scholarly journals Metabolomic signatures of long-term coffee consumption and risk of type 2 diabetes in women

Author(s):  
Dong Hang ◽  
Oana A. Zeleznik ◽  
Xiaosheng He ◽  
Marta Guasch-Ferre ◽  
Xia Jiang ◽  
...  

<b>Objective:</b> Coffee may protect against multiple chronic diseases, particularly type 2 diabetes, but the mechanisms remain unclear. <p><b>Research Design and Methods: </b>Leveraging dietary and metabolomic data in two large cohorts of women (the Nurses’ Health Study I and II), we identified and validated plasma metabolites associated with coffee intake in 1595 women. We then evaluated the prospective association of coffee-related metabolites with diabetes risk and the added predictivity of these metabolites for diabetes in two nested case-control studies (n=457 cases and 1371 controls). </p> <p><b>Results: </b>Of 461 metabolites, 34 were identified and validated to be associated with total coffee intake, including 13 positive associations (primarily trigonelline, polyphenol metabolites, and caffeine metabolites) and 21 inverse associations (primarily triacylglycerols and diacylglycerols). These associations were generally consistent for caffeinated and decaffeinated coffee, except for caffeine and its metabolites that were only associated with caffeinated coffee intake. The three cholesteryl esters positively associated with coffee intake showed inverse associations with diabetes risk, whereas the 12 metabolites negatively associated with coffee (five diacylglycerols and seven triacylglycerols) showed positive associations with diabetes. Adding the 15 diabetes-associated metabolites to classical risk factors-based prediction model increased the C-statistic from 0.79 (95% CI: 0.76, 0.83) to 0.83 (95% CI: 0.80, 0.86) (<i>P</i><0.001). Similar improvement was observed in the validation set.</p> <p><b>Conclusion: </b>Coffee consumption is associated with widespread metabolic changes, among which lipid metabolites may be critical for the anti- diabetes benefit of coffee. Coffee-related metabolites might help improve prediction of diabetes, but further validation studies <a>are </a>needed.</p>

2020 ◽  
Author(s):  
Dong Hang ◽  
Oana A. Zeleznik ◽  
Xiaosheng He ◽  
Marta Guasch-Ferre ◽  
Xia Jiang ◽  
...  

<b>Objective:</b> Coffee may protect against multiple chronic diseases, particularly type 2 diabetes, but the mechanisms remain unclear. <p><b>Research Design and Methods: </b>Leveraging dietary and metabolomic data in two large cohorts of women (the Nurses’ Health Study I and II), we identified and validated plasma metabolites associated with coffee intake in 1595 women. We then evaluated the prospective association of coffee-related metabolites with diabetes risk and the added predictivity of these metabolites for diabetes in two nested case-control studies (n=457 cases and 1371 controls). </p> <p><b>Results: </b>Of 461 metabolites, 34 were identified and validated to be associated with total coffee intake, including 13 positive associations (primarily trigonelline, polyphenol metabolites, and caffeine metabolites) and 21 inverse associations (primarily triacylglycerols and diacylglycerols). These associations were generally consistent for caffeinated and decaffeinated coffee, except for caffeine and its metabolites that were only associated with caffeinated coffee intake. The three cholesteryl esters positively associated with coffee intake showed inverse associations with diabetes risk, whereas the 12 metabolites negatively associated with coffee (five diacylglycerols and seven triacylglycerols) showed positive associations with diabetes. Adding the 15 diabetes-associated metabolites to classical risk factors-based prediction model increased the C-statistic from 0.79 (95% CI: 0.76, 0.83) to 0.83 (95% CI: 0.80, 0.86) (<i>P</i><0.001). Similar improvement was observed in the validation set.</p> <p><b>Conclusion: </b>Coffee consumption is associated with widespread metabolic changes, among which lipid metabolites may be critical for the anti- diabetes benefit of coffee. Coffee-related metabolites might help improve prediction of diabetes, but further validation studies <a>are </a>needed.</p>


Author(s):  
Jongeun Rhee ◽  
Erikka Loftfield ◽  
Neal D Freedman ◽  
Linda M Liao ◽  
Rashmi Sinha ◽  
...  

Abstract Background Coffee consumption has been associated with a reduced risk of some cancers, but the evidence for renal cell carcinoma (RCC) is inconclusive. We investigated the relationship between coffee and RCC within a large cohort. Methods Coffee intake was assessed at baseline in the National Institutes of Health–American Association of Retired Persons Diet and Health Study. Among 420 118 participants eligible for analysis, 2674 incident cases were identified. We fitted Cox-regression models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for coffee consumption vs non-drinkers. Results We observed HRs of 0.94 (95% CI 0.81, 1.09), 0.94 (0.81, 1.09), 0.80 (0.70, 0.92) and 0.77 (0.66, 0.90) for usual coffee intake of &lt;1, 1, 2–3 and ≥4 cups/day, respectively (Ptrend = 0.00003). This relationship was observed among never-smokers (≥4 cups/day: HR 0.62, 95% CI 0.46, 0.83; Ptrend = 0.000003) but not ever-smokers (HR 0.85, 95% CI 0.70, 1.05; Ptrend = 0.35; Pinteraction = 0.0009) and remained in analyses restricted to cases diagnosed &gt;10 years after baseline (HR 0.65, 95% CI 0.51, 0.82; Ptrend = 0.0005). Associations were similar between subgroups who drank predominately caffeinated or decaffeinated coffee (Pinteraction = 0.74). Conclusion In this investigation of coffee and RCC, to our knowledge the largest to date, we observed a 20% reduced risk for intake of ≥2 cups/day vs not drinking. Our findings add RCC to the growing list of cancers for which coffee consumption may be protective.


Circulation ◽  
2021 ◽  
Vol 143 (Suppl_1) ◽  
Author(s):  
Carolina Ochoa-Rosales ◽  
Niels van der Schaft ◽  
Kim V Braun ◽  
Frederick Ho ◽  
Fanny Petermann ◽  
...  

Background: Coffee intake has been linked to lower type 2 diabetes (T2D) risk. We hypothesized this may be mediated by coffee’s effects on inflammation. Methods: Using participants from the UK Biobank (UKB n=145370) and Rotterdam Study (RS n=7172) cohorts, we studied associations of coffee intake with incident T2D; longitudinally measured insulin resistance (HOMA IR); serum levels of inflammation markers; and the mediating role of inflammation. Statistical regression models were adjusted for sociodemographic, lifestyle and health factors. Results: The median follow up was 7 (UKB) and 9 (RS) years. An increase of one coffee cup/day was associated with 4-6% lower T2D risk (RS HR=0.94 [95% CI 0.90; 0.98]; UKB HR=0.96 [0.94; 0.98]); lower HOMA IR (RS β=-0.017 [-0.024; -0.010]); with lower C reactive protein (CRP) and higher adiponectin (Figure1). Consumers of filtered coffee had the lowest T2D risk (UKB HR=0.88 [0.83; 0.93]). CRP levels mediated 9.6% (UKB) and 3.4% (RS) of the total effect of coffee on T2D (Figure 1). Conclusions: We suggest that coffee’s beneficial effects on lower T2D risk are partially mediated by improvements in systemic inflammation.Figure 1. a CRP and a adiponectin refer to the effect of coffee intake on CRP and adiponectin levels. a CRP RS : β=-0.014 (-0.022; -0.005); UKBB a CRP UKB : β=-0.011 (-0.012; -0.009) and RS a adiponectin : β=0.025 (0.007; 0.042). b CRP and b adiponectin refer to the effect of coffee related levels in CRP and adiponectin on incident T2D, independent of coffee. RS b CRP : HR=1.17 (1.04; 1.31); UKB b CRP : HR=1.45 (1.37; 1.54); and b adiponectin : HR=0.58 (0.32; 0.83). c′ refers to coffee’ effect on T2D going directly or via others mediators. UKB c′ independent of CRP : HR=0.96 (0.94; 0.99); RS c′ independent of CRP : HR=0.94 (0.90; 0.99); and RS c′ independent of CRP+adiponectin : HR=0.90 (0.80; 1.01). Coffee related changes in CRP may partially explain the beneficial link between coffee and T2D, mediating a 3.4% (0.6; 4.8, RS) and 9.6% (5.7; 24.4, UKB). Evidence of mediation was also found for adiponectin.


Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
Hongyu Wu ◽  
Kimberly A Bertrand ◽  
Anna L Choi ◽  
Frank B Hu ◽  
Francine Laden ◽  
...  

Background: Animal experiments have suggested that exposure to persistent organic pollutants (POPs) may lead to increased risk of type 2 diabetes. Although recent human studies supported this hypothesis, evidence from prospective investigations is sparse. Objective: To examine the associations of plasma POP concentrations with risk of incident type 2 diabetes in a prospective setting among US women. Methods: Study population was comprised of participants from two independent nested case-control studies in the Nurses’ Health Study, in which major polychlorinated biphenyl (PCB 118, 138, 153, and 180), p-p'- dichlorodiphenyldichloroethylene (DDE), dichlorodiphenyltrichloroethane (DDT), and hexachlorobenzene (HCB) were measured. A non-parametric approach was used to derive standardized scores for plasma concentrations of lipid-adjusted POPs within each study to minimize between-study variation of the POP measurements. Risk of incident type 2 diabetes during the follow-up period (1990-2008) across the tertiles of the scores was examined. Results: Of 1,120 participants, we identified 48 incident type 2 diabetes cases. After adjusting for covariates assessed at blood draw in 1990, including smoking status, body mass index, and total fish intake, plasma HCB concentration was positively associated with type 2 diabetes risk: odds ratio (OR) (95% confidence interval [CI]) was 2.77 (1.17, 6.55, P for trend =0.022) comparing the highest vs. lowest tertile. Other POPs were not significantly associated with diabetes: the ORs (95% CI) were 1.10 (0.51, 2.34, P for trend =0.81) for p-p'-DDE, 0.93 (0.44, 1.95, P for trend =0.86) for DDT, and 0.88 (0.39, 1.97, P for trend =0.76) for sum of the 4 major PCBs, comparing the extreme tertiles. Conclusion: The significant association of plasma HCB concentration with diabetes risk supports a role of POP exposure in the etiology of type 2 diabetes. More prospective data are warranted to confirm these findings.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Danielle E Haslam ◽  
Dong Wang ◽  
Liming Liang ◽  
Rachel S Kelly ◽  
Clemens Wittenbecher ◽  
...  

Introduction: Puerto Rican (PR) adults living on the US mainland are at high risk for developing type 2 diabetes (T2D), and dietary factors may contribute to this increased risk. Network analysis is a data-reduction tool that can identify correlated clusters of co-regulated metabolites that reflect mechanisms underlying diet-T2D associations. Hypothesis: Diet quality will associate with T2D-associated metabolite clusters among PR adults. Methods: We used LC/MS to measure fasting plasma metabolites (>700) among Boston PR Health Study participants, aged 45-75 years, with (n=258) and without (n=421) T2D. We applied an unsupervised correlation network-based method to identify metabolite clusters within a global metabolite network and calculated a score for each cluster using a weighted sum of metabolite concentrations. To estimate diet quality, we calculated a modified version of a previously validated American Heart Association diet score (AHA-DS). Logistic regression was used to assess cross-sectional associations between metabolite clusters and prevalent T2D, and linear regression was used to assess associations between the continuous AHA-DS and T2D-associated metabolite clusters among controls, adjusting for potential confounders and correcting for multiple testing. Results: We identified 7 metabolite clusters that were associated with prevalent T2D ( p <0.05). For every 1-standard deviation (SD) increase in cluster score, the odds ratios for prevalent T2D and 95% confidence intervals were as the follows: acylcholines [0.40 (0.31, 0.50)], aromatic hydrocarbon derivatives [0.33 (0.22, 0.47)], sphingolipids [0.46 (0.33, 0.64)], tricarboxylic acid (TCA) cycle amino acids/peptides [0.39 (0.25, 0.62)], branched-chain amino acid metabolites [4.1 (2.9, 6.0)], acylcarnitines [1.8 (1.3, 2.5)], and TCA cycle/energy metabolites [2.0 (1.4, 3.0)]. The AHA-DS was only significantly associated with the acylcholine metabolites cluster [β (standard error) = 0.01 (0.004) SD increase in cluster score, p=0.02]. Conclusions: In individuals of PR descent, we identified a cluster of acylcholine metabolites where concentrations are higher among those with better diet quality and lower among those with prevalent T2D.


2008 ◽  
Vol 33 (6) ◽  
pp. 1269-1283 ◽  
Author(s):  
Rob M. van Dam

Numerous epidemiological studies have evaluated the association between coffee consumption and risk of type 2 diabetes, coronary heart disease, and various cancers. This paper briefly reviews the evidence for a relation between coffee consumption and these conditions, with particular attention to methodological issues. Several early studies suggested that coffee consumption could result in a marked increase in risk of coronary heart disease and several types of cancer. However, more recent prospective cohort studies that are less prone to selection and information bias have not confirmed these findings. High consumption of unfiltered types of coffee, such as French press and boiled coffee, has been shown to increase low-density-lipoprotein-cholesterol concentrations. In addition, limiting caffeinated coffee intake during pregnancy seems a prudent choice. However, evidence has been accumulating that frequent consumption of coffee may reduce risk of type 2 diabetes and liver cancer. Further experimental studies are warranted to elucidate the underlying mechanisms and possibly identify the components in coffee that are responsible for these putative effects. In sum, the currently available evidence on coffee and risk of cardiovascular diseases and cancer is largely reassuring, and suggests that, for the general population, addressing other health-related behaviors has priority for the prevention of chronic diseases.


2019 ◽  
Vol 29 (3) ◽  
pp. 579-584 ◽  
Author(s):  
Fateme Shafiei ◽  
Asma Salari-Moghaddam ◽  
Alireza Milajerdi ◽  
Bagher Larijani ◽  
Ahmad Esmaillzadeh

BackgroundResults from earlier publications on the association of coffee and caffeine and risk of ovarian cancer are inconsistent.ObjectiveTo evaluate the link between coffee, caffeine, caffeinated coffee, and decaffeinated coffee consumption and risk of ovarian cancer.MethodsWe searched PubMed/Medline, ISI Web of Science, Scopus, and Google Scholar to identify relevant publications up to April 2018. All case–control studies that considered coffee, caffeine, caffeinated coffee, or decaffeinated coffee as the exposure variables and ovarian cancer as the main outcome variable or as one of the outcomes were included in the systematic review. Publications in which odds ratios (ORs) or rate or risk ratios (RRs) and 95% confidence intervals (CIs) were reported, were included in the meta-analysis.ResultsA total of 22 case–control studies were included in the systematic review, and 20 studies in the meta-analysis. Overall, 40 140 participants, including 8568 patients with ovarian cancer, aged ≥ 17 years were included. Combining 21 effect sizes from 18 studies, no significant association was observed between total coffee intake and risk of ovarian cancer (OR=1.09; 95% CI 0.94 to 1.26). There was no significant association between total caffeine intake and ovarian cancer risk (OR=0.89; 95% CI 0.55 to 1.45). In addition, caffeinated coffee intake was not significantly associated with ovarian cancer (OR=1.05; 95% CI 0.87 to 1.28). However, combining effect sizes from five studies, we found an inverse significant association between decaffeinated coffee intake and risk of ovarian cancer (OR=0.72; 95% CI 0.58 to 0.90).ConclusionsOur findings indicated an inverse association between decaffeinated coffee consumption and risk of ovarian cancer. No significant association was found between coffee, caffeine or caffeinated coffee intake and risk of ovarian cancer.


2008 ◽  
Vol 100 (5) ◽  
pp. 1046-1053 ◽  
Author(s):  
Mark Hamer ◽  
Daniel R. Witte ◽  
Annhild Mosdøl ◽  
Michael G. Marmot ◽  
Eric J. Brunner

At least fourteen cohort studies have documented an inverse association between coffee consumption and risk of type 2 diabetes. We examined the prospective association between coffee and tea consumption and the risk of type 2 diabetes mellitus among British men (n 4055) and women (n 1768) from the Whitehall II cohort. During 11·7 years follow-up there were a total of 387 incident cases of diabetes confirmed by self-report of doctor's diagnosis or glucose tolerance tests. Despite an inverse association between coffee intake and 2 h post-load glucose concentration at the baseline assessment, combined caffeinated and decaffeinated coffee (hazard ratio (HR) 0·80; 95 % CI 0·54, 1·18) or only decaffeinated coffee intake (HR 0·65; 95 % CI 0·36, 1·16) was not significantly associated with diabetes risk at follow-up after adjustment for possible confounders. There was an association between tea intake and diabetes (HR 0·66; 95 % CI 0·61, 1·22; P < 0·05) after adjustment for age, gender, ethnicity and social status, which was not robust to further adjustments. There was, however, an association between combined intake of tea and coffee (two or more cups per day of both beverage) and diabetes (HR 0·68; 95 % CI 0·46, 0·99; P < 0·05) after full adjustment. In conclusion, relatively moderate intake (more than three cups per day) of coffee and tea were not prospectively associated with incidence of type 2 diabetes although there was evidence of a combined effect. The limited range of exposure and beverage consumption according to socio-economic class may explain these conflicting findings.


2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 1070-1070
Author(s):  
Carolina Ochoa-Rosales ◽  
Niels van der Schaft ◽  
Kim Braun ◽  
Frederick Ho ◽  
Fanny Petermann ◽  
...  

Abstract Objectives Given its popularity, there is an increasing interest in the study of coffee intake and its effect on health. Previous studies linked coffee consumption to lower type 2 diabetes (T2D) risk. However, potential underlying mechanisms remain unclear. We hypothesized that coffee's effects on systemic inflammation may play a role. We studied cross sectional and longitudinal associations of habitual coffee consumption with T2D risk and inflammation. Methods Participants from UK Biobank (UKB, n = 145,370) and Rotterdam Study (RS, n = 7172) cohorts were included. Coffee intake data were collected through self-administrated food frequency questionnaire or during home interviews. We studied associations of coffee intake with incident T2D using cox proportional hazard models; with longitudinally measured insulin resistance (HOMA IR) through linear mixed effect models; with serum baseline levels of inflammation markers using linear regressions; and the role of inflammation in coffee-T2D associations using mediation analysis. Models were adjusted for sociodemographic, lifestyle and health factors. Results were respectively expressed as hazard ratio (HR); β log transformed HOMA IR level; β log transformed ug/mL; and percentage mediated; and 95% confidence interval [95% CI]. Results UKB participants were 58% female and 55.2 years in average; RS were 59.7% female and 65.1 years. The median follow up was 7 (UKB) and 9 (RS) years. The modal coffee consumption was 0.5–2 cups/day (UKB) and 3–4 cups/day (RS). An increase of one coffee cup/day was associated with 4–6% lower T2D risk (RS HR 0.94 [95% CI 0.90; 0.98]; UKB HR 0.96 [0.94; 0.98]); lower HOMA IR (RS β −0.017 [−0.024; −0.010]); lower C reactive protein (CRP, RS β −0.014 [−0.022; −0.005]; UKBB β −0.011 [−0.012; −0.009] and higher adiponectin (RS β 0.025 [0.007; 0.042]. About coffee types, habitual consumers of filtered coffee had the lowest T2D risk (UKB HR 0.88 [0.83; 0.93]), compared to decaffeinated or instantaneous coffee. CRP levels mediated 9.6% (UKB) and 3.4% (RS) of the total effect of coffee on T2D. Adiponectin also showed evidence for mediation. Conclusions Coffee's beneficial effects on lower T2D risk may be partially mediated by improvements in systemic inflammation. Among coffee drinkers, filtered coffee may be of preference. Funding Sources Partially funded by the Institute for Scientific Information on Coffee.


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