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Biomedical subjects

J E Manson

Publications and source records attributed to J E Manson.

At least 181 records · Page 10Linked to original sources

Birth weight and adult hypertension and obesity in women.

BACKGROUND: Low birth weight has been associated with an increased risk of hypertension, and high birth weight has been associated with increased adult body mass index. Published studies on adults have included only a small number of women. METHODS AND RESULTS: We studied 71 100 women in the Nurses Health Study I (NHS I) who were 30 to 55 years of age in 1976 and 92 940 women in the Nurses' Health Study II (NHS II) who were 25 to 42 years of age in 1989. Information on birth weight, blood pressure, physician-diagnosed hypertension, and other relevant variables was collected by biennial mailed questionnaire. Ninety-five percent of the women were white. Compared with women in the middle category of birth weight (NHS I, 7.1 to 8.5 lb; NHS II, 7.0 to 8.4 lb), the age-adjusted odds ratio of hypertension in NHS I women with birth weights < 5.0 lb was 1.39 (95% CI, 1.29 to 1.50); in NHS II, for birth weights < 5.5 lb, the age-adjusted odds ratio was 1.43 (95% CI, 1.31 to 1.56). There was no material change in the estimates after adjustment for other risk factors. In addition, compared with women in NHS I who weighed 7.1 to 8.5 lb at birth, those who weighed > 10 lb had an age-adjusted odds ratio of 1.62 (95% CI, 1.38 to 1.90) of being in the highest (> 29.2 kg/m2) versus the lowest (< 21.9 kg/ m2) quintile of body mass index in midlife. Similar results were seen in the NHS II cohort. CONCLUSIONS: Early life exposures affecting birth weight may be important in the development of hypertension and obesity in adults.

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Postmenopausal estrogen and progestin use and the risk of cardiovascular disease.

BACKGROUND: Estrogen therapy in postmenopausal women has been associated with a decreased risk of heart disease. There is little information, however, about the effect of combined estrogen and progestin therapy on the risk of cardiovascular disease. METHODS: We examined the relation between cardiovascular disease and postmenopausal hormone therapy during up to 16 years of follow-up in 59,337 women from the Nurses' Health Study, who were 30 to 55 years of age at base line. Information on hormone use was ascertained with biennial questionnaires. From 1976 to 1992, we documented 770 cases of myocardial infarction or death from coronary disease in this group and 572 strokes. Proportional-hazards models were used to calculate relative risks and 95 percent confidence intervals, adjusted for confounding variables. RESULTS: We observed a marked decrease in the risk of major coronary heart disease among women who took estrogen with progestin (multivariate adjusted relative risk, 0.39; 95 percent confidence interval, 0.19 to 0.78) or estrogen alone (relative risk, 0.60; 95 percent confidence interval, 0.43 to 0.83), as compared with women who did not use hormones [corrected]. However, there was no significant association between stroke and use of combined hormones (multivariate adjusted relative risk, 1.09; 95 percent confidence interval, 0.66 to 1.80) or estrogen alone (relative risk, 1.27; 95 percent confidence interval, 0.95 to 1.69). CONCLUSIONS: The addition of progestin does not appear to attenuate the cardioprotective effects of postmenopausal estrogen therapy.

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Prospective study of oral contraceptives and hypertension among women in the United States.

BACKGROUND: Oral contraceptives induce hypertension in approximately 5% of users of high-dose pills that contain at least 50 micrograms estrogen and 1 to 4 mg progestin, and small increases in blood pressure have been reported even among users of modern low-dose formulations. However, neither the responsible hormone in the oral contraceptive nor particular subgroups of women who might be susceptible to the hypertensive effect of oral contraceptives have been identified. METHODS AND RESULTS: In a prospective cohort study in the United States, 68 297 female nurses aged 25 to 42 years and free of diagnosed hypertension, diabetes, coronary heart disease, stroke, and cancer at baseline were followed up for 4 years. During 231 006 person-years of follow-up, 1567 incident cases of hypertension were diagnosed. Compared with women who had never used oral contraceptives, the age-adjusted relative risk was 1.5 (95% CI = 1.2 to 1.8) for current use and 1.1 (95% CI = 0.9 to 1.2) for past use. After adjustment for age, body mass index, hormones cigarette smoking, family history of hypertension, parity, physical activity, alcohol intake, and ethnicity, current users of oral contraceptives had an increased risk of development of hypertension (RR = 1.8; 95% CI = 1.5 to 2.3) compared with women who had never used them. The multivariate relative risk for past users was 1.2 (95% CI = 1.0 to 1.4). There were no important modifying effects of age, family history of hypertension, ethnicity, or body mass index. CONCLUSIONS: Current users of oral contraceptives had a significant, moderately increased risk of hypertension. However, among this group, only 41.5 cases per 10 000 person-years could be attributed to oral contraceptive use. Risk decreased quickly with cessation of oral contraceptives, and past users appeared to have only a slightly increased risk.

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Lack of effect of long-term supplementation with beta carotene on the incidence of malignant neoplasms and cardiovascular disease.

BACKGROUND: Observational studies suggest that people who consume more fruits and vegetables containing beta carotene have somewhat lower risks of cancer and cardiovascular disease, and earlier basic research suggested plausible mechanisms. Because large randomized trials of long duration were necessary to test this hypothesis directly, we conducted a trial of beta carotene supplementation. METHODS: In a randomized, double-blind, placebo-controlled trial of beta carotene (50 mg on alternate days), we enrolled 22,071 male physicians, 40 to 84 years of age, in the United States; 11 percent were current smokers and 39 percent were former smokers at the beginning of the study in 1982. By December 31, 1995, the scheduled end of the study, fewer than 1 percent had been lost to follow-up, and compliance was 78 percent in the group that received beta carotene. RESULTS: Among 11,036 physicians randomly assigned to receive beta carotene and 11,035 assigned to receive placebo, there were virtually no early or late differences in the overall incidence of malignant neoplasms or cardiovascular disease, or in overall mortality. In the beta carotene group, 1273 men had any malignant neoplasm (except nonmelanoma skin cancer), as compared with 1293 in the placebo group (relative risk, 0.98; 95 percent confidence interval, 0.91 to 1.06). There were also no significant differences in the number of cases of lung cancer (82 in the beta carotene group vs. 88 in the placebo group); the number of deaths from cancer (386 vs. 380), deaths from any cause (979 vs. 968), or deaths from cardiovascular disease (338 vs. 313); the number of men with myocardial infarction (468 vs. 489); the number with stroke (367 vs. 382); or the number with any one of the previous three end points (967 vs. 972). Among current and former smokers, there were also no significant early or late differences in any of these end points. CONCLUSIONS: In this trial among healthy men, 12 years of supplementation with beta carotene produced neither benefit nor harm in terms of the incidence of malignant neoplasms, cardiovascular disease, or death from all causes.

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Self-reported breast implants and connective-tissue diseases in female health professionals. A retrospective cohort study.

OBJECTIVE: To evaluate the association of breast implants with connective-tissue diseases. DESIGN AND PARTICIPANTS: Retrospective cohort study of 395,543 female health professionals who completed mailed questionnaires for potential participation in the Women's Health Study. A total of 10,830 women reported breast implants and 11,805 reported connective-tissue diseases between 1962 and 1991. Cox proportional hazards regression models were used in analyses. MAIN OUTCOME MEASURE: Self-reported connective-tissue diseases. RESULTS: Compared with women who did not report breast implants, the relative risk (RR) of the combined end point of any connective-tissue disease among those who reported breast implants was 1.24 (95% confidence interval, 1.08 to 1.41, P = .0015). With respect to the individual diseases, the finding for other connective-tissue diseases (including mixed) was statistically significant (P = .017), the findings for rheumatoid arthritis, Sjogren's syndrome, dermatomyositis or polymyositis, or scleroderma were of borderline statistical significance (.05 < P < .10), and the finding for systemic lupus erythematosus was not statistically significant (P = .44). There were no clear trends in RR with increasing duration of breast implants. CONCLUSION: These self-reported data from female health professionals are compatible with prior reports from other cohort studies that exclude a large hazard, but do suggest small increased risks of connective-tissue diseases among women with breast implants. The very large sample size makes chance an unlikely explanation for the results, but bias due to differential overreporting of connective-tissue diseases or selective participation by affected women with breast implants remains a plausible alternative explanation. The major contribution of this and other observational analytic studies has been to exclude large risks of connective-tissue diseases following breast implants.

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Prospective assessment of breastfeeding and breast cancer incidence among 89,887 women.

BACKGROUND: The relation between breastfeeding and breast cancer risk has been examined in many studies; some have reported no association, and others a reduced risk, particularly among premenopausal women. In the only prospective cohort study, no association was found. We have assessed prospectively the association between breastfeeding and incidence of breast cancer among 89,887 women in the US Nurses' Health Study. METHODS: In 1986, participants were asked about the number of months they breastfed for all their children combined. Parous women with no history of cancer were included in this analysis. During 6 years of follow-up (513,015 person-years), 1,459 invasive breast cancer cases were diagnosed. FINDINGS: Relative to women who had never breastfed, no significant overall association was found--after adjusting for established risk factors for breast cancer--between a history of having breastfed and subsequent development of breast cancer (relative risk [RR] 0.93, 95% CI 0.83 -1.03). No inverse trend was observed with duration of breastfeeding; women who breastfed for 2 years of longer had a RR of 1.11 (0.90-1.38). Among women who had given birth only once, women who had breastfed their child experienced a lower incidence of breast cancer (RR 0.68, 0.46-1.00). Among premenopausal women, who tended to be near menopause due to the age structure of the cohort, the RR of breast cancer for those who had lactated was 1.16 (0.89-1.50). Premenopausal women who had lactated for 1 year or more had a RR of 1.10 (0.78-1.57). INTERPRETATION: These data suggest that there is no important overall association between breast-feeding and the occurrence of breast cancer.

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Coffee consumption and coronary heart disease in women. A ten-year follow-up.

OBJECTIVE--To assess the relationship between coffee consumption and risk of coronary heart disease (CHD) among women. DESIGN--Prospective cohort study with coffee consumption measured in 1980, 1984, and 1986, and follow-up through 1990. SETTING--Female registered nurses in the United States. PARTICIPANTS--A total of 85,747 US women 34 to 59 years of age in 1980 and without history of CHD, stroke, or cancer. MAIN OUTCOME MEASURE--Ten-year incidence of CHD (defined as nonfatal myocardial infarction or fatal CHD). RESULTS--During 10 years of follow-up we documented 712 cases of CHD. After adjustment for age, smoking, and other CHD risk factors, we found no evidence for any positive association between coffee consumption and risk of subsequent CHD. For women drinking six or more cups of caffeine-containing coffee per day in 1980, the relative risk was 0.95 (95% confidence interval, 0.73 to 1.26) compared with women who did not consume this beverage. Similarly, there was no association when the first 4 years of follow-up were excluded, when nonfatal and fatal CHD end points were examined separately, or when we updated coffee consumption in 1984 or 1986 and examined only CHD during the next 2-year interval. Further, there was no association with caffeine intake from all sources combined or with decaffeinated coffee consumption. CONCLUSIONS--These data indicate that coffee as consumed by US women is not an important cause of CHD.

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Diet and heart disease. The role of fat, alcohol, and antioxidants.

Overwhelming evidence indicates that the Western diet plays a major role in atherogenesis. Clinicians are only now beginning to tease out the precise components of the diet that are harmful or beneficial. With respect to fat intake, it remains unclear whether it is the amount or type of fat that promotes atherosclerotic disease. There appears to be a consistent positive association of cholesterol, saturated fat, and possibly trans-fatty acid intake and atherosclerotic disease. Although there is general agreement that reducing intake of these dietary components would be beneficial, controversy remains on what should replace these harmful fats. Some researchers advocate massive reductions in total fat consumption with replacement with carbohydrates for everyone, whereas others recommend a Mediterranean-style diet, which replaces saturated animal fats with vegetable fats. Very low-fat diets have been shown to lower the chance of a heart attack among those with severe coronary artery disease, but for the majority of Americans who do not have obvious artery disease, there is no convincing evidence that a very low-fat diet is optimal. There may be other adverse health effects of this Asian diet, such as increased rates of hemorrhagic stroke. Further research is required to refine thinking on the optimal composition of fats in diet. The effects of alcohol consumption on chronic diseases are complex. The strength and consistency of the observational and experimental evidence strongly suggests a causal link between light to moderate alcoholic beverage consumption and reduced risks of CHD. These reductions in risk of CHD appear to be mediated largely by raising HDL cholesterol levels, although additional mechanisms remain possible and do not appear to be beverage specific. Maximal benefit in terms of CHD appears to be at the level of one drink per day. From a public policy standpoint, whether the benefits for CHD persist at heavy drinking levels or are attenuated is moot because clear harm of heavy drinking in terms of overall mortality outweighs any benefits in the reduction of heart disease. Although the association of alcohol and CHD is likely to be causal, any individual or public health recommendations must consider the complexity of alcohol's metabolic, physiologic, and psychological effects. With alcohol, the differences between daily intake of small to moderate and large quantities may be the difference between preventing and causing disease. A discussion of alcohol intake should be a part of routine preventive counseling. Given the complex nature of alcohol disease relationships, alcohol consumption should not be viewed as a primary preventive strategy; also, it should not necessarily be viewed as an unhealthy behavior. Based on the totality of available evidence, antioxidants represent a possible but as yet unproven means to reduce risks of cardiovascular disease. Although it remains unclear whether supplementation of diet with antioxidant vitamins will reduce risks of atherosclerotic disease, most researchers agree that consumption of fruits and vegetables is an important part of a healthy diet. The U.S. Department of Agriculture recommends two to four servings of fruit and three to five servings of vegetables per day.

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Self-reported birthweight and history of having been breastfed among younger women: an assessment of validity.

BACKGROUND: Recent evidence suggests potential associations between birthweight and infant feeding history and risk of a variety of health outcomes during adulthood. Because studies may rely on self-reported birthweight and infant feeding history, it is important to assess the validity of this information. METHODS: The authors compared birthweights reported by a sample of 538 women, 27-44 years of age, participating in the Nurses' Healthy Study II (NHSII) cohort, with birthweights recalled by their mothers and with those from state birth records. In addition, we compared participants' self-reported history of having breastfed with their breastfeeding history reported by their mothers. RESULTS: For birthweight, the correlation between reports by the cohort participants and by their mothers was high (Spearman r = 0.75). Compared with weights recorded on state birth records, correlations were 0.74 for reports by cohort participants and 0.85 for reports by their mothers. When comparing NHSII participants' self-report of ever having been breastfed with their mothers' report, sensitivity was 82% and specificity was 86%. For duration of breastfeeding, the Spearman correlation between mother and daughter reports was 0.74. In analyses stratified by four ethnic groups (African-American, Asian, Caucasian, and Hispanic) we observed substantial differences in distribution of birthweight and breastfeeding patterns; however, the degree of validity in reporting them was similar. CONCLUSION: The validity of self-reported birthweight and breastfeeding history by these middle-aged women appears to be high.

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Obesity and cardiovascular disease.

Obesity is strongly associated with cardiac risk factors including elevated blood pressure, glucose intolerance, and dyslipidemia. Clinical trials have indicated that weight loss significantly improves these risk profiles. Epidemiologic studies consistently have shown that obesity is a strong risk factor for coronary heart disease in both men and women. In addition, abdominal adiposity may confer added risk for coronary heart disease. Although obesity is a modifiable and preventable cardiac risk factor, management of this disorder remains both challenging and vexing to clinicians. To prevent cardiovascular disease we must find ways to decrease the rising prevalence of obesity and to help overweight individuals achieve and sustain weight loss.

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Antioxidants and coronary heart disease: observational studies.

Observational studies have found that persons who consume large amounts of fruit and vegetables have lower rates of coronary heart disease. The strength of epidemiologic evidence, however, differs for each of the antioxidant vitamins. High intake of vitamin E from food or supplements has generally been associated with a lower incidence of coronary heart disease. The evidence for beta-carotene intake is inconsistent, with several studies finding a modest reduction in risk among persons with high intake, and others failing to find an association. Although many studies have examined the relationship between vitamin C intake and cardiovascular disease, no significant benefit was seen in any of the large studies that were able to control for other antioxidant intake or multivitamin use. Observational studies cannot discern whether the decreased risk observed is caused by the antioxidants themselves or other characteristics of the individuals who consume them. The epidemiologic associations may be due to other nutrients in antioxidant-rich foods, or other dietary or lifestyle factors. Randomized controlled trials are necessary to confirm or refute the observational data. On the basis of available evidence, we should recommend a healthy diet, rich in fruit and vegetables, but should not endorse vitamin supplementation unless conclusive evidence of benefit is demonstrated in clinical trials.

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Variability in diagnostic evaluation and criteria for gestational diabetes.

OBJECTIVE: To determine the frequency of screening for gestational diabetes mellitus (GDM) among a population receiving regular prenatal care and to assess the extent to which National Diabetes Data Group (NDDG) criteria for the diagnosis of GDM are used by practicing obstetricians. RESEARCH DESIGN AND METHODS: We studied participants in the Nurses' Health Study II, a large prospective cohort study of 116,678 nurses aged 25-42 years in 1989. A total of 422 women who reported a first diagnosis of GDM between 1989 and 1991 were sent supplementary questionnaires regarding diagnosis and treatment, and medical records were requested for a subset of 120 to validate self-reported GDM and assess criteria used for diagnosis. A sample of 100 women who reported a pregnancy not complicated by GDM were sent questionnaires addressing GDM screening and prenatal care. RESULTS: Among a sample of 93 women who reported a pregnancy not complicated by GDM and responded to the supplementary questionnaire, 16 (17%) reported no glucose loading test; 69% of unscreened women had one or more risk factors for GDM. Among a sample of 114 women who self-reported GDM in a singleton pregnancy and whose medical records were available for review, a physician diagnosis of GDM was confirmed in 107 (94%). Records and supplementary questionnaires indicated that oral glucose tolerance tests (OGTTs) were performed in 96 (86%) of these women. Of women with a physician diagnosis of GDM whose OGTT results were available, 25% failed to meet NDDG criteria for this diagnosis, although all had evidence of abnormal glucose homeostasis. CONCLUSIONS: Screening for GDM is not universal, even among a group of health professionals in whom screening prevalence is likely to be higher than in the general population. Diagnostic criteria for GDM among obstetricians in practice remain nonstandard despite NDDG recommendations. Better understanding of the implications of differing degrees of glucose intolerance and of varying GDM screening and management strategies is required to make policy recommendations for appropriate and cost-effective care.

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Prospective study of shift work and risk of coronary heart disease in women.

BACKGROUND: The purpose of this study was to examine prospectively the relation of shift work to risk of coronary heart disease (CHD) in a cohort of women. METHODS AND RESULTS: An ongoing prospective cohort of US female nurses, in whom we assessed (in 1988) the total number of years during which they worked rotating night shifts (at least three nights per month in addition to day and evening shifts), included 79,109 women, 42 to 67 years old in 1988, who were free of diagnosed CHD and stroke. Incident CHD was defined as nonfatal myocardial infarction and fatal CHD. During 4 years of follow-up (1988 to 1992), 292 cases of incident CHD (248 nonfatal myocardial infarction and 44 fatal CHD) occurred. The age-adjusted relative risk of CHD was 1.38 (95% CI, 1.08 to 1.76) in women who reported ever doing shift work compared with those who had never done so. The excess risk persisted after adjustment for cigarette smoking and a variety of other cardiovascular risk factors. Compared with women who had never done shift work, the multivariate adjusted relative risks of CHD were 1.21 (95% CI, 0.92 to 1.59) among women reporting less than 6 years and 1.51 (95% CI, 1.12 to 2.03) among those reporting 6 or more years of rotating night shifts. CONCLUSIONS: These data are compatible with the possibility that 6 or more years of shift work may increase the risk of CHD in women.

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Height and the risk of cardiovascular disease in women.

Height has been inversely associated with coronary heart disease in several prospective studies in men, but data in women are sparse. The relation between height and cardiovascular disease was examined in 14 years of follow-up data from the Nurses' Health Study, a prospective cohort of 121,700 US female nurses aged 30-55 years in 1976. The relative risks associating height with coronary heart disease (nonfatal myocardial infarction (n = 1,000), fatal myocardial infarction (n = 304), confirmed angina (n = 1,343), or coronary revascularization (n = 901)) were estimated after adjustment for a large number of cardiovascular risk factors, including age and body mass index. Compared with the shortest women (< or = 61 inches (< or = 1.55 m)), the relative risk of coronary heart disease was 0.82 (95% confidence interval (CI) 0.73-0.92) for women 62-63 inches (1.57-1.60 m) tall, 0.74 (95% CI 0.65-0.85) for women 64 inches (1.63 m) tall, 0.79 (95% CI 0.70-0.89) for women 65-66 inches (1.65-1.68 m) tall, and 0.73 (95% CI 0.65-0.83) for women 67 or more inches (> or = 1.70 m) tall (p for trend < 0.0001). The inverse association was more pronounced for angina/coronary revascularization (p for trend < 0.0001; relative risk for 67 or more inches = 0.67 (95% CI 0.58-0.78)) than for myocardial infarction (p for trend = 0.03; relative risk for 67 or more inches = 0.78 (95% CI 0.64-0.95)). No trend was evident for height in relation to risk of stroke. These data support the hypothesis that height is inversely related to risk of coronary heart disease in women.

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Psychosocial risk factors and nonfatal myocardial infarction.

BACKGROUND: Numerous psychosocial factors have been hypothesized to play a role in coronary heart disease. However, existing studies have yielded inconsistent results. METHODS AND RESULTS: The relations between type A personality as well as suppressed versus expressed anger and risk of nonfatal myocardial infarction (MI) were studied in 340 patients and 340 age-, sex-, and community-matched control subjects. Subjects were interviewed at home to assess behavioral and medical cardiovascular risk factors, and fasting blood samples were obtained. Type A personality was associated with nonfatal MI in crude matched-pair analysis (OR, 1.57; 95% CI, 1.12 to 2.20; P = .008). Adjusting for known cardiovascular risk factors (including treated hypertension, body mass index, treated diabetes, family history of premature MI, physical activity, smoking, alcohol, total calories per day, and saturated fat) did not substantially change the magnitude of the point estimate, although the finding was no longer statistically significant (OR, 1.43; 95% CI, 0.97 to 2.09; P = .069). Further adjustment for lipids, including total cholesterol, total HDL, its subfractions (HDL2, HDL3), LDL, VLDL, and triglycerides, markedly attenuated the association (OR, 1.12; 95% CI, 0.66 to 1.90; P = .687), an effect due almost entirely to HDL cholesterol. Suppressed anger was positively but not statistically significantly associated with increased risk of MI in crude matched-pair analysis (OR, 1.33; 95% CI, 0.98 to 1.81; P = .065), in analysis adjusted for behavioral and medical cardiovascular risk factors (OR, 1.26; 95% CI, 0.89 to 1.78; P = .193), or after adjustment for lipids (OR, 1.11; 95% CI, 0.67 to 1.82; P = .695). CONCLUSIONS: These findings suggest a possible association of type A but not suppressed anger with risk of nonfatal MI that may be mediated by alterations in HDL cholesterol level. If decreases in HDL are not in the same causal pathway, then the apparent association between type A personality and risk of MI is due to confounding, principally by HDL.

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