scholarly journals Caffeinated Coffee and Tea Consumption, Genetic Variation and Cognitive Function in the UK Biobank

2020 ◽  
Vol 150 (8) ◽  
pp. 2164-2174
Author(s):  
Marilyn C Cornelis ◽  
Sandra Weintraub ◽  
Martha Clare Morris

ABSTRACT Background Coffee and tea are the major contributors of caffeine in the diet. Evidence points to the premise that caffeine may benefit cognition. Objective We examined the associations of habitual regular coffee or tea and caffeine intake with cognitive function whilst additionally accounting for genetic variation in caffeine metabolism. Methods We included white participants aged 37–73 y from the UK Biobank who provided biological samples and completed touchscreen questionnaires regarding sociodemographic factors, medical history, lifestyle, and diet. Habitual caffeine-containing coffee and tea intake was self-reported in cups/day and used to estimate caffeine intake. Between 97,369 and 445,786 participants with data also completed ≥1 of 7 self-administered cognitive functioning tests using a touchscreen system (2006–2010) or on home computers (2014). Multivariable regressions were used to examine the association between coffee, tea, or caffeine intake and cognition test scores. We also tested interactions between coffee, tea, or caffeine intake and a genetic-based caffeine-metabolism score (CMS) on cognitive function. Results After multivariable adjustment, reaction time, Pairs Matching, Trail Making test B, and symbol digit substitution, performance significantly decreased with consumption of 1 or more cups of coffee (all tests P-trend < 0.0001). Tea consumption was associated with poor performance on all tests (P-trend < 0.0001). No statistically significant CMS × tea, CMS × coffee, or CMS × caffeine interactions were observed. Conclusions Our findings, based on the participants of the UK Biobank, provide little support for habitual consumption of regular coffee or tea and caffeine in improving cognitive function. On the contrary, we observed decrements in performance with intakes of these beverages which may be a result of confounding. Whether habitual caffeine intake affects cognitive function therefore remains to be tested.

Nutrients ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 1969
Author(s):  
Marilyn C. Cornelis ◽  
Sandra Weintraub ◽  
Martha Clare Morris

Clinical evidence points to the premise that caffeine may benefit cognition, but whether these findings extend to real life settings and amidst factors that impact caffeine metabolism is unclear. The aim of this study was to investigate the impact of recent caffeine drinking on cognitive ability while additionally accounting for lifestyle and genetic factors that impact caffeine metabolism. We included up to 434,900 UK Biobank participants aged 37–73 years, recruited in 2006–2010, who provided biological samples and completed touchscreen questionnaires regarding sociodemographic factors, medical history, lifestyle, and diet. Recent caffeine drinking (yes/no in the last hour) was recorded during a physical assessment. Participants completed at least one of four self-administered cognitive function tests using the touchscreen system: prospective memory (PM), pairs matching (Pairs), fluid intelligence (FI), and reaction time (RT). Multivariable regressions were used to examine the association between recent caffeine drinking and cognition test scores. We also tested interactions between recent caffeine drinking and a genetic caffeine-metabolism score (CMS) on cognitive function. Among white participants, recent caffeine drinking was associated with higher performance on RT but lower performance on FI, Pairs, and PM (p ≤ 0.004). Similar directions of associations for FI (p = 0.09), Pairs (p = 0.03), and PM (p = 0.34) were observed among non-white participants. No significant and consistent effect modification by age, sex, smoking, test time, habitual caffeine intake, or CMS was observed. Caffeine consumed shortly before tasks requiring shorter reaction times may improve task performance. Potential impairments in memory and reasoning tasks with recent caffeine drinking warrant further study.


2020 ◽  
Vol 150 (10) ◽  
pp. 2772-2788
Author(s):  
Marilyn C Cornelis ◽  
Rob M van Dam

ABSTRACT Background Mechanisms linking habitual consumption of coffee and tea to the development of type 2 diabetes and cardiovascular diseases remain unclear. Objectives We leveraged dietary, genetic, and biomarker data collected from the UK Biobank to investigate the role of different varieties of coffee and tea in cardiometabolic health. Methods We included data from ≤447,794 participants aged 37–73 y in 2006–2010 who provided a blood sample and completed questionnaires regarding sociodemographic factors, medical history, diet, and lifestyle. Multivariable linear regression was used to examine the association between coffee or tea consumption and blood concentrations of glycated hemoglobin, fasting glucose, total cholesterol, HDL cholesterol, LDL cholesterol, fasting triglycerides (TGs), apoA-1, apoB, lipoprotein-a, and C-reactive protein (CRP). Lifestyle and genetic factors affecting caffeine metabolism, responses, or intake were tested for interactions with beverage intake in relation to biomarker concentrations. Results Compared with coffee nonconsumers, each additional cup of coffee was significantly associated with higher total cholesterol, HDL-cholesterol, and LDL-cholesterol concentrations and lower TG and CRP concentrations in both men and women (P-trend < 0.002). Higher consumption of espresso coffee (≥2 compared with 0 cups/d) was associated with higher LDL cholesterol in men (β: 0.110 mmol/L; 95% CI: 0.058, 0.163 mmol/L) and women (β: 0.161 mmol/L; 95% CI: 0.088, 0.234 mmol/L), whereas no substantial association was observed for instant coffee. Compared with tea nonconsumers, higher tea consumption was associated with lower total and LDL cholesterol and apoB and higher HDL cholesterol (P-trend < 0.002); these associations were similar for black and green tea. Associations were not modified by genetics. Conclusions In the UK Biobank, consumption of certain coffee brews such as espresso had unfavorable associations with blood lipids, whereas consumption of tea had favorable associations. Findings were not modified by genetic variants affecting caffeine metabolism, suggesting a role of noncaffeine constituents of these beverages in cardiometabolic health.


2020 ◽  
Vol 129 ◽  
pp. 123-131 ◽  
Author(s):  
Jordan H. Creed ◽  
Stephanie A. Smith-Warner ◽  
Travis A. Gerke ◽  
Kathleen M. Egan

2019 ◽  
Vol 25 (10) ◽  
pp. 2422-2430 ◽  
Author(s):  
Douglas M. Ruderfer ◽  
Colin G. Walsh ◽  
Matthew W. Aguirre ◽  
Yosuke Tanigawa ◽  
Jessica D. Ribeiro ◽  
...  

Abstract Suicide accounts for nearly 800,000 deaths per year worldwide with rates of both deaths and attempts rising. Family studies have estimated substantial heritability of suicidal behavior; however, collecting the sample sizes necessary for successful genetic studies has remained a challenge. We utilized two different approaches in independent datasets to characterize the contribution of common genetic variation to suicide attempt. The first is a patient reported suicide attempt phenotype asked as part of an online mental health survey taken by a subset of participants (n = 157,366) in the UK Biobank. After quality control, we leveraged a genotyped set of unrelated, white British ancestry participants including 2433 cases and 334,766 controls that included those that did not participate in the survey or were not explicitly asked about attempting suicide. The second leveraged electronic health record (EHR) data from the Vanderbilt University Medical Center (VUMC, 2.8 million patients, 3250 cases) and machine learning to derive probabilities of attempting suicide in 24,546 genotyped patients. We identified significant and comparable heritability estimates of suicide attempt from both the patient reported phenotype in the UK Biobank (h2SNP = 0.035, p = 7.12 × 10−4) and the clinically predicted phenotype from VUMC (h2SNP = 0.046, p = 1.51 × 10−2). A significant genetic overlap was demonstrated between the two measures of suicide attempt in these independent samples through polygenic risk score analysis (t = 4.02, p = 5.75 × 10−5) and genetic correlation (rg = 1.073, SE = 0.36, p = 0.003). Finally, we show significant but incomplete genetic correlation of suicide attempt with insomnia (rg = 0.34–0.81) as well as several psychiatric disorders (rg = 0.26–0.79). This work demonstrates the contribution of common genetic variation to suicide attempt. It points to a genetic underpinning to clinically predicted risk of attempting suicide that is similar to the genetic profile from a patient reported outcome. Lastly, it presents an approach for using EHR data and clinical prediction to generate quantitative measures from binary phenotypes that can improve power for genetic studies.


BMJ Open ◽  
2019 ◽  
Vol 9 (12) ◽  
pp. e033011
Author(s):  
Drew M Altschul ◽  
Christina Wraw ◽  
Catharine R Gale ◽  
Ian J Deary

ObjectivesWe investigated how youth cognitive and sociodemographic factors are associated with the aetiology of overweight and obesity. We examined both onset (who is at early risk for overweight and obesity) and development (who gains weight and when).DesignProspective cohort study.SettingWe used data from the US National Longitudinal Study of Youth 1979 (NLSY) and the UK National Child Development Study (NCDS); most of both studies completed a cognitive function test in youth.Participants12 686 and 18 558 members of the NLSY and NCDS, respectively, with data on validated measures of youth cognitive function, youth socioeconomic disadvantage (eg, parental occupational class and time spent in school) and educational attainment. Height, weight and income data were available from across adulthood, from individuals’ 20s into their 50s.Primary and secondary outcome measuresBody mass index (BMI) for four time points in adulthood. We modelled gain in BMI using latent growth curve models to capture linear and quadratic components of change in BMI over time.ResultsAcross cohorts, higher cognitive function was associated with lower overall BMI. In the UK, 1 SD higher score in cognitive function was associated with lower BMI (β=−0.20, 95% CI −0.33 to −0.06 kg/m²). In America, this was true only for women (β=−0.53, 95% CI −0.90 to −0.15 kg/m²), for whom higher cognitive function was associated with lower BMI. In British participants only, we found limited evidence for negative and positive associations, respectively, between education (β=−0.15, 95% CI −0.26 to −0.04 kg/m²) and socioeconomic disadvantage (β=0.33, 95% CI 0.23 to 0.43 kg/m²) and higher BMI. Overall, no cognitive or socioeconomic factors in youth were associated with longitudinal changes in BMI.ConclusionsWhile sociodemographic and particularly cognitive factors can explain some patterns in individuals’ overall weight levels, differences in who gains weight in adulthood could not be explained by any of these factors.


2020 ◽  
Author(s):  
Sean J. Jurgens ◽  
Seung Hoan Choi ◽  
Valerie N. Morrill ◽  
Mark Chaffin ◽  
James P. Pirruccello ◽  
...  

AbstractBackgroundMany human diseases are known to have a genetic contribution. While genome-wide studies have identified many disease-associated loci, it remains challenging to elucidate causal genes. In contrast, exome sequencing provides an opportunity to identify new disease genes and large-effect variants of clinical relevance. We therefore sought to determine the contribution of rare genetic variation in a curated set of human diseases and traits using a unique resource of 200,000 individuals with exome sequencing data from the UK Biobank.Methods and ResultsWe included 199,832 participants with a mean age of 68 at follow-up. Exome-wide gene-based tests were performed for 64 diseases and 23 quantitative traits using a mixed-effects model, testing rare loss-of-function and damaging missense variants. We identified 51 known and 23 novel associations with 26 diseases and traits at a false-discovery-rate of 1%. There was a striking risk associated with many Mendelian disease genes including: MYPBC3 with over a 100-fold increased odds of hypertrophic cardiomyopathy, PKD1 with a greater than 25-fold increased odds of chronic kidney disease, and BRCA2, BRCA1, ATM and PALB2 with 3 to 10-fold increased odds of breast cancer. Notable novel findings included an association between GIGYF1 and type 2 diabetes (OR 5.6, P=5.35×10−8), elevated blood glucose, and lower insulin-like-growth-factor-1 levels. Rare variants in CCAR2 were also associated with diabetes risk (OR 13, P=8.5×10−8), while COL9A3 was associated with cataract (OR 3.4, P=6.7×10−8). Notable associations for blood lipids and hypercholesterolemia included NR1H3, RRBP1, GIGYF1, SCGN, APH1A, PDE3B and ANGPTL8. A number of novel genes were associated with height, including DTL, PIEZO1, SCUBE3, PAPPA and ADAMTS6, while BSN was associated with body-mass-index. We further assessed putatively pathogenic variants in known Mendelian cardiovascular disease genes and found that between 1.3 and 2.3% of the population carried likely pathogenic variants in known cardiomyopathy, arrhythmia or hypercholesterolemia genes.ConclusionsLarge-scale population sequencing identifies known and novel genes harboring high-impact variation for human traits and diseases. A number of novel findings, including GIGYF1,represent interesting potential therapeutic targets. Exome sequencing at scale can identify a meaningful proportion of the population that carries a pathogenic variant underlying cardiovascular disease.


2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1510-1510
Author(s):  
Huifeng Zhang ◽  
Janet Cade ◽  
Laura Hadie

Abstract Objectives In the largest study of its type, we tested for associations between red meat consumption and cognitive function using data from half a million participants enrolled into the UK Biobank cohort study. Methods Baseline data was obtained from the UK Biobank cohort, comprising half a million participants aged 37–73 years recruited between 2006 and 2010. The intake of red meat (frequency per week) was obtained using a self-reported food frequency questionnaire. Cognitive tests included the reaction-time (RT) test (reaction ability, N = 496, 695), fluid intelligence (FI) (reasoning ability, N = 165,467), the numeric memory test (short-term memory, N = 50,364), the pairs-matching (PM) test (visual-spatial memory, N = 482,650) and the prospective memory test (N = 171,509). Logistic and linear regression modelling was conducted with adjustment for potential confounders including age at recruitment, sex, ethnicity, Townsend deprivation index, smoking, alcohol, education, body mass index, physical activity level, sleeping hours, stroke history, and family history of dementia. Results Each additional portion per week of red-meat intake was associated with slower reaction time by 0.26 milliseconds (95% CI: 0.02, 0.50), lower FI score by 0.01 points (−0.02, −0.00), reduced numeric memory by 0.02 digits (−0.03, −0.01), and increased odds of incorrect prospective memory by 1% (0%, 2%). In men these associations were larger regarding the RT test (β = 0.54, [0.21, 0.87]), FI score (β = −0.02, [−0.03, −0.01]), and prospective memory (OR = 1.03, [1.01, 1.04]), while in women these were not significant. In terms of the PM test, a single additional portion of red-meat intake was associated with reduced incorrect matches by 0.004 pairs (−0.003, −0.006), both in men (β = −0.003, [−0.001, −0.005]) and women (β = −0.006, [−0.004, −0.008]). Conclusions In this cross-sectional analysis of the adult UK population, higher intake of red meat was associated with poorer cognitive function including reaction and reasoning ability, short-term and prospective memory especially among men; but not visual-spatial memory which showed a weak protective effect of red meat. Funding Sources The joint scholarship of University of Leeds and China Scholarship Council.


Author(s):  
Greg McInnes ◽  
Adam Lavertu ◽  
Katrin Sangkuhl ◽  
Teri E. Klein ◽  
Michelle Whirl-Carrillo ◽  
...  

AbstractPharmacogenetics (PGx) studies the influence of genetic variation on drug response. Clinically actionable associations inform guidelines created by the Clinical Pharmacogenetics Implementation Consortium (CPIC), but the broad impact of genetic variation on entire populations is not well-understood. We analyzed PGx allele and phenotype frequencies for 487,409 participants in the U.K. Biobank, the largest PGx study to date. For fourteen CPIC pharmacogenes known to influence human drug response, we find that 99.5% of individuals may have an atypical response to at least one drug; on average they may have an atypical response to 12 drugs. Non-European populations carry a greater frequency of variants that are predicted to be functionally deleterious; many of these are not captured by current PGx allele definitions. Strategies for detecting and interpreting rare variation will be critical for enabling broad application of pharmacogenetics.


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