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Biomedical subjects

M J Stampfer

Publications and source records attributed to M J Stampfer.

At least 181 records · Page 10Linked to original sources
PubMed1998

Nephrolithiasis and risk of hypertension in women.

Cross-sectional and prospective studies of men suggest a positive association between nephrolithiasis and hypertension. However, this association remains controversial in women. We conducted a prospective study of the relation between nephrolithiasis and the risk for hypertension in the Nurses' Health Study, a cohort of 89,376 women aged 34 to 59 years in 1980. Information on the history of nephrolithiasis, physician-diagnosed hypertension, and other relevant exposures was obtained by biennial mailed questionnaire. A history of nephrolithiasis before 1980 was reported by 2,558 women (2.9%), and a history of hypertension was reported by 11,883 women (13.3%). Among women without hypertension before 1980, 12,540 women reported a new diagnosis of hypertension between 1980 and 1992, during 711,039 person-years of follow-up. Compared with those without a history of nephrolithiasis, the age-adjusted relative risk (RR) for incident hypertension in women with such a history was 1.36 (95% confidence interval [CI], 1.20 to 1.43). After further adjustment for body mass index (BMI) and the intake of calcium, sodium, potassium, magnesium, caffeine, and alcohol, the RR was only slightly attenuated (RR=1.24; 95% CI, 1.13 to 1.37). In contrast, the occurrence of incident nephrolithiasis during follow-up was similar in women with hypertension at baseline compared with women without (adjusted odds ratio [OR]=1.01; 95% CI, 0.85 to 1.20). These data are consistent with the results obtained in men and support the hypothesis that a history of nephrolithiasis is associated with an increased risk for subsequent hypertension. Dietary factors, such as the intake of calcium, sodium, and potassium, do not explain this association. Unidentified pathogenic mechanisms common to nephrolithiasis and hypertension may be responsible for the development of both disorders.

Adult↗
PubMed1998

A common mutation in the methylenetetrahydrofolate reductase gene and risk of coronary heart disease: results among U.S. men.

OBJECTIVES: We examined the risk of coronary heart disease associated with homozygosity for the C677T mutation in the methylenetetrahydrofolate reductase gene. BACKGROUND: The mutation increases plasma homocysteine levels by impairing its remethylation. Increased plasma homocysteine is an independent risk factor for cardiovascular disease. METHODS: This was a case-control study nested within the Health Professionals Follow-up Study. In 1986, 44,940 U.S. male health professionals, aged 40 to 75 years and free from diagnosed cardiovascular disease, provided detailed information on usual dietary intake, including intake of folate, vitamins B2, B6 and B12, and methionine. Between 1993 and 1995, blood samples were provided by approximately 40% of the participants. We compared data from 500 men with nonfatal coronary heart disease, diagnosed between 1986 and 1992, with data from 500 age-matched control subjects who were free of diagnosed cardiovascular disease at the time of the matched case subject's diagnosis. RESULTS: Frequencies of homozygosity (+/+) and heterozygosity (+/-) for the mutation were 12.2% and 41.8% in case subjects and 14.4% and 40.0% in control subjects. With subjects homozygous (-/-) or heterozygous (+/-) for the wildtype allele as a reference and matched by age, the odds ratio of coronary heart disease was 0.83 (95% confidence interval, 0.57 to 1.19) for +/+ subjects. The odds ratio was unchanged after adjustment for smoking and other risk factors for coronary heart disease. Odds ratios were also calculated within strata for intake of vitamins involved in homocysteine metabolism or methionine, the metabolic precursor of homocysteine. The +/+ genotype was not directly associated with risk of coronary heart disease among men with low (that is, within the lowest quartile) intake (<301 microg/d) of folate, the substrate for methylenetetrahydrofolate reductase; low intake (<1.8 mg/d) of vitamin B2, the cofactor for methylenetetrahydrofolate reductase; low intake (<8.0 microg/d) of vitamin B12, the cofactor for remethylation; low intake (<2.1 mg/d) of vitamin B6, the cofactor in the catabolic pathway of homocysteine; or high intake (>2.4 g/d) of methionine. CONCLUSIONS: In this generally well-nourished population, men with the +/+ genotype for the C677T mutation in the methylenetetrahydrofolate reductase gene have no increase in risk of coronary heart disease, even when intake of folate or other B vitamins is low.

Adult↗
PubMed1998

Nephrolithiasis and risk of hypertension.

A positive association between nephrolithiasis and blood pressure has been suggested in previous studies. However, controversy remains, due to methodological problems in some of the previous studies and absence of prospective data. We evaluated the relationship between nephrolithiasis and the risk of hypertension in a cohort of 51,529 men followed prospectively for 8 years. Information was obtained by biennial mailed questionnaires. At baseline in 1986, 4111 (8.0%) subjects reported a history of nephrolithiasis and 11,623 (22.6%) a diagnosis of hypertension. A positive association was found between the two disorders (age adjusted odds ratio [OR]: 1.31; 95% confidence interval [CI]: 1.30 to 1.32). Among men who reported both disorders, 79.5% reported that the occurrence of nephrolithiasis was prior to or concomitant with the diagnosis of hypertension. Among men without hypertension at baseline, the odds ratio for incident hypertension in men with a history of nephrolithiasis compared with those without was 1.29 (95% CI: 1.12 to 1.41; adjusted for age, body mass index, and intake of calcium, sodium, potassium, magnesium, and alcohol). The occurrence of incident nephrolithiasis during follow-up was similar in men with hypertension at baseline compared with that in men without (adjusted OR: 0.99, 95% CI: 0.82 to 1.21). These data support the hypothesis that prior occurrence of nephrolithiasis increases the risk of subsequent hypertension.

Adult↗
PubMed1998

Diabetes mellitus and risk of prostate cancer (United States).

A lower risk of prostate cancer among diabetics has been suggested by several but not all studies. However, the studies have not always accounted for time since diagnosis of diabetes mellitus, or have not examined confounding factors such as diet and diagnostic bias. We thus examined this relationship in the Health Professionals Follow-Up Study from 1986 and 1994, in which 1,369 new cases of non-stage A1 prostate cancer were documented in 47,781 men. A prior history of a diagnosis of diabetes (mostly adult-onset) was associated with a reduced risk of prostate cancer (multivariate relative risk [RR] = 0.75; 95 percent confidence interval [CI] = 0.59-0.95) controlling for age, body mass index (wt/ht2) at age 21, and, in 1986, race, vasectomy, and intakes of total energy, total fat, calcium, fructose, and lycopene. After excluding the first year of follow-up after the diagnosis of diabetes, the RR was 0.63 (CI = 0.54-0.89). Prostate cancer was not reduced in the first five years after diagnosis (RR = 1.24, CI = 0.87-1.77), but was lower in the next five years (RR = 0.66, CI = 0.39-1.10) and lowest after 10 years (RR = 0.54, CI = 0.37-0.78); P-value for trend across time = 0.004. Similar associations were noted for advanced cases. Detection bias was unlikely to account for our findings. The basis of this relationship is unclear but may reflect hormonal changes related to diabetes, perhaps low testosterone levels.

Adult↗
PubMed1998

Folate and coronary heart disease.

Low folate intake is an important determinant of elevated blood levels of homocysteine. Because elevated homocysteine has been shown to be a possible graded risk factor for CHD, sufficient folate intake may be important in the prevention of CHD. The magnitude of the association between folate and CHD is consistent with its effects on homocysteine.

5,10-Methylenetetrahydrofolate Reductase (FADH2)↗
PubMed1998

Body size and risk of kidney stones.

A variety of factors influence the formation of calcium oxalate kidney stones, including gender, diet, and urinary excretion of calcium, oxalate, and uric acid. Several of these factors may be related to body size. Because men on average have a larger body size and a threefold higher lifetime risk of stone formation than women, body size may be an important risk factor for calcium oxalate stone formation. The association between body size (height, weight, and body mass index) and the risk of kidney stone formation was studied in two large cohorts: the Nurses' Health Study (NHS; n = 89,376 women) and the Health Professionals Follow-up Study (HPFS; n = 51,529 men). Information on body size, kidney stone formation, and other exposures of interest was obtained by mailed questionnaires. A total of 1078 incident cases of kidney stones in NHS during 14 yr of follow-up and a total of 956 cases in HPFS during 8 yr of follow-up were confirmed. In both cohorts, the prevalence of a stone disease history and the incidence of stone disease were directly associated with weight and body mass index. However, the magnitude of the associations was consistently greater among women. Specifically, the age-adjusted prevalence odds ratio for women with body mass index > or = 32 kg/m2 compared with 21 to 22.9 kg/m2 was 1.76 (95% confidence interval, 1.50 to 2.07), but 1.38 (95% confidence interval, 1.16 to 1.65) for the same comparison in men. For incident stone formation, the multivariate relative risks for the similar comparisons were 1.89 (1.51 to 2.36) for women and 1.19 (0.83 to 1.70) in men. Height was inversely associated with the prevalence of stone disease but was not associated with incident stone formation. These results suggest that body size is associated with the risk of stone formation and that the magnitude of risk varies by gender. Additional studies are necessary to determine whether a reduction in body weight decreases the risk of stone formation, particularly in women.

Adult↗
PubMed1998

Tooth loss and hormone use in postmenopausal women.

Nearly 32% of US women aged 65 to 69 have no teeth. Because some tooth loss may reflect systemic osteoporosis, and postmenopausal hormone therapy protects against osteoporosis, the authors examined the risk of tooth loss in relation to hormone use in a prospective study of 42,171 postmenopausal women. Overall, the risk of tooth loss was 24% lower in women who were currently using hormones, although there was little effect for women who had stopped taking hormones. This decreased risk for current hormone users was observed regardless of the duration of use and was similar for a variety of hormone preparations and doses. Although few studies have examined the issue, this research suggests that hormone therapy may reduce tooth loss.

Age Factors↗
PubMed1998

Risk factors for breast cancer in women with a breast cancer family history.

Family history (FH) is an important indicator of a woman's future risk of developing breast cancer. Using data collected in a large population-based case-control study (6705 cases and 9341 controls), we examined the associations of breast cancer with known risk factors in women reporting a first-degree FH (mother or sister), with an emphasis on lifestyle determinants that may be altered to reduce risk. First-degree FH was reported by 18.4% (n = 1234) of cases and 11.3% (n = 1058) of controls; the overall relative risk (RR) for breast cancer associated with a positive history was 1.70 [95% confidence interval (CI), 1.55-1.87] and 2.34 (95% CI, 1.80-3.02) for breast cancer at age 45 years or younger. Among women with a FH, statistically significant inverse associations were observed for increasing parity (RR per birth = 0.90; P < 0.0001), intake of carotene-rich foods (RR for >2000 IU/day = 0.73; P = 0.02), and strenuous activity as a young adult (RR per episode/week = 0.93; P = 0.02). Recent alcohol consumption increased risk (RR per 13 g/week = 1.21; P = 0.02), as did weight gain during adult life in postmenopausal women (RR per 5 kg = 1.08; P = 0.001). Breast-feeding for any duration was associated with a lower RR in parous, premenopausal women (RR = 0.59; P = 0.04). Associations for most risk factors with breast cancer were similar among women with and without a FH of breast cancer; however, a stronger inverse association was observed for parity in women with a positive history (P for interaction = 0.04). Based on these data, women with a FH may reduce their excess risk of breast cancer through adjustments in lifestyle and reproductive choices. The risk associated with FH of breast cancer seems to be largely independent of other known risk factors.

Adolescent↗
PubMed1998

The androgen receptor gene GGN microsatellite and prostate cancer risk.

The androgen receptor (AR) gene contains a polymorphic GGN microsatellite in exon 1, which encodes polyglycine in the amino terminus of the AR. Previous work has shown that a polymorphic region of CAG repeats also in exon 1 is inversely related to the ability of the AR to transactivate other genes and to prostate cancer risk. We investigated whether AR gene GGN repeat length is related to prostate cancer in a nested study of 582 cases and 794 controls matched on age and smoking status in the Physicians' Health Study. DNA was prepared from archived blood. Using PCR, the region surrounding the GGN repeat was amplified. Fluorescence-labeled primers were used such that the fragment produced could be sized using polyacrylamide gels and Genescan software. We estimated odds ratios and 95% confidence intervals from logistic models controlling for the matching variables for the relation between GGN repeat length and total prostate cancer and by stage/grade and by age at diagnosis. Among controls, the most frequent GGN repeat lengths were 23 (53.5%) and 24 (34.0%), with a range of 10-29. There was no statistically significant difference in the mean GGN repeat length between cases (23.13) and controls (23.05). However, cases had a narrower spread of repeats lengths (parametric test, P = 0.03; nonparametric test, P = 0.07) than controls, with fewer extreme lengths in either direction. The risk of total prostate cancer was slightly increased for a GGN repeat length of 23 compared to all others (odds ratio, 1.20; 95% confidence interval 0.97-1.49); risk did not vary by tumor stage/grade. For every one repeat deviation in either direction from 23, the risk of prostate cancer decreased by 8% (P = 0.04). Although the AR gene GGN repeat probably plays only a modest role in prostate cancer, the observed relation of this repeat with prostate cancer risk supports the evaluation of the effect of GGN repeat length on AR transactivation.

Adult↗
PubMed1998

Vitamin D receptor polymorphisms, circulating vitamin D metabolites, and risk of prostate cancer in United States physicians.

Prostatic cells express vitamin D receptor (VDR), which mediates the functions of 1,25-dihydroxyvitamin D. Two recent case-control studies suggested strong inverse associations between two VDR polymorphisms, TaqI and poly(A), and risk of prostate cancer. These two and a third polymorphism, BsmI, are closely linked. In a case-control study nested in the Physicians' Health Study, a randomized double-blind trial of aspirin and beta-carotene among 22,071 United States male physicians, we examined the associations between BsmI and TaqI and prostate cancer risk and whether the associations varied according to age and vitamin D metabolite levels among 372 incident cases and 591 controls. Among controls, the BB genotype was significantly associated with higher 1,25-dihydroxyvitamin D (median = 36.2 pg/ml for the BB versus 33.9 pg/ml for the bb genotype; P = 0.02), suggesting an association of the VDR polymorphisms with VDR function. Overall, we observed no significant associations of these VDR polymorphisms with prostate cancer risk: relative risk (RR) = 0.86 [95% confidence interval (CI) = 0.57-1.29] for the BB genotype and RR = 0.92 (95% CI = 0.69-1.22) for the Bb genotype, compared with the bb genotype (results were similar for the TaqI polymorphism). Stratification by age (< or = 61 and > 61 years) and tumor aggressiveness showed no significant associations. However, in an analysis restricted to men with plasma 25-hydroxyvitamin D below the median, we observed a 57% reduction (RR = 0.43, 95% CI = 0.19-0.98) in risk for those with the BB versus the bb genotype; the risk reduction was particularly marked among older men (RR = 0.18, 95% CI = 0.05-0.68). We did not observe this inverse association among men with 25-hydroxyvitamin D levels above the median, nor did we observe it among younger men.

Adult↗
PubMed1998

Risk of uterine leiomyomata among premenopausal women in relation to body size and cigarette smoking.

To investigate whether factors influencing ovarian function affect risk of uterine leiomyomata, we examined prospectively the association of new diagnoses confirmed by ultrasound or hysterectomy with body mass index, weight change, height, and cigarette smoking among 94,095 premenopausal women with intact uteri, who were ages 25-42 years at the start of follow-up in 1989. We assessed body mass index and cigarette smoking from responses on the study questionnaire completed just before diagnosis. During 322,775 person-years, 2,967 new cases of uterine leiomyomata confirmed by ultrasound or hysterectomy were reported. Risk among all cases confirmed by ultrasound or hysterectomy increased with increasing adult body mass index. The multivariate relative risks (RR) and 95% confidence intervals (CI) according to body mass index categories of <20.0, 20.0-21.9, 22.0-23.9, 24.0-25.9, 26.0-27.9, 28.0-29.9, and > or =30.0 were 0.90 (95% CI = 0.79-1.03), 1.00 (referent), 1.08 (95% CI = 0.97-1.21), 1.16 (95% CI = 1.03-1.31), 1.21 (95% CI = 1.05-1.40), 1.36 (95% CI = 1.16-1.59), and 1.23 (95% CI = 1.09-1.39), respectively. The RRs for hysterectomy-confirmed cases generally were higher. Similarly, risk was positively associated with weight gain since age 18 years. Body mass index at age 18 years, height, and cigarette smoking were unrelated to risk of uterine leiomyomata. Elevated adult body mass index is associated with a modest increased risk of uterine leiomyomata among premenopausal women.

Adult↗
PubMed1998

Lipoprotein (a), lipids, aspirin, and risk of myocardial infarction in the Physician's Health Study.

BACKGROUND: Previously reported data from the Physicians' Health Study indicate that there is no association between lipoprotein (a) level and subsequent risk of myocardial infarction among members of a large cohort of middle-aged men followed up prospectively for an average of 60.2 months. OBJECTIVE: To investigate whether this null finding is related to the generally favorable lipid profile of the cohort or to randomized assignment of aspirin. METHODS: In a follow-up analysis of 296 confirmed cases of myocardial infarction and 296 controls, we evaluated the association between lipoprotein (a) level and cardiovascular risk for those with and without hyperlipidemia as well as for those randomly allocated aspirin treatment and placebo. RESULTS: For those with total cholesterol levels > or = 200 mg/dl, the age-adjusted smoking-adjusted relative risks of a first myocardial infarction associated with lipoprotein (a) levels above the 25th, 50th, 75th, 90th, and 95th percentiles of the control distribution were 0.9, 1.1, 1.6, 1.7 and 1.0 (all NS; P for trend 0.5). Among those with total cholesterol levels < 200 mg/dl, the adjusted relative risks of myocardial infarction associated with these cutoff points were 0.9, 0.7, 1.2, 0.7, and 1.4 (all NS; P for trend 0.7). Analyses limited to those with total cholesterol levels > or = 240 mg/dl or to men with higher than normal total cholesterol: high-density lipoprotein ratios revealed similar null findings. We observed no significant interaction between total cholesterol and lipoprotein (a) levels for these groups. For those randomly allocated aspirin, the age-adjusted and smoking-adjusted relative risks of myocardial infarction associated with lipoprotein (a) levels above the 25th, 50th, 75th, 90th, and 95th percentile cutoff points were 0.9, 0.9, 1.5, 1.5, and 1.0 (all NS; P trend 0.9). For those randomly allocated placebo, the age-adjusted and smoking-adjusted relative risks of myocardial infarction associated with lipoprotein (a) levels were 0.8, 0.9, 1.4, 1.5, and 1.3 (all NS; P trend 0.9). There was no significant interaction between aspirin and lipoprotein (a) level for any of these groups. Similar null findings were observed in analyses evaluating evidence for there being a trend across increasing quartiles of lipoprotein (a). CONCLUSION: These prospective data indicate that neither levels of lipids nor aspirin treatment modified the lack of overall effect of lipoprotein (a) on the risk of a first myocardial infarction in the Physicians' Health Study.

Aspirin↗
PubMed1998

Can behavioral risk factors explain the difference in body mass index between African-American and European-American women?

African-American women are heavier than European-American women; the reasons are unknown. The purpose of this study was to examine potentially modifiable reasons for the weight difference among 86,326 female nurses. The determinants of body mass index (BMI) were modelled using the method of linear regression. The findings included the following: mean BMI (kg/m2) was 9.0% (95% CI, 7.8-10.1%) higher among African American (27.3) than among European-American women (25.1) (P<0.0001). However, recalled BMI at age 18 was equal in the two groups (21.4, P=0.98). Multivariate determinants of BMI include age, age 18 BMI, alcohol and calorie intake, exercise, marital status, parity, race, recent intentional weight loss, smoking, and television watching. Even after controlling for these factors, African-American women still had an 8.6% (95% CI, 7.7-9.5%) higher BMI than European-American women. Correction for error in measurement of physical activity attenuated this difference to 6.4% (95% CI, 5.0-7.8%). In conclusion, in this single occupation group, African-American women had a significantly higher BMI than European-American women. Age and measured behavioral factors did not explain this difference. However, imprecision in the measurement of diet and activity may explain this difference in part. Better measurement may help quantify the differences that are as yet unexplained.

Adolescent↗
PubMed1997

Dietary fat intake and the risk of coronary heart disease in women.

BACKGROUND: The relation between dietary intake of specific types of fat, particularly trans unsaturated fat and the risk of coronary disease remains unclear. We therefore studied this relation in women enrolled in the Nurses' Health Study. METHODS: We prospectively studied 80,082 women who were 34 to 59 years of age and had no known coronary disease, stroke, cancer, hypercholesterolemia, or diabetes in 1980. Information on diet was obtained at base line and updated during follow-up by means of validated questionnaires. During 14 years of follow-up, we documented 939 cases of nonfatal myocardial infarction or death from coronary heart disease. Mutivariate analyses included age, smoking status, total energy intake, dietary cholesterol intake, percentages of energy obtained from protein and specific types of fat, and other risk factors. RESULTS: Each increase of 5 percent of energy intake from saturated fat, as compared with equivalent energy intake from carbohydrates, was associated with a 17 percent increase in the risk of coronary disease (relative risk, 1.17; 95 percent confidence interval, 0.97 to 1.41; P=0.10). As compared with equivalent energy from carbohydrates, the relative risk for a 2 percent increment in energy intake from trans unsaturated fat was 1.93 (95 percent confidence interval, 1.43 to 2.61; P<0.001); that for a 5 percent increment in energy from monounsaturated fat was 0.81 (95 percent confidence interval, 0.65 to 1.00; P=0.05); and that for a 5 percent increment in energy from polyunsaturated fat was 0.62 (95 percent confidence interval, 0.46 to 0.85; P= 0.003). Total fat intake was not signficantly related to the risk of coronary disease (for a 5 percent increase in energy from fat, the relative risk was 1.02; 95 percent confidence interval, 0.97 to 1.07; P=0.55). We estimated that the replacement of 5 percent of energy from saturated fat with energy from unsaturated fats would reduce risk by 42 percent (95 percent confidence interval, 23 to 56; P<0.001) and that the replacement of 2 percent of energy from trans fat with energy from unhydrogenated, unsaturated fats would reduce risk by 53 percent (95 percent confidence interval, 34 to 67; P<.001). CONCLUSIONS: Our findings suggest that replacing saturated and trans unsaturated fats with unhydrogenated monounsaturated and polyunsaturated fats is more effective in preventing coronary heart disease in women than reducing overall fat intake.

Adult↗
PubMed1997

Dual effects of weight and weight gain on breast cancer risk.

CONTEXT: Breast cancer is a major cause of mortality among women. It is important to identify modifiable risk factors for this disease. OBJECTIVE: To examine body mass index (BMI) at the age of 18 years and at midlife and adult weight change in relation to breast cancer incidence and mortality. DESIGN: Cohort study. SETTING: A cohort of 95256 US female nurses aged 30 to 55 years who were followed up for 16 years. MAIN OUTCOME MEASURE: Incident and fatal breast cancer. RESULTS: During 1203498 person-years, 2517 incident breast cancers (60% postmenopausal) were documented. Higher current BMI was associated with lower breast cancer incidence before menopause and was minimally associated with incidence after menopause. However, a stronger positive relationship was seen among postmenopausal women who never used hormone replacement (relative risk=1.59 for BMI >31 kg/m2 vs < or = 20 kg/m2; 95% confidence interval, 1.09-2.32; P for trend <.001). Higher BMI at the age of 18 years was associated with lower breast cancer incidence both before and after menopause. Weight gain after the age of 18 years was unrelated to breast cancer incidence before menopause, but was positively associated with incidence after menopause. This increased risk with weight gain was limited to women who never used postmenopausal hormones; among these women, the relative risk was 1.99 (95% confidence interval, 1.43-2.76) for weight gain of more than 20 kg vs unchanged weight (P for trend <.001). Current BMI and weight gain were even more strongly associated with fatal postmenopausal breast cancer. In this population, the percentage of postmenopausal breast cancer accounted for by weight gain alone was approximately 16% and by hormone replacement therapy alone was 5%, but when the interaction between these variables was considered, together they accounted for about one third of postmenopausal breast cancers. CONCLUSIONS: Avoiding adult weight gain may contribute importantly to the prevention of breast cancer after menopause, particularly among women who do not use postmenopausal hormones.

Adolescent↗
PubMed1997

A prospective study of pregravid determinants of gestational diabetes mellitus.

CONTEXT: Gestational diabetes mellitus (GDM) affects 3% to 5% of pregnancies. Knowledge of risk factors for GDM is needed to identify possible preventive strategies. OBJECTIVE: To assess whether recognized determinants of noninsulin-dependent diabetes mellitus also may be markers for increased risk of GDM. DESIGN: Prospective cohort study. SETTING: The Nurses' Health Study II, which involves female US nurses aged 25 to 42 years at entry. PARTICIPANTS: The analyses included 14613 women without previous GDM or other known diabetes who reported a singleton pregnancy between 1990 and 1994. Of these women, 722 (4.9%) reported a new diagnosis of GDM. MAIN OUTCOME MEASURE: Self-report of GDM, validated by medical record review in a subset. RESULTS: In multivariate analyses including age, pregravid body mass index (BMI), and other GDM risk factors, the risk for GDM increased significantly with increasing maternal age (P for trend, <.01) and family history of diabetes mellitus (relative risk, 1.68; 95% confidence interval [CI], 1.39-2.04). Relative risks for GDM were 2.13 (95% CI, 1.65-2.74) for pregravid BMI of 25 to 29.9 kg/m2 and 2.90 (95% CI, 2.15-3.91) for BMI of 30 kg/m2 or more (vs BMI of <20 kg/m2). Risk for GDM increased with greater weight gain in early adulthood, and it also increased among nonwhite women. Pregravid current smokers had a relative risk for GDM of 1.43 (95% CI, 1.14-1.80), and pregravid vigorous exercise was associated with a nonsignificant reduction in GDM risk. CONCLUSIONS: Advanced maternal age, family history of diabetes mellitus, nonwhite ethnicity, higher BMI, weight gain in early adulthood, and cigarette smoking predict increased GDM risk. These observations may facilitate the identification of women at particular risk for GDM and suggest potential strategies for reducing this risk even before a woman becomes pregnant, such as avoiding substantial weight gain and smoking.

Adult↗
PubMed1997

Birth weight and risk of cardiovascular disease in a cohort of women followed up since 1976.

OBJECTIVE: To examine the association between birth weight and non-fatal adult cardiovascular disease while controlling for potential confounders such as socioeconomic group and adult lifestyle. DESIGN: Retrospective self report of birth weight in an ongoing longitudinal cohort of nurses followed up by postal questionnaire every two years. SETTING: Nurses' health study, a cohort of 121700 women followed up since 1976. MAIN OUTCOME MEASURES: Non-fatal cardiovascular disease, including myocardial infarction, coronary revascularisation, and stroke. RESULTS: Among the 70297 women free of cardiovascular disease at baseline who reported birth weight in the 1992 questionnaire there were 1309 first cases of non-fatal cardiovascular disease. Increasing birth weight was associated with decreasing risk of non-fatal cardiovascular disease. There were 1216 first cases of non-fatal cardiovascular disease among women who were singletons and had been born full term; their relative risks adjusted for several cardiovascular risk factors were 1.49 (95% confidence interval 1.05 to 2.10) for birth weight < 2268 g (< 5 lb 0 oz); 1.25 (0.98 to 1.61) for birth weight 2268-2495 g (5 lb 0 oz to 5 lb 8 oz); 1.12 (0.98 to 1.27) for birth weight > 2495-3175 g (> 5 lb 8 oz to 7 lb 0 oz); 1.00 (referent) for birth weight > 3175-3856 g (> 7 lb 0 oz to 8 lb 8 oz); 0.96 (0.80 to 1.15) for birth weight > 3856-4536 g (> 8 lb 8 oz to 10 lb 0 oz); and 0.68 (0.46 to 1.00) for birth weight > 4536 g (> 10 lb 0 oz) (P value for trend = 0.0004). The inverse trend was apparent for both coronary heart disease and stroke. CONCLUSIONS: These data provide strong evidence of an association between birth weight and adult coronary heart disease and stroke.

Adult↗