The primary desirable outcomes after bariatric surgery include low rates of perioperative and long-term complications, sustained and meaningful weight loss, significant improvement in quality of life, improvement or resolution of obesity-associated comorbidities, and extension of life span. All 5 outcomes have been shown to be feasible results of GBP performed at high-volume centers.5,11
Although modest weight loss has been shown to improve many of the metabolic complications of obesity,34,35
greater and long-term weight loss is likely necessary to obtain all of the long-term benefits observed with the operation.1
Our overall results of 60.2% EWL fit well within the range of 57% to 65% reported at 1 year in other large series of patients treated with GBP.1,5
Although some authors have suggested that the nadir of weight loss after GBP occurs at approximately 136,37
or 2 years after surgery,13,38
weight loss varies greatly among patients, 15% of whom may not lose enough weight to qualify as having a successful outcome. The very definition of successful weight loss varies among previous studies, with some using 50% EWL as a cutoff.14,39,40
We defined failure as 40% or less EWL because it was the cutoff used recently by Melton et al.18
Identified predictors of poor weight loss after GBP could be used to develop more specific guidelines for informing patients preoperatively about the likelihood of a suboptimal outcome and for guiding the decision to undertake bariatric surgery. They could also be used to develop better strategies to overcome modifiable risk factors. Our multivariate analysis shows that only the presence of diabetes and a larger pouch size were independently associated with poor weight loss. Like our study, others have found that patients with diabetes mellitus have poorer weight loss after GBP than do patients without diabetes.14,18,19
Although GBP is known to significantly improve or cure diabetes, we and others14,18,19
observed an independent effect of this disease on weight loss outcomes. One possible explanation is that most of these patients take exogenous insulin and/or drugs used to optimize glycemic control (sulfonylureas, meglitinides, and thiazolidinediones) that increase circulating insulin levels and/or insulin sensitivity. Because insulin is a known anabolic hormone that promotes lipogenesis, stimulation of triglyceride synthesis, adipocyte differentiation, and muscle synthesis,41–43
elevated levels may reduce the degree of weight loss after GBP. Other factors that may lead to weight gain in patients with diabetes include a “protective” increase in caloric intake to treat episodes of hypoglycemia, reduction of urinary glucose losses, and sodium and water retention that are a direct effect of insulin on the distal tubule in the kidney.43–50
These and the inherent metabolic derangements to glucose homeostasis that are caused by obesity likely converge to produce this effect.
Although strong evidence supports the importance of tight glycemic control in minimizing the microvascular complications of diabetes,43
the weight gain associated with the use of insulin and insulin secretagogues may create a vicious cycle and a risk of worsening the patient’s insulin resistance and other conditions. This combination of positive and negative effects is illustrated in results from the UK Prospective Diabetes Study,43
in which 3867 patients with newly diagnosed type 2 diabetes underwent analysis. Patients were randomized to receive intensive therapy with a sulfonylurea or insulin or to receive conventional therapy consisting of diet modification alone. The risks of any diabetes-related end point and diabetes-related death were 12% and 10% lower, respectively, in the intensive treatment group than in the conventional treatment group, whereas average weight gain was a significant 2.9 kg greater in the intensive treatment group. Moreover, patients in the intensive treatment group who received insulin gained more weight, with a mean weight gain of 4 kg greater than that observed in the patients who received sulfonylurea. These results are consistent with our findings that diabetes was an independent risk factor for poor weight loss and that patients receiving insulin were at higher risk of poor weight loss. Although GBP has proved to be very effective in improving insulin resistance and decreasing the need for medications even before significant weight loss is observed, and although it does so at better rates than any other nonsurgical or surgical treatment,1,51
a variable proportion of patients usually require some type of medication for proper postoperative glycemic control. This was true in our study, which found that most patients receiving oral medications or insulin before surgery were able to discontinue (74 of 114 patients [64.9%]) or significantly decrease (to <50% of preoperative doses) (103 of 114 [90.4%]) the use of medication for diabetes at 1 year of follow-up. Therefore, methods for achieving glycemic control that are not linked to weight gain, such as use of metformin hydrochloride, α-glucosidase inhibitors, and the newer class of diabetes medications such as glucagon-like peptide 1 receptor agonists (eg, exenatide) and the dipeptidyl-peptidase 4 inhibitors (eg, sitagliptin and vildagliptin), may be considered in patients who continue to need exogenous glucose control and thus may improve weight loss after GBP. The role of specific antidiabetic agents in weight loss after GBP should be the focus of future studies.
The restriction imposed by a small pouch size is one of the most important aspects of GBP. We know of only 1 other study that demonstrated an inverse correlation between initial gastric pouch size and EWL after GBP. In that study by Roberts et al,22
100 patients underwent GBP, had gastric pouch size measured, and had follow-up data available at 12 months. The mean pouch size (64 cm2
; range, 9–248 cm2
) was more than double what we measured in our series (mean, 26 cm2
; range, 7–78 cm2
). Although we attribute this difference to the likely variability in the pouch measurements obtained between the 2 studies, it also demonstrates the variability in how different surgeons in different centers create a gastric pouch. Roberts et al also found an inverse correlation between initial gastric pouch size and EWL (r
=−0.43) and that EWL was poorer in patients with larger pouches, results which support our findings. One other recent study29
attempted to determine the association between pouch size and EWL in 59 patients 1 year after GBP, in 4 groups according to pouch size. Madan et al29
failed to show a significant correlation, likely owing to a small sample size, to studying pouch sizes in groups, and to not controlling for other variables known to affect weight loss. Although pouch volume would be a preferable measurement compared with pouch area as was used in our study and the other studies mentioned, it was not feasible to obtain it routinely. Nevertheless, we believe that pouch area as measured using our methods is a useful surrogate for pouch volume, even allowing for individual differences in gastric wall distensibility. Many methods are used to estimate pouch size intraoperatively. According to a recent survey,25
70% of surgeons in the United States estimate pouch size by measuring the distance from the estimated location of the gastroesophageal junction to a variable distance in the lesser curvature of the stomach, and/or by the number of vessels in the lesser curvature; only about 20% use a sizing balloon. As the use of GBP continues to grow, we believe it is critical to stress the importance of and to teach the creation of the small gastric pouch and to better standardize the technique used for pouch creation.
Greater initial weight and BMI14,16,18,52
have previously been associated with poor EWL after GBP. A study of 494 morbidly obese patients, of whom 377 (76.3%) had complete follow-up at 1 year, found that higher initial weight and BMI were negatively associated with percentage of EWL because heavier patients lost a lower percentage of weight than did lighter patients (P
The following 2 main factors may support this finding in other series: a higher rate of other obesity-associated diseases with greater weight and BMI, and the fact that excess weight is by definition greater when weight and BMI are greater. Both factors may have put these patients at a disadvantage with respect to percentage of EWL. In contrast, in our study, greater initial weight and BMI were not found to be independent predictors of poor weight loss, showing that other factors are more important than initial weight and BMI.
Race was also not an independent factor predicting poor weight loss in our study, but others have found that association.16,17,53
A combination of a few known factors may explain poorer weight loss in black patients, such as differences in body composition, fat distribution, resting energy expenditure, and thermogenesis54
; higher diabetes prevalence55
; cultural and social environment56
; and the basic definition of ideal body weight that possibly underestimates the ideal body weight in black patients.56
Extending the alimentary and/or the biliopancreatic limb is one of the few technical variations of GBP that have been proposed to decrease the failure rate, but this effect has been shown only in patients with a BMI greater than 50.26,27,57
Several alimentary and/or the biliopancreatic limb lengths have been reported, and those alimentary limbsgreater than 200 cm have been associated with more complications. Nevertheless, extending the limb length is a technical aspect of the operation that needs further study, and we suggest that the better approach may be to tailor limb extension on the basis of individual patient characteristics.
Although our study is 1 of the largest single-center series currently available, with predictor variables and outcomes obtained in 85.9% of patients, the study population comes from a tertiary care medical center and its demographics and clinical characteristics may differ from those of other centers. Therefore, our findings should be validated in a multivariate analysis of a larger, independent data set. Another limitation was our inability to determine whether postoperative use of medications for diabetes had an effect on weight loss because only preoperative medication use was ascertained. Other factors that may have affected weight loss for which data were not available in the present study include physical activity level, measures of body composition, and fat distribution before or after surgery. These variables should receive greater emphasis in future studies. An additional relevant finding that may bias our results was the lower prevalence of 2 risk factors for poor weight loss among the 51 patients omitted from our analysis because they did not have 12 months of follow-up data. This suggests that our estimate of the prevalence of poor weight loss may be slightly high; however, it is unlikely that the associations between risk factors and poor weight loss differ in the omitted patients. Finally, although careful adjustment using multiple regression may remove most confounding by measured factors, in particular when a liberal criterion for adjustment is used, as in our study, it cannot balance unmeasured confounders.
We conclude that GBP provides good or excellent weight loss for most patients. However, diabetes mellitus and larger pouch size are independently associated with poor weight loss after GBP. Changes in the use of diabetes medications may reduce the risk of poor weight loss among diabetics undergoing GBP. Detailed attention to the creation of a small gastric pouch is essential for achieving the best results.