Reply to GC Chen et al

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Oct 24, 2018 - Reply to G-C Chen et al. Dear Editor: We appreciate Chen et al.'s comments on our meta-analysis (1) with regard to protein intakes and the risk ...
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LETTERS TO THE EDITOR

doi: 10.3945/ajcn.116.147470.

Reply to G-C Chen et al. Dear Editor: We appreciate Chen et al.’s comments on our meta-analysis (1) with regard to protein intakes and the risk of diabetes. We agree that some cases from the Dutch and Swedish cohorts of the European Prospective Investigation into Cancer and Nutrition (EPIC) study overlapped with those from the EPIC-InterAct case-cohort study (2–4). However, the total number of diabetes cases from the Dutch and Swedish cohort studies was larger than reported for these 2 countries in the EPICInterAct study, likely because EPIC-InterAct excluded participants without suitable blood samples (2–5). Given the disparities in diabetes cases, we included all 3 studies in the meta-analysis. In addition, we conducted a sensitivity analysis to determine pooled estimates for the remaining studies after the Swedish and Netherlands EPIC cohorts were removed, and the pooled RR was 1.08 (95% CI: 1.05, 1.11), which was similar to the overall result (RR: 1.09; 95% CI: 1.06, 1.13). We also agree that expressing protein intake as a continuous variable in the Women’s Health Initiative increased the weight of this study in the meta-analysis relative to other studies that analyzed protein intake as quantiles. As per several previous meta-analyses that included studies with exposure expressed as both continuous and categorical variables (6, 7), we chose to include the Women’s Health Initiative in our meta-analysis. Nevertheless, as shown in our Supplemental Table 4, the pooled RR for total protein intake and incident diabetes for the remaining studies after removing the Women’s Health Initiative was 1.12 (95% CI: 1.05, 1.18), which is consistent with the primary results (RR: 1.09; 95% CI: 1.06, 1.13) reported in our study. Chen et al. found a nonlinear relation between animal protein intake and incident diabetes, and this relation was independent of BMI, although additional adjustment for BMI attenuated this association. Animal protein intake (energy-adjusted) was expressed in grams per day in 2 studies included in their meta-analysis, and they converted this value to percentage of energy intake from animal protein so as to perform meta-analysis of the dose-response relation between each 5% of energy intake from animal protein and incident diabetes (4, 8). However, this conversion is questionable, because protein intake was calculated as a relative energyadjusted value where energy is kept constant. Another finding of great interest was that below an animal protein intake of 12% of total energy there was no significant association between animal protein intake and

diabetes. This may reflect the fact that individuals with lower animal protein intakes also consumed more plant protein because we observed a high inverse correlation between animal and plant protein intake in the Melbourne Collaborative Cohort Study (9). Of the studies included in the meta-analysis, plant protein intake was not adjusted for in 2 studies when analyzing the association between animal protein intake and incident diabetes (4, 8). Although this might have biased the association between animal protein intake and incident diabetes, it is reasonable to conclude that higher animal protein intake was associated with higher risk of diabetes. In brief, Chen et al. added some interesting new analyses to our analysis, and the overall conclusions are consistent. The authors did not report any potential conflicts of interest relevant to this letter.

Xianwen Shang David Scott Allison M Hodge Graham G Giles Peter R Ebeling Kerrie M Sanders From the Faculty of Medicine, Dentistry and Health Sciences, Melbourne Medical School-Western Campus (XS, e-mail: [email protected]), Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, Melbourne, Australia (AMH, GGG); Department of Medicine, School of Clinical Sciences at Monash Health, Monash University, Melbourne, Australia (DS, PRE); and Institute for Health and Ageing, Australian Catholic University, Melbourne, Australia (KMS).

REFERENCES 1. Shang X, Scott D, Hodge AM, English DR, Giles GG, Ebeling PR, Sanders KM. Dietary protein intake and risk of type 2 diabetes: results from the Melbourne Collaborative Cohort Study and a meta-analysis of prospective studies. Am J Clin Nutr 2016;104:1352–65. 2. Sluijs I, Beulens JW, van der AD, Spijkerman AM, Grobbee DE, van der Schouw YT. Dietary intake of total, animal, and vegetable protein and risk of type 2 diabetes in the European Prospective Investigation into Cancer and Nutrition (EPIC)-NL study. Diabetes Care 2010;33:43–8. 3. Ericson U, Sonestedt E, Gullberg B, Hellstrand S, Hindy G, Wirfalt E, Orho-Melander M. High intakes of protein and processed meat associate with increased incidence of type 2 diabetes. Br J Nutr 2013;109:1143–53. 4. van Nielen M, Feskens EJ, Mensink M, Sluijs I, Molina E, Amiano P, Ardanaz E, Balkau B, Beulens JW, Boeing H, , et al. Dietary protein intake and incidence of type 2 diabetes in Europe: the EPIC-InterAct case-cohort study. Diabetes Care 2014;37:1854–62. 5. Langenberg C, Sharp S, Forouhi NG, Franks PW, Schulze MB, Kerrison N, Ekelund U, Barroso I, Panico S, Tormo MJ, et al. Design and cohort description of the InterAct project: an examination of the interaction of genetic and lifestyle factors on the incidence of type 2 diabetes in the EPIC study. Diabetologia 2011;54:2272–82. 6. Strazzullo P, D’Elia L, Kandala NB, Cappuccio FP. Salt intake, stroke, and cardiovascular disease: meta-analysis of prospective studies. BMJ 2009;339:b4567. 7. Zhang Z, Xu G, Yang F, Zhu W, Liu X. Quantitative analysis of dietary protein intake and stroke risk. Neurology 2014;83:19–25. 8. Song Y, Manson JE, Buring JE, Liu S. A prospective study of red meat consumption and type 2 diabetes in middle-aged and elderly women: the Women’s Health Study. Diabetes Care 2004;27:2108–15. 9. Shang X, Scott D, Hodge A, English DR, Giles GG, Ebeling PR, Sanders KM. Dietary protein from different food sources, incident metabolic syndrome and changes in its components: an 11-year longitudinal study in healthy community-dwelling adults. Clin Nutr 2016 Oct 1 (Epub ahead of print; DOI: 10.1016/j.clnu.2016.09.024). doi: 10.3945/ajcn.116.149468.

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5. Ock´e MC, Larranaga N, Grioni S, van den Berg SW, Ferrari P, Salvini S, Benetou V, Linseisen J, Wirfalt E, Rinaldi S, et al. Energy intake and sources of energy intake in the European Prospective Investigation into Cancer and Nutrition. Eur J Clin Nutr 2009;63(Suppl 4):S3–15. 6. Orsini N, Li R, Wolk A, Khudyakov P, Spiegelman D. Meta-analysis for linear and nonlinear dose-response relations: examples, an evaluation of approximations, and software. Am J Epidemiol 2012;175:66–73. 7. Higgins JP, Thompson SG. Quantifying heterogeneity in a meta-analysis. Stat Med 2002;21:1539–58. 8. Egger M, Davey Smith G, Schneider M, Minder C. Bias in meta-analysis detected by a simple, graphical test. BMJ 1997;315:629–34. 9. Malik VS, Li Y, Tobias DK, Pan A, Hu FB. Dietary protein intake and risk of type 2 diabetes in US men and women. Am J Epidemiol 2016; 183:715–28. 10. Nanri A, Mizoue T, Kurotani K, Goto A, Oba S, Noda M, Sawada N, Tsugane S; Japan Public Health Center-Based Prospective Study Group. Low-carbohydrate diet and type 2 diabetes risk in Japanese men and women: the Japan Public Health Center-Based Prospective Study. PLoS One 2015;10:e0118377.