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Shana J Kim, Russell J de Souza, Vivian L Choo, Vanessa Ha, Adrian I Cozma, Laura Chiavaroli, Arash Mirrahimi, Sonia Blanco Mejia, Marco Di Buono, Adam M Bernstein, Lawrence A Leiter, Penny M Kris-Etherton, Vladimir Vuksan, Joseph Beyene, Cyril WC Kendall, David JA Jenkins, John L Sievenpiper, Effects of dietary pulse consumption on body weight: a systematic review and meta-analysis of randomized controlled trials, The American Journal of Clinical Nutrition, Volume 103, Issue 5, May 2016, Pages 1213–1223, https://doi.org/10.3945/ajcn.115.124677
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ABSTRACT
Background: Obesity is a risk factor for developing several diseases, and although dietary pulses (nonoil seeds of legumes such as beans, lentils, chickpeas, and dry peas) are well positioned to aid in weight control, the effects of dietary pulses on weight loss are unclear.
Objective: We summarized and quantified the effects of dietary pulse consumption on body weight, waist circumference, and body fat by conducting a systematic review and meta-analysis of randomized controlled trials.
Design: We searched the databases MEDLINE, Embase, CINAHL, and the Cochrane Library through 11 May 2015 for randomized controlled trials of ≥3 wk of duration that compared the effects of diets containing whole dietary pulses with those of comparator diets without a dietary pulse intervention. Study quality was assessed by means of the Heyland Methodologic Quality Score, and risk of bias was assessed with the Cochrane Risk of Bias tool. Data were pooled with the use of generic inverse-variance random-effects models.
Results: Findings from 21 trials (n = 940 participants) were included in the meta-analysis. The pooled analysis showed an overall significant weight reduction of −0.34 kg (95% CI: −0.63, −0.04 kg; P = 0.03) in diets containing dietary pulses (median intake of 132 g/d or ∼1 serving/d) compared with diets without a dietary pulse intervention over a median duration of 6 wk. Significant weight loss was observed in matched negative–energy-balance (weight loss) diets (P = 0.02) and in neutral–energy-balance (weight-maintaining) diets (P = 0.03), and there was low evidence of between-study heterogeneity. Findings from 6 included trials also suggested that dietary pulse consumption may reduce body fat percentage.
Conclusions: The inclusion of dietary pulses in a diet may be a beneficial weight-loss strategy because it leads to a modest weight-loss effect even when diets are not intended to be calorically restricted. Future studies are needed to determine the effects of dietary pulses on long-term weight-loss sustainability. This protocol was registered at clinicaltrials.gov as NCT01594567.
INTRODUCTION
Obesity has become a global epidemic. Obesity is a major risk factor for developing heart disease, hypertension, type 2 diabetes, and some cancers. According to the WHO, ≥2.8 million people die each year as a result of complications of obesity, which makes it one of the leading risk factors for global deaths (1). However, an important modifiable factor for obesity is the diet.
Previous studies have shown that the consumption of foods that are high in fiber and protein and low in the glycemic index (GI) promote weight loss and maintenance (2–4). Dietary pulses, the edible nonoil seeds of legumes, such as beans, lentils, chickpeas, and dry peas, are well positioned to aid in weight loss because they possess all of these ideal nutritional qualities as well as being low in saturated fat. Although the role of fiber and protein on weight control has previously been summarized and supported, the specific role of dietary pulses is uncertain. In addition, there has been evidence that dietary pulses increase satiety during meals; however, it is unclear whether this acute benefit translates into longer-term weight loss (5). Experimental trials have reported varying effects of dietary pulses on body weight (6–11), and few observational studies have assessed the association between dietary pulse consumption and weight (11). The only meta-analysis to evaluate the effects of dietary pulses on weight was conducted in 2002 (with 8 trials) and failed to support a role for dietary pulses reducing body weight (12). However, this study did not clearly document a search and selection strategy, which is a requirement for compliance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses and is in need of an update because several trials have been conducted since its publication in 2002.
Although the WHO has suggested the consumption of legumes to help reduce risks of obesity (1), other dietary guidelines have not provided a suggestive link between dietary pulse consumption and healthy body weight. Instead, there have been only general guidelines that have encouraged the frequent consumption of dietary pulses and legumes often (13, 14). In addition, optimal recommended daily intake is not known. To better inform guidelines for populations with rising obesity rates, we conducted a systematic review and meta-analysis of randomized controlled trials that have examined the effects of dietary pulse intake compared with the effects of a comparator diet on body weight. We further investigated the effects of dietary pulses on other measures of adiposity such as waist circumference and body fat percentage.
METHODS
Our protocol followed the guideline of the Cochrane Handbook for Systematic Reviews of Interventions (15), and findings are reported according to the guidelines of the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (16). This protocol was registered at clinicaltrials.gov as NCT01594567.
Data sources and searches
We searched MEDLINE (http://www.nlm.nih.gov/bsd/pmresources.html), Embase (https://www.embase.com), CINAHL (https://health.ebsco.com/products/the-cinahl-database), and the Cochrane Library (http://www.cochranelibrary.com/) through 11 May 2015 (see Supplemental Table 1 for the full search strategies for MEDLINE and Embase, with similar terms used for CINAHL and the Cochrane Library). The search was limited to human studies and had no language restrictions. Reference lists of selected studies and reviews were also searched to identify additional articles.
Study selection
We included randomized controlled trials that investigated the effect of exchanging whole dietary pulses for other dietary components on body weight, waist circumference, or body fat percentage in adults. Studies were excluded if they were not randomized, had a diet duration of <3 wk [adapted from the US Food and Drug Administration’s minimum duration for the effects of a soy intervention on other health claims (17)], used only dietary pulse extracts, or did not have the intention of using a calorically matched comparator arm (isocaloric). In cases in which other dietary components comprised part of the intervention, dietary pulses needed to make up >50% of the intervention. When multiple publications existed for the same study, the article with the most information was included (n = 2). Published abstracts were not included.
One reviewer (SJK) assessed the titles and abstracts of all identified studies. All studies that were potentially eligible for the systematic review after this assessment were reviewed in full text independently by a second reviewer (VLC) with discrepancies resolved by a senior author (RJdS) to obtain a consensus. The interrater agreement was quantified with the use of a κ score.
Data extraction and quality assessment
The 2 investigators independently extracted data from selected studies with the use of a standardized extraction form that was developed and piloted for use in other meta-analyses (18–21). The extraction form outlined information that needed to be recorded such as study design, blinding, sample size, participant characteristics, follow-up duration, types of dietary pulses used, dose of dietary pulse intake, comparator diet or food, adherence measures, macronutrient profile, funding source, and endpoint data.
The quality of each study was determined with the use of the Heyland Methodologic Quality Score (MQS), which scores the study quality on the domains of random assignment, blinding, dropout rate, sample-selection methods, analysis methods (intention to treat or per protocol), and protocol descriptions (22). Risk of bias for each individual study was assessed with the use of the Cochrane Risk of Bias tool (15). This tool determined the level of bias as either low (proper methods taken to reduce bias), high (improper methods creating bias), or unclear (insufficient information provided to determine the bias level) on the basis of sequence generation, allocation concealment, blinding, incomplete outcome data, and selective reporting. Authors were only contacted if additional information was necessary (n = 8). No ethical approval was required.
Statistical analysis
Baseline, end-of-study, and between-treatment differences in body weight, waist circumference, or body fat were recorded as means ± SDs. If not provided, between-treatment differences in change-from-baseline or end differences were calculated by subtracting means, and variance measures such as SEs were imputed with the use of published formulas (15). Missing SDs were imputed with the use of the pooled SD from other studies included in the analysis (15).
A generic inverse-variance method with random-effects models was used to calculate pooled mean differences and 95% CIs. Random-effects models were preferred over fixed-effect models even with no evidence of heterogeneity because random-effects models yield more-conservative estimates in the setting of between-studies heterogeneity. Change-from-baseline differences were preferred over end differences except when within-individual correlation coefficient values were missing. To mitigate a unit-of-analysis error in the analysis of a study that contained 4 comparison arms, we pooled the 3 intervention arms with the use of a weighted mean to create a single pairwise comparison. In addition, we present results separately according to the energy-balance setting as follows: in a negative–energy-balance setting, both dietary pulse and comparator arms were calorically restricted by 30–35% of total energy (i.e., weight-loss diets), and in a neutral–energy-balance setting, both dietary pulse and comparator arms had caloric intakes intended to meet their total energy needs (i.e., weight-maintaining diets). The significance level for an effect was set at P < 0.05.
We included crossover and parallel studies in the same pooled analysis. A paired analysis was applied to the analysis of crossover trials with the use of a within-individual correlation coefficient between treatments of 0.5 as described by Elbourne et al. (23). A sensitivity analysis was conducted with the use of different correlation coefficient values (0.25 and 0.75) to test for the robustness of the effect size. An additional sensitivity analysis included the removal of each single study from the meta-analyses one at a time and recalculation of the summary effect. An influential outlier was considered a study whose removal changed the magnitude of the pooled effect by >10%.
Between-study heterogeneity was detected with the use of Cochran’s Q statistic set at a significance level of P < 0.10 and was quantified with the use of the I2 statistic where I2 > 50% indicated a large amount of heterogeneity (15). Study design–level sources of heterogeneity were investigated by creating categorical subgroups according to a priori study-design features including study quality (MQS <8 or ≥8), study design (parallel or crossover), dose of dietary pulses given (<100 or ≥100 g/d), dietary pulse type (bean, chickpea, lentil, pea, or mixed), follow-up duration (<12 or ≥12 wk), saturated fat intake with a dietary pulse diet (<10% or ≥10%), fiber intake with a dietary pulse diet (<28 or ≥28 g/d), difference in saturated fat intake between the dietary pulse arm and comparator arm (greater than or less than the median of −0.4%), difference in fiber intake in the dietary pulse arm compared with in the comparator arm (greater than or less than the median of 8 g/d), baseline BMI (in kg/m2; greater than or less than the median of 30.2), and baseline body weight (greater than or less than the median of 79.3 kg). We also investigated whether the effect size was related to these a priori study-level values of possible effect modifiers such as the dose of dietary pulses, fiber intake, the change in fiber intake from baseline, saturated fat intake, and the change in saturated fat intake from baseline in the intervention arm. The significance of subgroup differences was assessed with the use of a continuous metaregression analysis (P < 0.05). Publication bias was investigated with the use of a visual inspection of funnel plots and Egger’s and Begg’s tests. All analyses were conducted with the use of RevMan version 5.2 software (The Nordic Cochrane Center, The Cochrane Collaboration) except for the metaregression analyses and tests for publication bias, which were conducted with the use of STATA version 12 software (StataCorp LP).
RESULTS
Search results
We identified 2924 potentially eligible articles (Figure 1), of which 2806 articles were excluded on the basis of the title or abstract. In total, 118 publications were retrieved in full and reviewed in duplicate to determine the final inclusion list. Of these 118 studies, 99 reports were excluded, which yielded a final total of 19 reports (with data for 21 trials) that were included in our pooled analysis for body weight (24–42). The search also yielded 6 reports that were included in our pooled analysis for waist circumference (24, 25, 30, 31, 33, 42) and body fat percentage (24, 25, 30–32, 42). The interrater κ was 0.83 with 94% agreement.
Summary of study search and selection. Reports were identified from MEDLINE (https://www.nlm.nih.gov/bsd/pmresources.html), Embase (http://www.embase.com), CINHAL (https://health.ebsco.com/products/the-cinahl-database), the Cochrane Library (http://www.cochranelibrary.com/) and through manual searches of reference lists of selected studies and reviews.
Summary of study search and selection. Reports were identified from MEDLINE (https://www.nlm.nih.gov/bsd/pmresources.html), Embase (http://www.embase.com), CINHAL (https://health.ebsco.com/products/the-cinahl-database), the Cochrane Library (http://www.cochranelibrary.com/) and through manual searches of reference lists of selected studies and reviews.
Trial characteristics
Characteristics of all included trials are shown in Table 1. The 19 publications reported results from 21 different trials with 940 participants. Most participants were middle aged (median age: 51.3 y; IQR: 46.6–56.6 y) men and women (median ratio of men to women: 1:0.9 in available trials). The median baseline BMI across studies was 30.2 (IQR: 27.6–31.4). The median number of participants per trial was 27 (IQR: 19–74) with a median follow-up length of 6 wk (IQR: 4–12 wk). Two of the 9 crossover designed trials did not have a washout period (35, 37).
Characteristics of randomized controlled trials included in the meta-analysis1
| Reference | Total subjects, n (M:F) | Age, y | BMI, kg/m2 | Design | Feeding2 | Pulse type | Dose,3 g/d | Comparator | Diet,4 % | Energy balance5 (% of energy) | Follow-up, wk | MQS6 |
| Abete et al., 2009 (24) | 18 (18:0) | 37.1 ± 8.07 | 31.6 ± 3.7 | Parallel | DA | Mixed | 113 | No pulses | 53:30:17 | Negative (30) | 8 | 9 |
| Abeysekara et al., 2012 (25) | 838,9 | 59.7 ± 6.3 | 27.5 ± 4.5 | Crossover | Supplement | Mixed | 250 | Usual diet | 49:37:1610 | Neutral | 8 | 9 |
| Anderson et al., 1984 (26) | 20 (20:0) | 54.0 ± 8.5 | Overweight11 | Parallel | Metabolic | Beans | 278 | Oat | 43:37:20 | Neutral | 3 | 5 |
| Anderson et al., 1990 (27) | ||||||||||||
| A | 6 (6:0) | 64.0 ± 2.4 | Overweight11 | Parallel | Metabolic | Bean | 113 | No pulses | 43:28:19 | Neutral | 4 | 5 |
| B | 9 (9:0) | 57.0 ± 9.0 | Overweight11 | Parallel | Metabolic | Bean | 113 | No pulses | 43:28:19 | Neutral | 4 | 5 |
| C | 9 (9:0) | 54.0 ± 9.0 | Overweight11 | Parallel | Metabolic | Bean | 152 | No pulses | 43:28:19 | Neutral | 4 | 5 |
| Belski et al., 2011 (28) | 93 (52:41) | 46.6 ± 9.7 | 31.4 ± 2.7 | Parallel | DA and supplement | Bean | 124 | Wheat | 39:32:2210 | Negative (35) | 48 | 8 |
| Crujeiras et al., 2007 (29) | 30 (17:13) | 36.0 ± 8.0 | 32.0 ± 5.3 | Parallel | DA | Mixed | 94 | No pulses | 50:30:20 | Negative (30) | 8 | 8 |
| Gravel et al., 2010 (30) | 114 (0:114) | 51.3 ± 8.7 | 29.9 ± 5.1 | Parallel | Supplement | Mixed | 81 | No pulses | 49:33:1710 | Neutral | 16 | 7 |
| Hermsdorff et al., 2011 (31) | 30 (17:13) | 36.0 ± 8.0 | 32.5 ± 4.5 | Parallel | DA | Mixed | 113 | No pulses | 53:30:17 | Negative (30) | 8 | 8 |
| Hodgson et al., 2010 (32) | 74 (26:48) | 57.9 ± 8.0 | 30.6 ± 3.5 | Parallel | Supplement | Bean | 132 | Wheat | 39:31:2410 | Neutral | 16 | 7 |
| Jenkins et al., 2012 (33) | 121 (61:60) | 59.5 ± 9.1 | 30.6 ± 6.3 | Parallel | DA | Mixed | 211 | Wheat | 45:23:3110 | Neutral | 12 | 8 |
| Jimenez-Cruz et al., 2004 (34) | 89 | 51.0 ± 3.0 | 30.7 ± 7.9 | Crossover | DA | Bean | 97 | High GI | 51:26:2310 | Neutral | 3 | 8 |
| Mackay and Ball, 1992 (35) | 39 (22:17) | 22.0–66.012 | 26.7 | Crossover | Supplement | Bean | 80 | Oat | 53:28:1710 | Neutral | 22 | 5 |
| Marinangeli and Jones, 2011 (36) | 23 (7:16) | 52.1 ± 10.6 | 30.2 ± 4.3 | Crossover | Metabolic | Pea | 138 | Wheat | 55:30:15 | Neutral | 4 | 6 |
| Nestel et al., 2004 (37) | 19 (9:10) | 56.6 ± 7.6 | 25.6 ± 3.2 | Crossover | Supplement | Chickpea | 140 | Wheat | 47:30:1910 | Neutral | 6 | 5 |
| Pittaway et al., 2006 (38) | 47 (19:28) | 53.0 ± 9.8 | 27.6 ± 4.1 | Crossover | DA and supplement | Chickpea | 140 | Wheat | 46:32:1810 | Neutral | 5, 613 | 5 |
| Pittaway et al., 2007 (39) | 27 (10:17) | 50.6 ± 10.5 | 28.8 ± 4.4 | Crossover | DA and supplement | Chickpea | 140 | Wheat | 44:34:1710 | Neutral | 5 | 6 |
| Saraf-Bank et al., 2015 (40) | 26 (12:14) | 50.0 ± 1.3 | 28.9 ± 0.9 | Crossover | DA and supplement | Mixed | 111 | No pulses | 66:20:1610 | Neutral | 6 | 8 |
| Tonstad et al., 2014 (41) | 1239 | 48.4 ± 10.7 | 36.5 ± 3.9 | Parallel | DA and supplement | Mixed | 250 | Low carb | 52:28:1910 | Neutral | 16 | 6 |
| Veenstra et al., 2010 (42)14 | ||||||||||||
| Chickpea | 19 (19:0) | 28.1 ± 5.9 | 25.2 ± 2.5 | Crossover | Supplement | Chickpea | 275 | Potato | 55:29:1510 | Neutral | 4 | 6 |
| Lentil | 19 (19:0) | Lentil | 53:29:1810 | |||||||||
| Pea | 20 (20:0) | Pea | 56:27:1710 | |||||||||
| Potato | 21 (21:0) | — | — | — | — |
| Reference | Total subjects, n (M:F) | Age, y | BMI, kg/m2 | Design | Feeding2 | Pulse type | Dose,3 g/d | Comparator | Diet,4 % | Energy balance5 (% of energy) | Follow-up, wk | MQS6 |
| Abete et al., 2009 (24) | 18 (18:0) | 37.1 ± 8.07 | 31.6 ± 3.7 | Parallel | DA | Mixed | 113 | No pulses | 53:30:17 | Negative (30) | 8 | 9 |
| Abeysekara et al., 2012 (25) | 838,9 | 59.7 ± 6.3 | 27.5 ± 4.5 | Crossover | Supplement | Mixed | 250 | Usual diet | 49:37:1610 | Neutral | 8 | 9 |
| Anderson et al., 1984 (26) | 20 (20:0) | 54.0 ± 8.5 | Overweight11 | Parallel | Metabolic | Beans | 278 | Oat | 43:37:20 | Neutral | 3 | 5 |
| Anderson et al., 1990 (27) | ||||||||||||
| A | 6 (6:0) | 64.0 ± 2.4 | Overweight11 | Parallel | Metabolic | Bean | 113 | No pulses | 43:28:19 | Neutral | 4 | 5 |
| B | 9 (9:0) | 57.0 ± 9.0 | Overweight11 | Parallel | Metabolic | Bean | 113 | No pulses | 43:28:19 | Neutral | 4 | 5 |
| C | 9 (9:0) | 54.0 ± 9.0 | Overweight11 | Parallel | Metabolic | Bean | 152 | No pulses | 43:28:19 | Neutral | 4 | 5 |
| Belski et al., 2011 (28) | 93 (52:41) | 46.6 ± 9.7 | 31.4 ± 2.7 | Parallel | DA and supplement | Bean | 124 | Wheat | 39:32:2210 | Negative (35) | 48 | 8 |
| Crujeiras et al., 2007 (29) | 30 (17:13) | 36.0 ± 8.0 | 32.0 ± 5.3 | Parallel | DA | Mixed | 94 | No pulses | 50:30:20 | Negative (30) | 8 | 8 |
| Gravel et al., 2010 (30) | 114 (0:114) | 51.3 ± 8.7 | 29.9 ± 5.1 | Parallel | Supplement | Mixed | 81 | No pulses | 49:33:1710 | Neutral | 16 | 7 |
| Hermsdorff et al., 2011 (31) | 30 (17:13) | 36.0 ± 8.0 | 32.5 ± 4.5 | Parallel | DA | Mixed | 113 | No pulses | 53:30:17 | Negative (30) | 8 | 8 |
| Hodgson et al., 2010 (32) | 74 (26:48) | 57.9 ± 8.0 | 30.6 ± 3.5 | Parallel | Supplement | Bean | 132 | Wheat | 39:31:2410 | Neutral | 16 | 7 |
| Jenkins et al., 2012 (33) | 121 (61:60) | 59.5 ± 9.1 | 30.6 ± 6.3 | Parallel | DA | Mixed | 211 | Wheat | 45:23:3110 | Neutral | 12 | 8 |
| Jimenez-Cruz et al., 2004 (34) | 89 | 51.0 ± 3.0 | 30.7 ± 7.9 | Crossover | DA | Bean | 97 | High GI | 51:26:2310 | Neutral | 3 | 8 |
| Mackay and Ball, 1992 (35) | 39 (22:17) | 22.0–66.012 | 26.7 | Crossover | Supplement | Bean | 80 | Oat | 53:28:1710 | Neutral | 22 | 5 |
| Marinangeli and Jones, 2011 (36) | 23 (7:16) | 52.1 ± 10.6 | 30.2 ± 4.3 | Crossover | Metabolic | Pea | 138 | Wheat | 55:30:15 | Neutral | 4 | 6 |
| Nestel et al., 2004 (37) | 19 (9:10) | 56.6 ± 7.6 | 25.6 ± 3.2 | Crossover | Supplement | Chickpea | 140 | Wheat | 47:30:1910 | Neutral | 6 | 5 |
| Pittaway et al., 2006 (38) | 47 (19:28) | 53.0 ± 9.8 | 27.6 ± 4.1 | Crossover | DA and supplement | Chickpea | 140 | Wheat | 46:32:1810 | Neutral | 5, 613 | 5 |
| Pittaway et al., 2007 (39) | 27 (10:17) | 50.6 ± 10.5 | 28.8 ± 4.4 | Crossover | DA and supplement | Chickpea | 140 | Wheat | 44:34:1710 | Neutral | 5 | 6 |
| Saraf-Bank et al., 2015 (40) | 26 (12:14) | 50.0 ± 1.3 | 28.9 ± 0.9 | Crossover | DA and supplement | Mixed | 111 | No pulses | 66:20:1610 | Neutral | 6 | 8 |
| Tonstad et al., 2014 (41) | 1239 | 48.4 ± 10.7 | 36.5 ± 3.9 | Parallel | DA and supplement | Mixed | 250 | Low carb | 52:28:1910 | Neutral | 16 | 6 |
| Veenstra et al., 2010 (42)14 | ||||||||||||
| Chickpea | 19 (19:0) | 28.1 ± 5.9 | 25.2 ± 2.5 | Crossover | Supplement | Chickpea | 275 | Potato | 55:29:1510 | Neutral | 4 | 6 |
| Lentil | 19 (19:0) | Lentil | 53:29:1810 | |||||||||
| Pea | 20 (20:0) | Pea | 56:27:1710 | |||||||||
| Potato | 21 (21:0) | — | — | — | — |
Carb, carbohydrate; DA, Dietary Advice; GI, glycemic index; MQS, Methodologic Quality Score
Metabolic feeding was the provision of all meals and study supplements (treatment and control foods) consumed in the study under controlled conditions. Supplement feeding was the provision of study supplements only. DA was the provision of counseling on treatment and control diets.
Pulse doses are given as cooked weight. We used the following conversion factors: 1 g dry pulses = 2.75 g cooked pulses; and 1 mL pulses = 0.76 g pulses.
Energy from carbohydrate:fat:protein intended for the intervention.
Negative energy balance refers to studies in which both dietary pulse and comparator arms were calorically restricted (i.e., weight-loss diets). Neutral energy balance refers to studies in which both dietary pulse and comparator arms had caloric intakes intended to meet their total energy needs (i.e., weight-maintaining diets).
Study quality was assessed with the use of the Heyland MQS. A score ≥8 was considered higher quality.
Mean ± SD (all such values).
n = 82 for the waist-circumference endpoint.
Sex of participants at end of study was not provided in the original article.
End-measured macronutrient intake in the intervention arm.
Baseline BMI was not given, but patients were described as overweight.
Range.
Pittaway et al. (38) performed the randomized controlled trial in 2 separate groups, one of which had 5 wk of follow-up, and the other of which had 6 wk of follow-up.
Veenstra et al. (42) had 3 different dietary pulse intervention arms in the same participants (crossover trial). The arm with the most participants (i.e., the control potato arm) was used to calculate the total meta-analysis participant number.
Characteristics of randomized controlled trials included in the meta-analysis1
| Reference | Total subjects, n (M:F) | Age, y | BMI, kg/m2 | Design | Feeding2 | Pulse type | Dose,3 g/d | Comparator | Diet,4 % | Energy balance5 (% of energy) | Follow-up, wk | MQS6 |
| Abete et al., 2009 (24) | 18 (18:0) | 37.1 ± 8.07 | 31.6 ± 3.7 | Parallel | DA | Mixed | 113 | No pulses | 53:30:17 | Negative (30) | 8 | 9 |
| Abeysekara et al., 2012 (25) | 838,9 | 59.7 ± 6.3 | 27.5 ± 4.5 | Crossover | Supplement | Mixed | 250 | Usual diet | 49:37:1610 | Neutral | 8 | 9 |
| Anderson et al., 1984 (26) | 20 (20:0) | 54.0 ± 8.5 | Overweight11 | Parallel | Metabolic | Beans | 278 | Oat | 43:37:20 | Neutral | 3 | 5 |
| Anderson et al., 1990 (27) | ||||||||||||
| A | 6 (6:0) | 64.0 ± 2.4 | Overweight11 | Parallel | Metabolic | Bean | 113 | No pulses | 43:28:19 | Neutral | 4 | 5 |
| B | 9 (9:0) | 57.0 ± 9.0 | Overweight11 | Parallel | Metabolic | Bean | 113 | No pulses | 43:28:19 | Neutral | 4 | 5 |
| C | 9 (9:0) | 54.0 ± 9.0 | Overweight11 | Parallel | Metabolic | Bean | 152 | No pulses | 43:28:19 | Neutral | 4 | 5 |
| Belski et al., 2011 (28) | 93 (52:41) | 46.6 ± 9.7 | 31.4 ± 2.7 | Parallel | DA and supplement | Bean | 124 | Wheat | 39:32:2210 | Negative (35) | 48 | 8 |
| Crujeiras et al., 2007 (29) | 30 (17:13) | 36.0 ± 8.0 | 32.0 ± 5.3 | Parallel | DA | Mixed | 94 | No pulses | 50:30:20 | Negative (30) | 8 | 8 |
| Gravel et al., 2010 (30) | 114 (0:114) | 51.3 ± 8.7 | 29.9 ± 5.1 | Parallel | Supplement | Mixed | 81 | No pulses | 49:33:1710 | Neutral | 16 | 7 |
| Hermsdorff et al., 2011 (31) | 30 (17:13) | 36.0 ± 8.0 | 32.5 ± 4.5 | Parallel | DA | Mixed | 113 | No pulses | 53:30:17 | Negative (30) | 8 | 8 |
| Hodgson et al., 2010 (32) | 74 (26:48) | 57.9 ± 8.0 | 30.6 ± 3.5 | Parallel | Supplement | Bean | 132 | Wheat | 39:31:2410 | Neutral | 16 | 7 |
| Jenkins et al., 2012 (33) | 121 (61:60) | 59.5 ± 9.1 | 30.6 ± 6.3 | Parallel | DA | Mixed | 211 | Wheat | 45:23:3110 | Neutral | 12 | 8 |
| Jimenez-Cruz et al., 2004 (34) | 89 | 51.0 ± 3.0 | 30.7 ± 7.9 | Crossover | DA | Bean | 97 | High GI | 51:26:2310 | Neutral | 3 | 8 |
| Mackay and Ball, 1992 (35) | 39 (22:17) | 22.0–66.012 | 26.7 | Crossover | Supplement | Bean | 80 | Oat | 53:28:1710 | Neutral | 22 | 5 |
| Marinangeli and Jones, 2011 (36) | 23 (7:16) | 52.1 ± 10.6 | 30.2 ± 4.3 | Crossover | Metabolic | Pea | 138 | Wheat | 55:30:15 | Neutral | 4 | 6 |
| Nestel et al., 2004 (37) | 19 (9:10) | 56.6 ± 7.6 | 25.6 ± 3.2 | Crossover | Supplement | Chickpea | 140 | Wheat | 47:30:1910 | Neutral | 6 | 5 |
| Pittaway et al., 2006 (38) | 47 (19:28) | 53.0 ± 9.8 | 27.6 ± 4.1 | Crossover | DA and supplement | Chickpea | 140 | Wheat | 46:32:1810 | Neutral | 5, 613 | 5 |
| Pittaway et al., 2007 (39) | 27 (10:17) | 50.6 ± 10.5 | 28.8 ± 4.4 | Crossover | DA and supplement | Chickpea | 140 | Wheat | 44:34:1710 | Neutral | 5 | 6 |
| Saraf-Bank et al., 2015 (40) | 26 (12:14) | 50.0 ± 1.3 | 28.9 ± 0.9 | Crossover | DA and supplement | Mixed | 111 | No pulses | 66:20:1610 | Neutral | 6 | 8 |
| Tonstad et al., 2014 (41) | 1239 | 48.4 ± 10.7 | 36.5 ± 3.9 | Parallel | DA and supplement | Mixed | 250 | Low carb | 52:28:1910 | Neutral | 16 | 6 |
| Veenstra et al., 2010 (42)14 | ||||||||||||
| Chickpea | 19 (19:0) | 28.1 ± 5.9 | 25.2 ± 2.5 | Crossover | Supplement | Chickpea | 275 | Potato | 55:29:1510 | Neutral | 4 | 6 |
| Lentil | 19 (19:0) | Lentil | 53:29:1810 | |||||||||
| Pea | 20 (20:0) | Pea | 56:27:1710 | |||||||||
| Potato | 21 (21:0) | — | — | — | — |
| Reference | Total subjects, n (M:F) | Age, y | BMI, kg/m2 | Design | Feeding2 | Pulse type | Dose,3 g/d | Comparator | Diet,4 % | Energy balance5 (% of energy) | Follow-up, wk | MQS6 |
| Abete et al., 2009 (24) | 18 (18:0) | 37.1 ± 8.07 | 31.6 ± 3.7 | Parallel | DA | Mixed | 113 | No pulses | 53:30:17 | Negative (30) | 8 | 9 |
| Abeysekara et al., 2012 (25) | 838,9 | 59.7 ± 6.3 | 27.5 ± 4.5 | Crossover | Supplement | Mixed | 250 | Usual diet | 49:37:1610 | Neutral | 8 | 9 |
| Anderson et al., 1984 (26) | 20 (20:0) | 54.0 ± 8.5 | Overweight11 | Parallel | Metabolic | Beans | 278 | Oat | 43:37:20 | Neutral | 3 | 5 |
| Anderson et al., 1990 (27) | ||||||||||||
| A | 6 (6:0) | 64.0 ± 2.4 | Overweight11 | Parallel | Metabolic | Bean | 113 | No pulses | 43:28:19 | Neutral | 4 | 5 |
| B | 9 (9:0) | 57.0 ± 9.0 | Overweight11 | Parallel | Metabolic | Bean | 113 | No pulses | 43:28:19 | Neutral | 4 | 5 |
| C | 9 (9:0) | 54.0 ± 9.0 | Overweight11 | Parallel | Metabolic | Bean | 152 | No pulses | 43:28:19 | Neutral | 4 | 5 |
| Belski et al., 2011 (28) | 93 (52:41) | 46.6 ± 9.7 | 31.4 ± 2.7 | Parallel | DA and supplement | Bean | 124 | Wheat | 39:32:2210 | Negative (35) | 48 | 8 |
| Crujeiras et al., 2007 (29) | 30 (17:13) | 36.0 ± 8.0 | 32.0 ± 5.3 | Parallel | DA | Mixed | 94 | No pulses | 50:30:20 | Negative (30) | 8 | 8 |
| Gravel et al., 2010 (30) | 114 (0:114) | 51.3 ± 8.7 | 29.9 ± 5.1 | Parallel | Supplement | Mixed | 81 | No pulses | 49:33:1710 | Neutral | 16 | 7 |
| Hermsdorff et al., 2011 (31) | 30 (17:13) | 36.0 ± 8.0 | 32.5 ± 4.5 | Parallel | DA | Mixed | 113 | No pulses | 53:30:17 | Negative (30) | 8 | 8 |
| Hodgson et al., 2010 (32) | 74 (26:48) | 57.9 ± 8.0 | 30.6 ± 3.5 | Parallel | Supplement | Bean | 132 | Wheat | 39:31:2410 | Neutral | 16 | 7 |
| Jenkins et al., 2012 (33) | 121 (61:60) | 59.5 ± 9.1 | 30.6 ± 6.3 | Parallel | DA | Mixed | 211 | Wheat | 45:23:3110 | Neutral | 12 | 8 |
| Jimenez-Cruz et al., 2004 (34) | 89 | 51.0 ± 3.0 | 30.7 ± 7.9 | Crossover | DA | Bean | 97 | High GI | 51:26:2310 | Neutral | 3 | 8 |
| Mackay and Ball, 1992 (35) | 39 (22:17) | 22.0–66.012 | 26.7 | Crossover | Supplement | Bean | 80 | Oat | 53:28:1710 | Neutral | 22 | 5 |
| Marinangeli and Jones, 2011 (36) | 23 (7:16) | 52.1 ± 10.6 | 30.2 ± 4.3 | Crossover | Metabolic | Pea | 138 | Wheat | 55:30:15 | Neutral | 4 | 6 |
| Nestel et al., 2004 (37) | 19 (9:10) | 56.6 ± 7.6 | 25.6 ± 3.2 | Crossover | Supplement | Chickpea | 140 | Wheat | 47:30:1910 | Neutral | 6 | 5 |
| Pittaway et al., 2006 (38) | 47 (19:28) | 53.0 ± 9.8 | 27.6 ± 4.1 | Crossover | DA and supplement | Chickpea | 140 | Wheat | 46:32:1810 | Neutral | 5, 613 | 5 |
| Pittaway et al., 2007 (39) | 27 (10:17) | 50.6 ± 10.5 | 28.8 ± 4.4 | Crossover | DA and supplement | Chickpea | 140 | Wheat | 44:34:1710 | Neutral | 5 | 6 |
| Saraf-Bank et al., 2015 (40) | 26 (12:14) | 50.0 ± 1.3 | 28.9 ± 0.9 | Crossover | DA and supplement | Mixed | 111 | No pulses | 66:20:1610 | Neutral | 6 | 8 |
| Tonstad et al., 2014 (41) | 1239 | 48.4 ± 10.7 | 36.5 ± 3.9 | Parallel | DA and supplement | Mixed | 250 | Low carb | 52:28:1910 | Neutral | 16 | 6 |
| Veenstra et al., 2010 (42)14 | ||||||||||||
| Chickpea | 19 (19:0) | 28.1 ± 5.9 | 25.2 ± 2.5 | Crossover | Supplement | Chickpea | 275 | Potato | 55:29:1510 | Neutral | 4 | 6 |
| Lentil | 19 (19:0) | Lentil | 53:29:1810 | |||||||||
| Pea | 20 (20:0) | Pea | 56:27:1710 | |||||||||
| Potato | 21 (21:0) | — | — | — | — |
Carb, carbohydrate; DA, Dietary Advice; GI, glycemic index; MQS, Methodologic Quality Score
Metabolic feeding was the provision of all meals and study supplements (treatment and control foods) consumed in the study under controlled conditions. Supplement feeding was the provision of study supplements only. DA was the provision of counseling on treatment and control diets.
Pulse doses are given as cooked weight. We used the following conversion factors: 1 g dry pulses = 2.75 g cooked pulses; and 1 mL pulses = 0.76 g pulses.
Energy from carbohydrate:fat:protein intended for the intervention.
Negative energy balance refers to studies in which both dietary pulse and comparator arms were calorically restricted (i.e., weight-loss diets). Neutral energy balance refers to studies in which both dietary pulse and comparator arms had caloric intakes intended to meet their total energy needs (i.e., weight-maintaining diets).
Study quality was assessed with the use of the Heyland MQS. A score ≥8 was considered higher quality.
Mean ± SD (all such values).
n = 82 for the waist-circumference endpoint.
Sex of participants at end of study was not provided in the original article.
End-measured macronutrient intake in the intervention arm.
Baseline BMI was not given, but patients were described as overweight.
Range.
Pittaway et al. (38) performed the randomized controlled trial in 2 separate groups, one of which had 5 wk of follow-up, and the other of which had 6 wk of follow-up.
Veenstra et al. (42) had 3 different dietary pulse intervention arms in the same participants (crossover trial). The arm with the most participants (i.e., the control potato arm) was used to calculate the total meta-analysis participant number.
All studies were randomized; however, the crossover trials by Anderson et al. (27) randomly assigned 3 groups of participants to receive graded doses of dietary pulses followed by a control diet. Because the treatment order was not randomly allocated, we used individual subject data to assign participants to treatment groups (stratified on weight and age), which minimized order effects and allowed these data to be analyzed as 3 separate trials. Most of the trial intervention arms used mixed (38%, n = 8) or bean dietary pulse types (38%, n = 8), whereas some trials used chickpeas (19%, n = 4), dried peas (10%, n = 2), or lentils (5%, n = 1) alone. The median dose of dietary pulses given was 132 g/d [0.5–0.75 cups/d or ∼1 serving/d (43, 44)] in cooked weight (IQR: 113–152 g/d).
In each of the trials, the dietary pulse intervention diet and comparator diet were isocaloric (matched for calories). As for the overall energy balance, 4 trials (19%) were designed to restrict caloric intake (by 30–35% of total energy) in both the dietary pulse and control arms (24, 28, 29, 31). We declared this assessment to be a matched negative–energy-balance diet comparison, which invoked a weight-loss diet. The other 17 trials were designed to provide matched neutral–energy-balance comparisons, which were intended to maintain weight.
According to the Heyland MQS, 8 of 19 publications (42%) were rated high quality (MQS ≥8). The individual risk-of-bias evaluation showed 7 reports had low risk of bias because the majority of their categories were rated as low risk. The remaining 12 reports were rated as having unclear risk of bias. High risk of bias was rated rarely across categories of reports (see Supplemental Figures 1 and 2 for the risk of bias summary figure and proportion graph, respectively).
Dietary pulses on body weight
The pooled effect of dietary pulses on body weight is shown in Figure 2. Compared with control diets, dietary pulses reduced body weight under both neutral–energy-balance (weight-maintaining) and negative–energy balance (weight-loss) diets [−0.29 kg (95% CI: −0.56, −0.03 kg; P = 0.03) and −1.74 kg (95% CI: −3.19, −0.30 kg; P = 0.02), respectively]. The overall pooled analysis showed that dietary pulse–containing arms had reduced body weight by −0.34 kg (95% CI: −0.63, −0.04 kg; P = 0.03) compared with that of control arms with low evidence of between-study heterogeneity (I2 = 9%, P-heterogeneity = 0.34).
Forest plot of randomized controlled trials investigating the effects of dietary pulses on body weight (kg). n = 940. Analyses were separated into subgroups of matched negative energy balance (in which both dietary pulse and comparator arms were calorically restricted by 30–35% of total energy; i.e., weight-loss diets) and matched neutral energy balance (in which both dietary pulse and comparator arms had caloric intakes intended to meet their total energy needs; i.e., weight-maintaining diets). The mean differences are represented by a square and 95% CIs by the line through the square. 95% CIs exceeding the plot’s bounds are represented by an arrowhead. Pooled effects are represented by diamonds and were estimated with the use of generic inverse variance random-effects models. Between-study heterogeneity was detected with the use of the Cochran’s Q statistic and quantified with the use of the I2 statistic. 1Weight (%) quantifies the contribution of a study to the overall pooled effect size. Each study was weighted according to the inverse of the variance of effect size.
Forest plot of randomized controlled trials investigating the effects of dietary pulses on body weight (kg). n = 940. Analyses were separated into subgroups of matched negative energy balance (in which both dietary pulse and comparator arms were calorically restricted by 30–35% of total energy; i.e., weight-loss diets) and matched neutral energy balance (in which both dietary pulse and comparator arms had caloric intakes intended to meet their total energy needs; i.e., weight-maintaining diets). The mean differences are represented by a square and 95% CIs by the line through the square. 95% CIs exceeding the plot’s bounds are represented by an arrowhead. Pooled effects are represented by diamonds and were estimated with the use of generic inverse variance random-effects models. Between-study heterogeneity was detected with the use of the Cochran’s Q statistic and quantified with the use of the I2 statistic. 1Weight (%) quantifies the contribution of a study to the overall pooled effect size. Each study was weighted according to the inverse of the variance of effect size.
The sensitivity analysis, in which each individual trial was removed, and the pooled effect was recalculated with the remaining 20 trials, did not largely affect the overall heterogeneity (I2 ≤ 13%, P-heterogeneity ≥ 0.29). Six studies were influential study outliers in that their removal altered the magnitude of the pooled effect in the remaining studies by >10% (25, 33, 36, 40–42). In addition, the removal of the studies of Jenkins et al. (33) and Saraf-Bank et al. (40) rendered the results no longer significant [−0.19 kg (95% CI: −0.51, 0.12 kg; P = 0.23) and −0.30 kg (95% CI: −0.63, 0.03 kg; P = 0.08), respectively; forest plots not shown). The sensitivity analysis with the use of different levels of correlation coefficients (0.25 and 0.75) for the crossover studies did not influence the weight-loss effect or heterogeneity in the overall pooled results.
Although our main analysis showed no evidence of heterogeneity, the lower power of heterogeneity tests conveyed that important subgroup effects may have been missed despite no statistical evidence of heterogeneity. Therefore, we undertook a priori subgroup analyses to explore the possibility that sources of heterogeneity went undetected (Figure 3). Only the MQS was a significant effect modifier of the weight-loss effect of dietary pulses. High-quality trials showed a 0.60-kg weight loss compared with lower-quality trials that showed a 0.05-kg weight gain (P = 0.04) (for a forest plot of only high-quality studies, see Supplemental Figure 3). We also observed a small but insignificant association for greater weight loss in the dietary pulse arm (0.58 kg) in studies with a parallel-study design (P = 0.07).
Subgroup analysis for mean differences (95% CIs) of the effects of dietary pulses on body weight. n = 940. The dashed line represents the pooled estimate for the overall primary analysis of dietary pulse intake on body weight. Within subgroup mean differences are the pooled effect estimates represented by a diamond. 95% CIs are represented by the line through the square and 95% CIs exceeding the plot’s bounds are represented by an arrowhead, and were estimated with the use of a meta-regression analysis. The residual I2 was estimated with the use of the Cochran’s Q statistic. P < 0.05 indicated that the effect size differed between levels of the subgroup. P values were based on independent-samples t tests of group means. 1The residual I2 is an estimate of the proportion of unexplained between-studies heterogeneity that remains after accounting for the variability in response because of the specific between-studies factor. For example, a residual I2 of 0% for Sat fat intake suggested that, after accounting for differences in the change in Sat fat intake between studies, there was no longer any evidence of unexplained heterogeneity. A residual I2 of 30% for baseline weight suggested that accounting for between-studies differences in the baseline weight of the enrolled participants did not contribute to a reduction of unexplained heterogeneity. 2Represents the I2 from the primary meta-analysis (Figure 2). 3Represents the P value for the primary meta-analysis (Figure 2).4Veenstra et al. (42) administered 3 different dietary pulse intervention arms within the same participants in a crossover design that yielded 23 dietary pulse types across 21 trials. 5Where 1 denotes bean, 2 denotes chickpea, 3 denotes lentil, 4 denotes pea, and 5 denotes mixed; 1 compared with 2: −0.18 (−1.27, 0.91), 1 compared with 3: −0.22 (−1.55, 1.11), 1 compared with 4: −0.49 (−1.52, 0.53), 1 compared with 5: 0.80 (−0.30, 1.90), 2 compared with 3: −0.04 (−1.45, 1.38), 2 compared with 4: −0.31 (−1.45, 0.82) 2 compared with 5: 0.98 (−0.22, 2.18), 3 compared with 4: −0.28 (−1.64, 1.08), 3 compared with 5: 1.02 (−0.40, 2.44), and 4 compared with 5: 1.29 (0.15, 2.43). MQS, Methodologic Quality Score; Sat, saturated.
Subgroup analysis for mean differences (95% CIs) of the effects of dietary pulses on body weight. n = 940. The dashed line represents the pooled estimate for the overall primary analysis of dietary pulse intake on body weight. Within subgroup mean differences are the pooled effect estimates represented by a diamond. 95% CIs are represented by the line through the square and 95% CIs exceeding the plot’s bounds are represented by an arrowhead, and were estimated with the use of a meta-regression analysis. The residual I2 was estimated with the use of the Cochran’s Q statistic. P < 0.05 indicated that the effect size differed between levels of the subgroup. P values were based on independent-samples t tests of group means. 1The residual I2 is an estimate of the proportion of unexplained between-studies heterogeneity that remains after accounting for the variability in response because of the specific between-studies factor. For example, a residual I2 of 0% for Sat fat intake suggested that, after accounting for differences in the change in Sat fat intake between studies, there was no longer any evidence of unexplained heterogeneity. A residual I2 of 30% for baseline weight suggested that accounting for between-studies differences in the baseline weight of the enrolled participants did not contribute to a reduction of unexplained heterogeneity. 2Represents the I2 from the primary meta-analysis (Figure 2). 3Represents the P value for the primary meta-analysis (Figure 2).4Veenstra et al. (42) administered 3 different dietary pulse intervention arms within the same participants in a crossover design that yielded 23 dietary pulse types across 21 trials. 5Where 1 denotes bean, 2 denotes chickpea, 3 denotes lentil, 4 denotes pea, and 5 denotes mixed; 1 compared with 2: −0.18 (−1.27, 0.91), 1 compared with 3: −0.22 (−1.55, 1.11), 1 compared with 4: −0.49 (−1.52, 0.53), 1 compared with 5: 0.80 (−0.30, 1.90), 2 compared with 3: −0.04 (−1.45, 1.38), 2 compared with 4: −0.31 (−1.45, 0.82) 2 compared with 5: 0.98 (−0.22, 2.18), 3 compared with 4: −0.28 (−1.64, 1.08), 3 compared with 5: 1.02 (−0.40, 2.44), and 4 compared with 5: 1.29 (0.15, 2.43). MQS, Methodologic Quality Score; Sat, saturated.
Metaregression analyses did not reveal any significant linear associations of between-study–level characteristics and the effect size in respect to the dose of dietary pulse intake, fiber intake, change in fiber intake from baseline, saturated fat intake, and change in saturated fat intake from baseline in the intervention arm (P ≥ 0.09) (Supplemental Table 2).
Dietary pulses and waist circumference and body fat
The pooled effect of 6 trials (n = 509 participants) that reported on dietary pulse consumption on waist circumference is shown in Figure 4. Diets that included dietary pulses did not significantly reduce waist circumference (−0.37 cm; 95% CI: −1.44, 0.71 cm; P = 0.51), but a trend was seen in 6 trials (n = 340 participants) that favored a reduction in body fat (−0.34%; 95% CI: −0.71, 0.03 cm; P = 0.07) (Figure 5). There was no evidence of significant heterogeneity for either endpoint (I2 = 43%, P-heterogeneity = 0.12 for waist circumference; I2 = 0%, P-heterogeneity = 0.97 for body fat).
Forest plot of randomized controlled trials investigating the effects of dietary pulses on waist circumference (cm). n = 509. Analyses were separated into subgroups of matched negative energy balance (in which both dietary pulse and comparator arms were calorically restricted by 30–35% of total energy; i.e., weight-loss diets) and matched neutral energy balance (in which both dietary pulse and comparator arms had caloric intakes intended to meet their total energy needs; i.e., weight-maintaining diets). The mean differences are represented by a square and 95% CIs by the line through the square. 95% CIs exceeding the plot’s bounds are represented by an arrowhead. Pooled effects are represented by diamonds and were estimated with the use of generic inverse variance random-effects models. Between-study heterogeneity was detected with the use of the Cochran’s Q statistic and quantified with the use of the I2 statistic. 1Weight (%) quantifies the contribution of a study to the overall pooled effect size. Each study was weighted according to the inverse of the variance of effect size.
Forest plot of randomized controlled trials investigating the effects of dietary pulses on waist circumference (cm). n = 509. Analyses were separated into subgroups of matched negative energy balance (in which both dietary pulse and comparator arms were calorically restricted by 30–35% of total energy; i.e., weight-loss diets) and matched neutral energy balance (in which both dietary pulse and comparator arms had caloric intakes intended to meet their total energy needs; i.e., weight-maintaining diets). The mean differences are represented by a square and 95% CIs by the line through the square. 95% CIs exceeding the plot’s bounds are represented by an arrowhead. Pooled effects are represented by diamonds and were estimated with the use of generic inverse variance random-effects models. Between-study heterogeneity was detected with the use of the Cochran’s Q statistic and quantified with the use of the I2 statistic. 1Weight (%) quantifies the contribution of a study to the overall pooled effect size. Each study was weighted according to the inverse of the variance of effect size.
Forest plot of randomized controlled trials investigating effects of dietary pulses on body fat (%). n = 340. Analyses were separated into subgroups of matched negative energy balance (in which both dietary pulse and comparator arms were calorically restricted by 30–35% of total energy; i.e., weight-loss diets) and matched neutral energy balance (in which both dietary pulse and comparator arms had caloric intakes intended to meet their total energy needs; i.e., weight-maintaining diets). The mean differences are represented by a square and 95% CIs by the line through the square. Pooled effects are represented by diamonds and were estimated with the use of generic inverse variance random-effects models. Between-study heterogeneity was detected with the use of the Cochran’s Q statistic and quantified with the use of the I2 statistic. 1Weight (%) quantifies the contribution of a study to the overall pooled effect size. Each study was weighted according to the inverse of the variance of effect size.
Forest plot of randomized controlled trials investigating effects of dietary pulses on body fat (%). n = 340. Analyses were separated into subgroups of matched negative energy balance (in which both dietary pulse and comparator arms were calorically restricted by 30–35% of total energy; i.e., weight-loss diets) and matched neutral energy balance (in which both dietary pulse and comparator arms had caloric intakes intended to meet their total energy needs; i.e., weight-maintaining diets). The mean differences are represented by a square and 95% CIs by the line through the square. Pooled effects are represented by diamonds and were estimated with the use of generic inverse variance random-effects models. Between-study heterogeneity was detected with the use of the Cochran’s Q statistic and quantified with the use of the I2 statistic. 1Weight (%) quantifies the contribution of a study to the overall pooled effect size. Each study was weighted according to the inverse of the variance of effect size.
For waist circumference, the removal of the study by Jenkins et al. (33) changed the effect direction (0.12 cm; 95% CI: −0.89, 1.13 cm; P = 0.82), whereas the removal of the study by Veenstra et al. (42) made the effect significant (−1.01%; 95% CI: −1.74%, −0.28%; P = 0.007). For body fat percentage, no studies were influential outliers. Metaregression analyses were not undertaken because of the small number of studies included for these endpoints.
Publication bias
We showed no evidence of funnel-plot asymmetry or statistical support for small-study effects across all trials with the use of either Egger’s or Begg’s tests (P > 0.05 for both) (Supplemental Figure 4).
DISCUSSION
The current systematic review and meta-analysis quantified the effects of dietary pulse consumption on weight loss in 21 randomized controlled trials in 940 predominately overweight or obese, middle-aged men and women. The pooled analysis showed an overall small but significant weight reduction of −0.34 kg in diets that contained dietary pulses (from 80 to 278 g/d; median intake: 132 g/d or ∼1 serving/d) compared with diets without a dietary pulse intervention over a median duration of 6 wk (P = 0.03). The stratification of our analysis into subgroups showed significant weight loss in the dietary pulse arm for negative–energy balance (weight-loss) conditions but also under neutral energy balance (weight maintaining) conditions (P ≤ 0.03). Our findings also provided some evidence that dietary pulse–containing diets may reduce body fat, which would support the WHO recommendations to consume legumes to reduce overweight and obesity (1).
We observed that high-quality trials of dietary pulse interventions yielded larger weight-loss effects than lower quality trials did, which was consistent with a need for careful attention to detail when designing and executing diet and weight-loss studies.
We showed that dietary pulses produced weight loss under conditions of neutral energy balance. The consumption of dietary pulses resulted in significant weight loss at the end of the trials although the interventions were designed to be weight-maintaining diets. This result indicated that dietary pulses may be effective for weight loss even when incorporated into a noncalorically restricted diet, thereby providing a potentially effective alternative for calorie-restricted–based diets that may be difficult to adhere to.
Our findings update the results of a much earlier meta-analysis. Anderson and Major (12) conducted the only meta-analysis that examined the effect of dietary pulses on weight in 8 trials in 2002. They failed to support a significant role for dietary pulses in reducing body weight and reported a 0.93% body weight reduction in the dietary pulse intervention relative to that in the control arms (approximated loss of 0.68 kg, P > 0.05) (12). However, the authors of the meta-analysis did not provide a clear description of their search and selection strategy, which makes it difficult to assess the study-selection bias. Although the absolute weight loss was greater than our reported value, the lack of significance may have been a result of low statistical power because our study added 16 new trials that have been published (24, 25, 28–34, 36–42) since the article by Anderson and Major (12).
Although there is currently limited evidence on dietary pulse consumption and body weight in observational studies, a cross-sectional study by Papanikolaou and Fulgoni (45) with the use of NHANES data reported that bean consumption was associated with a lower body weight and waist size, and individuals who consumed beans were 22% less likely to be obese (P = 0.03) than were those who did not consume beans. Although observational studies only support causation, Mollard et al. (46) published a randomized controlled trial that showed that a weight-maintaining diet that was high in dietary pulses reduced waist circumference to the same extent as did a calorie-restricted diet in 24 young-adult healthy men. This result also supports our findings in that dietary pulse consumption contributed to weight loss without explicit caloric restriction.
There are several mechanisms that could explain the weight loss seen in negative–energy-balanced (weight-loss) and neutral–energy-balanced (weight-maintaining) diets in our systematic review and meta-analysis. One mechanism may have been the satiating properties of dietary pulses (11, 47, 48). A recent systematic review and meta-analysis that evaluated 9 trials in 129 participants revealed a 31% increase in subjective satiety after a meal that contained dietary pulses compared with after a control meal, which was determined to be clinically meaningful (5). Dietary pulses may contribute to these satiety effects because of several physiologic properties, such as being high in fiber and protein and low in the GI. High-fiber foods such as dietary pulses contribute to the feeling of fullness because it increases the chewing time, thereby decreasing intake rates and stimulating early satiety signals (2). The soluble fibers in dietary pulses may also delay gastric emptying and the absorption of nutrients as they form viscous gels, thereby slowing their passage through the digestive system (2). The high-protein content of dietary pulses stimulates the secretion of the gastric hormones cholecystokinin and glucagon-like peptide-1, which causes the sensation of fullness (3). Last, low-GI diets regulate blood glucose concentrations and insulin release, which may prevent overeating and promote weight control (4, 6). These satiating effects may improve adherence to an energy-reduced diet and help prevent overeating in ad libitum settings.
The reduced bioavailability of calories from nutrients may be another means by which dietary pulses contribute to weight loss. Previous human trials have shown that high-fiber diets substantially reduce the absorption of fat and protein because they may lower the physical contact of the nutrients with intestinal villi (2), reduce the absorption in the gut due to the gel-forming properties of soluble fiber, or increase the rate of passage by insoluble fiber (49–51). Another important component that contributes to a reduced nutrient bioavailability is the properties of the cell walls of dietary pulses. White beans have been observed to have intact cell walls that encapsulate starch granules after digestion in the ileum that allows the internal content to escape digestion, thereby reducing their energy content (52). This protection provided by the cell walls in dietary pulses may be an important component in the reduction of the bioavailability of nutrients because the cell wall restricts the access of digestive enzymes to the dietary pulses’ internal starches (53).
There were several limitations to our analyses. Our sensitivity analyses indicated that the observed weight-loss effects were largely driven by one trial (33). This finding merits caution when interpreting our findings. Many of the trials were of short duration in terms of seeing an effective weight loss (range: 4–10 wk), which did not allow us to evaluate the long-term effects of dietary pulses on body weight or other endpoints. In addition, only 42% of the included reports were considered to be of high quality (MQS ≥8); however, our subgroup analysis showed a significant trend (P = 0.04) that favored greater weight loss in higher-quality reports, thus arguing against the undue weighting of less–methodologically rigorous trials. Last, the majority of trials were rated to have unclear risks of bias.
In conclusion, we showed modest weight loss with dietary pulse consumption in both explicitly calorie-restricted settings and in settings with intended weight maintenance. These findings are generalizable to a middle-aged, overweight and obese population and suggest that the incorporation of 1 serving of dietary pulses/d may be a useful weight-loss strategy in a normal or calorically reduced diet. Although the clinical significance of a <1-kg weight loss is likely marginal, this finding is encouraging because it suggests that dietary pulses do not lead to weight gain when incorporated into diets. The maintenance of reduced weight after weight loss remains a clinical challenge (54). Dietary pulses are satiating (5), affordable, and a sustainable source of protein and fiber that can be incorporated into weight-maintenance diets. Furthermore, there are additional health benefits of including dietary pulses in the diet that are related to cardiometabolic risk reduction because they improve markers of glycemic control (18), reduce LDL-cholesterol concentrations (19), and lower blood pressure (21), even without weight loss. Few randomized controlled trials have investigated the effects of dietary pulses on other measures of adiposity, such as waist circumference and body fat percentage. Future studies are warranted to clarify this effect. Additional long-term trials are also suggested to monitor the sustainability of the observed weight change.
The authors’ responsibilities were as follows—SJK and RJdS: wrote the manuscript and had primary responsibility for the final content of the manuscript; SJK, RJdS, and AIC: performed the statistical analysis; SJK and VLC: conducted the research; RJdS, MDB, AMB, LAL, PMK-E, VV, JB, CWCK, DJAJ, and JLS: designed the research; and all authors: contributed to the critical revision of the manuscript for important intellectual content and approved the final manuscript. At the time this manuscript was prepared, RJdS was funded by a Canadian Institutes of Health Research (CIHR) Postdoctoral Fellowship Award. He has received research support from the CIHR, the Calorie Control Council, the Canadian Foundation for Dietetic Research, and The Coca-Cola Company (investigator initiated, unrestricted grant). RJdS has served as an external resource person to WHO’s Nutrition Guidelines Advisory Group and received travel support from the WHO to attend group meetings. RJdS is the lead author of systematic reviews and meta-analyses commissioned by the WHO on the relation of saturated and trans fatty acids with health outcomes. VH has received funding from the CIHR, McMaster University, Province of Ontario, and the University of Toronto. She is the recipient of The Ashbaugh Graduate Scholarship. She has received payment from the WHO for work on a systematic review and meta-analysis commissioned by the WHO for work on the relation of saturated fatty acids with health outcomes. VH and her peers received a cash prize for placing second in the regional “Mission Impulsible” Competition, where they conceived and developed a marketable food product that contained dietary pulses. VH received a travel award to attend the “Journey Through Science Day” hosted by PepsiCo and the New York Academy of Sciences and received a Nutrica Travel Award from the Diabetes and Nutrition Study Group (DNSG) of the European Association for the Study of Diabetes (EASD). AIC has received research support from the CIHR and the WHO for work on a systematic review and meta-analysis commissioned by the WHO on the relation of saturated fatty acids with health outcomes and a travel award to attend a science day hosted by PepsiCo Inc. and the New York Academy of Sciences. He was funded by the Province of Ontario Graduate Scholarships and is funded by a CIHR Fredrick Banting and Charles Best Canada Graduate Scholarship and a Banting & Best Diabetes Centre (BBDC)-Novo Nordisk Studentship. LC has received research support from the CIHR and the Agricultural Bioproducts Innovation Program through the Pulse Research Network and from Saskatchewan Pulse Growers. LC is also a casual clinical research coordinator at Glycemic Index Laboratories Inc, which is a clinical research organization. VV holds the Canadian (2,410,556) and American (7,326.404) patents on medical use of a viscous fiber blend for reducing blood glucose for the treatment of diabetes, increasing insulin sensitivity, and the reduction of systolic blood pressure and blood lipids and is the vice president and part owner of Glycemic Index Laboratories Inc. and has received an in-kind donation of chia (in 2000) and salba (in 2001, 2009, and 2011) seeds for research and partial grant funding from companies who grow and distribute these products. JB has received research support from the CIHR, the Calorie Control Council, and The Coca-Cola Company (investigator initiated, unrestricted). CWCK has received research support from the Advanced Foods and Material Network, Agriculture and Agri-Food Canada, the Almond Board of California, the American Pistachio Growers, Barilla, the California Strawberry Commission, the Calorie Control Council, the CIHR, the Canola Council of Canada, The Coca-Cola Company (investigator initiated, unrestricted grant), the Hain Celestial Group, the International Tree Nut Council Nutrition Research and Education Foundation, the Kellogg Company, Kraft Foods Group Inc., Loblaw Companies Ltd., Orafti, Pulse Canada, Saskatchewan Pulse Growers, Solae, and Unilever. CWCK has received travel funding, consultant fees, or honoraria from Abbott Laboratories, the Almond Board of California, the American Peanut Council, the American Pistachio Growers, Barilla, Bayer, the Canola Council of Canada, The Coca-Cola Company, Danone, General Mills Inc., the International Tree Nut Council Nutrition Research and Education Foundation, the Kellogg Company, Loblaw Companies Ltd., the Nutrition Foundation of Italy, Oldways Preservation Trust, Orafti, Paramount Farms, the Peanut Institute, PepsiCo, Pulse Canada, Sabra Dipping Co., Saskatchewan Pulse Growers, Solae, Sun-Maid Growers of California, Tate & Lyle, and Unilever. CWCK is on the Dietary Guidelines Committee for the Diabetes Nutrition Study Group of the EASD and has served on the scientific advisory board for the Almond Board of California, the International Tree Nut Council, the Oldways Preservation Trust, Paramount Farms, and Pulse Canada. DJAJ has received research grants from Saskatchewan Pulse Growers, the Agricultural Bioproducts Innovation Program through the Pulse Research Network, the Advanced Foods and Material Network, Loblaw Companies Ltd., Unilever, Barilla, the Almond Board of California, Agriculture and Agri-Food Canada, Pulse Canada, Kellogg Canada Inc., Quaker Canada, Procter & Gamble Technical Centre Ltd., Bayer Consumer Care (Springfield, NJ), PepsiCo/Quaker Oats Company, International Nut & Dried Fruit, Soy Foods Association of North America, The Coca-Cola Company (investigator initiated, unrestricted grant), Solae, the Haine Celestial Group Inc., the Sanitarium Company, Orafti, the International Tree Nut Council Nutrition Research and Education Foundation, the Peanut Institute, the Canola and Flax Councils of Canada, the Calorie Control Council, the CIHR, the Canada Foundation for Innovation, and the Ontario Research Fund. DJAJ has been on the speaker’s panel, served on the scientific advisory board, or received travel support or honoraria from the Almond Board of California, Canadian Agriculture Policy Institute, Loblaw Companies Ltd., the Griffin Hospital (for the development of the NuVal scoring system; NuVal LLC), EPICURE, Danone, Saskatchewan Pulse Growers, the Sanitarium Company, Orafti, the American Peanut Council, the International Tree Nut Council Nutrition Research and Education Foundation, the Peanut Institute, Herbalife International, Pacific Health Laboratories, Barilla, Metagenics, Bayer Consumer Care, Unilever Canada and Netherlands, Solae LLC, the Kellogg Company, the Quaker Oats Company, Procter & Gamble, The Coca-Cola Company, Abbott Laboratories, the Canola Council of Canada, Dean Foods, the California Strawberry Commission, the Haine Celestial Group Inc., PepsiCo, the Alpro Foundation, Pioneer Hi-Bred International Inc., DuPont Nutrition & Health, Spherix Consulting and WhiteWave Foods, the Advanced Foods and Material Network, the Flax Council of Canada, the Nutritional Fundamentals for Health, Agriculture and Agri-Food Canada, the Canadian Agri-Food Policy Institute, Pulse Canada, the Soyfoods Association of North America, the Nutrition Foundation of Italy (NFI), Nutrasource Diagnostics, the McDougall Program, the Toronto Knowledge Translation Group (St. Michael’s Hospital), the Canadian College of Naturopathic Medicine, The Hospital for Sick Children, the Canadian Nutrition Society (CNS), the American Society of Nutrition (ASN), Arizona State University, the Paolo Sorbini Foundation, and the Institute of Nutrition, Metabolism and Diabetes. DJAJ received an honorarium from the USDA to present the 2013 WO Atwater Memorial Lecture and the 2013 Award for Excellence in Research from the International Nut and Dried Fruit Council. DJAJ received funding and travel support from the Canadian Society of Endocrinology and Metabolism to produce mini cases for the Canadian Diabetes Association (CDA) and is a member of the International Carbohydrate Quality Consortium. DJAJ’s wife, Alexandra L Jenkins, is a director and partner of Glycemic Index Laboratories Inc., and his sister, Caroline Brydson, received funding through a grant from the St. Michael’s Hospital Foundation to develop a cookbook for one of his studies. JLS has received research support from the CIHR, ASN, CDA, BBDC, Calorie Control Council, The Coca-Cola Company (investigator initiated, unrestricted), Dr. Pepper Snapple Group (investigator initiated, unrestricted), Pulse Canada, and the International Tree Nut Council Nutrition Research and Education Foundation. He has received travel funding, speaker fees, and/or honoraria from the American Heart Association, the American College of Physicians, ASN, the National Institute of Diabetes and Digestive and Kidney Diseases of the NIH, CDA, CNS, the University of South Carolina, the University of Alabama at Birmingham, the Oldways Preservation Trust, NFI, the Calorie Control Council, the Diabetes and Nutrition Study Group of the EASD, International Life Sciences Institute (ILSI) North America, ILSI Brazil, Abbott Laboratories, Pulse Canada, Canadian Sugar Institute, Dr. Pepper Snapple Group, The Coca-Cola Company, Corn Refiners Association, World Sugar Research Organisation, Dairy Farmers of Canada, and Società Italiana di Nutrizione Umana. He has consulting arrangements with Winston & Strawn LLP, Perkins Coie LLP, and Tate & Lyle. He is on the Clinical Practice Guidelines Expert Committee for Nutrition Therapy of both the CDA and EASD and serves on an ASN writing panel for a scientific statement on sugars. He is a member of the International Carbohydrate Quality Consortium and Board Member of the Diabetes and Nutrition Study Group of the EASD. He serves as an unpaid scientific advisor for the ILSI North America Food, Nutrition, and Safety Program and the Committee on Carbohydrates. JLS’s wife, Marcella Garsetti, is an employee of Unilever Canada. SJK, VLC, AM, SBM, MDB, AMB, LAL, and PMK-E reported no conflicts of interest related to the study.
FOOTNOTES
Supported by a Canadian Institutes of Health Research Knowledge Synthesis grant (119797). RJdS was supported by a Canadian Institutes of Health Research (CIHR) Postdoctoral Fellowship Award. VLC was supported by a Banting and Best Graduate Scholarship from the CIHR, Mary H. Beatty Fellowship. VH was supported by a Province of Ontario Graduate Scholarship. AIC was supported by a Province of Ontario Graduate Scholarship and by a CIHR-Fredrick Banting and Charles Best Canada Graduate Scholarship and Banting and Best Diabetes Centre-Novo Nordisk Studentship. AM was funded by a CIHR Canada Graduate Scholarship Master’s Award. DJAJ was supported by the Government of Canada through the Canada Research Chair Endowment. JLS was supported by a PSI Graham Farquharson Knowledge Translation Fellowship, Canadian Diabetes Association Clinician Scientist award, CIHR INMD/CNS New Investigator Partnership Prize, and Banting & Best Diabetes Centre Sun Life Financial New Investigator Award.
None of the sponsors had a role in any aspect of the current study, including the design and conduct of the study; collection, management, analysis, and interpretation of the data; and preparation, review, and approval of the manuscript.





