Dietary Fats and All-cause and Breast Cancer-specific Mortality among Women with Breast Cancer: The Western New York Exposures and Breast Cancer Study.

BACKGROUND: Study results of prediagnostic dietary fat intake and breast cancer mortality have been inconclusive. While dietary fat subtypes [saturated (SFA), polyunsaturated (PUFA), and monounsaturated (MUFA) fatty acids] may have different biological effects, there is little evidence regarding the association of dietary fat and fat subtype intake with mortality after breast cancer diagnosis. METHODS: Women with incident, pathologically confirmed invasive breast cancer and complete dietary data (n = 793) were followed in a population-based study, the Western New York Exposures and Breast Cancer study. Usual intake before diagnosis of total fat and subtypes were estimated from a food frequency questionnaire completed at baseline. HRs and 95% confidence intervals (CI) for all-cause and breast cancer-specific mortality were estimated with Cox proportional hazards models. Interactions by menopausal status, estrogen receptor (ER) status, and tumor stage were examined. RESULTS: Median follow-up time was 18.75 years; 327 (41.2%) participants had died. Compared with lower intake, greater intake of total fat (HR, 1.05; 95% CI, 0.65-1.70), SFA (1.31; 0.82-2.10), MUFA (0.99; 0.61-1.60), and PUFA (0.99; 0.56-1.75) was not associated with breast cancer-specific mortality. There was also no association with all-cause mortality. Results did not vary by menopausal status, ER status, or tumor stage. CONCLUSIONS: Prediagnostic intake of dietary fat and fat subtypes was not associated with either all-cause or breast cancer mortality in a population-based cohort of breast cancer survivors. IMPACT: Understanding factors affecting survival among women diagnosed with breast cancer is critically important. Dietary fat intake prior to diagnosis may not impact that survival.

Associations of intakes of magnesium and calcium and survival among women with breast cancer: results from Western New York Exposures and Breast Cancer (WEB) Study.

Magnesium (Mg) and calcium (Ca) antagonizes each other in (re) absorption, cell cycle regulation, inflammation, and many other physiologic activities. However, few studies have investigated the association between magnesium and calcium intakes and breast cancer survival, and the interaction between calcium and magnesium intake. In a cohort of 1,170 women with primary, incident, and histologically confirmed breast cancer from Western New York State, we examined the relationship between intakes of these two minerals and survival. Cox regression models were used to estimate hazard ratios (HR) and 95% confidence intervals (95% CI). Mean follow-up time was 87.4 months after breast cancer diagnosis; there were 170 deaths identified. After adjustment for known prognostic factors, and intakes of energy, total vitamin D and total calcium, higher dietary intake of magnesium was inversely associated with risk of all-cause mortality (HR = 0.50, 95% CI, 0.28-0.90 for highest vs. lowest tertile; p trend = 0.02). Likewise, a marginal association was found for total Magnesium intake from foods and supplements combined (HR = 0.58, 95% CI, 0.31-1.08; p trend = 0.09). The inverse association of higher total magnesium intake with all-cause mortality was primarily presented among postmenopausal women and was stronger among women who had a high Ca:Mg intake ratio (>2.59). There were no clear associations for prognosis with intake of calcium. We found that magnesium intake alone may improve overall survival following breast cancer, and the association may be stronger among those with high Ca:Mg intake ratio.

NIH state-of-the-science conference statement: Preventing Alzheimer's disease and cognitive decline.

OBJECTIVE: To provide health care providers, patients, and the general public with a responsible assessment of currently available data on prevention of Alzheimer's disease and cognitive decline. PARTICIPANTS: A non-Department of Health and Human Services, nonadvocate 15-member panel representing the fields of preventive medicine, geriatrics, internal medicine, neurology, neurological surgery, psychiatry, mental health, human nutrition, pharmacology, genetic medicine, nursing, health economics, health services research, family caregiving, and a public representative. In addition, 20 experts from pertinent fields presented data to the panel and conference audience. EVIDENCE: Presentations by experts and a systematic review of the literature prepared by the Duke University Evidence-based Practice Center, through the Agency for Healthcare Research and Quality. Scientific evidence was given precedence over anecdotal experience. CONFERENCE PROCESS: The panel drafted its statement based on scientific evidence presented in open forum and on published scientific literature. The draft statement was presented on the final day of the conference and circulated to the audience for comment. The panel released a revised statement later that day at http://consensus.nih.gov. This statement is an independent report of the panel and is not a policy statement of the NIH or the Federal Government. CONCLUSIONS: Cognitive decline and Alzheimer's disease are major causes of morbidity and mortality worldwide and are substantially burdensome to the affected persons, their caregivers, and society in general. Extensive research over the past 20 years has provided important insights on the nature of Alzheimer's disease and cognitive decline and the magnitude of the problem. Nevertheless, there remain important and formidable challenges in conducting research on these diseases, particularly in the area of prevention. Currently, firm conclusions cannot be drawn about the association of any modifiable risk factor with cognitive decline or Alzheimer's disease. Highly reliable consensus-based diagnostic criteria for cognitive decline, mild cognitive impairment, and Alzheimer's disease are lacking, and available criteria have not been uniformly applied. Evidence is insufficient to support the use of pharmaceutical agents or dietary supplements to prevent cognitive decline or Alzheimer's disease. We recognize that a large amount of promising research is under way; these efforts need to be increased and added to by new understandings and innovations (as noted in our recommendations for future research). For example, ongoing studies including (but not limited to) studies on antihypertensive medications, omega-3 fatty acids, physical activity, and cognitive engagement may provide new insights into the prevention or delay of cognitive decline or Alzheimer's disease. This important research needs to be supplemented by further studies. Large-scale population-based studies and randomized controlled trials (RCTs) are critically needed to investigate strategies to maintain cognitive function in individuals at risk for decline, to identify factors that may delay the onset of Alzheimer's disease among persons at risk, and to identify factors that may slow the progression of Alzheimer's disease among persons in whom the condition is already diagnosed.

Effects of long-term selenium supplementation on the incidence of type 2 diabetes: a randomized trial.

BACKGROUND: Findings from animal models suggest that selenium supplementation improves glucose metabolism. OBJECTIVE: To examine the effect of long-term selenium supplementation on the incidence of type 2 diabetes. DESIGN: Secondary analysis of a randomized, double-blind, placebo-controlled trial. SETTING: Areas of low selenium consumption of the eastern United States. PATIENTS: 1202 persons seen in dermatology clinics who did not have type 2 diabetes at baseline. INTERVENTION: Oral administration of selenium, 200 microg/d, or placebo. MEASUREMENTS: Incidence of type 2 diabetes. RESULTS: During an average follow-up of 7.7 years (SD, 2.7), type 2 diabetes developed in 58 selenium recipients and 39 placebo recipients (incidence, 12.6 cases per 1000 person-years vs. 8.4 cases per 1000 person-years, respectively; hazard ratio, 1.55 [95% CI, 1.03 to 2.33]). The lack of benefit of selenium supplementation on the incidence of type 2 diabetes persisted in analyses stratified by age, sex, body mass index, and smoking status. An exposure-response gradient was found across tertiles of baseline plasma selenium level, with a statistically significantly increased risk for type 2 diabetes in the highest tertile of baseline plasma selenium level (hazard ratio, 2.70 [CI, 1.30 to 5.61]). LIMITATIONS: Diabetes was a secondary outcome in the parent trial. Diagnoses of diabetes were self-reported but were validated in most participants. The sample was mostly older and white. CONCLUSIONS: Selenium supplementation does not seem to prevent type 2 diabetes, and it may increase risk for the disease. Click here for related information on selenium.

Calcium/vitamin D supplementation and cardiovascular events.

BACKGROUND: Individuals with vascular or valvular calcification are at increased risk for coronary events, but the relationship between calcium consumption and cardiovascular events is uncertain. We evaluated the risk of coronary and cerebrovascular events in the Women's Health Initiative randomized trial of calcium plus vitamin D supplementation. METHODS AND RESULTS: We randomized 36,282 postmenopausal women 50 to 79 years of age at 40 clinical sites to calcium carbonate 500 mg with vitamin D 200 IU twice daily or to placebo. Cardiovascular disease was a prespecified secondary efficacy outcome. During 7 years of follow-up, myocardial infarction or coronary heart disease death was confirmed for 499 women assigned to calcium/vitamin D and 475 women assigned to placebo (hazard ratio, 1.04; 95% confidence interval, 0.92 to 1.18). Stroke was confirmed among 362 women assigned to calcium/vitamin D and 377 assigned to placebo (hazard ratio, 0.95; 95% confidence interval, 0.82 to 1.10). In subgroup analyses, women with higher total calcium intake (diet plus supplements) at baseline were not at higher risk for coronary events (P=0.91 for interaction) or stroke (P=0.14 for interaction) if assigned to active calcium/vitamin D. CONCLUSIONS: Calcium/vitamin D supplementation neither increased nor decreased coronary or cerebrovascular risk in generally healthy postmenopausal women over a 7-year use period.

Dietary lignan intakes and risk of breast cancer by tumor estrogen receptor status.

We examined the association of dietary lignan intake with estrogen receptor negative (ER-) and ER positive (ER+) breast cancer risk in a breast cancer case-control study. Among premenopausal women only, there was a reduced risk of ER- breast cancer for those in the highest compared to the lowest quartile of lignan intake suggesting that the observed negative association of lignans with breast cancer may be limited to ER- tumors.

Effects of selenium supplementation on cardiovascular disease incidence and mortality: secondary analyses in a randomized clinical trial.

Despite the documented antioxidant and chemopreventive properties of selenium, studies of selenium intake and supplementation and cardiovascular disease have yielded inconsistent findings. The authors examined the effect of selenium supplementation (200 microg daily) on cardiovascular disease incidence and mortality through the entire blinded phase of the Nutritional Prevention of Cancer Trial (1983-1996) among participants who were free of cardiovascular disease at baseline (randomized to selenium: n = 504; randomized to placebo: n = 500). Selenium supplementation was not significantly associated with any of the cardiovascular disease endpoints during 7.6 years of follow-up (all cardiovascular disease: hazard ratio (HR) = 1.03, 95% confidence interval (CI): 0.78, 1.37; myocardial infarction: HR = 0.94, 95% CI: 0.61, 1.44; stroke: HR = 1.02, 95% CI: 0.63, 1.65; all cardiovascular disease mortality: HR = 1.22, 95% CI: 0.76, 1.95). The lack of significant association with cardiovascular disease endpoints was also confirmed when analyses were further stratified by tertiles of baseline plasma selenium concentrations. These findings indicate no overall effect of selenium supplementation on the primary prevention of cardiovascular disease in this population.

The association between osteoporosis and alveolar crestal height in postmenopausal women.

BACKGROUND: Evidence supporting an association between osteoporosis and loss of alveolar crestal bone is limited. This study investigated that association in a large cohort of postmenopausal women. METHODS: A cohort of 1,341 postmenopausal women aged 53 to 85 were assessed for alveolar crestal height (ACH) and bone density. ACH was determined from oral radiographs with subjects dichotomized by disease severity. Bone density was assessed by dual energy x-ray absorptiometry, with severity determined by worst T score measured (normal >-1.00; low -1.00 to -2.00; moderate -2.01 to -2.49; osteoporotic <-2.5). RESULTS: Compared to subjects in the normal T-score group, the odds of worse ACH increased by 39%, 59%, and 230% for those in the low, moderate, and osteoporotic groups, respectively. Adjustment for weight, education, hormone use, calcium or vitamin D supplementation, and smoking did not appreciably change the findings. Further adjustment for age attenuated the association, with osteoporotic subjects having a 1.9-fold increase of being in the worst ACH group (95% confidence interval [CI] 1.19 to 3.05). After age stratification, in women younger than 70 there was a significant trend by decreasing T-score category (P <0.02). Osteoporotic subjects had worse ACH (odds ratio [OR] = 1.95; 95% CI 1.20 to 3.17). In women aged 70 and older, worse ACH was 2.5- to 4.6-fold increased for decreasing T-score category. After adjustment, the OR (95% CI) for the low, moderate, and osteoporotic groups were 2.66 (1.12 to 6.29), 2.31 (0.89 to 6.01), and 3.57 (1.42 to 8.97), respectively (P trend = 0.026). CONCLUSIONS: This study found a strong and consistent association between T score and ACH in postmenopausal women. Increasing age is an important modifier of that association.

The Association Between Osteoporosis and Alveolar Crestal Height in Postmenopausal Women.

BACKGROUND: Evidence supporting an association between osteoporosis and loss of alveolar crestal bone is limited. This study investigated that association in a large cohort of postmenopausal women. METHODS: A cohort of 1,341 postmenopausal women aged 53 to 85 were assessed for alveolar crestal height (ACH) and bone density. ACH was determined from oral radiographs with subjects dichotomized by disease severity. Bone density was assessed by dual energy x-ray absorptiometry, with severity determined by worst T score measured (normal >-1.00; low -1.00 to -2.00; moderate -2.01 to -2.49; osteoporotic <-2.5). RESULTS: Compared to subjects in the normal T-score group, the odds of worse ACH increased by 39%, 59%, and 230% for those in the low, moderate, and osteoporotic groups, respectively. Adjustment for weight, education, hormone use, calcium or vitamin D supplementation, and smoking did not appreciably change the findings. Further adjustment for age attenuated the association, with osteoporotic subjects having a 1.9-fold increase of being in the worst ACH group (95% confidence interval [CI] 1.19 to 3.05). After age stratification, in women younger than 70 there was a significant trend by decreasing T-score category (P <0.02). Osteoporotic subjects had worse ACH (odds ratio [OR] = 1.95; 95% CI 1.20 to 3.17). In women aged 70 and older, worse ACH was 2.5- to 4.6-fold increased for decreasing T-score category. After adjustment, the OR (95% CI) for the low, moderate, and osteoporotic groups were 2.66 (1.12 to 6.29), 2.31 (0.89 to 6.01), and 3.57 (1.42 to 8.97), respectively (P trend = 0.026). CONCLUSIONS: This study found a strong and consistent association between T score and ACH in postmenopausal women. Increasing age is an important modifier of that association.