87 research outputs found

    Healthy Lifestyle in the Primordial Prevention of Cardiovascular Disease Among Young Women

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    AbstractBackgroundOverall mortality rates from coronary heart disease (CHD) in the United States have declined in recent decades, but the rate has plateaued among younger women. The potential for further reductions in mortality rates among young women through changes in lifestyle is unknown.ObjectivesThe aim of this study was to estimate the proportion of CHD cases and clinical cardiovascular disease (CVD) risk factors among young women that might be attributable to poor adherence to a healthy lifestyle.MethodsA prospective analysis was conducted among 88,940 women ages 27 to 44 years at baseline in the Nurses’ Health Study II who were followed from 1991 to 2011. Lifestyle factors were updated repeatedly by questionnaire. A healthy lifestyle was defined as not smoking, a normal body mass index, physical activity ≥ 2.5 h/week, television viewing ≤ 7 h/week, diet in the top 40% of the Alternative Healthy Eating Index–2010, and 0.1 to 14.9 g/day of alcohol. To estimate the proportion of CHD and clinical CVD risk factors (diabetes, hypertension, and hypercholesterolemia) that could be attributed to poor adherence to a healthy lifestyle, we calculated the population-attributable risk percent.ResultsDuring 20 years of follow-up, we documented 456 incident CHD cases. In multivariable-adjusted models, nonsmoking, a healthy body mass index, exercise, and a healthy diet were independently and significantly associated with lower CHD risk. Compared with women with no healthy lifestyle factors, the hazard ratio for CHD for women with 6 lifestyle factors was 0.08 (95% confidence interval: 0.03 to 0.22). Approximately 73% (95% confidence interval: 39% to 89%) of CHD cases were attributable to poor adherence to a healthy lifestyle. Similarly, 46% (95% confidence interval: 43% to 49%) of clinical CVD risk factor cases were attributable to a poor lifestyle.ConclusionsPrimordial prevention through maintenance of a healthy lifestyle among young women may substantially lower the burden of CVD

    Changes in Alcohol Consumption and Subsequent Risk of Type 2 Diabetes in Men

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    Objective -The objective of this study was to investigate the association of four-year changes in alcohol consumption with subsequent risk of type 2 diabetes. Research Design and Methods - We prospectively examined 38,031 men from the Health Professionals Follow-up Study free of diagnosed diabetes or cancer in 1990. Alcohol consumption was reported on food frequency questionnaires and updated every four years. Results - A total of 1905 cases of type 2 diabetes occurred during 428,497 person-years of follow-up. A 7.5 g/day (~half a glass) increase in alcohol consumption over four years was associated with lower diabetes risk among initial nondrinkers (multivariable hazard ratio [HR] 0.78; 95% confidence interval [CI] 0.60-1.00) and drinkers initially consumin

    Intake of specific fruits and vegetables in relation to risk of estrogen receptor-negative breast cancer among postmenopausal women. Breast Cancer Res

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    Abstract In previous studies of postmenopausal women, overall intake of fruits and vegetables groups has been inversely associated with estrogen receptor-negative (ER-) breast cancer. In this analysis, we prospectively examined the associations of specific fruits and vegetables with risk of ER-postmenopausal breast cancer among 75,929 women aged 38-63 years at baseline and followed for up to 24 years. Dietary data were collected seven times during this period. Cox proportional hazard models were used, adjusting for potential confounders, including a modified Alternate Mediterranean Diet score. We ascertained 792 incident cases of ER-postmenopausal breast cancer. The multivariate relative risk (RR) for every 2 servings/week consumption for total berries was 0.82 (95 % CI = 0.71-0.96, p = 0.01), and the RR for women who consumed at least one serving of blueberries a week was 0.69 (95 % CI = 0.50-0.95, p = 0.02) compared with non-consumers. Also, the RR for consuming at least 2 servings of peaches/ nectarines per week was 0.59 (95 % CI = 0.37-0.93, p = 0.02). Risk of ER-breast cancer was not associated with intakes of other specific fruits or vegetables. In conclusion, higher intake of berries and peaches was associated with lower risk of ER-breast cancer among postmenopausal women. These results are considered exploratory and need to be confirmed in further studies

    Validation of a risk prediction tool for coronary heart disease in middle-aged women

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    Background: Health risk appraisal tools may be useful for identifying individuals who would benefit from lifestyle changes and increased surveillance. We evaluated the validity of the Your Disease Risk tool (YDR) for estimating relative risk of coronary heart disease (CHD) among middle-aged women. Methods: We included 55,802 women in the Nurses’ Health Study who completed a mailed questionnaire about risk factors in 1994 and had no history of heart disease at that time. Participants were followed through 2004 for the occurrence of CHD. We estimated each woman’s 10-year relative risk of CHD using YDR, and we compared the estimated YDR relative risk category (ranging from “very much below average” to “very much above average”) to the observed relative risk for each category using logistic regression. We also examined the discriminatory accuracy of YDR using concordance statistics (c-statistics). Results: There were 1165 CHD events during the 10-year follow-up period. Compared to the “about average” category, the observed age-adjusted relative risk was 0.43 (95 % confidence interval: 0.33, 0.56) for the “very much below average” category and 2.48 (95 % confidence interval: 1.68, 3.67) for the “very much above average” category. The age-adjusted c-statistic for the model including the YDR relative risk category was 0.71 (95 % confidence interval: 0.69, 0.72). The model performed better in younger than older women. Conclusion: The YDR tool appears to have moderate validity for estimating 10-year relative risk of CHD in this population of middle-aged women. Further research should aim to improve the tool’s performance and to examine its validity in other populations. Electronic supplementary material The online version of this article (doi:10.1186/s12905-015-0250-x) contains supplementary material, which is available to authorized users

    Bachelors, Divorcees, and Widowers: Does Marriage Protect Men from Type 2 Diabetes?

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    While research has suggested that being married may confer a health advantage, few studies to date have investigated the role of marital status in the development of type 2 diabetes. We examined whether men who are not married have increased risk of incident type 2 diabetes in the Health Professionals Follow-up Study. Men (n = 41,378) who were free of T2D in 1986, were followed for ≤22 years with biennial reports of T2D, marital status and covariates. Cox proportional hazard models were used to compare risk of incident T2D by marital status (married vs unmarried and married vs never married, divorced/separated, or widowed). There were 2,952 cases of incident T2D. Compared to married men, unmarried men had a 16% higher risk of developing T2D (95%CI:1.04,1.30), adjusting for age, family history of diabetes, ethnicity, lifestyle and body mass index (BMI). Relative risks (RR) for developing T2D differed for divorced/separated (1.09 [95%CI: 0.94,1.27]), widowed (1.29 [95%CI:1.06,1.57]), and never married (1.17 [95%CI:0.91,1.52]) after adjusting for age, family history of diabetes and ethnicity. Adjusting for lifestyle and BMI, the RR for T2D associated with widowhood was no longer significant (RR:1.16 [95%CI:0.95,1.41]). When allowing for a 2-year lag period between marital status and disease, RRs of T2D for widowers were augmented and borderline significant (RR:1.24 [95%CI:1.00,1.54]) after full adjustment. In conclusion, not being married, and more specifically, widowhood was more consistently associated with an increased risk of type 2 diabetes in men and this may be mediated, in part, through unfavorable changes in lifestyle, diet and adiposity

    A prospective analysis of circulating saturated and monounsaturated fatty acids and risk of non-Hodgkin lymphoma

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    Circulating saturated (SFA) and monounsaturated fatty acids (MUFA), which are predominantly derived from endogenous metabolism, may influence non-Hodgkin lymphoma (NHL) risk by modulating inflammation or lymphocyte membrane stability. However, few biomarker studies have evaluated NHL risk associated with these fats. We conducted a prospective study of 583 incident NHL cases and 583 individually matched controls with archived pre-diagnosis red blood cell (RBC) specimens in the Nurses\u27 Health Study (NHS) and Health Professionals Follow-up Study (HPFS). RBC membrane fatty acid levels were measured using gas chromatography. Using multivariable logistic regression, we estimated odds ratios (OR) and 95% confidence intervals (CI) for risk of NHL and major NHL subtypes including T cell NHL (T-NHL), B cell NHL (B-NHL) and three individual B-NHLs: chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL), diffuse large B-cell lymphoma (DLBCL) and follicular lymphoma. RBC SFA and MUFA levels were not associated with NHL risk overall. However, RBC very long chain SFA levels (VLCSFA; 20:0, 22:0, 23:0) were inversely associated with B-NHLs other than CLL/SLL; ORs (95% CIs) per standard deviation (SD) increase in level were 0.81 (0.70, 0.95) for 20:0, 0.82 (0.70, 0.95) for 22:0, and 0.82 (0.70, 0.96) for 23:0 VLCSFA. Also, both VLCSFA and MUFA levels were inversely associated with T-NHL [ORs (95% CIs) per SD: VLCSFA, 0.63 (0.40, 0.99); MUFA, 0.63 (0.40, 0.99)]. The findings of inverse associations for VLCSFAs with B-NHLs other than CLL/SLL and for VLCSFA and MUFA with T-NHL suggest an influence of fatty acid metabolism on lymphomagenesis

    The association between betaine and choline intakes and the plasma concentrations of homocysteine in women

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    Elevated total homocysteine (tHcy), a risk factor for many chronic diseases, can be remethylated to methionine by folate. Alternatively, tHcy can be metabolized by other 1-carbon nutrients, ie, betaine and its precursor, choline

    Haptoglobin Genotype Is a Consistent Marker of Coronary Heart Disease Risk Among Individuals With Elevated Glycosylated Hemoglobin

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    ObjectivesThis study sought to investigate into the biologically plausible interaction between the common haptoglobin (Hp) polymorphism rs#72294371 and glycosylated hemoglobin (HbA1c) on risk of coronary heart disease (CHD).BackgroundStudies of the association between the Hp polymorphism and CHD report inconsistent results. Individuals with the Hp2-2 genotype produce Hp proteins with an impaired ability to prevent oxidative injury caused by elevated HbA1c.MethodsHbA1c concentration and Hp genotype were determined for 407 CHD cases matched 1:1 to controls (from the NHS [Nurses' Health Study]) and in a replication cohort of 2,070 individuals who served as the nontreatment group in the ICARE (Prevention of Cardiovascular Complications in Diabetic Patients With Vitamin E Treatment) study, with 29 CHD events during follow-up. Multivariate models were adjusted for lifestyle and CHD risk factors as appropriate. A pooled analysis was conducted of NHS, ICARE, and the 1 previously published analysis (a cardiovascular disease case-control sample from the Strong Heart Study).ResultsIn the NHS, Hp2-2 genotype (39% frequency) was strongly related to CHD risk only among individuals with elevated HbA1c (≥6.5%), an association that was similar in the ICARE trial and the Strong Heart Study. In a pooled analysis, participants with both the Hp2-2 genotype and elevated HbA1c had a relative risk of 7.90 (95% confidence interval: 4.43 to 14.10) for CHD compared with participants with both an Hp1 allele and HbA1c <6.5% (p for interaction = 0.004), whereas the Hp2-2 genotype with HbA1c <6.5% was not associated with risk (relative risk: 1.34 [95% confidence interval: 0.73 to 2.46]).ConclusionsHp genotype was a significant predictor of CHD among individuals with elevated HbA1c

    Saturated Fats Compared With Unsaturated Fats and Sources of Carbohydrates in Relation to Risk of Coronary Heart Disease A Prospective Cohort Study

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    AbstractBackgroundThe associations between dietary saturated fats and the risk of coronary heart disease (CHD) remain controversial, but few studies have compared saturated with unsaturated fats and sources of carbohydrates in relation to CHD risk.ObjectivesThis study sought to investigate associations of saturated fats compared with unsaturated fats and different sources of carbohydrates in relation to CHD risk.MethodsWe followed 84,628 women (Nurses’ Health Study, 1980 to 2010), and 42,908 men (Health Professionals Follow-up Study, 1986 to 2010) who were free of diabetes, cardiovascular disease, and cancer at baseline. Diet was assessed by a semiquantitative food frequency questionnaire every 4 years.ResultsDuring 24 to 30 years of follow-up, we documented 7,667 incident cases of CHD. Higher intakes of polyunsaturated fatty acids (PUFAs) and carbohydrates from whole grains were significantly associated with a lower risk of CHD comparing the highest with lowest quintile for PUFAs (hazard ratio [HR]: 0.80, 95% confidence interval [CI]: 0.73 to 0.88; p trend <0.0001) and for carbohydrates from whole grains (HR: 0.90, 95% CI: 0.83 to 0.98; p trend = 0.003). In contrast, carbohydrates from refined starches/added sugars were positively associated with a risk of CHD (HR: 1.10, 95% CI: 1.00 to 1.21; p trend = 0.04). Replacing 5% of energy intake from saturated fats with equivalent energy intake from PUFAs, monounsaturated fatty acids, or carbohydrates from whole grains was associated with a 25%, 15%, and 9% lower risk of CHD, respectively (PUFAs, HR: 0.75, 95% CI: 0.67 to 0.84; p < 0.0001; monounsaturated fatty acids, HR: 0.85, 95% CI: 0.74 to 0.97; p = 0.02; carbohydrates from whole grains, HR: 0.91, 95% CI: 0.85 to 0.98; p = 0.01). Replacing saturated fats with carbohydrates from refined starches/added sugars was not significantly associated with CHD risk (p > 0.10).ConclusionsOur findings indicate that unsaturated fats, especially PUFAs, and/or high-quality carbohydrates can be used to replace saturated fats to reduce CHD risk
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