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Biomedical subjects

M J Stampfer

Publications and source records attributed to M J Stampfer.

At least 289 records · Page 16Linked to original sources
PubMed1995

Mutation in the gene coding for coagulation factor V and the risk of myocardial infarction, stroke, and venous thrombosis in apparently healthy men.

BACKGROUND: A specific point mutation in the gene coding for coagulation factor V is associated with resistance to degradation by activated protein C, a recently described abnormality of coagulation that may be associated with an increased risk of venous thrombosis. Whether this mutation also predisposes patients to arterial thrombosis is unknown, as is the value of screening for the mutation in order to define the risk of venous thrombosis among unselected healthy people. METHODS: Among 14,916 apparently healthy men in the Physicians' Health Study who provided base-line blood samples, 374 had myocardial infarctions, 209 had strokes, and 121 had deep venous thrombosis, pulmonary embolism, or both, during a mean follow-up of 8.6 years. We determined whether a mutation at nucleotide position 1691 of the factor V gene was present or absent in these 704 men and in an equal number of matched participants who remained free of vascular disease. RESULTS: The prevalence of heterozygosity for the mutation among men who had myocardial infarctions (6.1 percent, P = 0.9) or strokes (4.3 percent, P = 0.4) was similar to that among men who remained free of vascular disease (6.0 percent). However, the prevalence of the mutation was significantly higher among men who had venous thrombosis, pulmonary embolism, or both (11.6 percent, P = 0.02). In adjusted analyses, the relative risk of venous thrombosis among men with the mutation was 2.7 (95 percent confidence interval, 1.3 to 5.6; P = 0.008). This increased risk was seen with primary venous thrombosis (relative risk, 3.5; 95 percent confidence interval, 1.5 to 8.4; P = 0.004) but not with secondary venous thrombosis (relative risk, 1.7; 95 percent confidence interval, 0.6 to 5.3; P = 0.3), and it was most apparent among older men. Specifically, the prevalence of the mutation among men over the age of 60 in whom primary venous thrombosis developed was 25.8 percent (relative risk, 7.0; 95 percent confidence interval, 2.6 to 19.1; P < 0.001). CONCLUSIONS: In a large cohort of apparently healthy men, the presence of a specific point mutation in the factor V gene was associated with an increased risk of venous thrombosis, particularly primary venous thrombosis. The presence of the mutation was not associated with an increased risk of myocardial infarction or stroke. This mutation appears to be the most common inherited factor thus far recognized that predisposes patients to venous thrombosis.

Aged↗
PubMed1995

Prospective study of toenail selenium levels and cancer among women.

BACKGROUND: Inverse associations between selenium status and cancer risk have been observed in animal studies, ecologic studies, and some case-control and prospective studies. Whereas results of some prospective studies have suggested an overall inverse relationship between selenium levels and cancer, other prospective studies have failed to confirm this finding. Prospective data on women are particularly limited because fewer women than men have been studied prospectively. PURPOSE: The aim of this study was to prospectively examine the relationship between selenium levels in toenails (previously shown to reflect selenium intake) and incidence of cancer among women. METHODS: The Nurses' Health Study cohort began in 1976 with 121,700 female nurses aged 30-55 years living in 11 U.S. states. In 1982, we requested toenail clippings from the members of the cohort, and 62,641 participants with no history of cancer returned these clippings. During 41 months of follow-up, 503 cases of cancer other than breast cancer (results previously reported) or nonmelanoma skin cancer were analyzed. For each case patient, a control subject was chosen from women who remained free of diagnosed cancer, matched by age and by date of nail return. RESULTS: No inverse association was observed between selenium levels in toenails and cancer risk. The age- and smoking-adjusted relative risk (RR), comparing the highest with the lowest quintile of toenail selenium level, was 1.44 (95% confidence interval [CI] = 0.97-2.13), and the trend across quintiles was marginally significant (two-sided P = .06). Comparing the highest with the lowest decile, the RR (age- and smoking-adjusted) was 1.77 (95% CI = 1.04-3.02). When these data were combined with the data from 434 breast cancer case patients and their matched control subjects identified in parallel from this same cohort, the RR comparing the highest with the lowest quintile was 1.24 (95% CI = 0.93-1.65). Toenail selenium level was not inversely associated with cancer at any major site, including uterine cancer, colorectal cancer, melanoma, ovarian cancer, or lung cancer (after adjusting for smoking); in fact, nonsignificant positive associations were observed at several sites. CONCLUSIONS: Toenail selenium levels were not inversely associated with cancer risk in this study. IMPLICATIONS: These data, in conjunction with previous findings of no association between toenail selenium status and breast cancer risk, strongly suggest that higher selenium intake within the range consumed by most U.S. women (as reflected by toenail selenium levels) is not protective against overall cancer incidence in women.

Adult↗
PubMed1995

A prospective evaluation of an angiotensin-converting-enzyme gene polymorphism and the risk of ischemic heart disease.

BACKGROUND: In a previous study, men with a history of myocardial infarction were found to have an increased prevalence of homozygosity for the deletional allele (D) of the angiotensin-converting-enzyme (ACE) gene. The D allele is associated with higher levels of ACE, which may predispose a person to ischemic heart disease. We investigated the association between the ACE genotype and the incidence of myocardial infarction, as well as other manifestations of ischemic heart disease, in a large, prospective cohort of U.S. male physicians. METHODS: In the Physicians' Health Study, ischemic heart disease as defined by angina, coronary revascularization, or myocardial infarction developed in 1250 men by 1992. They were matched with 2340 controls according to age and smoking history. Zygosity for the deletion-insertion (D-I) polymorphism of the ACE gene was determined by an assay based on the polymerase chain reaction. Data were analyzed for both matched pairs and unmatched samples, with adjustment for the effects of known or suspected risk factors by conditional and nonconditional logistic regression, respectively. RESULTS: The ACE genotype was not associated with the occurrence of either ischemic heart disease or myocardial infarction. The adjusted relative risk associated with the D allele was 1.07 (95 percent confidence interval, 0.96 to 1.19; P = 0.24) for ischemic heart disease and 1.05 (95 percent confidence interval, 0.89 to 1.25; P = 0.56) for myocardial infarction, if an additive mode of inheritance is assumed. Additional analyses assuming dominant and recessive effects of the D allele also failed to show any association, as did the examination of low-risk subgroups. CONCLUSIONS: In a large, prospectively followed population of U.S. male physicians, the presence of the D allele of the ACE gene conferred no appreciable increase in the risk of ischemic heart disease or myocardial infarction.

Alleles↗
PubMed1995

Prospective study of cigarette smoking, alcohol use, and the risk of diabetes in men.

OBJECTIVE: To examine the association between smoking, alcohol consumption, and the incidence of non-insulin dependent diabetes mellitus in men of middle years and older. DESIGN: Cohort questionnaire study of men followed up for six years from 1986. SETTING: The health professionals' follow up study being conducted across the United States. SUBJECTS: 41,810 male health professionals aged 40-75 years and free of diabetes, cardiovascular disease, and cancer in 1986 and followed up for six years. MAIN OUTCOME MEASURE: Incidence of non-insulin dependent diabetes mellitus diagnosed in the six years. RESULTS: During 230,769 person years of follow up 509 men were newly diagnosed with diabetes. After controlling for known risk factors men who smoked 25 or more cigarettes daily had a relative risk of diabetes of 1.94 (95% confidence interval 1.25 to 3.03) compared with non-smokers. Men who consumed higher amounts of alcohol had a reduced risk of diabetes (P for trend < 0.001). Compared with abstainers men who drank 30.0-49.9 g of alcohol daily had a relative risk of diabetes of 0.61 (95% confidence interval 0.44 to 0.91). CONCLUSIONS: Cigarette smoking may be an independent, modifiable risk factor for non-insulin dependent diabetes mellitus. Moderate alcohol consumption among healthy people may be associated with increased insulin sensitivity and a reduced risk of diabetes.

Adult↗
PubMed1995

Physical activity, obesity, and risk for colon cancer and adenoma in men.

OBJECTIVE: To determine whether physical inactivity and obesity increase risk for colon cancer and adenomas, which are precursors of cancer, and whether the abdominal distribution of obesity is an independent risk factor for these events. DESIGN: Prospective cohort study. SETTING: United States. PATIENTS: 47,723 male health professionals, 40 to 75 years of age, who responded to a questionnaire mailed in 1986. MEASUREMENTS: Questionnaires in 1986 about physical activity level and body mass index, and questionnaires in 1987 (31,055 respondents) about waist and hip circumferences. Between 1986 and 1992, 203 new patients were diagnosed with colon cancer and 586 were diagnosed with adenomas. RESULTS: Physical activity was inversely associated with risk for colon cancer (high compared with low quintiles of average energy expenditure from leisure-time activities: relative risk, 0.53 [95% CI, 0.32 to 0.88], P for trend = 0.03) after adjustment for age; history of colorectal polyp; previous endoscopy; parental history of colorectal cancer; smoking; body mass; use of aspirin; and intake of red meat, dietary fiber, folate, and alcohol. Body mass index was directly associated with risk for colon cancer independently of physical activity level. Waist circumference and waist-to-hip ratio were strong risk factors for colon cancer (waist-to-hip ratio > or = 0.99 compared with waist-to-hip ratio < 0.90: multivariate relative risk, 3.41 [CI, 1.52 to 7.66], P for trend = 0.01; waist circumference > or = 43 inches compared with waist circumference < 35 inches: relative risk, 2.56 [CI, 1.33 to 4.96], P for trend < 0.001). These associations persisted even after adjustment for body mass and physical activity. Similar associations were seen between obesity and physical inactivity and adenomas of 1 cm or more, but no association was observed for smaller adenomas. Height was also associated with a higher risk for colon cancer (height > or = 73 inches compared with height < or = 68 inches: multivariate relative risk, 1.76 [CI, 1.13 to 2.74], P for trend = 0.02). CONCLUSIONS: The results support an inverse association between physical activity and risk for colon cancer, whereas height and obesity, particularly abdominal adiposity, are associated with an elevated risk.

Adenoma↗
PubMed1995

Alcohol, low-methionine--low-folate diets, and risk of colon cancer in men.

BACKGROUND: Methylation of DNA, which may have a role in the regulation of gene expression, depends on dietary folate and methionine. Because aberrant DNA methylation may contribute to the initiation or progression of colon cancer, we hypothesized that deficient intakes of folate or methionine and high consumption of alcohol, an antagonist of methyl-group metabolism, increase risk of colon neoplasia. Previously, a high-alcohol and low-methionine--low-folate (methyl-deficient) diet was shown to be related to a higher risk of colon adenomas, precursors of cancer. PURPOSE: Our goal was to determine if ingestion of a high-alcohol, methyl-deficient diet is related directly to risk of colon cancer. METHODS: We assessed dietary intake for a 1-year period for a cohort of 47,931 U.S. male health professionals, 40-75 years old and free of diagnosed cancer in 1986. We assessed diet by using a validated, semiquantitative food-frequency questionnaire. During 6 years of follow-up, we documented 205 new cases of colon cancer in this cohort. RESULTS: Current alcohol intake was directly related to risk of colon cancer (multivariate relative risk [RR] = 2.07; 95% confidence interval [CI] = 1.29-3.32, for > 2 drinks versus < or = 0.25 drink daily; P trend = .005), and past drinkers were also at higher risk (RR = 1.95; 95% CI = 1.22-3.10). Individually, folate and methionine intakes were weakly inversely associated with risk of colon cancer. An adverse effect of a high-alcohol, low-methyl diet was not observed among regular users of aspirin, who have previously been shown to be at lower risk for colon cancer. Combinations of high alcohol and low methionine and folate intakes yielded striking associations for total colon cancer (RR = 3.30 [95% CI = 1.58-6.88] comparing high-methyl diets with low-methyl diets among nonusers of aspirin) and for cancers of the distal colon (RR = 7.44; 95% CI = 1.72-32.1). Among men with high intakes of folate or methionine, alcohol levels of > 2 drinks daily were not associated with risk of colon cancer. The increased risk of colon cancer associated with alcohol and methyl-deficient diets was not confounded by smoking; intakes of fat, red meat, and fiber; level of physical activity; multivitamin or aspirin use; and body mass index. CONCLUSIONS: These findings support the hypothesis that substantial consumption of alcohol, when combined with inadequate intakes of folate and methionine, may increase risk of colon cancer and confirm similar findings in adenomas. IMPLICATIONS: These data provide further support of recommendations to avoid excess alcohol consumption and to increase dietary folate to lower the risk of colon cancer.

Adenoma↗
PubMed1995

Weight, weight change, and coronary heart disease in women. Risk within the 'normal' weight range.

OBJECTIVE--To assess the validity of the 1990 US weight guidelines for women that support a substantial gain in weight at approximately 35 years of age and recommend a range of body mass index (BMI) (defined as weight in kilograms divided by the square of height in meters) from 21 to 27 kg/m2, in terms of coronary heart disease (CHD) risk in women. DESIGN--Prospective cohort study. SETTING--Female registered nurses in the United States. PARTICIPANTS--A total of 115,818 women aged 30 to 55 years in 1976 and without a history of previous CHD. MAIN OUTCOME MEASURE--Incidence of CHD defined as nonfatal myocardial infarction or fatal CHD. RESULTS--During 14 years of follow-up, 1292 cases of CHD were ascertained. After controlling for age, smoking, menopausal status, postmenopausal hormone use, and parental history of CHD and using as a reference women with a BMI of less than 21 kg/m2, relative risks (RRs) and 95% confidence intervals (CIs) for CHD were 1.19 (0.97 to 1.44) for a BMI of 21 to 22.9 kg/m2, 1.46 (1.20 to 1.77) for a BMI of 23 to 24.9 kg/m2, 2.06 (1.72 to 2.48) for a BMI of 25 to 28.9 kg/m2, and 3.56 (2.96 to 4.29) for a BMI of 29 kg/m2 or more. Women who gained weight from 18 years of age were compared with those with stable weight (+/- 5 kg) in analyses that controlled for the same variables as well as BMI at 18 years of age. The RRs and CIs were 1.25 (1.01 to 1.55) for a 5- to 7.9-kg gain, 1.64 (1.33 to 2.04) for an 8- to 10.9-kg gain, 1.92 (1.61 to 2.29) for an 11- to 19-kg gain, and 2.65 (2.17 to 3.22) for a gain of 20 kg or more. Among women with the BMI range of 18 to 25 kg/m2, weight gain after 18 years of age remained a strong predictor of CHD risk. CONCLUSIONS--Higher levels of body weight within the "normal" range, as well as modest weight gains after 18 years of age, appear to increase risks of CHD in middle-aged women. These data provide evidence that current US weight guidelines may be falsely reassuring to the large proportion of women older than 35 years who are within the current guidelines but have potentially avoidable risks of CHD.

Adult↗
PubMed1995

A prospective evaluation of plasma prostate-specific antigen for detection of prostatic cancer.

OBJECTIVE: To evaluate the validity of prostate-specific antigen (PSA) in identifying men who subsequently were or were not clinically diagnosed with prostate cancer, assess optimal test cutoff, measure lead time, and estimate relative risks (RRs) associated with discrete PSA levels. DESIGNS: Nested case-control study of men providing plasma samples before a 10-year follow-up. SETTING: The Physicians' Health Study, an ongoing randomized trial that enrolled 22,071 men aged 40 to 84 years in 1982. PARTICIPANTS: A total of 366 men (cases) diagnosed with prostate cancer and 1098 men (three controls per case), matched by age, randomly selected from all cohort members at risk at the time of case diagnosis. MAIN OUTCOME MEASURES: Sensitivity and specificity for each year of follow-up and for aggressive and nonaggressive cancers separately. RESULTS: At a cutoff of 4.0 ng/mL, sensitivity for the entire 10-year follow-up was 46% for total cases. Sensitivities for detection of total, aggressive, and nonaggressive cancers occurring in the first 4 years were 73%, 87%, and 53%. Overall, specificity was 91% and changed little by year of follow-up. Optimal validity was achieved at a cutoff of 3.3 ng/mL. Estimated mean lead time for all cancers was 5.5 years. Only 40% of cancers detected more than 5 years from baseline were nonaggressive. Compared with men with PSA levels less than 1.0 ng/mL, those with PSA levels between 2.0 and 3.0 ng/mL had an RR of 5.5 (95% confidence interval, 3.7 to 9.2). CONCLUSIONS: A single PSA measurement had a relatively high sensitivity and specificity for detection of prostate cancers that arose within 4 years. Prostate-specific antigen values less than the usual cutoff were associated with substantial increases in risk compared with the lowest levels. Final evaluation of PSA screening must also consider cost and the ability of current treatments to improve the prognosis of screen-detected cases.

Adult↗
PubMed1995

A prospective study of plasma hormone levels, nonhormonal factors, and development of benign prostatic hyperplasia.

We assessed the relation of plasma hormone levels and nonhormonal factors with subsequent occurrence of surgical treatment for benign prostatic hyperplasia (BPH) among participants in the Physicians' Health Study. Frozen plasma samples, collected at the study onset, were available for 320 men who developed surgically treated BPH up to 9 years later and for 320 age-matched controls. Plasma testosterone (T), dihydrotestosterone (DHT), androstenedione, estradiol (E2), and estrone (E1) were measured for each case-control pair. In unadjusted analyses, none of the hormones or hormone ratios were associated with BPH; for example, for T and E2 the odds ratios (OR) comparing the highest quintile (Q5) with the lowest (Q1) were 0.74 (95% CI = 0.42, 1.30) and 1.07 (95% CI = 0.51, 2.22), respectively. However, in multivariate analyses controlling diastolic blood pressure, exercise, alcohol, E1, and DHT:T ratio, we observed a strong trend for increasing risk across quintiles for E2 (Q5 vs. Q1 OR = 3.56, P trend = 0.009), and a weak inverse trend for E1 (Q5 vs Q1 OR = 0.51, P trend = 0.07). The excess risk associated with E2 was confined to men with relatively low androgen levels. Three nonhormonal factors previously suspected as risk factors were independently associated with surgical BPH in these data. The OR for a 1-mm Hg difference in diastolic blood pressure was 1.04 (95% CI = 1.01, 1.07). Alcohol use and infrequent exercise were inversely associated with risk of BPH surgery; however, risk estimates were not consistent across categories of exercise and alcohol frequency. Our results indicate that normal variation in circulating androgen levels does not influence development of BPH, but that variation in estrogen levels might be important.

Adult↗
PubMed1995

Diet, alcohol, and smoking and the occurrence of hyperplastic polyps of the colon and rectum (United States).

Hyperplastic polyps of the colon reveal a geographic distribution similar to that of colorectal cancer and adenomatous polyps. However, unlike adenomas--known precursors of colorectal cancer--little is known about the etiology or clinical significance of the hyperplastic polyp. In this prospective study, we set out to determine the main dietary and other lifestyle factors in the United States that might be associated with this lesion. Hyperplastic polyps of the distal colon and rectum were diagnosed in 219 of 12,922 men of the Health Professionals Follow-up Study having had an endoscopic procedure between 1986 and 1992, and 175 of 15,339 women of the Nurses' Health Study who had undergone an endoscopy for a variety of reasons between 1980 and 1990. After adjusting for age, family history of colon cancer, history of previous endoscopy, and total energy intake using multiple logistic regression, those consuming 30 g or more of alcohol per day were at increased risk relative to nondrinkers among men (relative risk [RR] = 1.69; 95 percent confidence interval [CI] = 1.01-2.80) and women (RR = 1.79, CI = 1.02-3.15). Current smoking also was found to be associated strongly positively with hyperplastic polyps in men (RR = 2.45, CI = 1.59-3.75) and women (RR = 1.96, CI = 1.16-2.86). High intake of folate was associated inversely with risk in both men (RR = 0.74, CI = 0.49-1.11, between high and low intakes of folate) and women (RR = 0.45, CI = 0.28-0.74, between high and low intakes of folate). Among macronutrients, a suggestive increase in risk existed with intake of animal fat, although this was attenuated in the full multivariate model (RR[men] = 1.48, CI = 0.94-2.41, and RR[women] = 1.22, CI = 0.77-1.94) between high and low quantities of animal fat intake. These prospective data provide evidence of associations between low folate intake, alcohol consumption, and current cigarette smoking, and risk of hyperplastic polyps of the distal colon and rectum. These same factors also have been found to be related to adenoma and cancer of the colon. The hyperplastic polyp is an indicator of populations at high risk for colorectal carcinoma, and it also may serve as a marker for factors that influence neoplastic evolution.

Adult↗
PubMed1995

Reproductive factors and family history of breast cancer in relation to plasma estrogen and prolactin levels in postmenopausal women in the Nurses' Health Study (United States).

Parity, age at first birth, age at menarche, and a family history of breast cancer have each been associated consistently with breast cancer risk. Whether this increase in risk is mediated, at least in part, through changes in endogenous hormone levels is unclear. We conducted a cross-sectional study of the relationships between these factors and plasma hormone levels in 216 healthy postmenopausal women in the Nurses' Health Study (United States). The hormones evaluated were estradiol, percent and total free estradiol, percent and total bioavailable estradiol, estrone, estrone sulfate, and prolactin. After controlling for age, body mass index (weight/height2), and alcohol use, we observed inverse associations between estrone sulfate and parity (r = -0.15, P = 0.03) and between percent bioavailable estradiol and age at first birth (r = -0.17, P = 0.02). Although women with a family history of breast cancer tended to have higher estrogen levels compared with women without such history, the differences were not statistically significant. Age at menarche was not related significantly to any of the hormones. These data provide some additional evidence that the inverse relationship observed between parity and breast cancer risk may be mediated, at least in part, through decreased estrogen levels. Our data do not support a substantial influence of either family history of breast cancer or age at menarche on postmenopausal estrogen or prolactin levels.

Adult↗
PubMed1995

A prospective study of plasma fish oil levels and incidence of myocardial infarction in U.S. male physicians.

OBJECTIVES: This study evaluated whether increased intake of fish oils (eicosapentaenoic and docosahexaenoic acids) might reduce the risk of coronary heart disease. BACKGROUND: Observational and clinical studies have suggested that increased intake of fish oils, as reflected in plasma levels of fish oils, may reduce the risk of myocardial infarction. METHODS: A nested case-control study was conducted among the 14,916 participants in the Physicians' Health Study with a sample of plasma before randomization. Each participant with myocardial infarction occurring during the first 5 years of follow-up was matched by smoking status and age with a randomly chosen control participant who had not developed coronary heart disease. RESULTS: Mean levels of fish oils (with 95% confidence interval [CI] for paired differences and p values) in case and control participants, expressed as percent of total fatty acids, were, for eicosapentaenoic acid, 0.26 versus 0.25 (95% CI -0.03 to 0.05, p = 0.70) in cholesterol esters and 0.56 versus 0.54 (95% CI -0.04 to 0.09, p = 0.44) in phospholipids, and for docosahexaenoic acid, 0.23 versus 0.24 (95% CI -0.07 to 0.04, p = 0.64) in cholesterol esters and 2.22 versus 2.14 (95% CI -0.10 to 0.27, p = 0.36) in phospholipids. Results adjusted for major cardiovascular risk factors showed a very similar lack of association between fish oil levels and the incidence of myocardial infarction. CONCLUSIONS: These results indicate no beneficial effect of increased fish oil consumption on the incidence of a first myocardial infarction. However, the effect of very high levels of fish oils could not be evaluated.

Adjuvants, Immunologic↗
PubMed1995

Discrimination in absorption or transport of beta-carotene isomers after oral supplementation with either all-trans- or 9-cis-beta-carotene.

Human subjects (n = 24) were supplemented with 100 mg beta-carotene/d for 6 d, either as synthetic all-trans-beta-carotene or a natural beta-carotene preparation derived from the alga Dunaliella salina, which consists of a 50:50 mixture of all-trans- and 6-cis-beta-carotene. This loading dose was followed by a 23-d maintenance dose consisting of alternate-day supplementation with 50 mg all-trans-beta-carotene or either 66 or 100 mg of the natural 50:50 isomeric mixture. The loading dose resulted in significant increases in plasma concentrations of both isomers, with the all-trans-beta-carotene-supplemented group showing a 7.2- and 5.0-fold increase in the all-trans and 9-cis concentrations in plasma, respectively. The group receiving the 50:50 mixture showed a 4.0- and 3.7-fold increase in the all-trans and 9-cis concentrations in plasma, respectively, without any apparent dose-dependency. However, even with the 50:50 mixture, the 9-cis concentrations were only a small fraction of the total plasma beta-carotene. Results after an additional 23-d period of alternate-day supplementation were not significantly different from those described above for the 6-d supplementation. Increases in low-density-lipoprotein concentrations of total beta-carotene correlated strongly with the increases seen in plasma concentrations. Lipid-soluble antioxidants vitamin E and ubiquinol were unaffected by beta-carotene supplementation. However, the amount of lycopene in the low-density lipoprotein decreased during this supplementation period. A strong discrimination between these two geometric isomers of beta-carotene was demonstrated, although the tissue site of discrimination was not determined.

Administration, Oral↗
PubMed1995

Epidemiologic evidence for vitamin E in prevention of cardiovascular disease.

Ecologic studies of vitamin E have shown that regions with relatively low dietary vitamin E tend to have higher rates of coronary heart disease (CHD), but it is difficult to adjust for other risk factors. Cross-sectional studies in individuals have yielded conflicting results, as have prospective studies based on stored blood samples. Two large prospective studies found that persons who had used vitamin E supplements for > or = 2 y had approximately 40% lower rates of CHD. Short durations and doses of < 100 IU/d had no significant effect. The effect of dietary vitamin E was modest and nonsignificant. Adjustment for a wide array of other coronary risk factors had little effect on the findings, which were specific for vitamin E and not other supplements. The only large, randomized trial found no material reduction in CHD risk for 50 IU vitamin E/d. The epidemiologic evidence suggests that high doses of vitamin E may reduce the risk of CHD.

Animals↗
PubMed1995

Prospective studies of homocysteine and cardiovascular disease.

The link between vascular disease and elevated homocysteine levels has been recognized for more than 30 years, and an association with moderately elevated levels has been suspected for 20 years. The initial investigations were case series, cross-sectional, and case-control studies. Those studies consistently suggest a strong positive relationship between moderate hyperhomocysteinemia and risk of vascular disease. However, a major limitation of these types of study design is that the possibility of elevated homocysteine levels being influenced by the disease or its treatment cannot be ruled out. In case-control studies there is always concern about the appropriateness of the control group. These issues pose much less of a problem in prospective designs. Prospective studies also offer the opportunity to study various manifestations of cardiovascular disease at the same time. However, prospective studies tend to be more expensive and time-consuming, perhaps explaining the smaller number of prospective studies and why the first was not published until 1992. The distinct limitations and advantages of prospective studies are also reviewed.

Aged↗
PubMed1995

Prospective study of physical activity and the risk of symptomatic diverticular disease in men.

The relationship between physical activity and risk of symptomatic diverticular disease has not been investigated directly. This association was examined in a prospective cohort of 47,678 American men, 40 to 75 years of age, and free of diagnosed diverticular disease, colon or rectal polyp, ulcerative colitis, and cancer before 1988. During four years of follow up, 382 newly diagnosed cases of symptomatic diverticular disease were documented. After adjustment for age, energy adjusted dietary fibre, and energy adjusted total fat, overall physical activity was inversely associated with the risk of symptomatic diverticular disease (for highest versus lowest extremes, relative risk (RR) = 0.63 (95% confidence interval (CI) 0.45, 0.88). Most of the inverse association was attributable to vigorous activity, for extreme categories RR = 0.60 (95% CI 0.41, 0.87). For activity that was not vigorous the RR was 0.93 (95% CI 0.67, 1.69). Several specific activities were inversely associated with the risk of diverticular disease, but jogging and running combined was the only individual activity that was statistically significant (p for trend = 0.03). For men in the lowest quintile for dietary fibre intake and total physical activity (compared with those in the opposite extreme), the RR was 2.56 (95% CI 1.36, 4.82). Physical activity, along with a high fibre diet, may be an important factor in the prevention of symptomatic diverticular disease.

Adult↗
PubMed1995

Childhood socioeconomic status and risk of cardiovascular disease in middle aged US women: a prospective study.

OBJECTIVE: To examine prospectively the relationship of childhood socioeconomic status and risk of cardiovascular disease in middle aged women. DESIGN: A prospective cohort of women with 14 years follow up data (1976-90). SUBJECTS: A total of 117,006 registered female nurses aged 30 to 55 years in 1976 and free of diagnosed coronary heart disease, stroke, and cancer at baseline. MAIN OUTCOME MEASURES: Incident fatal coronary heart disease, non-fatal myocardial infarction, and stroke (fatal and non-fatal). RESULTS: Low socioeconomic status in childhood was associated with a modestly increased risk of incident non-fatal myocardial infarction and total cardiovascular disease in adulthood. Compared with middle aged women from white collar childhood backgrounds, the age adjusted risk of total cardiovascular disease for women from blue collar backgrounds was 1.13 (95% CI 1.02, 1.24) and that of non-fatal myocardial infarction was 1.23 (95% CI 1.06, 1.42). No significant increase in risk was observed for stroke or fatal coronary heart disease. Adjustment for differences in family and personal past medical history, medication use, exercise, alcohol intake, diet, birth weight, being breastfed in infancy, and adult socioeconomic circumstance somewhat attenuated the increased risks observed for women from blue collar childhood socioeconomic backgrounds. In multivariate analysis, women whose fathers had been manual labourers had the highest relative risk of total coronary heart disease (RR = 1.53; 95% CI 1.09, 2.16) and non-fatal myocardial infarction (RR = 1.67; 95% CI 1.11, 2.53) when compared with women whose fathers had been employed in the professions. CONCLUSION: In this group lower childhood socioeconomic status was associated with a small but significant increase in the risk of total coronary heart disease as well as non-fatal myocardial infarction. For women from the most socioeconomically disadvantaged childhood backgrounds, the association is not explained by differences in a large number of cardiovascular risk factors, by differences in adult socioeconomic status, or by differences in indices of nutrition during gestation or infancy.

Adult↗