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Review Article |

Coffee, Decaffeinated Coffee, and Tea Consumption in Relation to Incident Type 2 Diabetes Mellitus:  A Systematic Review With Meta-analysis FREE

Rachel Huxley, DPhil; Crystal Man Ying Lee, PhD; Federica Barzi, PhD; Leif Timmermeister; Sebastien Czernichow, MD, PhD; Vlado Perkovic, MD, PhD; Diederick E. Grobbee, MD, PhD; David Batty, PhD; Mark Woodward, PhD
[+] Author Affiliations

Author Affiliations: The George Institute for International Health, The University of Sydney, Sydney, Australia (Drs Huxley, Lee, Barzi, Czernichow, Perkovic, Batty, and Woodward and Mr Timmermeister); Department of Public Health, Avicenne Hospital, University of Paris 13, Paris, France (Dr Czernichow); The Julius Center for Health Sciences and Primary Care, Utrecht University Medical Center, Utrecht, the Netherlands (Dr Grobbee); Medical Research Council Social & Public Health Sciences Unit, University of Glasgow, Glasgow, Scotland (Dr Batty); and Mount Sinai School of Medicine, New York, New York (Dr Woodward).


Arch Intern Med. 2009;169(22):2053-2063. doi:10.1001/archinternmed.2009.439.
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Published online

Background  Coffee consumption has been reported to be inversely associated with risk of type 2 diabetes mellitus. Similar associations have also been reported for decaffeinated coffee and tea. We report herein the findings of meta-analyses for the association between coffee, decaffeinated coffee, and tea consumption with risk of diabetes.

Methods  Relevant studies were identified through search engines using a combined text word and MeSH (Medical Subject Headings) search strategy. Prospective studies that reported an estimate of the association between coffee, decaffeinated coffee, or tea with incident diabetes between 1966 and July 2009.

Results  Data from 18 studies with information on 457 922 participants reported on the association between coffee consumption and diabetes. Six (N = 225 516) and 7 studies (N = 286 701) also reported estimates of the association between decaffeinated coffee and tea with diabetes, respectively. We found an inverse log-linear relationship between coffee consumption and subsequent risk of diabetes such that every additional cup of coffee consumed in a day was associated with a 7% reduction in the excess risk of diabetes relative risk, 0.93 [95% confidence interval, 0.91-0.95]) after adjustment for potential confounders.

Conclusions  Owing to the presence of small-study bias, our results may represent an overestimate of the true magnitude of the association. Similar significant and inverse associations were observed with decaffeinated coffee and tea and risk of incident diabetes. High intakes of coffee, decaffeinated coffee, and tea are associated with reduced risk of diabetes. The putative protective effects of these beverages warrant further investigation in randomized trials.

Figures in this Article

By 2025, the number of in individuals estimated to be affected by type 2 diabetes mellitus (DM) will increase by 65% to reach an estimated 380 million individuals worldwide, with the greatest burden being shouldered by the lower- and middle-income countries of the Asia-Pacific region.1 Diabetes mellitus causes substantial morbidity and mortality in those affected and is associated with enormous economic, health, and societal costs.2,3 Moreover, compared with unaffected individuals, those with DM are at greatly elevated risk of other chronic illnesses, including cardiovascular disease, in which cases DM more than doubles the risk of having a heart attack or stroke.4,5 Therefore, the identification of modifiable risk factors for the primary prevention of DM is of considerable public health importance.

Despite considerable research attention, the role of specific dietary and lifestyle factors remains uncertain, although obesity6,7 and physical inactivity8 have consistently been reported to raise the risk of DM. Observational epidemiologic studies have also suggested that high dietary intakes of fat, especially trans-fats,9 and red meat10,11 are independently associated with reduced insulin sensitivity and increased risk of DM, and conversely, that high intakes of whole grains may be protective.5,9,12 Other studies have highlighted the potential role that high intakes of coffee and tea may have on reducing the likelihood of developing DM.

An earlier meta-analysis suggested that individuals with the highest level of coffee consumption have approximately one-third the risk of DM compared with those with the lowest levels of consumption.13 However, since that review was published, the amount of information that is now available on the relationship between coffee consumption and subsequent risk of DM has more than doubled.1424 Furthermore, several studies have also published data suggesting that decaffeinated coffee and tea may confer benefits similar to those of regular coffee consumption, although there has been no systematic evaluation of the evidence for these beverages.16,17 Hence, the purpose of the current report is to update the previous meta-analysis of the association between coffee consumption and risk of DM and to conduct a supplementary overview of the evidence for decaffeinated coffee and tea consumption on subsequent risk.

LITERATURE SEARCH

We performed a systematic review of available literature according to the MOOSE guidelines.25 Relevant studies published between 1966 and July 2009 were identified from CINAHL, EMBASE, PubMed, and the Cochrane Library using a combined text and the following MeSH heading search strategies: (caffeine OR coffee OR decaffeinated OR tea) AND (diabetes OR NIDDM OR adult-onset diabetes OR glucose) AND (cohort OR case-control). References from these studies, as well from the previous reviews, were also scrutinized to identify other relevant studies. There was no language restriction.

STUDY SELECTION AND DATA EXTRACTION

Studies were included in this systematic review if they had published quantitative estimates (including variability) of the association between intake of total coffee, decaffeinated coffee, total tea (including green and black) with new-onset (incident) DM. Findings had to be adjusted for at least age and body mass index (BMI). We excluded all animal studies and, in humans, studies of type 1 DM. Given that a disease may plausibly affect dietary intake (reverse causality), we also excluded all cross-sectional studies and those case-control studies with no information on incident DM. Furthermore, we excluded studies that classified consumption only into a binary variable (ie, yes or no) without specifying the number of cups of beverage consumed per day. The literature research and data extraction were conducted by 2 of the us (C.M.Y.L. and L.T.). Where there was disagreement over the eligibility of the study, 3 more of us reviewed the article (R.H., F.B., and S.C.), and a consensus was reached.

DATA SYNTHESIS AND ANALYSIS

Given that most studies reported the association between beverage consumption and DM for more than 1 level of intake, an a priori decision was made to pool the estimates of relative risk (RR) that corresponded as closely as possible to between 3 and 4 cups of coffee, decaffeinated coffee, or tea per day, compared with none. A test for linear trend of effects across coffee consumption categories was performed by regressing each log RR on the ordered categorical variable for coffee in 5 levels using a random-effect meta-regression model. A log-linear association between cups per day and RR was fitted using generalized least squares.26

For studies of specific types of tea (black, green, and oolong), only 1 estimate of the association with DM was reported, and hence, we report on the association with DM comparing tea drinkers with non–tea drinkers. Summary estimates were obtained by means of a random-effects model, and studies were weighted according to an estimate of statistical size defined as the inverse of the variance of the log RR.27 The percentage of variability across studies attributable to heterogeneity rather than chance was estimated using the I2 statistic.28,29 Possible sources of heterogeneity were investigated by comparing summary results obtained when studies were grouped according to statistical size, sex, method of diagnosis of DM, and level of adjustment. Publication bias was assessed taking, for each study, the RR and 95% confidence interval (CI) corresponding to the highest category of coffee consumption using the Egger test.30 All analyses were performed using Stata software, version 10 (StataCorp LP, College Station, Texas).

STUDY CHARACTERISTICS

The search strategy identified a total of 2435 articles, of which 847 were duplicates. After a review of 1588 abstracts, 120 reports were reviewed in full (Figure 1), and 20 of these, all cohort studies, were included in our review.1424,3140 The sample size ranged from 910 to 88 259 and totaled 517 325 individuals, among whom there were 21 897 cases of new-onset DM (Table A and Table B). Cohorts were drawn from diverse populations, including Singapore,20 Puerto Rico,15 the United Kingdom,17 Finland,14,18,31,32 the United States,16,2123,3436 Japan,17,40 the Netherlands,38,39 and Sweden33 but included predominantly white populations, with 21% of the data derived from Asian cohorts (n = 110 147). The studies represented both the general population and specific occupational groups. Age at commencement of the studies ranged from 20 to 98 years, and the median duration of follow-up ranged from 2 to 20 years.

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Figure 1.

Flowchart for identifying eligible studies.

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Table Graphic Jump LocationTable. Characteristics of Studies Reporting on the Association Between Coffee, Decaffeinated Coffee, or Tea and Subsequent Type 2 DM
Table Graphic Jump LocationTable. Characteristics of Studies Reporting on the Association Between Coffee, Decaffeinated Coffee, or Tea and Subsequent Type 2 DM (cont)
MEASUREMENT OF EXPOSURE AND OUTCOME

Apart from 1 study, which used 24-hour dietary recall to obtain an estimate of coffee consumption,15 all of the remaining studies used self-reported food frequency or self-administered questionnaires. Diabetes mellitus was ascertained using self-report of physician diagnoses, routinely collected hospital admission records, or direct measurement using an oral glucose tolerance test. Studies quantified the association between beverage intake and DM using RR with accompanying 95% CIs. With few exceptions, all studies controlled extensively for a range of potential confounders. Although some studies recruited men and women, not all reported sex-specific analyses; those that did were entered separately into the meta-analysis, resulting in a total of 37 estimates of the relationship between coffee, decaffeinated coffee, and tea with risk of DM.

ASSOCIATION BETWEEN COFFEE CONSUMPTION AND DM

A total of 23 estimates from 18 studies (5 studies reported sex-specific estimates) with information on 457 922 participants reported on the association between coffee consumption and subsequent risk of DM. There was evidence of a significant inverse log-linear association such that every additional cup of coffee consumed in a day was associated with a 7% reduction in the excess risk of DM (RR, 0.93 [95% CI, 0.91-0.95]) (P < .001) (Figure 2). In categorical analysis, the pooled summary estimate from these studies indicated that drinking 3 to 4 cups of coffee per day was associated with an approximate 25% lower risk of DM than drinking none or 2 or fewer cups per day (RR, 0.76 [95% CI, 0.69-0.82]) (Figure 3). There was evidence of significant heterogeneity across studies (P = .01) that was not explained by differences in the strength of effect between men and women (RR, 0.78 [95% CI, 0.70-0.87] and 0.71 [95% CI, 0.62-0.81], respectively) (P = .24 for heterogeneity); the region where the study was conducted (Europe RR, 0.84 [95% CI, 0.75-0.94] vs the United States RR, 0.73 [95% CI, 0.62-0.85]) (P = .15 for heterogeneity); or the method of diagnosis (national register or oral glucose tolerance test RR, 0.85 [95% CI, 0.74-0.98] vs self-report RR, 0.72 [95% CI, 0.66-0.79]) (P = .05 for heterogeneity).

Place holder to copy figure label and caption
Figure 2.

The relationship between coffee consumption and subsequent type 2 diabetes mellitus in different categories of coffee consumption. The center of each black square is placed at the summary point estimate; the area of the square is proportional to the statistical size; and each vertical line shows the 95% confidence interval about the summary estimate.

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Place holder to copy figure label and caption
Figure 3.

Association between coffee, decaffeinated coffee, and tea consumption and subsequent type 2 diabetes mellitus in published cohort studies (adjusted in all cases at least for age, sex, and body mass index). The studies are sorted by statistical size, defined by the inverse of the variance of the relative risk (RR). The center of each black square is placed at the point estimate; the area of the square is proportional to the statistical size; and each horizontal line shows the 95% confidence interval (CI) for the estimate for each study. Pheter indicates P value for heterogeneity.

Graphic Jump Location

Restriction of the analysis to those 11 studies that reported both age- and sex-adjusted estimates and estimates that were adjusted for other potential confounders (Table A and Table B) indicated that the observed association was unaffected by the level of adjustment in the crude model (RR, 0.75 [95% CI, 0.67-0.85]) vs in the maximally adjusted model (RR, 0.76 [95% CI, 0.70-0.84]) (P = .81 for heterogeneity).

There was some evidence of publication bias found by the Egger test (P = .08) such that the smaller studies tended to report greater effect sizes than did the larger studies (P = .01 for trend) (Figure 4). The summary risk estimate from the 6 largest estimates (defined as having a statistical study weight ≥35) of drinking 3 to 4 cups of coffee per day compared with drinking none or fewer than 2 cups per day was RR, 0.85 (95% CI, 0.75-0.96), while from the 7 smallest estimates (defined as having a statistical study weight <20), it was RR, 0.62 (95% CI, 0.48-0.79).

Place holder to copy figure label and caption
Figure 4.

Impact of study size on summary estimates of the relative risk between coffee consumption and subsequent type 2 diabetes mellitus adjusted in all cases at least for age, sex, and body mass index. The center of each black square is placed at the summary point estimate; the area of the square is proportional to the statistical size; and each horizontal line shows the 95% confidence interval about the summary estimate.

Graphic Jump Location
ASSOCIATION BETWEEN DECAFFEINATED COFFEE CONSUMPTION AND SUBSEQUENT RISK OF DM

Six studies (N = 225 516 participants) reported on the association between decaffeinated coffee consumption and subsequent risk of DM. The pooled summary estimates from these studies indicated that individuals who drank more than 3 to 4 cups of decaffeinated coffee per day had an approximate one-third lower risk of DM than those consuming no decaffeinated coffee (RR, 0.64 [95% CI, 0.54-0.77]) (Figure 3). There was little evidence for either significant heterogeneity across included studies (P = .31) or publication bias (P = .57 for Egger test).

ASSOCIATION BETWEEN TEA CONSUMPTION AND SUBSEQUENT RISK OF DM

A total of 7 studies (N = 286 701 participants) reported on the association between tea consumption and subsequent risk of DM. Pooled summary estimates indicated that individuals who drank more than 3 to 4 cups of tea per day had an approximate one-fifth lower risk of DM than those consuming no tea (RR, 0.82 [95% CI, 0.73-0.94]) (Figure 3). There was little evidence for significant heterogeneity across included studies (P = .46) and no evidence to indicate the presence of publication bias (P = .11 for Egger test). For studies of tea and decaffeinated coffee, there was insufficient data to permit examination of a dose-response relation. It was also not possible to examine the potential effect of confounding on the relationship because none of the studies reported both age- and multivariate-adjusted estimates.

The findings from this meta-analysis, based on over 500 000 individuals with over 21 000 cases of new-onset DM, confirm an inverse association between coffee consumption and subsequent risk of DM: every additional cup of coffee consumed in a day was associated with 5% to 10% lower risk of incident DM after adjustment for potential confounders. However, this may be an overestimate of the true magnitude of the association owing to the presence of small-study bias.

Furthermore, in the first overview of which we are aware, we were able to demonstrate similar inverse associations between consumption of decaffeinated coffee and tea with risk of incident DM. For example, individuals consuming more than 3 to 4 cups of tea a day had a one-fifth lower risk of subsequent DM than non–tea drinkers; those consuming a similar amount of decaffeinated coffee had a one-third lower risk than nonconsumers. However, in the study by Greenberg and colleagues,16 consumption of decaffeinated coffee was associated with a significant 40% reduction in the risk of DM only in those aged 60 years or younger. In older individuals, the direction of association was reversed such that there was a significant 40% increase in risk. The observed age-related effect may have been a statistical artifact driven by subgroup analysis. However, we were unable to examine the effect by age, and the possibility that the association between coffee and DM risk is age dependent warrants further investigation.

That the apparent protective effect of tea and coffee consumption appears to be independent of a number of potential confounding variables raises the possibility of direct biological effects. Our findings suggest that any protective effects of coffee and tea are unlikely to be solely effects of caffeine, but rather, as has been speculated previously, they likely involve a broader range of chemical constituents present in these beverages, such as magnesium,41 lignans,42 and chlorogenic acids.43 The effects of these coffee components on glucose metabolism and insulin sensitivity from both animal studies and in vitro experiments have been extensively reviewed elsewhere.44 While these components have been demonstrated to have beneficial effects on biological pathways intimately involved in glucose homeostasis and insulin secretion, how these findings relate to in vivo effects in humans is uncertain. Because most of the studies included in this review did not provide data on the effects of these beverages or their components on measures of hyperglycemia and insulin sensitivity, we cannot provide further evidence on the mechanisms involved. In studies that reported data on insulin sensitivity, findings were conflicting, with some suggesting that coffee use increased sensitivity to insulin,38,45 while others reported no effect.46 There have been few randomized trials of the effects of coffee on glucose and insulin, but 1 randomized crossover trial of 4 weeks' duration of high coffee consumption reported an increase in fasting insulin levels but no effect on fasting glucose concentration.47

Possible mechanisms of action for tea on DM may involve 1 or more physiologic pathways. For example, tea catechins have been shown to inhibit the carbohydrate digestive enzymes, which suggests that glucose production may be decreased in the gastrointestinal system resulting in lower levels of glucose and insulin.48 Black, green, and oolong tea have also been reported to increase insulin sensitivity by increasing insulin-stimulated glucose uptake in adipocytes.49 There has also been the suggestion that green tea may prevent damage to pancreatic beta cells.50,51 There have been several small clinical intervention studies conducted that have examined the effects of tea consumption on biomarkers of glucoregulatory control, but the results from these studies have been inconsistent. Some studies have reported a significant reduction in plasma glucose and hemoglobin A1c levels,52,53 while others have reported no effect on any aspect of glucoregulatory control.54 Given that dietary polyphenols are rapidly metabolized, one explanation for the discrepant findings between these studies may have been the measurement of the effects of tea on biomarkers at different times after its consumption. For example, catechin concentrations in human plasma reach their maximum level at 2 hours after ingestion of green tea but are undetectable after 24 hours.55

That there is a causal inverse association between coffee consumption and subsequent risk of DM is further supported by the presence of a dose-response relationship. In those consuming more than 6 cups of coffee per day, the risk of new-onset DM was reduced by approximately 40% compared with non–coffee drinkers, while among those who drank less than 1 cup per day, the risk was only marginally reduced to about 4% compared with coffee abstainers. Moreover, estimates were quite similar across studies despite the diversity in populations. Of note, this similarity was presence in spite of the likely presence of marked variation between studies in types of coffee and tea and their preparation (eg, filtered vs unfiltered, cup size, cup strength, addition of milk or sugar, and other variations). Finally, the results were consistent between studies regardless of which method of diagnosis of DM was used (ie, self-report vs national register or oral glucose tolerance test).

An inherent weakness of all observational studies and meta-analyses thereof is the possibility that any association is due to the presence of confounding. However, because high levels of coffee and tea consumption have been reported to be associated with risk behaviors that are positively associated with the risk of developing DM (such as low levels of physical activity56 and cigarette smoking57), it might be speculated that adjustment for such risk factors would strengthen the relationship as has been reported. We examined the impact of confounding on the relationship between coffee consumption and subsequent risk of DM by comparing crude and adjusted estimates of effect from only those studies that reported both estimates and observed that adjustment for potential confounders had no material impact (either a strengthening or a weakening) on the estimate of effect. However, we were unable to conduct a similar analysis for tea consumption because studies only reported the adjusted estimate. Tea drinkers may be more health conscious than coffee drinkers, and it is therefore plausible that some of the observed beneficial effect of tea on DM risk is due in part to other health-promoting behaviors (eg, regular physical activity, weight maintenance, and nonsmoking) that may or may not have been taken into consideration in the original studies.

A further major limitation of this analysis is the reliance on published data, which precluded more detailed analysis of the effect of adjustment for confounders at an individual level or for specific confounders separately. In this regard, it is possible that individuals who consume extreme quantities of coffee differ in other important dietary and sociologic aspects from more moderate coffee consumers, but to examine this issue any further would require an individual participant data meta-analysis. Therefore, the possibility that coffee consumption may be acting as a surrogate marker of some other dietary or lifestyle risk factor cannot be fully excluded.

Finally, although the studies included in this review were all population based, only 20% of the cohorts were from nonwhite populations, which somewhat limits the generalizability of the study findings to largely Western populations. This is an important consideration given that the pattern of beverage consumption and background risk of DM may differ across ethnic groups.

In conclusion, high intake of coffee, decaffeinated coffee, and/or tea is associated with a material reduction in the risk of new-onset DM. If such beneficial effects were observed in interventional trials to be real, the implications for the millions of individuals who have DM, or who are at future risk of developing it, would be substantial. For example, the identification of the active components of these beverages would open up new therapeutic pathways for the primary prevention of DM. It could also be envisaged that we will advise our patients most at risk for DM to increase their consumption of tea and coffee in addition to increasing their levels of physical activity and weight loss.

Correspondence: Rachel Huxley, DPhil, The George Institute for International Health, PO Box M201, Missenden Road, Sydney, NSW 2050, Australia (rhuxley@george.org.au).

Accepted for Publication: August 14, 2009.

Author Contributions: Dr Huxley had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis. Study concept and design: Huxley, Czernichow, Perkovic, and Grobbee. Acquisition of data: Timmermeister. Analysis and interpretation of data: Huxley, Lee, Barzi, Timmermeister, Perkovic, Batty, and Woodward. Drafting of the manuscript: Huxley, Barzi, Timmermeister, Czernichow, Grobbee, Batty, and Woodward. Critical revision of the manuscript for important intellectual content: Huxley, Lee, Czernichow, Perkovic, Grobbee, and Batty. Statistical analysis: Lee, Barzi, Grobbee, and Woodward. Administrative, technical, and material support: Perkovic. Study supervision: Huxley and Barzi.

Financial Disclosure: None reported.

Funding/Support: Dr Huxley is supported by a Career Development Award from the National Heart Foundation of Australia. This work was additionally supported by grant 402903 from the National Health and Medical Research Council of Australia (Dr Lee); a Research Career Development Fellowship from the UK Wellcome Trust (Dr Batty); and a research grant from Institut Servier, France and Assistance Publique-Hopitaux de Paris (Dr Czernichow).

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Tuomilehto  JHu  GBidel  SLindstrom  JJousilahti  P Coffee consumption and risk of type 2 diabetes mellitus among middle-aged Finnish men and women. JAMA 2004;291 (10) 1213- 1219
PubMed Link to Article
van Dam  RMDekker  JMNijpels  GStehouwer  CDBouter  LMHeine  RJHoorn study, Coffee consumption and incidence of impaired fasting glucose, impaired glucose tolerance, and type 2 diabetes: the Hoorn Study. Diabetologia 2004;47 (12) 2152- 2159
PubMed
van Dam  RMFeskens  EJM Coffee consumption and risk of type 2 diabetes mellitus. Lancet 2002;360 (9344) 1477- 1478
PubMed Link to Article
Kato  MNoda  MInoue  MKadowaki  TTsugane  SJPHC Study Group, Psychological factors, coffee and risk of diabetes mellitus among middle-aged Japanese: a population-based prospective study in the JPHC study cohort. Endocr J 2009;56 (3) 459- 468
PubMed Link to Article
U.S. Department of Agriculture ARS, USDA National Nutrient Database for Standard Reference Release 17. http://www.nal.usda.gov/fnic/foodcomp/Data/SR17/sr17.html. Accessed August 11, 2009
Milder  IEArts  ICvan de Putte  BVenema  DPHollman  PC Lignan contents of Dutch plant foods: a database including lariciresinol, pinoresinol, secoisolariciresinol and metairesinol. Br J Nutr 2005;93 (3) 393- 402
PubMed Link to Article
Clifford  MN Cholorogenic acids and other cinnamates: nature, occurrence and dietary burden. J Sci Food Agric 1999;79 (5) 362- 372
Link to Article
van Dam  RM Coffee and type 2 diabetes: from bean to beta-cells. Nutr Metab Cardiovasc Dis 2006;16 (1) 69- 77
PubMed Link to Article
Agardh  EECarlsson  SAhlbom  A  et al.  Coffee consumption, type 2 diabetes and impaired glucose tolerance in Swedish men and women. J Intern Med 2004;255 (6) 645- 652
PubMed Link to Article
Soriguer  FRojo-Martinez  Gde Antonio  IE Coffee consumption and type 2 diabetes mellitus. Ann Intern Med 2004;141 (4) 321- 323
PubMed Link to Article
van Dam  RMPasman  WJVerhoef  P Effects of coffee consumption on fasting blood glucose and insulin concentrations: randomized controlled trials in healthy volunteers. Diabetes Care 2004;27 (12) 2990- 2992
PubMed Link to Article
Kobayashi  YSuzuki  MSatsu  H  et al.  Green tea polyphenols inhibit the sodium-dependent glucose transporter of intestinal epithelial cells by a competitive mechanism. J Agric Food Chem 2000;48 (11) 5618- 5623
PubMed Link to Article
Waltner-Law  MEWang  XLLaw  BKHall  RKNawano  MGranner  DK Epigallocatechin gallate, a constituent of green tea, represses hepatic glucose production. J Biol Chem 2002;277 (38) 34933- 34940
PubMed Link to Article
Kao  YHChang  HHLee  MJChen  CL Tea, obesity and diabetes. Mol Nutr Food Res 2006;50 (2) 188- 210
PubMed Link to Article
Crespy  VWilliamson  G A review of the health effects of green tea catechins in in vivo animal models. J Nutr 2004;134 (12) ((suppl)) 3431S- 3440S
PubMed
Hosoda  KWang  MFLiao  ML  et al.  Antihyperglycemic effect of oolong tea in type 2 diabetes. Diabetes Care 2003;26 (6) 1714- 1718
PubMed Link to Article
Fukino  YIkeda  AMaruyama  KAoki  NOkubo  TIso  H Randomized controlled trial for an effect of green tea-extract powder supplementation on glucose abnormalities. Eur J Clin Nutr 2008;62 (8) 953- 960
PubMed Link to Article
Ryu  OHLee  JLee  KW  et al.  Effects of green tea consumption on inflammation, insulin resistance and pulse wave velocity in type 2 diabetes patients. Diabetes Res Clin Pract 2006;71 (3) 356- 358
PubMed Link to Article
Henning  SMNiu  YLee  NH  et al.  Bioavailability and antioxidant activity of tea flavanols after consumption of green tea, black tea, or a green tea extract supplement. Am J Clin Nutr 2004;80 (6) 1558- 1564
PubMed
Bassuk  SSManson  JE Epidemiological evidence for the role of physical activity in reducing risk of type 2 diabetes and cardiovascular disease. J Appl Physiol 2005;99 (3) 1193- 1204
PubMed Link to Article
Perry  IJ Commentary: smoking and diabetes; accumulating evidence of a causal link. Int J Epidemiol 2001;30 (3) 554- 555
PubMed Link to Article

Figures

Place holder to copy figure label and caption
Figure 1.

Flowchart for identifying eligible studies.

Graphic Jump Location
Place holder to copy figure label and caption
Figure 2.

The relationship between coffee consumption and subsequent type 2 diabetes mellitus in different categories of coffee consumption. The center of each black square is placed at the summary point estimate; the area of the square is proportional to the statistical size; and each vertical line shows the 95% confidence interval about the summary estimate.

Graphic Jump Location
Place holder to copy figure label and caption
Figure 3.

Association between coffee, decaffeinated coffee, and tea consumption and subsequent type 2 diabetes mellitus in published cohort studies (adjusted in all cases at least for age, sex, and body mass index). The studies are sorted by statistical size, defined by the inverse of the variance of the relative risk (RR). The center of each black square is placed at the point estimate; the area of the square is proportional to the statistical size; and each horizontal line shows the 95% confidence interval (CI) for the estimate for each study. Pheter indicates P value for heterogeneity.

Graphic Jump Location
Place holder to copy figure label and caption
Figure 4.

Impact of study size on summary estimates of the relative risk between coffee consumption and subsequent type 2 diabetes mellitus adjusted in all cases at least for age, sex, and body mass index. The center of each black square is placed at the summary point estimate; the area of the square is proportional to the statistical size; and each horizontal line shows the 95% confidence interval about the summary estimate.

Graphic Jump Location

Tables

Table Graphic Jump LocationTable. Characteristics of Studies Reporting on the Association Between Coffee, Decaffeinated Coffee, or Tea and Subsequent Type 2 DM
Table Graphic Jump LocationTable. Characteristics of Studies Reporting on the Association Between Coffee, Decaffeinated Coffee, or Tea and Subsequent Type 2 DM (cont)

References

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PubMed Link to Article
Bidel  SSilventoinen  KHu  GLee  DHKaprio  JTuomilehto  J Coffee consumption, serum gamma-glutamyltransferase and risk of type II diabetes. Eur J Clin Nutr 2008;62 (2) 178- 185
PubMed Link to Article
Fuhrman  BJSmit  ECrespo  CGarcia-Palmieri  M Coffee intake and risk of incident diabetes in Puerto Rican men: results from the Puerto Rico Heart Health Program. Public Health Nutr 2009;12 (6) 842- 848
PubMed Link to Article
Greenberg  JAAxen  KVSchnoll  RBoozer  CN Coffee, tea and diabetes: the role of weight loss and caffeine. Int J Obes (Lond) 2005;29 (9) 1121- 1129
PubMed Link to Article
Hamer  MWitte  DRMosdol  AMarmot  MGBrunner  EJ Prospective study of coffee and tea consumption in relation to risk of type 2 diabetes mellitus among men and women: the Whitehall II study. Br J Nutr 2008;100 (5) 1046- 1053
PubMed Link to Article
Hu  GJousilahti  PPeltonen  MBidel  STuomilehto  J Joint association of coffee consumption and other factors to the risk of type 2 diabetes: a prospective study in Finland. Int J Obes (Lond) 2006;30 (12) 1742- 1749
PubMed Link to Article
Iso  HDate  CWakai  KFukui  MTamakoshi  AJACC Study Group, The relationship between green tea and total caffeine intake and risk for self-reported type 2 diabetes among Japanese adults. Ann Intern Med 2006;144 (8) 554- 562
PubMed Link to Article
Odegaard  AOPereira  MAKoh  WPArakawa  KLee  HPYu  MC Coffee, tea, and incident type 2 diabetes: the Singapore Chinese Health Study. Am J Clin Nutr 2008;88 (4) 979- 985
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Paynter  NPYeh  H-CVoutilainen  S  et al.  Coffee and sweetened beverage consumption and the risk of type 2 diabetes mellitus: the atherosclerosis risk in communities study. Am J Epidemiol 2006;164 (11) 1075- 1084
PubMed Link to Article
Pereira  MAParker  EDFolsom  AR Coffee consumption and risk of type 2 diabetes mellitus: an 11-year prospective study of 28 812 postmenopausal women. Arch Intern Med 2006;166 (12) 1311- 1316
PubMed Link to Article
Smith  BWingard  DLSmith  TCKritz-Silverstein  DBarrett-Connor  E Does coffee consumption reduce the risk of type 2 diabetes in individuals with impaired glucose? Diabetes Care 2006;29 (11) 2385- 2390
PubMed Link to Article
van Dam  RMWillett  WCManson  JEHu  FB Coffee, caffeine, and risk of type 2 diabetes: a prospective cohort study in younger and middle-aged U.S. women. Diabetes Care 2006;29 (2) 398- 403
PubMed Link to Article
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Orsini  NBellocco  RGreenland  S Generalized least squares for trend estimation of summarized dose-response data. Stata J 2006;6 (1) 40- 57
Woodward  M Epidemiology: Study Design and Data Analysis. 2nd ed. Boca Raton, FL Chapman & Hall/CRC2005;
Higgins  JPThompson  SGDeeks  JJAltman  DG Measuring inconsistency in meta-analyses. BMJ 2003;327 (7414) 557- 560
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Higgins  JPThompson  SG Quantifying heterogeneity in a meta-analysis. Stat Med 2002;21 (11) 1539- 1558
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Egger  MDavey Smith  GSchneider  MMinder  C Bias in meta-analysis detected by a simple, graphical test. BMJ 1997;315 (7109) 629- 634
PubMed Link to Article
Carlsson  SHammar  NGrill  VKaprio  J Coffee consumption and risk of type 2 diabetes in Finnish twins. Int J Epidemiol 2004;33 (3) 616- 617
PubMed Link to Article
Reunanen  AHeliovaara  MAho  K Coffee consumption and risk of type 2 diabetes mellitus. Lancet 2003;361 (9358) 702- 703
PubMed Link to Article
Rosengren  ADotevall  AWilhelmsen  LThelle  DJohansson  S Coffee and incidence of diabetes in Swedish women: a prospective 18-year follow-up study. J Intern Med 2004;255 (1) 89- 95
PubMed Link to Article
Salazar-Martinez  EWillett  WCAscherio  A  et al.  Coffee consumption and risk for type 2 diabetes mellitus. Ann Intern Med 2004;140 (1) 1- 8
PubMed Link to Article
Saremi  ATulloch-Reid  MKnowler  WC Coffee consumption and the incidence of type 2 diabetes. Diabetes Care 2003;26 (7) 2211- 2212
PubMed Link to Article
Song  YManson  JEBuring  JESesso  HDLiu  S Associations of dietary flavonoids with risk of type 2 diabetes, and markers of insulin resistance and systemic inflammation in women: a prospective study and cross-sectional analysis. J Am Coll Nutr 2005;24 (5) 376- 384
PubMed Link to Article
Tuomilehto  JHu  GBidel  SLindstrom  JJousilahti  P Coffee consumption and risk of type 2 diabetes mellitus among middle-aged Finnish men and women. JAMA 2004;291 (10) 1213- 1219
PubMed Link to Article
van Dam  RMDekker  JMNijpels  GStehouwer  CDBouter  LMHeine  RJHoorn study, Coffee consumption and incidence of impaired fasting glucose, impaired glucose tolerance, and type 2 diabetes: the Hoorn Study. Diabetologia 2004;47 (12) 2152- 2159
PubMed
van Dam  RMFeskens  EJM Coffee consumption and risk of type 2 diabetes mellitus. Lancet 2002;360 (9344) 1477- 1478
PubMed Link to Article
Kato  MNoda  MInoue  MKadowaki  TTsugane  SJPHC Study Group, Psychological factors, coffee and risk of diabetes mellitus among middle-aged Japanese: a population-based prospective study in the JPHC study cohort. Endocr J 2009;56 (3) 459- 468
PubMed Link to Article
U.S. Department of Agriculture ARS, USDA National Nutrient Database for Standard Reference Release 17. http://www.nal.usda.gov/fnic/foodcomp/Data/SR17/sr17.html. Accessed August 11, 2009
Milder  IEArts  ICvan de Putte  BVenema  DPHollman  PC Lignan contents of Dutch plant foods: a database including lariciresinol, pinoresinol, secoisolariciresinol and metairesinol. Br J Nutr 2005;93 (3) 393- 402
PubMed Link to Article
Clifford  MN Cholorogenic acids and other cinnamates: nature, occurrence and dietary burden. J Sci Food Agric 1999;79 (5) 362- 372
Link to Article
van Dam  RM Coffee and type 2 diabetes: from bean to beta-cells. Nutr Metab Cardiovasc Dis 2006;16 (1) 69- 77
PubMed Link to Article
Agardh  EECarlsson  SAhlbom  A  et al.  Coffee consumption, type 2 diabetes and impaired glucose tolerance in Swedish men and women. J Intern Med 2004;255 (6) 645- 652
PubMed Link to Article
Soriguer  FRojo-Martinez  Gde Antonio  IE Coffee consumption and type 2 diabetes mellitus. Ann Intern Med 2004;141 (4) 321- 323
PubMed Link to Article
van Dam  RMPasman  WJVerhoef  P Effects of coffee consumption on fasting blood glucose and insulin concentrations: randomized controlled trials in healthy volunteers. Diabetes Care 2004;27 (12) 2990- 2992
PubMed Link to Article
Kobayashi  YSuzuki  MSatsu  H  et al.  Green tea polyphenols inhibit the sodium-dependent glucose transporter of intestinal epithelial cells by a competitive mechanism. J Agric Food Chem 2000;48 (11) 5618- 5623
PubMed Link to Article
Waltner-Law  MEWang  XLLaw  BKHall  RKNawano  MGranner  DK Epigallocatechin gallate, a constituent of green tea, represses hepatic glucose production. J Biol Chem 2002;277 (38) 34933- 34940
PubMed Link to Article
Kao  YHChang  HHLee  MJChen  CL Tea, obesity and diabetes. Mol Nutr Food Res 2006;50 (2) 188- 210
PubMed Link to Article
Crespy  VWilliamson  G A review of the health effects of green tea catechins in in vivo animal models. J Nutr 2004;134 (12) ((suppl)) 3431S- 3440S
PubMed
Hosoda  KWang  MFLiao  ML  et al.  Antihyperglycemic effect of oolong tea in type 2 diabetes. Diabetes Care 2003;26 (6) 1714- 1718
PubMed Link to Article
Fukino  YIkeda  AMaruyama  KAoki  NOkubo  TIso  H Randomized controlled trial for an effect of green tea-extract powder supplementation on glucose abnormalities. Eur J Clin Nutr 2008;62 (8) 953- 960
PubMed Link to Article
Ryu  OHLee  JLee  KW  et al.  Effects of green tea consumption on inflammation, insulin resistance and pulse wave velocity in type 2 diabetes patients. Diabetes Res Clin Pract 2006;71 (3) 356- 358
PubMed Link to Article
Henning  SMNiu  YLee  NH  et al.  Bioavailability and antioxidant activity of tea flavanols after consumption of green tea, black tea, or a green tea extract supplement. Am J Clin Nutr 2004;80 (6) 1558- 1564
PubMed
Bassuk  SSManson  JE Epidemiological evidence for the role of physical activity in reducing risk of type 2 diabetes and cardiovascular disease. J Appl Physiol 2005;99 (3) 1193- 1204
PubMed Link to Article
Perry  IJ Commentary: smoking and diabetes; accumulating evidence of a causal link. Int J Epidemiol 2001;30 (3) 554- 555
PubMed Link to Article

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