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      Is the Association Between Parity and Coronary Heart Disease Due to Biological Effects of Pregnancy or Adverse Lifestyle Risk Factors Associated With Child-Rearing? : Findings From the British Women’s Heart and Health Study and the British Regional Heart Study

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          Abstract

          Parity is associated with coronary heart disease (CHD) risk. In the present study, we assessed the associations between number of children and CHD in both women and men. A total of 4286 women and 4252 men aged 60 to 79 years from 24 British towns were studied. Number of children was positively associated with body mass index and waist-hip ratio in both sexes. In women but not in men, number of children was inversely associated with high-density lipoprotein cholesterol and was positively associated with triglycerides and diabetes. For both sexes, similar "J" shaped associations between number of children and CHD were observed, with the prevalence lowest among those with 2 children and increasing linearly with each additional child beyond 2. For those with at least 2 children, each additional child increased the age-adjusted odds of CHD by 30% (odds ratio, 1.30; 95% confidence interval, 1.17 to 1.44) for women and by 12% for men (odds ratio, 1.12; 95% confidence interval, 1.02 to 1.22). Adjustment for obesity and metabolic risk factors attenuated the associations between greater number of children and CHD in both sexes, although in women some association remained. Lifestyle risk factors associated with child-rearing lead to obesity and result in increased CHD in both sexes; biological responses of pregnancy may have additional adverse effects in women.

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          Most cited references18

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          Pregnancy complications and maternal cardiovascular risk: opportunities for intervention and screening?

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            Cardiovascular disease in women with polycystic ovary syndrome at long-term follow-up: a retrospective cohort study.

            Polycystic ovary syndrome (PCOS) is associated with higher prevalence of cardiovascular risk factors but the relative prevalence of cardiovascular disease in women with PCOS has not previously been reported. We have compared cardiovascular mortality and morbidity in middle-aged women previously diagnosed with PCOS and age-matched control women. A retrospective cohort study of women diagnosed with PCOS in the United Kingdom before 1979. Seventy cohort members died before 31 March 1999. Morbidity data were collected from 319 women with PCOS and 1060 age-matched control women. Sixty-one women with PCOS and 63 control women attended a clinical examination. Data were collected from death certificates, general practitioners' records and questionnaires with measurement of cardiovascular risk factors in a subsample of questionnaire respondents. All-cause and cardiovascular mortality in the cohort were similar to women in the general population (standardized mortality ratios (95% CI): 93 (72-117) and 78 (45-124), respectively). Women with PCOS had higher levels of several cardiovascular risk factors: diabetes (P = 0.002) hypertension (P = 0.04), hypercholesterolaemia (P < 0.001), hypertriglyceridaemia (P = 0.02) and increased waist:hip ratio (P = 0.004). After adjustment for BMI, odds ratios (OR) were 2.2 (0.9-5. 2) for diabetes, 1.4 (0.9-2.0) for hypertension and 3.2 (1.7-6.0) for hypercholesterolaemia. A history of coronary heart disease (CHD) was not significantly more common in women with PCOS (crude OR (95%CI) 1.5 (0.7-2.9)) but the crude OR for cerebrovascular disease was 2.8 (1.1-7.1). At long-term follow-up, a history of nonfatal cerebrovascular disease and cardiovascular risk factors including diabetes are more prevalent among women with polycystic ovary syndrome. Morbidity and mortality from of coronary heart disease among women with polycystic ovary syndrome is not as high as previously predicted. This finding challenges our understanding of the aetiology of coronary heart disease in women.
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              Physical activity and hemostatic and inflammatory variables in elderly men.

              Physical activity is associated with lower risk of cardiovascular disease, but the mechanisms are uncertain. Hemostatic and inflammatory markers have been linked with risk of cardiovascular disease. We therefore examined the relationship between physical activity and hemostatic and inflammatory variables. In 1998 to 2000, 20 years after the initial screening of 7735 men 40 to 59 years old from general practices in 24 British towns, 4252 subjects (77% of available survivors, now 60 to 79 old) attended for reexamination. A fasting blood sample was available in 4088 men. All men on warfarin (n=134) and men with incomplete data on physical activity (n=144) were excluded, leaving 3810 men for analysis. Physical activity showed a significant and inverse dose-response relationship with fibrinogen, plasma and blood viscosity, platelet count, coagulation factors VIII and IX, von Willebrand factor, fibrin D-dimer, tissue plasminogen activator antigen, C-reactive protein, and white cell count, even after adjustment for possible confounders. The effects were similar in men with and without prevalent cardiovascular disease. No relationship was seen with activated partial thromboplastin time, activated protein C resistance, hematocrit, or factor VII. An examination of changes in physical activity between baseline and 20 years later showed that inactive men who took up at least light physical activity had levels of blood variables approaching those who remained at least lightly active. Those who became inactive showed levels more similar to those who remained inactive. These data suggest that the benefit of physical activity on cardiovascular disease may be at least partly a result of effects on hemostasis and inflammation.
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                Author and article information

                Journal
                Circulation
                Circulation
                Ovid Technologies (Wolters Kluwer Health)
                0009-7322
                1524-4539
                March 11 2003
                March 11 2003
                : 107
                : 9
                : 1260-1264
                Affiliations
                [1 ]From the Department of Social Medicine, University of Bristol (D.A.L., S.E., G.D.S.); the Department of Primary Care and Population Sciences, Royal Free Hospital School of Medicine (J.R.E., G.W., M.W.); and the Department of Public Health Sciences, St George’s Hospital Medical School (P.W.), Bristol, UK.
                Article
                10.1161/01.CIR.0000053441.43495.1A
                12628945
                0506006e-8b16-4811-b085-723e6f739464
                © 2003
                History

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