Eur J Nutr DOI 10.1007/s00394-015-1139-z
REVIEW
Coffee consumption and the risk of cutaneous melanoma: a meta‑analysis Jia Wang1 · Xutong Li2 · Dongfeng Zhang1
Received: 20 September 2015 / Accepted: 11 December 2015 © Springer-Verlag Berlin Heidelberg 2015
Abstract Purpose Results from epidemiologic studies on coffee consumption and the risk of cutaneous melanoma are inconsistent. We conducted a meta-analysis to assess the associations between the consumption of total coffee, caffeinated coffee and decaffeinated coffee and the risk of cutaneous melanoma, respectively. Methods A literature search was performed in PubMed, Web of Science and EMBASE for relevant articles published up to August 2015. Pooled relative risks (RRs) with 95 % confidence intervals (CIs) were calculated with a random-effects model. Dose–response relationship was assessed by restricted cubic spline. Results Twelve studies involving 832,956 participants for total coffee consumption, 5 studies involving 717,151 participants for caffeinated coffee consumption and 6 studies involving 718,231 participants for decaffeinated coffee consumption were included in this meta-analysis. Compared with the lowest level of consumption, the pooled RRs were 0.80 (95 % CI 0.69–0.93, I2 = 53.5 %), 0.85 (95 % CI 0.71–1.01, I2 = 65.0 %) and 0.92 (95 % CI 0.81–1.05, I2 = 0.0 %) for the consumption of total coffee, caffeinated coffee and decaffeinated coffee, respectively. In subgroup Electronic supplementary material The online version of this article (doi:10.1007/s00394-015-1139-z) contains supplementary material, which is available to authorized users. * Dongfeng Zhang [email protected]; [email protected] 1
Department of Epidemiology and Health Statistics, The Medical College of Qingdao University, No. 38 Dengzhou Road, Qingdao 266021, China
2
Department of Oncology, Second Affiliated Hospital, The Medical College of Qingdao University, Qingdao, China
analysis by study design, the pooled RRs in cohort studies and case–control studies were 0.83 (95 % CI 0.72–0.97) and 0.74 (95 % CI 0.51–1.07) for total coffee consumption, respectively. Dose–response analysis suggested cutaneous melanoma risk decreased by 3 % [0.97 (0.93–1.00)] and 4 % [0.96 (0.92–1.01)] for 1 cup/day increment of total coffee and caffeinated coffee consumption, respectively. Conclusions This meta-analysis suggests that coffee consumption may reduce the risk of cutaneous melanoma. Keywords Coffee · Caffeinated coffee · Cutaneous melanoma · Meta-analysis
Introduction Cutaneous melanoma is a kind of malignant neoplasm derived from cells that can produce melanin. It may occur in the skin of any part of the body. It occurs mostly in adults and may be idiopathic or from a pigmented nevus or malignant lentigo. Melanomas commonly metastasize to the regional lymph nodes, liver, lungs, and brain. Over the past several decades, the incidence of cutaneous melanoma has increased faster than any other cancers in Caucasian population [1, 2]. In 2015, the estimated new cases and deaths of cutaneous melanoma will be 73,870 and 9940 in the USA, respectively [3]. Solar ultraviolet (UV) radiation and the number of UV-induced sunburns have been confirmed to be the risk factors for cutaneous melanoma [4, 5], but smoking [6] and retinol intake [7] are revealed to be inversely associated with cutaneous melanoma. Coffee, as the most widely consumed beverage around the world, contains several bioactive compounds, such as caffeine, diterpenes, polyphenols, volatile aroma and heterocyclic substances [8]. Many epidemiological studies
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have revealed that coffee consumption is associated with reduced risks of cancers, such as prostate cancer [9], endometrial cancer [10], colorectal cancer [11] and liver cancer [12]. However, the relationship between coffee consumption and the risk of cutaneous melanoma still remains controversial [13–21]. One prospective study [15] reported that coffee consumption could reduce the risk of cutaneous melanoma. However, two other prospective studies [17, 20] showed no significant association between coffee consumption and the risk of cutaneous melanoma. Metaanalysis refers to the statistical analysis of a large collection of analysis results from individual studies for the purpose of integrating the findings. By combining results from relevant studies, meta-analysis can obtain more precise estimate [22]. Results from a meta-analysis by Yew et al. [23] indicated that regular coffee consumption could decrease the risk of cutaneous melanoma and decaffeinated coffee consumption had no effect on cutaneous melanoma. In their meta-analysis, the association between caffeinated coffee consumption and the risk of cutaneous melanoma was not analyzed separately, and dose–response analysis was not adopted to explore the relationship between coffee consumption and the risk of cutaneous melanoma quantitatively. Therefore, we systematically conducted a meta-analysis to: (1) further explore the effect of coffee consumption on the risk of cutaneous melanoma, including total coffee, caffeinated coffee and decaffeinated coffee and (2) evaluate the possible dose–response relationships of the consumption of total coffee and caffeinated coffee and the risk of cutaneous melanoma.
Eur J Nutr
multivariate-adjusted relative risk (RR) with 95 % confidence interval (CI) was provided; (5) the most recent and complete study was selected if data from the same population had been published more than once. Two investigators searched and reviewed all identified studies independently. If the two investigators disagreed about the eligibility of an article, it was resolved by debating with a third reviewer. Data extraction and quality assessment
Materials and methods
The following information was extracted from each study by two investigators independently: the first author’s name, publication year, country where the study was conducted, study design, follow-up duration, age range or mean age at baseline, sample size and number of cases, the type of coffee, RR (we presented all results as RR for simplicity) with 95 % CI for the highest versus lowest category of the consumption of total coffee, caffeinated coffee and decaffeinated coffee and adjustment for potential confounders. For dose–response analysis, the number of cases and participants or person-years, and RR (95 % CI) for each category of total coffee and caffeinated coffee were extracted. The median or mean level of total coffee and caffeinated coffee for each category was assigned to the corresponding RR for every study. If the upper boundary of the highest category was not provided, we supposed that the boundary had the same amplitude as the contiguous category [24]. We extracted RRs adjusted for the most confounders in the original studies. The study quality was assessed using the NewcastleOttawa quality assessment scale (http://www.ohri.ca/programs/clinical_epidemiology/oxford.asp).
Literature search strategy
Statistical analysis
We conducted a literature search to identify relevant available articles from PubMed (from 1950), Web of Science (from 1950) and EMBASE (from 1974) up to August 2015 without any restrictions (including language restriction and study design etc.). Search terms included “coffee” (or “caffeinated coffee” or “decaffeinated coffee” or “beverage” or “drink”) and “cutaneous melanoma” (or “melanoma” or “skin cancer” or “skin neoplasm”). We also reviewed the reference lists of the included studies for undetected relevant studies.
Pooled measure was calculated as the inverse varianceweighted mean of the logarithm of RR with 95 % CI to assess the strength of associations between the consumption of total coffee, caffeinated coffee and decaffeinated coffee and the risk of cutaneous melanoma, respectively. The DerSimonian and Laird random effect model (REM) was used to combine study-specific RRs (95 % CIs) [25]. The I2 was adopted to describe the proportion of total variation in study estimates that is due to heterogeneity rather than chance [26]. I2 lies between 0 % and 100 %, and I2 values of 25, 50 and 75 % represent low, moderate and high heterogeneity, respectively [27]. Meta-regression with restricted maximum likelihood estimation was performed to explore the potentially important covariates that might exert substantial impacts on between-study heterogeneity [28]. Subgroup analysis was performed by study design and continent where the studies were conducted.
Inclusion criteria The inclusion criteria were as follows: (1) original research from observational studies; (2) the exposure of interest was total coffee, caffeinated coffee or decaffeinated coffee; (3) the outcome of interest was cutaneous melanoma; (4)
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If the between-study heterogeneity could not be explained by meta-regression and subgroup analysis, the leave-oneout sensitivity analysis [29] was performed to evaluate the key studies that have important impacts on between-study heterogeneity. Influence analysis was performed with one study removed at a time to assess whether the results could have been affected markedly by a single study [30]. Smallstudy effect was assessed with visual inspection of the funnel plot and Egger’s test [31]. For dose–response analysis, a two-stage random-effects dose–response meta-analysis [32] was performed to compute the trend from the correlated log RR estimates across levels of total coffee and caffeinated coffee, respectively. In the first stage, a restricted cubic spline model with three knots at the 10th, 50th and 90th percentiles [33] of the levels of total coffee and caffeinated coffee was estimated using generalized least-square regression, taking into account the correlation within each set of published RRs [34]. Then the study-specific estimates were combined using the restricted maximum likelihood method in a multivariate random-effects meta-analysis [35]. A P value for
nonlinearity was calculated by testing the null hypothesis that the coefficient of the second spline is equal to 0. All statistical analyses were performed with STATA version 12.0 (Stata Corporation, College Station, TX, USA). All reported probabilities (P values) were two-sided with P 1). However, in other cohorts involving female or both genders combined, the RR estimates were smaller than 1 (RR 7 times/week, respectively. But in other studies included in this meta-analysis, the coffee consumption was divided into at least three categories, and the levels of the lowest and highest consumption ranged from 0 to ≤2 cups/day and >2 cups/day to ≥7 cups/day, respectively. The different category of coffee consumption may contribute to the between-study heterogeneity. After excluding the two studies [13, 21], no heterogeneity was left, and the inverse association did not change substantially, suggesting that the result was stable. This is a meta-analysis with dose–response analysis to explore the associations between the consumption of total coffee, caffeinated coffee and decaffeinated coffee and the risk of cutaneous melanoma. The strength of this metaanalysis includes the large number of participants included, increasing the statistical power of the study to detect this modest decrease in risk of cutaneous melanoma. Second, RRs that reflected the greatest degree of control for potential confounders were extracted, indicating that the results were more credible. Third, a significantly inverse association was found in cohort studies, implying a potential causal relationship between total coffee consumption and the risk of cutaneous melanoma. Forth, after excluding two studies that had strong impacts on between-study heterogeneity for total coffee consumption, the betweenstudy heterogeneity reduced to 0.0 %, and the result did not
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change substantially, suggesting that the result was stable. Fifth, dose–response analyses were conducted to explore the relationships between the consumption of total coffee and caffeinated coffee and the risk of cutaneous melanoma quantitatively. However, there are some limitations in this meta-analysis. First, although major confounders had been adjusted for in the included studies, other unknown confounders might result in exaggerated or underestimated association. And confounders adjusted for in each study were different, which might affect the observed association. As a metaanalysis of observational studies, misclassification of coffee consumption could be of concern. In addition, residual confounding owing to measurement error in the assessment of confounding factors or unmeasured confounding should be considered. Thus the results from this meta-analysis should be interpreted with caution. Second, although coffee consumption was measured in a cups/day scale in included studies except for two [13, 17], the variation of cup size may have an impact on the observed association. Third, we did not get statistically significant associations between the consumption of caffeinated coffee and decaffeinated coffee and the risk of cutaneous melanoma. This might be caused by the relatively small number of studies and cases that reduced the statistical power to detect statistically significant associations. Forth, the production and preparation methods of coffee vary across the geographical region. Coffee can be divided into several types by different preparation methods, such as Scandinavian boiled coffee, Turkish/Greek coffee, French press coffee, Espresso coffee, Mocha coffee, Percolated coffee and Drip-filtered coffee, etc. [46]. The different preparation methods can change the content of diterpenes in coffee. Oil droplets containing diterpenes are released from ground coffee beans by brewing. In paper-filtered coffee, diterpenes are retained by a paper filter largely during filtering [47]. But other brews, such as Scandinavian boiled coffee and Middle Eastern coffee types, are decanted directly from the boiling state into the cup without applying a filter at all [48]. A study [46] indicates that the mean concentrations of diterpenes in boiled coffee and French press coffee range from 3 to 4 mg per cup. However, the levels of diterpenes in filtered coffee are very low. And the levels of diterpenes in boiled coffee are about twice as high as in Italian espresso [46]. In addition, limited data showed no association between decaffeinated coffee consumption and the risk of cutaneous melanoma in this meta-analysis, indicating that production method can also be of concern in assessing the coffee-cutaneous melanoma association. However, only one [17] of the included studies had considered the effect of different brewing methods, which prevent us from further exploration. In conclusion, this meta-analysis suggested that coffee consumption may reduce the risk of cutaneous melanoma,
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and cutaneous melanoma risk decreased by 3 % for 1 cup/ day increment of total coffee consumption. Compliance with ethical standards Conflict of interest On behalf of all authors, the corresponding author states that there is no conflict of interest.
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Eur J Nutr Research in D (2004) Risk of melanoma and vitamin A, coffee and alcohol: a case–control study from Italy. Eur J Cancer Prev 13(6):503–508 17. Nilsson LM, Johansson I, Lenner P, Lindahl B, Van Guelpen B (2010) Consumption of filtered and boiled coffee and the risk of incident cancer: a prospective cohort study. Cancer Causes Control 21(10):1533–1544. doi:10.1007/s10552-010-9582-x 18. Osterlind A, Tucker MA, Stone BJ, Jensen OM (1988) The Danish case–control study of cutaneous malignant melanoma. IV. No association with nutritional factors, alcohol, smoking or hair dyes. Int J Cancer 42(6):825–828 19. Veierod MB, Thelle DS, Laake P (1997) Diet and risk of cutaneous malignant melanoma: a prospective study of 50,757 Norwegian men and women. Int J Cancer 71(4):600–604 20. Wu H, Reeves KW, Qian J, Sturgeon SR (2015) Coffee, tea, and melanoma risk among postmenopausal women. Eur J Cancer Prev 24(4):347–352. doi:10.1097/CEJ.0000000000000093 21. Wu S, Han J, Song F, Cho E, Gao X, Hunter DJ, Qureshi AA (2015) Caffeine intake, coffee consumption, and risk of cutaneous malignant melanoma. Epidemiology. doi:10.1097/ EDE.0000000000000360 22. Glass GV (1976) Primary, secondary, and meta-analysis of research. Educ Res 5:3–8 23. Yew YW, Lai YC, Schwartz RA (2015) Coffee consump tion and melanoma: a systematic review and meta-analysis of observational studies. Am J Clin Dermatol. doi:10.1007/ s40257-015-0165-1 24. Larsson SC, Orsini N (2011) Coffee consumption and risk of stroke: a dose-response meta-analysis of prospective studies. Am J Epidemiol 174(9):993–1001. doi:10.1093/aje/kwr226 25. DerSimonian R, Laird N (1986) Meta-analysis in clinical trials. Control Clin Trials 7(3):177–188 26. Higgins JP, Thompson SG (2002) Quantifying heterogeneity in a meta-analysis. Stat Med 21(11):1539–1558. doi:10.1002/ sim.1186 27. Higgins JP, Thompson SG, Deeks JJ, Altman DG (2003) Measuring inconsistency in meta-analyses. BMJ 327(7414):557–560. doi:10.1136/bmj.327.7414.557 28. Higgins JP, Thompson SG (2004) Controlling the risk of spurious findings from meta-regression. Stat Med 23(11):1663–1682. doi:10.1002/sim.1752 29. Patsopoulos NA, Evangelou E, Ioannidis JP (2008) Sensitivity of between-study heterogeneity in meta-analysis: proposed metrics and empirical evaluation. Int J Epidemiol 37(5):1148–1157. doi:10.1093/ije/dyn065 30. Tobias A (1999) Assessing the influence of a single study in the meta-analysis estimate. Stata Tech Bull 47:15–17 31. Egger M, Davey Smith G, Schneider M, Minder C (1997) Bias in meta-analysis detected by a simple, graphical test. BMJ 315(7109):629–634 32. Orsini N, Li R, Wolk A, Khudyakov P, Spiegelman D (2012) Meta-analysis for linear and nonlinear dose-response relations: examples, an evaluation of approximations, and software. Am J Epidemiol 175(1):66–73. doi:10.1093/aje/kwr265 33. Harrell FE Jr, Lee KL, Pollock BG (1988) Regression models in clinical studies: determining relationships between predictors and response. J Natl Cancer Inst 80(15):1198–1202 34. Orsini N, Bellocco R (2006) Generalized least squares for trend estimation of summarized dose–response data. Stata J 6:40–57
35. Jackson D, White IR, Thompson SG (2010) Extending DerSimonian and Laird’s methodology to perform multivariate random effects meta-analyses. Stat Med 29(12):1282–1297. doi:10.1002/ sim.3602 36. Lu YP, Lou YR, Peng QY, Xie JG, Conney AH (2004) Stimulatory effect of topical application of caffeine on UVB-induced apoptosis in the epidermis of p53 and Bax knockout mice. Cancer Res 64(14):5020–5027. doi:10.1158/0008-5472. CAN-04-0760 37. Lu YP, Lou YR, Xie JG, Peng QY, Zhou S, Lin Y, Shih WJ, Conney AH (2007) Caffeine and caffeine sodium benzoate have a sunscreen effect, enhance UVB-induced apoptosis, and inhibit UVB-induced skin carcinogenesis in SKH-1 mice. Carcinogenesis 28(1):199–206. doi:10.1093/carcin/bgl112 38. Gude RP, Menon LG, Rao SG (2001) Effect of Caffeine, a xanthine derivative, in the inhibition of experimental lung metastasis induced by B16F10 melanoma cells. J Exp Clin Cancer Res 20(2):287–292 39. Tsuchiya H, Tomita K, Yasutake H, Ueda Y, Tanaka M, Sasaki T (1989) Growth inhibition and differentiation of murine melanoma B16-BL6 cells caused by the combination of cisplatin and caffeine. Jpn J Cancer Res 80(12):1246–1251 40. Denkert C, Kobel M, Berger S, Siegert A, Leclere A, Trefzer U, Hauptmann S (2001) Expression of cyclooxygenase 2 in human malignant melanoma. Cancer Res 61(1):303–308 41. Goulet AC, Einsphar JG, Alberts DS, Beas A, Burk C, Bhattacharyya A, Bangert J, Harmon JM, Fujiwara H, Koki A, Nelson MA (2003) Analysis of cyclooxygenase 2 (COX-2) expression during malignant melanoma progression. Cancer Biol Ther 2(6):713–718 42. Kang NJ, Lee KW, Shin BJ, Jung SK, Hwang MK, Bode AM, Heo YS, Lee HJ, Dong Z (2009) Caffeic acid, a phenolic phytochemical in coffee, directly inhibits Fyn kinase activity and UVB-induced COX-2 expression. Carcinogenesis 30(2):321– 330. doi:10.1093/carcin/bgn282 43. Lee KA, Chae JI, Shim JH (2012) Natural diterpenes from coffee, cafestol and kahweol induce apoptosis through regulation of specificity protein 1 expression in human malignant pleural mesothelioma. J Biomed Sci 19:60. doi:10.1186/1423-0127-19-60 44. Lee KJ, Jeong HG (2007) Protective effects of kahweol and cafestol against hydrogen peroxide-induced oxidative stress and DNA damage. Toxicol Lett 173(2):80–87. doi:10.1016/j. toxlet.2007.06.008 45. Munafo MR, Flint J (2004) Meta-analysis of genetic asso ciation studies. Trends Genet 20(9):439–444. doi:10.1016/j. tig.2004.06.014 46. Urgert R, van der Weg G, Kosmeijer-Schuil TG, van de Bovenkamp P, Hovenier R, Katan MB (1995) Levels of the cholesterolelevating diterpenes cafestol and kahweol in various coffee brews. J Agric Food Chem 43:2167–2172 47. Ratnayake WM, Hollywood R, O’Grady E, Stavric B (1993) Lipid content and composition of coffee brews prepared by different methods. Food Chem Toxicol 31(4):263–269 48. IARC Working Group (1991) Coffee, tea, mate, methylxanthines and methylglyoxal. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Lyon, 27 February to 6 March 1990. IARC Monogr Eval Carcinog Risks Hum 51:1–513
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REVIEW
Coffee consumption and the risk of cutaneous melanoma: a meta‑analysis Jia Wang1 · Xutong Li2 · Dongfeng Zhang1
Received: 20 September 2015 / Accepted: 11 December 2015 © Springer-Verlag Berlin Heidelberg 2015
Abstract Purpose Results from epidemiologic studies on coffee consumption and the risk of cutaneous melanoma are inconsistent. We conducted a meta-analysis to assess the associations between the consumption of total coffee, caffeinated coffee and decaffeinated coffee and the risk of cutaneous melanoma, respectively. Methods A literature search was performed in PubMed, Web of Science and EMBASE for relevant articles published up to August 2015. Pooled relative risks (RRs) with 95 % confidence intervals (CIs) were calculated with a random-effects model. Dose–response relationship was assessed by restricted cubic spline. Results Twelve studies involving 832,956 participants for total coffee consumption, 5 studies involving 717,151 participants for caffeinated coffee consumption and 6 studies involving 718,231 participants for decaffeinated coffee consumption were included in this meta-analysis. Compared with the lowest level of consumption, the pooled RRs were 0.80 (95 % CI 0.69–0.93, I2 = 53.5 %), 0.85 (95 % CI 0.71–1.01, I2 = 65.0 %) and 0.92 (95 % CI 0.81–1.05, I2 = 0.0 %) for the consumption of total coffee, caffeinated coffee and decaffeinated coffee, respectively. In subgroup Electronic supplementary material The online version of this article (doi:10.1007/s00394-015-1139-z) contains supplementary material, which is available to authorized users. * Dongfeng Zhang [email protected]; [email protected] 1
Department of Epidemiology and Health Statistics, The Medical College of Qingdao University, No. 38 Dengzhou Road, Qingdao 266021, China
2
Department of Oncology, Second Affiliated Hospital, The Medical College of Qingdao University, Qingdao, China
analysis by study design, the pooled RRs in cohort studies and case–control studies were 0.83 (95 % CI 0.72–0.97) and 0.74 (95 % CI 0.51–1.07) for total coffee consumption, respectively. Dose–response analysis suggested cutaneous melanoma risk decreased by 3 % [0.97 (0.93–1.00)] and 4 % [0.96 (0.92–1.01)] for 1 cup/day increment of total coffee and caffeinated coffee consumption, respectively. Conclusions This meta-analysis suggests that coffee consumption may reduce the risk of cutaneous melanoma. Keywords Coffee · Caffeinated coffee · Cutaneous melanoma · Meta-analysis
Introduction Cutaneous melanoma is a kind of malignant neoplasm derived from cells that can produce melanin. It may occur in the skin of any part of the body. It occurs mostly in adults and may be idiopathic or from a pigmented nevus or malignant lentigo. Melanomas commonly metastasize to the regional lymph nodes, liver, lungs, and brain. Over the past several decades, the incidence of cutaneous melanoma has increased faster than any other cancers in Caucasian population [1, 2]. In 2015, the estimated new cases and deaths of cutaneous melanoma will be 73,870 and 9940 in the USA, respectively [3]. Solar ultraviolet (UV) radiation and the number of UV-induced sunburns have been confirmed to be the risk factors for cutaneous melanoma [4, 5], but smoking [6] and retinol intake [7] are revealed to be inversely associated with cutaneous melanoma. Coffee, as the most widely consumed beverage around the world, contains several bioactive compounds, such as caffeine, diterpenes, polyphenols, volatile aroma and heterocyclic substances [8]. Many epidemiological studies
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have revealed that coffee consumption is associated with reduced risks of cancers, such as prostate cancer [9], endometrial cancer [10], colorectal cancer [11] and liver cancer [12]. However, the relationship between coffee consumption and the risk of cutaneous melanoma still remains controversial [13–21]. One prospective study [15] reported that coffee consumption could reduce the risk of cutaneous melanoma. However, two other prospective studies [17, 20] showed no significant association between coffee consumption and the risk of cutaneous melanoma. Metaanalysis refers to the statistical analysis of a large collection of analysis results from individual studies for the purpose of integrating the findings. By combining results from relevant studies, meta-analysis can obtain more precise estimate [22]. Results from a meta-analysis by Yew et al. [23] indicated that regular coffee consumption could decrease the risk of cutaneous melanoma and decaffeinated coffee consumption had no effect on cutaneous melanoma. In their meta-analysis, the association between caffeinated coffee consumption and the risk of cutaneous melanoma was not analyzed separately, and dose–response analysis was not adopted to explore the relationship between coffee consumption and the risk of cutaneous melanoma quantitatively. Therefore, we systematically conducted a meta-analysis to: (1) further explore the effect of coffee consumption on the risk of cutaneous melanoma, including total coffee, caffeinated coffee and decaffeinated coffee and (2) evaluate the possible dose–response relationships of the consumption of total coffee and caffeinated coffee and the risk of cutaneous melanoma.
Eur J Nutr
multivariate-adjusted relative risk (RR) with 95 % confidence interval (CI) was provided; (5) the most recent and complete study was selected if data from the same population had been published more than once. Two investigators searched and reviewed all identified studies independently. If the two investigators disagreed about the eligibility of an article, it was resolved by debating with a third reviewer. Data extraction and quality assessment
Materials and methods
The following information was extracted from each study by two investigators independently: the first author’s name, publication year, country where the study was conducted, study design, follow-up duration, age range or mean age at baseline, sample size and number of cases, the type of coffee, RR (we presented all results as RR for simplicity) with 95 % CI for the highest versus lowest category of the consumption of total coffee, caffeinated coffee and decaffeinated coffee and adjustment for potential confounders. For dose–response analysis, the number of cases and participants or person-years, and RR (95 % CI) for each category of total coffee and caffeinated coffee were extracted. The median or mean level of total coffee and caffeinated coffee for each category was assigned to the corresponding RR for every study. If the upper boundary of the highest category was not provided, we supposed that the boundary had the same amplitude as the contiguous category [24]. We extracted RRs adjusted for the most confounders in the original studies. The study quality was assessed using the NewcastleOttawa quality assessment scale (http://www.ohri.ca/programs/clinical_epidemiology/oxford.asp).
Literature search strategy
Statistical analysis
We conducted a literature search to identify relevant available articles from PubMed (from 1950), Web of Science (from 1950) and EMBASE (from 1974) up to August 2015 without any restrictions (including language restriction and study design etc.). Search terms included “coffee” (or “caffeinated coffee” or “decaffeinated coffee” or “beverage” or “drink”) and “cutaneous melanoma” (or “melanoma” or “skin cancer” or “skin neoplasm”). We also reviewed the reference lists of the included studies for undetected relevant studies.
Pooled measure was calculated as the inverse varianceweighted mean of the logarithm of RR with 95 % CI to assess the strength of associations between the consumption of total coffee, caffeinated coffee and decaffeinated coffee and the risk of cutaneous melanoma, respectively. The DerSimonian and Laird random effect model (REM) was used to combine study-specific RRs (95 % CIs) [25]. The I2 was adopted to describe the proportion of total variation in study estimates that is due to heterogeneity rather than chance [26]. I2 lies between 0 % and 100 %, and I2 values of 25, 50 and 75 % represent low, moderate and high heterogeneity, respectively [27]. Meta-regression with restricted maximum likelihood estimation was performed to explore the potentially important covariates that might exert substantial impacts on between-study heterogeneity [28]. Subgroup analysis was performed by study design and continent where the studies were conducted.
Inclusion criteria The inclusion criteria were as follows: (1) original research from observational studies; (2) the exposure of interest was total coffee, caffeinated coffee or decaffeinated coffee; (3) the outcome of interest was cutaneous melanoma; (4)
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If the between-study heterogeneity could not be explained by meta-regression and subgroup analysis, the leave-oneout sensitivity analysis [29] was performed to evaluate the key studies that have important impacts on between-study heterogeneity. Influence analysis was performed with one study removed at a time to assess whether the results could have been affected markedly by a single study [30]. Smallstudy effect was assessed with visual inspection of the funnel plot and Egger’s test [31]. For dose–response analysis, a two-stage random-effects dose–response meta-analysis [32] was performed to compute the trend from the correlated log RR estimates across levels of total coffee and caffeinated coffee, respectively. In the first stage, a restricted cubic spline model with three knots at the 10th, 50th and 90th percentiles [33] of the levels of total coffee and caffeinated coffee was estimated using generalized least-square regression, taking into account the correlation within each set of published RRs [34]. Then the study-specific estimates were combined using the restricted maximum likelihood method in a multivariate random-effects meta-analysis [35]. A P value for
nonlinearity was calculated by testing the null hypothesis that the coefficient of the second spline is equal to 0. All statistical analyses were performed with STATA version 12.0 (Stata Corporation, College Station, TX, USA). All reported probabilities (P values) were two-sided with P 1). However, in other cohorts involving female or both genders combined, the RR estimates were smaller than 1 (RR 7 times/week, respectively. But in other studies included in this meta-analysis, the coffee consumption was divided into at least three categories, and the levels of the lowest and highest consumption ranged from 0 to ≤2 cups/day and >2 cups/day to ≥7 cups/day, respectively. The different category of coffee consumption may contribute to the between-study heterogeneity. After excluding the two studies [13, 21], no heterogeneity was left, and the inverse association did not change substantially, suggesting that the result was stable. This is a meta-analysis with dose–response analysis to explore the associations between the consumption of total coffee, caffeinated coffee and decaffeinated coffee and the risk of cutaneous melanoma. The strength of this metaanalysis includes the large number of participants included, increasing the statistical power of the study to detect this modest decrease in risk of cutaneous melanoma. Second, RRs that reflected the greatest degree of control for potential confounders were extracted, indicating that the results were more credible. Third, a significantly inverse association was found in cohort studies, implying a potential causal relationship between total coffee consumption and the risk of cutaneous melanoma. Forth, after excluding two studies that had strong impacts on between-study heterogeneity for total coffee consumption, the betweenstudy heterogeneity reduced to 0.0 %, and the result did not
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change substantially, suggesting that the result was stable. Fifth, dose–response analyses were conducted to explore the relationships between the consumption of total coffee and caffeinated coffee and the risk of cutaneous melanoma quantitatively. However, there are some limitations in this meta-analysis. First, although major confounders had been adjusted for in the included studies, other unknown confounders might result in exaggerated or underestimated association. And confounders adjusted for in each study were different, which might affect the observed association. As a metaanalysis of observational studies, misclassification of coffee consumption could be of concern. In addition, residual confounding owing to measurement error in the assessment of confounding factors or unmeasured confounding should be considered. Thus the results from this meta-analysis should be interpreted with caution. Second, although coffee consumption was measured in a cups/day scale in included studies except for two [13, 17], the variation of cup size may have an impact on the observed association. Third, we did not get statistically significant associations between the consumption of caffeinated coffee and decaffeinated coffee and the risk of cutaneous melanoma. This might be caused by the relatively small number of studies and cases that reduced the statistical power to detect statistically significant associations. Forth, the production and preparation methods of coffee vary across the geographical region. Coffee can be divided into several types by different preparation methods, such as Scandinavian boiled coffee, Turkish/Greek coffee, French press coffee, Espresso coffee, Mocha coffee, Percolated coffee and Drip-filtered coffee, etc. [46]. The different preparation methods can change the content of diterpenes in coffee. Oil droplets containing diterpenes are released from ground coffee beans by brewing. In paper-filtered coffee, diterpenes are retained by a paper filter largely during filtering [47]. But other brews, such as Scandinavian boiled coffee and Middle Eastern coffee types, are decanted directly from the boiling state into the cup without applying a filter at all [48]. A study [46] indicates that the mean concentrations of diterpenes in boiled coffee and French press coffee range from 3 to 4 mg per cup. However, the levels of diterpenes in filtered coffee are very low. And the levels of diterpenes in boiled coffee are about twice as high as in Italian espresso [46]. In addition, limited data showed no association between decaffeinated coffee consumption and the risk of cutaneous melanoma in this meta-analysis, indicating that production method can also be of concern in assessing the coffee-cutaneous melanoma association. However, only one [17] of the included studies had considered the effect of different brewing methods, which prevent us from further exploration. In conclusion, this meta-analysis suggested that coffee consumption may reduce the risk of cutaneous melanoma,
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and cutaneous melanoma risk decreased by 3 % for 1 cup/ day increment of total coffee consumption. Compliance with ethical standards Conflict of interest On behalf of all authors, the corresponding author states that there is no conflict of interest.
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