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Clinical Nutrition xxx (2017) 1e8

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Contents lists available at ScienceDirect 56
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Clinical Nutrition 59
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journal homepage: http://www.elsevier.com/locate/clnu 61
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Meta-analyses 64
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1 Dietary ber intake and risk of metabolic syndrome: A meta-analysis 66
2 67
3 Q4 of observational studies 68
4 69
5 Q3 Baozhu Wei a, 1, Yang Liu b, 1, Xuan Lin b, Ying Fang b, Jing Cui b, Jing Wan a, * 70
6 a 71
Department of Cardiology, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, China
7 b 72
Department of Endocrinology, China Resource and WISCO General Hospital, Wuhan, China
8 73
9 74
10 75
a r t i c l e i n f o s u m m a r y
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12 77
Article history: Background & aims: Epidemiological studies show inconsistent ndings on the association of dietary
13 Received 31 January 2017 ber intake with risk of metabolic syndrome (MetS). Herein, we aim to conduct a meta-analysis of 78
14 Accepted 21 October 2017 published studies to determine the role of dietary ber in prevention of MetS. 79
15 Methods: A systematical search in PubMed and Embase databases through December 2016, together 80
16 Keywords: with reference scrutiny of relevant literature, was performed to identify studies for inclusion. We 81
Dietary ber
17 aggregated the odds ratios (ORs) with 95% condence intervals (CIs) of MetS using a random effect 82
Metabolic syndrome
18 model. Doseeresponse relationship between ber intake and MetS was also evaluated. 83
Meta-analysis
19 Results: This meta-analysis included 8 cross-sectional and 3 cohort studies, totaling 28,241 participants
Prevention 84
20 and 9140 MetS cases. The highest versus lowest ber intake was associated with a reduced risk of MetS
85
(OR: 0.85, 95% CI: 0.79e0.92; P 0.005), with moderate heterogeneity (I2 64%, P 0.001) across
21 86
studies. The benet of ber intake was signicant among cross-sectional studies (OR: 0.85, 95% CI: 0.78
22 87
e0.92; P < 0.001) but not among cohort studies (OR: 0.86, 95% CI: 0.70e1.06; P 0.16). In doseeresponse
23 88
analysis, we found a curvilinear relationship between ber consumption and prevalence of MetS.
24 Compared with non-ber intake, the ORs (95% CIs) of MetS across ber intake levels were 0.85 (0.79 89
25 e0.91), 0.76 (0.67e0.85), 0.73 (0.65e0.83), and 0.73 (0.65e0.82) for 10, 20, 30, and 40 g/d, respectively. 90
26 Conclusions: Dietary ber intake is associated with less likelihood of having MetS. Additional large, 91
27 prospective studies are warranted to enhance our ndings. 92
28 2017 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved. 93
29 94
30 95
31 96
32 97
33 98
1. Introduction pointed out that MetS is correlated with enhanced risks of common
34 99
cancers, such as breast and colorectal cancers [5]. Due to these
35 100
Metabolic syndrome (MetS) represents a concurrence of inter- features, controlling the development of MetS is of great signi-
36 101
related metabolic disorders, including abdominal obesity, dyslipi- cance for public health. Among the various preventive strategies
37 102
demia, hypertension, and hyperglycemia. The incidence of MetS against MetS, lifestyle modications, especially healthy diet, have
38 103
has rapidly increased worldwide, with an estimated prevalence of been attracting great attentions. Dietary consumptions of vegeta-
39 104
35% in the United States, 18%e34% in Europe, and 13%e41% in Asia bles, fruits, sh, dairy products, coffee, and tea have offered a
40 105
[1]. Globally, there is approximately 20%e25% of the world's adult protective role against MetS development [6e8].
41 106
population suffering from this syndrome [2]. MetS has been found Dietary ber, an important ingredient of a healthy diet, is
42 107
to confer elevated risks of cardiovascular disorders, type 2 diabetes commonly obtained from consuming cereals, fruits, and vegetables.
43 108
mellitus, and all deaths [3,4]. In addition, some evidence also Accumulating evidence suggest that intake of dietary ber can
44 109
reduce risks of cardiovascular disease, type 2 diabetes mellitus, and
45 110
some cancers [9]. More importantly, dietary ber has salutary ef-
46 111
Abbreviations: AHRQ, Agency for Healthcare Research Quality; ATP, Adult fects on individual components of MetS, including body weight
47 112
Treatment Panel; IDF, International Diabetes Federation; MetS, metabolic syn- regulation, lipid reduction, improved glucose metabolism, and
48 113
drome; NOS, Newcastle-Ottawa Scale. blood pressure control [10]. Dietary ber also suppresses oxidative
49 * Corresponding author. No. 169 Donghu Road, Wuchang District, Wuhan City 114
stress and inammation [11], both of which have been linked to the
50 Q1 430071, Hubei Province, China. Fax: 86 027 67813073. 115
E-mail address: wanjing2017@163.com (J. Wan). development of MetS [12]. However, whether this nutrient is
51 116
1
Both authors contributed equally to this work. associated with the overall risk of MetS remains unclear. A
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53 118
https://doi.org/10.1016/j.clnu.2017.10.019
54 0261-5614/ 2017 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved. 119

Please cite this article in press as: Wei B, et al., Dietary ber intake and risk of metabolic syndrome: A meta-analysis of observational studies,
Clinical Nutrition (2017), https://doi.org/10.1016/j.clnu.2017.10.019
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2 B. Wei et al. / Clinical Nutrition xxx (2017) 1e8

1 mounting body of studies has been performed to explore the quality. Any disagreements in data abstraction and quality evalua- 66
2 relationship of ber intake with MetS, but the results are incon- tion were resolved by consensus between the 2 reviewers or 67
3 sistent. Some of them showed that dietary ber was inversely consulting with a third reviewer (X.L.). 68
4 correlated with risk of MetS [13e18], while others not [19e23]. 69
5 Herein, we performed this meta-analysis to comprehensively es- 2.4. Statistical analyses 70
6 timate the association of ber intake with MetS. We hypothesized 71
7 that high consumption of dietary ber may reduce the prevalence The summarized risk estimates of MetS were reported as OR 72
8 of MetS. with its 95% condence interval (CI). We pooled the risk estimates 73
9 of MetS for highest versus lowest total ber and ber subtypes 74
10 2. Materials and methods intakes using a random effect model. The study by Hosseinpour- 75
11 Niazi et al. [20] did not provide the separate risks of MetS for sol- 76
12 2.1. Search strategy uble and insoluble bers; thus, we used the data of their previous 77
13 report [27] instead, to evaluate the effect of ber subtypes. Het- 78
14 This study was performed followed the Meta-analysis Of erogeneity across the included studies was detected by the 79
15 Observational Studies in Epidemiology guideline [24]. We system- Cochrane Q test, with a P value < 0.1 suggesting signicance. We 80
16 atically searched the PubMed and Embase databases from incep- also reported the heterogeneity as low, moderate, and high with I2 81
17 tion to December 2016 to identify publications for inclusion. The values of 25%, 50%, and 75%, respectively [28]. 82
18 MeSH terms used included dietary ber and metabolic syn- Subgroup analyses were performed according to sample size 83
19 drome X. We combined these terms with free text word searches (2000 or <2000), study design (cross-sectional or cohort studies), 84
20 that included ber, bre, metabolic syndrome, MetS, car- location (America, Europe, or Asia), MetS denition (ATP III or other 85
21 diometabolic, and cardiovascular risk factor (see detailed search criteria), degree of adjustment (10 or <10 variables), and mean 86
22 strategy in Supplementary Table 1). The reference lists of retrieved age (60 or <60 years). Sensitivity analyses, including removals of 87
23 literature were also checked for including additional studies. Only individual study, low-quality studies, and studies of diabetic pa- 88
24 studies that were published in English with full-text form available tients, were conducted to appraise the robustness of our results. 89
25 were enrolled in this meta-analysis. The search process was per- Publication bias was evaluated by funnel plot analyses and further 90
26 formed by 2 independent investigators (B.W. and Y.L.). conrmed by Egger's tests. If there was publication bias, we used 91
27 the trim and ll strategy to adjust the funnel plot and then re- 92
28 2.2. Eligibility of studies computed the results [29]. 93
29 To assess the potential doseeresponse pattern between ber 94
30 Studies that met all of the following conditions were included: intake and MetS risk, we performed a 2-stage random-effects 95
31 1) the study design was cohort, caseecontrol, or cross-sectional; 2) doseeresponse meta-analysis. In the rst stage, we estimated a 96
32 the exposure of interest was dietary ber intake; 3) the outcome of restricted cubic spline model with 3 knots at the 10th, 50th, and 97
33 interest included MetS; 4) the risk estimates of MetS, such as odds 90th percentiles of the ber intake using generalized least-square 98
34 ratios (ORs) or risk ratios (RRs), have been reported. We also regression, considering the correlation within each set of pub- 99
35 planned to include randomized trials that investigated the impacts lished ORs as proposed by Orsini et al. [30]. Then the study-specic 100
36 of ber supplementation on risk of MetS; however, no randomized ORs were pooled using the restricted maximum likelihood method 101
37 trials met this requirement. For doseeresponse analysis, the risk in a random-effects meta-analysis [31]. A P-value for nonlinearity 102
38 effect size should be provided for 3 quantitative categories of ber was calculated by testing the null hypothesis that the coefcient of 103
39 intake, and the numbers of cases and participants or person-years the second spline is equal to 0. 104
40 for each category were also available (or details were provided to All data analyses were realized with STATA 12.0 (StataCorp, 105
41 calculate them). Reviews, abstracts, comments, unpublished re- College Station, TX, USA) and R 3.2.5 (The R Foundation for Statis- 106
42 sults, and studies of children or adolescents were excluded. When tical Computing, Vienna, Austria) softwares, and P values < 0.05 107
43 reports pertained to overlapping participants, we included only the were considered as signicant. 108
44 study with larger population to avoid duplication of data. 109
45 3. Results 110
46 2.3. Data collection and quality evaluation 111
47 3.1. Search process 112
48 Two reviewers (B.W. and Y.L.) independently extracted the in- 113
49 formation on study characteristics, including study author, publi- We initially identied 1786 publications, of which 729 dupli- 114
50 cation year, study design and population, number of participants cates and 993 irrelevant studies were discarded. Among the 115
51 and cases, percentage of men, baseline age, MetS denition criteria, remaining 64 articles selected for full-text reading, 53 articles that 116
52 ascertainments of ber intake and Mets, study location, and factors failed to meet the eligibility criteria were eliminated. Besides, the 117
53 adjusted in multivariable models. The maximally adjusted risk es- study by Moreno-Franco et al. [22] reported only the separate risks 118
54 timates were also recorded for pooling analyses. When necessary, of MetS for soluble and insoluble bers, thus it was treated as 2 119
55 the corresponding authors of the included studies were e-mailed individual reports. In total, 11 studies [13e23] with 12 reports were 120
56 for missing data. To evaluate the methodological quality, we used included in the nal analyses (Fig. 1). 121
57 an 11-item checklist recommended by Agency for Healthcare 122
58 Research Quality (AHRQ) [25] for cross-sectional studies and 3.2. Study characteristics and quality evaluation 123
59 Newcastle-Ottawa Scale (NOS) [26] for cohort studies. For each 124
60 cross-sectional study, an item of AHRQ checklist can score 1 point if The baseline characteristics of eligible studies are listed in 125
61 it was answered yes; otherwise, score 0 point. The NOS score for Table 1. Briey, the set of studies consists of 8 cross-sectional and 3 126
62 each cohort study was calculated according to 3 major aspects: cohort studies, totaling 28,241 participants and 9140 MetS cases. 127
63 selection of participants (0e4 points), adjustment for confounders The age range was 18e84 years, and men accounted for 54% of the 128
64 (0e2 points), and ascertainment of outcomes (0e3 points). A study total participants. Five studies were conducted in America, 3 in 129
65 with an AHRQ score 8 or NOS score 7 was regarded as of high Europe, and 3 in Asia. With regard to MetS denition, 8 studies 130

Please cite this article in press as: Wei B, et al., Dietary ber intake and risk of metabolic syndrome: A meta-analysis of observational studies,
Clinical Nutrition (2017), https://doi.org/10.1016/j.clnu.2017.10.019
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B. Wei et al. / Clinical Nutrition xxx (2017) 1e8 3

1 66

Idenficaon
2 67
3 68
Records idenfied from Records idenfied from
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databases search (n = 1778) other sources (n=8)
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6 71
7 72
8 Records aer duplicates removed (n=1057) 73
9 74
Screening

10 75
11 76
Records screened (n = 1057)
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13 78
14 993 records were excluded 79
15 based on tles or abstracts 80
16 81
Eligibility

17 Records selected for full-text 82


18 reading (n = 64) 83
19 84
20 85
21 53 records excluded: 86
22 4 review arcles 87
23 27 did not study fiber intake as an exposure 88
24 15 did not study MetS as an outcome 89
25 90
4 duplicated samples or cohorts
26 91
2 no risk esmates reported
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28 1 study of adolescents 93
Inclusion

29 94
30 Studies included in this 95
31 96
meta-analysis (n = 11)
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33 98
Fig. 1. Flow diagram of study search process.
34 99
35 100
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adopted the Adult Treatment Panel III (ATP III) criteria or its P 0.09). Also, the stratied analysis based on study design indi-
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adapted version [32,33], 3 studies adopted the International Dia- cated that the association between ber intake and prevalence of
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betes Federation (IDF) criteria [34], and 1 study used the harmo- MetS was signicant among cross-sectional studies (OR: 0.85, 95%
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nized denition [35]. Of the included reports, all performed health CI: 0.78e0.92; P < 0.001) but not among cohort studies (OR: 0.86,
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examination to ascertain MetS conditions, and 6 assessed dietary 95% CI: 0.70e1.06, P 0.16). Other subanalyses, such as that for
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factors using food frequency questionnaire. The most commonly sample size, MetS denition, degree of adjustment, and mean age,
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adjusted confounders in the studies were age, gender, smoking, showed consistent results. Relevant details are exhibited in Table 2.
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alcohol consumption, and total calorie intake.
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The detailed quality assessment is shown in Supplementary 3.4. Sensitivity analyses and publication bias
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Tables 2 and 3. In general, there were 5 of the cross-sectional
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studies [13e16,21] and 2 of the cohort studies [19,20] having a Sensitivity analysis by excluding each study in sequence had no
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high quality. The mean AHRQ score was 7.5 for cross-sectional inuence on the overall results. Exclusion of low-quality studies
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studies and the mean NOS score was 7.3 for cohort studies. [17,18,22,23] or studies of diabetic patients [15,18,23] did not alter
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50 the inverse relationship between ber intake and MetS. The funnel 115
51 3.3. High versus low analyses plot was visually asymmetric with the P value of Egger's 116
52 test 0.001, suggesting the potential of publication bias. After 117
53 Data pooling indicated that compared to the lowest intake, the introducing the trim and ll strategy to correct this bias, the 118
54 highest intake of dietary ber was correlated with a decreased overall risk estimate was still signicant in favor of dietary ber 119
55 prevalence of MetS (OR: 0.85, 95% CI: 0.79e0.92, P 0.005; Fig. 2), intake (OR: 0.90, 95% CI: 0.83e0.98, P 0.02; Supplementary 120
56 with moderate heterogeneity across the studies (I2 64%, Fig. 1). 121
57 P 0.001). Among ber subtypes, the summarized OR (95% CI) of 122
58 developing MetS was 0.80 (0.67e0.96) for cereal ber, 0.85 3.5. Doseeresponse analyses 123
59 (0.77e0.94) for fruit ber, 1.07 (0.88e1.31) for vegetable ber, 0.78 124
60 (0.62e0.98) for soluble ber, and 0.55 (0.42e0.73) for insoluble Eight studies [13,14,16,17,19e22] were selected for the dosee 125
61 ber (Figs. 3 and 4). response meta-analysis. We found a nonlinear association between 126
62 In the subgroup analysis for study locations, inverse associations dietary ber intake and risk of MetS (P for nonlinearity < 0.001; 127
63 of dietary ber intake with MetS were seen in America (OR: 0.84, Fig. 5). The summarized OR (95% CI) of MetS for a ber intake of 10, 128
64 95% CI: 0.73e0.97, P 0.01) and in Europe (OR: 0.62, 95% CI: 20, 30, and 40 g/d was 0.85 (0.79e0.91), 0.76 (0.67e0.85), 0.73 129
65 0.49e0.79, P < 0.001), but not in Asia (OR: 0.94, 95% CI: 0.88e1.01, (0.65e0.83), and 0.73 (0.65e0.82), respectively. Additionally, we 130

Please cite this article in press as: Wei B, et al., Dietary ber intake and risk of metabolic syndrome: A meta-analysis of observational studies,
Clinical Nutrition (2017), https://doi.org/10.1016/j.clnu.2017.10.019
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4 B. Wei et al. / Clinical Nutrition xxx (2017) 1e8

1 also assumed a linear relationship between dietary ber and MetS. 66

ATP, Adult Treatment Panel; BDHQ, brief diet history questionnaire; BMI, body mass index; CVD, cardiovascular disease; DM, diabetes mellitus; FFQ, food frequency questionnaire; HE, health examination; IDF, International
Age, sex, BMI, smoking, physical activity, intake of total energy,
protein, fat, cholesterol, dairy products, meat, poultry, and sh
2 The result suggested that the odds of MetS decreased by 11% (OR: 67

Sex, DM duration, physical activity, and total energy intake


3 0.89, 95% CI: 0.82e0.96) for each 10-g/d increment in total ber 68

Age, sex, race, smoking, education, and total energy intake

Age, sex, smoking, drinking, physical activity, and intake


4 intake. 69

Age, sex, BMI, smoking, physical activity, dialysis mode


Age, sex, DM duration, smoking, drinking, leisure time,

and duration, steroids dose, menopausal status, family


history of diabetes and stroke, and total energy intake
Age, sex, smoking, drinking, studies completed level,
physical activity, and intake of carbohydrate and fat

physical activity, work type, and total energy intake


5 70
Age, sex, BMI, smoking, drinking, physical activity,

physical activity, hypoglycemic agents, and intake


Age, sex, DM, smoking, drinking, physical activity,

Age, sex, race, education, BMI, smoking, drinking,


education, marital status, and total energy intake
6 4. Discussion 71

Sex, BMI, hypertension, and total energy intake


and intake of total energy, fat, and magnesium

7 72
8 There are limited studies that have examined the role of dietary 73
9 ber in preventing MetS. The ndings from our meta-analysis 74

of total energy, fat, and multivitamin.


10 reveal an inverse relationship between consumption of dietary - 75
11 ber and risk of MetS when comparing the highest versus lowest 76
12 categories. Moreover, we also observe a curvilinear correlation of 77
13 ber intake with prevalence of MetS. 78
of total energy and fat

14 Previous studies have suggested a protective role of ber-rich 79


15 food or diet in the development of MetS. Whole-grain consump- 80
16 tion was reported to be associated with a lower risk of having MetS, 81
Adjustment

17 while intake of rened-grain (containing low ber) appeared to 82


18 increase the prevalence of MetS [36]. A recent randomized trial also 83
19 showed that dietary ber enriched rice cakes decreased the num- 84
20 ber of MetS components [37]. Similarly, adherence to Mediterra- 85
Location

21 nean diet, which is high in whole-grains, fresh fruits, vegetables, 86


Brazil
Brazil
Spain

Japan

Spain
Italy

22 and legumes, may reduce the incidence of MetS [38]. In addition, 87


USA

USA

USA
Iran

Iran

23 Carlson et al. performed a cross-sectional analysis enrolling 2128 88


adolescents, and found that high intakes of dietary ber might
Outcome

24 89
25 lower the risk of MetS [39]. We did not include this study in our 90
HE
HE
HE

HE

HE

HE

HE
HE

HE

HE

HE

26 analysis because of the potential metabolic differences between 91


27 adults and adolescents. 92
Dietary records
Dietary records
Dietary history
Ascertainment

Dietary recalls

28 There are several plausible explanations for the favorable im- 93


29 pacts of dietary ber on MetS development. Firstly, it is found that 94
Exposure

30 ber intake confers improvements in individual components of 95


BDHQ
FFQ

FFQ

FFQ

FFQ

FFQ

FFQ

31 MetS [10]. These effects may be attributed to the fact that ber 96
32 intake induces increased satiety, delayed gastric emptying, reduced 97
Harmonized

33 absorption of macronutrients, and improved insulin sensitivity 98


ATP III IDF
denition

denition

34 [10]. Secondly, dietary ber has been shown to exert protective 99


ATP III

ATP III

ATP III
ATP III

ATP III

ATP III

ATP III
MetS

35 roles against oxidative stress by suppress of ROS generation [11]. It 100


IDF
IDF

36 is well known that oxidative stress is involved in the pathogenesis 101


61 (mean)
60 (mean)

37 of MetS [40]. Thirdly, ber supplementation can favorably affect the 102
(years)

45e64

55e80

18e30

20e50
19e84

26e82

40e55

38 phylogenetic structure and functional capacity of gut microbiome 103


Diabetes Federation; MetS, metabolic syndrome; NA, not applicable; RT, renal transplantation.
20

18
Age

39 [41]. Previous studies have indicated that alterations in microbial 104


40 community and functional shifts of gut microbiome lead to sys- 105
Men

50.9
48.6
47.2

44.9

44.6

56.7

46.0

95.1

62.5
54.8

45.5

41 106
(%)

temic inammation and insulin resistance, thus promoting the


42 development of MetS [42]. Therefore, the observed benets of ber 107
3780/10,473
(MetS/total)
Participants

43 intake may be, at least in part, mediated through its regulation of 108
2397/4399
384/1653

575/4192

240/1582

605/2834

377/1592

109/175
174/214
437/967

44 gut microbiome. 109


62/160

45 Among ber subtypes, we observed reduced risks of MetS for 110


46 cereal and fruit bers, but not for vegetable ber. Consistent with 111
our nding, some included studies also revealed the neutral effects
National population

47 112
of vegetable ber on insulin resistance and MetS [20,21]. Besides,
Patients after RT

48 113
Healthy adults

Healthy adults

Healthy adults

Healthy adults
Adults at high

no association was detected of vegetable ber intake with incident


Workers free

49 114
DM patients
DM patients
DM patients
risk of CVD
Population

50 coronary heart disease [43] and type 2 diabetes mellitus [44]. The 115
of CVD

51 potential biological mechanisms for the lack of signicant nding 116


for vegetable ber remain unclear. It is likely that the common
Baseline characteristics of the included studies.

52 117
53 nutrient-poor starchy vegetables, such as potatoes and peas, may 118
Cross-sectional

Cross-sectional

Cross-sectional

Cross-sectional

Cross-sectional
Cross-sectional
Cross-sectional

Cross-sectional

54 lead to high glycemic load, which has been shown to increase the 119
55 incidence of MetS [45]. Thus, the benets of vegetable ber may be 120
Design

Cohort

Cohort

Cohort

56 offset by some adverse impact of starchy vegetables. However, 121


57 because of the limited studies available for analysis of vegetable 122
58 ber, this result should be interpreted with caution. Future studies 123
Steemburgo 2009 [18]

59 124
Carnethon 2004 [19]

concerning these issues are needed.


McKeown 2004 [21]
Study (author, year)

Hosseinpour-Niazi
Grooms 2013 [16]

60 The quality of included studies was relatively high, but moder- 125
Cabello-Saavedra

Noori 2010 [17]


Moreno-Franco

Silva 2011 [23]


Fujii 2013 [15]

61 ate heterogeneity was detected across studies. We found that the 126
Bo 2006 [13]

2014 [14]

2015 [20]

2014 [22]

62 heterogeneity was decreased among studies using either the ATP III 127
63 criteria or other criteria, suggesting that different denition 128
Table 1

64 methods of MetS may account for the heterogeneity in our study. 129
65 Nevertheless, an inverse correlation between ber intake and risk 130

Please cite this article in press as: Wei B, et al., Dietary ber intake and risk of metabolic syndrome: A meta-analysis of observational studies,
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Fig. 2. Odds ratio of MetS for the highest versus lowest intake of dietary ber.
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of MetS was identied in both subsets of the diagnostic criteria. but not signicantly affect our ndings. Because the age ranges of
30 95
Although the prevalence of MetS was lower when using the ATP III participants in the studies differ so much from each other, we also
31 96
criteria than the IDF criteria and harmonized denition, there is performed a subanalysis according to the mean age. The benecial
32 97
generally good concordance between all these 3 MetS criteria [46]. effects of ber intake on MetS were present in adults older or
33 98
This fact may explain why moderate heterogeneity was observed younger than 60 years, suggesting that our result is less likely to be
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65 Fig. 3. Odds ratio of MetS for the highest versus lowest intake of cereal, fruit, and vegetable bers. 130

Please cite this article in press as: Wei B, et al., Dietary ber intake and risk of metabolic syndrome: A meta-analysis of observational studies,
Clinical Nutrition (2017), https://doi.org/10.1016/j.clnu.2017.10.019
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6 B. Wei et al. / Clinical Nutrition xxx (2017) 1e8

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23 Fig. 4. Odds ratio of MetS for the highest versus lowest intake of soluble and insoluble bers. 88
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inuenced by the age difference. In addition to adults, previous ber and MetS, and each 10 g/d increase in ber intake was found
26 91
studies have also conrmed the favorable impacts of dietary ber to be associated with a decreased risk of MetS.
27 92
on physiologic activities in elderly persons, including metabolic Our work has several strengths. To date, this is the rst meta-
28 93
properties and microbiome functions [47]. Thus, dietary ber can analysis that explored the relationship between dietary ber
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function well in both adults and the elderly, although potential intake and prevalence of MetS. In addition, the inverse association
30 95
differences in metabolism and microbial composition are seen of ber intake with MetS was observed not only considering ber
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between these 2 age groups. intake as a categorical variable but also in a doseeresponse pattern.
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In doseeresponse meta-analysis, there appears to be no addi- However, we should not ignore the limitations of the current study.
33 98
tional reduction in odds of MetS if the ber intake is increased over First of all, the recall and selection bias cannot be eliminated
34 99
30 g/d. A possible explanation is that excessive ber intake may owning to the observational nature of included studies. Cohort
35 100
negatively affect the salutary nutrients intake by extending satiety studies are less susceptible to such bias, but only 3 cohort studies
36 101
and binding up minerals through ber-related phytates and oxa- were included in our study, and the summary estimate of these
37 102
lates [48]. It should be noted that there are few risk estimates studies was not signicant. Secondly, there are few studies avail-
38 103
available for the ber intake levels of more than 30 g/d, potentially able to perform stratied analyses by ber subtypes and other
39 104
leading to mis-modeling of the exact doseeresponse relationship. variables, which may cause inaccurate evaluations of their effects
40 105
Therefore, we also assumed a linear correlation between dietary on risk of MetS. Likewise, due to the lack of relevant data, we cannot
41 106
conduct subanalyses by some important covariates, such as gender.
42 107
43 108
Table 2
44 Subgroup analyses for the association between ber intake and MetS. 109
45 110
Subgroup No. of Heterogeneity Pooled estimates
46 111
reports
47 I2 P OR (95% CI) P 112
48 Sample size 113
49  2000 4 74.7 0.01 0.86 (0.74, 0.99) 0.03 114
50 < 2000 8 62.3 0.01 0.72 (0.57, 0.89) 0.003 115
Study design
51 Cross-sectional 9 72.1 <0.001 0.85 (0.78, 0.92) <0.001
116
52 Cohort 3 0 0.50 0.86 (0.70, 1.06) 0.16 117
53 Location 118
54 America 5 70.2 0.01 0.84 (0.73, 0.97) 0.01 119
Europe 4 3.5 0.38 0.62 (0.49, 0.79) <0.001
55 120
Asia 3 2.8 0.36 0.94 (0.88, 1.01) 0.09
56 MetS denition 121
57 ATP III 9 10.3 0.35 0.76 (0.68, 0.85) <0.001 122
58 Other 4 49.4 0.12 0.94 (0.89, 0.98) 0.01 123
59 Degree of adjustment 124
10 confounders 4 0 0.52 0.95 (0.91, 0.99) 0.01
60 <10 confounders 8 74.5 <0.001 0.74 (0.63, 0.88) <0.001
125
61 Mean age 126
62 60 year 4 60.6 0.05 0.93 (0.88, 0.99) 0.02 127
63 <60 year 7 10.9 0.35 0.76 (0.65, 0.90) 0.001 128
64 ATP, Adult Treatment Panel; CI, condence interval; MetS, metabolic syndrome; OR, 129
65 odds ratio. Fig. 5. Doseeresponse analysis for the association between ber intake and MetS. 130

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1 Thirdly, publication bias is present in our work because small [9] Dahl WJ, Stewart ML. Position of the Academy of Nutrition and Dietetics: 66
health implications of dietary ber. J Acad Nutr Diet 2015;115:1861e70.
2 studies with null ndings is less likely to be published. However, 67
[10] Satija A, Hu FB. Cardiovascular benets of dietary ber. Curr Atheroscler Rep
3 the result remained signicant in favor of ber intake after intro- 2012;14:505e14. 68
4 ducing the trim and ll method to adjust publication bias. [11] Ghanim H, Batra M, Abuaysheh S, Green K, Makdissi A, Kuhadiya N, et al. Anti- 69
5 Fourthly, the results of doseeresponse analysis may be unstable inammatory and ROS suppressive effects of the addition of ber to a high fat 70
high calorie meal. J Clin Endocrinol Metab 2016. https://doi.org/10.1210/
6 when some biases are present, including publication bias, as jc.2016-2669. published online December 1. 71
7 mentioned by Orsini et al. [30]. [12] Fernandez-Garcia JC, Cardona F, Tinahones FJ. Inammation, oxidative stress 72
8 In conclusion, dietary ber intake is associated with a decreased and metabolic syndrome: dietary modulation. Curr Vasc Pharmacol 2013;11: 73
906e19.
9 risk of MetS. The result supports the current recommendation of [13] Bo S, Durazzo M, Guidi S, Carello M, Sacerdote C, Silli B, et al. Dietary mag-
74
10 ber intake for preventing chronic disease. Considering the limi- nesium and ber intakes and inammatory and metabolic indicators in 75
11 tations of this meta-analysis, additional large, prospective studies middle-aged subjects from a population-based cohort. Am J Clin Nutr 76
2006;84:1062e9.
12 are warranted to enhance our ndings, especially regarding the [14] Cabello-Saavedra E, Bes-Rastrollo M, Martinez JA, Diez-Espino J, Buil-
77
13 effect of vegetable ber and the doseeresponse relationship be- Cosiales P, Serrano-Martinez M, et al. Macronutrient intake and metabolic 78
14 tween ber intake and MetS. syndrome in subjects at high cardiovascular risk. Ann Nutr Metab 2010;56: 79
152e9.
15 80
[15] Fujii H, Iwase M, Ohkuma T, Ogata-Kaizu S, Ide H, Kikuchi Y, et al. Impact of
16 Statement of authorship dietary ber intake on glycemic control, cardiovascular risk factors and 81
17 chronic kidney disease in Japanese patients with type 2 diabetes mellitus: the 82
Fukuoka Diabetes Registry. Nutr J 2013;12:159.
18 J.W. conceived and designed the study. B.W. and Y.L. acquired 83
[16] Grooms KN, Ommerborn MJ, Pham DQ, Djousse L, Clark CR. Dietary ber
19 the data. B.W., Y.L., and X.L. did statistic analysis. B.W. drafted the intake and cardiometabolic risks among US adults, NHANES 1999e2010. Am J 84
20 manuscript. Y.F. and J.C. made critical revision of the manuscript for Med 2013;126:1059e1067.e1-4. 85
21 [17] Noori N, Nafar M, Poorrezagholi F, Ahmadpoor P, Samadian F, Firouzan A, et al. 86
key intellectual content, with support from J.W. All authors Dietary intakes of ber and magnesium and incidence of metabolic syndrome
22 approved the nal version of this article. in rst year after renal transplantation. J Ren Nutr 2010;20:101e11. 87
23 [18] Steemburgo T, Dall'Alba V, Almeida JC, Zelmanovitz T, Gross JL, de 88
24 Azevedo MJ. Intake of soluble bers has a protective role for the presence of 89
Funding sources metabolic syndrome in patients with type 2 diabetes. Eur J Clin Nutr 2009;63:
25 127e33.
90
26 This work was supported by a grant from the National Natural [19] Carnethon MR, Loria CM, Hill JO, Sidney S, Savage PJ, Liu K, et al. Risk factors 91
27 for the metabolic syndrome: the coronary artery risk development in young 92
Science Foundation of China to Jing Wan [NSFC, Grant No. adults (CARDIA) study, 1985-2001. Diabetes Care 2004;27:2707e15.
28 81670409]. [20] Hosseinpour-Niazi S, Mirmiran P, Mirzaei S, Azizi F. Cereal, fruit and vegetable
93
29 bre intake and the risk of the metabolic syndrome: a prospective study in the 94
30 Tehran Lipid and Glucose Study. J Hum Nutr Diet 2015;28:236e45. 95
Q2 Conict of interest [21] McKeown NM, Meigs JB, Liu S, Saltzman E, Wilson PW, Jacques PF. Carbo-
31 96
hydrate nutrition, insulin resistance, and the prevalence of the metabolic
32 syndrome in the Framingham offspring cohort. Diabetes Care 2004;27: 97
The authors declare no conict of interest.
33 538e46. 98
[22] Moreno Franco B, Leon Latre M, Andres Esteban EM, Ordovas JM,
34 99
Acknowledgements Casasnovas JA, Penalvo JL. Soluble and insoluble dietary bre intake and risk
35 factors for metabolic syndrome and cardiovascular disease in middle-aged 100
36 adults: the AWHS cohort. Nutr Hosp 2014;30:1279e88. 101
The authors thank Qr. Cheng Qian (Department of Cardiology, [23] Silva FM, Steemburgo T, de Mello VD, Tonding SF, Gross JL, Azevedo MJ. High
37 102
Zhongnan Hospital of Wuhan University, Wuhan, China) for dietary glycemic index and low ber content are associated with metabolic
38 syndrome in patients with type 2 diabetes. J Am Coll Nutr 2011;30:141e8. 103
providing statistical assistance.
39 [24] Stroup DF, Berlin JA, Morton SC, Olkin I, Williamson GD, Rennie D, et al. Meta- 104
40 analysis of observational studies in epidemiology: a proposal for reporting. 105
41 Appendix A. Supplementary data Meta-analysis of Observational Studies in Epidemiology (MOOSE) group.
106
JAMA 2000;283:2008e12.
42 [25] Zeng X, Zhang Y, Kwong JS, Zhang C, Li S, Sun F, et al. The methodological 107
43 Supplementary data related to this article can be found at quality assessment tools for preclinical and clinical studies, systematic review 108
44 https://doi.org/10.1016/j.clnu.2017.10.019. and meta-analysis, and clinical practice guideline: a systematic review. J Evid
109
Based Med 2015;8:2e10.
45 [26] Wells GA, Shea B, O'Connell D, Peterson J, Welch V, Losos M, et al. The 110
46 References Newcastle-Ottawa Scale (NOS) for assessing the quality of nonrandomised 111
studies in meta-analyses. (Accessed 10 January 2017, at http://www.ohri.ca/
47 112
[1] Dai L, Goncalves CM, Lin Z, Huang J, Lu H, Yi L, et al. Exploring metabolic programs/clinical_epidemiology/oxford.asp).
48 syndrome serum free fatty acid proles based on GC-SIM-MS combined with [27] Hosseinpour-Niazi S, Mirmiran P, Sohrab G, Hosseini-Esfahani F, Azizi F. In- 113
49 random forests and canonical correlation analysis. Talanta 2015;135:108e14. verse association between fruit, legume, and cereal ber and the risk of 114
[2] Eckel RH, Grundy SM, Zimmet PZ. The metabolic syndrome. Lancet 2005;365: metabolic syndrome: tehran lipid and glucose study. Diabetes Res Clin Pract
50 115
1415e28. 2011;94:276e83.
51 [3] O'Neill S, O'Driscoll L. Metabolic syndrome: a closer look at the growing [28] Chen LH, Wang YF, Xu QH, Chen SS. Omega-3 fatty acids as a treatment for 116
52 epidemic and its associated pathologies. Obes Rev 2015;16:1e12. non-alcoholic fatty liver disease in children: a systematic review and meta- 117
53 [4] Li Z, Yang X, Yang J, Yang Z, Wang S, Sun F, et al. The cohort study on pre- analysis of randomized controlled trials. Clin Nutr 2016. https://doi.org/ 118
diction of incidence of all-cause mortality by metabolic syndrome. PLoS One 10.1016/j.clnu.2016.12.009. published online December 23.
54 2016;11:e0154990. [29] Duval S, Tweedie R. A nonparametric trim and ll method of accounting for 119
55 [5] Mendonca FM, de Sousa FR, Barbosa AL, Martins SC, Araujo RL, Soares R, et al. publication bias in meta-analysis. J Am Stat Assoc 2000;95:89e98. 120
56 Metabolic syndrome and risk of cancer: which link? Metabolism 2015;64: [30] Orsini N, Li R, Wolk A, Khudyakov P, Spiegelman D. Meta-analysis for linear 121
182e9. and nonlinear dose-response relations: examples, an evaluation of approxi-
57 mations, and software. Am J Epidemiol 2012;175:66e73.
122
[6] Cheraghi Z, Mirmiran P, Mansournia MA, Moslehi N, Khalili D, Nedjat S. The
58 association between nutritional exposures and metabolic syndrome in the [31] Jackson D, White IR, Thompson SG. Extending DerSimonian and Laird's 123
59 Tehran Lipid and Glucose Study (TLGS): a cohort study. Public Health methodology to perform multivariate random effects meta-analyses. Stat Med 124
2016;140:163e71. 2010;29:1282e97.
60 [32] Expert panel on detection, evaluation, and treatment of high blood cholesterol
125
[7] Kim YS, Xun P, He K. Fish consumption, long-chain omega-3 polyunsaturated
61 fatty acid intake and risk of metabolic syndrome: a meta-analysis. Nutrients in adults. Executive summary of the third report of the national cholesterol 126
62 2015;7:2085e100. education program (NCEP) expert Panel on detection, evaluation, and treat- 127
[8] Marventano S, Salomone F, Godos J, Pluchinotta F, Del Rio D, Mistretta A, et al. ment of high blood cholesterol in adults (adult treatment Panel III). JAMA
63 128
Coffee and tea consumption in relation with non-alcoholic fatty liver and 2001;285:2486e97.
64 metabolic syndrome: a systematic review and meta-analysis of observational [33] Grundy SM, Cleeman JI, Daniels SR, Donato KA, Eckel RH, Franklin BA, et al. 129
65 studies. Clin Nutr 2016;35:1269e81. Diagnosis and management of the metabolic syndrome: an American heart 130

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8 B. Wei et al. / Clinical Nutrition xxx (2017) 1e8

1 association/national heart, lung, and blood institute scientic statement. Cir- [41] Holscher HD, Caporaso JG, Hooda S, Brulc JM, Fahey Jr GC, Swanson KS. Fiber 23
culation 2005;112:2735e52. supplementation inuences phylogenetic structure and functional capacity of
2 24
[34] Alberti KG, Zimmet P, Shaw J. Metabolic syndromeea new world-wide de- the human intestinal microbiome: follow-up of a randomized controlled trial.
3 nition. A consensus statement from the International Diabetes Federation. Am J Clin Nutr 2015;101:55e64. 25
4 Diabet Med 2006;23:469e80. [42] Festi D, Schiumerini R, Eusebi LH, Marasco G, Taddia M, Colecchia A. Gut 26
5 [35] Alberti KG, Eckel RH, Grundy SM, Zimmet PZ, Cleeman JI, Donato KA, et al. microbiota and metabolic syndrome. World J Gastroenterol 2014;20: 27
Harmonizing the metabolic syndrome: a joint interim statement of the in- 16079e94.
6 ternational diabetes federation task force on epidemiology and prevention; [43] Wu Y, Qian Y, Pan Y, Li P, Yang J, Ye X, et al. Association between dietary ber 28
7 national heart, lung, and blood institute; American heart association; world intake and risk of coronary heart disease: a meta-analysis. Clin Nutr 2015;34: 29
8 heart federation; international atherosclerosis society; and international as- 603e11. 30
sociation for the study of obesity. Circulation 2009;120:1640e5. [44] Yao B, Fang H, Xu W, Yan Y, Xu H, Liu Y, et al. Dietary ber intake and risk of
9 [36] Georgoulis M, Kontogianni MD, Margariti A, Tiniakos D, Fragopoulou E, type 2 diabetes: a dose-response analysis of prospective studies. Eur J Epi-
31
10 Zaropoulou R, et al. Associations between dietary intake and the presence of demiol 2014;29:79e88. 32
11 the metabolic syndrome in patients with non-alcoholic fatty liver disease. [45] Juanola-Falgarona M, Salas-Salvado J, Buil-Cosiales P, Corella D, Estruch R, 33
J Hum Nutr Diet 2015;28:409e15. Ros E, et al. Dietary glycemic index and glycemic load are positively associated
12 [37] Yoon NR, Yoon S, Lee SM. Rice cakes containing dietary ber supplemented with risk of developing metabolic syndrome in middle-aged and elderly
34
13 with or without artemisia annua and gynura procumbens merr. alleviated the adults. J Am Geriatr Soc 2015;63:1991e2000. 35
14 risk factors of metabolic syndrome. Clin Nutr Res 2016;5:79e88. [46] Erasmus RT, Soita DJ, Hassan MS, Blanco-Blanco E, Vergotine Z, Kegne AP, et al. 36
[38] Grosso G, Stepaniak U, Micek A, Topor-Madry R, Steer D, Szafraniec K, et al. High prevalence of diabetes mellitus and metabolic syndrome in a South
15 37
A Mediterranean-type diet is associated with better metabolic prole in urban African coloured population: baseline data of a study in Bellville, Cape Town.
16 Polish adults: results from the HAPIEE study. Metabolism 2015;64:738e46. S Afr Med J 2012;102:841e4. 38
17 [39] Carlson JJ, Eisenmann JC, Norman GJ, Ortiz KA, Young PC. Dietary ber and [47] Donini LM, Savina C, Cannella C. Nutrition in the elderly: role of ber. Arch 39
nutrient density are inversely associated with the metabolic syndrome in US Gerontol Geriatr 2009;49(Suppl 1):61e9.
18 40
adolescents. J Am Diet Assoc 2011;111:1688e95. [48] Comerford KB, Ayoob KT, Murray RD, Atkinson SA. The role of avocados in
19 [40] Bonomini F, Rodella LF, Rezzani R. Metabolic syndrome, aging and involve- complementary and transitional feeding. Nutrients 2016. https://doi.org/ 41
20 ment of oxidative stress. Aging Dis 2015;6:109e20. 10.3390/nu8050316. published online May 21. 42
21 43
22 44

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