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Background: Ultra-processed food (UPF) consumption has been associated with higher cardiovascular disease (CVD) and mortality risks.Objectives: The aim of this study was to assess the relationship between UPF consumption and incident dyslipidemia in older adults, where evidence is limited.Methods: We studied a prospective cohort of 1082 community-dwelling adults in Spain, older than 60 (mean age, 68 ± 6 years old). Participants (52% were women) were recruited between 2008-10 and followed up to 2015. At baseline, food intake data were collected using a validated computerized face-to-face dietary history. UPFs were identified according to the nature and extent of their industrial processing (NOVA classification). Triglycerides, HDL cholesterol, and LDL cholesterol were measured in fasting plasma samples collected at baseline and at follow-up. Statistical analyses were performed with logistic regression adjusted for the main potential confounders.Results: Among those free of corresponding dyslipidemia at baseline, and after a follow-up of between 5 to 7 years, 60 (out of 895) developed incident hypertriglyceridemia (≥150 mg/dL), 112 (out of 878) had low HDL cholesterol (<40 in men/<50 mg/dL in women), and 54 (out of 472) had high LDL cholesterol (>129 mg/dL). The mean percentage of UPF consumption was 19% ± 11% of total energy intake. Those in the highest versus the lowest tertile of energy intake from UPFs had more than twice the odds of incident hypertriglyceridemia (OR, 2.66; 95% CI: 1.20-5.90; P-trend, 0.011) or low HDL cholesterol (OR, 2.23; 95% CI: 1.22-4.05; P-trend, 0.012). UPF consumption was not associated with high LDL cholesterol plasma concentrations.Conclusions: Although UPF consumption in Spain was low among older adults, high consumption of UPFs was clearly associated with incident dyslipidemia. The increase in CVD risk recently found to be associated with UPF consumption might be mediated by these atherogenic lipid abnormalities. [ABSTRACT FROM AUTHOR]

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. [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]

The consumption of sweetened beverages such as soft drinks has been associated with adverse effects on markers of cardiovascular risk. We examined the hypothesis that high consumption of sweetened beverages increases the risk of stroke. We followed 32,575 women aged 49-83 y and 35,884 men aged 45-79 y without cardiovascular disease, cancer, or diabetes at baseline. The consumption of sweetened beverages, including sugar-sweetened and artificially sweetened soft drinks and juice drinks, was assessed by using a food-frequency questionnaire. Stroke cases were ascertained by linkage to the Swedish Inpatient Register and the Swedish Cause of Death Register. The data were analyzed by using a Cox proportional hazards regression model. We ascertained 3510 incident cases of stroke, including 2588 cerebral infarctions, 349 intracerebral hemorrhages, 156 subarachnoid hemorrhages, and 417 unspecified strokes, during a mean follow-up of 10.3 y. Sweetened beverage consumption was significantly positively associated with risk of total stroke and cerebral infarction but not with hemorrhagic stroke. The multivariable RRs comparing ≥2 (median: 2.1) servings/d (200 mL/serving) with 0.1 to <0.5 (median: 0.3) servings/d were 1.19 (95% CI: 1.04, 1.36) for total stroke and 1.22 (95% CI: 1.04, 1.42) for cerebral infarction. These findings suggest that sweetened beverage consumption is positively associated with the risk of stroke. [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]

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]

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., (© 2016 American Society for Nutrition.)

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.