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Dietary selenium intake and mortality in two population-based cohort studies of 133 957 Chinese men and women

Published online by Cambridge University Press:  20 May 2016

Jiang-Wei Sun
Affiliation:
School of Public Health, Fudan University, Shanghai, People’s Republic of China Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, No. 25 Lane 2200, Xie Tu Road, Shanghai 200032, People’s Republic of China
Xiao-Ou Shu
Affiliation:
Division of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN, USA
Hong-Lan Li
Affiliation:
Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, No. 25 Lane 2200, Xie Tu Road, Shanghai 200032, People’s Republic of China
Wei Zhang
Affiliation:
Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, No. 25 Lane 2200, Xie Tu Road, Shanghai 200032, People’s Republic of China
Jing Gao
Affiliation:
Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, No. 25 Lane 2200, Xie Tu Road, Shanghai 200032, People’s Republic of China
Long-Gang Zhao
Affiliation:
Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, No. 25 Lane 2200, Xie Tu Road, Shanghai 200032, People’s Republic of China
Wei Zheng
Affiliation:
Division of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN, USA
Yong-Bing Xiang*
Affiliation:
Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, No. 25 Lane 2200, Xie Tu Road, Shanghai 200032, People’s Republic of China
*
*Corresponding author: Email ybxiang@shsci.org
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Abstract

Objective

To investigate the potential influence of dietary Se intake on mortality among Chinese populations.

Design

We prospectively evaluated all-cause, CVD and cancer mortality risks associated with dietary Se intake in participants of the Shanghai Women’s Health Study (SWHS) and the Shanghai Men’s Health study (SMHS). Dietary Se intake was assessed by validated FFQ during in-person interviews. Cox proportional hazards models were used to calculate hazard ratios (HR) and 95 % CI.

Setting

Urban city in China.

Subjects

Chinese adults (n 133 957).

Results

During an average follow-up of 13·90 years in the SWHS and 8·37 years in the SMHS, 5749 women and 4217 men died. The mean estimated dietary Se intake was 45·48 μg/d for women and 51·34 μg/d for men, respectively. Dietary Se intake was inversely associated with all-cause mortality and CVD mortality in both women and men, with respective HR for the highest compared with the lowest quintile being 0·79 (95 % CI 0·71, 0·88; Ptrend<0·0001) and 0·80 (95 % CI 0·66, 0·98; Ptrend=0·0268) for women, and 0·79 (95 % CI 0·70, 0·89; Ptrend=0·0001) and 0·66 (95 % CI 0·54, 0·82; Ptrend=0·0002) for men. No significant associations were observed for cancer mortality in both women and men. Results were similar in subgroup and sensitivity analyses.

Conclusions

Dietary Se intake was inversely associated with all-cause and cardiovascular mortality in both sexes, but not cancer mortality.

Type
Research Papers
Copyright
Copyright © The Authors 2016 

Se, which is an essential trace element to maintain optimal human health, is incorporated into selenoproteins that have a wide variety of effects, ranging from antioxidant and anti-inflammatory effects to the production of active thyroid hormone( Reference Rayman 1 ). Low Se status has been associated with increased mortality from cancer, poor immune function, male infertility and cognitive decline( Reference Rayman 1 , Reference Papp, Lu and Holmgren 2 ). Meta-analyses of observational studies have provided some evidence for a beneficial effect of Se levels on bladder cancer( Reference Amaral, Cantor and Silverman 3 ), prostate cancer( Reference Etminan, FitzGerald and Gleave 4 ), lung cancer( Reference Zhuo, Smith and Steinmaus 5 ) and CHD( Reference Flores-Mateo, Navas-Acien and Pastor-Barriuso 6 ), but findings from randomized trials have been mixed. Besides, randomized trials assessing the use of supplements for primary prevention usually need long periods to affect health outcomes significantly and thus observational studies, such as cohort studies, may facilitate assessment of the association between long-term nutritional status and health outcomes.

Although several prospective studies have explored the association between Se levels and all-cause mortality, their findings have been mixed with some studies showing an effect of increasing Se on decreasing risk( Reference Lauretani, Semba and Bandinelli 7 Reference Bleys, Navas-Acien and Guallar 10 ) and some not( Reference Wei, Abnet and Qiao 11 ). Researchers often focused on the association between all-cause mortality and the Se concentration in serum or plasma. Few studies exist in the literature examining the association between dietary Se intake and all-cause and cause-specific mortality. Moreover, dietary intake of Se varies widely worldwide owing to variability in the Se content of soil and hence of plant foods and animal forage( Reference Rayman 12 ). In China, the level of Se intake exhibits huge variation ranging from toxic (approximately 5 mg/d in areas of Enshi County) or adequate–marginally adequate (approximately 30–90 μg /d) to low or deficient intake (Heilongjiang Province: 7–11 μg/d)( Reference Rayman 12 , Reference Combs 13 ).

Therefore, using data collected in the Shanghai Women’s Health Study (SWHS) and the Shanghai Men’s Health Study (SMHS), we assessed the average level of dietary Se intake in Shanghai and prospectively investigated the potential long-term associations of dietary Se intake with all-cause, cardiovascular and cancer mortality risks in middle-aged and older Chinese adults.

Methods

Study population

Participants from the SWHS and the SMHS were included in the analysis. Details regarding the designs and methods used in these studies have been described elsewhere( Reference Zheng, Chow and Yang 14 , Reference Shu, Li and Yang 15 ). Briefly, between March 1997 and May 2000, a total of 74 941 women aged 40–70 years were recruited for the SWHS (participation rate: 92·7 %); and between April 2002 and June 2006, a total of 61 480 men aged 40–74 years with no previous history of cancer were recruited for the SMHS (participation rate: 74·1 %). In-person interviews were conducted to obtain information on sociodemographic factors, dietary and lifestyle habits, physical activity and medical history using structured questionnaires. Anthropometric measurements including weight, height, and waist and hip circumferences were also conducted at baseline.

We excluded from the analysis participants who were immediately lost to follow-up after study enrolment (five women and fourteen men), had missing data for any of covariates of interest (957 women and 1135 men), and 125 women and 228 men with extreme energy intake (<3347 or >17 573 kJ/d (<800 or >4200 kcal/d) for men; <2092 or >14 644 kJ/d (<500 or >3500 kcal/d) for women). The resulting analytic cohort included 73 854 women and 60 103 men.

Dietary assessment

In both the SWHS and the SMHS, usual dietary intakes were assessed using semi-quantitative FFQ. The FFQ used in the SWHS included seventy-seven items that covered 85·6 % of foods commonly consumed in urban Shanghai in 1996( Reference Shu, Yang and Jin 16 ). A similar but extended FFQ with eighty-one items was used in the SMHS which captured 88·8 % of commonly consumed foods( Reference Villegas, Yang and Liu 17 ). During the in-person interviews, participants were asked about how frequently they consumed the food or food group during the preceding year (five categories: daily, weekly, monthly, yearly or never) and then followed by a question on the amount of food consumed each time, in liangs (1 liang=50 g). Each participant was also asked about whether he or she had taken supplements (vitamin A, B, C or E; a multivitamin; or calcium) at least three times per week continuously for more than 2 months.

The Chinese food composition tables( Reference Yang, Wang and Pan 18 ) were used to calculate daily intakes of total energy and nutrients. The reproducibility and validity of the FFQ in the SMHS/SWHS were determined using monthly (SMHS; n 12) or biweekly (SWHS; n 24) 24 h dietary recall evaluation over a 1-year period. The correlation coefficients for micronutrients ranged from 0·33 to 0·58 in the SMHS( Reference Villegas, Yang and Liu 17 ) and from 0·41 to 0·59 in the SWHS( Reference Shu, Yang and Jin 16 ).

Follow-up and outcome ascertainment

Study participants were followed up by in-person surveys every two to three years and annual record linkage with the Shanghai Vital Statistics Registry. For the SWHS, the response rates for the first, second, third and fourth surveys were 99·8%, 98·7%, 96·7% and 92·3 %, respectively. For the SMHS, the response rates for the first and second surveys were 97·6% and 93·7 %, respectively. All possible matches identified through the linkage were verified by home visits. The underlying cause of death was determined primarily on the basis of death certificate data from the Shanghai Vital Statistics Unit and coded according to the International Classification of Diseases, Ninth Revision (ICD-9). Our primary end point was death from any cause. We also examined deaths from CVD (ICD-9 codes: 390–459) and cancer (ICD-9 codes: 140–208).

Statistical analysis

Dietary Se intake was adjusted for total energy using the nutrient density method( Reference Willett, Howe and Kushi 19 ) and then categorized by quintile distribution, with the lowest quintile serving as the reference group. We used Cox proportional hazards regression models to determine the association of dietary Se intake with total and cause-specific mortality, with person-years as the underlying time metric. The proportional hazards assumption was evaluated using Schoenfeld residual plots and no evidence of violation was observed. Tests for linear trend across quintiles were estimated by assigning the median intake value for the quintile to each person and including this as a continuous variable in the regression model. Person-years of follow-up were calculated as the interval between baseline recruitment and the date of death, loss to follow-up or 31 December 2012, whichever was earlier.

We presented risk estimates separately for men and women. In minimally adjusted models, we included age and energy intake as covariates. In multivariable-adjusted models, we further adjusted for the following baseline factors: birth cohort (1920s, 1930s, 1940s, 1950s, 1960s); level of education (four categories: elementary school or less, middle school, high school, college or above); income (four categories: low, low to middle, middle to high, high); marital status (four categories); occupation (housewife (women only), manual, clerical, professional), BMI (four categories: <18·5 kg/m2, 18·5–24 kg/m2, 24–28 kg/m2, ≥28 kg/m2); physical activity (quartiles of MET-h/week per year, where MET=metabolic equivalent of task); energy-adjusted fat intake (g/4184 kJ (1000 kcal) per d, continuous); use of any vitamin supplement (yes/no); smoking status (for men: never, ever, current; for women: never, ever); drinking status (for men: never, ever, current; for women: never, ever); status with regard to a history of hypertension (yes/no), diabetes (yes/no), CHD (yes/no) and stroke (yes/no); and family history of cancer (yes/no). For women, menopausal status (yes/no) was also included in multivariate models.

To minimize the influence of possible reverse causation owing to the presence of chronic diseases at baseline, sensitivity analyses were conducted by excluding the first 2 years of follow-up and restricting the analyses to participants who did not have a history of hypertension, diabetes, CHD or stroke at baseline, or family history of cancer. We also restricted the analysis among lifetime non-smokers to eliminate the potential confounding effect of cigarette smoking on the association between dietary Se intake and death. In secondary analyses, we examined associations among pre-specified baseline subgroups based on the following: BMI, drinking status, use of any supplement; and in women, menopausal status.

Analyses were performed with the statistical software package SAS version 9.2. Statistical tests were two-sided, and P values of less than 0·05 were considered statistically significant.

Results

Se intake and dietary, lifestyle factors

The average estimated dietary Se intake was 45·48 μg/d for women and 51·34 μg/d for men, which is close to the recommended nutrient intake level of 50 μg/d for the Chinese population( Reference Yang, Wang and Pan 18 ). Compared with participants in the lowest quintile of Se density intake, those in the highest quintile were younger, with lower BMI and were less likely to exercise, but had higher total energy and fat intakes, family income and educational level. They were also more likely to use multivitamin supplements, but less likely to have a history of hypertension, CHD and stroke. Men in the highest quintile were also more likely to smoke and consume alcoholic drinks (Table 1).

Table 1 Baseline characteristics by energy-adjusted quintile of selenium intake in the Shanghai Women’s Health Study (SWHS; 1997–2000) and the Shanghai Men’s Health Study (SMHS; 2002–2006)

The median and cut-off points for the quintile of Se intake in the SWHS were 15·86 (7·19–19·04), 21·16 (19·05–23·15), 25·18 (23·16–27·31), 30·02 (27·32–33·35) and 42·22 (33·36–124·64) μg/4184 kJ (1000 kcal) per d and in the SMHS were 16·46 (7·43–19·36), 21·33 (19·37–23·20), 25·09 (23·21–27·11), 29·72 (27·12–32·91) and 41·70 (32·92–165·38) μg/4184 kJ (1000 kcal) per d.

High educational level was defined as college or above.

High income was defined as a family income greater than 30 000 Yuan per year for women or a personal income greater than 2000 Yuan per month for men.

§ Physical activity: metabolic equivalent of task (MET)-h/week per year (1 MET-h=15 min of moderate-intensity activity).

|| Use of any vitamin A, B, C or E supplements, multivitamins or calcium.

Dietary Se intake and total mortality

During an average follow-up of 13·90 years in the SWHS and 8·37 years in the SMHS, we documented 9966 deaths from all causes (4217 men and 5749 women), including 3154 deaths from CVD (1402 men and 1752 women) and 4352 deaths from cancer (1798 men and 2554 women).

Age- and energy-adjusted and multivariate-adjusted analyses showed a significant inverse association between dietary Se intake and total mortality among both men and women (Table 2). Multivariate-adjusted hazard ratios (HR) for total death among women across the lowest to the highest quintile of Se intake were 1·00 (reference), 0·96 (95 % CI 0·89, 1·03), 0·92 (95 % CI 0·84, 1·00), 0·90 (95 % CI 0·82, 0·99) and 0·79 (95 % CI 0·71, 0·88), respectively (P<0·0001 for trend across categories). The corresponding HR among men were 1·00 (reference), 0·91 (95 % CI 0·83, 0·99), 0·86 (95 % CI 0·78, 0·95), 0·82 (95 % CI 0·73, 0·91) and 0·79 (95 % CI 0·70, 0·89), respectively (P=0·0001 for trend across categories).

Table 2 Association of dietary selenium intake with total and cause-specific mortality in the Shanghai Women’s Health Study (SWHS; 1997–2000) and the Shanghai Men’s Health Study (SMHS; 2002–2006)

HR, hazard ratio.

* P values for trend were estimated by assigning the median intake value for the quintile to each person and including this as a continuous variable in the model.

Dietary intakes were adjusted for energy intake using the nutrient density method and expressed as per μg/4184 kJ (1000 kcal) per d.

Adjusted for age and total energy intake.

§ Adjusted for age, birth cohort, education, income, marital status, occupation, BMI, physical activity, total energy intake, dietary fat intake, supplement use, smoking status, drinking status, status with regard to a history of hypertension, diabetes, CHD or stroke, family history of cancer and menopausal status (women only).

Dietary Se intake and CVD and cancer mortality

In multivariate analyses, Se intake was inversely associated with CVD mortality in both men and women. The HR for the highest v. lowest quintile were 0·80 (95 % CI 0·66, 0·98; P for trend=0·0268) among women and 0·66 (95 % CI 0·54, 0·82; P for trend=0·0002) among men. In contrast, no significant associations between Se intake and deaths from cancer were observed in both women and men.

Sensitivity and subgroup analyses

The significant inverse association between Se intake and all-cause mortality remained largely unchanged when we excluded the first 2 years of follow-up (628 men and 441 women; see online supplementary material, Table S1); excluded participants with hypertension (17 940 men and 17 544 women), diabetes (3767 men and 3216 women), CHD (3069 men and 5411 women) or stroke at baseline (2265 men and 853 women), or family history of cancer (17 062 men and 19 710 women); excluded participants who had ever smoked (41 900 men and 2059 women); excluded participants who had ever drunk (20 231 men); and excluded participants who reported use of any supplement at the baseline survey (10 480 men and 22 940 women; Table S2).

In stratified analyses, we found similar inverse associations between dietary Se intake and all-cause mortality across subgroups defined by menopause status (P=0·6543 for interaction) and BMI (P=0·8968 for interaction in men, P=0·8259 for interaction in women). We noted significant interactions between waist-to-hip ratio and Se intake with respect to total death (P=0·0399 for interaction in men, P<0·0001 for interaction in women); stronger associations were observed among men and women who had lower waist-to-hip ratio (≤0·90 for men, HR=0·71 (95 % CI 0·60, 0·84); ≤0·85 for women, HR=0·76 (95 % CI 0·67, 0·87)) than among those who had high waist-to-hip ratio (HR=0·87 (95 % CI 0·73, 1·03) for men; HR=0·83 (95 % CI 0·69, 1·00) for women; see online supplementary material, Table S3).

Discussion

In the current analysis of two large population-based cohorts involving 133 957 participants living in Shanghai, China, we found a significant inverse association between dietary Se intake and all-cause and CVD mortality, after adjusting for potential confounders. Compared with the lowest quintile, women in the highest quintile of Se intake had a 21 % lower risk of all-cause mortality and a 20 % lower risk of CVD mortality, whereas men in this category of consumption had a 21 % and a 34 % lower risk, respectively. No association was found between Se intake and cancer mortality for either men or women.

Our finding of a significant inverse association between dietary Se intake and all-cause mortality is generally consistent with findings from most previous prospective studies on plasma or serum Se level and mortality. In an analysis of 1389 elderly French participants in the Etude du Vieillissement Arteriel (EVA), low plasma Se at baseline was positively associated with all-cause mortality (relative risk (RR)=1·54 (95 % CI 1·25, 1·88))( Reference Akbaraly 9 ). In the Invecchiare in Chianti, adults in the lowest quartile of Se had higher mortality risk compared with those in the highest quartile (RR=1·60 (95 % CI 1·04, 2·47))( Reference Lauretani, Semba and Bandinelli 7 ). A non-linear association between Se level and all-cause mortality was observed in 13 887 US adult participants followed up for up to 12 years in the Third National Health and Nutrition Examination Survey( Reference Bleys, Navas-Acien and Guallar 10 ). By contrast, in a cohort analysis of 1103 participants in LinXian( Reference Wei, Abnet and Qiao 11 ), China, no association was noted between baseline serum Se (mean 73 μg/l) and all-cause mortality (RR=0·93 (95 % CI 0·72, 1·19)). Moreover, in a meta-analysis of randomized controlled trials, Se given alone or in combination with other supplements had no significant effect on mortality in seventeen trials (RR=0·97 (95 % CI 0·91, 1·03))( Reference Bjelakovic, Nikolova and Gluud 20 ), such as the Nutritional Prevention of Cancer (NPC) trial (median baseline plasma Se: 114 ng/ml)( Reference Clark, Combs and Turnbull 21 ) and the Selenium and Vitamin E Cancer Prevention Trial (SELECT; median baseline serum Se: 136 μg/l)( Reference Lippman, Klein and Goodman 22 ).

Se may protect against CVD by preventing oxidative modification of lipids, inhibiting platelet aggregation, reducing inflammation( Reference Rayman 1 , Reference Rayman 23 ) and improving functional capillary recruitment( Reference Buss, Marinho and Maranhão 24 ). Although a meta-analysis of observational studies showed a significant inverse association between Se concentration and risk of CHD( Reference Flores-Mateo, Navas-Acien and Pastor-Barriuso 6 ), randomized trials using Se in combination with other antioxidants have not shown a significant protective effect on CVD or mortality( Reference Flores-Mateo, Navas-Acien and Pastor-Barriuso 6 , Reference Lippman, Klein and Goodman 22 ). However, most of these large prevention trials did not consider baseline nutrition level in their inclusion criteria and Se was given in combination with other vitamins and minerals in all but two trials( Reference Stranges, Marshall and Trevisan 25 , Reference Korpela, Kumpulainen and Jussila 26 ).

In contrast with previous prospective studies, our analysis of the SWHS and the SMHS data found no association between dietary Se intake and cancer mortality. In meta-analyses of observational studies, the pooled RR risk comparing the highest with the lowest category of Se levels was 0·61 (95 % CI, 0·32, 0·95) for bladder cancer( Reference Amaral, Cantor and Silverman 3 ) and 0·74 (95 % CI, 0·57, 0·97)( Reference Zhuo, Smith and Steinmaus 5 ) for lung cancer. For prostate cancer, a more significant protective association was detected between Se and risk of advanced, rather than localized or low-grade, prostate cancer( Reference Peters and Takata 27 ). However, results from the recent randomized controlled trials have failed to provide evidence of a beneficial effect of Se supplementation on risk of all cancers, prostate cancer or other site-specific cancers( Reference Vinceti, Dennert and Crespi 28 ). In the NPC trial, Se supplementation was associated with a statistically significant decrease in total cancer mortality, total cancer incidence and incidence of lung, colorectal and prostate cancers( Reference Duffield-Lillico, Reid and Turnbull 29 ). However, with longer follow-up time, the differences in lung and colorectal cancer became statistically non-significant. Another randomized controlled trial, SELECT, found no evidence of effects on the incidence of prostate, lung or any cancer overall at or beyond 5 years of follow-up with Se supplementation( Reference Lippman, Klein and Goodman 22 ).

Differences in baseline Se plasma or serum levels of the populations studied might account for the observed differences. Beyond a specific Se concentration, additional Se intake does not result in additional reduction of mortality and human studies have provided evidence of a U-shaped association between intake or status and health outcomes( Reference Bleys, Navas-Acien and Guallar 10 , Reference Duffield-Lillico, Reid and Turnbull 29 ). Moreover, because published randomized trials used a wide variety of supplements, in different doses, with different objectives and populations, and with short duration of follow-up time and small sample size, the power to detect the health effects of Se was slightly limited.

The underlying biological mechanism by which low dietary Se intake contributes to an increased mortality risk may be related to the increased oxidative stress and inflammation effects( Reference Ray, Semba and Walston 8 ). Higher Se levels may potentially protect against oxidative stress and reduce pro-inflammation cytokines and other markers of inflammation, including C-reactive protein, by incorporation into selenoproteins such as glutathione peroxidase and seleneprotein S (SEPS 1)( Reference Rayman 30 ). Low Se may compromise health by decreasing the synthesis and activity of deiodinase, the enzyme that transforms thyroxine into the biologically active triiodothyronine( Reference Beckett 31 ). Moreover, low Se status may be implicated in the pathogenesis of atherosclerosis through its effects on regulating the cyclo-oxygenase and lipoxygenase pathways of the arachidonic acid cascade in endothelial cells( Reference Rayman 23 ). In the Uppsala Longitudinal Study of Adult Men, high concentrations of serum Se predicted reduced levels of urinary F2-isoprostane, a biomarker of lipid peroxidation and oxidative stress( Reference Helmersson, Arnlov and Vessby 32 ).

Strengths of our study include the population-based, prospective design with high participation and retention rates and detailed information on diet. The extensive data on possible risk factors for mortality allowed comprehensive adjustments for confounders. Results from the various sensitivity and subgroup analyses we carried out yielded similar results throughout, which suggests that our findings are fairly robust. However, several limitations of our study also merit consideration. First, as with any nutritional epidemiological study, measurement errors in self-reported dietary data introduced by FFQ, which are most likely non-differential, may have attenuated estimates for the associations. Second, because dietary and lifestyle factors interact in complex ways with each other, we cannot entirely separate the effect of dietary Se from those of other nutrients and foods, and thus we cannot completely rule out the possibility that some unmeasured confounders or residual confounding accounted for the observed associations. Third, Se intake from supplements was not taken into account in our analysis. However, the associations between Se intake and mortality did not change substantially after exclusion of supplement users. Fourth, dietary intake assessed at baseline may have been affected by preclinical conditions. Nevertheless, excluding the first 2 years of follow-up and participants with chronic diseases at baseline did not alter the results. Fifth, since Se levels in foods may vary between geographic regions due to the Se content of the soil where the food was produced, serum or plasma Se levels would have been preferable to estimate Se exposure. However, owing to constraints on resources, serum or plasma Se levels were not measured for the participants in our study. We expect that the errors in dietary Se assessment would be random and likely lead to an attenuation of the true effect rather than create an artificial effect when none existed. Sixth, it is not known whether participants’ diet during the baseline year reflected their diet during the biologically relevant period. Thus, although an inverse association between Se exposure and mortality was found in some observational studies, including our study, this cannot be taken as evidence of a causal relationship and our results should be interpreted with caution.

Conclusion

In conclusion, we found that increased dietary Se intake was associated with lower all-cause and CVD mortality risk among Chinese men and women, consistent with previous observational studies, suggesting that individuals in the lower categories of Se exposure may benefit from increased Se intake.

Acknowledgements

Acknowledgements: The authors would like to thank the participants of the SMHS and the SWHS for their invaluable contribution to this work. Financial support: This work was supported by the State Key Laboratory of Oncogene and Related Genes (grant number 91-15-10) and the Shanghai Health Bureau Key Disciplines and Specialties Foundation, and the US National Institutes of Health (grant numbers R37 CA070867 and UM1 CA182910, R01 CA082729 and UM1 CA173640). All funders had no role in the design, analysis or writing of this article. Conflict of interest: None. Authorship: Y.-B.X. conceived and designed the study, and was responsible for final editing and approval of the manuscript. J.-W.S., H.-L.L., W. Zhang and L.-G.Z. analysed the data. J.-W.S. wrote the first draft. All authors critically reviewed the manuscript and approved the final version. Ethics of human subject participation: This study was conducted according to the guidelines laid down in the Declaration of Helsinki and all procedures involving human subjects were approved by the all relevant Institutional Review Boards. Written informed consent was obtained from all participants.

Supplementary material

To view supplementary material for this article, please visit http://dx.doi.org/10.1017/S1368980016001130

References

1. Rayman, MP (2012) Selenium and human health. Lancet 379, 12561268.CrossRefGoogle ScholarPubMed
2. Papp, LV, Lu, J, Holmgren, A et al. (2007) From selenium to selenoproteins: synthesis, identity, and their role in human health. Antioxid Redox Signal 9, 775806.CrossRefGoogle ScholarPubMed
3. Amaral, AFS, Cantor, KP, Silverman, DT et al. (2010) Selenium and bladder cancer risk: a meta-analysis. Cancer Epidemiol Biomarkers Prev 19, 24072415.CrossRefGoogle ScholarPubMed
4. Etminan, M, FitzGerald, JM, Gleave, M et al. (2005) Intake of selenium in the prevention of prostate cancer: a systematic review and meta-analysis. Cancer Causes Control 16, 11251131.CrossRefGoogle ScholarPubMed
5. Zhuo, H, Smith, AH & Steinmaus, C (2004) Selenium and lung cancer: a quantitative analysis of heterogeneity in the current epidemiological literature. Cancer Epidemiol Biomarkers Prev 13, 771778.CrossRefGoogle ScholarPubMed
6. Flores-Mateo, G, Navas-Acien, A, Pastor-Barriuso, R et al. (2006) Selenium and coronary heart disease: a meta-analysis. Am J Clin Nutr 84, 762773.CrossRefGoogle ScholarPubMed
7. Lauretani, F, Semba, RD, Bandinelli, S et al. (2008) Low plasma selenium concentrations and mortality among older community-dwelling adults: the InCHIANTI Study. Aging Clin Exp Res 20, 153158.CrossRefGoogle ScholarPubMed
8. Ray, AL, Semba, RD, Walston, J et al. (2006) Low serum selenium and total carotenoids predict mortality among older women living in the community: the women’s health and aging studies. J Nutr 136, 172176.CrossRefGoogle ScholarPubMed
9. Akbaraly, NT (2005) Selenium and mortality in the elderly: results from the EVA study. Clin Chem 51, 21172123.CrossRefGoogle ScholarPubMed
10. Bleys, J, Navas-Acien, A & Guallar, E (2008) Serum selenium levels and all-cause, cancer, and cardiovascular mortality among US adults. Arch Intern Med 168, 404410.CrossRefGoogle ScholarPubMed
11. Wei, WQ, Abnet, CC, Qiao, YL et al. (2004) Prospective study of serum selenium concentrations and esophageal and gastric cardia cancer, heart disease, stroke, and total death. Am J Clin Nutr 79, 8085.CrossRefGoogle ScholarPubMed
12. Rayman, MP (2008) Food-chain selenium and human health: emphasis on intake. Br J Nutr 100, 254268.CrossRefGoogle ScholarPubMed
13. Combs, GF (2001) Selenium in global food systems. Br J Nutr 85, 517547.CrossRefGoogle ScholarPubMed
14. Zheng, W, Chow, WH, Yang, G et al. (2005) The Shanghai Women’s Health Study: rationale, study design, and baseline characteristics. Am J Epidemiol 162, 11231131.CrossRefGoogle ScholarPubMed
15. Shu, X, Li, H, Yang, G et al. (2015) Cohort profile: the Shanghai Men’s Health Study. Int J Epidemiol 44, 810818.CrossRefGoogle ScholarPubMed
16. Shu, XO, Yang, G, Jin, F et al. (2004) Validity and reproducibility of the food frequency questionnaire used in the Shanghai Women’s Health Study. Eur J Clin Nutr 58, 1723.CrossRefGoogle ScholarPubMed
17. Villegas, R, Yang, G, Liu, D et al. (2007) Validity and reproducibility of the food-frequency questionnaire used in the Shanghai Men’s Health Study. Br J Nutr 97, 9931000.CrossRefGoogle ScholarPubMed
18. Yang, YX, Wang, GY & Pan, XC (2002) China Food Composition 2002. Beijing: Peking University Medical Press.Google Scholar
19. Willett, WC, Howe, GR & Kushi, LH (1997) Adjustment for total energy intake in epidemiologic studies. Am J Clin Nutr 65, 4 Suppl., 1220S1228S.CrossRefGoogle ScholarPubMed
20. Bjelakovic, G, Nikolova, D, Gluud, LL et al. (2012) Antioxidant supplements for prevention of mortality in healthy participants and patients with various diseases. Cochrane Database Syst Rev 3, CD007176.Google Scholar
21. Clark, LC, Combs, GJ, Turnbull, BW et al. (1996) Effects of selenium supplementation for cancer prevention in patients with carcinoma of the skin. A randomized controlled trial. Nutritional Prevention of Cancer Study Group. JAMA 276, 19571963.CrossRefGoogle ScholarPubMed
22. Lippman, SM, Klein, EA, Goodman, PJ et al. (2009) Effect of selenium and vitamin E on risk of prostate cancer and other cancers: the Selenium and Vitamin E Cancer Prevention Trial (SELECT). JAMA 301, 3951.CrossRefGoogle Scholar
23. Rayman, MP (2000) The importance of selenium to human health. Lancet 356, 233241.CrossRefGoogle ScholarPubMed
24. Buss, C, Marinho, C, Maranhão, PA et al. (2013) Long-term dietary intake of selenium, calcium, and dairy products is associated with improved capillary recruitment in healthy young men. Eur J Nutr 52, 10991105.CrossRefGoogle ScholarPubMed
25. Stranges, S, Marshall, JR, Trevisan, M et al. (2006) Effects of selenium supplementation on cardiovascular disease incidence and mortality: secondary analyses in a randomized clinical trial. Am J Epidemiol 163, 694699.CrossRefGoogle ScholarPubMed
26. Korpela, H, Kumpulainen, J, Jussila, E et al. (1989) Effect of selenium supplementation after acute myocardial infarction. Res Commun Chem Pathol Pharmacol 65, 249252.Google ScholarPubMed
27. Peters, U & Takata, Y (2008) Selenium and the prevention of prostate and colorectal cancer. Mol Nutr Food Res 52, 12611272.CrossRefGoogle ScholarPubMed
28. Vinceti, M, Dennert, G, Crespi, CM et al. (2014) Selenium for preventing cancer. Cochrane Database Syst Rev 3, CD005195.Google Scholar
29. Duffield-Lillico, AJ, Reid, ME, Turnbull, BW et al. (2002) Baseline characteristics and the effect of selenium supplementation on cancer incidence in a randomized clinical trial: a summary report of the Nutritional Prevention of Cancer Trial. Cancer Epidemiol Biomarkers Prev 11, 630639.Google Scholar
30. Rayman, MP (2009) Selenoproteins and human health: insights from epidemiological data. Biochim Biophys Acta 1790, 15331540.CrossRefGoogle ScholarPubMed
31. Beckett, GJ (2005) Selenium and endocrine systems. J Endocrinol 184, 455465.CrossRefGoogle ScholarPubMed
32. Helmersson, J, Arnlov, J, Vessby, B et al. (2005) Serum selenium predicts levels of F2-isoprostanes and prostaglandin F in a 27 year follow-up study of Swedish men. Free Radic Res 39, 763770.CrossRefGoogle Scholar
Figure 0

Table 1 Baseline characteristics by energy-adjusted quintile of selenium intake in the Shanghai Women’s Health Study (SWHS; 1997–2000) and the Shanghai Men’s Health Study (SMHS; 2002–2006)

Figure 1

Table 2 Association of dietary selenium intake with total and cause-specific mortality in the Shanghai Women’s Health Study (SWHS; 1997–2000) and the Shanghai Men’s Health Study (SMHS; 2002–2006)

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