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Biomedical subjects

Walter C Willett

Publications and source records attributed to Walter C Willett.

At least 19 recordsLinked to original sources
PubMed2007

A prospective cohort study of red wine consumption and risk of prostate cancer.

In light of recent, strong inverse findings between lifetime red wine consumption and prostate cancer among younger men, we revisited our previous cohort analysis to more thoroughly investigate red wine consumption and prostate cancer in the Health Professionals Follow-up Study (HPFS). In 1986, HPFS participants reported their average consumption of red wine, white wine, beer and liquor during the past year, and their change in alcohol consumption over the prior 10 years. Prostate cancer diagnoses were ascertained on each biennial questionnaire and confirmed by medical record review. Between 1986 and 2002, 3,348 cases of prostate cancer were diagnosed among 45,433 eligible participants. Using men who did not consume red wine as the reference, no linear trend was observed between red wine consumption and prostate cancer in the full analytic cohort (p-trend = 0.57). Among men with unchanged alcohol consumption in the prior 10 years, and those additionally <65 years of age, slightly lower risks were observed for men who consumed 4 glasses/week, resulting in a lack of linear trend. These findings suggest that red wine does not contribute appreciably to the etiology of prostate cancer.

Adult↗
PubMed2007

Smoking, hypertension, alcohol consumption, and risk of abdominal aortic aneurysm in men.

Despite the known protective association between moderate alcohol consumption and ischemic heart disease, little is known about the effects of alcohol consumption on abdominal aortic aneurysms (AAA). The authors analyzed prospective, biennially updated data for a cohort of 39,352 US men from 1986 to 2002. The association of incident AAA diagnosis with alcohol consumption in grams per day was assessed at baseline and by using alcohol consumption data updated every 4 years, controlling for previously reported cardiovascular risk factors. During 576,374 person-years of follow-up, 376 newly diagnosed cases of AAA were demonstrated. After adjustment for other risk factors for AAA, including smoking, hypertension, and body mass index, alcohol consumption at baseline was independently associated with AAA diagnosis (p for trend = 0.03), with a maximum hazard ratio of 1.21 (95% confidence interval: 0.78, 1.87) for > or =30.0 g (approximately > or =2 standard drinks) of daily alcohol consumption. This association was stronger when the updated alcohol consumption data were assessed rather than simply baseline exposure (p for trend = 0.02); the hazard ratio for the highest level of intake (> or =30.0 g/day) was 1.65 (95% confidence interval: 1.03, 2.64). Small numbers limited analyses by beverage type, but liquor demonstrated the strongest positive association with AAA.

Adult↗
PubMed2007

Plasma adiponectin concentrations and risk of incident breast cancer.

INTRODUCTION: Previous retrospective case-control studies suggest that adiponectin, an obesity-related hormone, is inversely associated with breast cancer risk, particularly in postmenopausal women; however, no prospective studies exist. Therefore, we conducted a prospective case-control study nested within the Nurses' Health Study (NHS) and NHSII cohorts examining the association between plasma adiponectin concentrations and breast cancer risk. MATERIALS AND METHODS: Blood samples were collected from 1989 through 1990 (NHS) and 1996 through 1999 (NHSII); adiponectin was measured by RIA. The analysis included 1477 breast cancer cases diagnosed after blood collection and before June 2000 (NHS) or June 2003 (NHSII) who had one or two controls (n=2196) matched on age, menopausal status, postmenopausal hormone (PMH) use, fasting, and time of day and month of blood collection. We adjusted for body mass index at age 18, weight change from age 18 to blood draw, family history of breast cancer, history of benign breast disease, duration of PMH use, ages at menarche and first birth, and parity. RESULTS: Although we observed no association between adiponectin and breast cancer risk overall, there was a nearly significant interaction by menopausal status (P=0.08), with a relative risk, top vs. bottom quartile of 0.73 (95% confidence interval, 0.55-0.98; P trend=0.08) among postmenopausal women and 1.30 (95% confidence interval, 0.80-2.10; P trend=0.09) for premenopausal women. Among postmenopausal women, adiponectin appeared more strongly inversely associated in women who never used PMH (P heterogeneity=0.05) and women with low circulating estradiol levels (P heterogeneity=0.05). DISCUSSION: Our results suggest that adiponectin may be inversely associated with postmenopausal breast cancer risk, particularly in a low-estrogen environment.

Adiponectin↗
PubMed2007

Alcohol consumption and breast cancer risk in the Women's Health Study.

The authors assessed the association between moderate alcohol consumption and breast cancer risk in the Women's Health Study (United States, 1992-2004). During an average of 10 years of follow-up, 1,484 cases of total breast cancer (1,190 invasive and 294 in situ) were documented among 38,454 women who, at baseline, were free of cancer and cardiovascular disease and provided detailed dietary information, including alcohol consumption, for the preceding 12 months. Higher alcohol consumption was associated with a modest increase in breast cancer risk; the multivariable relative risks for > or =30 g/day of alcohol vs. none were 1.32 (95% confidence interval (CI): 0.96, 1.82) for total breast cancer and 1.43 (95% CI: 1.02, 2.02) for invasive breast cancer. An increased risk was limited to estrogen receptor (ER)- and progesterone receptor (PR)-positive tumors; the multivariable relative risks for an increment of 10 g/day of alcohol were 1.11 (95% CI: 1.03, 1.20) for ER+PR+ tumors (804 cases), 1.00 (95% CI: 0.81, 1.24) for ER+PR- tumors (125 cases), and 0.99 (95% CI: 0.82, 1.20) for ER-PR- tumors (167 cases). The association also seemed strongest among those taking postmenopausal hormones currently, but the test for interaction was not significant. The findings from this prospective study suggest that moderate alcohol consumption increases breast cancer risk.

Alcohol Drinking↗
PubMed2007

Diet and breast cancer.

Clarification of the role of diet in breast cancer pathogenesis is important in order to identify modifiable risk factors on which to focus prevention efforts. Excess weight and weight gain in adult life are related to higher risk of postmenopausal breast cancer, and weight loss after menopause is associated with substantially reduced risk. Even moderate alcohol consumption contributes considerably to excess breast cancer risk, which can likely be mitigated with adequate folate intake. Diet during early life may play a substantial role in later cancer risk, but data are limited. In addition, physical activity and the prevention of weight gain can improve survival after a breast cancer diagnosis.

Body Mass Index↗
PubMed2007

Dietary fatty acid intakes and the risk of ovulatory infertility.

BACKGROUND: Pharmacologic activation of the peroxisome proliferator-activated receptor gamma (PPAR-gamma) improves ovulatory function in women with polycystic ovary syndrome, and specific dietary fatty acids can affect PPAR-gamma activity. OBJECTIVE: The objective of the study was to assess whether the intakes of total fat, cholesterol, and major types of fatty acids affect the risk of ovulatory infertility. DESIGN: We conducted a prospective cohort study of 18 555 married, premenopausal women without a history of infertility who attempted a pregnancy or became pregnant between 1991 and 1999. Diet was assessed twice during follow-up by using a food-frequency questionnaire. RESULTS: During follow-up, 438 incidents of ovulatory infertility were reported. In logistic regression analyses, intakes of total fat, cholesterol, and most types of fatty acids were not related to ovulatory infertility. Each 2% increase in the intake of energy from trans unsaturated fats, as opposed to that from carbohydrates, was associated with a 73% greater risk of ovulatory infertility after adjustment for known and suspected risk factors for this condition [relative risk (RR) = 1.73; 95% CI: 1.09, 2.73]. Obtaining 2% of energy intake from trans fats rather than from n-6 polyunsaturated fats was associated with a similar increase in the risk of ovulatory infertility (RR = 1.79; 95% CI: 1.11, 2.89). In addition, obtaining 2% of energy from trans fats rather than from monounsaturated fats was associated with a more than doubled risk of ovulatory infertility (RR = 2.31; 95% CI: 1.09, 4.87). CONCLUSION: trans Unsaturated fats may increase the risk of ovulatory infertility when consumed instead of carbohydrates or unsaturated fats commonly found in nonhydrogenated vegetable oils.

Adult↗
PubMed2006

Statin drugs and risk of advanced prostate cancer.

BACKGROUND: Statins are commonly used cholesterol-lowering drugs that have proapoptotic and antimetastatic activities that could affect cancer risk or progression. Results from previous epidemiologic studies of the association between statin use and cancer have been inconsistent. We investigated the association of statin use with total and advanced prostate cancer, the latter being the most important endpoint to prevent. METHODS: We analyzed data from an ongoing prospective cohort study of 34,989 US male health professionals who were cancer free in 1990 and were followed to 2002. Participants reported their use of cholesterol-lowering drugs on biennial questionnaires. Prostate cancer diagnosis was confirmed by medical record review. Multivariable-adjusted relative risks (RRs) were estimated from Cox proportional hazards regression models. Statistical tests were two-sided. RESULTS: During 376,939 person-years of follow-up, we ascertained 2579 prostate cancer cases, 316 of which were advanced (regionally invasive, metastatic, or fatal). The age-standardized incidence rates of advanced prostate cancer were 38 and 89 per 100,000 person-years in current statin users and in past or never users, respectively. The multivariable-adjusted relative risk of advanced disease was 0.51 (95% confidence interval [CI] = 0.30 to 0.86) and of metastatic or fatal disease was 0.39 (95% CI = 0.19 to 0.77) for current statin use compared with no current use. The associations remained after adjusting for prostate-specific antigen screening history (advanced disease: RR = 0.57, 95% CI = 0.30 to 1.11; metastatic or fatal disease: RR = 0.35, 95% CI = 0.14 to 0.92). Risk of advanced disease was lower with longer statin use (P(trend) = .003); compared with never use, the relative risk for less than 5 years of use was 0.60 (95% CI = 0.35 to 1.03) and for 5 or more years of use was 0.26 (95% CI = 0.08 to 0.83). We found no association between statin use and risk of total prostate cancer (RR = 0.96, 95% CI = 0.85 to 1.09). CONCLUSIONS: In this cohort of male health professionals, use of statin drugs was not associated with risk of prostate cancer overall but was associated with a reduced risk of advanced (especially metastatic or fatal) prostate cancer.

Aged↗
PubMed2006

Dietary carotenoids and risk of colorectal cancer in a pooled analysis of 11 cohort studies.

Dietary carotenoids have been hypothesized to protect against epithelial cancers. The authors analyzed the associations between intakes of specific carotenoids (alpha-carotene, beta-carotene, beta-cryptoxanthin, lutein + zeaxanthin, and lycopene) and risk of colorectal cancer using the primary data from 11 cohort studies carried out in North America and Europe. Carotenoid intakes were estimated from food frequency questionnaires administered at baseline in each study. During 6-20 years of follow-up between 1980 and 2003, 7,885 incident cases of colorectal cancer were diagnosed among 702,647 participants. The authors calculated study-specific multivariate relative risks and then combined them using a random-effects model. In general, intakes of specific carotenoids were not associated with colorectal cancer risk. The pooled multivariate relative risks of colorectal cancer comparing the highest quintile of intake with the lowest ranged from 0.92 for lutein + zeaxanthin to 1.04 for lycopene; only for lutein + zeaxanthin intake was the result borderline statistically significant (95% confidence interval: 0.84, 1.00). The associations observed were generally similar across studies, for both sexes, and for colon cancer and rectal cancer. These pooled data did not suggest that carotenoids play an important role in the etiology of colorectal cancer.

Carotenoids↗
PubMed2006

Cancer incidence and mortality and vitamin D in black and white male health professionals.

Blacks have been documented to have low vitamin D levels. We thus examined whether total cancer incidence and mortality rates differ between Blacks and Whites in a population of male health professionals, and particularly for digestive system cancers (oral, esophagus, stomach, pancreas, and colorectum), which have been most consistently linked to poor vitamin D status. Second, we examined whether Blacks might be more susceptible to these cancers if they concurrently had other risk factors for hypovitaminosis D. In the Health Professionals Follow-up Study, from 1986 to 2002, 99 of 481 Black men and 7,019 of 43,468 White men were diagnosed with cancer. Adjusting for multiple dietary, lifestyle, and medical risk factors, using Cox modeling, Black men were at higher risk of total cancer incidence [relative risk (RR), 1.32; 95% confidence interval (95% CI), 1.08-1.61; P = 0.007] and total cancer mortality (RR, 1.89; 95% CI, 1.40-2.56; P < 0.0001) and especially digestive system cancer mortality (RR, 2.24; 95% CI, 1.35-3.70). Compared with Whites with relatively few risk factors for hypovitaminosis D, Blacks also with few risk factors for hypovitaminosis D were not at appreciably higher risk of total cancer incidence (RR, 0.95; 95% CI, 0.60-1.51) or mortality (RR, 1.55; 95% CI, 0.91-2.62), but Black men with additional risk factors for poorer vitamin D status had a much higher cancer incidence (RR, 1.57; 95% CI, 1.16-2.11) and mortality risk (RR, 2.27; 95% CI, 1.57-3.28). This pattern was even more pronounced for digestive system cancer. Our results suggest that the high frequency of hypovitaminosis D in Blacks may be an important, and easily modifiable, contributor to their higher risk of cancer incidence and mortality.

Adult↗
PubMed2006

Weight cycling and risk of gallstone disease in men.

BACKGROUND: The long-term effect of repeated intentional weight loss and weight regain on the risk of gallstone disease in men is not clear. METHODS: Participants in the Health Professionals Follow-up Study provided information on intentional weight loss during the previous 4 years in 1992. Weight cyclers were men who had intentional weight loss and weight regain. Men free of gallstone disease at baseline were followed from 1992 to 2002. On biennial questionnaires the participants reported newly diagnosed gallstone disease. RESULTS: During 264,760 person-years of follow-up we ascertained 1222 cases of symptomatic gallstones. We examined the effect of weight cycling on the risk of gallstone disease. The multivariate relative risk of weight cyclers, compared with weight maintainers, after adjusting for potential confounding variables, including body mass index, was 1.11 (95% confidence interval [CI], 0.94-1.31) in light cyclers, 1.18 (95% CI, 0.97-1.43) in moderate cyclers, and 1.42 (95% CI, 1.11-1.81) in severe cyclers. We further examined the effect of number of cycling episodes. Among weight cyclers, the relative risk associated with having more than 1 weight cycle, compared with weight maintainers, was 1.10 (95% CI, 0.88-1.37) in light cyclers, 1.28 (95% CI, 1.03-1.59) in moderate cyclers, and 1.51 (95% CI, 1.13-2.02) in severe cyclers. CONCLUSIONS: Our findings suggest that weight cycling, independent of body mass index, may increase the risk of gallstone disease in men. Larger weight fluctuation and more weight cycles are associated with greater risk.

Adult↗
PubMed2006

Longitudinal study on the role of body size in premenopausal breast cancer.

BACKGROUND: A high body mass index (BMI) has been related to a reduced risk of breast cancer in premenopausal women. The mechanisms underlying this association have not been elucidated. METHODS: We explored whether factors affecting ovulation may explain the inverse association between BMI (calculated as weight in kilograms divided by the square of height in meters) and breast cancer in 113,130 premenopausal participants in the Nurses' Health Study II. During 1,225,520 person-years of prospective follow-up between 1989 and 2003, 1398 incident cases of invasive breast cancer were diagnosed. Weight, height, ovulatory infertility, menstrual cycle patterns, and a multitude of covariates were assessed throughout follow-up. Cox proportional hazards regression was used to compute hazard ratios and 95% confidence intervals (CIs). RESULTS: We observed a significant linear inverse trend between current BMI and breast cancer incidence (P<.001) that was not explained by menstrual cycle characteristics or infertility due to an ovulatory disorder (covariate-adjusted hazard ratio for breast cancer in women with a BMI > or =30 vs 20.0-22.4, 0.81; 95% CI, 0.68-0.96). We found BMI at age 18 years to be the strongest predictor of breast cancer incidence (covariate-adjusted hazard ratio for breast cancer in women with a BMI at age 18 years > or =27.5 vs 20.0-22.4, 0.57; 95% CI, 0.41-0.81). CONCLUSIONS: Body size during the early phases of adult life seems to be particularly important in the development of premenopausal breast cancer. Factors other than anovulation are likely to mediate the protection conferred by a high BMI.

Adult↗
PubMed2006

Parental age at delivery and incidence of breast cancer: a prospective cohort study.

BACKGROUND: Studies on parental age at delivery in relation to breast cancer risk have had mixed results, but prospective data are limited. No study has explored the associations with subtypes of breast cancer defined by hormonal receptor status. METHODS: 109,773 women in the Nurses' Health Study were followed from 1976 to 2002. We used Cox proportional hazards model to examine the association between parental age at delivery and daughters' risk of breast cancer. RESULTS: 6,827 incident cases of invasive breast cancer occurred in this cohort during 2,581,098 person-years. Adjusting for other early life exposures and family history of breast cancer, the hazard ratio for breast cancer in women born to mothers aged 21-25, 26-30, 31-35, and > or =36 years was, respectively, 1.08 (95% CI: 0.99-1.18), 1.12 (95% CI: 1.03-1.23), 1.17 (95% CI: 1.06-1.29), and 1.12 (95% CI: 1.01-1.25), compared to women born to mothers aged < or =20 years (P for trend = 0.008). Similarly, advanced paternal age was associated with increased incidence of breast cancer (P for trend = 0.03), but the association disappeared when conditioning on maternal age. The positive association between maternal age and incidence of breast cancer was stronger for estrogen receptor-positive and progesterone receptor-positive tumors (P for trend = 0.003) than for tumors with both receptors negative (P for trend = 0.78), and was more consistent among postmenopausal women, women without a family history and women who were first born. CONCLUSION: Our findings support a modest positive association between maternal age and daughter's risk of breast cancer, possibly mediated by hormonal factors.

Adult↗
PubMed2006

Alcohol consumption and ovarian cancer risk in a population-based case-control study.

Alcohol consumption has been investigated as a possible risk factor for ovarian cancer in several epidemiological studies, with inconsistent findings. Recent studies have suggested that the association between alcohol consumption and ovarian cancer may vary according to histologic subtype of ovarian cancer and type of alcohol consumed (e.g., wine, beer, or liquor). We examined these associations in a population-based case-control study comprised of 762 incident cases of epithelial ovarian cancer and 6,271 population controls from Massachusetts and Wisconsin aged 40-79 years. Women reported their usual alcohol consumption as young adults (20-30 years of age) and in the recent past. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated. There was no significant association of ovarian cancer with increasing alcohol consumption either during ages 20-30 years (p trend 0.42) or in the recent past (p trend 0.83). Regular drinking of beer (1 drink/day or more) during ages 20-30 (OR 1.55, 95% CI 1.07-2.26), though not liquor (OR 1.35, 95% CI 0.86-2.11) or wine (OR 0.99, 95% CI 0.49-2.00), was associated with a statistically significant increase in risk of invasive tumors, whereas no significant relationships were observed for recent drinking, regardless of alcohol type. The elevated risk for early adult regular drinking was confined to serous invasive tumors (OR 1.52, 95% CI 1.01-2.30), though results for other subtypes were based on sparse data and results were imprecise. In this study, neither total alcohol consumption as a young adult nor recently was associated with an increase in the risk of ovarian cancer.

Adenocarcinoma, Mucinous↗
PubMed2006

Red meat intake and risk of breast cancer among premenopausal women.

BACKGROUND: The association between red meat intake and breast cancer is unclear, but most studies have assessed diet in midlife or later. Although breast tumors differ clinically and biologically by hormone receptor status, few epidemiologic studies of diet have made this distinction. METHODS: Red meat intake and breast cancer risk were assessed among premenopausal women aged 26 to 46 years in the Nurses' Health Study II. Red meat intake was assessed with a food frequency questionnaire administered in 1991, 1995, and 1999, with respondents followed up through 2003. Breast cancers were self-reported and confirmed by review of pathologic reports. RESULTS: During 12 years of follow-up of 90,659 premenopausal women, we documented 1021 cases of invasive breast carcinoma. Greater red meat intake was strongly related to elevated risk of breast cancers that were estrogen and progesterone receptor positive (ER+/PR+; n = 512) but not to those that were estrogen and progesterone receptor negative (ER-/PR-; n = 167). Compared with those eating 3 or fewer servings per week of red meat, the multivariate relative risks (95% confidence intervals) for ER+/PR+ breast cancer with increasing servings of red meat intake were 1.14 (0.90-1.45) for more than 3 to 5 or fewer servings per week, 1.42 (1.06-1.90) for more than 5 per week to 1 or fewer servings per day, 1.20 (0.89-1.63) for more than 1 to 1.5 or fewer servings per day, and 1.97 (1.35-2.88) for more than 1.5 servings per day (test for trend, P = .001). The corresponding relative risks for ER-/PR- breast cancer were 1.34 (0.89-2.00), 1.21 (0.73-2.00), 0.69 (0.39-1.23), and 0.89 (0.43-1.84) (test for trend, P = .28). Higher intakes of several individual red meat items were also strongly related to elevated risk of ER+/PR+ breast cancer. CONCLUSION: Higher red meat intake may be a risk factor for ER+/PR+ breast cancer among premenopausal women.

Adult↗
PubMed2006

Low-carbohydrate-diet score and the risk of coronary heart disease in women.

BACKGROUND: Low-carbohydrate diets have been advocated for weight loss and to prevent obesity, but the long-term safety of these diets has not been determined. METHODS: We evaluated data on 82,802 women in the Nurses' Health Study who had completed a validated food-frequency questionnaire. Data from the questionnaire were used to calculate a low-carbohydrate-diet score, which was based on the percentage of energy as carbohydrate, fat, and protein (a higher score reflects a higher intake of fat and protein and a lower intake of carbohydrate). The association between the low-carbohydrate-diet score and the risk of coronary heart disease was examined. RESULTS: During 20 years of follow-up, we documented 1994 new cases of coronary heart disease. After multivariate adjustment, the relative risk of coronary heart disease comparing highest and lowest deciles of the low-carbohydrate-diet score was 0.94 (95% confidence interval [CI], 0.76 to 1.18; P for trend=0.19). The relative risk comparing highest and lowest deciles of a low-carbohydrate-diet score on the basis of the percentage of energy from carbohydrate, animal protein, and animal fat was 0.94 (95% CI, 0.74 to 1.19; P for trend=0.52), whereas the relative risk on the basis of the percentage of energy from intake of carbohydrates, vegetable protein, and vegetable fat was 0.70 (95% CI, 0.56 to 0.88; P for trend=0.002). A higher glycemic load was strongly associated with an increased risk of coronary heart disease (relative risk comparing highest and lowest deciles, 1.90; 95% CI, 1.15 to 3.15; P for trend=0.003). CONCLUSIONS: Our findings suggest that diets lower in carbohydrate and higher in protein and fat are not associated with increased risk of coronary heart disease in women. When vegetable sources of fat and protein are chosen, these diets may moderately reduce the risk of coronary heart disease.

Adult↗
PubMed2006

Intake of the major carotenoids and the risk of epithelial ovarian cancer in a pooled analysis of 10 cohort studies.

Carotenoids, found in fruits and vegetables, have the potential to protect against cancer because of their properties, including their functions as precursors to vitamin A and as antioxidants. We examined the associations between intakes of alpha-carotene, beta-carotene, beta-cryptoxanthin, lutein/zeaxanthin and lycopene and the risk of invasive epithelial ovarian cancer. The primary data from 10 prospective cohort studies in North America and Europe were analyzed and then pooled. Carotenoid intakes were estimated from a validated food frequency questionnaire administered at baseline in each study. Study-specific relative risks (RR) were estimated using the Cox proportional hazards model and then combined using a random-effects model. Among 521,911 women, 2,012 cases of ovarian cancer occurred during a follow-up of 7-22 years across studies. The major carotenoids were not significantly associated with the risk of ovarian cancer. The pooled multivariate RRs (95% confidence intervals) were 1.00 (0.95-1.05) for a 600 microg/day increase in alpha-carotene intake, 0.96 (0.93-1.03) for a 2,500 microg/day increase in beta-carotene intake, 0.99 (0.97-1.02) for a 100 microg/day increase in beta-cryptoxanthin intake, 0.98 (0.94-1.03) for a 2,500 microg/day increase in lutein/zeaxanthin intake and 1.01 (0.97-1.05) for a 4,000 microg/day increase in lycopene intake. These associations did not appreciably differ by study (p-values, tests for between-studies heterogeneity >0.17). Also, the observed associations did not vary substantially by subgroups of the population or by histological type of ovarian cancer. These results suggest that consumption of the major carotenoids during adulthood does not play a major role in the incidence of ovarian cancer.

Breast Neoplasms↗