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Background The implication of calcium and magnesium in drinking water for cardiovascular disease is unclear. Objectives To assess the association of the concentration of calcium and magnesium in drinking water with incidence of myocardial infarction and stroke, accounting for dietary mineral intake. Methods We linked drinking water monitoring data to residential information of 26,733 women from the population-based Swedish Mammography Cohort, who completed a 96-item FFQ at baseline. Drinking water was categorized into low (magnesium <10 mg/L and calcium <50 mg/L) or high (magnesium ≥10 mg/L or calcium ≥50 mg/L) mineral concentration. Incident cases of myocardial infarction and stroke types were ascertained 1998–2019 using the National Patient Register. Results The mean ± SD concentration of calcium and magnesium in drinking water was 29 ± 7 mg/L and 5 ± 1 mg/L in the low-exposed area and 52 ± 20 mg/L and 10 ± 3 mg/L in the high-exposed area, respectively. During 16 years of follow-up, we ascertained 2023, 2279, and 452 cases of myocardial infarction, ischemic stroke, and hemorrhagic stroke, respectively. High drinking water calcium and magnesium was associated with lower risk of ischemic and hemorrhagic stroke HRs of 0.87 (95% CI: 0.80, 0.95) and 0.78 (95% CI: 0.65, 0.95), whereas the HR for myocardial infarction was 0.93 (95% CI: 0.85, 1.02). In separate analyses, only drinking water magnesium, not calcium, remained associated with ischemic stroke (HR: 0.69; 95% CI: 0.54, 0.88). Conclusions Drinking water with a high concentration of calcium and magnesium, particularly magnesium, may lower the risk of stroke in postmenopausal women. [ABSTRACT FROM AUTHOR]

BACKGROUND: Per- and polyfluoroalkyl substances (PFAS) are widespread and persistent pollutants that have been associated with elevated cholesterol levels. However, data on incident cardiovascular disease (CVD) is lacking. OBJECTIVES: We investigated the association of exposure to PFAS with risk of myocardial infarction and stroke and, subsidiary, with baseline blood lipids. METHODS: This population-based nested case–control study included first incident myocardial infarction and stroke cases with matched controls from two Swedish cohorts: the Swedish Mammography Cohort-Clinical (SMC-C) and the Cohort of 60-year-olds (60YO). Baseline blood sampling occurred during 2003–2009 and 1997–1999 with follow-up through 2017 and 2014 for the SMC-C and the 60YO, respectively. Eight plasma PFAS concentrations were measured using targeted liquid chromatography–triple quadrupole mass spectrometry. Five of these were quantifiable in both cohorts; individual values and their standardized sum were categorized into tertiles based on the controls. First incident myocardial infarction (푛=345) and ischemic stroke (푛=354) cases were ascertained via linkage to the National Inpatient Register and the Cause of Death Register. Controls were randomly selected from each cohort after matching for age, sex, and sample date. Baseline blood lipids were measured in plasma or serum after overnight fasting. RESULTS: Among the 1,528 case–control subjects, the mean (standard deviation) age was 66 (7.7) y and 67% of them were women. In multivariable-adjusted analyses, the third tertile of the standardized sum of five PFAS associated with higher cholesterol and lower triglyceride levels among controls at baseline (푛=631). The corresponding results were odds ratios=0:70 [95% confidence interval (CI): 0.53, 0.93] for CVD, 0.60 (95% CI: 0.39, 0.92) for myocardial infarction, and 0.83 (95% CI: 0.46, 1.50) for stroke. DISCUSSION: This study indicated that exposure to PFAS, although associated with increased cholesterol levels, did not associate with an increased risk of myocardial infarction, stroke, or their composite end point. The findings improve our knowledge on potential health effects of environmental contaminants in the CVD context. [ABSTRACT FROM AUTHOR]

BACKGROUND: Although randomized controlled trials (RCTs) have demonstrated that high fluoride increases bone mineral density (BMD) and skeletal fragility, observational studies of low-dose chronic exposure through drinking water (<1.5 mg/L, the maximum recommended by the World Health Organization) have been inconclusive. OBJECTIVE: We assessed associations of fluoride in urine, and intake via diet and drinking water, with BMD and fracture incidence in postmenopausal women exposed to drinking water fluoride ≤ mg/L. METHODS: Data were from participants in the Swedish Mammography Cohort-Clinical, a population-based prospective cohort study. At baseline (2004-2009), fluoride exposure was assessed based on urine concentrations (푛=4,306) and estimated dietary intake (including drinking water) (푛=4,072), and BMD was measured using dual energy X-ray absorptiometry. Incident fractures were ascertained via register-linkage through 2017. Residential history was collected to identify women with long-term consistent drinking water exposures prior to baseline. RESULTS: At baseline, mean urine fluoride was 1.2 mg/g creatinine (±1.9) and mean dietary intake was 2.2 mg/d (±0:9), respectively. During follow up, 850, 529, and 187 cases of any fractures, osteoporotic fractures, and hip fractures, respectively, were ascertained. Baseline BMD was slightly higher among women in the highest vs. lowest tertiles of exposure. Fluoride exposures were positively associated with incident hip fractures, with multivariable-adjusted hazard ratios of 1.50 (95% CI: 1.04, 2.17) and 1.59 (95% CI: 1.10, 2.30), for the highest vs. lowest tertiles of urine fluoride and dietary fluoride, respectively. Associations with other fractures were less pronounced for urine fluoride, and null for dietary fluoride. Restricting the analyses to women with consistent long-term drinking water exposures prior to baseline strengthened associations between fractures and urinary fluoride. DISCUSSION: In this cohort of postmenopausal women, the risk of fractures was increased in association with two separate indicators of fluoride exposure. Our findings are consistent with RCTs and suggest that high consumption of drinking water with a fluoride concentration of ~1 mg/L may increase both BMD and skeletal fragility in older women [ABSTRACT FROM AUTHOR]

BACKGROUND: Chlorination is globally used to produce of safe drinking water. Chlorination by-products are easily formed, and there are indications that these are associated with adverse reproductive outcomes. OBJECTIVES: We conducted a nationwide register-based prospective study to assess whether gestational exposure to the four most common chlorination by-products [total trihalomethanes (TTHMs)] via tap water was associated with risk of small for gestational age (SGA), preterm delivery, and very preterm delivery. To date, this is one of the largest studies assessing drinking water TTHM-associated adverse reproductive outcomes. METHODS: We included all singleton births 2005-2015 (live and stillbirths) of mothers residing in Swedish localities having >10,000 inhabitants, ≤2 operating waterworks, adequate information on chlorination treatment, and a sufficient number of routine TTHM measurements in tap water. Individual maternal second and third trimester exposure was obtained by linking TTHM measurements to residential history, categorized into no chlorination, <5, 5-15, and >15 µg TTHM/L. Outcomes and covariates were obtained via the linkage to Swedish health and administrative registers. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated by logistic regression using inverse probability weighting. We stratified the analyses by chlorination treatment (chloramine, hypochlorite). RESULTS: Based on approximately 500,000 births, we observed a TTHM dose-dependent association with increased risk of SGA, confined to treatment with hypochlorite, corresponding to a multivariable-adjusted OR=1.20 (95% CI: 1.08, 1.33) comparing drinking water TTHM >15 µg to the unexposed. Similar results were obtained when, instead of unexposed, the lowest exposure category (<5 µg/L TTHM) was used as reference. No clear associations were observed for preterm delivery and very preterm delivery. DISCUSSION: Chlorination by-products exposure via drinking water was associated with increased risk of SGA in areas with hypochlorite treatment. [ABSTRACT FROM AUTHOR]

Given the importance of prevention of complications in type 2 diabetes (T2D), we aimed to examine changes over time in consumption of fruits, vegetables and juice among men who were diagnosed with T2D in comparison with men without diabetes. The prospective Cohort of Swedish Men, aged 45–79 years in 1997, was used to examine changes in diet after diagnosis of T2D. Dietary intake was assessed using FFQ in 1997 and 2009. In all, 23 953 men who were diabetes free at baseline (1997) and completed both FFQ were eligible to participate in the study. Diagnosis of T2D was reported by subjects and ascertained through registers. Multivariable linear mixed models were used to examine changes in mean servings/week over time. In total, 1741 men developed T2D during the study period. Increased consumption of vegetables and fruits was observed among those who developed T2D (equivalent to 1·6 servings/week, 95 % CI 1·08, 2·03) and men who remained diabetes free (0·7 servings/week, 95 % CI 0·54, 0·84). Consumption of juice decreased by 0·6 servings/week (95 % CI −0·71, −0·39) among those who developed T2D and increased by 0·1 servings/week (95 % CI 0·05, 0·15) in those who were diabetes free. Changes over time and between groups were statistically significant. Although improvements in diet were observed, only 36 % of those with T2D and 35 % of those without diabetes consumed ≥5 servings of fruits and vegetables/d in 2009. [ABSTRACT FROM PUBLISHER]

Purpose: Epidemiological evidence on the association between fish consumption and risk of type 2 diabetes is heterogeneous across geographical regions. Differences related to fish consumption pattern could possibly help explain the discrepancy between the findings. We therefore aimed to investigate the association between fish consumption (total, fried, specific fish items) and type 2 diabetes incidence, taking exposure to contaminants present in fish (polychlorinated biphenyls and methyl mercury) into consideration. Methods: The population-based Cohort of Swedish Men, including 35,583 men aged 45-79 years, was followed from 1998 to 2012. We estimated hazard ratios (HRs) with 95 % confidence intervals (CIs) using Cox proportional hazards models. Results: During 15 years of follow-up, 3624 incident cases were identified. Total fish consumption (≥4 servings/week vs. <1 serving/week) was not associated with type 2 diabetes in multivariable-adjusted analysis (HR 1.00; 95 % CI 0.85-1.18); however, a statistically non-significant inverse association was observed after adjustment for dietary contaminant exposures (HR 0.79; 95 % CI 0.60-1.04). Fried fish (≥6 servings/month vs. ≤1 servings/month) and shellfish consumption (≥1 serving/week vs. never/seldom) were associated with HRs of 1.14 (95 % CI 1.03-1.31) and 1.21 (95 % CI 1.07-1.36), respectively. Conclusions: We observed no overall association between total fish consumption and type 2 diabetes. The results indicated that dietary contaminants in fish may influence the relationship. Fried fish and shellfish consumption were associated with higher type 2 diabetes incidence. These findings suggest that more specific advice on fish species sub-types (varying in contamination) and preparation methods may be warranted. [ABSTRACT FROM AUTHOR]

Background: Conflicting evidence associates diet acidity with the incidence of chronic diseases such as hypertension, diabetes, kidney disease, and bone-mineral disorders. It is currently unknown whether dietary acidity is associated with death.Objective: We investigated the association of dietary acid load with the risk of all-cause and cardiovascular disease (CVD) mortality.Methods: We used data from 2 prospective cohorts, the Swedish Mammography Cohort and the Cohort of Swedish Men, which included 36,740 women and 44,957 men aged 45-84 y at the start of a 15-y follow-up period (1998-2012). Acid load was estimated from food-frequency questionnaires by use of the validated potential renal acid load (PRAL) algorithm. Deaths were ascertained via record linkage. Associations of PRAL with mortality were modeled by use of restricted cubic splines.Results: The median PRAL was 0.65 mEq/d (range: -109 to 81.5 mEq/d) in women and 12.3 mEq/d (-111 to 121 mEq/d) in men. During a mean of 13.5 ± 3.3 y of follow-up, there were 8576 and 13,332 deaths, of which 3203 and 5427 were attributed to cardiovascular causes in woman and men, respectively. In both sexes, a nonlinear U-shaped relation was observed, with higher mortality rates for both dietary acid and alkali excess. Compared with neutral PRAL (0 mEq/d), the HRs for all-cause mortality for the 10th and 90th percentiles of PRAL were 1.05 (95% CI: 1.01, 1.10) and 1.03 (95% CI: 0.98, 1.08), respectively, in women. The corresponding results for men were HRs 1.01 (95% CI: 1.00, 1.02) and 1.04 (95% CI: 1.00, 1.08) respectively. This relation was slightly stronger for CVD mortality.Conclusions: Excess diet alkalinity and acidity both showed weak associations with higher mortality in Swedish adults. An acid-base balanced diet was associated with the lowest mortality, but the magnitude of mortality reduction was modest. The Swedish Mammography Cohort was registered at clinicaltrials.gov as NCT01127698 The Cohort of Swedish Men was registered at clinicaltrials.gov as NCT01127711. [ABSTRACT FROM AUTHOR]

Objective: To examine whether chocolate consumption is associated with a reduced risk of ischaemic heart disease, we used data from a prospective study of Swedish adults and we performed a meta-analysis of available prospective data.Methods and Results: The Swedish prospective study included 67 640 women and men from the Cohort of Swedish Men and the Swedish Mammography Cohort who had completed a food-frequency questionnaire and were free of cardiovascular disease at baseline. Myocardial infarction (MI) cases were ascertained through linkage with the Swedish National Patient and Cause of Death Registers. PubMed and EMBASE databases were searched from inception until 4 February 2016 to identify prospective studies on chocolate consumption and risk of ischaemic heart disease.Results: The results from eligible studies were combined using a random-effects model. During follow-up (1998-2010), 4417 MI cases were ascertained in the Swedish study. Chocolate consumption was inversely associated with MI risk. Compared with non-consumers, the multivariable relative risk for those who consumed ≥3-4 servings/week of chocolate was 0.87 (95% CI 0.77 to 0.98; p for trend =0.04). Five prospective studies on chocolate consumption and ischaemic heart disease were identified. Together with the Swedish study, the meta-analysis included six studies with a total of 6851 ischaemic heart disease cases. The overall relative risk for the highest versus lowest category of chocolate consumption was 0.90 (95% CI 0.82 to 0.97), with little heterogeneity among studies (I(2)=24.3%).Conclusions: Chocolate consumption is associated with lower risk of MI and ischaemic heart disease. [ABSTRACT FROM AUTHOR]

Aims: We examined the hypothesis that high adherence to a Mediterranean diet reduces the risk of developing heart failure (HF) as well as the risk of death from HF.Methods and Results: The study population comprised 37 308 men from the Cohort of Swedish Men who were free from cardiovascular disease at baseline. The modified Mediterranean diet (mMED) score was created from a self-administered food frequency questionnaire, based on consumption of presumed beneficial/detrimental foods, on a 0-8 scale. Incident HF events were ascertained by linkage to the Swedish National Patient and the Cause of Death Registers. Relative risks (RR) with 95% confidence intervals (CI), adjusted for potential confounders, were estimated by Cox proportional hazards regression models. We identified 146 deaths from HF and 1269 incident HF events over a median follow-up of 10.9 years (1998-2008). The mMED score was inversely associated with risk of HF (multivariable RR for the highest vs. lowest quartile 0.69, 95% CI 0.57, 0.83); the corresponding RR of HF mortality was 0.55 (95% CI 0.31, 0.98). The multivariable RR for every two-point increment in the mMED score was 0.85 (95% CI 0.78, 0.91) for incidence of HF and 0.78 (95% CI 0.62, 0.98) for mortality from HF, respectively.Conclusions: High adherence to a Mediterranean diet was associated with a lower risk of HF and mortality from HF in men. Further studies are needed to replicate these findings in other populations. [ABSTRACT FROM AUTHOR]

The prevalence of obesity is increasing in most parts of the world. The objective of this study was to examine whether changes in food patterns were associated with changes in BMI among women over 9 y. Data were from 33,840 women participating in the Swedish Mammography Cohort in 1987 and 1997. Diet was assessed with a FFQ at both time points and 4 food patterns were derived using confirmatory factor analysis (Healthy, Western/Swedish, Alcohol, and Sweets). Our exposure variables were defined as change in factor score for each food pattern from 1987 to 1997. Our outcome variable was defined as change in BMI during the same period, and we also examined change in weight. Normal weight and overweight women had positive changes in weight and BMI during follow-up, whereas obese women had negative changes in BMI and weight; we observed a significant interaction between change in food patterns and baseline BMI. Obese subjects who increased their factor score for the Healthy pattern had larger decreases in BMI (beta = -0.18 kg/m(2) for a 1 unit increase in SD score, CI: -0.26 to -0.10; P < 0.0001), whereas normal weight and overweight women who increased their Healthy pattern score had smaller increases in BMI (-0.05 kg/m(2) and -0.11 kg/m(2), respectively; P < 0.05 for both). Obese women who increased their Healthy pattern score >3 SD had almost a 4 kg decrease in weight and a 1 unit decrease in BMI at follow-up. In conclusion, changes in eating patterns were significantly related to changes in BMI over 9 y and the effect was modified by baseline BMI. Pattern analysis is helpful in generating hypotheses regarding the role of diet in obesity, and additional research is needed to understand which elements of our patterns are protective or risk factors for weight gain. [ABSTRACT FROM AUTHOR]

Cadmium is a well-known nephrotoxic agent in food and tobacco, but the exposure level that is critical for kidney effects in the general population is not defined. Within a population-based women's health survey in southern Sweden (Women's Health in the Lund Area, WHILA), we investigated cadmium exposure in relation to tubular and glomerular function, from 1999 through early 2000 in 820 women (71% participation rate) 53-64 years of age. Multiple linear regression showed cadmium in blood (median, 0.38 µg/L) and urine (0.52 µg/L; density adjusted = 0.67 µg/g creatinine) to be significantly associated with effects on renal tubules (as indicated by increased levels of human complex-forming protein and N-acetyl-β-d-glucosaminidase in urine), after adjusting for age, body mass index, blood lead, diabetes, hypertension, and regular use of nephrotoxic drugs. The associations remained significant even at the low exposure in women who had never smoked. We also found associations with markers of glomerular effects: glomerular filtration rate and creatinine clearance. Significant effects were seen already at a mean urinary cadmium level of 0.6 µg/L (0.8 µg/g creatinine). Cadmium potentiated diabetes-induced effects on kidney. In conclusion, tubular renal effects occurred at lower cadmium levels than previously demonstrated, and more important, glomerular effects were also observed. Although the effects were small, they may represent early signs of adverse effects, affecting large segments of the population. Subjects with diabetes seem to be at increased risk. [ABSTRACT FROM AUTHOR]

Links between specific foods and the risk of renal cell carcinoma (RCC) are not well established. Dietary patterns may be a better predictor of RCC risk. Our aim was to identify and examine major dietary patterns and their relation to the risk of RCC in a large prospective cohort study of Swedish women. Complete dietary information was available from a FFQ from 46,572 women aged 40-76 y at baseline. We conducted factor analysis to identify dietary patterns. Cox proportional hazard models were used to estimate rate ratios (RRs) and 95% CIs. During a mean of 14.3 y of follow-up, we identified 93 cases of RCC. We observed 3 major dietary patterns in the cohort: Healthy (vegetables, tomato, fish, fruits, poultry, whole grains), Western (sweets, processed meat, refined grains, margarine/butter, high-fat dairy products, fried potato, soft drinks, meat) and Drinker (wine, hard liquor, beer, snacks) pattern. Higher Healthy pattern scores were not significantly associated with decreased risk of RCC (highest vs. lowest tertile AR = 0.81; 95% Cl 0.45-1.48 and RR = 0.54; 95% Cl 0.27-1.10 among women ⩽ 65 y). There was a suggestion of an inverse association between the Drinker pattern and RCC risk (RR comparing the 2nd and 3rd with the first tertile, 0.56; 95% Cl, 0.34-0.95; and 0.72; 95% Cl, 0.42-1.22, respectively, P = 0.08 by Wald test); the association was clearer among women ⩽ 65 y (P = 0.02 by Wald test). Our data suggest an inverse association between Drinker pattern and the risk of RCC. [ABSTRACT FROM AUTHOR]

• Improved efficiency in drinking water treatment may reduce gastrointestinal illness. • SMS is a data collection tool that is easy to use, with a high response rate. • Reduced gastrointestinal illness was observed among children, but not in adults. There are indications that drinking water may contribute to endemic gastrointestinal illness (GII) even when the drinking water quality meets current standards, but the knowledge is limited. In this population-based prospective study, we assessed if changes in municipal drinking water production affected the GII incidence, by collecting self-reported GII episodes among the population in two municipalities during calendar time-specific inter-annual periods. About 2600 adults in central Sweden and 2600 adults (including 700 households with children aged 0–9 years) in Southwest Sweden, were followed during a baseline and a follow-up period in 2012–2016. Monthly reports of episodes and symptoms of GII were collected by SMS. The following drinking water related changes were assessed: Change 1 (adults) ; a municipality with a groundwater treatment, changed to a different groundwater source with UV treatment; Change 2 (adults) ; a municipality with a surface water treatment changed to a groundwater source with UV treatment; and Change 3a (adults) and 3b (children): a municipality with a surface water treatment changed to a new surface water source, having a treatment with a higher pathogen reduction. We observed no evidence that changes in raw water source and/or improved pathogen removal in the drinking water treatment affected the risk of GII among adults. Among children aged 0–9 years participating in Change 3b, we observed a 24% relative risk reduction in GII incidence. These results suggest that improved water treatment may reduce the disease burden of GII in children even in settings in which water treatment efficacy meets current quality standards. [ABSTRACT FROM AUTHOR]

There is inconclusive evidence for an association between per- and polyfluoroalkyl substances (PFAS) and fetal growth. We conducted a nation-wide register-based cohort study to assess the associations of the estimated maternal exposure to the sum (PFAS4) of perfluorooctane sulfonic acid (PFOS), perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA) and perfluorohexane sulfonic acid (PFHxS) with birthweight as well as risk of small- (SGA) and large-for-gestational-age (LGA). We included all births in Sweden during 2012–2018 of mothers residing ≥ four years prior to partus in localities served by municipal drinking water where PFAS were measured in raw and drinking water. Using a one-compartment toxicokinetic model we estimated cumulative maternal blood levels of PFAS4 during pregnancy by linking residential history, municipal PFAS water concentration and year-specific background serum PFAS concentrations in Sweden. Individual birth outcomes and covariates were obtained via register linkage. Mean values and 95 % confidence intervals (CI) of β coefficients and odds ratios (OR) were estimated by linear and logistic regressions, respectively. Quantile g-computation regression was conducted to assess the impact of PFAS4 mixture. Among the 248,804 singleton newborns included, no overall association was observed for PFAS4 and birthweight or SGA. However, an association was seen for LGA, multivariable-adjusted OR 1.08 (95% CI: 1.01–1.16) when comparing the highest PFAS4 quartile to the lowest. These associations remained for mixture effect approach where all PFAS, except for PFOA, contributed with a positive weight. We observed an association of the sum of PFAS4 – especially PFOS – with increased risk of LGA, but not with SGA or birthweight. The limitations linked to the exposure assessment still require caution in the interpretation. [ABSTRACT FROM AUTHOR]

Persistent organic pollutants (POPs) have been associated with type 2 diabetes (T2D), but causality is uncertain. Within longitudinal population-based data from northern Sweden, we assessed how POPs associated with T2D prospectively and cross-sectionally, and further investigated factors related to individual changes in POP concentrations. For 129 case-controls pairs matched by age, sex and date of sampling, plasma concentrations of hexachlorobenzene (HCB), dichlorodiphenyl-dichloroethylene (p,p'-DDE), dioxin-like (DL) polychlorinated biphenyl congeners (PCB-118 and PCB-156), and non-dioxin like (NDL-PCB: PCB-74, -99, -138 -153, −170, −180, −183 and PCB-187) were analyzed twice (baseline and follow-up, 9–20 years apart). The cases received their T2D diagnose between baseline and follow-up. Prospective (using baseline data) and cross-sectional (using follow-up data) odds ratios (ORs) for T2D on lipid standardized POPs (HCB, p,p'-DDE, ∑DL-PCBs, ∑NDL-PCBs) were estimated using conditional logistic regression, adjusting for body mass index (BMI) and plasma lipids. The influence of BMI, weight-change, and plasma lipids on longitudinal changes in POP concentrations were evaluated among non-diabetic individuals (n = 306). POPs were associated with T2D in both the prospective and cross-sectional assessments. Of a standard deviation increase in POPs, prospective ORs ranged 1.42 (95% CI: 0.99, 2.06) for ∑NDL-PCBs to 1.55 (95% CI: 1.01, 2.38) for HCB (p < 0.05 only for HCB), and cross-sectional ORs ranged 1.62 (95% CI: 1.13; 2.32) for p,p'-DDE to 2.06 (95% CI: 1.29, 3.28) for ∑DL-PCBs (p < 0.05 for all POPs). In analyses of non-diabetic individuals, higher baseline BMI, decreased weight and decreased plasma lipid concentrations were associated with a slower decrease of POPs. Cases had, besides a higher BMI, reduced cholesterol and weight gain at follow-up compared to controls, which can explain the higher ORs in the cross-sectional assessments. The association between POPs and T2D was confirmed, but an indication that individuals body fat history might influence POP-T2D associations weakens the epidemiological support for a causal association. It also warrants studies based on other exposure metrics than biomonitoring. In addition, we note that a cross-sectional design overestimates the ORs if T2D cases have successfully intervened on weight and/or blood lipids, as changes in these factors cause changes in POPs. • Plasma POP concentrations associates with increased risk of type 2 diabetes. • POPs were measured twice, before and after diagnosis. • BMI, changes in weight and plasma lipids can influence the associations. • Causality is uncertain as past body fat may affect both POP concentrations and type 2 diabetes risk. [ABSTRACT FROM AUTHOR]

Background Fish consumption may promote cardiovascular health. The role of major food contaminants, such as polychlorinated biphenyls (PCBs) common in fatty fish, is unclear. We assessed the association between dietary PCB exposure and risk of myocardial infarction taking into account the intake of long-chain omega-3 fish fatty acids. Methods In the prospective population-based Swedish Mammography Cohort, 33,446 middle-aged and elderly women, free from cardiovascular disease, cancer and diabetes at baseline (1997) were followed-up for 12 years. Validated estimates of dietary PCB exposure and intake of fish fatty acids (eicosapentaenoic acid and docosahexaenoic acid; EPA-DHA) were obtained via a food frequency questionnaire at baseline. Results During follow-up 1386 incident cases of myocardial infarction were ascertained through register-linkage. Women in the highest quartile of dietary PCB exposure (median 286 ng/day) had a multivariable-adjusted RR of myocardial infarction of 1.21 (95% confidence interval [CI], 1.01-1.45) compared to the lowest quartile (median 101 ng/day) before, and 1.58 (95% CI, 1.10-2.25) after adjusting for EPA-DHA. Stratification by low and high EPA-DHA intake, resulted in RRs 2.20 (95% CI, 1.18-4.12) and 1.73 (95% CI, 0.81-3.69), respectively comparing highest PCB tertile with lowest. The intake of dietary EPA-DHA was inversely associated with risk of myocardial infarction after but not before adjusting for dietary PCB. Conclusion Exposure to PCBs was associated with increased risk of myocardial infarction, while some beneficial effect was associated with increasing EPA and DHA intake. To increase the net benefits of fish consumption, PCB contamination should be reduced to a minimum. [ABSTRACT FROM AUTHOR]

Cadmium is a widespread environmental pollutant, which is associated with increased risk of osteoporosis. It has been proposed that cadmium's toxic effect on bone is exerted via impaired activation of vitamin D, secondary to the kidney effects. To test this, we assessed the association of cadmium-induced bone and kidney effects with serum 1,25-dihydroxyvitamin D (1,25(OH)2D); measured by enzyme immunoassay. For the assessment, we selected 85 postmenopausal women, based on low (0.14–0.39μg/L) or high (0.66–2.1μg/L) urinary cadmium, within a cross-sectional population-based women's health survey in Southern Sweden. We also measured 25-hydroxy vitamin D, cadmium in blood, bone mineral density and several markers of bone remodeling and kidney effects. Although there were clear differences in both kidney and bone effect markers between women with low and high cadmium exposure, the 1,25(OH)2D concentrations were not significantly different (median, 111pmol/L (5–95th percentile, 67–170pmol/L) in low- and 125pmol/L (66–200pmol/L) in high-cadmium groups; p=0.08). Also, there was no association between 1,25(OH)2D and markers of bone or kidney effects. It is concluded that the low levels of cadmium exposure present in the studied women, although high enough to be associated with lower bone mineral density and increased bone resorption, were not associated with lower serum concentrations of 1,25(OH)2D. Hence, decreased circulating levels of 1,25(OH)2D are unlikely to be the proposed link between cadmium-induced effects on kidney and bone. [Copyright &y& Elsevier]

Background: The EAT-Lancet diet was created to support dietary transition towards sustainable diets. Current evidence indicates that adherence to the EAT-Lancet diet may reduce mortality risk, yet how adherence may impact dietary exposure to food contaminants remains unexplored. We aimed to estimate the association between adherence to the EAT-Lancet diet and i) all-cause, cardiovascular-, and cancer-mortality and ii) predicted dietary exposure to the following food contaminants: cadmium, methylmercury, polychlorinated biphenyls (PCBs), and pesticide residues., Methods: We used self-reported dietary data from a 96-item food frequency questionnaire of two population-based cohorts - the Cohort of Swedish Men (n = 35,687) and the Swedish Mammography Cohort (n = 32,488). The EAT-Lancet Adherence Index (EAI) was created by scoring consumption of the 14 dietary components included in the EAT-Lancet diet (totalling 0-14 points). Cox proportional hazards regression models were applied to assess the association between EAI and mortality outcomes, presented as multivariable-adjusted hazard ratios (HR) and 95 % confidence intervals (CI). Descriptive statistics were used to characterise predicted exposure to food contaminants, and the correlations between EAI and food contaminants assessed using Spearman's rank correlation., Results: Increased adherence to the EAT-Lancet diet was associated with a lower risk of all-cause mortality (per 3-point increase in EAI: HR = 0.93; CI:0.90,0.97 and HR = 0.91; CI:0.87,0.95 for men and women, respectively) and cardiovascular-mortality (corresponding HR = 0.94; CI:0.88,1.00 and HR = 0.93; CI:0.87,1.00). No clear association was found with cancer-mortality. Increasing EAI was correlated with increased predicted dietary exposure to cadmium, methylmercury, PCBs, and pesticide residues and their median predicted dietary exposures were greater in the high adherence group, compared to the low adherence group., Conclusion: High adherence to the EAT-Lancet diet is associated with a reduction in risk of all-cause and cardiovascular-mortality, but also increased dietary exposure to food contaminants., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Cardiovascular disease (CVD) development may be linked to persistent organic pollutants (POPs), including organochlorine compounds (OCs) and perfluoroalkyl and polyfluoroalkyl substances (PFAS). To explore underlying mechanisms, we investigated metabolites, proteins, and genes linking POPs with CVD risk. We used data from a nested case-control study on myocardial infarction (MI) and stroke from the Swedish Mammography Cohort - Clinical ( n = 657 subjects). OCs, PFAS, and multiomics (9511 liquid chromatography-mass spectrometry (LC-MS) metabolite features; 248 proteins; 8110 gene variants) were measured in baseline plasma. POP-related omics features were selected using random forest followed by Spearman correlation adjusted for confounders. From these, CVD-related omics features were selected using conditional logistic regression. Finally, 29 (for OCs) and 12 (for PFAS) unique features associated with POPs and CVD. One omics subpattern, driven by lipids and inflammatory proteins, associated with MI (OR = 2.03; 95% CI = 1.47; 2.79), OCs, age, and BMI, and correlated negatively with PFAS. Another subpattern, driven by carnitines, associated with stroke (OR = 1.55; 95% CI = 1.16; 2.09), OCs, and age, but not with PFAS. This may imply that OCs and PFAS associate with different omics patterns with opposite effects on CVD risk, but more research is needed to disentangle potential modifications by other factors.

Tobacco smoking is an important risk factor for peripheral artery disease (PAD), but it remains unknown whether smokeless tobacco, such as Swedish snuff (snus), is also associated with this disease. We used data from the Cohort of Swedish Men including 24,085 men. Individuals were grouped into never, past, and current snus dippers as well as never, past quitting ≥ 10 years, past, quitting < 10 years, and current smokers. Incident PAD cases were defined by linkage of the cohort with the Swedish National Patient Register. Cox proportional hazards regression was used to analyze the data. Over a mean follow-up period of 9.1 years (from July 1, 2009 to December 31, 2019), 655 incident PAD cases were ascertained. Cigarette smoking but not Swedish snus dipping was associated with an increased risk of PAD. Compared with never snus dippers, the hazard ratio of PAD was 0.95 (95% confidence interval [CI] 0.73-1.24) for past snus dippers and 0.88 (95% CI 0.66-1.17) for current snus dippers. Compared to never smokers, the hazard ratio of PAD was 1.38 (95% CI 1.14-1.68) for past smoker who stopped smoking for ≥ 10 years, 2.61 (95% CI 1.89-3.61) for past smoker who stopped smoking for < 10 years, and 4.01 (95% CI 3.17, 5.08) for current smoker. In conclusion, cigarette smoking but not Swedish snus dipping increases the risk of PAD., (© 2022. The Author(s).)

Background and Aims: Inflammation has been revealed to facilitate thrombogenesis and to increase the risk of venous thromboembolism (VTE). However, limited data are available on the association between the anti-inflammatory diet and incident VTE. We conducted a cohort analysis to examine this association and to further examine whether this association is modified by smoking status, a trigger of systemic inflammation., Methods and Results: We used data from two cohorts including 81,507 middle-aged and older Swedish adults without previous VTE at baseline. An empirically validated anti-inflammatory diet index (AIDI), based on 12 foods with anti-inflammatory potential and 5 foods with pro-inflammatory potential, was employed to estimate the anti-inflammatory potential of diet. Hazard ratios (HRs), with corresponding 95% confidence intervals (CIs), of VTE were estimated by Cox proportional hazards regression models. During a mean follow-up of 17.8-years, 5241 VTE cases were diagnosed. Compared with individuals in the lowest quartile of the AIDI (score ≤4), those in the highest quartile (score ≥8) had a 9% (95% CI, 0-17%) lower risk of VTE. The inverse association was observed in current and past smokers (HR between the two extreme quartiles, 0.80, 95% CI, 0.70-0.91) but not in never smokers (HR, 1.03, 95% CI, 0.91-1.17). French fries (HR per serving, 1.33, 95% CI, 1.06, 1.67) but no other foods included in AIDI was associated with VTE., Conclusion: The study suggests that a consumption of foods with high anti-inflammatory potential may play a role in the prevention of VTE in smokers., Competing Interests: Declaration of competing interest All authors declare no conflict of interest with the exception for SMD who receives research support from RenalytixAI and personal consulting fees from Calico Labs, outside the scope of the current research., (Copyright © 2021 The Author(s). Published by Elsevier B.V. All rights reserved.)

Background: There is conflicting evidence regarding the association between fish intake and type 2 diabetes (T2D) incidence, possibly owing to measurement errors in self-reported intake and coexposure to persistent organic pollutants (POPs) present in fish., Objective: The aim of this study was to identify plasma metabolites associated with fish intake and to assess their association with T2D risk, independently of POPs, in Swedish adults., Methods: In a case-control study nested in the Swedish Västerbotten Intervention Programme, fasting plasma samples from 421 matched T2D case-control pairs of men and women aged 30-60 y at baseline and 10-y follow-up samples from a subset of 149 pairs were analyzed using untargeted metabolomics. Moreover, 16 plasma POPs were analyzed for the 149 pairs who had repeated samples available. Fish-related plasma metabolites were identified using multivariate modelling and partial correlation analysis. Reproducibility of metabolites and metabolite patterns, derived via principal component analysis (PCA), was assessed by intraclass correlation. A unique component of metabolites unrelated to POPs was dissected by integrating metabolites and POPs using 2-way orthogonal partial least squares regression. ORs of T2D were estimated using conditional logistic regression., Results: We identified 31 metabolites associated with fish intake that had poor to good reproducibility. A PCA-derived metabolite pattern strongly correlated with fish intake (ρ = 0.37, P < 0.001) but showed no association with T2D risk. Integrating fish-related metabolites and POPs led to a unique metabolite component independent of POPs, which tended to be inversely associated with T2D risk (OR: 0.75; 95% CI: 0.54, 1.02, P = 0.07). This component mainly consisted of metabolites reflecting fatty fish intake., Conclusions: Our results suggest that fatty fish intake may be beneficial for T2D prevention, after removing the counteractive effects of coexposure to POPs in Swedish adults. Integrating metabolite markers and POP exposures appears a promising approach to advance the understanding of associations between fish intake and T2D incidence., (Copyright © American Society for Nutrition 2019.)

Background: Beneficial effects of fish consumption on heart failure (HF) may be modified by contaminants in fish. Polychlorinated biphenyls (PCBs) are of particular concern as they have been associated with well-established risk factors of HF, but current data are limited., Objectives: We aimed to assess the association between dietary PCB exposure and risk of HF, accounting for dietary intake of long-chain omega-3 fish fatty acids., Design: We used the prospective population-based research structure SIMPLER (previously the Swedish Mammography Cohort and Cohort of Swedish Men) comprising 32,952 women and 36,546 men, free from cancer, cardiovascular disease and diabetes at baseline in 1997. Validated estimates of dietary PCBs and long-chain omega-3 fish fatty acids [eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA)] were obtained via a food frequency questionnaire at baseline. Incident cases of HF were ascertained through register linkage., Results: During an average of 12 years of follow-up, we ascertained 2736 and 3128 incident cases of HF in women and men, respectively. In multivariable-adjusted models, mutually adjusted for PCBs and EPA-DHA, the relative risk (RR) for dietary PCB exposure was 1.48 (95% CI 1.12-1.96) in women and 1.42 (95% CI 1.08-1.86) in men, comparing extreme quintiles. Corresponding RRs for EPA-DHA intake were 0.71 (95% CI 0.54-0.93) and 0.82 (95% CI 0.63-1.07), respectively., Conclusions: Dietary exposure to PCBs was associated with an increased risk of HF in both women and men. EPA-DHA intake was associated with a lower risk of HF in women, with a similar tendency in men., (Copyright © 2019 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background: Perfluoroalkyl substances (PFAS) have drawn much attention due to bioaccumulation potential and their current omnipresence in human blood. We assessed whether plasma PFAS, suspected to induce endocrine-disrupting effects, were prospectively associated with clinical type 2 diabetes (T2D) risk., Methods: We established a nested case-control study within the Swedish prospective population-based Västerbotten Intervention Programme cohort. Several PFAS were measured in plasma from a subset of 124 case-control pairs at baseline (during 1990-2003) and at 10-year follow-up. T2D cases were matched (1:1) according to gender, age and sample date with participants without T2D (controls). Conditional logistic regressions were used to prospectively assess risk of T2D by baseline PFAS plasma concentrations. Associations between long-term PFAS plasma levels (mean of baseline and follow-up) and insulin resistance (HOMA2-IR) and beta-cell function (HOMA2-B%) at follow-up were prospectively explored among 178 and 181 controls, respectively, by multivariable linear regressions., Results: After adjusting for gender, age, sample year, diet and body mass index, the odds ratio of T2D for the sum of PFAS (Σ z-score PFAS) was 0.52 (95% confidence interval, CI: 0.20, 1.36), comparing third with first tertile; and 0.92 (95% CI: 0.84, 1.00) per one standard deviation increment of sum of log-transformed PFAS. Among the controls, the adjusted β of HOMA2-IR and HOMA-B% for the sum of PFAS were -0.26 (95% CI: -0.52, -0.01) and -9.61 (95% CI: -22.60, 3.39) respectively comparing third with first tertile., Conclusions: This prospective nested case-control study yielded overall inverse associations between individual PFAS and risk of T2D, although mostly non-significant. Among participants without T2D, long-term PFAS exposure was prospectively associated with lower insulin resistance., (Copyright © 2019 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Persistent organochlorine pollutants (POPs) have shown to be involved in the atherosclerotic process and to cause endothelial cell dysfunction. To assess longitudinally whether plasma concentrations of different POPs were associated with blood pressure and risk of hypertension in middle-aged women and men. Study subjects were 850 participants in the VIP (Västerbotten Intervention Programme) with 2 blood samples and blood pressure measurements, 10 years apart, during 1990 to 2003 (baseline) and during 2000 to 2013 (follow-up). Dioxin-like and nondioxin-like polychlorinated biphenyls (DL-PCBs, NDL-PCBs) and p,p'-dichlorodiphenyldichloroethylene (DDE) were measured. Associations were assessed using generalized estimating equations. At baseline sampling 49% and at follow-up 64% had hypertension. DL-PCBs and DDE, but not NDL-PCBs or hexachlorobenzene, were associated with hypertension. Only the association for DL-PCBs remained statistically significant after lipid-standardization and adjustment for body mass index and total serum lipids. The multivariable-adjusted odds ratio of hypertension based on repeated measurements were 1.52 (95% confidence interval, 1.08-2.13) for DL-PCBs (third versus first tertile of lipid-standardized POPs). In stratified adjusted analyses, odds ratio for those born after 1950 increased to 3.99 (95% confidence interval, 2.15-7.43), whereas no association was observed among those born earlier. Based on repeated measurements, the accumulated exposure to DL-PCBs and DDE, although less clear for the latter, may disrupt the normal blood pressure levels and increase the odds of hypertension. Moreover, individuals experiencing early-life POP exposure may be at elevated risk of vascular POP effects., (© 2018 The Authors.)

Background and Aims: The Mediterranean diet, which is palatable and easily achievable, has been associated with lower all-cause and cardiovascular disease (CVD) incidence and mortality. Data on heart failure (HF) and stroke types are lacking. The aim was to examine a Mediterranean diet in relation to incidence of myocardial infarction (MI), HF and stroke types in a Swedish prospective cohort., Methods: In a population-based cohort of 32,921 women, diet was assessed through a self-administered questionnaire. The modified Mediterranean diet (mMED) score was created based on high consumption of vegetables, fruits, legumes, nuts, whole grains, fermented dairy products, fish and monounsaturated fat, moderate intakes of alcohol and low consumption of red meat, on a 0-8 scale. Relative risks (RR) with 95% confidence intervals (CI), adjusted for potential confounders, were estimated by Cox proportional hazards regression models., Results: During 10 y of follow-up (1998-2008), 1109 MIs, 1648 HFs, 1270 ischemic strokes and 262 total hemorrhagic strokes were ascertained. A high adherence to the mMED score (6-8), compared to low, was associated with a lower risk of MI (RR: 0.74, 95% CI: 0.61-0.90, p = 0.003), HF (RR: 0.79, 95% CI: 0.68-0.93, p = 0.004) and ischemic stroke (RR: 0.78, 95% CI: 0.65-0.93, p = 0.007), but not hemorrhagic stroke (RR: 0.88, 95% CI: 0.61-1.29, p = 0.53)., Conclusions: Better adherence to a Mediterranean diet was associated with lower risk of MI, HF and ischemic stroke. The Mediterranean diet is most likely to be beneficial in primary prevention of all major types of atherosclerosis-related CVD., (Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.)

Background: Some studies have found that egg consumption is associated with a higher risk of ischemic heart disease in patients with diabetes. Epidemiologic studies of egg consumption in relation to risk of heart failure (HF) and stroke types are scarce., Objective: The aim of this study was to examine whether egg consumption is associated with incidence of HF, myocardial infarction (MI), or stroke types., Design: In prospective cohorts of 37,766 men (Cohort of Swedish Men) and 32,805 women (Swedish Mammography Cohort) who were free of cardiovascular disease (CVD), egg consumption was assessed at baseline with a food-frequency questionnaire. Incident CVD cases were identified through linkage with the Swedish National Patient and Cause of Death Registers. The data were analyzed with the use of a Cox proportional hazards regression model., Results: During 13 y of follow-up, we ascertained 1628 HFs, 3262 MIs, 2039 ischemic strokes, and 405 hemorrhagic strokes in men and 1207 HFs, 1504 MIs, 1561 ischemic strokes, and 294 hemorrhagic strokes in women. There was no statistically significant association between egg consumption and risk of MI or any stroke type in either men or women or HF in women. In men, consumption of ≤6 eggs/wk was not associated with HF risk; however, daily egg consumption (≥1/d) was associated with a 30% higher risk of HF (RR: 1.30; 95% CI: 1.01, 1.67). Egg consumption was not associated with any CVD outcome in individuals with diabetes., Conclusions: Daily egg consumption was not associated with risk of MI or any stroke type in either men or women or with HF in women. Consumption of eggs ≥1 time/d, but not less frequent consumption, was associated with an elevated risk of HF in men., (© 2015 American Society for Nutrition.)

Objective: To examine the impact of a healthy lifestyle on stroke risk in men at higher risk of stroke because of other cardiovascular diseases or conditions., Methods: Our study population comprised 11,450 men in the Cohort of Swedish Men who had a history of hypertension, high cholesterol levels, diabetes, heart failure, or atrial fibrillation. Participants had completed a questionnaire about diet and lifestyle and were free from stroke and ischemic heart disease at baseline (January 1, 1998). We defined a healthy lifestyle as a low-risk diet (≥5 servings/d of fruits and vegetables and <30 g/d of processed meat), not smoking, ≥150 min/wk of physical activity, body mass index of 18.5 to 25 kg/m(2), and low to moderate alcohol consumption (>0 to ≤30 g/d). Ascertainment of stroke cases was accomplished through linkage with the National Inpatient Register and the Swedish Cause of Death Register., Results: During a mean follow-up of 9.8 years, we ascertained 1,062 incident stroke cases. The risk of total stroke and stroke types decreased with increasing number of healthy lifestyle factors. The multivariable relative risk of total stroke for men who achieved all 5 healthy lifestyle factors compared with men who achieved 0 or 1 factor was 0.28 (95% confidence interval 0.14-0.55). The corresponding relative risks (95% confidence interval) were 0.31 (0.15-0.66) for ischemic stroke and 0.32 (0.04-2.51) for hemorrhagic stroke., Conclusions: A healthy lifestyle is associated with a substantially reduced risk of stroke in men at higher risk of stroke., (© 2015 American Academy of Neurology.)

Objective: We investigated whether younger age at natural menopause confers a risk of heart failure. We also examined a possible modifying effect of tobacco smoking., Methods: This study used the population-based Swedish Mammography Cohort; 22,256 postmenopausal women with information on age at natural menopause were followed from 1997 through 2011. First event of heart failure was ascertained through the Swedish National Patient Register and the Cause of Death Register. Cox proportional hazards regression analyses were conducted to estimate multivariable-adjusted hazard ratios (HRs) and 95% CIs., Results: During a mean follow-up of 13 years, we ascertained 2,532 first events of heart failure hospitalizations and deaths. The mean age at menopause was 51 years. Early natural menopause (40-45 y), compared with menopause at ages 50 to 54 years, was significantly associated with heart failure (HR, 1.40; 95% CI, 1.19 to 1.64). In analyses stratified by smoking status, similar HRs were observed for this age group among never smokers (HR, 1.33; 95% CI, 1.06 to 1.66) and ever smokers (HR, 1.39; 95% CI, 1.09 to 1.78). Among ever smokers, increased incidence (HR, 1.25; 95% CI, 1.06 to 1.47) of heart failure could be detected even among those who entered menopause at ages 46 to 49 years. We found a significant interaction between age at natural menopause and smoking (P = 0.019)., Conclusions: This study indicates that women who experience early natural menopause are at increased risk for developing heart failure and that smoking can modify the association by increasing the risk even among women who enter menopause around ages 46 to 49 years.

The kidney is widely regarded as the critical organ for cadmium toxicity, however, considerable uncertainty remains regarding the clinical significance of the renal effects of cadmium at low levels of exposure. Food is the primary source of cadmium exposure in the general population with tobacco representing an important additional source. We aimed to assess the association between dietary cadmium exposure and chronic kidney disease (CKD) incidence in two large population-based, prospective cohorts of men (Cohort of Swedish Men (COSM)) and women (The Swedish Mammography Cohort (SMC)) with no history of kidney disease. At baseline 1997, men (45-79 years) and women (48-83 years), completed a self-administered questionnaire on diet and lifestyle. Dietary cadmium exposure for each individual was estimated using dietary data and concentrations of cadmium in food. During 13 years of follow-up, we ascertained 599 incident cases of CKD among men (in 481,591 person-years) and 253 cases among women (in 415,432 person-years) through linkage of the cohorts to national inpatient and outpatient registers. Hazard ratios (HR) were calculated using the Cox proportional-hazard regression model. Estimated dietary cadmium exposure was not associated with increased CKD incidence among men HR 0.97 (95% confidence interval (CI): 0.77-1.21) or women HR 0.74 (95% CI: 0.53-1.04), comparing highest tertile with lowest. Our results do not support a strong association between dietary cadmium exposure and CKD at the exposure levels seen in the general population., (Copyright © 2014 Elsevier GmbH. All rights reserved.)

Background: The toxic metal cadmium is suggested to increase the risk of cardiovascular disease, but only one incidence study has explored this association. We evaluated the association between quartiles of food frequency questionnaire-based estimates of cadmium exposure from food (the predominant source of exposure to the metal) and incident cardiovascular disease and its subtypes., Methods: From the population-based Swedish Mammography cohort, 33,333 women were followed prospectively from baseline (1997) through 2010. We estimated relative risks (RRs) with 95% confidence intervals (CIs) using Cox proportional hazard models., Results: During 12 years of follow-up, we identified 3155 incident cases of total cardiovascular disease (1322 cases of myocardial infarction and 1833 cases of total stroke [1485 ischemic and 208 hemorrhagic stroke]). Dietary cadmium exposure was not associated with risk of total cardiovascular disease, myocardial infarction, or total stroke or its subtypes. For total cardiovascular disease, the multivariable-adjusted RR comparing the highest quartile of cadmium exposure with the lowest was 0.96 (95% CI = 0.85-1.09). The corresponding RRs were 1.07 (0.88-1.29) for myocardial infarction, 0.90 (0.76-1.05) for total stroke, 0.89 (0.74-1.06) for ischemic stroke, and 1.11 (0.68-1.80) for hemorrhagic stroke., Conclusions: Our study lends no support to an overall association between low-level exposure to cadmium via food and incident cardiovascular disease.

The relation between dairy foods, particularly specific foods, and risk of cardiovascular disease (CVD) remains unclear. We examined the association between total, as well as specific, dairy food intakes and incidence of myocardial infarction (MI) in a prospective population-based cohort. We followed 33,636 women (aged 48-83 y), free from CVD, cancer, and diabetes at baseline (1997), in the Swedish Mammography Cohort. Consumption of milk, cultured milk/yogurt, cheese, cream, crème fraiche, and butter was obtained from a validated self-administered FFQ at baseline. We used Cox proportional hazards regression models to estimate HRs and 95% CIs, adjusted for relevant CVD risk factors. MI incidence was ascertained from national registries. Over 11.6 y of follow-up, we ascertained 1392 cases of MI. When the highest quintile was compared with the lowest quintile, total dairy food intake was inversely associated with MI risk [multivariable adjusted HR: 0.77 (95% CI: 0.63, 0.95)]. Among specific dairy food products, total cheese was inversely associated [HR: 0.74 (95% CI: 0.60, 0.91)] and butter used on bread but not on cooking was positively associated [HR: 1.34 (95% CI: 1.02, 1.75)] with MI risk. Other specific dairy food products were not significantly associated with MI risk. No differences were observed between consumption of specific low-fat and high-fat dairy foods, expressed as either absolute intakes or intakes relative to the total, and MI risk. Failure to consider dairy foods as a heterogeneous group in future studies could hamper important insights of relevance for the development of dietary guidelines.

Background: There are no previous studies investigating the effect of all dietary antioxidants in relation to myocardial infarction. The total antioxidant capacity of diet takes into account all antioxidants and synergistic effects between them. The aim of this study was to examine how total antioxidant capacity of diet and antioxidant-containing foods were associated with incident myocardial infarction among middle-aged and elderly women., Methods: In the population-based prospective Swedish Mammography Cohort of 49-83-year-old women, 32,561 were cardiovascular disease-free at baseline. Women completed a food-frequency questionnaire, and dietary total antioxidant capacity was calculated using oxygen radical absorbance capacity values. Information on myocardial infarction was identified from the Swedish Hospital Discharge and the Cause of Death registries. Hazard ratios (HR) and 95% confidence intervals (CI) were calculated using Cox proportional hazard models., Results: During the follow-up (September 1997-December 2007), we identified 1114 incident cases of myocardial infarction (321,434 person-years). In multivariable-adjusted analysis, the HR for women comparing the highest quintile of dietary total antioxidant capacity to the lowest was 0.80 (95% CI, 0.67-0.97; P for trend=0.02). Servings of fruit and vegetables and whole grains were nonsignificantly inversely associated with myocardial infarction., Conclusions: These data suggest that dietary total antioxidant capacity, based on fruits, vegetables, coffee, and whole grains, is of importance in the prevention of myocardial infarction., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Osteoporosis and its main health outcome, fragility fractures, are large and escalating public health problems. Cadmium, a widespread food contaminant, is a proposed risk factor; still the association between estimated dietary cadmium exposure and bone mineral density (BMD) has never been assessed. Within a sub-cohort of the Swedish Mammography Cohort, we assessed dietary cadmium exposure based on a food frequency questionnaire (1997) and urinary cadmium (2004-2008) in relation to total-body BMD and risk of osteoporosis and fractures (1997-2009) among 2676 women (aged 56-69 years). In multivariable-adjusted linear regression, dietary cadmium was inversely associated with BMD at the total body and lumbar spine. After further adjustment for dietary factors important for bone health and cadmium bioavailability--calcium, magnesium, iron and fiber, the associations became more pronounced. A 32% increased risk of osteoporosis (95% CI: 2-71%) and 31% increased risk for any first incident fracture (95% CI: 2-69%) were observed comparing high dietary cadmium exposure (≥13 μg/day, median) with lower exposures (<13 μg/day). By combining high dietary with high urinary cadmium (≥0.50 μg/g creatinine), odds ratios among never-smokers were 2.65 (95% CI: 1.43-4.91) for osteoporosis and 3.05 (95% CI: 1.66-5.59) for fractures. In conclusion, even low-level cadmium exposure from food is associated with low BMD and an increased risk of osteoporosis and fractures. The partial masking of the associations by essential nutrients indicates important interplay between dietary factors and contaminants present in food. In separate analyses, dietary and urinary cadmium underestimated the association with bone effects., (Copyright © 2012 Elsevier Inc. All rights reserved.)