Background: In several short-term studies, coffee consumption has been associated with impairment of endothelial function. Objective: The objective was to assess the relation between long-term caffeinated and decaffeinated filtered coffee consumption and markers of inflammation and endothelial dysfunction. Design: We conducted a cross-sectional study of 730 healthy women and 663 women with type 2 diabetes from the Nurses’ Health Study I cohort, who were aged 43–70 y and free of cardiovascular disease and cancer at the time blood was drawn (1989–1990). Dietary intake was assessed with a validated food-frequency questionnaire in 1986 and 1990. Results: About 77% of the healthy women consumed ≥1 cup (237 mL) caffeinated coffee/mo and 75% consumed ≥1 cup decaffeinated coffee/mo; the corresponding intakes for women with type 2 diabetes were 74% and 63%, respectively. In healthy women, no appreciable differences in plasma concentrations of the markers were found across categories of caffeinated coffee intake. In women with type 2 diabetes, higher caffeinated coffee consumption was associated with lower plasma concentrations of E-selectin (adjusted percentage change per 1 cup/d increment = −3.2%; P = 0.05) and C-reactive protein (adjusted percentage change = −10.2%; P < 0.001). Higher decaffeinated coffee consumption was associated with lower plasma concentrations of E-selectin (adjusted percentage change = −2.5%; P = 0.08) and C-reactive protein (adjusted percentage change = −7.9%; P = 0.02) only in healthy women. The results were similar when we also adjusted the models for other dietary factors and blood lipids and when we excluded participants with hypertension or hypercholesterolemia. Conclusions: These results indicate that neither caffeinated nor decaffeinated filtered coffee has a detrimental effect on endothelial function. In contrast, the results suggest that coffee consumption is inversely associated with markers of inflammation and endothelial dysfunction.

Background: The role of the Mediterranean diet among individuals with previous cardiovascular disease (CVD) is uncertain.Objective: The aim of this s

Coffee consumption has been linked to various beneficial and detrimental health effects, but data on its relation with mortality are sparse. To assess the association between coffee consumption and mortality from cardiovascular disease (CVD), cancer, and all causes during 18 years of follow-up in men and 24 years of follow-up in women. Sex-specific Cox proportional hazard models were used to investigate the association between coffee consumption and incidence of all-cause and disease-specific mortality in a prospective cohort study. Health Professionals Follow-up Study and Nurses' Health Study. 41 736 men and 86 214 women with no history of CVD or cancer at baseline. Coffee consumption was assessed first in 1986 for men and in 1980 for women and then every 2 to 4 years through 2004. Investigators documented 6888 deaths (2049 due to CVD and 2491 due to cancer) among men and 11 095 deaths (2368 due to CVD and 5011 due to cancer) among women. After adjustment for age, smoking, and other CVD and cancer risk factors, the relative risks for all-cause mortality in men across categories of coffee consumption (<1 cup per month, 1 cup per month to 4 cups per week, 5 to 7 cups per week, 2 to 3 cups per day, 4 to 5 cups per day, and ≥6 cups per day) were 1.0, 1.07 (95% CI, 0.99 to 1.16), 1.02 (CI, 0.95 to 1.11), 0.97 (CI, 0.89 to 1.05), 0.93 (CI, 0.81 to 1.07), and 0.80 (CI, 0.62 to 1.04), respectively (P for trend = 0.008). For women, the relative risks were 1.0, 0.98 (CI, 0.91 to 1.05), 0.93 (CI, 0.87 to 0.98), 0.82 (CI, 0.77 to 0.87), 0.74 (CI, 0.68 to 0.81), and 0.83 (CI, 0.73 to 0.95), respectively (P for trend < 0.001). This inverse association was mainly due to a moderately reduced risk for CVD mortality and was independent of caffeine intake. By contrast, coffee consumption was not statistically significantly associated with risk for cancer death after adjustment for potential confounders. Decaffeinated coffee consumption was associated with a small reduction in all-cause and CVD mortality. Coffee consumption was estimated from self-report; thus, some measurement error is inevitable. Regular coffee consumption was not associated with an increased mortality rate in either men or women. The possibility of a modest benefit of coffee consumption on all-cause and CVD mortality needs to be further investigated.

Background: The long-term effects of caffeine intake on weight have not been examined prospectively. Objective: The objective was to assess the relation between caffeine intake and 12-y weight change. Design: We conducted a prospective study of 18 417 men and 39 740 women, with no chronic diseases at baseline, who were followed from 1986 to 1998. Caffeine intake was assessed repeatedly every 2–4 y. Weight change was calculated as the difference between the self-reported weight in 1986 and in 1998. Results: The participants reported a change in caffeine intake that varied across quintiles, from decreases of 296 and 342 mg/d to increases of 213 and 143 mg/d in men and women, respectively. Age-adjusted models showed a lower mean weight gain in participants who increased their caffeine consumption than in those who decreased their consumption, but the differences between extreme quintiles were small: −0.43 kg (95% CI: −0.17, −0.69) in men and −0.41 kg (95% CI: −0.20, −0.62) in women. After adjustment for potential confounders and baseline and change in total energy intake and other nutrients and foods, the differences remained similar for men and diminished slightly for women (men: −0.43 kg; 95% CI: −0.17, −0.68; women: −0.35; 95% CI: −0.14, −0.56). An increase in coffee and tea consumption was also associated with less weight gain. In men, the association between caffeine intake and weight was stronger in younger participants (P for interaction < 0.001); in women, the association was stronger in those who had a body mass index (in kg/m²) ≥25, who were less physically active, or who were current smokers (P for interaction < 0.001). Conclusion: Increases in caffeine intake may lead to a small reduction in long-term weight gain.

There is emerging evidence of the role of certain nutrients as risk factors for frailty. However, people eat food, rather than nutrients, and no previous study has examined the association between dietary patterns empirically derived from food consumption and the risk of frailty in older adults. This is a prospective cohort study of 1,872 non-institutionalized individuals aged ≥60 years recruited between 2008 and 2010. At baseline, food consumption was obtained with a validated diet history and, by using factor analysis, two dietary patterns were identified: a ‘prudent’ pattern, characterized by high intake of olive oil and vegetables, and a ‘Westernized’ pattern, with a high intake of refined bread, whole dairy products, and red and processed meat, as well as low consumption of fruit and vegetables. Participants were followed-up until 2012 to assess incident frailty, defined as at least three of the five Fried criteria (exhaustion, weakness, low physical activity, slow walking speed, and unintentional weight loss). Over a 3.5-year follow-up, 96 cases of incident frailty were ascertained. The multivariate odds ratios (95% confidence interval) of frailty among those in the first (lowest), second, and third tertile of adherence to the prudent dietary pattern were 1, 0.64 (0.37–1.12), and 0.40 (0.2–0.81), respectively; P-trend = 0.009. The corresponding values for the Westernized pattern were 1, 1.53 (0.85–2.75), and 1.61 (0.85–3.03); P-trend = 0.14. Moreover, a greater adherence to the Westernized pattern was associated with an increasing risk of slow walking speed and weight loss. In older adults, a prudent dietary pattern showed an inverse dose-response relationship with the risk of frailty while a Westernized pattern had a direct relationship with some of their components. Clinical trials should test whether a prudent pattern is effective in preventing or delaying frailty.

Background— Data on the association between coffee consumption and risk of stroke are sparse. We assessed the association between coffee consumption and the risk of stroke over 24 years of follow-up in women. Methods and Results— We analyzed data from a prospective cohort of 83 076 women in the Nurses’ Health Study without history of stroke, coronary heart disease, diabetes, or cancer at baseline. Coffee consumption was assessed first in 1980 and then repeatedly every 2 to 4 years, with follow-up through 2004. We documented 2280 strokes, of which 426 were hemorrhagic, 1224 were ischemic, and 630 were undetermined. In multivariable Cox regression models with adjustment for age, smoking status, body mass index, physical activity, alcohol intake, menopausal status, hormone replacement therapy, aspirin use, and dietary factors, the relative risks (RRs) of stroke across categories of coffee consumption (<1 cup per month, 1 per month to 4 per week, 5 to 7 per week, 2 to 3 per day, and ≥4 per day) were 1, 0.98 (95% CI, 0.84 to 1.15), 0.88 (95% CI, 0.77 to 1.02), 0.81 (95% CI, 0.70 to 0.95), and 0.80 (95% CI, 0.64 to 0.98) ( P for trend=0.003). After further adjustment for high blood pressure, hypercholesterolemia, and type 2 diabetes, the inverse association remained significant. The association was stronger among never and past smokers (RR for ≥4 cups a day versus <1 cup a month, 0.57; 95% CI, 0.39 to 0.84) than among current smokers (RR for ≥4 cups a day versus <1 cup a month, 0.97; 95% CI, 0.63 to 1.48). Other drinks containing caffeine such as tea and caffeinated soft drinks were not associated with stroke. Decaffeinated coffee was associated with a trend toward lower risk of stroke after adjustment for caffeinated coffee consumption (RR for ≥2 cups a day versus <1 cup a month, 0.89; 95% CI, 0.73 to 1.08; P for trend=0.05). Conclusions— Long-term coffee consumption was not associated with an increased risk of stroke in women. In contrast, our data suggest that coffee consumption may modestly reduce risk of stroke.