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Keywords:

  • diet;
  • pregnancy;
  • randomised controlled trial;
  • systematic review;
  • meta-analysis

Abstract

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Acknowledgements
  9. Source of funding
  10. Conflict of interest
  11. Contributions
  12. References
  13. Supporting Information

Dietary intake during pregnancy influences maternal health. Poor dietary practices during pregnancy have been linked to maternal complications. The objective was to determine the effect of dietary intervention before or during pregnancy on pregnancy outcomes. A systematic review was conducted without date restrictions. Randomised controlled trials (RCTs) evaluating whole diet or dietary components and pregnancy outcomes were included. Two authors independently identified papers for inclusion and assessed methodological quality. Meta-analysis was conducted separately for each outcome using random effects models. Results were reported by type of dietary intervention: (1) counselling; (2) food and fortified food products; or (3) combination (counselling + food); and collectively for all dietary interventions. Results were further grouped by trimester when the intervention commenced, nutrient of interest, country income and body mass index. Of 2326 screened abstracts, a total of 28 RCTs were included in this review. Dietary counselling during pregnancy was effective in reducing systolic [standardised mean difference (SMD) −0.26, 95% confidence interval (CI) −0.45 to −0.07; P < 0.001] and diastolic blood pressure (SMD −0.57, 95% CI −0.75 to −0.38; P < 0.001). Macronutrient dietary interventions were effective in reducing the incidence of preterm delivery (SMD −0.19, 95% CI −0.34 to −0.04; P = 0.01). No effects were seen for other outcomes. Dietary interventions showed some small, but significant differences in pregnancy outcomes including a reduction in the incidence of preterm birth. Further high-quality RCTs, investigating micronutrient provision from food, and combination dietary intervention, are required to identify maternal diet intakes that optimise pregnancy outcomes.


Introduction

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Acknowledgements
  9. Source of funding
  10. Conflict of interest
  11. Contributions
  12. References
  13. Supporting Information

The association between early life nutrition and long-term health has been of interest for decades (Bhutta 2013). There is an abundance of evidence to suggest that when a woman has a good state of health and nutrition prior to and during pregnancy, there is a greater chance of a successful pregnancy and birth outcome (Goldberg 2002; Erick 2008; Ritchie & King 2008; Nichols-Richardson 2011). Inadequate nutrition during this time, particularly the first trimester, impairs fetal growth (Antal et al. 1997; Derbyshire et al. 2006; Northstone et al. 2008) and has long-term negative consequences for the mother and the developing fetus (Godfrey & Robinson 1998; Moore et al. 2004; Northstone et al. 2008; Derbyshire et al. 2009).

Gestational diabetes mellitus (GDM) and pregnancy hypertensive disorders are among the most common complications of pregnancy (Sibai 2003; Zhang et al. 2006) affecting 2–5% (Gilmartin et al. 2008), and 10% (Roberts et al. 2011) of all pregnancies, respectively. Pregnancies complicated by these metabolic conditions are associated with adverse maternal, fetal and neonatal outcomes (Brown et al. 2000; Östlund et al. 2003; Roberts et al. 2003, 2005). GDM is associated with an increased risk of pregnancy hypertensive disorders and caesarean section (American Diabetes Association 2003), while increasing the risk of neonatal outcomes: intrauterine fetal death, preterm delivery and fetal macrosomia (American Diabetes Association 2003). In the United States, pregnancy hypertensive disorders, are one of the leading causes of maternal death (Peters & Flack 2004), associated with an increased risk of placental abruption, ante- and post-partum haemorrhage, and acute renal or hepatic failure for the mother (National High Blood Pressure Education Program Working Group on High Blood Pressure in Pregnancy 2000). Pregnancy hypertensive disorders are also associated with preterm birth, intrauterine growth restriction and perinatal death for the neonate (Brown et al. 2000, Roberts et al. 2003, National High Blood Pressure Education Program Working Group on High Blood Pressure in Pregnancy 2000, Lowe et al. 2009). Maternal diet is one of the key risk factors for developing pregnancy hypertensive disorders and GDM and therefore may be a key preventative strategy on these and other pregnancy outcomes (King 2006). However, little is known about the effectiveness of dietary intervention during pregnancy (Roseboom et al. 2011).

The objective of this study was to synthesise the best of the available evidence by conducting a systematic review and meta-analysis, to determine whether dietary interventions have any effect on pregnancy outcome. Dietary interventions could consist of dietary counselling, food and/or fortified food products, or a combination of both, administered either before or during pregnancy.

Key messages

  • Dietary counselling during pregnancy reduces maternal blood pressure, but not hypertensive disorders.
  • Dietary interventions focused on modifying macronutrient intakes during pregnancy reduces the incidence of preterm delivery.
  • Further research is needed to elucidate the role of maternal diet, particularly micronutrient provision and combination dietary interventions to optimise pregnancy outcomes.

Materials and methods

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Acknowledgements
  9. Source of funding
  10. Conflict of interest
  11. Contributions
  12. References
  13. Supporting Information

The review protocol was developed using the Cochrane Handbook for Systematic Reviews of Interventions (The Cochrane Collaboration 2011) and Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) for reporting the methods and outcomes (Liberati et al. 2009; Moher et al. 2009).

Eligibility criteria

Table 1 highlights the inclusion and exclusion criteria for the selection of publications. Any publication identified in the search reporting one or more pregnancy, neonatal or infant outcomes was considered. At least three randomised controlled trials (RCTs) needed to be identified for each outcome for inclusion in the results to allow for meta-analysis. The outcome definitions were those used by the authors; however, where multiple definitions existed between publications, the term was used broadly. For example, preterm delivery included those classified as <36 weeks gestation (de Groot et al. 2004), <37 weeks (Mora et al. 1978; Rush et al. 1980; McDonald et al. 1981; Kafatos et al. 1989; Van Buul et al. 1997; Smuts et al. 2003b; Khoury et al. 2005; Bech et al. 2007; Aaltonen et al. 2008; Thornton et al. 2009; Vinter et al. 2011) and unspecified (Mardones-Santander et al. 1988; Briley et al. 2002; Smuts et al. 2003a; Quinlivan et al. 2011). Nutrient deficiencies were excluded from this review as they were considered risk factors rather than clinical outcomes. This review focuses on dietary intake from food, rather than nutritional supplement use. Publications that targeted the whole diet, single food groups, individual food and fortified foods were included. Fortified foods included the provision of one or more foods that has essential vitamins and/or minerals added to enhance the foods nutritional content; for example docosahexaenoic acid (DHA) added to a cereal-based bar to increase the omega 3 fatty acid content. Fortified foods modify both the macro- (carbohydrate, protein, fat) and micronutrient (vitamins and minerals) content of the maternal diet. Supplement-only trials including the provision of a pill, capsule or tablet containing vitamins, minerals or amino acids were excluded. The types of dietary interventions included dietary counselling, modifying or providing food and fortified food products, or a combination of both.

Table 1. Criteria for the selection of studies
InclusionExclusion
  1. *American Dietetic Association Quality Criteria Checklist for Primary Research (see Academy of Nutrition and Dietetics 2012).

Studies that reported any pregnancy, neonatal or infant outcomes in preconception or pregnant women, any age, weight or body mass index, without date limits.Health conditions that may influence dietary intake (i.e. unrepresentative sample such as gestational diabetes).
At least three randomised controlled trials per outcome.Studies published in languages other than English.
Any healthy, human population.Studies in animals.
Randomised or pseudo-randomised controlled trials on dietary interventions, including counselling, food and/or both provided by any health professional.Case study, editorial, conference proceeding.
Any intensity, frequency or timing of intervention.Studies on gestational weight gain.
Positive or neutral methodological quality.*Trials solely on nutrient supplementation (i.e. tablet form; no macronutrient change).
Multiple births.
Duplicate populations (the data reporting the smaller number of participants for the same pregnancy outcome was excluded).
Negative methodological quality.*

Search strategy

A research librarian (DB) guided the systematic search for publications in December 2011. The search was conducted without date limits, using 10 electronic databases: EMBASE; Pre-Medline; MEDLINE; Proquest; Web of Science; CINAHL; Scopus; The Cochrane Library; Mosby Index; and Maternity and Infant Care. The following MeSH terms, words and combinations of words were searched: pregnancy; diet OR food OR beverage OR nutrient OR macro-nutrient OR micro-nutrient; and randomised controlled trial OR randomized controlled trial. Keywords were searched as free text in the title, abstract, or topic and combined using the Boolean operator ‘AND’. Our MeSH terms were intentionally broad so as to capture as many dietary interventions and outcomes as possible. Preconception was defined as up to 3 months before pregnancy; however, we did not explicitly include ‘preconception’ as a search term in isolation from the term ‘pregnancy’. Limits included English language and humans. Additional publications were identified from the reference lists of included papers. All primary trials included in systematic reviews and meta-analyses were independently assessed for eligibility. Outcomes were divided into two groups: pregnancy (this paper), and neonatal and infant (presented elsewhere).

Selection process

All records identified were first assessed for eligibility based on the information contained in the title and abstract, by two independent reviewers (EG and AH), as recommended by the PRISMA guidelines for systematic reviews of randomised trials (Liberati et al. 2009). When multiple publications were available for the same trial, the publication reporting the greatest number of participants for each outcome was selected. The full text of all publications that appeared to meet the eligibility screening (Table 1) was retrieved and subjected to a second assessment for relevance (EG and AH). Any discrepancy in assessment between reviewers was resolved through discussion. Selected full texts were then assessed for methodological quality by two independent reviewers (EG and SD) using the Quality Criteria Checklist for Primary Research in the American Dietetic Association Evidence Analysis Manual (Academy of Nutrition and Dietetics 2012). Any discrepancies were discussed. The Quality Criteria Checklist includes 10 structured validity questions that address scientific quality and soundness, including bias, confounding and the appropriateness of the interventions and measures. The Quality Criteria Checklist enabled a systematic and objective rating to be given to each publication. The highest methodological quality papers were designated ‘Positive’, meeting most of the validity criteria including all priority criteria (Academy of Nutrition and Dietetics 2012). ‘Neutral’ quality publications met most of the validity criteria, but failed one or more of the four priority criteria, indicating the study was not exceptionally strong (Academy of Nutrition and Dietetics 2012). ‘Negative’ publications failed to meet six or more of the validity criteria (Academy of Nutrition and Dietetics 2012) and were excluded from the results.

Data extraction

One reviewer (EG) extracted relevant data from all included publications, with a second independent reviewer (AH/JL) extracting data from approximately half to ensure accuracy. The following variables were data extracted: study design, aim, quality, participant characteristics, intervention type, dietary modification, assessment, compliance and outcome. For the meta-analysis, one reviewer (EG) extracted the data from each publication into an Excel spread sheet, verified by a second reviewer (AB) for the following variables: author, year, outcome, type of intervention, trimester when the intervention commenced, nutrient of interest (macro- or micronutrient), body mass index (BMI; underweight/nutritional risk, overweight/obese, or no restriction), country income (high or low), quality rating (positive or neutral), participant numbers per group and by outcome, mean, standard deviation, 95% confidence interval (CI), median, range and odds ratio where possible for each outcome. Trials were divided into either macro- or micronutrient, depending on their focus. For example, an intervention using a high-energy and high-protein beverage would be classified ‘macronutrient’, while an intervention targeting calcium using either dairy or fortified orange juice would be classified ‘micronutrient’. BMI was defined according to the baseline nutritional status of the mother. The Organisation for Economic Co-operation and Development (OECD) criteria (The World Bank Group 2012) was used to classify ‘high-’ and ‘low-’ income countries. Corresponding authors were emailed for additional data or clarification when needed. In trials reporting a range of gestational ages at study commencement, the most advanced week was used to calculate length of intervention.

Statistical analysis

The main measure of effect was the standardised mean difference (SMD). The SMD is determined by taking the difference in the mean outcome between the intervention and control group in one publication, and dividing it by the pooled standard deviation for the outcome across the whole trial. The SMD accounts for differences in variance between studies by allowing the size of the intervention effect in each publication to be expressed relative to the variability observed within that study. A secondary measure of effect, the raw mean difference (RMD), presented in the common units for each outcome [e.g. weeks gestation, mmHg for blood pressure (BP) ] was also included. Trials containing more than one intervention (Rush et al. 1980; Ross et al. 1985; Chan et al. 2006), or control group (Smuts et al. 2003a) had their effects averaged, as there were no significant differences on pregnancy outcomes (Lipsey & Wilson 2001). Dichotomised outcomes had the log-odds and standard errors converted to SMD via the method created by Hasselblad and Hedges (1995; Chinn 2000). Means and variance were approximated for trials reporting medians using the method reported by Hozo et al. (2005). Trials reporting outcomes with zero counts for both intervention and control groups were excluded from the analysis. For outcomes reporting zero counts for one intervention group only, the Firth penalized likelihood method was used to approximate the odds ratio (Firth 1993; Heinze & Schemper 2002) and 95% CIs.

Meta-analyses were performed for each outcome and dietary intervention type using a random effects model with random weights applied for each study. Subgroup analyses were performed for each outcome by dietary intervention, trimester when the intervention commenced, nutrient of interest, BMI and country income. The I2 statistic was applied to describe the total variation in study estimates because of heterogeneity. Funnel plots were used as a visual tool for investigating the presence of potential bias and Egger's test used to test for funnel plot asymmetry (Egger et al. 1997). Statistical analyses were performed using the metan command in the statistical software package Intercooled Stata, version 12 (Stata, College Station, Texas, USA) (StataCorp 2011). P-values ≤0.01 were considered statistically significant to adjust for the multiple comparisons that were made.

Results

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Acknowledgements
  9. Source of funding
  10. Conflict of interest
  11. Contributions
  12. References
  13. Supporting Information

Description of studies

The trial selection process is summarised in Fig. 1. Of the 2326 papers screened, data were extracted from 28 publications, which included 8322 participants. The earliest published study was in 1978 (Mora et al. 1978) and the latest in 2011 (Luoto et al. 2011; Courville et al. 2011; Quinlivan et al. 2011; Vinter et al. 2011). Twenty-four publications were performed in high-income OECD countries: 10 in the United States, 3 each in Finland, Denmark and the Netherlands, and 1 each in Australia, Norway, Italy, Greece and Chile (Supporting Information Table S1).

figure

Figure 1. Flow diagram for the selection of included studies.

aNot a study means not a study design of interest. It includes observational trials, editorials and conference papers.

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The methodological quality and characteristics of included publications are shown in Supporting Information Table S1. All studies were of positive or neutral quality according to the American Dietetic Association Quality Criteria Checklist (Academy of Nutrition and Dietetics 2012). Fourteen publications compared dietary counselling with standard antenatal care (no intervention) (Kafatos et al. 1989; Van Buul et al. 1997; Knuist et al. 1998; Briley et al. 2002; Bonomo et al. 2005; Khoury et al. 2005; Chan et al. 2006; O'Connor & Whaley 2007; Wolff et al. 2008; Asbee et al. 2009; Thornton et al. 2009; Luoto et al. 2010; Quinlivan et al. 2011; Vinter et al. 2011). Twelve publications evaluated the effect of specific food and fortified food products (Mora et al. 1978, 1979; Rush et al. 1980; McDonald et al. 1981; Metcoff et al. 1985; Ross et al. 1985; Mardones-Santander et al. 1988; Smuts et al. 2003a,b; de Groot et al. 2004; Bech et al. 2007; Courville et al. 2011), two of which came from the Columbian Longitudinal Study of Malnutrition and Intellectual Development (Mora et al. 1978, 1979). Two publications from the Finnish Mother–Infant Nutrition and Probiotic Intervention assessed the effect of combined dietary counselling, and food and fortified food products (Aaltonen et al. 2008; Luoto et al. 2010).

All but one publication (McDonald et al. 1981) studied the effect of dietary intervention during pregnancy on pregnancy outcomes. McDonald et al. (1981) included pre-pregnancy (periconception) dietary intervention. Twenty (of 28) publications, included two groups: dietary intake (intervention) vs. usual care or dietary intake (control). Dietary intervention during the second and third trimester was the most frequently reported period of intervention (22 publications). Dietary intervention ranged in duration from 10 (Rush et al. 1980) to greater than 40 weeks (pre-pregnancy intervention) (McDonald et al. 1981). Dietitians or nutritionists were the most frequent dietary intervention providers (12 publications) and macronutrients (24 publications) were more commonly targeted in the intervention than micronutrients (4 publications). Fourteen publications did not report any dietary data (Metcoff et al. 1985; Ross et al. 1985; Van Buul et al. 1997; Knuist et al. 1998; Smuts et al. 2003a,b; Bonomo et al. 2005; Bech et al. 2007; O'Connor & Whaley 2007; Asbee et al. 2009; Thornton et al. 2009; Courville et al. 2011; Quinlivan et al. 2011; Vinter et al. 2011), with 12 of these not conducting nutritional assessments during the intervention period (Metcoff et al. 1985; Ross et al. 1985; Van Buul et al. 1997; Knuist et al. 1998; Smuts et al. 2003a,b; Bonomo et al. 2005; Bech et al. 2007; O'Connor & Whaley 2007; Asbee et al. 2009; Thornton et al. 2009; Vinter et al. 2011). Six trials (7 publications) recruited women who were underweight or nutritionally at risk (Mora et al. 1978, 1979; Rush et al. 1980; McDonald et al. 1981; Metcoff et al. 1985; Ross et al. 1985; Mardones-Santander et al. 1988), while four trials recruited overweight or obese women as their target population (Wolff et al. 2008; Thornton et al. 2009; Quinlivan et al. 2011; Vinter et al. 2011). The pregnancy outcomes included: hypertensive disorders (pregnancy-induced hypertension and preeclampsia), BP, GDM, caesarean section, length of gestation, preterm and post-term delivery.

Effects of dietary intervention

Table 2 shows the effect of dietary intervention components and all dietary intervention trials on meta-analysed pregnancy outcomes. There was one trial (2 publications) in our review on the combination (counselling + food) dietary intervention (Aaltonen et al. 2008; Luoto et al. 2010). Aaltonen et al. (2008) analysed the effect of combination dietary intervention on the pregnancy outcomes preeclampsia, GDM, BP, length of gestation, preterm and post-term (Aaltonen et al. 2008), while Luoto et al. (2010) analysed combination dietary intervention and caesarean section only (Luoto et al. 2010). However, because of insufficient data for pooling, this trial was meta-analysed as part of all dietary interventions only.

Table 2. Effect of dietary interventions during pregnancy on pregnancy outcomes*
 Number of trials (references)Number of participantsIntervention Number or Mean ± SDControl Number or Mean ± SDSMD (95% CI)RMDP-valueI2 (%)
IntCon
  1. BP, blood pressure; CI, confidence interval; Con, control; Int, intervention; NA, not applicable; RMD, raw mean difference; SD, standard deviation; SMD, standardised mean difference.

  2. *The main measure of effect was SMD. The SMD was determined by taking the difference in the mean of an outcome between the intervention and control group in one publication, and dividing it by the pooled standard deviation for the outcome across the whole trial. The trials by Metcoff et al. (1985) and Mora et al. (1979) were not included in the meta-analysed outcome: length of gestation, as authors did not present results. The secondary measure of effect was RMD. Categorical outcomes are reported as odds ratios. §The total number of participants (Int + Con) was 3307. The trial by Metcoff et al. (1985) provided withdrawals for the trial (n = 61); however, it did not specify participant withdrawals per Int and Con group. Because authors did not provide this data, all enrolled participants were included in the number of participants (n = 3368).

Dietary counselling         
Hypertensive disorders7 (Van Buul et al. 1997; Khoury et al. 2005; Wolff et al. 2008; Asbee et al. 2009; Thornton et al. 2009; Luoto et al. 2011; Vinter et al. 2011)8117917796−0.12 (−0.30 to 0.06)0.850.200
Systolic BP (mmHg)3 (Chan et al. 2006; Wolff et al. 2008; Vinter et al. 2011)225207115.65 ± 5.80117.81 ± 7.61−0.26 (−0.45 to −0.07)−0.66<0.0010
Diastolic BP (mmHg)3 (Chan et al. 2006; Wolff et al. 2008; Vinter et al. 2011)22520771.81 ± 4.3175.02 ± 6.50−0.57 (−0.75 to −0.38)−2.76<0.0010
Gestational diabetes6 (Wolff et al. 2008; Asbee et al. 2009; Thornton et al. 2009; Luoto et al. 2011; Quinlivan et al. 2011; Vinter et al. 2011)624582191172−0.27 (−0.72 to 0.17)0.700.2369
Length of gestation (weeks)12 (Kafatos et al. 1989; Van Buul et al. 1997; Knuist et al. 1998; Bonomo et al. 2005; Khoury et al. 2005; Chan et al. 2006; O'Connor & Whaley 2007; Wolff et al. 2008; Asbee et al. 2009; Thornton et al. 2009; Luoto et al. 2011; Vinter et al. 2011)1577152639.60 ± 1.4039.49 ± 1.590.06 (−0.05 to 0.16)0.080.2949
Preterm delivery7 (Kafatos et al. 1989; Van Buul et al. 1997; Briley et al. 2002; Khoury et al. 2005; Thornton et al. 2009; Quinlivan et al. 2011; Vinter et al. 2011)8848753356−0.25 (−0.56 to 0.05)0.670.1019
Post-term delivery1 (Thornton et al. 2009)1161161516−0.04 (−0.46 to 0.38)0.950.85NA
Caesarean section6 (Knuist et al. 1998; Bonomo et al. 2005; Wolff et al. 2008; Asbee et al. 2009; Thornton et al. 2009; Vinter et al. 2011)680667206206−0.02 (−0.17 to 0.14)0.990.8512
Food and food products        
Hypertensive disorders2 (Smuts et al. 2003a,b)160184610−0.29 (−0.86 to 0.29)1.040.330
Gestational diabetes3 (Smuts et al. 2003a,b; de Groot et al. 2004)200223470.20 (−0.50 to 0.89)0.860.580
Length of gestation (weeks)7 (Ross et al. 1985; Mardones-Santander et al. 1988; Smuts et al. 2003a,b; de Groot et al. 2004; Bech et al. 2007; Courville et al. 2011)1399§895§39.68 ± 1.0939.65 ± 1.370.09 (−0.13 to 0.25)0.250.2748
Preterm delivery7 (Mora et al. 1978; Rush et al. 1980; McDonald et al. 1981; Smuts et al. 2003a,b; de Groot et al. 2004; Bech et al. 2007)16201349170145−0.10 (−0.23 to 0.04)0.880.160
Post-term delivery2 (Mora et al. 1978; McDonald et al. 1981)3153101826−0.16 (−0.68 to 0.36)0.760.5443
Caesarean section3 (Smuts et al. 2003a,b; de Groot et al. 2004)1892132335−0.15 (−0.48 to 0.17)0.820.350
Combination        
Hypertensive disorders1 (Aaltonen et al. 2008)868556−0.11 (−0.79 to 0.56)0.830.74NA
Systolic BP (mmHg)1 (Aaltonen et al. 2008)8685116 ± 14.10112 ± 110.32 (0.01 to 0.62)4.000.04NA
Diastolic BP (mmHg)1 (Aaltonen et al. 2008)868570 ± 9.6069.00 ± 9.200.11 (−0.20 to 0.41)1.000.49NA
Gestational diabetes1 (Aaltonen et al. 2008)8685860.17 (−0.44 to 0.77)1.290.59NA
Length of gestation (weeks)1 (Aaltonen et al. 2008)868538.25 ± 1.9839.69 ± 1.4−0.55 (−0.84 to −0.26)−1.43<0.001NA
Preterm delivery1 (Aaltonen et al. 2008)8685410.78 (−0.44 to 2.00)3.820.21NA
Post-term delivery1 (Aaltonen et al. 2008)868501−0.62 (−2.40 to 1.16)0.330.50NA
Caesarean section1 (Luoto et al. 2010)777612110.05 (−0.44 to 0.54)1.070.85NA
All dietary interventions        
Hypertensive disorders101057106088112−0.13 (−0.30 to 0.04)0.840.120
Systolic BP (mmHg)4311292115.74 ± 7.87116.35 ± 8.46−0.12 (−0.45 to 0.21)−0.350.4871
Diastolic BP (mmHg)431129271.36 ± 5.6373.51 ± 7.18−0.40 (−0.79 to −0.01)−0.450.0480
Gestational diabetes10910890203185−0.12 (−0.44 to 0.20)0.820.4752
Length of gestation (weeks)203062250639.60 ± 1.3139.55 ± 1.510.04 (−0.06 to 0.14)0.100.4261
Preterm delivery1525902309207202−0.13 (−0.27 to 0.02)0.840.0915
Post-term delivery45175113343−0.16 (−0.42 to 0.11)0.790.240
Caesarean section10946956241252−0.03 (−0.16 to 0.10)0.980.650

Pregnancy hypertensive disorders

Seven RCTs studied the effect of dietary counselling on pregnancy hypertensive disorders (n = 1602 women) (Van Buul et al. 1997; Khoury et al. 2005; Wolff et al. 2008; Asbee et al. 2009; Thornton et al. 2009; Luoto et al. 2010; Vinter et al. 2011), with two trials reporting more than one hypertensive outcome (Wolff et al. 2008; Thornton et al. 2009). Trials examining the effect of dietary counselling on pregnancy hypertensive disorders included: three trials on pregnancy-induced hypertension (Van Buul et al. 1997; Wolff et al. 2008; Thornton et al. 2009), four trials on preeclampsia/eclampsia (Wolff et al. 2008; Asbee et al. 2009; Thornton et al. 2009; Luoto et al. 2010), and two trials combining pregnancy-induced hypertension and preeclampsia (Khoury et al. 2005; Vinter et al. 2011). Two RCTs studied the effect of food and fortified food products on pregnancy hypertensive disorders (n = 344 women) (Smuts et al. 2003a,b). Meta-analysis demonstrated no effect of dietary intervention components or all dietary interventions combined on pregnancy hypertensive disorders, with no evidence of heterogeneity or bias.

Maternal BP

Three RCTs studied the effect of dietary counselling on maternal BP (systolic and diastolic) (n = 432 women) (Chan et al. 2006; Wolff et al. 2008; Vinter et al. 2011). Meta-analysis demonstrated significant effects for a reduction in both systolic (SMD −0.26, 95% CI −0.45 to −0.07; P < 0.001; I2 = 0%) (Fig. 2) and diastolic BP (SMD −0.57, 95% CI −0.75 to −0.38; P < 0.001; I2 = 0%) for dietary counselling (Fig. 3). Using RMD, this roughly translates to a mean change in systolic and diastolic BP of −0.66 mmHg and −2.76 mmHg, respectively, although, this could vary by population. Meta-analysis demonstrated an effect for all dietary interventions combined on diastolic BP, with very high heterogeneity (I2 = 80%), and no evidence of bias. The four trials contributing to this analysis all commenced in the second trimester. Therefore, any effect from earlier or later intervention during pregnancy could not be determined.

figure

Figure 2. Standardised mean difference (SMD) for systolic blood pressure and dietary counselling in pregnancy. The overall effect size was estimated by SMD. The black dot represents the point estimate, and square size the weight of each study in the meta-analysis and the horizontal lines represent the 95% confidence interval (CI). The vertical solid line represents the line of no effect. The diamond represents the overall pooled estimate effect of dietary counselling on systolic blood pressure.

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figure

Figure 3. Standardised mean difference (SMD) for diastolic blood pressure and dietary counselling in pregnancy. The overall effect size was estimated by SMD. The black dot represents the point estimate, and square size the weight of each study in the meta-analysis and the horizontal lines represent the 95% confidence interval (CI). The vertical solid line represents the line of no effect. The diamond represents the overall pooled estimate effect of dietary counselling on diastolic blood pressure.

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GDM

Six RCTs studied the effect of dietary counselling on GDM (n = 1206 women) (Wolff et al. 2008; Asbee et al. 2009; Thornton et al. 2009; Luoto et al. 2010; Quinlivan et al. 2011; Vinter et al. 2011). Three RCTs studied the effect of food and fortified food products on GDM (n = 423 women) (Smuts et al. 2003a,b; de Groot et al. 2004). Meta-analysis demonstrated no effect of dietary intervention components or all dietary interventions combined on GDM. The data showed heterogeneity (I2 = 52%), with no presence of bias.

Caesarean section

Six RCTs studied the effect of dietary counselling on caesarean section (n = 1347 women) (Knuist et al. 1998; Bonomo et al. 2005; Wolff et al. 2008; Asbee et al. 2009; Thornton et al. 2009; Vinter et al. 2011). Three RCTs studied the effect of food and fortified food products on caesarean section (n = 402 women) (Smuts et al. 2003a,b; de Groot et al. 2004). Meta-analysis demonstrated no effect of dietary intervention components or all dietary interventions combined on caesarean section, with no evidence of heterogeneity or bias.

Length of gestation

Twelve RCTs studied the effect of dietary counselling on length of gestation (n = 3103 women) (Kafatos et al. 1989; Van Buul et al. 1997; Knuist et al. 1998; Bonomo et al. 2005; Khoury et al. 2005; Chan et al. 2006; O'Connor & Whaley 2007; Wolff et al. 2008; Asbee et al. 2009; Thornton et al. 2009; Luoto et al. 2010; Vinter et al. 2011). Nine RCTs studied the effect of food and fortified food products on length of gestation (n = 3307 women) (Mora et al. 1979; Metcoff et al. 1985; Ross et al. 1985; Mardones-Santander et al. 1988; Smuts et al. 2003a,b; de Groot et al. 2004; Bech et al. 2007; Courville et al. 2011), with seven of these trials meta-analysed (n = 2294). There were no effects of dietary intervention components or all dietary interventions combined on length of gestation. The data showed heterogeneity (I2 = 61%), with no evidence of bias.

Fourteen RCTs (n = 4728) studied the effect of dietary intervention on preterm delivery (Mora et al. 1978; Rush et al. 1980; McDonald et al. 1981; Kafatos et al. 1989; Van Buul et al. 1997; Briley et al. 2002; Smuts et al. 2003a,b; de Groot et al. 2004; Khoury et al. 2005; Bech et al. 2007; Thornton et al. 2009; Quinlivan et al. 2011; Vinter et al. 2011). Seven RCTs studied the effect of dietary counselling on preterm delivery (n = 1759 women) (Kafatos et al. 1989; Van Buul et al. 1997; Briley et al. 2002; Khoury et al. 2005; Thornton et al. 2009; Quinlivan et al. 2011; Vinter et al. 2011): the other seven trials provided food and fortified food products (n = 2969) (Mora et al. 1978; Rush et al. 1980; McDonald et al. 1981; Smuts et al. 2003a,b; de Groot et al. 2004; Bech et al. 2007). Meta-analysis demonstrated no effect of dietary intervention components or all dietary interventions combined, with no evidence of heterogeneity or bias.

One RCT studied the effect of dietary counselling on post-term delivery (n = 232 women) (Thornton et al. 2009). Two RCTs studied the effect of food and fortified food products on post-term delivery (n = 625 women) (Mora et al. 1978; McDonald et al. 1981). Meta-analysis found no effect of dietary intervention components or all dietary interventions combined on post-term delivery, with no evidence of heterogeneity or bias.

Sub-analysis: trimester when the intervention commenced, nutrient of interest, BMI and country income

There were very few effects of diet on pregnancy outcome by trimester when the intervention commenced, nutrient of interest, BMI and country income subgroupings (Table 3). This was largely due to the small number of outcomes where three or more trials contributed data for each group. The trials for trimester when the intervention commenced on diastolic BP, and high-income country on hypertensive disorders, systolic and diastolic BP, GDM and caesarean section did not differ from the results presented in Table 2, therefore have not been repeated.

Table 3. Subgroup analyses for pregnancy outcomes in evaluation of dietary intervention during pregnancy*
 Number of trialsSMD (95% CI)RMDP-value
  1. BMI, body mass index; BP, blood pressure; CI, confidence interval; RMD, raw mean difference; SMD, standardised mean difference. *The main measure of effect was SMD. Meta-analysis focused on outcomes with three or more trials contributing data to pooled results. There were no studies for subgroup analyses for trimester commencement: one on systolic BP and diastolic BP, and three on hypertensive disorders, systolic BP, diastolic BP and gestational diabetes; or nutrient of interest: micronutrients on gestational diabetes and post-term delivery; BMI: underweight/nutritional risk on hypertensive disorders, systolic BP, diastolic BP and caesarean section; or country income: low on hypertensive disorders, systolic BP, diastolic BP, gestational diabetes and caesarean section. The secondary measure of effect was RMD. Categorical outcomes are reported as odds ratios. Micronutrient of interest is sodium. §All weight categories included those trials not restricting BMI within the target population. Micronutrient of interest is calcium. **The trials by Metcoff et al. (1985) and Mora et al. (1979) were not included in the meta-analysed outcome: length of gestation, as authors did not present results.

Hypertensive disorders    
Trimester when the intervention commenced    
One1−0.16 (−1.70 to 1.39)0.760.84
Two9−0.13 (−0.30 to 0.04)0.840.13
Nutrient of interest    
Macronutrients9−0.16 (−0.34 to 0.02)0.800.08
Micronutrient10.04 (−0.37 to 0.45)1.050.86
BMI    
Overweight and obese3−0.30 (−0.63 to 0.02)0.690.07
All weight categories§7−0.03 (−0.25 to 0.18)0.960.76
Systolic BP (mmHg)    
Nutrient of interest    
Macronutrients3−0.05 (−0.45 to 0.35)−0.280.81
Micronutrient§1−0.39 (−0.87 to 0.10)−3.510.12
BMI    
Overweight and obese2−0.24 (−0.44 to −0.03)−0.510.02
All weight categories2−0.01 (−0.07 to 0.68)−0.430.98
Diastolic BP (mmHg)    
Nutrient of interest    
Macronutrients3−0.38 (−0.88 to 0.12)−1.430.13
Micronutrient1−0.48 (−0.96 to 0.00)−3.500.05
BMI    
Overweight and obese2−0.58 (−0.78 to −0.38)−2.69<0.001
All weight categories2−0.15 (−0.72 to 0.41)−0.920.60
Gestational diabetes    
Trimester when the intervention commenced    
One1−0.77 (−2.57 to 1.02)0.260.40
Two9−0.10 (−0.43 to 0.23)0.830.55
Nutrient of interest    
Macronutrients10−0.12 (−0.44 to 0.20)0.820.47
BMI    
Overweight and obese4−0.42 (−0.91 to 0.06)0.570.09
All weight categories60.22 (−0.00 to 0.43)1.110.05
Length of gestation (weeks)**    
Trimester when the intervention commenced    
One20.11 (−1.31 to 1.53)−0.060.88
Two170.06 (−0.05 to 0.17)0.140.30
Three1−1.44 (−1.64 to −1.23)−0.20<0.001
Nutrient of interest    
Macronutrients150.01 (−0.10 to 0.13)0.030.83
Micronutrients50.11 (−0.08 to 0.31)0.310.27
BMI    
Underweight/nutritional risk20.00 (‒0.21 to 0.21)0.001.00
Overweight and obese30.02 (−0.14 to 0.18)0.000.83
All weight categories150.05 (−0.07 to 0.18)0.130.41
Country income    
Low20.00 (−0.21 to 0.21)0.001.00
High180.05 (−0.06 to 0.15)0.110.40
Preterm delivery    
Trimester when the intervention commenced    
One1−0.44 (−1.22 to 0.34)0.490.27
Two13−0.13 (−0.30 to 0.05)0.840.17
Three1−0.08 (−0.41 to 0.26)0.890.66
Nutrient of interest    
Macronutrients13−0.19 (−0.34 to −0.04)0.790.01
Micronutrients20.10 (−0.16 to 0.37)1.180.44
BMI    
Underweight/nutritional risk3−0.15 (−0.32 to 0.01)0.830.07
Overweight and obese3−0.04 (−0.48 to 0.41)0.940.88
All weight categories9−0.16 (−0.46 to 0.14)0.800.32
Country income    
Low2−0.13 (−0.44 to 0.17)0.830.40
High13−0.13 (−0.30 to 0.05)0.820.17
Post-term delivery    
Trimester when the intervention commenced    
One10.20 (−0.52 to 0.91)1.380.59
Two2−0.07 (−0.48 to 0.34)0.910.73
Three1−0.36 (−0.76 to 0.04)0.570.08
Nutrient of interest    
Macronutrients4−0.16 (−0.42 to 0.11)0.790.24
BMI    
Underweight/nutritional risk2−0.16 (−0.68 to 0.36)0.760.54
Overweight and obese1−0.04 (−0.46 to 0.38)0.950.85
All weight categories1−0.62 (−2.40 to 1.16)0.330.50
Country income    
Low2−0.16 (−0.68 to 0.36)0.760.54
High2−0.07 (−0.48 to 0.34)0.910.73
Caesarean section    
Trimester when the intervention commenced    
One1−0.48 (−1.03 to 0.08)0.560.09
Two8−0.02 (−0.16 to 0.13)0.990.84
Three10.04 (−0.24 to 0.31)1.040.80
Nutrient of interest    
Macronutrients9−0.00 (−0.14 to 0.13)1.000.96
Micronutrients1−0.18 (−0.52 to 0.15)0.770.28
BMI    
Overweight and obese30.10 (−0.11 to 0.31)1.050.36
All weight categories7−0.10 (−0.26 to 0.06)0.890.41

Trials altering the macronutrient composition of dietary interventions demonstrated a reduction in the incidence of preterm delivery (P = 0.01). Using RMD, this translates to a 21% reduction (0.79 odds ratio) in the incidence of preterm birth.

Discussion

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Acknowledgements
  9. Source of funding
  10. Conflict of interest
  11. Contributions
  12. References
  13. Supporting Information

Summary of main findings

To develop appropriate dietary guidelines for pregnancy we need to understand the effects of diet and dietary modification on a range of pregnancy outcomes. This systematic review summarises the best available evidence of dietary intervention during pregnancy on pregnancy outcomes. Results indicate that dietary interventions during pregnancy, particularly dietary counselling, slightly reduce BP (0.66 mmHg systolic and 2.76 mmHg diastolic), but not hypertensive disorders. Dietary interventions focusing on macronutrient intake reduce the incidence of preterm delivery (21% decrease in the odds), while interventions commencing in the second trimester reduce diastolic BP (0.45 mmHg). No other significant effects were observed for the other pregnancy outcomes.

Interpretation

The effect on BP was not consistent across trial populations. There were variations in the types of dietary intervention and the effect of specific nutrient components. There was no heterogeneity for dietary intervention components, but considerate heterogeneity for all dietary interventions combined. Dietary counselling interventions shown to lower BP varied in frequency from one to 10 sessions. Target populations ranged from adolescent girls (Chan et al. 2006) to obese women (Wolff et al. 2008; Vinter et al. 2011), limiting the generalisability of the findings to a broader group of women of child-bearing age. Those interventions shown to be effective in reducing BP included a balanced diet complying with National recommendations (Vinter et al. 2011), energy intake individualised for the needs of the mother (Wolff et al. 2008) and modifying calcium intake (Chan et al. 2006). Identifying specific components of successful interventions can assist in understanding how the intervention exerts its effect (Michie et al. 2011). Calcium has been studied in large supplemental trials (Palacios & Pena-Rosas 2011), demonstrating a reduction in the risk of hypertensive disorders during pregnancy, particularly for women at high-risk or with low calcium intakes (Hofmeyr et al. 2010; Palacios & Pena-Rosas 2011; Imdad & Bhutta 2012). Our review identified no effect of dietary intervention on hypertensive disorders. However, the pooled trials involved whole diet recommendations, or the modification of fat intake, and there were no trials on hypertensive disorders specifically targeting calcium intake.

Like the results in our review, calcium intake has been shown to lower BP among pregnant women (Carroli et al. 1994; Van Mierlo et al. 2006; Hofmeyr et al. 2010; Palacios & Pena-Rosas 2011), and the effects appear stronger in women with low calcium intakes prior to intervention (Carroli et al. 1994; Van Mierlo et al. 2006; Hofmeyr et al. 2010; Palacios & Pena-Rosas 2011). Calcium intakes were not analysed for each included study as part of this review. The effect of low calcium during pregnancy is thought to exert its effect via an increase in parathyroid hormone secretion, which increases intracellular calcium, smooth muscle contractibility and/or releases renin from the kidney, leading to vasoconstriction and retention of sodium (Hacker et al. 2012). These physiological changes (from low calcium intakes during pregnancy) increase BP and potentially contribute to the development of hypertensive disorders (Hacker et al. 2012). Women beginning pregnancy with adequate intakes of at least 1000 mg calcium per day may not need additional amounts, while those with suboptimal intakes (<500 mg per day) may benefit from intervention (Hacker et al. 2012).

Our review also found that women consuming a balanced diet, including enough energy based on their individual requirements, had lower BP, paralleling current lifestyle recommendations for individuals with high BP (National Institutes of Health 2003). The effect size of 1–3 mmHg was very small compared with using antihypertensive agents (Patel et al. 2012). However, the effect was evident in normotensive rather than hypertensive women. Furthermore, treatment with antihypertensive drugs during pregnancy carries known and unknown risks to the fetus, because these drugs cross the placenta (e.g. nifedapine is Category C) (Department of Health, 2014). Therefore, any reductions in BP gained from dietary intervention offers clear advantages when BP is of clinical concern.

Macronutrient interventions demonstrating a reduction in the incidence of preterm delivery varied in frequency and included supplemental beverages (Rush et al. 1980; McDonald et al. 1981), dietary counselling on the nutritional needs during pregnancy (Kafatos et al. 1989; Briley et al. 2002; Quinlivan et al. 2011), limiting cholesterol and reducing saturated fat (Khoury et al. 2005), GDM-specific dietary recommendations (Thornton et al. 2009), providing DHA-fortified eggs (Smuts et al. 2003a,b), and a range of energy- and protein-based foods (Mora et al. 1978). Observational studies (Kramer 1987; Institute of Medicine 1990; Rush 2001) have reported that energy intake may be strongly and positively associated with a reduced risk of preterm birth. Our review confirms these findings, demonstrating a reduction in the incidence of preterm birth with macronutrient or whole diet intervention.

The pooled studies on preterm delivery showed little evidence of heterogeneity, with a narrow spread of data and overlapping CIs. Six of the macronutrient dietary interventions were conducted in low-income populations (Mora et al. 1978; Rush et al. 1980; McDonald et al. 1981; Kafatos et al. 1989; Briley et al. 2002; Quinlivan et al. 2011). Four interventions contained small sample sizes of less than 125 pregnant women (Briley et al. 2002; Smuts et al. 2003a; de Groot et al. 2004; Quinlivan et al. 2011) meaning these trials were individually underpowered. Of the 13 RCTs contributing data, only two trials (Kafatos et al. 1989; Khoury et al. 2005) demonstrated statistically significant effects in their respective publications. Based on the pooled dietary interventions, there were particular nutrients impacting on the result rather than the type of intervention. Modifying fat intake, particularly long-chain polyunsaturated fatty acids (LC-PUFA) were shown to reduce the incidence of preterm delivery (Smuts et al. 2003a,b; Khoury et al. 2005). Paralleling these findings, Horvath et al. (2007), Szajewska et al. (2006) and a recent Cochrane Review (Makrides et al. 2012) concluded that women allocated to LC-PUFA supplementation had longer gestation than women receiving placebo or no treatment, which remained true for both low- and high-risk pregnancies. Observational studies, mainly in populations with high consumption of seafood, have also suggested that marine LC-PUFA intake during pregnancy promotes longer gestation (Olsen et al. 1986, 1990, 1993). DHA and arachidonic acid are essential nutrients that are supplied during pregnancy to the fetus by preferential placental transfer (Al et al. 1995; Otto et al. 1997; Berghaus et al. 2000; Larquè et al. 2003). The mechanism behind their role in increasing gestational length may be an imbalance between DHA and arachidonic acid, which is associated with disturbances in the production of prostacyclin and thromboxane involved in the initiation of labour (Herrera 2002). Therefore, adequate dietary intake or supplementation of LC-PUFA may prolong gestational length, and in turn, decrease the risk of preterm delivery (Horvath et al. 2007).

The conversion of each publication's results to SMD for statistical inference effectively creates a common scale that would otherwise not be possible because of the differences in variance between publications. The SMD express differences as units of standard deviations, and thus cannot be used to interpret absolute or relative differences in clinically meaningful outcomes (e.g. for BP, the absolute reduction in mmHg). Therefore, we have also provided the RMD to give some indication of effect size in the standard units for each outcome, including odds ratios for outcomes like pre- and post-term delivery.

Implications for practice and research

Dietary intervention during pregnancy slightly reduces maternal BP and the incidence of preterm delivery. No strong evidence was found for any effect of dietary intervention during pregnancy on the other outcomes. To develop appropriate dietary guidelines for pregnancy, we need to understand the role of everyday diet on pregnancy. This review advances our understanding of the role of nutrition for a healthy pregnancy by observing small reductions in BP and slight increases in the length of gestation. Further research, with larger sample sizes and robust methodology is required to better understand. Quantifying dietary intakes before, during and after an intervention would provide an important measure of compliance with the dietary intervention regime, which was lacking from most of the included trials (n = 14).

Limitations

This systematic review is broader in scope when compared with other published systematic reviews and meta-analyses (Dodd et al. 2010; Streuling et al. 2010; Tanentsapf et al. 2011; Oteng-Ntim et al. 2012; Thangaratinam et al. 2012), and the quality of the included studies was mostly positive. Gestational weight gain was not included as an outcome in this review, as others have focused on this (Dodd et al. 2010; Streuling et al. 2010; Tanentsapf et al. 2011; Oteng-Ntim et al. 2012; Thangaratinam et al. 2012). Despite the broad scope of this review, very few trials contributed data to each pregnancy outcome, with the exception of length of gestation (n = 12). For this reason, some of the outcomes were not reported and others are underpowered, particularly with the subgroup analysis. Dietary intervention trials should measure and report on a range of pregnancy outcomes so the effects of diet on pregnancy outcomes can be determined. There was heterogeneity for BP, GDM and length of gestation only, which was not explained by subgroup analyses, but may be due to the varying intensity and duration of included trials.

Conclusion

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Acknowledgements
  9. Source of funding
  10. Conflict of interest
  11. Contributions
  12. References
  13. Supporting Information

There is evidence that dietary intervention during pregnancy can reduce maternal BP and the incidence of preterm delivery. Interventions focusing on national recommendations and modifying calcium, saturated fat and cholesterol are the most promising dietary interventions to reduce BP and the incidence of preterm delivery. Further large high-quality RCTs investigating combination dietary intervention and micronutrient provision from food are needed. Future trials beginning in preconception and spanning for the duration of pregnancy, as well as between pregnancies are needed to advance our understanding of optimal nutrition for maternal–child health.

Acknowledgements

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Acknowledgements
  9. Source of funding
  10. Conflict of interest
  11. Contributions
  12. References
  13. Supporting Information

The authors thank Research Librarian Debbie Booth for her assistance with the database searches; Accredited Practising Dietitians Samantha Diamond and Jun Lai for their assistance with assessing methodological quality and data extraction.

Source of funding

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Acknowledgements
  9. Source of funding
  10. Conflict of interest
  11. Contributions
  12. References
  13. Supporting Information

EG is funded by an Australian Postgraduate Award (PhD scholarship) provided by the University of Newcastle, New South Wales.

Contributions

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Acknowledgements
  9. Source of funding
  10. Conflict of interest
  11. Contributions
  12. References
  13. Supporting Information

EG, AB, JEB, AJH designed research; EG and AJH conducted research; EG and AB analysed data; EG wrote the paper and had primary responsibility for final content. All authors read and approved the final paper.

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  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Acknowledgements
  9. Source of funding
  10. Conflict of interest
  11. Contributions
  12. References
  13. Supporting Information
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Supporting Information

  1. Top of page
  2. Abstract
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Acknowledgements
  9. Source of funding
  10. Conflict of interest
  11. Contributions
  12. References
  13. Supporting Information
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Table S1. Characteristics of included studies in a systematic review of dietary interventions during pregnancy on pregnancy outcomes

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