Background: The association between coffee consumption and incident hypertension remained inconsistent.
Objective: This study aimed to examine the association of consumption of coffee, including different types (instant and ground) and with different additives, with new-onset hypertension, and evaluate whether genetic variation in caffeine metabolism and inflammation may modify the association.
Design: This study utilized a prospective cohort design.
Participants/setting: A total of 98 765 participants free of hypertension enrolled in the UK Biobank between 2006 and 2010 were included. Dietary coffee consumption was collected using 24-hour dietary recall questionnaires.
Main outcome measures: The study outcome was new-onset hypertension, ascertained by self-reported medical conditions, hospital inpatient records, death registers, and primary care records.
Statistical analyses performed: Cox proportional hazards models were used to estimate hazard ratio and 95% CI. Potential modifying effects were assessed by likelihood ratio testing.
Results: During a median follow-up of 12.1 years, 7090 (7.2%) new-onset cases of hypertension were documented. Overall, regardless of coffee type (instant or ground) and whether adding milk to coffee, there was a U-shaped association between unsweetened coffee consumption and new-onset hypertension, with a 14% to 18% reduction of hypertension risk at >1 to ≤4 drinks per day, whereas a null association was observed between sweetened coffee consumption and the risk of new-onset hypertension. Relative to coffee nonconsumers, the adjusted hazard ratio (95% CI) of new-onset hypertension for participants who drinking unsweetened coffee 1 or fewer, >1 to 2, >2 to 3, >3 to 4, and >4 drinks/day were 0.92 (95% CI 0.85 to 1.00), 0.82 (95% CI 0.76 to 0.89), 0.86 (95% CI 0.79 to 0.96), 0.86 (95% CI 0.77 to 0.96), and 0.88 (95% CI 0.78 to 0.99), respectively. Moreover, a stronger inverse association between moderate consumption of unsweetened coffee and new-onset hypertension was found in participants with higher C-reactive protein levels (P for interaction =.012), whereas an individual's genetic variation in caffeine metabolism did not significantly modify the association (P for interaction = .453).
Conclusions: Regardless of the type of coffee (instant or ground) or the addition of milk to coffee, moderate consumption of unsweetened coffee (>1 to ≤4 drinks/day), but not sweetened coffee, was associated with a lower risk of new-onset hypertension.
Background: Ultraprocessed foods (UPF) consumption has been associated with depression risk, but its association with depression persistence is unclear.
Objective: The objective of this study was to evaluate the association of UPF consumption with depression persistence and incidence.
Design: The Brazilian Longitudinal Study of Adult Health is a multicenter prospective cohort study with 3 waves (2008-2010, 2012-2014, and 2017-2019). Baseline percentage of energy from UPF, measured using a food frequency questionnaire, was divided into quartiles.
Participants/setting: Civil servants aged 35 to 74 years at baseline were included in the Brazilian Longitudinal Study of Adult Health. Participants with Parkinson disease, dementia, stroke history, extreme energy intake, and missing dietary or depression data at baseline were excluded.
Main outcome measures: Depression was based on the Clinical Interview Schedule-Revised, depression persistence on depression status at each wave and depression incidence on time to first depression diagnosis.
Statistical analyses performed: Clustering large applications algorithm, multinomial logistic regression, Cox proportional-hazard models, and partition substitution model were performed.
Results: Among 13 870 participants free from depression at baseline, 731 (5.3%) had depression after 8 years of follow-up. Participants in Cluster 1 did not have depression in any wave, in Cluster 2 had depression in 1 wave, and in Cluster 3 had persistent depression in 2 or more waves. Compared with the first quartile of UPF consumption, participants in Quartiles 2, 3, and 4 had a 1.30 (95% CI 1.29 to 1.31), 1.39 (95% CI 1.38 to 1.40), and 1.58 (95% CI 1.56 to 1.60) higher odds of persistent depression (P = .019), respectively. Compared with the first UPF quartile, participants in Quartiles 3 and 4 had a 1.32 (95% CI 1.07 to 1.64) and 1.30 (95% CI 1.04 to 1.61) higher risk of incident depression (P = .017), respectively. Substituting 5%, 10%, and 20% of UPF with unprocessed/minimally processed foods and culinary ingredients was associated with a 6%, 11%, and 22% decreased depression incidence, respectively.
Conclusions: Higher consumption of UPF at baseline was associated with higher odds of persistent depression and higher risk of incident depression over 8 years of follow-up.