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Derivation and external validation of a risk score for clinically important declines in health and function among two longitudinal cohorts of women in the mid-life.
Solomon, DH, Santacroce, L, Shadyab, A, Haring, B, Burnett-Bowie, SM, Karvonen-Gutierrez, C, Colvin, A, Jackson, R, LeBoff, MS, Ruppert, K, et al
BMJ open. 2023;(8):e069149
Abstract
OBJECTIVES Women in mid-life often develop chronic conditions and experience declines in physical health and function. Identifying factors associated with declines provides opportunity for targeted interventions. We derived and externally validated a risk score for clinically important declines over 10 years among women ages 55-65 using the Physical Component Summary Score (PCS) of the SF-36. DESIGN Derivation and validation of a risk score. SETTING Two longitudinal cohorts from sites in the USA were used. PARTICIPANTS Women from the Study of Women's Health Across the Nation (SWAN) and women from the Women's Health Initiative (WHI) Observational Study and/or clinical trials. OUTCOME MEASURES A clinically important decline over 10 years among women ages 55-65 using the PCS of the SF-36 predictors was measured at the beginning of the 10 years of follow-up. RESULTS Seven factors-lower educational attainment, smoking, higher body mass index, history of cardiovascular disease, history of osteoarthritis, depressive symptoms and baseline PCS level-were found to be significant predictors of PCS decline among women in SWAN with an area under the curve (AUC)=0.71 and a Brier Score=0.14. The same factors were associated with a decline in PCS in WHI with an AUC=0.64 and a Brier Score=0.18. Regression coefficients from the SWAN analysis were used to estimate risk scores for PCS decline in both cohorts. Using a threshold of a 30% probability of a significant decline, the risk score created a binary test with a specificity between 89%-93% and an accuracy of 73%-79%. CONCLUSIONS Seven clinical variables were used to create a valid risk score for PCS declines that was replicated in an external cohort. The risk score provides a method for identifying women at high risk for a significant mid-life PCS decline.
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Associations of Biomarker-Calibrated Healthy Eating Index-2010 Scores with Chronic Disease Risk and Their Dependency on Energy Intake and Body Mass Index in Postmenopausal Women.
Neuhouser, ML, Pettinger, M, Tinker, LF, Thomson, C, Van Horn, L, Haring, B, Shikany, JM, Stefanick, ML, Prentice, RL, Manson, JE, et al
The Journal of nutrition. 2023;(12):2808-2817
Abstract
BACKGROUND Prior studies examined associations between the Healthy Eating Index (HEI) and chronic disease risk based on self-reported diet without measurement error correction. OBJECTIVE Our objective was to test associations between biomarker calibration of the food-frequency questionnaire (FFQ)-derived HEI-2010 with incident cardiovascular disease (CVD), cancer, and type 2 diabetes (T2D) among Women's Health Initiative (WHI) participants. METHODS Data were derived from WHI postmenopausal women (n = 100,374) aged 50-79 y at enrollment (1993-1998) at 40 US clinical centers, linked to nutritional biomarker substudies and outcomes over subsequent decades of follow-up. Baseline or year 1 FFQ-derived HEI-2010 scores were calibrated with nutritional biomarkers and participant characteristics (e.g., BMI) for systematic measurement error correction. Calibrated data were then used in HR models examining associations with incidence of CVD (total, subtypes, mortality), cancer (total, subtypes, mortality), and T2D in WHI participants with approximately 2 decades of follow-up. Models were multivariable-adjusted with further adjustment for BMI and doubly labeled water (DLW)-calibrated energy. RESULTS Multivariable-adjusted HRs modeled a 20% increment in HEI-2010 score in relation to outcomes. HRs were modest using uncalibrated HEI-2010 scores (HRs = 0.91-1.09). Using biomarker-calibrated HEI-2010, 20% increments in scores yielded multivariable-adjusted HRs (95% CIs) of 0.75 (0.60, 0.93) for coronary heart disease; 0.75 (0.61, 0.91) for myocardial infarction; 0.96 (0.92, 1.01) for stroke; 0.88 (0.75, 1.02) for CVD mortality; 0.81 (0.70, 0.94) for colorectal cancer; 0.81 (0.74, 0.88) for breast cancer; 0.79 (0.73, 0.87) for cancer mortality; and 0.45 (0.36-0.55) for T2D. Except for cancer mortality and T2D incidence, results became null when adjusted for DLW-calibrated energy intake and BMI. CONCLUSIONS Biomarker calibration of FFQ-derived HEI-2010 was associated with lower CVD and cancer incidence and mortality and lower T2D incidence in postmenopausal women. Attenuation after adjustment with BMI and DLW-calibrated energy suggests that energy intake and/or obesity are strong drivers of diet-related chronic disease risk in postmenopausal women. The Women's Health Initiative is registered at clinicaltrials.gov at NCT00000611.
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Somatic Mutations and Clonal Hematopoiesis as Drivers of Age-Related Cardiovascular Risk.
Haring, B, Wissel, S, Manson, JE
Current cardiology reports. 2022;(8):1049-1058
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Abstract
PURPOSE OF REVIEW Clonal hematopoiesis of indeterminate potential (CHIP) has been identified as a novel cardiovascular risk factor. Here we review the relationship of lifestyle and environmental risk factors predisposing to somatic mutations and CHIP and provide an overview on age-related cardiovascular outcomes. RECENT FINDINGS CHIP has been associated with accelerated atherosclerosis and cardiovascular disease in both epidemiological and experimental studies. The most commonly mutated candidate driver genes are DNMT3A, TET2, JAK2, and ASXL1. The underlying mechanisms appear predominantly related to inflammatory pathways. Although age is the dominant risk factor for developing CHIP, emerging evidence suggests that other factors such as smoking, obesity/type 2 diabetes, or an unhealthy diet play a role in the occurrence of somatic mutations. Evidence suggests a strong link between vascular risk factors, somatic hematopoietic mutations, and age-related cardiovascular disease. Further studies on CHIP biology are required to identify targeted interventions for risk reduction in patients with CHIP and inform the utility of screening strategies.
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Association of Major Dietary Protein Sources With All-Cause and Cause-Specific Mortality: Prospective Cohort Study.
Sun, Y, Liu, B, Snetselaar, LG, Wallace, RB, Shadyab, AH, Kroenke, CH, Haring, B, Howard, BV, Shikany, JM, Valdiviezo, C, et al
Journal of the American Heart Association. 2021;10(5):e015553
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Plain language summary
Dietary recommendations for human health focusing on total protein intake without considering specific protein sources may be simplistic and insufficient. The aim of this study was to investigate whether different dietary protein sources would be differentially associated with mortality risk. The study is based on data from a large prospective cohort study with up to 18-years of follow-up to investigate the risks of all-cause and cause-specific mortality in relation to animal and plant protein intake, and major sources of dietary protein. Results indicate that intake of plant protein and substitution of animal protein with plant protein, were associated with lower risk of all-cause, cardiovascular disease, and dementia mortality. Furthermore, substitution of red meat, eggs, dairy products, or legumes with nuts was associated with lower risk of all-cause mortality. Authors conclude that their findings support the need for consideration of protein sources, in addition to the amount of protein intake, in future dietary guidelines.
Abstract
Background Dietary recommendations regarding protein intake have been focused on the amount of protein. However, such recommendations without considering specific protein sources may be simplistic and insufficient. Methods and Results We included 102 521 postmenopausal women enrolled in the Women's Health Initiative between 1993 and 1998, and followed them through February 2017. During 1 876 205 person-years of follow-up, 25 976 deaths occurred. Comparing the highest with the lowest quintile, plant protein intake was inversely associated with all-cause mortality (hazard ratio [HR], 0.91 [0.86, 0.96]), cardiovascular disease mortality (HR, 0.88 [0.79, 0.97]), and dementia mortality (HR, 0.79 [0.67, 0.94]). Among major protein sources, comparing the highest with the lowest quintile of consumption, processed red meat (HR, 1.06 [1.01, 1.10]) or eggs (HR, 1.14 [1.10, 1.19]) was associated with higher risk of all-cause mortality. Unprocessed red meat (HR, 1.12 [1.02, 1.23]), eggs (HR, 1.24 [1.14, 1.34]), or dairy products (HR, 1.11 [1.02, 1.22]) was associated with higher risk of cardiovascular disease mortality. Egg consumption was associated with higher risk of cancer mortality (HR, 1.10 [1.02, 1.19]). Processed red meat consumption was associated with higher risk of dementia mortality (HR, 1.20 [1.05, 1.32]), while consumption of poultry (HR, 0.85 [0.75, 0.97]) or eggs (HR, 0.86 [0.75, 0.98]) was associated with lower risk of dementia mortality. In substitution analysis, substituting of animal protein with plant protein was associated with a lower risk of all-cause mortality, cardiovascular disease mortality, and dementia mortality, and substitution of total red meat, eggs, or dairy products with nuts was associated with a lower risk of all-cause mortality. Conclusions Different dietary protein sources have varying associations with all-cause mortality, cardiovascular disease mortality, and dementia mortality. Our findings support the need for consideration of protein sources in future dietary guidelines.
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The risk of cardiovascular events with increased apolipoprotein CIII: A systematic review and meta-analysis.
Wyler von Ballmoos, MC, Haring, B, Sacks, FM
Journal of clinical lipidology. 2015;(4):498-510
Abstract
BACKGROUND Apolipoprotein CIII (apoC-III) is an atherogenic protein found on HDL, VLDL and LDL. OBJECTIVE The objective of this study is to review the literature on the association of blood apoC-III level with cardiovascular events and the dose-response relationship for this association. METHODS AND RESULTS MEDLINE, EMBASE, BIOSIS, CINAHL, Clinicaltrials.gov, grey-literature sources, contact with investigators, and reference lists of studies, without language restrictions, were reviewed. Twelve studies (5 retrospective and 7 prospective) with a total of 3163 cases of cardiovascular events met inclusion criteria for this systematic review. The pooled standardized mean difference showed significantly higher levels of apoC-III in the non-HDL fraction of plasma (representing apoC-III in VLDL and LDL) in those with cardiovascular disease compared with controls; no difference for apoC-III levels in HDL; and, a trend toward higher total plasma apoC-III in the cases. Pooled risk estimates from the meta-analysis were 2.48 (1.48-4.32; non-HDL apoC-III), 1.09 (0.65-1.82; HDL apoC-III), and 1.33 (1.07-1.66; total apoC-III) for a cardiovascular event with a 5-mg/dL increase in apoC-III. CONCLUSIONS The current body of literature includes several methodologically sound studies that together provide consistent evidence for an association of cardiovascular events with blood apoC-III level in total plasma or in VLDL and LDL. More data are needed to determine importance of levels of apoC-III in specific lipoproteins for cardiovascular risk assessment and management and to elucidate the interaction between triglycerides and apoC-III in relation to risk of cardiovascular disease.
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Healthy dietary interventions and lipoprotein (a) plasma levels: results from the Omni Heart Trial.
Haring, B, von Ballmoos, MC, Appel, LJ, Sacks, FM
PloS one. 2014;(12):e114859
Abstract
BACKGROUND Increased lipoprotein(a) [Lp(a)] levels are associated with atherosclerotic cardiovascular disease. Studies of dietary interventions on changes in Lp(a) are sparse. We aimed to compare the effects of three healthy dietary interventions differing in macronutrient content on Lp(a) concentration. METHODS Secondary analysis of a randomized, 3-period crossover feeding study including 155 (89 blacks; 66 whites) individuals. Participants were given DASH-type healthy diets rich in carbohydrates [Carb], in protein [Prot] or in unsaturated fat [Unsat Fat] for 6 weeks each. Plasma Lp(a) concentration was assessed at baseline and after each diet. RESULTS Compared to baseline, all interventional diets increased mean Lp(a) by 2 to 5 mg/dl. Unsat Fat increased Lp(a) less than Prot with a difference of 1.0 mg/dl (95% CI, -0.5, 2.5; p = 0.196) in whites and 3.7 mg/dl (95% CI, 2.4, 5.0; p < 0.001) in blacks (p-value between races = 0.008); Unsat Fat increased Lp(a) less than Carb with a difference of -0.6 mg/dl, 95% CI, -2.1, 0.9; p = 0.441) in whites and -1.5 mg/dl (95% CI, -0.2, -2.8; p = 0.021) in blacks (p-value between races = 0.354). Prot increased Lp(a) more than Carb with a difference of 0.4 mg/dl (95% CI, -1.1, 1.9; p = 0.597) in whites and 2.2 mg/dl (95%CI, 0.9, 3.5; p = 0.001) in blacks (p-value between races = 0.082). CONCLUSION Diets high in unsaturated fat increased Lp(a) levels less than diets rich in carbohydrate or protein with greater changes in blacks than whites. Our results suggest that substitutions with dietary mono- and polyunsaturated fatty acids in healthy diets may be preferable over protein or carbohydrates with regards to Lp(a). TRIAL REGISTRATION Clinicaltrials.gov NCT00051350.