Cheese and Healthy Diet: Associations With Incident Cardio-Metabolic Diseases and All-Cause Mortality in the General Population.
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ABSTRACT:
SUBMITTER: Dekker LH
PROVIDER: S-EPMC6927928 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:AimsAlthough absolute (AID) and functional iron deficiency (FID) are known risk factors for patients with cardiovascular (CV) disease, their relevance for the general population is unknown. The aim was to assess the association between AID/FID with incident CV disease and mortality in the general population.Methods and resultsIn 12 164 individuals from three European population-based cohorts, AID was defined as ferritin < 100 μg/L or as ferritin < 30 μg/L (severe AID), and FID was defined as ferritin < 100 μg/L or ferritin 100-299 μg/L and transferrin saturation < 20%. The association between iron deficiency and incident coronary heart disease (CHD), CV mortality, and all-cause mortality was evaluated by Cox regression models. Population attributable fraction (PAF) was estimated. Median age was 59 (45-68) years; 45.2% were male. AID, severe AID, and FID were prevalent in 60.0%, 16.4%, and 64.3% of individuals. AID was associated with CHD [hazard ratio (HR) 1.20, 95% confidence interval (CI) 1.04-1.39, P = 0.01], but not with mortality. Severe AID was associated with all-cause mortality (HR 1.28, 95% CI 1.12-1.46, P < 0.01), but not with CV mortality/CHD. FID was associated with CHD (HR 1.24, 95% CI 1.07-1.43, P < 0.01), CV mortality (HR 1.26, 95% CI 1.03-1.54, P = 0.03), and all-cause mortality (HR 1.12, 95% CI 1.01-1.24, P = 0.03). Overall, 5.4% of all deaths, 11.7% of all CV deaths, and 10.7% of CHD were attributable to FID.ConclusionsIn the general population, FID was highly prevalent, was associated with incident CHD, CV death, and all-cause death, and had the highest PAF for these events, whereas AID was only associated with CHD and severe AID only with all-cause mortality. This indicates that FID is a relevant risk factor for CV diseases in the general population.
| S-EPMC8712835 | biostudies-literature
Project description:Various individual diet and lifestyle factors are associated with mortality. Investigating these factors collectively may help clarify whether dietary and lifestyle patterns contribute to life expectancy. We investigated the association of previously described evolutionary-concordance and Mediterranean diet pattern scores and a novel evolutionary-concordance lifestyle pattern score with all-cause and cause-specific mortality in the prospective Iowa Women's Health Study (1986-2012). We created the diet pattern scores from Willett FFQ responses, and the lifestyle pattern score from self-reported physical activity, BMI and smoking status, and assessed their associations with mortality, using multivariable Cox proportional hazards regression. Of the 35 221 55- to 69-year-old cancer-free women at baseline, 18 687 died during follow-up. The adjusted hazard ratios (HR) and 95 % CI for all-cause, all CVD, and all-cancer mortality among participants in the highest relative to the lowest quintile of the evolutionary-concordance lifestyle score were, respectively, 0·52 (95 % CI 0·50, 0·55), 0·53 (95 % CI 0·49, 0·57) and 0·51 (95 % CI 0·46, 0·57). The corresponding findings for the Mediterranean diet score were HR 0·85 (95 % CI 0·82, 0·90), 0·83 (95 % CI 0·76, 0·90) and 0·93 (95 % CI 0·84, 1·03), and for the evolutionary-concordance diet score they were close to null and not statistically significant. The lowest estimated risk was among those in the highest joint quintile of the lifestyle score and either diet score (both Pinteraction <0·01). Our findings suggest that (1) a more Mediterranean-like diet pattern and (2) a more evolutionary-concordant lifestyle pattern, alone and in interaction with a more evolutionary-concordant or Mediterranean diet pattern, may be inversely associated with mortality.
| S-EPMC6581641 | biostudies-literature
Project description:BackgroundThe associations of the proportion of vigorous physical activity (VPA) to moderate to vigorous physical activity (MVPA) with incident cardiovascular disease (CVD) and all-cause mortality are unclear.MethodsThe present study included 366,566 participants (aged 40-69 years) without baseline CVD from the UK biobank during 2006 to 2010. Cox regression was used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) for risks of outcomes.ResultsDuring a median 11.8 years of follow-up, among 366,566 participants (mean age [SD]: 56.0 [8.1]), 31,894 incident CVD and 19,823 total deaths were documented. Compared with no VPA, 0%-30% of VPA to MVPA was associated with 12% and 19% lower risks of incident CVD (HR, 0.88 [95% CI, 0.86-0.91]) and all-cause mortality (HR, 0.81 [95% CI, 0.78-0.84]), respectively. Furthermore, we found that the maximum reduction of risks of incident CVD and all-cause mortality occurred at performing approximately 30% of VPA to MVPA (P < 0.001). Compared with participants reporting the lowest levels of MVPA (moderate physical activity [MPA], 0-150 min/week; VPA, 0-75 min/week), those performing 150-300 min/week of MPA and ≥ 150 min/week of VPA experienced the lowest risk of incident CVD (HR, 0.87 [95% CI, 0.79-0.95]) and all-cause mortality (HR, 0.71 [95% CI, 0.63-0.80]). Interestingly, we found that smokers yielded more cardiovascular benefits than non-smokers by performing a higher volume of VPA.ConclusionsComparing with UK adults reporting no VPA, engaging in 30% of VPA was associated with the lowest risk of incident CVD and all-cause mortality.
| S-EPMC9745930 | biostudies-literature
Project description:BACKGROUND:Income volatility is on the rise and presents a growing public health problem. Because in many epidemiological studies income is measured at a single point in time, the association of long-term income volatility with incident cardiovascular disease (CVD) and mortality has not been adequately explored. The goal of this study was to examine associations of income volatility from 1990 to 2005 with incident CVD and all-cause mortality in the subsequent 10 years. METHODS:The Coronary Artery Risk Development in Young Adults Study is an ongoing prospective cohort study conducted within urban field centers in Birmingham, AL; Chicago, IL; Minneapolis, MN; and Oakland, CA. We studied 3937 black and white participants 23 to 35 years of age in 1990 (our study baseline). Income volatility was defined as the intraindividual SD of the percent change in income across 5 assessments from 1990 to 2005. An income drop was defined as a decrease of ?25% from the previous visit and less than the participant's average income from 1990 to 2005. CVD events (fatal and nonfatal) and all-cause mortality between 2005 and 2015 were adjudicated with the use of medical records and death certificates. CVD included primarily acute events related to heart disease and stroke. RESULTS:A total of 106 CVD events and 164 deaths occurred between 2005 and 2015 (incident rate, 2.76 and 3.66 per 1000 person-years, respectively). From Cox models adjusted for sociodemographic, behavioral, and CVD risk factors, higher income volatility and more income drops were associated with greater CVD risk (high versus low volatility: hazard ratio, 2.07; 95% CI, 1.10-3.90; ?2 versus 0 income drops: hazard ratio, 2.54; 95% CI, 1.24-5.19) and all-cause mortality (high versus low volatility: hazard ratio, 1.78; 95% CI,1.03-3.09; ?2 versus 0 income drops: hazard ratio, 1.92; 95% CI, 1.07-3.44). CONCLUSIONS:In a cohort of relatively young adults, income volatility and drops during a 15-year period of formative earning years were independently associated with a nearly 2-fold risk of CVD and all-cause mortality.
| S-EPMC6370510 | biostudies-literature
Project description:To examine the associations of three understudied hemostatic factors--D-dimer, factor VIII(c), and plasmin-antiplasmin (PAP) complex--with incident cardiovascular disease (CVD) and all cause mortality in the Multiethnic Study of Atherosclerosis cohort. Hemostatic factors were measured at baseline in 45-84-year-old patients (n = 6,391) who were free of clinically recognized CVD. Over 4.6 years of follow-up, we identified 307 CVD events, 207 hard coronary heart disease events, and 210 deaths. D-dimer, factor VIII(c), and PAP were not associated with CVD incidence after adjustment for other risk factors. In contrast, each factor was associated positively with total mortality, and D-dimer and factor VIII(c) were associated positively with cancer mortality. When modeled as ordinal variables and adjusted for risk factors, total mortality was greater by 33% (95% CI 15-54) for each quartile increment of D-dimer, 26% (11-44) for factor VIIIc, and 20% (4-38) for PAP. This prospective cohort study did not find D-dimer, factor VIII(c), or PAP to be risk factors for CVD. Instead, elevated levels of these three hemostatic factors were associated independently with increased risk of death. Elevated D-dimer and factor VIII(c) were associated with increased cancer death.
| S-EPMC2950108 | biostudies-literature
Project description:ObjectiveTo examine whether overall lifestyles mediate associations of socioeconomic status (SES) with mortality and incident cardiovascular disease (CVD) and the extent of interaction or joint relations of lifestyles and SES with health outcomes.DesignPopulation based cohort study.SettingUS National Health and Nutrition Examination Survey (US NHANES, 1988-94 and 1999-2014) and UK Biobank.Participants44 462 US adults aged 20 years or older and 399 537 UK adults aged 37-73 years.ExposuresSES was derived by latent class analysis using family income, occupation or employment status, education level, and health insurance (US NHANES only), and three levels (low, medium, and high) were defined according to item response probabilities. A healthy lifestyle score was constructed using information on never smoking, no heavy alcohol consumption (women ≤1 drink/day; men ≤2 drinks/day; one drink contains 14 g of ethanol in the US and 8 g in the UK), top third of physical activity, and higher dietary quality.Main outcome measuresAll cause mortality was the primary outcome in both studies, and CVD mortality and morbidity in UK Biobank, which were obtained through linkage to registries.ResultsUS NHANES documented 8906 deaths over a mean follow-up of 11.2 years, and UK Biobank documented 22 309 deaths and 6903 incident CVD cases over a mean follow-up of 8.8-11.0 years. Among adults of low SES, age adjusted risk of death was 22.5 (95% confidence interval 21.7 to 23.3) and 7.4 (7.3 to 7.6) per 1000 person years in US NHANES and UK Biobank, respectively, and age adjusted risk of CVD was 2.5 (2.4 to 2.6) per 1000 person years in UK Biobank. The corresponding risks among adults of high SES were 11.4 (10.6 to 12.1), 3.3 (3.1 to 3.5), and 1.4 (1.3 to 1.5) per 1000 person years. Compared with adults of high SES, those of low SES had higher risks of all cause mortality (hazard ratio 2.13, 95% confidence interval 1.90 to 2.38 in US NHANES; 1.96, 1.87 to 2.06 in UK Biobank), CVD mortality (2.25, 2.00 to 2.53), and incident CVD (1.65, 1.52 to 1.79) in UK Biobank, and the proportions mediated by lifestyle were 12.3% (10.7% to 13.9%), 4.0% (3.5% to 4.4%), 3.0% (2.5% to 3.6%), and 3.7% (3.1% to 4.5%), respectively. No significant interaction was observed between lifestyle and SES in US NHANES, whereas associations between lifestyle and outcomes were stronger among those of low SES in UK Biobank. Compared with adults of high SES and three or four healthy lifestyle factors, those with low SES and no or one healthy lifestyle factor had higher risks of all cause mortality (3.53, 3.01 to 4.14 in US NHANES; 2.65, 2.39 to 2.94 in UK Biobank), CVD mortality (2.65, 2.09 to 3.38), and incident CVD (2.09, 1.78 to 2.46) in UK Biobank.ConclusionsUnhealthy lifestyles mediated a small proportion of the socioeconomic inequity in health in both US and UK adults; therefore, healthy lifestyle promotion alone might not substantially reduce the socioeconomic inequity in health, and other measures tackling social determinants of health are warranted. Nevertheless, healthy lifestyles were associated with lower mortality and CVD risk in different SES subgroups, supporting an important role of healthy lifestyles in reducing disease burden.
| S-EPMC8044922 | biostudies-literature
Project description:Background and aimsThere is limited evidence about the association of healthy lifestyle and all-cause mortality in individuals with metabolic associated fatty liver disease (MAFLD). We aimed to examine this association and compare it with the association in those without MAFLD.MethodsA prospective cohort study was performed and linked mortality data through 2019 in the National Health Nutrition Examination Survey (NHANES 1999-2010). A healthy lifestyle score was constructed from cigarette smoking, alcohol drinking, healthy eating score, and leisure-time physical activity. Risk stratification was conducted in participants with MAFLD by fibrosis biomarkers and liver enzymes. Survey-weight adjusted Cox regression was used to estimate adjusted hazard ratios (HRs) and confidence intervals (CIs) for all-cause mortality associated with healthy lifestyle.ResultsThere was a protective association between healthy lifestyle and all-cause mortality in participants with MAFLD (HR per 1-unit increase of healthy lifestyle score 0.77 [95% CI 0.69-0.85]), with no difference from the association in participants without MAFLD (HR 0.77 [0.72-0.82]). In participants with MAFLD, the associations tended to be stronger in those with lower risk of advanced fibrosis (HR per 1-unit increase of healthy lifestyle score 0.64 [0.50-0.79] for low NAFLD fibrosis score [NFS] and 0.84 [0.75-0.93] for high NFS, p-value for interaction 0.02), but did not differ by liver enzymes. The results for non-alcoholic fatty liver disease (NAFLD) mirrored those for MAFLD.ConclusionsHealthy lifestyle showed protective associations with all-cause mortality regardless of MAFLD status, and the associations tended to be stronger in those with lower risk of advanced fibrosis. Timely lifestyle modification matters for individuals with MAFLD.
| S-EPMC9609442 | biostudies-literature
Project description:ImportanceAlthough the associations between processed meat intake and cardiovascular disease (CVD) and all-cause mortality have been established, the associations of unprocessed red meat, poultry, or fish consumption with CVD and all-cause mortality are still uncertain.ObjectiveTo identify the associations of processed meat, unprocessed red meat, poultry, or fish intake with incident CVD and all-cause mortality.Design, setting, and participantsThis cohort study analyzed individual-level data of adult participants in 6 prospective cohort studies in the United States. Baseline diet data from 1985 to 2002 were collected. Participants were followed up until August 31, 2016. Data analyses were performed from March 25, 2019, to November 17, 2019.ExposuresProcessed meat, unprocessed red meat, poultry, or fish intake as continuous variables.Main outcomes and measuresHazard ratio (HR) and 30-year absolute risk difference (ARD) for incident CVD (composite end point of coronary heart disease, stroke, heart failure, and CVD deaths) and all-cause mortality, based on each additional intake of 2 servings per week for monotonic associations or 2 vs 0 servings per week for nonmonotonic associations.ResultsAmong the 29 682 participants (mean [SD] age at baseline, 53.7 [15.7] years; 13 168 [44.4%] men; and 9101 [30.7%] self-identified as non-white), 6963 incident CVD events and 8875 all-cause deaths were adjudicated during a median (interquartile range) follow-up of 19.0 (14.1-23.7) years. The associations of processed meat, unprocessed red meat, poultry, or fish intake with incident CVD and all-cause mortality were monotonic (P for nonlinearity ≥ .25), except for the nonmonotonic association between processed meat intake and incident CVD (P for nonlinearity = .006). Intake of processed meat (adjusted HR, 1.07 [95% CI, 1.04-1.11]; adjusted ARD, 1.74% [95% CI, 0.85%-2.63%]), unprocessed red meat (adjusted HR, 1.03 [95% CI, 1.01-1.06]; adjusted ARD, 0.62% [95% CI, 0.07%-1.16%]), or poultry (adjusted HR, 1.04 [95% CI, 1.01-1.06]; adjusted ARD, 1.03% [95% CI, 0.36%-1.70%]) was significantly associated with incident CVD. Fish intake was not significantly associated with incident CVD (adjusted HR, 1.00 [95% CI, 0.98-1.02]; adjusted ARD, 0.12% [95% CI, -0.40% to 0.65%]). Intake of processed meat (adjusted HR, 1.03 [95% CI, 1.02-1.05]; adjusted ARD, 0.90% [95% CI, 0.43%-1.38%]) or unprocessed red meat (adjusted HR, 1.03 [95% CI, 1.01-1.05]; adjusted ARD, 0.76% [95% CI, 0.19%-1.33%]) was significantly associated with all-cause mortality. Intake of poultry (adjusted HR, 0.99 [95% CI, 0.97-1.02]; adjusted ARD, -0.28% [95% CI, -1.00% to 0.44%]) or fish (adjusted HR, 0.99 [95% CI, 0.97-1.01]; adjusted ARD, -0.34% [95% CI, -0.88% to 0.20%]) was not significantly associated with all-cause mortality.Conclusions and relevanceThese findings suggest that, among US adults, higher intake of processed meat, unprocessed red meat, or poultry, but not fish, was significantly associated with a small increased risk of incident CVD, whereas higher intake of processed meat or unprocessed red meat, but not poultry or fish, was significantly associated with a small increased risk of all-cause mortality. These findings have important public health implications and should warrant further investigations.
| S-EPMC7042891 | biostudies-literature
Project description:BACKGROUND:Many studies investigated the association between miR-146a rs2910164 polymorphisms and risk of ischemic cardio-cerebrovascular diseases. However, the results were inconsistent. METHODS:We searched the PubMed, EMBASE, Cochrane library, Web of Science, Chinese National Knowledge Infrastructure, VIP, and Wanfang databases for appropriate studies. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated to evaluate the associations. Heterogeneity, sensitivity, and publication bias were conducted to measure the robustness of our findings.All analyses were based on previous published studies, thus, no ethical approval and patient consent are required. RESULTS:We conducted a meta-analysis to evaluate the relationship between miR-146a rs2910164 polymorphisms and risk of ischemic cardio-cerebrovascular diseases. A total of 26 related studies involving 11,602 cases and 14,016 controls were identified and included in our meta-analysis. After considering the heterogeneity of the global analysis, we inferred that rs2910164 polymorphisms were associated with a lower risk of coronary heart disease (CHD) significantly in all genetic models. In addition, it was also found that the miR-146a rs2910164 polymorphisms were associated with the low risk of ischemic cardio-cerebrovascular diseases in large sample size subgroup analysis. CONCLUSION:These results indicate that miR-146a rs2910164 polymorphisms were significantly associated with a lower risk of ischemic cardio-cerebrovascular. The miR-146a rs29101164 might be recommended as a predictor for susceptibility of ischemic cardio-cerebrovascular diseases.
| S-EPMC6824813 | biostudies-literature
Project description:ObjectivesThe purpose of this study was to compare the risks of incident heart failure (HF) among a variety of chronic inflammatory diseases (CIDs) and to determine whether risks varied by severity of inflammation within each CID.BackgroundIndividuals with CIDs are at elevated risk for cardiovascular diseases, but data are limited regarding risk for HF.MethodsAn electronic health records database from a large urban medical system was examined, comparing individuals with CIDs with frequency-matched controls without CIDs, all of whom were receiving regular outpatient care. Rates of incident HF were determined by using the Kaplan-Meier method and subsequently used multivariate-adjusted proportional hazards models to compare HF risks for each CID. Exploratory analyses determined HF risks by proxy measurement of CID severity.ResultsOf 37,636 patients (n = 18,278 patients with CIDs; and n = 19,358 controls without CIDs) there were 960 incident HF cases over a median of 3.6 years. Risks for incident HF were significantly or borderline significantly elevated for patients with systemic sclerosis (hazard ratio [HR]: 7.26; 95% confidence interval [CI]: 5.72 to 9.21; p < 0.01), systemic lupus erythematosus (HR: 3.15; 95% CI: 2.41 to 4.11; p < 0.01), rheumatoid arthritis (HR: 1.39; 95% CI: 1.13 to 1.71; p < 0.01), and human immunodeficiency virus (HR: 1.28; 95% CI: 0.99 to 1.66; p = 0.06). There was no association between psoriasis or inflammatory bowel disease and incident HF, although patients with those CIDs with higher levels of C-reactive protein had higher risks for HF than controls.ConclusionsSystemic sclerosis and systemic lupus erythematosus were associated with the highest risks of HF, followed by rheumatoid arthritis and HIV. Measurements of inflammation were associated with HF risk across different CIDs.
| S-EPMC7261254 | biostudies-literature