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Letters to the Editor / Nutrition 31 (2015) 1055–1059
Correction of data errors and reanalysis of “The effect of glucomannan on body weight in overweight or obese children and adults: A systematic review of randomized controlled trials” To the Editor: Recently, some of us (BMZ, AC, HS) published a metaanalysis of the effect of glucomannan on body weight [1]. Others of us (PL, TS, DBA), upon reading the article, noticed that the SDs reported in Figure 2 spanned two orders of magnitude, were surprised by this, and checked the original papers. Upon doing so, we noticed discrepancies between the data in Figure 2 and the data reported in one of the original papers [2] and contacted the authors of the two papers in question [1,2]. After discussion and checking, differences were detected in the data from one of the original papers (Keithley et al.) included in the meta-analysis [2]. These inaccuracies were then corrected and the meta-analytical statistics recomputed with the corrected data, which resulted in some changes in the meta-analytical conclusions. We describe those corrections and revised results and conclusions here.
Description of the error(s) Figure 2 in the meta-analysis [1] reported the SDs for the changes of body weights from different studies. However, the reported SDs from the study by Keithley et al. [2] were incorrect. Specifically, the reported SDs in the meta-analysis [1] were 0.18 and 0.08 for the glucomannan (GM) and placebo groups after a 2-wk treatment, and 0.08 and 0.43 for the GM and placebo groups after an 8-wk treatment. These values are different from those reported in the original study [2], in which they were 0.04, 0.02, 0.06, and 0.07, respectively (see last paragraph on page 3). Rather, the SDs reported in the meta-analysis [1] were obtained from the communication between authors of
these two papers [1,2]. We found that the SDs from both papers [1,2] were incorrect. As a result, related 95% confidence intervals (CIs) for the mean difference (MD) in Figure 2 in the metaanalysis [1] were also incorrect. The correct SDs in the study by Keithley et al. [2] based on individual change scores are 1.02 and 1.34 for the GM and placebo groups, respectively, after the 2-wk treatment, and 1.91 and 1.62 for the GM and placebo groups after the 8 wk-treatment. We also found that the body mass index (BMI) values for this publication [2] were initially calculated and reported inappropriately. These were corrected after another communication between the authors and are provided here.
Revised results with the error(s) corrected Data for weight change in the GM group compared with placebo group were recomputed using correct SDs (Fig. 1). No significant differences in weight loss between groups were noted after the 2-wk treatment (MD, 0.21; 95% CI, 0.47 to 0.89), nor after the 8-wk treatment (MD, 0.03; 95% CI, 1.04 to 0.98). The effect of treatment after 2 wk that was originally reported as statistically significant in the meta-analysis published turned out to be insignificant after the correction. However, the clinical significance of the effect reported in the first place was still negligible. Corrected data for BMI change in the GM group compared with the placebo group were recomputed. Originally, no significant effect of treatment (after 2 and 8 wk) was noted. Once correction was made with the new data, there was a statistically significant difference in favor of placebo (MD, 0.27; 95% CI, 0.43 to 0.11) after 2 wk, and in line with previously reported results, no statistically significant differences in effect after 8 wk were observed (MD, 0.26; 95% CI, 0.68 to 0.16). Similar to the difference in weight loss between the study groups, BMI change seemed to have little clinical significance due to very small values despite the reported statistically significant effect.
Conclusion We were glad to have this opportunity to work together to correct these errors and hope the results are useful to the scientific community.
Fig. 1. Weight change in GM group versus placebo group after 2, 4, 5, 8, and 12 wk of intervention (data recomputed for weeks 2 and 8). Negative number indicates weight increase.
Letters to the Editor / Nutrition 31 (2015) 1055–1059
Acknowledgments Supported in part by NIH grants R25 HL124208 and P30 DK056336. The opinions expressed are those of the authors and do not necessarily represent those of the NIH or any other organization. References [1] Zalewski BM, Chmielewska A, Szajewska H. The effect of glucomannan on body weight in overweight or obese children and adults: A systematic review of randomized controlled trials. Nutrition 2015;31:437–442.e2. [2] Keithley JK, Swanson B, Mikolaitis SL, Demeo M, Zeller JM, Fogg L, et al. Safety and efficacy of glucomannan for weight loss in overweight and moderately obese adults. J Obes 2013;2013:610908.
Bart1omiej M. Zalewski, M.D. Anna Chmielewska, M.D., Ph.D. Hania Szajewska, M.D., Ph.D. Department of Pediatrics The Medical University of Warsaw, Warsaw, Poland Joyce K. Keithley, D.N.Sc. College of Nursing Rush University Medical Center, Chicago, IL Peng Li, Ph.D. TaShauna U. Goldsby, Ph.D. David B. Allison, Ph.D. Office of Energetics and Nutrition Obesity Research Center University of Alabama at Birmingham Birmingham, AL http://dx.doi.org/10.1016/j.nut.2015.02.008
Food at will after pancreaticoduodenectomies. Re. “Perioperative nutritional support of patients undergoing pancreatic surgery in the age of ERAS” To the Editor: In an article recently published in Nutrition [1], Bozzetti and Mariani challenge the recommendation to allow “food at will” following pancreaticoduodenectomies (PDs) in our recent enhanced recovery after surgery (ERAS) guidelines [2,3]. Instead, Bozzetti and Mariani suggested we adhere to the ESPEN guidelines for enteral [4] and parenteral [5] nutrition in surgical patients, dating from 2006 and 2009. Their article [1] suggests a discrepancy between the ERAS and the ESPEN guidelines. This is, in fact, an artificially created controversy because the ERAS guidelines were fully endorsed by the ESPEN Society and by the International Association for Surgical Metabolism and Nutrition (IASMEN, part of the International Surgical Society). It is for
The authors are members of the ERAS Study Group and have authored several ERAS society recommendations.
1057
this reason and because it was aimed to reach the surgical and nutritional community that it was agreed upon by the Editorsin-Chief of the World Journal of Surgery and Clinical Nutrition to publish the ERAS guidelines simultaneously in these two journals as a legitimate double publication. The endorsement by the two societies is specifically mentioned in both papers [2,3]. Several of the authors of the earlier ESPEN guidelines were also involved in the more recent ERAS guidelines. It would therefore seem that the ERAS guidelines are an updated version of the ESPEN guidelines. They focus on a more specific patient population than the earlier ESPEN guidelines, which addressed gastrointestinal surgery in general and not PDs specifically. From this perspective, the conclusions of the Bozzetti and Mariani article are not correct: The ERAS guidelines are the ESPEN guidelines. The ERAS guidelines do not involve “oral feeding” as Bozzetti and Mariani claim. Feeding is a nonvolitional and nonphysiological process. Eating is the opposite: It is a volitional, normal process that elicits physiological reflexes central to digestion and that is associated with “a host of pleasurable phenomena” [6]. Feeding involves the use of a catheter or a tube, put into a vein or the gut and with inherent risks for complications that are well documented. Feeding almost always implies use of an artificial, industrially produced solution that carries as many nutritional components and core elements as we are able to put into it. The ERAS group recommends that patients are allowed to eat normal food at will after PD, but that they are advised to begin cautiously and advance according to tolerance. We do not recommend routine pre- or postoperative artificial nutritiondimmune-enhanced or notdin uncomplicated cases. For the “standard patient,” this ERAS approach is feasible, safe, and the best practice. This does not mean the ERAS group encourages unsupervised oral intake and we do recognize that selected subgroups of PD patients will need some form of artificial nutritional support. For the first few postoperative days, the ERAS regimen will certainly provide patients with fewer calories than one would be able to infuse through a central venous catheter or a feeding jejunostomy. We believe that this is more than balanced by the positive effects of eating normal food the normal way and by the absence of catheter- or infusion-related complications [7]. It is of note that Bozzetti and Mariani do not cite a recent systematic review dedicated to this very issue [8] that concludes in full accordance with the ERAS guidelines. Also, we would like to point to the only randomized controlled trial (RCT) to compare needle catheter jejunostomies with oral intake at will in upper major abdominal surgery, with >80 PD patients showing no increase in morbidity when oral diet at will was allowed [9]. Weight loss before major surgery is very well documented as a risk factor for complications. Quite another question is whether preoperative artificial nutritional therapy will confer any effect beyond increased weight. We are not aware of any adequately designed RCT (double-blind with a valid control group by the standards of today), in major, upper abdominal cancer surgery that shows preoperative artificial feeding to lower the risk for postoperative complications in patients who are allowed food. Based on studies in traditional care, the ESPEN guidelines [4,5] give such a recommendation “Grade A” and the same is the case for immune-enhanced enteral nutrition [4]. These are issues that lend themselves perfectly to investigation by the gold standard (i.e., an RCT) [10], and hence we should accept nothing less. The ESPEN guidelines were assembled by a group of very experienced clinicians and scientists and based on the literature
Letters to the Editor / Nutrition 31 (2015) 1055–1059
Correction of data errors and reanalysis of “The effect of glucomannan on body weight in overweight or obese children and adults: A systematic review of randomized controlled trials” To the Editor: Recently, some of us (BMZ, AC, HS) published a metaanalysis of the effect of glucomannan on body weight [1]. Others of us (PL, TS, DBA), upon reading the article, noticed that the SDs reported in Figure 2 spanned two orders of magnitude, were surprised by this, and checked the original papers. Upon doing so, we noticed discrepancies between the data in Figure 2 and the data reported in one of the original papers [2] and contacted the authors of the two papers in question [1,2]. After discussion and checking, differences were detected in the data from one of the original papers (Keithley et al.) included in the meta-analysis [2]. These inaccuracies were then corrected and the meta-analytical statistics recomputed with the corrected data, which resulted in some changes in the meta-analytical conclusions. We describe those corrections and revised results and conclusions here.
Description of the error(s) Figure 2 in the meta-analysis [1] reported the SDs for the changes of body weights from different studies. However, the reported SDs from the study by Keithley et al. [2] were incorrect. Specifically, the reported SDs in the meta-analysis [1] were 0.18 and 0.08 for the glucomannan (GM) and placebo groups after a 2-wk treatment, and 0.08 and 0.43 for the GM and placebo groups after an 8-wk treatment. These values are different from those reported in the original study [2], in which they were 0.04, 0.02, 0.06, and 0.07, respectively (see last paragraph on page 3). Rather, the SDs reported in the meta-analysis [1] were obtained from the communication between authors of
these two papers [1,2]. We found that the SDs from both papers [1,2] were incorrect. As a result, related 95% confidence intervals (CIs) for the mean difference (MD) in Figure 2 in the metaanalysis [1] were also incorrect. The correct SDs in the study by Keithley et al. [2] based on individual change scores are 1.02 and 1.34 for the GM and placebo groups, respectively, after the 2-wk treatment, and 1.91 and 1.62 for the GM and placebo groups after the 8 wk-treatment. We also found that the body mass index (BMI) values for this publication [2] were initially calculated and reported inappropriately. These were corrected after another communication between the authors and are provided here.
Revised results with the error(s) corrected Data for weight change in the GM group compared with placebo group were recomputed using correct SDs (Fig. 1). No significant differences in weight loss between groups were noted after the 2-wk treatment (MD, 0.21; 95% CI, 0.47 to 0.89), nor after the 8-wk treatment (MD, 0.03; 95% CI, 1.04 to 0.98). The effect of treatment after 2 wk that was originally reported as statistically significant in the meta-analysis published turned out to be insignificant after the correction. However, the clinical significance of the effect reported in the first place was still negligible. Corrected data for BMI change in the GM group compared with the placebo group were recomputed. Originally, no significant effect of treatment (after 2 and 8 wk) was noted. Once correction was made with the new data, there was a statistically significant difference in favor of placebo (MD, 0.27; 95% CI, 0.43 to 0.11) after 2 wk, and in line with previously reported results, no statistically significant differences in effect after 8 wk were observed (MD, 0.26; 95% CI, 0.68 to 0.16). Similar to the difference in weight loss between the study groups, BMI change seemed to have little clinical significance due to very small values despite the reported statistically significant effect.
Conclusion We were glad to have this opportunity to work together to correct these errors and hope the results are useful to the scientific community.
Fig. 1. Weight change in GM group versus placebo group after 2, 4, 5, 8, and 12 wk of intervention (data recomputed for weeks 2 and 8). Negative number indicates weight increase.
Letters to the Editor / Nutrition 31 (2015) 1055–1059
Acknowledgments Supported in part by NIH grants R25 HL124208 and P30 DK056336. The opinions expressed are those of the authors and do not necessarily represent those of the NIH or any other organization. References [1] Zalewski BM, Chmielewska A, Szajewska H. The effect of glucomannan on body weight in overweight or obese children and adults: A systematic review of randomized controlled trials. Nutrition 2015;31:437–442.e2. [2] Keithley JK, Swanson B, Mikolaitis SL, Demeo M, Zeller JM, Fogg L, et al. Safety and efficacy of glucomannan for weight loss in overweight and moderately obese adults. J Obes 2013;2013:610908.
Bart1omiej M. Zalewski, M.D. Anna Chmielewska, M.D., Ph.D. Hania Szajewska, M.D., Ph.D. Department of Pediatrics The Medical University of Warsaw, Warsaw, Poland Joyce K. Keithley, D.N.Sc. College of Nursing Rush University Medical Center, Chicago, IL Peng Li, Ph.D. TaShauna U. Goldsby, Ph.D. David B. Allison, Ph.D. Office of Energetics and Nutrition Obesity Research Center University of Alabama at Birmingham Birmingham, AL http://dx.doi.org/10.1016/j.nut.2015.02.008
Food at will after pancreaticoduodenectomies. Re. “Perioperative nutritional support of patients undergoing pancreatic surgery in the age of ERAS” To the Editor: In an article recently published in Nutrition [1], Bozzetti and Mariani challenge the recommendation to allow “food at will” following pancreaticoduodenectomies (PDs) in our recent enhanced recovery after surgery (ERAS) guidelines [2,3]. Instead, Bozzetti and Mariani suggested we adhere to the ESPEN guidelines for enteral [4] and parenteral [5] nutrition in surgical patients, dating from 2006 and 2009. Their article [1] suggests a discrepancy between the ERAS and the ESPEN guidelines. This is, in fact, an artificially created controversy because the ERAS guidelines were fully endorsed by the ESPEN Society and by the International Association for Surgical Metabolism and Nutrition (IASMEN, part of the International Surgical Society). It is for
The authors are members of the ERAS Study Group and have authored several ERAS society recommendations.
1057
this reason and because it was aimed to reach the surgical and nutritional community that it was agreed upon by the Editorsin-Chief of the World Journal of Surgery and Clinical Nutrition to publish the ERAS guidelines simultaneously in these two journals as a legitimate double publication. The endorsement by the two societies is specifically mentioned in both papers [2,3]. Several of the authors of the earlier ESPEN guidelines were also involved in the more recent ERAS guidelines. It would therefore seem that the ERAS guidelines are an updated version of the ESPEN guidelines. They focus on a more specific patient population than the earlier ESPEN guidelines, which addressed gastrointestinal surgery in general and not PDs specifically. From this perspective, the conclusions of the Bozzetti and Mariani article are not correct: The ERAS guidelines are the ESPEN guidelines. The ERAS guidelines do not involve “oral feeding” as Bozzetti and Mariani claim. Feeding is a nonvolitional and nonphysiological process. Eating is the opposite: It is a volitional, normal process that elicits physiological reflexes central to digestion and that is associated with “a host of pleasurable phenomena” [6]. Feeding involves the use of a catheter or a tube, put into a vein or the gut and with inherent risks for complications that are well documented. Feeding almost always implies use of an artificial, industrially produced solution that carries as many nutritional components and core elements as we are able to put into it. The ERAS group recommends that patients are allowed to eat normal food at will after PD, but that they are advised to begin cautiously and advance according to tolerance. We do not recommend routine pre- or postoperative artificial nutritiondimmune-enhanced or notdin uncomplicated cases. For the “standard patient,” this ERAS approach is feasible, safe, and the best practice. This does not mean the ERAS group encourages unsupervised oral intake and we do recognize that selected subgroups of PD patients will need some form of artificial nutritional support. For the first few postoperative days, the ERAS regimen will certainly provide patients with fewer calories than one would be able to infuse through a central venous catheter or a feeding jejunostomy. We believe that this is more than balanced by the positive effects of eating normal food the normal way and by the absence of catheter- or infusion-related complications [7]. It is of note that Bozzetti and Mariani do not cite a recent systematic review dedicated to this very issue [8] that concludes in full accordance with the ERAS guidelines. Also, we would like to point to the only randomized controlled trial (RCT) to compare needle catheter jejunostomies with oral intake at will in upper major abdominal surgery, with >80 PD patients showing no increase in morbidity when oral diet at will was allowed [9]. Weight loss before major surgery is very well documented as a risk factor for complications. Quite another question is whether preoperative artificial nutritional therapy will confer any effect beyond increased weight. We are not aware of any adequately designed RCT (double-blind with a valid control group by the standards of today), in major, upper abdominal cancer surgery that shows preoperative artificial feeding to lower the risk for postoperative complications in patients who are allowed food. Based on studies in traditional care, the ESPEN guidelines [4,5] give such a recommendation “Grade A” and the same is the case for immune-enhanced enteral nutrition [4]. These are issues that lend themselves perfectly to investigation by the gold standard (i.e., an RCT) [10], and hence we should accept nothing less. The ESPEN guidelines were assembled by a group of very experienced clinicians and scientists and based on the literature
