Eur J Nutr

DOI 10.1007/s00394-016-1306-x

ORIGINAL CONTRIBUTION

Effects of low‑glycemic‑index diets in pregnancy on maternal

and newborn outcomes in pregnant women: a meta‑analysis
of randomized controlled trials
Ru Zhang1 · Shufen Han1 · Guo‑Chong Chen1 · Zeng‑Ning Li2 · Irma Silva‑Zolezzi3 ·
Gerard Vinyes Parés4 · Yi Wang4 · Li‑Qiang Qin1 

Received: 5 April 2016 / Accepted: 27 August 2016

© Springer-Verlag Berlin Heidelberg 2016

Abstract  more than 8 trials. Compared with control diets, low-GI

Purpose Maternal diet with a high glycemic index (GI) diets significantly reduced FBG (weight mean differences
is associated with fetal overgrowth and higher infant body (WMD)  =  −0.18 mmol/L, 95 % CI: −0.33, −0.02), 2-h
adiposity. Effects of low-GI diet on maternal and newborn postprandial glucose level (WMD =  −0.33 mmol/L,
outcomes have been assessed in both healthy pregnancy 95 % CI: −0.54, −0.12), and the proportion of LGA
and gestational diabetes mellitus, but the results remain (RR  = 0.52, 95 % CI: 0.31, 0.89). A lower GWG
inconclusive. This meta-analysis aimed to examine the (WMD  =  −0.69 kg, 95 % CI: −1.74, 0.36) and birth
effects of low-GI diets on maternal and newborn outcomes. weight (WMD =  −0.10 kg, 95 % CI: −0.23, 0.03) were
Methods PubMed, Clinical Trials, and Cochrane Library also observed without significant differences. Heterogene-
databases were searched for relevant randomized trials up ity was observed in the GWG, FBG, and birth weight anal-
to January 2016. Random- or fixed-effects models were yses. Low-GI diets did not affect other maternal and new-
used to calculate combined treatment effects. born outcomes. In subgroup and sensitivity analyses, the
Results A total of 11 trials involving 1985 women were intervention effects of low GI on GWG and FBG varied.
eligible for analysis. This meta-analysis assessed 7 mater- Conclusions  Low-GI diets may have beneficial effects on
nal and 11 newborn outcomes. Of these, gestational weight maternal outcomes for those at risk of developing high glu-
gain (GWG), fasting blood glucose (FBG), newborn birth cose levels, without causing adverse effects on newborn
weight, ponderal index (PI), proportion of macrosomia, outcomes. However, results should be interpreted with cau-
and large for gestational age (LGA) were investigated in tion because of the evidence of heterogeneity and limited
number of studies.
Electronic supplementary material  The online version of this
article (doi:10.1007/s00394-016-1306-x) contains supplementary
Keywords  Low glycemic index · Pregnancy outcomes ·
material, which is available to authorized users. Randomized controlled trials · Meta-analysis

* Yi Wang
[email protected]
Introduction
* Li‑Qiang Qin
[email protected]
The nutritional status of the mother during pregnancy plays
1
Department of Nutrition and Food Hygiene, School of Public a vital role in fetal growth and development, with glucose
Health, Soochow University, 199 Renai Road, Dushu Lake as the main energy substrate [1]. However, different carbo-
Higher Education Town, Suzhou 215123, China hydrate foods produce varied glycemic responses, which
2
Department of Nutrition, First Hospital of Hebei Medical influence maternal blood glucose concentrations [2]. In
University, Shijiazhuang 050031, China 1981, Jenkins [3] proposed the use of glycemic index (GI)
3
Nutrition and Health Research, Nestlé Research Center, to rank postprandial glycemic responses to the equivalent
Lausanne, Switzerland portions of carbohydrates in different foods. Carbohydrates
4
Nestlé Research Center, Beijing 100095, China are then classified according to their induced glycemic

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responses as either high or low GI. Among these two types Study selection
of carbohydrates, those with low GI produce low glyce-
mic response, e.g., whole grain breads, cereals, and nuts, Studies were selected based on the following criteria: (1)
whereas high-GI foods produce a high glycemic response, The study design was a RCT; (2) the study was conducted
e.g., refined grains, desserts, and soft drinks. Alterations in in pregnant women (≥18 years old, with a singleton preg-
maternal metabolism provide nutrients in excess of those nancy); (3) the study comprised a control or a comparison
required for normal fetal growth and for maternal and fetal group, and the intervention was low-GI diet with dietary GI
energy requirements. In this context, the presence of any level; (4) the dietary intervention was more than 4 weeks; and
degree of abnormal glucose tolerance represents an altered (5) pregnancy outcomes included maternal or newborn out-
environment for the growth of the fetus [4]. A dietary comes providing data for statistical analysis. Maternal out-
intake of carbohydrates with low GI induces individuals to comes included the following: GWG, fasting blood glucose
obtain normal gestational weight gain (GWG) and normal (FBG), 2-h postprandial glucose (2-h PG), glycated Hb A1c
infant birth weight, whereas carbohydrates with high GI (HbA1c), gestational age at delivery, proportion of pregnant
results in feto-placental overgrowth and predisposition to women who use insulin, and proportion of cesarean delivery.
fetal macrosomia [5]. Newborn outcomes included the following: birth weight, pon-
Previous systematic reviews and meta-analyses dem- deral index (PI), head circumference, body length, abdominal
onstrated that low-GI diets may reduce insulin require- circumference, proportion of large for gestational age (LGA;
ments and birth weight without adverse effects on preg- birth weight >90th centile), small for gestational age (SGA;
nant women with gestational diabetes mellitus (GDM), birth weight <10th centile), macrosomia (birth weight >4 kg),
suggesting that low-GI diets are an appropriate dietary prematurity, birth centile, and birthweight centile.
intervention for GDM when glucose load is controlled
[6, 7]. As the research in this field is active and fast- Data extraction and quality assessment
moving, a number of recent randomized controlled tri-
als (RCTs) have been published to assess the effects of The following characteristics of each study were recorded:
dietary GI on maternal and newborn outcomes in preg- the first author’s name, publication year, country of origin,
nant women with or without GDM. However, these tri- sample size, study design details, participant characteristics
als yielded varied results because of the differences in (mean age, body weight, body mass index (BMI), health
the study design and participant characteristics [8–18]. status, and gestation age at recruitment), dietary GI level,
Thus, the feasibility of using low-GI diets to replace cur- and maternal or newborn outcomes mentioned above. If
rent recommended pregnant diets remains inconclusive. more than one time point for the follow-up was reported,
The present study aims to analyze the overall effects data from the longest period were used. The Jadad scale
of low-GI diets on maternal and newborn outcomes in was used to assess the methodological quality of each
pregnant women regardless of their health status by con- included trial by assigning scores ranging from 0 to 5 for
ducting a meta-analysis of RCTs. reported randomization, blinding, and withdrawal [20].
Two authors (R-Z and LQ-Q) independently conducted the
literature search, study selection, and data extraction. Any
Materials and methods divergence was resolved by discussion.

Literature search Statistical analysis

This study was performed in accordance with Preferred For binary data, combined relative risk (RR) with 95 %
Reporting Items for Systematic Reviews and Meta-Analy- confidence interval (CI) was evaluated. For continuous
ses (PRISMA) [19]. A systematic literature search for Eng- data, weighted mean difference (WMD) with 95 % CIs was
lish publications was conducted in the databases of Pub- calculated. Standard deviations (SDs) for net changes were
Med, Clinical Trials, and the Cochrane Central Register of obtained from the baseline in each group. If not reported,
controlled Trials up to January 2016. Search terms included they were derived from standard errors, median and inter-
glycemic index, glycemic load, carbohydrates combining quartile ranges by using a standard formula [21]. If SDs for
with pregnancy, and gravidas. The search was limited to the baseline and final values were only provided, SDs were
human clinical trials. A manual search was also performed imputed according to the method of Follmann et al. [22]
using the reference lists of original articles and recent with an assumed correlation coefficient of 0.5.
reviews. Authors of the original studies were not contacted The heterogeneity of the effect size among studies was
for additional information. tested using the Cochran’s Q test at the P < 0.10 level of

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significance. We calculated I2 values, a quantitative meas- abstracts because they were animal studies and reviews,
ure of inconsistency across studies [23]. A random-effects and did not follow a randomized design. After reviewing
model was used when P < 0.10 at the Q test; otherwise, a the full text of the remaining 27 articles, 16 were excluded.
fixed-effects model was applied [24]. To explore the pos- The main reasons for which were as follows: Diet was not
sible influences of study designs and participant character- the primary intervention, the dietary GI levels were not
istics on the combined effect sizes, we further conducted reported, and pregnancy outcomes were not of our inter-
pre-specified subgroup analyses using stratified outcomes est. Walsh et al. [12] and Macgowan et al. [26] reported the
from ≥8 trials. In addition, we investigated the influence results from the same trial (the ROLO study), and the study
of a single study on the overall risk estimate by omitting of Walsh et al. was included because of the larger popula-
one study in each turn. Potential publication bias was tion size. Clapp et al. [5, 27] provided additional informa-
assessed using Begg’s funnel plots and the Egger’s regres- tion for the previous article [18]. To obtain sufficient data,
sion test [25]. All analyses were performed using STATA we used supplementary data in one systematic review [7],
version 12.0 (StataCorp, College Station, TX, USA). which were not reported in the original study [17], instead
P < 0.05 was considered statistically significant, except of contacting authors for additional information. Eleven
otherwise specified. RCTs were selected for the final analysis [8–18]. The flow-
chart of literature search is presented in Fig. 1.

Results Study characteristics

Literature search The characteristics of the selected trials are presented in

Table  1. Of the 11 trials published from 1997 to 2016, 5
We initially identified 339 potentially eligible publications, were conducted in Australia, 2 in the USA, and 1 each in
most of which were excluded after browsing titles and Ireland, Mexico, Canada, and China. Only 1 trial followed

Fig. 1  Flowchart for selection

of eligible studies
Records identified through Additional records identified
Idenficaon

database searching through other sources

(n =341) (n =6)

Records after duplicates removed

(n =339)
Screening

Records screened Records excluded

(n =339) (n =312)

13 excluded:
Full-text articles assessed Diet was not the primary
for eligibility
Eligibility

intervention (n=5)
(n =27) GI levels were not reported (n=7)
Duplicate study (n=1)

Studies included in Pregnancy outcomes were not of

qualitative synthesis interest (n=3)
(n =14)
Included

Studies included in
quantitative synthesis
(meta-analysis)
(n =11)

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Table 1  Characteristics of the included randomized controlled trials in this meta-analysis
Author Location Design Status Sample Age Weight BMI Baseline Gestation weeks at GI Jadad
size (years) (kg) (kg/m2) FBG (mmol/L) recruitment score
Intervention Control

Markovic [8] Australia O At high risk of 72/67 34.7 NR 25.2 NR 17.6 (14–20) 50.4 ± 4.7 57.7 ± 5.1 2
GDM
Ma [9] China O GDM 41/42 30 (18–45) NR 21.5 4.88 27.7 (24–26) 50.1 ± 2.2 53.8 ± 2.5 3
Moses [10] Australia P, O Healthy 296/280 29.9 67.1 24.5 NR 16.5 (<20) 52.8 ± 5.2 55.8 ± 5.0 3
Perichart-Perera Mexico P, SB GDM 61/46 32.1 74 31.1 5.5 21.7 (≤29) 47.2 ± 6.9 48.6 ± 8.4 3
[11]
Walsh [12] Ireland O Previously 372/387 32 73.6 26.8 4.5 12.9 (< 18) 56.0 ± 3.8 57.7 ± 3.9 2
delivered a
macrosomic
infant
Grant [13] Canada O GDM and IGTP 23/24 34 (18–45) NR 26.5 4.74 29 (> 28) 49 ± 3.9 58 ± 2.4 2
Louie [14] Australia P, DB GDM 47/45 33.2 (18–45) NR 24 4.65 29.3 (20–32) 47 ± 6.9 53 ± 6.7 4
Rhodes [15] USA SB Overweight or 25/21 33.5 85.8 31.7 4.25 19.7 (13–28) 51.8 ± 6.9 58.0 ± 4.3 3
obese
Moses [16] Australia O GDM 31/32 31(18–40) 85 32.4 4.65 30.1 (28–32) 48 ± 5.0 56.0 ± 6.2 3
Moses [17] Australia O Healthy 32/30 29.9 (21–40) 69.9 25.5 4.35 12–16 51 ± 5.7 58 ± 5.5 1
Clapp [18] USA O Healthy 10/10 34.5 62.3 NR NR >8 71 ± 2.4 84 ± 2.4 2

DB double blind, GDM gestational diabetes mellitus, IGTP impaired glucose tolerance of pregnancy, NR not reported, O open label, P parallel, SB single blind
Eur J Nutr
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a double-blind design and 2 applied a single-blind design. abdominal circumference (MWD =  −0.65 cm, 95 % CI:
Sample sizes varied from 20 to 576, with a total of 1985 −2.23, 0.92, n  = 3), SGA(RR = 1.33, 95 % CI: 0.71,
pregnant women. The mean age of pregnant women 2.50, n  = 6), macrosomia (RR = 0.95, 95 % CI: 0.83,
ranged from 29.9 to 34.7 years, and mean BMI from 21.5 1.09, n = 8), prematurity (RR = 0.70, 95 % CI: 0.39, 1.28,
to 32.4 kg/m2. Five trials were conducted in pregnant n  = 5), birth centile (MWD =  −7.87, 95 % CI: −21.92,
women with GDM, pregestational type 2 diabetes mellitus 6.19, n  = 3), and birthweight centile (MWD =  −1.22,
(T2DM), or impaired glucose tolerance during pregnancy. 95 % CI: −4.46, 2.02, n  = 3) (Supplementary Fig. 2).
The other trials studied healthy pregnant women (n  = 3), Significant heterogeneity was observed for the analysis
overweight/obese pregnant women (n  = 1), women who of birth weight (P < 0.001, I2  = 80.7 %), PI (P  = 0.009,
previously delivered a macrosomic infant (n  = 1), and I2 = 62.6 %), body length (P = 0.002, I2 = 73.5 %), head
women who were at high risk of GDM (n  = 1). Die- circumference (P  = 0.005, I2  = 73.3 %), abdominal cir-
tary intervention was initially conducted from 12.9 to cumference (P < 0.001, I2  = 91.9 %), and birth centile
30.1 weeks of gestation, and five trials continued the inter- (P = 0.005, I2 = 81.1 %).
vention until delivery. The dietary GI ranged from 47 to 71
(median 50.4) in the intervention groups and from 48.6 to Subgroup and sensitivity analyses
84 (median 57.7) in the control groups. Nine trials meas-
ured the dietary intake by using 3-day diet records, and GWG, FBG, birth weight, LGA, macrosomia, and PI were
other two used 24-h dietary recalls. Most participants in investigated in 9, 8, 11, 8, 8, and 8 trials, respectively. Sub-
the control group received healthy eating diet advice. The group analysis was performed on these six outcomes. The
Jadad scale of these trials ranged from 1 to 4. The charac- significant decrease in maternal FBG was diminished when
teristics of maternal and newborn outcomes in the included trials were limited to blind design, BMI ≥25 kg/m2, and GI
trials are given in Table 2. difference <7. Low-GI diets did not affect FBG when trials
were stratified by GDM condition. The significant decrease
Effects of low‑GI diets on maternal outcomes in GWG by low-GI diets was observed when the analysis
was limited to trials with a GI difference ≥7. On the other
Low-GI diet significantly reduced FBG (WMD =  hand, the results of birth weight, LGA, macrosomia, and PI
−0.18 mmol/L, 95 % CI: −0.33, −0.02, n  = 8) (Fig. 2) by any stratification were consistent with the overall esti-
and 2-h PG (n = −0.33 mmol/L, 95 % CI: −0.54, −0.12, mates (Table 2).
n = 4), but did not affect HbA1c levels (WMD = 0.02 %, Sensitivity analyses were performed to examine the
95 % CI: −0.03, 0.08, n  = 3). Low-GI diets produced effect of a single trial on the overall results by omit-
somewhat lower GWG (WMD =  −0.69 kg, 95 % CI: ting one trial in each turn. When the study of Walsh et al.
−1.74, 0.36, n  = 9) than control diets without significant [12] was excluded, maternal FBG reduction became
difference (Fig. 3). In contrast, no significant change was more pronounced (WMD =  −0.28 mmol/L, 95 % CI:
observed in gestational age at delivery (MWD = 0.03, −0.36, −0.20) without heterogeneity across the stud-
95 % CI: −0.14, 0.20, n = 5), proportion of cesarean deliv- ies (P  = 0.190, I2  = 31.2 %). In addition, omitting the
ery (RR = 1.07, 95 % CI: 0.75, 1.53, n = 5), and insulin trial by Ma et al. [9] resulted in less reduction in FBG by
use (RR = 1.01, 95 % CI: 0.77, 1.33, n = 3) (Supplemen- 0.13 mmol/L (95 % CI: −0.29, 0.02) and in 2-h PG by
tary Fig. 1). GWG (P = 0.027, I2 = 53.8 %) and FBG anal- 0.21 mmol/L (95 % CI: −0.49, 0.07). When the study of
yses (P < 0.001, I2 = 73.7 %) showed heterogeneity across Moses et al. [17] was excluded, reduced GWG became
studies. significant (WMD =  −0.99 kg, 95 % CI: −1.95, −0.03)
without heterogeneity across the studies (P  = 0.122,
Effects of low‑GI diets on newborn outcomes I2 = 38.6 %). When the trial by Perichart-Perera et al. [11]
was excluded, low-GI diet significantly decreased prematu-
The meta-analysis results showed a borderline significant rity (RR = 0.45, 95 % CI: 0.20, 0.99).
reduction in birth weight (WMD =  −0.10 kg, 95 % CI:
−0.23, 0.03, n  = 11) (Fig. 4) and a significant reduction Publication bias
in the proportion of LGA (RR = 0.52, 95 % CI: 0.31, 0.89,
n = 8) (Fig. 5). No differences were observed in other new- No publication bias was found as assessed by Begg’s fun-
born outcomes, including PI (MWD = −0.07 kg/m3, 95 % nel plot and Egger’s test, except a possible publication bias
CI: −0.71, 0.57, n = 8), body length (MWD = −0.05 cm, for analyses 2-h PG (Egger’s test, P = 0.004), LGA (Egg-
95 % CI: −0.66, 0.55, n  = 6), head circumference er’s test, P = 0.014), SGA (Egger’s test, P = 0.044), and
(MWD  =  −0.13 cm, 95 % CI: −0.68, 0.41, n  = 5), macrosomia (Egger’s test, P = 0.033).

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Table 2  Results of subgroup analyses according to trial or participant characteristics

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GWG (kg) FBG (mmol/L) Birth weight (kg) LGA Macrosomia Ponderal index(kg/m3)

N WMD P I2 N WMD P I2 N WMD P I2 N RR P I2 N RR P I2 N RR P I2

(95 % (%) (95 % CI) (%) (95 % CI) (%) (95 % CI) (%) (95 % CI) (%) (95 % CI) (%)
CI)

Total 9 −0.69 0.027 53.8 8 −0.18 0 73.7 11 −0.10 0 80.7 8 0.52 (0.31, 0.083 44.4 8 0.95 (0.83, 0.873 0 8 −0.07 0.009 62.6
(−1.74, (−0.33, (−0.23, 0.89) 1.09) (−0.71,
0.36) −0.02) 0.03) 0.57)
Study design
 Open 7 −0.66 0.008 65.2 5 −0.23 0 81.7 8 −0.14 0 83.7 5 0.39 (0.12, 0.089 50.5 5 0.96 (0.84, 0.853 0 6 −0.29 0.004 70.7
(−2.02, (−0.40, (−0.29, 1.31) 1.11) (−1.10,
0.70) −0.05) 0.01) 0.53)
 Blind 2 −0.91 0.907 0 3 0.05 0.132 50.7 3 0.03 0.013 77 3 1.31 (0.50, 0.386 0 3 0.61 (0.20, 0.562 0 2 0.42 0.344 0
(−2.62, (−0.45, (−0.31, 3.41) 1.87) (−0.44,
0.80) 0.54) 0.37) 1.29)
BMI (kg/m2)
 <25 3 −0.61 0.804 0 2 −0.30 0.480 0 3 −0.02 0.692 0 1 2.87 (0.61, 2 0.40 (0.08, 0.775 0 2 0.20 1.000 0
(−1.82, (−0.39, (−0.05, 13.50) 1.98) (−0.20,
0.60) −0.21) 0.09) 0.60)
 ≥25 5 −0.28 0.050 57.8 5 −0.08 0.187 35.2 7 −0.03 0.028 57.5 6 0.53 (0.27, 0.431 0 6 0.97 (0.84, 0.871 0 5 0.18 0.069 53.9
(−1.69, (−0.25, (−0.16, 1.02) 1.11) (−0.74,
1.14) 0.09) 0.11) 1.09)
GDM
 No 6 −0.70 0.005 70.5 4 −0.19 0.15 43.6 6 −0.09 0 89.3 4 0.26 (0.07, 0.135 46.1 3 0.98 (0.85, 0.685 0 6 −0.33 0.006 69.4
(−2.23, (−0.39, (−0.27, 1.06) 1.13) (−1.18,
0.83) 0.02) 0.08) 0.51)
 Yes 3 −0.75 0.873 0 4 −0.14 0.045 62.8 5 −0.11 0.712 0 4 1.29 (0.58, 0.668 0 5 0.47 (0.18, 0.997 0 2 0.50 0.328 0
(−2.10, (−0.38, (−0.23, 2.89) 1.23) (−0.28,
0.61) 0.10) 0.02) 1.27)
GI difference
 <7 5 −1.13 0.667 0 5 −0.12 0 82.8 6 0.01 0.085 48.4 3 1.37 (0.56, 0.386 0 5 0.97 (0.84, 0.721 0 4 0.24 0.775 0
(−4.47, (−0.32, (−0.08, 3.40) 1.11) (–0.14,
2.21) 0.07) 0.09) 0.63)
 ≥7 4 −1.26 0.011 73.2 3 −0.30 0.534 0 5 −0.31 0 87.9 5 0.30 (0.14, 0.089 50.5 3 0.62 (0.25, 0.978 0 4 −0.56 0..002 80.4
(−1.83, (−0.51, (−0.72, 0.62) 1.53) (−1.88,
−0.69) −0.09) 0.10) 0.76)

GWG gestational weight gain, FBG fasting blood glucose, LGA large for gestational age, BMI body mass index, GDM gestational diabetes mellitus, GI glycemic index
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Fig. 2  Meta-analysis of the FBG WMD (95% CI) Weight (%)

effect of low-glycemic-index
(GI) diets on gestational weight Ma (2014) -0.31 (-0.40, -0.22) 23.91
gain (GWG) as compared to the
control. WMD weighted mean Perichart-Perera (2012) 0.40 (-0.11, 0.91) 6.89
difference (kg)
Walsh (2012) -0.06 (-0.13, 0.01) 24.97

Grant (2011) -0.13 (-0.56, 0.30) 8.68

Louie (2011) -0.20 (-0.49, 0.09) 13.61

Rhodes (2010) 0.00 (-3.34, 3.34) 0.21

Moses (2006) -0.30 (-0.57, -0.03) 14.38

Clapp (1997) -0.50 (-0.99, -0.01) 7.34

Overall (I-squared = 73.7%, p = 0.000) -0.18 (-0.33, -0.02) 100.00

-1 -.5 0 .5 1

Fig. 3  Meta-analysis of the GWG WMD (95% CI) Weight %

effect of low-glycemic-index
(GI) diets on maternal fast- Markovic (2016) 0.30 (-1.63, 2.23) 13.63
ing blood glucose (FBG) as
Ma (2014) -0.47 (-2.18, 1.24) 15.18
compared to the control. WMD
weighted mean difference Moses (2014) -0.10 (-2.76, 2.56) 9.66
(mmol/L)
Walsh (2012) -1.50 (-2.16, -0.84) 23.05
Louie (2011) -1.20 (-3.43, 1.03) 11.81

Rhodes (2010) -0.50 (-3.17, 2.17) 9.63

Moses (2009) -1.70 (-18.56, 15.16) 0.38

Moses (2006) 1.40 (-0.63, 3.43) 13.00

Clapp (1997) -7.90 (-12.98, -2.82) 3.65
Overall (I-squared = 53.8%, p = 0.027) -0.69 (-1.74, 0.36) 100.00

-8 -4 0 4

Fig. 4  Meta-analysis of the Birth weight WMD (95% CI) Weight (%)

effect of low-glycemic-index
(GI) diets on newborn birth Markovic (2016) 0.05 (-0.11, 0.21) 12.03
weight as compared to the Ma (2014) -0.06 (-0.25, 0.13) 10.98
control. WMD weighted mean
Moses (2014) 0.03 (-0.05, 0.11) 13.93
difference (kg)
Perichart-Perera (2012) -0.24 (-0.48, 0.00) 9.67
Walsh (2012) 0.03 (-0.04, 0.10) 13.99
Grant (2011) -0.21 (-0.70, 0.29) 4.63
Louie (2011) 0.00 (-0.28, 0.28) 8.69
Rhodes (2010) 0.37 (0.04, 0.70) 7.45
Moses (2009) -0.05 (-1.29, 1.19) 1.00
Moses (2006) -0.23 (-0.46, 0.00) 9.90
Clapp (1997) -0.98 (-1.30, -0.66)7.74
Overall (I-squared = 80.7%, p = 0.000) -0.10 (-0.23, 0.03) 100.00

-2 0 2

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Fig. 5  Meta-analysis of the LGA RR (95% CI) Weight (%)

effect of low-glycemic-index
(GI) diets on proportion of large Markovic (2016) 0.92 (0.13, 6.35) 5.74
for gestational age (LGA) as Perichart-Perera (2012) 1.15 (0.20, 6.55) 6.26
compared to the control. RR
relative risk Louie (2011) 2.87 (0.61, 13.50) 5.64

Grant (2011) 0.74 (0.14, 3.94) 7.85

Rhodes (2010) 0.58 (0.11, 3.16) 8.84

Moses (2009) 1.03 (0.23, 4.73) 8.15

Moses (2006) 0.09 (0.01, 0.69) 28.51

Clapp (1997) 0.05 (0.00, 0.72) 29.00

Overall (I-squared = 44.4%, p = 0.083) 0.52 (0.31, 0.89) 100.00

.1 1 5

Discussion and dinner in pregnant women with GDM were signifi-

cantly lower after administering low-GI staple diets than
Maternal dietary macronutrient intake throughout preg- those after providing normal diabetic control diet. This trial
nancy affects maternal metabolism and in utero envi- was not included in the present study because it is a short-
ronment. As glucose is a major energy substrate for fetal term intervention with no other outcomes evaluated [33].
growth, varying degrees of glucose intolerance, even if The present meta-analysis showed a significant reduction in
less than that conventionally required for the diagnosis of FBG by 0.18 mmol/L and 2 h PG by 0.33 mmol/L, which
gestational diabetes, will result in alterations in utero envi- suggested the beneficial effects of low-GI diets beyond
ronment and thus will influence fetal growth and adiposity postprandial glucose. The current results updated the pre-
[28]. Oostdam et al. [29] evaluated six types of intervention vious meta-analysis including only 3 trials, in which the
during pregnancy in the prevention of GDM using meta- lowering effect of low-GI diet on maternal FBG was not
analysis; the results showed that dietary intervention, such observed [29]. However, the subgroup analysis revealed
as low-GI diet advice, may reduce GDM incidence com- that the effects of low-GI diets on FBG diminished when
pared with the standard care. A previous systemic review trials were stratified by GDM condition and gestation week
also reported that low-GI diets may reduce the need for at recruitment. This observation may be explained by a low
insulin in pregnant women with GDM [6]; this finding was statistical power resulting from the limited number of tri-
confirmed by a recent meta-analysis [7]. als in each subgroup (n  = 4). It is important to note that
So far, both reviews excluded trials conducted among the intervention in GDM group usually started after GDM
healthy women and the number of selected trials was less diagnosis around 24–28 weeks, which leaves a very short
than five. In fact, women with even a mildly elevated blood time window for any intervention. Nevertheless, the minor
glucose level have a higher risk of giving birth to a LGA improvement in circulating blood glucose is effective to
infant [29]. Beneficial effects on birth weight were already reduce excessive newborn weight.
observed in pregnant women without GDM after low-GI Excessive GWG is considered a risk factor not only for
diets [18]. Thus, in the present updated meta-analysis, we GDM but also for excessive fetal growth [34, 35]. High
have included participants of healthy pregnant women, GWG was related to long-term adverse health outcomes
women with gestational hyperglycemia, and women with for the mother–newborn pair [36]. Mourtakos et al. [37]
pregestational T2DM. Moreover, the pregnancy outcomes found that excessive GWG was associated with a higher
in the present meta-analysis included 7 maternal and 11 risk of greater infant size at birth and a higher BMI status
newborn outcomes, which were more comprehensive than at the ages of 2 and 8 years. Sridhar et al. [38] also demon-
the previous relevant studies. strated that GWG outside the recommendations increased
Maternal hyperglycemia and hyperglycemic excursions the odds of childhood overweight and obesity, independ-
(during fasting, after a glucose load, and postprandial) ent of several potential confounders, such as birth weight.
could lead to adverse pregnancy and offspring outcomes Thus, gestational weight must be controlled in a rational
[30–32]. By definition, a low-GI diet is expected to lower range. A recent meta-analysis has shown that a low-GI
postprandial glucose when glucose load is controlled. A diet promoted weight loss in overweight or obese people
recent trial found that glucose levels after breakfast, lunch, [39]. Therefore, a low-GI diet may also provide benefits

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to weight management during pregnancy. Dietary inter- could be related to a relative small number of trials and low
ventions have shown the greatest reduction in gestational quality of evidence.
weight gain compared to other methods. Although reduced Some observational epidemiological studies also sup-
GWG did not reach significant in the present meta-anal- ported the present findings. A prospective cohort study
ysis, the low-GI diets significantly decreased GWG by on 13,110 eligible women in the Nurses’ Health Study II
0.99 kg compared with the control group when the study found that women whose dietary GI was higher than 57
of Moses et al. [17] was excluded. Moses study was the units had a 30 % increased risk of developing GDM com-
source of heterogeneity in GWG analysis, and low-GI diet pared with participants whose dietary GI was lower than 51
caused higher GWG compared with the control group. units [42]. A cohort including 1082 gravidas in the Camden
However, that result may be wrested by the significant Study found that GI was positively and significantly related
lower BMI in the low-GI diet group than in the control to maternal plasma glucose, HbA1c, and infant birth weight
group (24.4 vs. 26.6 kg/m2, P = 0.04). A recent 6-month [43]. A recent prospective cohort study during the 10 years
randomized trial conducted on women with previous of follow-up has shown that higher intake of nuts, which
GDM found that subjects in the low-GI group lost an aver- are typical low-GI food sources [44], was associated with
age of 1.3 kg compared with the 0.1 kg in the conventional a significantly lower risk of GDM by 27 % as a result of
healthy dietary recommendation [40]. The present analy- improved insulin sensitivity [45]. These results highlighted
sis revealed inconsistent results on GWG and FBG, sug- the clinical importance of dietary sources in assessing the
gesting that the effects of low-GI diets on GWG and FBG health effects of low-GI diets.
appeared to be related to study design and characteristics The current meta-analysis was primarily limited by con-
of participants. This result was consistent with previous siderable heterogeneity across studies, such as the main
meta-analysis on patients with GDM [7]. outcomes of GWG and FBG and birth weight, which com-
In theory, reduced FBG by low-GI diet in the present plicated the interpretation of the findings. The heteroge-
meta-analysis could decrease newborn birth weight. Horan neity can be attributed to study design and characteristics
et al. [28] found that low-GI dietary intervention in preg- of participants. Most included RCTs used an open-label
nancy had a beneficial effect on neonatal central adiposity design. As such, blinding of the treatment to the par-
as determined using the ratio of waist to length. The mater- ticipants or investigator is difficult, perhaps impossible,
nal dietary GI even affects childhood health. Okubo et al. because of the nature of dietary intervention/advice design.
[41] found that maternal dietary GI in early pregnancy was More importantly, the methods of intervention and control
positively associated with fat mass at 4 and 6 years of age. may be the source of heterogeneity. Regarding interven-
In the present meta-analysis, a borderline significant reduc- tion, these RCTs differed in values of dietary GI and some-
tion in birth weight of 0.12 kg was observed. In a previous times in co-interventions. For example, all participants in
meta-analysis on 4 trials, low-GI diets reduced the newborn the Clapp study participated in an exercise program before
birth weight (WMD −0.16 kg, 95 % CI: −0.25, −0.08) and after pregnancy, which may reinforce the effect of the
compared with control diets in pregnant women with dietary intervention [18]. On the other hand, three studies
GDM [7]. However, in the present subgroup for women declared that low-GI diets for intervention were supported
with GDM with recent trials added, the reduction in new- or supplied by relevant companies [13, 15, 16]. Regarding
born weight was still retained in borderline significance. In control, high-GI dietary advice [14, 16–18] or low-fat die-
fact, the disadvantage of birth weight reduction should be tary advice [15] was used in some trials. In general, high-
considered, particularly in pregnant women who are under- GI diets, rather than normal diets, are the dominant diet in
weight, at nutritional risk, or from a low-income country. individuals living in the Western industrialized societies
Participants in the included trials did not suffer from appar- [27]. Other limitations, which also resulted in heterogene-
ent malnutrition. Thus, the issue of low birth weight did not ity, included different criteria for screening and diagno-
fall within the scope of this study. Besides, women exhib- sis of GDM, start of counseling in first or second trimes-
ited reduced risk of having an LGA infant after administer- ter, and frequency of counseling that varied from twice
ing with low-GI diets in the present meta-analysis, which is only to weekly during pregnancy. Finally, the SDs of the
consistent with Oostdam et al. [29]. In addition to the bor- net changes were not available in some trials. SDs were
derline significant reduction in birth weight and LGA, low- derived from the standard errors, median and interquartile
GI diets minimally affected the other 9 newborn outcomes. ranges, or standard deviations for the initial and final val-
The current results were generally consistent with these of ues. These methods employed may not be ideal and result
previous studies, in which no effects were observed in the in some inaccuracies.
majority of outcomes. However, Viana et al. [7] found that Based on the current available evidence, we concluded
pregnant women with GDM used insulin less frequently. that low-GI diets may have beneficial effects on mater-
The partial discrepancy among these meta-analysis results nal outcomes without causing adverse effects on newborn

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outcomes in general pregnant women. The risk of adverse 11. Perichart-Perera O, Balas-Nakash M, Rodriguez-Cano A, Legor-
pregnancy outcomes can be reduced by low-GI dietary reta-Legorreta J, Parra-Covarrubias A, Vadillo-Ortega F (2012)
Low glycemic index carbohydrates versus all types of carbohy-
intervention because of the controlled maternal blood glu- drates for treating diabetes in pregnancy: a randomized clinical
cose level. However, the results should be interpreted with trial to evaluate the effect of glycemic control. Int J Endocrinol
caution because of the evidence of heterogeneity across 2012:296017
studies, possible publication bias, and limited number of 12. Walsh JM, McGowan CA, Mahony R, Foley ME, McAuliffe
FM (2012) Low glycaemic index diet in pregnancy to prevent
studies. Hence, large, well-designed, intervention RCTs macrosomia (ROLO study): randomised control trial. BMJ
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RG (2011) Effect of a low glycaemic index diet on blood glucose
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Compliance with ethical standards  Pract 91:15–22
14. Louie JCY, Markovic TP, Perera N, Foote D, Petocz P, Ross GP,
Brand-Miller JC (2011) A randomized controlled trial investigating
Conflict of interest Irma Silva-Zolezzi is employee of Nestlé the effects of a low-glycemic index diet on pregnancy outcomes in
Research Center, Lausanne. Gerard Vinyes Parés and Yi Wang are gestational diabetes mellitus. Diabetes Care 34:2341–2346
employees of Nestlé Research Center Beijing. The authors state that 15. Rhodes ET, Pawlak DB, Takoudes TC, Ebbeling CB, Feldman
there is no conflict of interest. HA, Lovesky MM, Cooke EA, Leidig MM, Ludwig DS (2010)
Effects of a low-glycemic load diet in overweight and obese
pregnant women a pilot randomized controlled trial. Am J Clin
Nutr 92:1306–1315
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