In this study involving long-term follow-up of more than 400,000 adults, coffee consumption was inversely associated with total mortality and mortality due to heart disease, respiratory disease, ...stroke, injuries and accidents, diabetes, and infections, but not cancer.
Coffee is one of the most widely consumed beverages, both in the United States and worldwide. Since coffee contains caffeine, a stimulant, coffee drinking is not generally considered to be part of a healthy lifestyle. However, coffee is a rich source of antioxidants
1
and other bioactive compounds, and studies have shown inverse associations between coffee consumption and serum biomarkers of inflammation
2
and insulin resistance.
3
,
4
Considerable attention has been focused on the possibility that coffee may increase the risk of heart disease,
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,
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particularly since drinking coffee has been associated with increased low-density lipoprotein cholesterol levels
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and short-term increases in . . .
Increased attention in dietary research and guidance has been focused on dietary patterns, rather than on single nutrients or food groups, because dietary components are consumed in combination and ...correlated with one another. However, the collective body of research on the topic has been hampered by the lack of consistency in methods used. We examined the relationships between 4 indices—the Healthy Eating Index–2010 (HEI-2010), the Alternative Healthy Eating Index–2010 (AHEI-2010), the alternate Mediterranean Diet (aMED), and Dietary Approaches to Stop Hypertension (DASH)—and all-cause, cardiovascular disease (CVD), and cancer mortality in the NIH-AARP Diet and Health Study (n = 492,823). Data from a 124-item food-frequency questionnaire were used to calculate scores; adjusted HRs and 95% CIs were estimated. We documented 86,419 deaths, including 23,502 CVD- and 29,415 cancer-specific deaths, during 15 y of follow-up. Higher index scores were associated with a 12–28% decreased risk of all-cause, CVD, and cancer mortality. Specifically, comparing the highest with the lowest quintile scores, adjusted HRs for all-cause mortality for men were as follows: HEI-2010 HR: 0.78 (95% CI: 0.76, 0.80), AHEI-2010 HR: 0.76 (95% CI: 0.74, 0.78), aMED HR: 0.77 (95% CI: 0.75, 0.79), and DASH HR: 0.83 (95% CI: 0.80, 0.85); for women, these were HEI-2010 HR: 0.77 (95% CI: 0.74, 0.80), AHEI-2010 HR: 0.76 (95% CI: 0.74, 0.79), aMED HR: 0.76 (95% CI: 0.73, 0.79), and DASH HR: 0.78 (95% CI: 0.75, 0.81). Similarly, high adherence on each index was protective for CVD and cancer mortality examined separately. These findings indicate that multiple scores reflect core tenets of a healthy diet that may lower the risk of mortality outcomes, including federal guidance as operationalized in the HEI-2010, Harvard’s Healthy Eating Plate as captured in the AHEI-2010, a Mediterranean diet as adapted in an Americanized aMED, and the DASH Eating Plan as included in the DASH score.
Abstract
Background
Ambient air pollution is a modifiable risk factor for cardiovascular disease, yet uncertainty remains about the size of risks at lower levels of fine particulate matter (PM2.5) ...exposure which now occur in the USA and elsewhere.
Methods
We investigated the relationship of ambient PM2.5 exposure with cause-specific cardiovascular disease mortality in 565 477 men and women, aged 50 to 71 years, from the National Institutes of Health-AARP Diet and Health Study. During 7.5 x 106 person-years of follow up, 41 286 cardiovascular disease deaths, including 23 328 ischaemic heart disease (IHD) and 5894 stroke deaths, were ascertained using the National Death Index. PM2.5 was estimated using a hybrid land use regression (LUR) geostatistical model. Multivariate Cox regression models were used to estimate relative risks (RRs) and 95% confidence intervals (CI).
Results
Each increase of 10 μg/m3 PM2.5 (overall range, 2.9–28.0 μg/m3) was associated, in fully adjusted models, with a 16% increase in mortality from ischaemic heart disease hazard ratio (HR) 1.16; 95% CI 1.09-1.22 and a 14% increase in mortality from stroke (HR 1.14; CI 1.02-1.27). Compared with PM2.5 exposure <8 μg/m3 (referent), risks for CVD were increased in relation to PM2.5 exposures in the range of 8–12 μg/m3 (CVD: HR 1.04; 95% CI 1.00-1.08), in the range 12–20 μg/m3 (CVD: HR 1.08; 95% CI 1.03-1.13) and in the range 20+ μg/m3 (CVD: HR 1.19; 95% CI 1.10-1.28). Results were robust to alternative approaches to PM2.5 exposure assessment and statistical analysis.
Conclusions
Long-term exposure to fine particulate air pollution is associated with ischaemic heart disease and stroke mortality, with excess risks occurring in the range of and below the present US long-term standard for ambient exposure to PM2.5 (12 µg/m3), indicating the need for continued improvements in air pollution abatement for CVD prevention.
ABSTRACT
Background
A limited number of studies have evaluated self-reported dietary intakes against objective recovery biomarkers.
Objective
The aim was to compare dietary intakes of multiple ...Automated Self-Administered 24-h recalls (ASA24s), 4-d food records (4DFRs), and food-frequency questionnaires (FFQs) against recovery biomarkers and to estimate the prevalence of under- and overreporting.
Design
Over 12 mo, 530 men and 545 women, aged 50–74 y, were asked to complete 6 ASA24s (2011 version), 2 unweighed 4DFRs, 2 FFQs, two 24-h urine collections (biomarkers for protein, potassium, and sodium intakes), and 1 administration of doubly labeled water (biomarker for energy intake). Absolute and density-based energy-adjusted nutrient intakes were calculated. The prevalence of under- and overreporting of self-report against biomarkers was estimated.
Results
Ninety-two percent of men and 87% of women completed ≥3 ASA24s (mean ASA24s completed: 5.4 and 5.1 for men and women, respectively). Absolute intakes of energy, protein, potassium, and sodium assessed by all self-reported instruments were systematically lower than those from recovery biomarkers, with underreporting greater for energy than for other nutrients. On average, compared with the energy biomarker, intake was underestimated by 15–17% on ASA24s, 18–21% on 4DFRs, and 29–34% on FFQs. Underreporting was more prevalent on FFQs than on ASA24s and 4DFRs and among obese individuals. Mean protein and sodium densities on ASA24s, 4DFRs, and FFQs were similar to biomarker values, but potassium density on FFQs was 26–40% higher, leading to a substantial increase in the prevalence of overreporting compared with absolute potassium intake.
Conclusions
Although misreporting is present in all self-report dietary assessment tools, multiple ASA24s and a 4DFR provided the best estimates of absolute dietary intakes for these few nutrients and outperformed FFQs. Energy adjustment improved estimates from FFQs for protein and sodium but not for potassium. The ASA24, which now can be used to collect both recalls and records, is a feasible means to collect dietary data for nutrition research.
Outdoor fine particulate matter (≤ 2.5 μm; PM2.5) has been identified as a global health threat, but the number of large U.S. prospective cohort studies with individual participant data remains ...limited, especially at lower recent exposures.
We aimed to test the relationship between long-term exposure PM2.5 and death risk from all nonaccidental causes, cardiovascular (CVD), and respiratory diseases in 517,041 men and women enrolled in the National Institutes of Health-AARP cohort.
Individual participant data were linked with residence PM2.5 exposure estimates across the continental United States for a 2000-2009 follow-up period when matching census tract-level PM2.5 exposure data were available. Participants enrolled ranged from 50 to 71 years of age, residing in six U.S. states and two cities. Cox proportional hazard models yielded hazard ratio (HR) estimates per 10 μg/m3 of PM2.5 exposure.
PM2.5 exposure was significantly associated with total mortality (HR = 1.03; 95% CI: 1.00, 1.05) and CVD mortality (HR = 1.10; 95% CI: 1.05, 1.15), but the association with respiratory mortality was not statistically significant (HR = 1.05; 95% CI: 0.98, 1.13). A significant association was found with respiratory mortality only among never smokers (HR = 1.27; 95% CI: 1.03, 1.56). Associations with 10-μg/m3 PM2.5 exposures in yearly participant residential annual mean, or in metropolitan area-wide mean, were consistent with baseline exposure model results. Associations with PM2.5 were similar when adjusted for ozone exposures. Analyses of California residents alone also yielded statistically significant PM2.5 mortality HRs for total and CVD mortality.
Long-term exposure to PM2.5 air pollution was associated with an increased risk of total and CVD mortality, providing an independent test of the PM2.5-mortality relationship in a new large U.S. prospective cohort experiencing lower post-2000 PM2.5 exposure levels.
Thurston GD, Ahn J, Cromar KR, Shao Y, Reynolds HR, Jerrett M, Lim CC, Shanley R, Park Y, Hayes RB. 2016. Ambient particulate matter air pollution exposure and mortality in the NIH-AARP Diet and Health cohort. Environ Health Perspect 124:484-490; http://dx.doi.org/10.1289/ehp.1509676.
Celotno besedilo
Dostopno za:
CEKLJ, DOBA, IZUM, KILJ, NUK, OILJ, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK, VSZLJ
OBJECTIVE: To investigate the relationship between diabetes and future risk of Parkinson's disease (PD) among older U.S. adults. RESEARCH DESIGN AND METHODS: A prospective study of self-reported ...diabetes in 1995 and 1996 in relation to PD diagnosed after 1995 among 288,662 participants of the National Institutes of Health-AARP Diet and Health Study. Multivariate odds ratio (OR) and 95% CI were derived from logistic regression models. RESULTS: A total of 1,565 participants with PD diagnosed after 1995 were included in the analysis. After adjustment for potential confounders, PD risk was ~40% higher (OR = 1.41 95% CI 1.20-1.66) among diabetic patients than among participants without diabetes. Further analysis showed that the risk elevation was largely limited to individuals who had diabetes for more than 10 years at the time of baseline survey (1.75 1.36-2.25). The association with diabetes was seen for both participants with PD diagnosed between 1995 and 1999 and participants with PD diagnosed after 2000. In addition, similar results were obtained after excluding participants with stroke, heart disease, cancers, or poor or fair health status and in subgroup analyses by age, sex, smoking status, and coffee consumption. CONCLUSIONS: This large study showed that diabetes was associated with a higher future risk of PD and the nature of this association warrants further investigation.
Higher physical activity levels have been associated with a lower risk of developing various cancers and all‐cancer mortality, but the impact of pre‐diagnosis physical activity on cancer‐specific ...death has not been fully characterized. In the prospective National Institutes of Health‐AARP Diet and Health Study with 293,511 men and women, we studied prediagnosis moderate to vigorous intensity leisure time physical activity (MVPA) in the past 10 years and cancer‐specific mortality. Over a median 12.1 years, we observed 15,001 cancer deaths. Using Cox proportional hazards regression, we estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for MVPA with cancer mortality overall and by 20 specific cancer sites, adjusting for relevant risk factors. Compared to participants reporting never/rare MVPA, those reporting >7 hr/week MVPA had a lower risk of total cancer mortality (HR = 0.89, 95% CI 0.84–0.94; p‐trend <0.001). When analyzed by cancer site‐specific deaths, comparing those reporting >7 hr/week of MVPA to those reporting never/rare MVPA, we observed a lower risk of death from colon (HR = 0.70; 95% CI 0.57–0.85; p‐trend <0.001), liver (0.71; 0.52–0.98; p‐trend = 0.012) and lung cancer (0.84; 0.77–0.92; p‐trend <0.001) and a significant p‐trend for non‐Hodgkins lymphoma (0.80; 0.62–1.04; p‐trend = 0.017). An unexpected increased mortality p‐trend with increasing MVPA was observed for death from kidney cancer (1.42; 0.98–2.03; p‐trend = 0.016). Our findings suggest that higher prediagnosis leisure time physical activity is associated with lower risk of overall cancer mortality and mortality from multiple cancer sites. Future studies should confirm observed associations and further explore timing of physical activity and underlying biological mechanisms.
What's new?
Despite evidence that physical activity reduces risk of multiple chronic diseases, including cancer, as much as one‐third of the U.S. population is inactive. In this study, the authors explored associations between pre‐diagnosis physical activity and cancer mortality. They found that higher pre‐diagnosis leisure‐time physical activity is associated with a decreased risk of overall cancer mortality, and particularly mortality from cancers of the colon, liver, lung, and non‐Hodgkin's lymphoma.
Background
Advanced glycation end products (AGEs) are reactive metabolites produced as a by‐product of sugar metabolism and are consumed through the diet in high‐fat and highly processed foods. They ...are associated with chronic inflammatory diseases, and evidence suggests that they play a role in carcinogenesis. The authors evaluated the association of dietary AGE intake and the risk of postmenopausal invasive breast cancer.
Methods
This was a prospective cohort study of 183,548 postmenopausal women in the National Institutes of Health‐AARP Diet and Health Study. The main outcome was incident invasive breast cancer. AGE intake was estimated from food‐frequency questionnaires. Incident breast cancer cases were identified through state cancer registries. Cox proportional hazards regression models were used to estimate hazard ratios (HRs) and 95% confidence intervals for developing breast cancer according to AGE intake quintiles. Multivariable regression models were adjusted for breast cancer risk factors.
Results
The mean follow‐up was 12.8 years, and 9851 breast cancers (1978 advanced stage) were identified. The median AGE daily intake was 5932 kilo units per 100 kilocalories (KU/1000 kcal). Women with higher intake tended to have lower education levels, higher body mass index, less physical activity, were current smokers, and had higher fat and meat intake. The highest quintile of AGE intake (compared with the lowest) was associated with an increased risk of breast cancer (HR, 1.09; 95% CI, 1.02‐1.16; P = .03) after adjusting for breast cancer risk factors and particularly was associated with 37% of advanced‐stage tumors (HR, 1.37; 95% CI, 1.09‐1.74; P < .02) after adjusting for risk factors and fat and meat intake.
Conclusions
Dietary AGEs may play a role in the development of postmenopausal breast cancer.
Advanced glycation end products (AGEs) are reactive metabolites produced as a by‐product of sugar metabolism and consumed through diet in high‐fat and highly processed foods. AGEs play a role in carcinogenesis, and the consumption of dietary AGEs may increase the risk of breast cancer.
Purpose
Although a growing body of evidence supports an early-life contribution to prostate cancer (PCa) development, few studies have investigated early-life diet, and only three have examined ...early-life dairy product intake, a promising candidate risk factor because of its known/suspected influence on insulin-like growth factor levels and height.
Methods
We used recalled dietary data from 162,816 participants in the NIH-AARP Diet and Health Study to investigate associations for milk, cheese, ice cream, total dairy, and calcium intake at ages 12–13 years with incident total (
n
= 17,729), advanced (
n
= 2,348), and fatal PCa (
n
= 827) over 14 years of follow-up. We calculated relative risks (RRs) and 95% confidence intervals (CIs) by Cox proportional hazards regression.
Results
We observed suggestive positive trends for milk, dairy, and calcium intake with total and/or advanced PCa (
p
-trends = 0.016–0.148). These trends attenuated after adjustment for additional components of adolescent diet, particularly red meat and vegetables/potatoes. In contrast, suggestive inverse trends were observed for cheese and ice cream intake with total and/or advanced PCa (
p
-trends = 0.043–0.153), and for milk, dairy, and calcium intake with fatal PCa (
p
-trend = 0.045–0.117).
Conclusion
Although these findings provide some support for a role of adolescent diet in increasing PCa risk, particularly for correlates of milk intake or overall dietary patterns, our protective findings for cheese and ice cream intake with PCa risk and mortality, and for all dairy products with PCa mortality, suggest alternative explanations, such as the influence of early-life socioeconomic status, and increased PCa screening, earlier detection, and better PCa care.
Observational studies report inconsistent associations of fat and fatty acids with prostate cancer.
We investigated associations between dietary fats and fatty acids and risk of prostate cancer in ...the NIH-American Association of Retired Persons (AARP) Diet and Health Study. Diet was assessed at baseline with self-administered food-frequency questionnaires. Cases were determined by linkage with state cancer registries. HR and 95% confidence intervals (CI) were estimated with Cox proportional hazards models.
Among 288,268 men with average follow-up of nine years, 23,281 prostate cancer cases (18,934 nonadvanced and 2,930 advanced including 725 fatal cases) were identified. Total fat and mono- and polyunsaturated fat intakes were not associated with incidence of prostate cancer. Saturated fat intake was related to increased risk of advanced prostate cancer (HRQuintile 5 vs. Qunitile 1 (Q1 vs. Q5), 1.21; 95% CI, 1.00-1.46; Ptrend = 0.03) and fatal prostate cancer (HRQ5 vs. Q1, 1.47; 95% CI, 1.01-2.15; Ptrend = 0.04). α-Linolenic acid (ALA) intake was related to increased risk of advanced prostate cancer (HRQ5 vs. Q1, 1.17; 95% CI, 1.04-1.31; Ptrend = 0.01). Eicosapentanoic acid (EPA) intake was related to decreased risk of fatal prostate cancer (HRQ5 vs. Q1, 0.82; 95% CI, 0.64-1.04; Ptrend = 0.02).
Our study suggests that the associations of fat and fatty acids differ by prostate cancer severity. Saturated fat, ALA, and EPA intakes were related to the risk of advanced or fatal prostate cancer but not to nonadvanced prostate cancer.
Identifying factors associated with advanced prostate cancer could reduce morbidity and mortality.
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