We could not evaluate the effect of folic acid treatment on plasma zinc or copper concentrations. Because of these limitations, our study was just hypothesis-generating. These findings need to be further examined and confirmed in future studies.
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