AARP Diet Research Articles

Adiposity, Adult Weight Change, and Postmenopausal Breast Cancer Risk

Obesity is a risk factor for postmenopausal breast cancer, but the role of the timing and amount of adult weight change in breast cancer risk is unclear. We prospectively examined the relations of adiposity and adult weight change to breast cancer risk among 99 039 postmenopausal women in the National Institutes of Health-AARP Diet and Health Study. Anthropometry was assessed by self-report in 1996. Through 2000, 2111 incident breast cancer cases were ascertained. Current body mass index (BMI) (calculated as weight in kilograms divided by height in meters squared), BMI at ages 50 and 35 years, and waist-hip ratio were associated with increased breast cancer risk, particularly in women not using menopausal hormone therapy (MHT). Weight gained between age 18 years and the current age, between ages 18 and 35 years, between ages 35 and 50 years, and between age 50 years and the current age was consistently associated with increased breast cancer risk in MHT nonusers (relative risk [RR], 2.15; 95% confidence interval [CI], 1.35-3.42 for a >/=50-kg weight gain between age 18 years and the current age vs stable weight) but not in current MHT users. Risk associated with adult weight change was stronger in women with later vs earlier age at menarche (RR, 4.20; 95% CI, 2.05-8.64 for >/=15 years vs RR, 1.51; 95% CI, 1.11-2.06 for 11-12 years; P = .007 for interaction). In MHT nonusers, the associations with current BMI and adult weight change were stronger for advanced disease than for nonadvanced disease (P = .009 [current BMI] and .21 [weight gain] for heterogeneity) and were stronger for hormone receptor-positive than hormone receptor-negative tumors (P < .001 for heterogeneity). Weight gain throughout adulthood is associated with increased postmenopausal breast cancer risk in MHT nonusers.

Re: Multivitamin Use and Risk of Prostate Cancer in the National Institutes of Health AARP Diet and Health Study

Re: Multivitamin Use and Risk of Prostate Cancer in the National Institutes of Health AARP Diet and Health Study

Response: Re: Multivitamin Use and Risk of Prostate Cancer in the National Institutes of Health AARP Diet and Health Study

Response: Re: Multivitamin Use and Risk of Prostate Cancer in the National Institutes of Health AARP Diet and Health Study

Calcium, Dairy Foods, and Risk of Incident and Fatal Prostate Cancer: The NIH-AARP Diet and Health Study

Calcium and dairy foods in relation to prostate cancer were examined in the National Institutes of Health (NIH)-AARP (formerly known as the American Association of Retired Persons) Diet and Health Study (1995/1996-2001). Diet was assessed with a food frequency questionnaire at baseline. Multivariate relative risks and 95% confidence intervals were estimated by Cox regression. During up to 6 years of follow-up (n = 293,888), the authors identified 10,180 total prostate cancer cases (8,754 nonadvanced, 1,426 advanced, and 178 fatal cases). Total and supplemental calcium were unrelated to total and nonadvanced prostate cancer. However, a statistically nonsignificant positive association with total calcium was observed for advanced (> or = 2,000 vs. 500-<750 mg/day: relative risk (RR) = 1.25, 95% confidence interval (CI): 0.91, 1.71; p(trend) = 0.06) and fatal (> or = 1,000 vs. 500-<750 mg/day: RR = 1.39, 95% CI: 0.92, 2.09; p(trend) = 0.10) prostate cancer. Skim milk, but not other dairy foods, was associated with increased risk of advanced prostate cancer (> or = 2 vs. zero servings/day: RR = 1.23, 95% CI: 0.99, 1.54; p(trend) = 0.01). In contrast, calcium from nondairy foods was associated with lower risk of nonadvanced prostate cancer (> or = 600 vs. < 250 mg/day: RR = 0.82, 95% CI: 0.68, 0.99; p(trend) = 0.04). Although the authors cannot definitively rule out a weak association for aggressive prostate cancer, their findings do not provide strong support for the hypothesis that calcium and dairy foods increase prostate cancer risk.

Fruit and vegetable intake and esophageal cancer in a large prospective cohort study

Changing patterns of esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EAC) incidence worldwide suggest distinct etiologies. Although associations between fruit and vegetable intake and both ESCC and EAC have been found in multiple ecological and case-control studies, few prospective studies have investigated these associations. We prospectively examined these associations in 490,802 participants of the National Institutes of Health (NIH)-AARP Diet and Health Study using Cox models adjusted for age, alcohol intake, body mass index, cigarette smoking, education, physical activity and total energy intake. We present hazard ratios and 95% confidence intervals per serving per 1,000 calories. During 2,193,751 person years of follow-up, 103 participants were diagnosed with ESCC and 213 participants with EAC. We found a significant inverse association between total fruit and vegetable intake and ESCC risk (HR: 0.78, 95% CI: 0.67-0.91), but not EAC risk (0.98, 0.90-1.08). In models mutually adjusted for fruit and vegetable intake, the protective association with ESCC was stronger for fruits (0.73, 0.57-0.93) than for vegetables (0.84, 0.66-1.07). When we examined botanical subgroups, we observed significant protective associations for ESCC and intake of Rosacea (apples, peaches, nectarines, plums, pears and strawberries) and Rutaceae (citrus fruits). A significant inverse association between EAC and Chenopodiaceae (spinach) intake was observed. Results from our study suggest that the relation of fruit and vegetable intake and esophageal cancer risk may vary by histologic type.

Multivitamin Use and Risk of Prostate Cancer in the National Institutes of Health-AARP Diet and Health Study

Multivitamin supplements are used by millions of Americans because of their potential health benefits, but the relationship between multivitamin use and prostate cancer is unclear. We prospectively investigated the association between multivitamin use and risk of prostate cancer (localized, advanced, and fatal) in 295,344 men enrolled in the National Institutes of Health (NIH)-AARP Diet and Health Study who were cancer free at enrollment in 1995 and 1996. During 5 years of follow-up, 10,241 participants were diagnosed with incident prostate cancer, including 8765 localized and 1476 advanced cancers. In a separate mortality analysis with 6 years of follow-up, 179 cases of fatal prostate cancer were ascertained. Multivitamin use was assessed at baseline as part of a self-administered, mailed food-frequency questionnaire. Relative risks (RRs) and 95% confidence intervals (CIs) were calculated by use of Cox proportional hazards regression, adjusted for established or suspected prostate cancer risk factors. No association was observed between multivitamin use and risk of localized prostate cancer. However, we found an increased risk of advanced and fatal prostate cancers (RR = 1.32, 95% CI = 1.04 to 1.67 and RR = 1.98, 95% CI = 1.07 to 3.66, respectively) among men reporting excessive use of multivitamins (more than seven times per week) when compared with never users. The incidence rates per 100,000 person-years for advanced and fatal prostate cancers for those who took a multivitamin more than seven times per week were 143.8 and 18.9, respectively, compared with 113.4 and 11.4 in never users. The positive associations with excessive multivitamin use were strongest in men with a family history of prostate cancer or who took individual micronutrient supplements, including selenium, beta-carotene, or zinc. These results suggest that regular multivitamin use is not associated with the risk of early or localized prostate cancer. The possibility that men taking high levels of multivitamins along with other supplements have increased risk of advanced and fatal prostate cancers is of concern and merits further evaluation.

Dietary fiber and whole-grain consumption in relation to colorectal cancer in the NIH-AARP Diet and Health Study

Background: Whether the intake of dietary fiber can protect against colorectal cancer is a long-standing question of considerable public health import, but the epidemiologic evidence has been inconsistent.Objective: The objective was to investigate the relation between dietary fiber and whole-grain food intakes and invasive colorectal cancer in the prospective National Institutes of Health–AARP Diet and Health Study.Design: The analytic cohort consisted of 291 988 men and 197 623 women aged 50–71 y. Diet was assessed with a self-administered food-frequency questionnaire at baseline in 1995–1996; 2974 incident colorectal cancer cases were identified during 5 y of follow-up. The Cox proportional hazards model was used to estimate the relative risks (RRs) and 95% CIs.Results: Total dietary fiber intake was not associated with colorectal cancer. The multivariate RR for the highest compared with the lowest intake quintile (RRQ5-Q1) was 0.99 (95% CI: 0.85, 1.15; P for trend = 0.96). In analyses of fiber from different food sources, only fiber from grains was associated with a lower risk of colorectal cancer (multivariate RRQ5-Q1: 0.86; 95% CI: 0.76, 0.98; P for trend = 0.01). Whole-grain intake was inversely associated with colorectal cancer risk: the multivariate RRQ5-Q1 was 0.79 (95% CI: 0.70, 0.89) for the whole cohort (P for trend < 0.001). The association with whole grain was stronger for rectal than for colon cancer.Conclusions: In this large prospective cohort study, total dietary fiber intake was not associated with colorectal cancer risk, whereas whole-grain consumption was associated with a modest reduced risk.

Body Mass and Colorectal Cancer Risk in the NIH-AARP Cohort

In most studies, body mass index (BMI) has been associated with increased risk of colorectal or colon cancer in men, but the relation is weaker and less consistent for women, possibly because of interactions with age or hormone replacement therapy. The authors examined the relation between BMI and colorectal cancer incidence in a large, prospective US cohort of 307,708 men and 209,436 women from the NIH-AARP Diet and Health Study. During follow-up of the cohort from 1995 to 2000, 2,314 cases of colorectal cancer were observed in men and 1,029 in women. BMI was related to increased risk of incident colon cancer, but not rectal cancer, for both men and women. For men, relative risks of colon cancer for a BMI of 18.5-<23, 23-<25, 25-<27.5, 27.5-<30, 30-<32.5, 32.5-<35, 35-<40, and > or = 40 kg/m(2) were 1.0 (referent), 1.11, 1.22, 1.44, 1.53, 1.57, 1.71, and 2.39, respectively (95% confidence interval: 1.59, 3.58; p-trend < 0.0005). Corresponding relative risks for women were 1.0, 1.20, 1.29, 1.31, 1.28, 1.13, 1.46, and 1.49 (95% confidence interval: 0.98, 2.25; p-trend = 0.02). BMI was related to colon cancer risk for younger (aged 50-66 years) but not older (aged 67-71 years) women. The association was not modified by hormone replacement therapy in women or physical activity in men or women.

Menopausal Hormone Therapy and Ovarian Cancer Risk in the National Institutes of Health–AARP Diet and Health Study Cohort

Menopausal Hormone Therapy and Ovarian Cancer Risk in the National Institutes of Health–AARP Diet and Health Study Cohort

Menopausal Hormone Therapy and Ovarian Cancer Risk in the National Institutes of Health–AARP Diet and Health Study Cohort

Recent studies offer conflicting data on risks of ovarian cancer in users of menopausal hormone therapy. Some findings of increased risks associated with unopposed estrogen use are based on older studies of women with intact uteri, and small sample size and incomplete exposure information have limited the data on estrogen plus progestin associations. The National Institutes of Health-AARP Diet and Health Study Cohort included 97,638 women aged 50-71 years at baseline who completed two questionnaires (1995-1996 and 1996-1997). We identified 214 incident ovarian cancers among these women through the year 2000 using data from state cancer registries and mortality indexes. We estimated relative risks (RRs) of ovarian cancer for detailed hormone therapy exposures using multivariable proportional hazards regression models. All statistical tests were two-sided. Use of unopposed estrogen for fewer than 10 years was not associated with ovarian cancer. Compared with use of no hormone therapy, use of unopposed estrogen for 10 or more years was statistically significantly associated with ovarian cancer among all women (RR = 1.89, 95% confidence interval [CI] = 1.22 to 2.95; P = .004; 56 versus 72 ovarian cancers per 100,000 person-years, respectively) and, albeit not statistically significantly, among women with hysterectomy (n = 19,359, RR = 1.70, 95% CI = 0.87 to 3.31; P = .06). Among the 73,483 women with intact uteri, 51,698 had used no hormone therapy or only estrogen plus progestin. Compared with no hormone therapy use, 5 or more years of use of sequential (progestin for < 15 days per cycle; RR = 3.09, 95% CI = 1.68 to 5.68; P < .001; 49 versus 108 per 100,000 person-years) or continuous (progestin for > or = 15 days per cycle; RR = 1.82, 95% CI = 1.03 to 3.23; P = .02; 49 versus 66 per 100,000 person-years) estrogen plus progestin regimens were statistically significantly associated with ovarian cancer. Long durations of use of unopposed estrogen and of estrogen plus progestin, especially sequential regimens, are associated with increased ovarian cancer risk. These data expand the range of possible risks associated with menopausal hormone therapy.

A nomogram for the transfer factor for carbon monoxide in the lungs.

<h3>Background:</h3> Limited evidence suggests that adiposity and lack of physical activity may increase the risk of chronic obstructive pulmonary disease (COPD). We investigated the relation of body size and physical activity with incidence of COPD. <h3>Methods:</h3> We obtained data on anthropometric measurements and physical activity from 113 279 participants in the National Institutes of Health–AARP Diet and Health Study who reported no diagnosis of COPD at baseline (1995–1996). We estimated associations between these measurements and subsequent diagnosis of COPD between 1996 and 2006, with extensive adjustment for smoking and other potentially confounding variables. <h3>Results:</h3> Participants reported 3648 new COPD diagnoses during follow-up. The incidence of COPD was higher in both severely obese (body mass index [BMI]D≥ 35) and underweight (BMID&lt; 18.5) participants, but after adjustment for waist circumference, only underweight remained positively associated with COPD (relative risk [RR]D1.56, 95% confidence interval [CI]D1.15–2.11). Larger waist circumference (highest v. normal categories, adjusted RRD1.72, 95% CID1.37–2.16) and higher waist–hip ratio (highest v. normal categories, adjusted RRD1.46, 95% CID1.23–1.73) were also positively associated with COPD. In contrast, hip circumference (highest v. normal categories, adjusted RR 0.78, 95% CI 0.62–0.98) and physical activity (≥ 5 v. 0 times/wk, adjusted RRD0.71, 95% CID0.63–0.79) were inversely associated with COPD. <h3>Interpretation:</h3> Obesity, in particular abdominal adiposity, was associated with an increased risk of COPD, and increased hip circumference and physical activity were associated with a decreased risk of COPD. These findings suggest that following guidelines for a healthy body weight, body shape and physical activity decrease the risk of COPD.