Diet or exercise, or both, for preventing excessive weight gain in pregnancy
Abstract
Background
This is an update of a Cochrane review first published in 2012, Issue 4. Excessive weight gain during pregnancy is associated with poor maternal and neonatal outcomes including gestational diabetes, hypertension, caesarean section, macrosomia, and stillbirth. Diet or exercise interventions, or both, may reduce excessive gestational weight gain (GWG) and associated poor outcomes; however, evidence from the original review was inconclusive.
Objectives
To evaluate the effectiveness of diet or exercise, or both, interventions for preventing excessive weight gain during pregnancy and associated pregnancy complications.
Search methods
We searched the Cochrane Pregnancy and Childbirth Group's Trials Register (5 November 2014), contacted investigators of the previously identified ongoing studies and scanned reference lists of retrieved studies.
Selection criteria
Randomised controlled trials (RCTs) of diet or exercise, or both, interventions for preventing excessive weight gain in pregnancy.
Data collection and analysis
Two review authors independently assessed trials for inclusion and risk of bias, extracted data and checked them for accuracy. We organised RCTs according to the type of interventions and pooled data using the random‐effects model in the Review Manager software. We also performed subgroup analyses according to the initial risk of adverse effects related to poor weight control. We performed sensitivity analysis to assess the robustness of the findings.
Main results
We included 65 RCTs, out of which 49 RCTs involving 11,444 women contributed data to quantitative meta‐analysis. Twenty studies were at moderate‐to‐high risk of bias. Study interventions involved mainly diet only, exercise only, and combined diet and exercise interventions, usually compared with standard care. Study methods varied widely; therefore, we estimated the average effect across studies and performed sensitivity analysis, where appropriate, by excluding outliers and studies at high risk of bias.
Diet or exercise, or both, interventions reduced the risk of excessive GWG on average by 20% overall (average risk ratio (RR) 0.80, 95% confidence interval (CI) 0.73 to 0.87; participants = 7096; studies = 24; I² = 52%). This estimate was robust to sensitivity analysis, which reduced heterogeneity, therefore we graded this evidence as high‐quality. Interventions involving low glycaemic load diets, supervised or unsupervised exercise only, or diet and exercise combined all led to similar reductions in the number of women gaining excessive weight in pregnancy.
Women receiving diet or exercise, or both interventions were more likely to experience low GWG than those in control groups (average RR 1.14, 95% CI 1.02 to 1.27; participants = 4422; studies = 11; I² = 3%; moderate‐quality evidence). We found no difference between intervention and control groups with regard to pre‐eclampsia (RR 0.95, 95% CI 0.77 to 1.16; participants = 5330; studies = 15; I² = 0%; high‐quality evidence); however, maternal hypertension (not a pre‐specified outcome) was reduced in the intervention group compared with the control group overall (average RR 0.70, 95% CI 0.51 to 0.96; participants = 5162; studies = 11; I² = 43%; low‐quality evidence).
There was no clear difference between groups with regard to caesarean delivery overall (RR 0.95, 95% CI 0.88 to 1.03; participants = 7534; studies = 28; I² = 9%; high‐quality evidence); although the effect estimate suggested a small difference (5%) in favour of the interventions. In addition, for combined diet and exercise counselling interventions there was a 13% (‐1% to 25%) reduction in this outcome (borderline statistical significance).
We found no difference between groups with regard to preterm birth overall (average RR 0.91, 95% CI 0.68 to 1.22; participants = 5923; studies = 16; I² = 16%; moderate‐quality evidence); however limited evidence suggested that these effect estimates may differ according to the types of interventions, with a trend towards an increased risk for exercise‐only interventions.
We found no clear difference between intervention and control groups with regard to infant macrosomia (average RR 0.93, 95% CI 0.86 to 1.02; participants = 8598; studies = 27; I² = 0%; high‐quality evidence), although the effect estimate suggested a small difference (7% reduction) in favour of the intervention group. The largest effect size occurred in the supervised exercise‐only intervention group (RR 0.81, 95% CI 0.64 to 1.02; participants = 2445; studies = 7; I² = 0%), which approached statistical significance (P = 0.07). Furthermore, in subgroup analysis by risk, high‐risk women (overweight or obese women, or women with or at risk of gestational diabetes) receiving combined diet and exercise counselling interventions experienced a 15% reduced risk of infant macrosomia (average RR 0.85, 95% CI 0.73 to 1.00; participants = 3252; studies = nine; I² = 0; P = 0.05; moderate‐quality evidence)
There were no differences in the risk of poor neonatal outcomes including shoulder dystocia, neonatal hypoglycaemia, hyperbilirubinaemia, or birth trauma (all moderate‐quality evidence) between intervention and control groups; however, infants of high‐risk women had a reduced risk of respiratory distress syndrome if their mothers were in the intervention group (RR 0.47, 95% CI 0.26 to 0.85; participants = 2256; studies = two; I² = 0%; moderate‐quality evidence).
Authors' conclusions
High‐quality evidence indicates that diet or exercise, or both, during pregnancy can reduce the risk of excessive GWG. Other benefits may include a lower risk of caesarean delivery, macrosomia, and neonatal respiratory morbidity, particularly for high‐risk women receiving combined diet and exercise interventions. Maternal hypertension may also be reduced. Exercise appears to be an important part of controlling weight gain in pregnancy and more research is needed to establish safe guidelines. Most included studies were carried out in developed countries and it is not clear whether these results are widely applicable to lower income settings.
PICOs
Plain language summary
Diet and exercise interventions for preventing excessive weight gain during pregnancy
The issue
A large proportion of women gain more weight than is recommended during pregnancy. Excessive weight gain in pregnancy is associated with complications such as diabetes, high blood pressure, caesarean section, and large babies. This review aimed to determine whether diet or exercise measures,or both, could prevent excessive gestational weight gain (GWG), and if they were safe.
How we conducted the review
This is an update of a review first published in 2012 and is current to November 2014 and included randomised controlled trials (RCTs) only in the updated review. We grouped studies according to the types of interventions, and according to the types of participants, i.e. normal weight women (the low‐risk group), all pregnant women (the mixed‐risk group), and overweight or obese women, or women with or at risk of gestational diabetes (the high‐risk group).
Findings
We included 65 randomised controlled trials, of which 49 trials involving 11,444 women contributed data. Twenty studies were at a moderate‐to high‐risk of bias. The diets tested were low sugar (low glycaemic load), diabetic, low‐calorie or low‐fat diets, with or without food diaries and regular weighing. The exercise interventions were most often of moderate intensity and involving regular walking, dance or aerobic classes. The comparison or control group generally received standard care. Overall, weight management interventions led to a reduction in the number of women gaining excess weight by a fifth (20%; range 13% to 27%) over the pregnancy. We considered this evidence to be high‐quality.
Overall, we found no clear benefits of all diet or exercise interventions, or both, on other outcomes including pre‐eclampsia, caesarean section, preterm birth, and having a baby weighing more than 4 kg (macrosomia), although we could not rule out a small effect on caesarean section (5% reduction) and macrosomia (7% reduction), particularly for women receiving combined diet and exercise counselling interventions. There was a tendency for supervised exercise‐only interventions to reduce macrosomia too. Maternal hypertension (high blood pressure) was also reduced with the interventions. We found no clear differences between study groups with regard to most infant complications, except that for high‐risk women the babies born to the women in the intervention group were less likely to experience breathing difficulties (respiratory distress syndrome) than babies in the control group. This evidence was mostly of a moderate quality.
The studies had differences in the types of interventions, types of participants (for example in terms of body mass index (BMI), number of previous pregnancies and age), delivery of the intervention (whether the intervention was incorporated into antenatal visits or delivered separately by a dietician), timing of the measurements, timing of commencement of the intervention (first, second or third trimester), the intensity of the intervention, and how it was monitored or supervised. Most included studies were carried out in developed countries and it is not clear whether these results are widely applicable to lower income settings.
Conclusions
We found high‐quality evidence that diet or exercise interventions, or both, help to reduce excessive weight gain in pregnancy. They may also reduce caesarean deliveries, especially with combined diet and exercise interventions, and maternal hypertension. In addition, the chances of having a baby over 4 kg and the chances of the newborn having breathing difficulties after birth may be reduced, especially in overweight and obese women. Moderate‐intensity exercise appears to be an important part of weight‐control strategies in pregnancy; however, more research is needed on side‐effects to inform safe guidelines.
Authors' conclusions
Summary of findings
| All diet and/or exercise interventions compared to standard/other care for preventing excessive weight gain in pregnancy | ||||||
| Patient or population: pregnant women | ||||||
| Outcomes | Illustrative comparative risks* (95% CI) | Relative effect | No of Participants | Quality of the evidence | Comments | |
| Assumed risk | Corresponding risk | |||||
| Standard/other care | All diet and/or exercise interventions | |||||
| Excessive weight gain | Study population | RR 0.80 | 7096 | ⊕⊕⊕⊕ | ||
| 453 per 1000 | 362 per 1000 | |||||
| Mean GWG (kg) | Mean difference not estimated | Due to substantial heterogeneity among studies, we did not consider the pooled estimate to be meaningful. Limited subgroup analyses suggested that effect estimates might differ according to risk group. | ||||
| Low weight gain | Study population | RR 1.14 | 4422 | ⊕⊕⊕⊝ MODERATE2 | ||
| 227 per 1000 | 259 per 1000 | |||||
| Preterm birth | Study population | RR 0.91 | 5923 | ⊕⊕⊕⊝ | ||
| 57 per 1000 | 52 per 1000 | |||||
| Pre‐eclampsia | Study population | RR 0.95 | 5330 | ⊕⊕⊕⊕ | ||
| 66 per 1000 | 62 per 1000 | |||||
| Caesarean delivery | Study population | RR 0.95 | 7534 | ⊕⊕⊕⊕ | ||
| 288 per 1000 | 274 per 1000 | |||||
| Macrosomia Infant birthweight > 4000 g | Study population | RR 0.93 | 8598 | ⊕⊕⊕⊕ | ||
| 178 per 1000 | 166 per 1000 | |||||
| *The basis for the assumed risk was the median control group risk across studies. The corresponding risk (and its 95% confidence interval) is based on the assumed risk in the comparison group and the relative effect of the intervention (and its 95% CI). | ||||||
| GRADE Working Group grades of evidence | ||||||
| 1Although heterogeneity was moderate‐to‐high (I² = 52%), the RR was robust to sensitivity analysis, which was associated with less heterogeneity (I² ‐ 40%), therefore we did not downgrade this evidence 2Downgraded due to imprecision of results according to types of intervention (‐1) 3Downgraded due to risk of bias concerns and concerns that data could not be included in the analysis due to studies excluding women with or at risk of preterm birth post‐randomisation from analysis (Cordero 2014; Di Carlo 2014; Murtezani 2014; Rauh 2013). This omission might have led to publication bias in the review's 'preterm birth' outcome (‐1) | ||||||
| Intervention type | Risk group | EGWG | Mean GWG | Low GWG | Preterm birth | Caesarean | Pre‐eclampsia | Macrosomia |
| All interventions (max 36 studies) | Overall | 20% reduction (13 to 27%) | Not estimated | 14% increase (2% to 27%) | NS | NS | NS | BS (7% reduction, ‐2% to 14%) |
| Low GL diet (max 5 studies) | Overall | 23% reduction (9% to 33%) | Not estimated | NS | BS in favour of the intervention | NS | NA | NS |
| Low | 40% reduction (6% to 52%) | NS | NS | NS | NS | NA | NA | |
| Mixed | 21% reduction (1 study) | NS | NA | NS | NS | NA | NS | |
| High | NS | NS | NS | NS | NS | NA | NS | |
| Diet and exercise counselling (max 13 studies) | Overall | 14% reduction (2% to 25%) | Not estimated | NS | NS | BS (13% reduction; ‐1% to 25%) | NS | NS |
| Low | 28% reduction (5% to 45%) | NS | NS | NS | NS | NS | NS | |
| Mixed | NS | 1.80 kg reduction (0.24 to 3.36 kg) | NA | NS | BS (34% reduction; ‐5% to 59%) | NA | NS | |
| High | NS | 0.71 kg reduction (0.08 to 1.34) | NS | NS | BS (11% reduction; ‐4 to 24%) | NS | 15% reduction (0% to 27%) | |
| Exercise (supervised or unsupervised) only (max 10 studies) | Overall | 21% reduction (11% to 30%) | Not estimated | BS (19% increase; 0% to 41%) | NS | NS | NS | NS |
| Low | BS (31%; ‐2 to 53%) | 1.50 kg reduction (0,92 to 2.08 kg; one study only) | 29% increase; 6% to 42%) | BS (one study) | NS | NA | ||
| Mixed | 23% reduction (12% to 34%) | 1.35 kg reduction (0.89 to 1.80) | NS | NS | NS | NS | BS* (19% reduction; ‐2% to 36%) | |
| High | 16% reduction (5% to 27%) | NS | NS | NS | NS | NS | NS | |
| Unsupervised exercise only (max 3 studies) | Overall | 17% reduction (3% to 29%) | Not estimated | NS | NS | NS | NS | NS |
| Supervised exercise only (max 7 studies) | Overall | 25% reduction (11% to 37%) | Not estimated | BS (21% increase; ‐1% to 52%) | NS (trend in favour of control) | NS | NS | BS (19% reduction;‐2% to 36%) |
| Diet and supervised exercise (max 5 studies) | Overall | 29% reduction (15% to 41%) | NS | NS | NA | NS | NS | NS |
| Low | NS | 3.33 kg reduction (1,21 to 5.45; one study only) | NA | NA | Not estimable | NA | NA | |
| Mixed | 36% reduction (16% to 52%) | 1.69 kg reduction (0.11 to 3.48) | NS | NA | NS | NA | NS | |
| High | NS | NS | NA | NA | NS | NA | NS | |
| Diet counselling/other (max 7 studies) | Overall | NS | Not estimated | NS | NS | NS | NS | NS |
| Mixed | NS | NA | NA | NS | NS | NS | NA | |
| High | NS | NA | NA | NS | NS | NS | NS | |
| Finding are presented with reference to the intervention group * Sensitivity analysis suggested that there may be a statistically significant difference in favour of the intervention for the mixed‐risk subgroup. Abbreviations: NA = not available; NS = not statistically significant (P ≥ 0.05); BS = borderline significance | ||||||||
Background
Description of the condition
Pregnancy weight gain guidelines
In 2009, the Institute of Medicines (IOM) in the United States updated earlier guidelines on weight gain during pregnancy (Medicine 1990; Medicine 2009). The report set out specific ranges of weight gain for women with different prepregnancy weights: suggesting that underweight women (body mass index (BMI) less than 18.5 kg/m²) gain 28 lbs to 40 lbs (12.5 kg to 18 kg); normal weight women (BMI 18.5 kg/m² to 24.9 kg/m²) gain 25 lbs to 35 lbs (11.5 kg to 16 kg); whereas overweight women (BMI 25 kg/m² to 29.9 kg/m²) were advised to gain between 15 lbs and 25 lbs (7 kg to 11.5 kg) and obese women (BMI at least 30 kg/m²) to gain between 11 lbs and 20 lbs (5 kg to 9 kg) (Medicine 2009).
Previous guidelines from the IOM (Medicine 1990) had been widely adopted but not universally accepted. However, a review of relevant information confirmed that pregnancy weight gain within the IOM's recommended ranges was associated with the best outcomes for both mothers and infants, and that weight gain within the IOM's recommended ranges is not harmful for the mothers or for their infants (Abrams 2000).
No official recommendations or clinical guidelines for weight gain during pregnancy exist in the United Kingdom (UK) (Ford 2001). However, a report from the UK Centre for Maternal and Child Enquiries (CMACE 2010) suggested a more comprehensive guidance for the care of overweight and obese women, and recommended weighing women in the third trimester and again when women are admitted in labour. Guidelines in other countries have also recommended monitoring weight gain in pregnancy. In Sweden, it has been recommended that the optimal gestational weight gain for Swedish women is 4 kg to 10 kg for BMI less than 20, 2 kg to 10 kg for BMI 20 to 24.9; less than 9 kg for women with a BMI of 25 to 29.9, and less than 6 kg for women with a BMI of 30 or more (Cedergren 2007). Maternal weight gain recommendations based on data from high‐income countries may not be applicable to Asian women, who appear to have lower weight gains compared with women in Europe and North America (Abrams 1995; Siega‐Riz 1993). Weight gain limits for Chinese women, taking ethnic‐specific differences into account, have been recommended as 13 kg to 16.7 kg, 11 kg to 16.4 kg, and 7.1 kg to 14.4 kg respectively for women of low (BMI less than 19), moderate (BMI 19 to 23.5), and high (BMI greater than 23.5) BMI (Wong 2000).
Trends in pregnancy weight gain
Although the 1990 IOM guidelines have now been promoted for two decades it has been estimated that over this time only 30% to 40% of pregnant women in the United States gain gestational weight within the IOM recommended ranges (Abrams 2000; Cogswell 1999; Medicine 1990; Olson 2003). Furthermore, gestational weight gain above the guidelines is more common than gestational weight gain below (Stotland 2006). Several studies on gestational weight gain in the USA and Europe indicate that about 20% to 40% of women are gaining weight above the recommendations (Cedergren 2006; Medicine 2009; Olson 2003) and the prevalence of excessive gestational weight gain is increasing (Abrams 2000; Rhodes 2003; Schieve 1998). A retrospective cohort study undertaken to examine the trend in weight gain during pregnancy of 1,463,936 women over 16 years in North Carolina found that the proportion of women gaining excessive gestational weight (more than 18 kg) increased from 15.5% in 1988 to 19.5% in 2003; an additional 40 women per 1000 gained excessive weight by 2003 (Helms 2006). The recent IOM report summarised the situation in a number of countries; compared with two decades earlier "Women today are also heavier; a greater percentage of them are entering pregnancy overweight or obese, and many are gaining too much weight during pregnancy" (Medicine 2009).
Weight gain during pregnancy is generally inversely proportional to prepregnancy weight category. Although underweight women are least likely to exceed weight gain recommendations, obese women tend to gain less weight than normal and overweight women (Abrams 1989; Bianco 1998; Edwards 1996; Walling 2006). Two large population‐based studies, in Sweden and the United States, found that approximately 30% of average and overweight women had high‐gestational weight gain, compared with 20% of obese women (Cedergren 2006; Cogswell 1995).
Pregnancy weight gain and outcomes for mothers and infants
It is well known from large studies in a number of countries that excessive weight gain during pregnancy is associated with multiple maternal and neonatal complications. Retrospective cohort studies have examined the relationship between gestational weight gain and adverse neonatal outcomes among infants born at term. Gestational weight gain above the upper limit of the IOM guideline has been associated with a low five‐minute Apgar score, seizure, hypoglycaemia, polycythaemia, meconium aspiration syndrome and large‐for‐gestational age compared with women within weight gain guidelines (Hedderson 2006; Stotland 2006). For obese women, low‐gestational weight gain has been shown to decrease the risk of several undesirable outcomes including pre‐eclampsia, caesarean section, instrumental delivery, and large‐for‐gestational‐age births; whereas, excessive weight gain increased the risk for caesarean delivery in all maternal BMI classes (Cedergren 2006).
Findings from a national study in the UK revealed that compared with pregnant women in general, obese pregnant women were at increased risk of having a co‐morbidity diagnosed before or during pregnancy (in particular pregnancy‐induced hypertension and gestational diabetes), were at increased risk of having induction of labour and a caesarean birth, were more likely to have postpartum haemorrhage, and their babies were at increased risk of stillbirth, neonatal death, of being large‐for‐gestational age and more likely to be admitted for special care (CMACE 2010).
A number of studies have concluded that excessive gestational weight gain increases postpartum weight retention (Gunderson 2000; Keppel 1993; Polley 2002; Rooney 2002; Rossner 1997; Scholl 1995) and is related to a two‐ to three‐fold increase in the risk of becoming overweight after delivery (Gunderson 2000). Moreover, mothers who gained more weight during pregnancy have been shown to have children at higher risk of being overweight in early childhood (Oken 2007).
Description of the intervention
Pregnancy may be an optimal time to inform and challenge women to change their eating habits and physical activities, and thereby prevent excessive weight gain. Dietary control, exercise and eating behaviour modification are the main elements for controlling weight. Dietary interventions include low glycaemic, energy‐restricted, diabetic, healthy eating, low carbohydrate and other diets. Regular exercise is an important part of a healthy lifestyle and most guidelines support moderate‐intensity physical activity during pregnancy (Evenson 2014).
How the intervention might work
Diet and exercise interventions are recommended components of weight control programs in the general population. Diet interventions work mainly by limiting energy intake, whereas exercise interventions work by using energy. If one utilises more energy than one takes in, one creates an energy deficit, which facilitates the use of stored energy.
Why it is important to do this review
Pregnancy results in dramatic physiological changes, with weight gain occurring as part of the normal pregnancy process. This normal occurrence and expectation of weight gain in pregnancy can make it difficult for a woman of any prepregnancy weight to maintain her weight within recommended limits. Thus, pregnancy is a time when women especially need clear guidance on how best to maintain a healthy weight, in a way that will be safe for both mother and baby. Given the increasing prevalence and negative consequences of excessive gestational weight gain, preventing excessive weight gain during pregnancy is becoming increasingly important. The previous version of this review found weak evidence to support diet and exercise interventions to reduce gestational weight gain; however, findings were inconsistent and interventions heterogeneous. Despite this and another systematic review that included randomised and non‐randomised studies (Thangaratinam 2012), it remains unclear which types of interventions will yield the best outcomes for mothers and their infants, and whether interventions work equally for all risk groups. Pregnancy offers an ideal opportunity to support women towards a healthier lifestyle; however, strategies for reducing weight gain in the non‐pregnant population may not be suitable for use in pregnancy. The aim of this review was to determine whether diet or exercise interventions, or both, for preventing excessive weight gain are effective and safe in pregnancy and to stimulate further research in this field.
Objectives
To evaluate the effectiveness and safety of diet or exercise, or both, interventions for preventing excessive weight gain during pregnancy.
Methods
Criteria for considering studies for this review
Types of studies
Randomised controlled trials (RCTs) and cluster‐RCTs. Quasi‐RCTs were not eligible.
Types of participants
Pregnant women of any BMI. We considered studies recruiting women with normal BMIs to have a 'low risk' of weight‐related complications at baseline, those recruiting women from the general population including women of any BMI to have a 'mixed‐risk' status, and studies of overweight and/or obese women, or high‐risk women, as defined by the investigators, to have a 'high‐risk' status.
Types of interventions
Any diet or exercise, or both, intervention (e.g. healthy eating plan, low glycaemic diet, exercise intervention, health education, lifestyle counselling) compared with standard or routine care for preventing excessive weight gain in pregnancy. We organised our main comparison into different intervention types, as follows:
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diet counselling only versus routine care;
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diet and exercise counselling versus routine care;
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diet interventions (e.g. low glycaemic diet) versus routine care;
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exercise (supervised or unsupervised) interventions only versus routine care;
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diet and supervised exercise interventions versus routine care.
We defined diet as a special selection of food, or energy intake, to which a participant was restricted. Exercise interventions included any activity requiring physical effort, carried out to sustain or improve health and fitness.
Types of outcome measures
Primary outcomes
Excessive weight gain as defined by investigators.
Secondary outcomes
For the mothers
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Weight gain.
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Low weight gain as defined by investigators.
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Preterm birth.
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Preterm prelabour rupture of membranes.
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Pre‐eclampsia/eclampsia.
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Hypertension (not prespecified).
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Induction of labour.
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Caesarean delivery.
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Postpartum complication including postpartum haemorrhage, wound infection, endometritis, need for antibiotics, perineal trauma, thromboembolic disease, maternal death.
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Behaviour modification outcomes: diet, physical activity.
For the newborns
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Birthweight (not prespecified).
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Birthweight greater than 4000 g or greater than the 90th centile for gestational age and infant sex (macrosomia).
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Birthweight less than 2500 g or less than the 10th centile for gestational age and infant sex.
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Complication related to macrosomia including hypoglycaemia, hyperbilirubinaemia, infant birth trauma (palsy, fracture, shoulder dystocia), respiratory distress syndrome.
Long‐term health outcomes
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Maternal weight retention postpartum.
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Childhood weight.
Gestational diabetes, an important outcome of many interventions aimed at preventing excessive weight gain in pregnancy, is the primary outcome of separate Cochrane reviews (Crane 2013; Han 2012; Tieu 2008) and is therefore not included in this review.
Search methods for identification of studies
The following methods section of this review is based on a standard template used by the Cochrane Pregnancy and Childbirth Group.
Electronic searches
We searched the Cochrane Pregnancy and Childbirth Group’s Trials Register by contacting the Trials Search Co‐ordinator (5 November 2014).
The Cochrane Pregnancy and Childbirth Group’s Trials Register is maintained by the Trials Search Co‐ordinator and contains trials identified from:
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monthly searches of the Cochrane Central Register of Controlled Trials (CENTRAL);
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weekly searches of MEDLINE (Ovid);
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weekly searches of Embase (Ovid);
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handsearches of 30 journals and the proceedings of major conferences;
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weekly current awareness alerts for a further 44 journals plus monthly BioMed Central email alerts.
Details of the search strategies for CENTRAL, MEDLINE and Embase, the list of handsearched journals and conference proceedings, and the list of journals reviewed via the current awareness service can be found in the ‘Specialized Register’ section within the editorial information about the Cochrane Pregnancy and Childbirth Group.
Trials identified through the searching activities described above are each assigned to a review topic (or topics). The Trials Search Co‐ordinator searches the register for each review using the topic list rather than keywords.
Searching other resources
For this update, we also contacted investigators of the previously identified ongoing studies by email to enquire about any new or imminent publications.
We searched the reference lists of retrieved studies.
We did not apply any language or date restrictions.
Data collection and analysis
For methods used in the previous version of this review, seeMuktabhant 2012.
For this update, we used the following methods based on a standard template used by the Cochrane Pregnancy and Childbirth Group for assessing the reports that were identified as a result of the updated search.
Selection of studies
Two review authors (Benja Muktabhant (BM); Theresa Lawrie (TL)) independently assessed for inclusion all the potential studies identified as a result of the search strategy. We resolved any disagreement through discussion or, if required, we consulted the third review author (Pisake Lumbiganon (PL)).
Data extraction and management
Using Microsoft Excel®, we designed a spreadsheet to collect study data and piloted it with two studies. Thereafter, two review authors (BM, TL) extracted data from included studies using the piloted form. We resolved discrepancies through discussion or, if required, we consulted a third review author (PL). Data were entered into Review Manager software (RevMan 2014) by one review author (TL) and checked for accuracy by another (BM).
For studies that reported results for obese and overweight women separately, we combined these data for the 'high‐risk women' subgroup.
Assessment of risk of bias in included studies
Two review authors (BM, TL) independently assessed risk of bias for each study using the criteria outlined in the Cochrane Handbook for Systematic Reviews of Interventions (Higgins 2011). Any disagreement was resolved by discussion or by involving a third assessor (PL or Malinee Laopaiboon (ML)).
(1) Random sequence generation (checking for possible selection bias)
We described for each included study the method used to generate the allocation sequence in sufficient detail to allow an assessment of whether it should produce comparable groups.
We assessed the method as:
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low risk of bias (any truly random process, e.g. random number table; computer random number generator);
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high risk of bias (any non‐random process, e.g. odd or even date of birth; hospital or clinic record number);
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unclear risk of bias.
(2) Allocation concealment (checking for possible selection bias)
We described for each included study the method used to conceal allocation to interventions prior to assignment and assessed whether intervention allocation could have been foreseen in advance of, or during recruitment, or changed after assignment.
We assessed the methods as:
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low risk of bias (e.g. telephone or central randomisation; consecutively numbered sealed opaque envelopes);
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high risk of bias (open random allocation; unsealed or non‐opaque envelopes, alternation; date of birth);
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unclear risk of bias.
(3.1) Blinding of participants and personnel (checking for possible performance bias)
We described for each included study the methods used, if any, to blind study participants and personnel from knowledge of which intervention a participant received. We considered that studies were at low risk of bias if they were blinded, or if we judged that the lack of blinding unlikely to affect results. We assessed blinding separately for different outcomes or classes of outcomes.
We assessed the methods as:
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low, high or unclear risk of bias for participants;
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low, high or unclear risk of bias for personnel.
(3.2) Blinding of outcome assessment (checking for possible detection bias)
We described for each included study the methods used, if any, to blind outcome assessors from knowledge of which intervention a participant received. We assessed blinding separately for different outcomes or classes of outcomes.
We assessed methods used to blind outcome assessment as:
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low, high or unclear risk of bias.
(4) Incomplete outcome data (checking for possible attrition bias due to the amount, nature and handling of incomplete outcome data)
We described for each included study, and for each outcome or class of outcomes, the completeness of data including attrition and exclusions from the analysis. We stated whether attrition and exclusions were reported and the numbers included in the analysis at each stage (compared with the total randomised participants), reasons for attrition or exclusion where reported, and whether missing data were balanced across groups or were related to outcomes. Where sufficient information was reported, or could be supplied by the trial authors, we planned to re‐include missing data in the analyses which we undertook.
We assessed methods as:
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low risk of bias (e.g. no missing outcome data; missing outcome data balanced across groups);
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high risk of bias (e.g. numbers or reasons for missing data imbalanced across groups; ‘as treated’ analysis done with substantial departure of intervention received from that assigned at randomisation);
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unclear risk of bias.
(5) Selective reporting (checking for reporting bias)
We described for each included study how we investigated the possibility of selective outcome reporting bias and what we found.
We assessed the methods as:
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low risk of bias (where it is clear that all of the study’s pre‐specified outcomes and all expected outcomes of interest to the review have been reported);
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high risk of bias (where not all the study’s pre‐specified outcomes have been reported; one or more reported primary outcomes were not pre‐specified; outcomes of interest are reported incompletely and so cannot be used; study fails to include results of a key outcome that would have been expected to have been reported);
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unclear risk of bias.
(6) Other bias (checking for bias due to problems not covered by (1) to (5) above)
We described for each included study any important concerns we had about other possible sources of bias.
(7) Overall risk of bias
We made explicit judgements about whether studies were at high risk of bias, according to the criteria given in the Handbook (Higgins 2011). With reference to (1) to (6) above, we attempted to assess the likely magnitude and direction of the bias and whether we considered it is likely to impact on the findings. We explored the impact of the level of bias through undertaking sensitivity analyses ‐ seeSensitivity analysis.
Measures of treatment effect
Dichotomous data
For dichotomous data, we presented results as summary risk ratios with 95% confidence intervals.
Continuous data
We used the mean difference if outcomes were measured in the same way between trials. We used the standardised mean difference to combine trials that measured the same outcome, but used different methods.
Unit of analysis issues
Cluster‐randomised trials
We included cluster‐randomised trials in the analyses along with individually‐randomised trials provided that cluster‐RCT data were adjusted for clustering and any baseline imbalances. We considered it reasonable to combine the results from both if there was little heterogeneity between the study designs and the interaction between the effect of intervention and the choice of randomisation unit was considered to be unlikely. We assessed risk of bias of these trials with particular attention to imbalances in baseline characteristics between the comparison arms, loss of clusters and appropriate analyses, and we acknowledged heterogeneity in the randomisation unit, performing sensitivity analyses to investigate the effects of including these studies on review findings.
Other issues
For studies that included three arms, we divided the control group into two equal groups and considered each comparison separately. If the number of events in the control group was an odd number, to reduce the risk of overestimating effects in favour of the intervention group, we halved it and rounded it down; for odd denominators (total number of participants in the control group), we rounded these numbers upwards for the same reason.
Dealing with missing data
For included studies, we noted levels of attrition. We imputed data for studies where results were incompletely reported, e.g. if percentages and denominators were known, but the number of events was missing. For all outcomes, we carried out, as far as possible, analyses on an intention‐to‐treat basis, that is, we attempted to include all participants randomised to each group in the analyses. The denominator for each outcome in each trial was the number randomised minus any participants whose outcomes were known to be missing.
Assessment of heterogeneity
We assessed statistical heterogeneity in each meta‐analysis using the Tau², I² and Chi² statistics. We regarded heterogeneity as substantial if an I² was greater than 30% and either a Tau² was greater than zero, or there was a low P value (less than 0.10) in the Chi² test for heterogeneity. If we identified heterogeneity above 30%, we explored it by sensitivity and subgroup analyses.
Assessment of reporting biases
Where there were 10 or more studies in the meta‐analysis, we investigated reporting biases (such as publication bias) using funnel plots, which we assessed visually for asymmetry. If asymmetry was suggested by a visual assessment, we performed exploratory analyses to investigate it.
Data synthesis
We carried out statistical analysis using the Review Manager software (RevMan 2014). We used random‐effects meta‐analysis to produce an overall summary, if an average treatment effect across trials.was considered clinically meaningful The random‐effects summary was treated as the average of the range of possible treatment effects and we considered the clinical implications of treatment effects differing between trials. If the average treatment effect was not clinically meaningful, we did not combine trials. The results of these random‐effects analyses are presented as the average treatment effect with 95% confidence intervals and estimates of I².
Subgroup analysis and investigation of heterogeneity
Subgroup analyses according to risk were not specified in the original review protocol. We conducted subgroup analyses according to the risk of adverse effects related to poor weight control with the high‐risk group comprising only overweight and obese women, or women with or at risk of diabetes mellitus; a mixed‐risk group comprising women in the general population, including women of any body mass indices (BMIs), and a low‐risk group comprising normal weight women or women with BMIs of less than 25 kg/m2. Where possible, we performed subgroup analysis for the following outcomes.
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Excessive gestational weight gain (GWG)
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Mean GWG
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Low GWG
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Preterm birth
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Caesarean section
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Pre‐eclampsia
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Macrosomia
For these analyses, we assessed subgroup differences by interaction tests available within RevMan (RevMan 2014) and reported the results of subgroup analyses quoting the Chi² statistic and P value, and the interaction test I² value.
We explored heterogeneity by organising studies within comparisons according to the types of interventions.
Sensitivity analysis
We carried out sensitivity analyses to explore the effect of trial quality by excluding studies with risk of bias concerns from the analyses in order to assess whether this made any difference to the overall result.
Quality of evidence
Following meta‐analysis, the quality of the evidence was assessed using the GRADE approach (Schunemann 2009) for the following key outcomes.
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Excessive GWG
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Mean GWG
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Low GWG
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Preterm birth
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Caesarean section
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Pre‐eclampsia
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Macrosomia
'Summary of findings' tables were created using this feature in RevMan 2014 with a summary of the intervention effect and a measure of quality produced for each of the above outcomes using the GRADE approach (GRADE 2014). The GRADE approach uses five considerations to assess the quality of the body of evidence for each outcome. We downgraded the evidence from 'high quality' by one level for serious (or by two levels for very serious) limitations, depending on assessments for risk of bias, indirectness of evidence, serious inconsistency, imprecision of effect estimates or potential publication bias.
Results
Description of studies
SeeCharacteristics of included studies; Characteristics of excluded studies; Characteristics of studies awaiting classification; Characteristics of ongoing studies.
Results of the search
The original search identified 63 potential studies, of which we included 28 and excluded 12 studies in the original review (Muktabhant 2012). Two studies remained unclassified and 21 studies were ongoing.
Searches updated to November 2014 identified 169 eligible records. Of these 169 records, we included 102 records (pertaining to 41 new RCTs), and excluded 19 records (pertaining to 10 new studies, and one previously excluded study). Twelve of the 169 records were new reports of five previously included RCTs (Barakat 2011; Callaway 2010; Laitinen 2009; Luoto 2011; Phelan 2011), 36 records were of ongoing RCTs, and one record remained unclassified for this update (requiring translation from Farsi).
For this update, we excluded two previously included quasi‐RCTs (Bechtel‐Blackwell 2002; Moses 2006) and two RCTs that involved anti‐suppressant drugs (Boileau 1968; Silverman 1971), which had previously been included under a broader title (see Differences between protocol and review).
Therefore, in summary, we included a total of 65 RCTs in this update (41 new and 24 previously included). Forty‐nine studies (29 newly included) contributed data to quantitative synthesis. Twelve RCTs that had been identified as ongoing in the previous review have now been published, leaving 40 ongoing RCTs altogether (including new and previously included ongoing trials not yet reported) for this update (Characteristics of ongoing studies).
Included studies
Out of 65 included studies, two studies were cluster‐RCTs (Luoto 2011; Rauh 2013); all other studies were RCTs. We were able to adjust data for one cluster‐RCT (Luoto 2011; Appendix 1) and used adjusted data in meta‐analyses, however we were unable to adjust data from Rauh 2013, which therefore did not contribute to meta‐analyses. Seven RCT reports were conference abstracts (Angel 2011; Bisson 2014; Bogaerts 2012; Leiferman 2011; Marcinkevage 2012; Mujsindi 2014; Szmeja 2011). One of these studies (Leiferman 2011), also generated a substudy in the form of a PhD thesis (Nodine 2011), which we have linked to this study in the references section. When reported in full, these seven RCTs may yet contribute data to future versions of this review; however, in general, we gleaned very little methodological information and no usable data from the abstracts. We have included information about these trials in the Characteristics of included studies tables, but they are not otherwise discussed in the sections below.
Participants
Two studies (Bogaerts 2012; Leiferman 2011) did not report the number of participants. The remaining 63 included studies involved at least 13,523 pregnant participants, and the number of participants in each study ranged from 12 (Magee 1990) to more than 2000 (Dodd 2014). Fifty‐five out of 65 studies reported age and body mass index (BMI) at baseline and these were similar between study and control groups, with a few exceptions (see Risk of bias in included studies). Four studies recruited only nulliparous women (Althuizen 2013; Haakstad 2011; Murtezani 2014; Pinzon 2012). Most studies recruited women less than 20 weeks' gestation (48/65; 74%), with 27/65 (42%) studies recruiting women less than or equal to 14 weeks' gestation. Thirteen studies recruited participants after 20 weeks' gestation, namely Rhodes 2010 (13 to 28 weeks); Ferrara 2011 (approximately 31 weeks on average); Louie 2011 (20 to 32 weeks); Angel 2011 (more than 20 weeks); Hui 2012, Hui 2006 and Jackson 2011 (up to 26 weeks); Magee 1990 (13 to 38 weeks); Moses 2009 (approximately 30 weeks on average); Pollak 2014 (up to 21 weeks); Stafne 2012 (18 to 22 weeks); Thornton 2009 (12 to 28 weeks); Vitolo 2011 (10 to 29 weeks). Gestation at recruitment was not clear for the remainder (Bogaerts 2012; Leiferman 2011; Mujsindi 2014; Quinlivan 2011).
Studies included participants of various weight categories with 'normal weight' generally defined as a BMI greater than 18 and less than 25 kg/m², 'overweight' was considered to be greater than or equal to 25 kg/m² and less than 30 kg/m², and 'obese' was considered to be a BMI of greater than or equal to 30 kg/m². Thirty‐four studies recruited women from the 'general population' (i.e. of various BMIs) and the proportion of women with normal BMIs varied widely across study samples reporting this baseline characteristic, from 15% to 79% of participants. Most of these studies did not report results for high‐ (overweight/obese women) and low‐risk (normal BMI) women separately; however, for eight of these studies (Althuizen 2013; Hui 2014; Jeffries 2009; Phelan 2011; Polley 2002; Ronnberg 2014; Ruiz 2013; Vitolo 2011), main outcomes were reported separately for women with low/normal versus overweight/obese prepregnancy weights; therefore, where possible, we used relevant data from these studies for meta‐analyses pertaining to low, mixed‐risk and high‐risk groups. One study (ROLO 2012) recruited only secundigravid women who had previously given birth to a baby with macrosomia and reported certain outcomes separately for women in all weight categories.
Among 31 studies recruiting women in high‐risk groups, 24 studies recruited overweight and obese women, or obese women only (Angel 2011; Bisson 2014; Bogaerts 2012; Callaway 2010; Dodd 2014; Guelinckx 2010; Kong 2014; Magee 1990; Marcinkevage 2012; Mujsindi 2014; Nascimento 2012; Oostdam 2012; Petrella 2013; Poston 2013; Pollak 2014; Quinlivan 2011; Renault 2014; Rhodes 2010; Santos 2005; Szmeja 2011; Thornton 2009; Vesco 2013; Vinter 2012; Wolff 2008); and seven recruited women with, or defined as at high risk of, gestational diabetes (Ferrara 2011; Harrison 2013; Korpi‐Hyovalti 2011; Louie 2011; Luoto 2011; Moses 2009; Rae 2000).
Settings
Most studies were conducted in high‐income countries, including Australia (Callaway 2010; Dodd 2014; Harrison 2013; Jeffries 2009; Louie 2011; Moses 2009; Moses 2014; Quinlivan 2011; Szmeja 2011; Wilkinson 2012), Belgium (Bogaerts 2012; Guelinckx 2010), Canada (Hui 2006; Hui 2012; Hui 2014; Hui 2014; Ruchat 2012), Denmark (Renault 2014; Vinter 2012; Wolff 2008), Finland (Korpi‐Hyovalti 2011; Laitinen 2009; Luoto 2011), Germany (Rauh 2013), Ireland (ROLO 2012), Italy (Di Carlo 2014; Petrella 2013), Kosovo (Murtezani 2014), Norway (Haakstad 2011), Sweden (Petrov Fieril 2014; Ronnberg 2014), The Netherlands (Althuizen 2013; Oostdam 2012), Spain (Barakat 2011; Cordero 2014; Ruiz 2013), the United Kingdom (Poston 2013) and the United States of America (USA) (Angel 2011; Asbee 2009; Bisson 2014; Clapp 2002a; Clapp 2002b; Ferrara 2011; Hawkins 2014; Kieffer 2014; Kong 2014; Leiferman 2011; Magee 1990; Marcinkevage 2012; Mujsindi 2014; Phelan 2011; Pollak 2014; Polley 2002; Price 2012; Rhodes 2010; Thornton 2009; Vesco 2013). Two of these studies (Hui 2006; Polley 2002) recruited women with low‐, or low‐middle incomes in Canada and the USA, respectively. Of the six studies conducted in low‐income countries, four were conducted in Brazil (De Oliveria Melo 2012; Nascimento 2012; Santos 2005; Vitolo 2011), one was conducted in Columbia (Pinzon 2012) and one was conducted in Taiwan (Huang 2011).
Interventions
All the interventions considered in this review included modifying or restricting diet or increasing exercise, or both; however there was considerable variation in the interventions used, which included:
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diet only (eight studies): low glycaemic load (GL) diet versus conventional healthy eating or routine or other care: Angel 2011; Clapp 2002a; Louie 2011; Moses 2009; Moses 2014; Rhodes 2010; ROLO 2012; one study evaluated a supervised low calorie diet (Magee 1990);
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diet and exercise counselling (25 studies): Asbee 2009; Althuizen 2013; Bogaerts 2012; Dodd 2014; Ferrara 2011; Guelinckx 2010; Harrison 2013; Hawkins 2014; Huang 2011; Jackson 2011; Kieffer 2014; Korpi‐Hyovalti 2011; Luoto 2011; Marcinkevage 2012; Mujsindi 2014; Petrella 2013; Phelan 2011; Pollak 2014; Polley 2002; Quinlivan 2011; Rauh 2013; Renault 2014; Szmeja 2011; Vesco 2013; Wilkinson 2012;
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exercise interventions (e.g. supervised exercise, individualised exercise programs, dance classes, provision of pedometers or treadmills) (20 studies): Barakat 2011; Bisson 2014; Callaway 2010; Clapp 2002b; Cordero 2014; De Oliveria Melo 2012; Haakstad 2011; Kong 2014; Leiferman 2011; Murtezani 2014; Nascimento 2012; Oostdam 2012; Petrov Fieril 2014; Pinzon 2012; Poston 2013; Price 2012; Renault 2014; Ruiz 2013; Ronnberg 2014; Santos 2005;
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diet and supervised exercise interventions (five studies): Hui 2006; Hui 2012; Hui 2014; Ruchat 2012; Vinter 2012;
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diet counselling/other (seven studies): Di Carlo 2014; Jeffries 2009; Laitinen 2009; Rae 2000; Thornton 2009; Vitolo 2011; Wolff 2008.
Interventions varied in intensity. Control groups mostly comprised routine or standard care (which also varied considerably in different settings and was not always well‐described). Hui 2006 compared a supervised group exercise and diet intervention with an exercise and diet information pack. Clapp 2002b compared different exercise intensities at different stages of pregnancy. Some studies included more than two arms (De Oliveria Melo 2012; Laitinen 2009; Guelinckx 2010; Renault 2014).
Outcomes
Gestational weight gain (GWG) or excessive GWG, or both, were reported as primary or secondary outcomes in 75% of included studies. Excessive GWG was usually defined according to prevailing IOM guidelines. Generally, baseline weight was measured at recruitment; however, several studies used self‐reported prepregnancy weight as the baseline measurement (e.g. Di Carlo 2014; Haakstad 2011; Hui 2012; Louie 2011; Moses 2014; Oostdam 2012). The final weight measurement was either collected by researchers at the last clinic or hospital visit (usually greater than or equal to 36 weeks) or from medical records. Several studies collected these follow‐up weight data earlier than 36 weeks, including Vesco 2013 (34 weeks), Oostdam 2012 (32 weeks), Harrison 2013 (28 weeks), and Petrov Fieril 2014 (25 weeks). The latter study included mean weight as an outcome, but not mean weight gain.
Other reported outcomes included postpartum weight retention, macrosomia, infant birthweight, gestational diabetes, pre‐eclampsia/hypertension, diet and physical activity (PA) behaviour, breastfeeding, biochemical parameters, e.g. serum insulin levels, and various other maternal and neonatal outcomes.
Excluded studies
Initially, we excluded 26 studies (12 previously excluded, 10 new excluded and four previously included). One previously excluded study (Moses 2007), was a follow‐up of a previously included study (Moses 2006) and these two reports are now listed together, reducing the number of excluded studies to 25 studies. The main reasons for exclusion were as follows.
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Non‐randomised study or quasi‐RCT: Bechtel‐Blackwell 2002; Breslow 1963; Daley 2014; Davenport 2011; Graham 2014; Gray‐Donald 2000; Kinnunen 2007; Maitland 2014; Mohebi 2009; Moses 2006; Mottola 2010; Olson 2004; Stutzman 2010; Walker 1966.
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Participants included non‐pregnant or postpartum women: Campbell 2004; Faucher 2008; Hausenblas 2008; Te Morenga 2011; Wisner 2006.
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Not a diet or exercise intervention: Asemi 2011; Boileau 1968; Hauner 2012; Ismail 1990; Lindsay 2014; Silverman 1971.
Risk of bias in included studies
Details of the methodological quality of each study are given in Characteristics of included studies, Figure 1, and Figure 2. Studies were considered to be potentially at a moderate‐to‐high risk of bias if they were assessed to be at 'high risk' for at least one of the risk of bias items below, excluding blinding, as most studies were open‐label. We considered 35/65 studies (54%) to be at a low risk of bias overall, and 20/65 (29%) to be at a moderate‐to‐high risk of bias overall (Asbee 2009; Barakat 2011; Callaway 2010; Cordero 2014; Di Carlo 2014; Ferrara 2011; Luoto 2011; Murtezani 2014; Nascimento 2012; Oostdam 2012; Petrov Fieril 2014; Pinzon 2012; Price 2012; Rauh 2013; Ruchat 2012; Santos 2005; Stafne 2012; Vitolo 2011; Wilkinson 2012; Wolff 2008). Five of the latter studies (Callaway 2010; Pinzon 2012; Rauh 2013; Vitolo 2011; Wilkinson 2012) did not contribute to quantitative analysis in this update. The remaining 10 studies were at an unclear risk of bias (Angel 2011; Bisson 2014; Bogaerts 2012; Korpi‐Hyovalti 2011; Leiferman 2011; Magee 1990; Marcinkevage 2012; Mujsindi 2014; Polley 2002; Szmeja 2011).
Methodological quality summary: review authors' judgements about each methodological quality item for each included study.
Methodological quality graph: review authors' judgements about each methodological quality item presented as percentages across all included studies.
Allocation
Out of 65 studies, 45 (69%) were assessed as being at low risk of bias for generation of the randomisation sequence and 34 (52%) used methods that we judged to be at a low risk of bias for allocation concealment. The remaining studies (25%) were at an unclear risk of selection bias.
Blinding
Twenty‐four out of 65 studies (37%) had taken some steps to implement performance or detection blinding, or both. Achieving participant and personnel blinding of treatment allocation for diet and exercise interventions was indicated to be not feasible in several studies and was not described in many others. Where studies were described as open‐label or unblinded, we classified these as at a high risk of bias for this item; however, it was difficult to ascertain whether the lack of blinding, or unsuccessful blinding, impacted on outcomes or resulted in any systematic bias. In addition, the studies that did not describe blinding were probably unblinded. For these reasons we did not use blinding as a criterion in the overall assessment of individual study bias but rather took into account other types of bias.
Incomplete outcome data
We assessed 29/65 studies (45%) to be at a low risk of attrition bias. Fourteen studies (22%) (Callaway 2010; Cordero 2014; Di Carlo 2014; Ferrara 2011; Luoto 2011; Oostdam 2012; Petrov Fieril 2014; Pinzon 2012; Price 2012; Ruchat 2012; Santos 2005; Stafne 2012; Wilkinson 2012; Wolff 2008) had high attrition (greater than 20%) overall, or for the intervention or control group only, or for certain outcomes, and we considered these to be at a high risk of bias accordingly. In the remaining studies, loss of outcome data was either not stated or was less than 20% but there were other concerns (e.g. imbalance in attrition between arms) and for these we considered the risk of bias to be unclear.
Selective reporting
It was difficult to assess bias associated with the outcome reporting bias as we did not have access to the study protocols of most studies and we did not know whether results for all outcomes where data had been collected had been reported; we therefore assessed many of these studies as being unclear for the outcome reporting bias. However, we considered Cordero 2014 and Di Carlo 2014 to be at a potentially high risk of reporting bias as only per protocol findings were reported. During the course of these studies, women with preterm labour were excluded, therefore, this potential side‐effect could not be evaluated. In addition, Cordero 2014 additionally excluded data from women with poor adherence to the intervention; therefore, the reported results may be biased in the direction of the intervention.
Other potential sources of bias
Six studies had important baseline imbalances in the characteristics of the women in the intervention and control groups (Barakat 2011; Cordero 2014; Di Carlo 2014; Price 2012; Rauh 2013; Santos 2005) that might have impacted the results in favour of the intervention. Barakat 2011, Cordero 2014,Di Carlo 2014 and Price 2012 did not adjust results for these imbalances and we therefore considered them to be at a potentially high risk of bias. Cordero 2014 additionally had an unexplained difference in intervention and control group sizes. Rauh 2013 is discussed below under 'Assessment of cluster‐RCTs'.
In Price 2012, control participants were told not to exercise because it would blur the distinction between the groups. This contributed to high drop‐out rates in the control group and bias in favour of the intervention, whilst making results less applicable by enforcing no exercise. Oostdam 2012 had issues with adherence to the intervention, which may have biased results in favour of the control group.
Most studies involving an exercise component excluded women at risk of miscarriage or preterm birth at screening. However, four studies excluded women with or at risk of preterm birth post‐randomisation from analysis (Cordero 2014; Di Carlo 2014; Murtezani 2014; Rauh 2013). This omission might have led to publication bias in the review's 'preterm birth' outcome. Any other potential sources of bias were noted in the Characteristics of included studies.
Assessment of cluster‐RCTs
Two trials were cluster‐RCTs (Luoto 2011; Rauh 2013).
Recruitment bias: In Rauh 2013, intervention and control groups differed substantially in size as "During recruitment it turned out that it was easier to recruit women for the intervention group than for the control group, yielding a 2:1 ratio", instead of 1:1. In Luoto 2011, more than 20% and 30% in the intervention and control arms, respectively, were excluded from analysis based on oral glucose tolerance tests conducted between eight and 12 weeks' gestation. Only 40% and 47% of women in intervention and control groups, respectively, who were assessed as preliminary eligible were analysed.
Baseline imbalances: Baseline imbalances were limited to differences in educational levels between arms in Luoto 2011. However, in Rauh 2013, baseline characteristics differed significantly with regard to pregravid BMI (P = 0.003) and BMI at booking (P = 0.008), with a higher proportion of women in the control group considered obese or overweight (16.2% versus 31.4%; P = 0.009). In addition, mean age was younger and gestational age at booking was significantly earlier in the intervention clusters.
Loss of clusters: There was no loss of clusters in either study.
Analysis methods: Both Luoto 2011 and Rauh 2013 reported adjusting the summary effect size for clusters and baseline imbalances. However, outcome data for both studies needed to be estimated for use in meta‐analysis, and this was not possible for Rauh 2013, due to insufficient data and the lack of an intracluster correlation coefficient. The results reported in Rauh 2013 favoured the intervention arm for weight gain outcomes (Appendix 2), and although these were adjusted for BMI, age and clustering, there may also have been other (unknown) differences between the women in these groups. We therefore considered this study to be at potentially high risk of bias; however, Rauh 2013 data did not contribute to meta‐analyses.
Comparability with individually‐randomised trials: These trials were comparable to individually‐randomised trials except that large differences in study group sizes occurred in Rauh 2013. Study investigators reported that the clusters (gynaecology practices) differed significantly in size; the result was that 227 versus 129 women were eligible for the intervention and control clusters, respectively.
Overall assessment: We assessed these cluster‐RCTs as moderate‐to‐high risk of bias. Adjusted Luoto 2011 data were used in meta‐analyses; however, Rauh 2013 data could not be adjusted and were therefore not used.
Effects of interventions
See: Summary of findings for the main comparison All diet and/or exercise interventions compared to standard/other care for preventing excessive weight gain in pregnancy; Summary of findings 2 Comparative table of findings by intervention type
We compared diet or exercise, or both, interventions together (comparisons 1) organised by types of interventions (see Table 1 for the rationale for study categories). We also analysed each intervention category separately stratified for risk (comparisons 2, 3, 4, and 5 ) for all women (i.e. a mixed‐risk population), low risk, and high‐risk women.
| Number | Study ID | Experimental intervention (unless otherwise stated, the control intervention was routine care) | Participants analysed | Contributed data | ||
| Low risk | Mixed risk | High risk | ||||
| Diet counselling/other | ||||||
| 1 | The intervention involved a supervised personalised diet plan meeting both personal preferences and specific gestational needs with the average caloric intake being 1916 kcal. The only fat allowed was olive oil. Participants in the intervention group underwent monthly follow‐up appointments with a dietician who monitored their weight gain and discussed issues. Control group received standard brochure on healthy eating. | 120 | / | |||
| 2. | Women were given a personalised weight measurement card, advised of their optimal gestational weight gain based on their BMI at the time of recruitment and the United States IOM guidelines, and instructed to record their weight at 16, 20, 24, 28, 30, 32 and 34 weeks' gestation. | 236 | / | / | ||
| 3. | Dietary counselling was given by a dietitian at each study visit and aimed to modify dietary intake to conform with that currently recommended, particular attention being paid to the quality of dietary fat. Study visits took place 3 times during pregnancy and at 1, 6 and 12 months postpartum. | 171 | / | |||
| 4. | This was a multi‐faceted intervention that included weighing on arrival and a brief dietary intervention by a food technologist at every antenatal visit. Other aspects of the intervention involved continuity of care provider and psychological assessment. | 124 | / | |||
| 5. | The intervention comprised instruction in a moderately energy restricted diabetic diet providing between 1590‐1776 kcal (70% RDA). | 117 | / | |||
| 6. | Participants were counselled in nutrition and monitored by a registered dietitian and given a detailed nutrition program similar to a diabetic diet. | 232 | / | |||
| 7. | Intervention comprise a healthy diet according to the official Danish dietary recommendations (% fat, protein, CHO, 30%, 15%‐20%, 50%‐55%). The energy intake was restricted based on individually estimated energy requirements and estimated energetic cost of fetal growth. | 50 | / | |||
| Low GL diet | ||||||
| 8. | Participants were randomised to either a low‐glycaemic diet (aboriginal diet) or high‐glycaemic diet (cafeteria diet). | 20 | / | |||
| 9. | Intervention was a healthy low‐GL diet of protein (15%‐25%), fat (25%‐30%) and carbohydrate (40%‐45%) (versus healthy high‐fibre diet with moderate GL, similar to population average). Participants attended at least 3 face‐to‐face visits with the study dietician for monitoring adherence and encouragement. Intervention began after 29th week. | 92 | / | |||
| 10. | Low‐GL diet versus high‐GL diet. The dietary advice by dietitian was individualised with specific mention of the energy and nutrient balance to achieve normal weight gain during the 3rd trimester. | 63 | / | |||
| 11. | The intervention involved a low glycaemic diet from 12 to 16 weeks' gestation for the remainder of pregnancy (compared with conventional healthy eating). Women received a detailed dietary education tailored for the group assignment at baseline ‐ there were no difference in the macronutrient distribution in the diets, only the substitution of carbohydrate‐rich foods with low GL alternatives in the experimental group. Information booklets were provided. 4 contact points with a research dietician were planned (first visit, phone call, midway and final visits) to collect data and ensure adherence. | 576 | / | |||
| 12. | Nutrition education, dietary counselling, and a low‐GL diet (vs a low‐fat diet). | 50 | / | |||
| 13. | Low‐GL dietary intervention given by a dietitian involving 1 dietary education session lasting 2 hours in groups of 2 ‐6 women at baseline. Follow‐up reinforcement sessions were held at 28 and 34 weeks' gestation. Women also received written resources about low‐GL foods. | 759 | / | / | / | |
| Diet and exercise counselling | ||||||
| 14. | The intervention involved counselling by members of the research team consisting of 5 x 15 minute sessions on weight, physical activity and diet. Interventions were face‐to‐face at 18, 22, 30, and 36 weeks' gestation, with a telephone session at 8 weeks postpartum. Counsellors discussed how to control weight gain during and after pregnancy, and how to maintain a healthy lifestyle. | 219 | / | / | ||
| 15 | At the initial visit, participants met with a registered dietician to receive a standardised counselling session, including information on pregnancy‐specific dietary and lifestyle choices. Participants were instructed to engage in moderate‐intensity exercise at least 3 times per week and preferably 5 times per week. Weight gain was reviewed at each routine antenatal visit. | 100 | / | |||
| 16. | Comprehensive dietary and lifestyle intervention (counselling) (n = 1108) Intervention involved meetings and home visits with advice on dietary, exercise, and behavioural strategies delivered by a dietician and trained research assistants. Exercise advice primarily encouraged women to increase their amount of walking and incidental activity. | 2212 | / | |||
| 17. | Lifestyle intervention involved 3 in‐person sessions and up to 15 telephone calls with counselling re diet, physical activity and breast‐feeding up to 12 months postpartum. The intervention was delivered by 2 dietitians. Participants were encouraged to engage in moderate‐intensity physical activity for 150 minutes per week and received written materials about food size, foods with low GL or low fat, and how to read food labels were discussed, | 197 | / | |||
| 18. | 2 intervention arms: 1 involved a brochure only, the other involved a brochure and counselling by a trained nutritionist in 3 group sessions. A maximum of 5 women were brought together in these 1‐hour sessions, which were scheduled at 15, 20, and 32 weeks of pregnancy. The sessions provided participants with recommendations on a balanced, healthy diet, and physical activity specifically designed for the study to limit weight gain. | 124 | / | |||
| 19. | Intervention provided dietary advice, simple healthy eating, and "physical activity messages" and weight gain self‐monitoring. Also included "regular self‐weighing as a key behavioural strategy". | 203 | / | |||
| 20. | A lifestyle intervention consisting of a culturally and linguistically modified, motivationally targeted, individually tailored 6‐month prenatal programme. Educators encouraged women to achieve guidelines for physical activity, decrease saturated fat and increase dietary fibre. The intervention consisted of 6 monthly in‐person behavioural counselling sessions and 5 telephone booster sessions with follow‐up to 6 weeks postpartum. Women were encourage to achieve ≥ 30 minutes of moderate‐intensity activity on most days of the week through walking and developing a more active lifestyle. | 68 | / | |||
| 21. | The intervention was delivered at regularly scheduled clinic visits by nurses with training in nutrition and physical fitness. The nurse discussed with each participant how to design an individualised diet and physical activity plan. The intervention consisted of 6 1‐to‐1 counselling sessions: 1 primary session (about 30–40 minutes) at the 16‐week gestation visit, and 5 1‐to‐1 booster sessions (at 28 gestational weeks, 36–38 gestational weeks, before hospital discharge after a 3 to 7‐day stay, 6 weeks' postpartum and 3 months postpartum). After each clinic visit, women in the experimental groups were sent a personalised graph of their weight changes. At the 1st session, the experimental groups also received a researcher‐prepared brochure that provided detailed information on weight management goals during pregnancy and postpartum. | 160 | / | |||
| 22. | Individual dietary advice tailored to each participant at 6 visits to include a low fat diet rich in vegetables, fruit and berries. Moderate‐intensity physical exercise was encouraged at 6 exercise counselling sessions. | 60 | / | |||
| 23. | Individual counselling on physical activity and diet and weight gain. At the first visit the recommendations for gestational weight gain were discussed and an appropriate weight gain graph was selected to guide the participant in monitoring her weight gain. Physical activity counselling was implemented at 8–12 weeks' gestation and the dietary counselling session occurred at 16–18 weeks' gestation. Physical activity counselling was enhanced at 4, and diet counselling at 3 subsequent visits. | 399 | / | |||
| 24. | Lifestyle intervention involving a caloric restricted diet (1500 kcal/day) and mild exercise 30 minutes/day, 3 times per week monitored by a pedometer. | 63 | / | |||
| 25. | The Fit for Delivery intervention included a face‐to‐face visit with an interventionist at the onset of treatment who discussed appropriate weight gains during pregnancy, physical activity (30 minutes of walking most days of the week), and calorie goals (20 kcal/kg). Emphasis was placed on decreasing high fat foods, increasing physical activity, and daily self‐monitoring. Women also received personalised weight graphs after each clinic visit, automated supportive postcards and 3 supportive phone calls. | 401 | / | / | ||
| 26. | Intervention conducted at routine clinic visits by staff with training in nutrition or psychology involved education about weight gain, healthy eating, and exercise, and individual graphs of their weight gain. After each clinic visit, women were sent a personalised graph of their weight gain. | 110 | / | / | ||
| 27. | A lifestyle intervention (diet plus exercise) involving 1 1‐to‐1 counselling session with a health trainer and then weekly group sessions for 8 consecutive weeks from 19 weeks' gestation. Sessions delivered by health trainers involved diet and exercise advice informed by psychological models of health behaviour. Dietary advice focused on increased consumption of foods with a low‐dietary GL, and reduction of saturated fats. Physical activity advice encouraged women to increase daily walking activity at moderate‐intensity level, setting goals monitored by a pedometer. Women also received a DVD of a pregnancy specific exercise regimen. | 154 | / | |||
| 28. | A 3‐arm study with 2 intervention groups. 1 intervention involved unsupervised exercise only (women were given a pedometer), the other involved diet and exercise counselling only. The diet and exercise intervention included follow‐up on a hypocaloric Mediterranean‐style diet. Instruction was given by a dietician every 2 weeks with alternating outpatient visits and phone calls, including weight measurement, encouragement and correcting advice on exercise and diet. | 389 | / | |||
| 29. | Intervention involved a 45‐minute diet consultation with an individualised caloric goal, a second individualised session, weekly group meetings with weigh ins, food/activity logs. Women are encouraged to accumulate at least 30 minutes of moderate‐intensity activity per day. Pedometers recorded steps with a target of 10,000 steps daily and were only provided to the intervention group. | 114 | / | |||
| Unsupervised exercise intervention | ||||||
| 30. | Unsupervised exercise intervention involved a walking program on treadmill or other setting for a minimum of 150 min/week. Women were loaned treadmills for the study and steps monitored. | 42 | / | |||
| 31. | A 3‐arm study with 2 intervention groups. 1 intervention involved unsupervised exercise only (women were given a pedometer), the other involved diet and exercise counselling. The physical activity intervention included encouragement or increase physical activity, aiming at a daily step count of 11,000, monitored by pedometer assessment on 7 consecutive days, every 4 weeks. | 389 | / | |||
| 32. | Intervention involved prescribed exercise to be at a "moderate level of exertion for approximately 30 min/day". | 374 | / | / | / | |
| Supervised exercise intervention | ||||||
| 33. | Intervention involved 35‐ to 45‐minute exercise sessions 3 times per week from the start of the pregnancy (weeks 6‐9) to the end of the 3rd trimester (weeks 38‐39) ‐ an average of 85 training sessions. Exercise intensity was light‐to‐moderate and was supervised by a fitness specialist in groups of 10‐12 women. | 80 | / | |||
| 34. | A supervised exercise program consisting of aerobic and toning exercises for 3 sessions per week. 2 weekly sessions were performed on land (60 minutes) and 1 session was aquatic based (50 minutes). Program commenced from 10‐14 weeks to the end of the third trimester. Sessions were supervised by a qualified fitness specialist and an obstetrician. | 257 | / | |||
| 35. | Supervised moderate‐intensity exercise (initiated at 13 weeks or 20 weeks) vs control . Sessions consisted of warming up and stretching exercises, followed by supervised walking 3 times a week in the open air. Supervised by physical education professionals and medical, physiotherapy and nursing students. | 187 | / | |||
| 36. | Exercise (60 minutes supervised aerobic dance at least twice a week for a minimum of 12 weeks) (n = 52). Women in the exercise group were advised to have moderate, self‐imposed physical activity on the remaining weekdays. | 105 | / | |||
| 37. | The exercise training program started in the second trimester and was continued until the end of pregnancy. Each session consisted of 40‐45 minutes of aerobic and strength exercise. Individuals were supervised by certified aerobic‐instructors, and each session included a maximum of 10 participants. Intensity was moderate‐to‐vigorous; supine postures and Valsalva manoeuvres were avoided. | 63 | / | |||
| 38. | Intervention consisted of a supervised exercise program guided by a trained physical therapist in weekly classes with light‐to‐moderate‐intensity exercise for 40 minutes. It also included home exercise counselling which was to be performed 5 times per week (consisting of a sequence of 22 exercises or walking). | 82 | / | |||
| 39. | A supervised exercise intervention comprising 2 sessions of aerobic and strengthening exercises per week; each exercise session lasted for 60 minutes from 20 weeks' gestation. | 101 | / | |||
| 40. | Intervention group received supervised resistance exercise twice a week, with light barbells and weight plates in a group setting, performed at an activity level equivalent to within moderate–to‐vigorous between weeks 14 to 25 gestation, and was self‐adjusted. In addition, walking, cycling, water‐gymnastics, Pilates, yoga and home exercises that included pelvic floor training were recommended. | 72 | / | |||
| 41. | Intervention involved a program of supervised aerobic training of 45‐60 minutes, 4 days per week. | 62 | / | |||
| 42. | Intervention involved light‐to moderate‐intensity supervised aerobic and resistance exercises (including pelvic floor exercises) performed 3 days a week (50‐55 minutes per session) from 9 weeks to weeks 38‐39. Exercise sessions involved 8‐10 participants. | 962 | / | / | / | |
| 43 | The intervention consisted of a program of supervised physical exercise of 60 minutes duration, performed 3 times per week for 12 weeks. | 72 | / | |||
| 44. | intervention comprised a 12‐week regular standardised exercise program including aerobic activity, strength training, and balance exercises. The exercise program followed standard recommendations and included moderate‐intensity to high‐intensity activity 3 or more days per week. Physiotherapist‐supervised training sessions of 60 minutes in groups of 8‐15 women were offered once per week. | 702 | / | |||
| Supervised exercise and diet intervention | ||||||
| 45. | Exercise intervention involved a weekly supervised group session including floor aerobics, stretching and strength exercises, and similar home‐based exercise 3‐5 times/week for 30‐45 minutes per session. A video was provided to participants to assist with home‐based exercise. Diet intervention involved a computer‐assisted food choice map interview and a personalised plan by a dietician. | 46 | / | |||
| 46. | Exercise intervention involved an exercise regimen comprising 3 to 5 times per week, including a weekly supervised community‐based session and multiple home sessions, of mild‐to‐moderate exercise for 30 to 45 minutes. Program started between 20‐26 weeks. Group exercise sessions including aerobics were held in community centres and instructors were licensed fitness trainers. 2 dietary interviews with counselling were provided. | 190 | / | |||
| 47. | Lifestyle intervention (diet counselling and a supervised exercise program) vs control. Intervention included "a community‐based exercise program specifically designed for pregnant women was provided". An exercise regimen, 3 to 5 times per week including a weekly exercise session and home sessions with DVD instruction of mild‐to‐moderate aerobic exercise for 30 to 45 minutes was recommended. Program started between 20‐26 weeks and continued to 36 weeks. Group exercise sessions including aerobics were held in community centres and instructors were licensed fitness trainers. 2 dietary interviews with dietician counselling using a Food Choice Map were provided (baseline and 2 months later). Control group received standard care. | 113 | / | / | ||
| 48. | Moderate‐intensity exercise 3‐4 times per week, including 1 supervised session (versus low‐intensity exercise in the form of a walking program 3‐4 times per week). All participants received a diet plan based on a modified diabetic diet. | 49 | / | |||
| 49. | A lifestyle intervention consisting of dietary counselling and exercise. The intervention involved dietary advise on 4 occasions (15, 20, 28 and 35 weeks) by a dietician. Energy requirements were personalised for each participant. Exercise intervention included a pedometer and free gym membership for 6 months. Participants were encouraged to do 30‐60 minutes moderate‐physical activity daily. In addition, at the gym they had 1 supervised aerobic class with a physiotherapist for 1 hour each week. | 304 | / | |||
BMI: body mass index
CHO: carbohydrate
GL: glycaemic load
IOM: Institute of Medicine
RDA: recommended dietary allowance
1. Diet and/or exercise interventions vs routine care in all pregnant women
Forty‐nine studies involving 11,444 participants contributed data to these analyses. A maximum of 36 studies contributed data to Comparison 1 analyses. Funnel plots were asymmetrical for most analyses.
1.1 Excessive gestational weight gain (GWG)
Diet or exercise, or both, interventions resulted in an average risk reduction of excessive GWG of 20% in favour of the intervention group (risk ratio (RR) 0.80, 95% confidence interval (CI) 0.73 to 0.87; participants = 7096; studies = 24; I² = 52%; Analysis 1.1). Reductions in favour of the intervention arms were consistent across the different types of intervention groups, except for the heterogenous group comprising 'diet counselling or other interventions', with the largest reduction occurring with 'supervised exercise and diet' interventions.
Sensitivity analysis
When we removed five studies with risk of bias concerns from the meta‐analysis (Cordero 2014; Di Carlo 2014; Ferrara 2011; Hui 2006; Ruchat 2012), heterogeneity was reduced and the average overall effect in favour of the intervention group was robust to the original result (RR 0.82, 95% CI 0.76 to 0.89; participants = 6437; studies = 19; I² = 40%). In addition, when we pooled data from exercise only interventions (supervised and unsupervised), findings were similar (RR 0.79, 95% CI 0.70 to 0.89; participants = 1901; studies = six; I² = 0%).
Quality of the evidence
We graded this evidence as high quality.
1.2 Mean gestational weight gain (GWG)
Thirty‐six studies reported this outcome; however, due to substantial heterogeneity we did not pool these data (Analysis 1.2). Thirteen studies reported significant differences in mean GWG between intervention and control groups in favour of the interventions, with five studies reporting mean differences in GWG in excess of 5 kg (Clapp 2002a; Di Carlo 2014; Thornton 2009; Quinlivan 2011; Wolff 2008). The remainder of studies found no significant difference in mean GWG between groups.
1.3 Low weight gain
Women in the intervention group were significantly more likely to experience low GWG compared with the control group (average RR 1.14, 95% CI 1.02 to 1.27; participants = 4422; studies = 11; I² = 3%; Analysis 1.3). Results according to types of interventions were not statistically significant, with wide confidence intervals and a consistent trend in favour of the control group. However, when data from the supervised and unsupervised exercise groups were combined the effect was of borderline statistical significance (RR 1.19, 95% CI 1.00 to 1.41; participants = 1565; studies = four; I² = 0%).
Sensitivity analysis
There were no serious risk of bias concerns for this analysis.
Quality of the evidence
We graded this evidence as moderate quality.
1.4 Preterm birth
There was no statistically significant difference between intervention and control groups for preterm birth outcomes (average RR 0.91, 95% CI 0.68 to 1.22; participants = 5923; studies = 16; I² = 16%; Analysis 1.4). Point estimates for exercise only interventions favoured the control groups; however, when data from the supervised and unsupervised groups were combined the trend was not statistically significant (RR 1.59, 95% CI 0.76 to 3.33; participants = 1358; studies = five; I² = 0%).
Sensitivity analysis
When two studies with risk of bias concerns were excluded from the analysis (Price 2012; Petrella 2013), results were similar to the original analysis (average RR 0.88, 95% CI 0.70 to 1.10; participants = 5800; studies = 14; I² = 0%).
Quality of the evidence
We downgraded this evidence to moderate quality due to risk of bias concerns arising from potential under‐reporting (in at least four studies, women at risk of preterm birth were withdrawn; see Risk of bias in included studies).
1.5 Pre‐eclampsia
There was no statistically significant difference between the intervention and control groups with regard to pre‐eclampsia (average RR 0.95, 95% CI 0.77 to 1.16; participants = 5330; studies = 15; I² = 0%; Analysis 1.5).
Quality of the evidence
We graded the quality of this evidence as high.
1.6 Hypertension (not prespecified)
Maternal hypertension occurred significantly more frequently in the control group compared with the intervention group (average RR 0.70, 95% CI 0.51 to 0.96; participants = 5162; studies = 11; I² = 43%; Analysis 1.6).
Sensitivity analysis and investigation of heterogeneity
When we excluded three studies (Petrella 2013; Price 2012; Stafne 2012) with risk of bias concerns, the result remained in favour of the interventions; however it was no longer statistically significant (RR 0.74, 95% CI 0.53 to 1.02; participants = 4314; studies = eight; I² = 44%). Heterogeneity could not be attributed to differences between the different types of interventions. We investigated heterogeneity further below, by subgrouping studies by participant risk group.
Quality of the evidence
We downgraded the evidence to low quality due to inconsistency and risk of bias concerns.
1.7 Induction of labour
There was no statistically significant difference between intervention and control groups for this outcome (average RR 1.06, 95% CI 0.94 to 1.19; participants = 3832; studies = eight; I² = 9%; Analysis 1.7).
Quality of the evidence
We graded the quality of this evidence as high.
1.8 Caesarean delivery
There was no statistically significant difference in the risk of caesarean section between intervention and control groups (average RR 0.95, 95% CI 0.88 to 1.03; participants = 7534; studies = 28; I² = 9%; Analysis 1.8); although the point estimate favoured a small reduction in favour of the intervention group. Effect estimates for supervised and unsupervised exercise interventions only, alone or combined, were robust to the overall findings. However, for the diet and exercise counselling interventions, the effect estimate approached statistical significance with a 13% reduction in caesarean delivery in the intervention group (RR 0.87, 95% CI 0.75 to 1.01; participants = 3406; studies = 9; I² = 15%; P = 0.06).
Sensitivity analysis
When we excluded two studies with risk of bias concerns (Di Carlo 2014; Price 2012), the results moved further toward the null (average RR 0.97, 95% CI 0.91 to 1.04; participants = 7323; studies = 26; I² = 2%).
Quality of the evidence
We graded the quality of this evidence as high, although effects may differ according to types of interventions.
1.9 and 1.10 Maternal postpartum weight retention (mean [kg] and rate)
Diet or exercise, or both, interventions on average were not associated with less postpartum weight retention in kilograms compared with the controls (average mean difference (MD) ‐1.12, 95% CI ‐2.49 to 0.25; participants = 818; studies = 7; I² = 55%; Analysis 1.9); however, pooled data from five studies indicated significantly lower rates of postpartum weight retention in the intervention group (average RR 0.78, 95% CI 0.63 to 0.97; participants = 902; studies = five; I² = 63%, Analysis 1.10).
Sensitivity analysis and investigation of heterogeneity
Time frames for these assessments ranged from six weeks to six months postpartum which may have accounted for the heterogeneity. Several studies had risk of bias concerns (mainly attrition bias) for these outcomes; therefore, we did not perform sensitivity analysis.
Quality of the evidence
We graded this evidence as low quality due to inconsistency and risk of bias concerns.
1.11 to 1.13 Behaviour modification outcomes (diet and physical activity)
Energy and fibre intake
Data on mean energy intake were available for 12 studies and revealed a statistically significant difference in energy intake (in kilojoules) between intervention and control groups (average MD ‐570.77, 95% CI ‐894.28 to ‐247.26; participants = 4065; studies = 12; I² = 73%;Analysis 1.11). Similarly, fibre intake in grams was significantly higher in the intervention group (MD 1.53, 95% CI 0.94 to 2.12; participants = 3466; studies = 8; I² = 0%; Analysis 1.12).
Physical activity score at 26 to 29 weeks
Women in the intervention group revealed higher physical activity scores on average compared with controls (average standardised mean difference (SMD) 0.40, 95% CI 0.18 to 0.61; participants = 2851; studies = 9; I² = 75%; Analysis 1.13).
Quality of evidence
We graded evidence relating to behaviour modification outcomes as low quality due to heterogeneity and risk of bias concerns, particularly detection (mainly self‐reported outcomes) and attrition bias.
1.14 Infant birthweight greater than 4000 g
There was no statistically significant difference in the risk of macrosomia (birthweight greater than 4000 g) between intervention and control groups overall (average RR 0.93, 95% CI 0.86 to 1.02; participants = 8598; studies = 27; I² = 0%, Analysis 1.14), although the trend favoured the intervention groups. For the 'supervised exercise' intervention group, the effect in favour of the intervention bordered on statistical significance (average RR 0.81, 95% CI 0.64 to 1.02; participants = 2445; studies = seven; I² = 0%; P = 0.07), but not when supervised and unsupervised exercise interventions were combined (RR 0.87, 95% CI 0.71 to 1.07; participants = 2674; studies = nine; I² = 0%).
Sensitivity analysis
Results were similar when we performed sensitivity analysis by excluding seven studies (Cordero 2014;Ferrara 2011; Luoto 2011; Murtezani 2014; Stafne 2012; Ruchat 2012) with risk of bias concerns from the analysis (average RR 0.92, 95% CI 0.82 to 1.04; participants = 7021; studies = 20; I² = 11%).
Quality of the evidence
We graded the evidence as high, although further research may reveal important differences between intervention types.
1.15 Infant birthweight greater than 90th centile
There was no statistically significant difference in the risk of large‐for‐gestational‐age infants between intervention and control groups (average RR 0.92, 95% CI 0.80 to 1.05; participants = 4525; studies = 18; I² = 0%; Analysis 1.15); however, the effect in the diet and exercise counselling group non‐significantly favoured the intervention (RR 0.87, 95% CI 0.74 to 1.02; participants = 2777; studies = 6; I2 = 0%).
Quality of the evidence
We graded the quality of this evidence as high.
1.16 Mean birthweight (g)
There was no statistically significant difference in mean birthweight between intervention and control groups (average MD 12.20, 95% CI ‐15.26 to 39.65; participants = 8350; studies = 29; I² = 44%; Analysis 1.16).
Sensitivity analysis and investigation of heterogeneity
There were many risk of bias concerns for this outcome (e.g. due to post‐randomisation exclusions of women with preterm birth in several studies) but the overall result remained fairly robust to exclusion of high‐risk studies.
Quality of the evidence
We graded the quality of the evidence as moderate due to inconsistency.
1.17 and 1.18 Infant birthweight less 2500 g or less than 10th centile
There was no statistically significant difference between groups with respect to birthweight less than 2500 g (average RR 0.88, 95% CI 0.67 to 1.14; participants = 4834; studies = 12; I² = 0%; Analysis 1.17) or small‐for‐gestational‐age infants (average (RR 1.09, 95% CI 0.61 to 1.94; participants = 662; studies = seven; I² = 0%, Analysis 1.18).
Quality of the evidence
We downgraded the quality of this evidence to moderate due to potential risk of bias concerns relating mainly to the limited reporting of this outcome.
1.19 Shoulder dystocia
There was no statistically significant difference in the risk of shoulder dystocia between intervention and control groups (average RR 1.02, 95% CI 0.57 to 1.83; participants = 3253; studies = four; I² = 8%, Analysis 1.19).
Quality of the evidence
We graded this evidence as moderate quality due to imprecision.
1.20 Neonatal hypoglycaemia
There was no statistically significant difference in the risk of neonatal hypoglycaemia between intervention and control groups (average RR 0.95, 95% CI 0.76 to 1.18; participants = 2601; studies = four; I² = 0%); Analysis 1.20).
Quality of the evidence
We graded this evidence as moderate quality due to indirectness (may not apply to all types of interventions).
1.21 Neonatal birth trauma
There was no statistically significant difference between intervention and control groups (average RR 0.89, 95% CI 0.35 to 2.30; participants = 2256; studies = two; I² = 0%; Analysis 1.21). Both included studies (Dodd 2014; Vesco 2013) were diet and exercise counselling interventions and were conducted in high‐risk populations.
Quality of the evidence
We graded this evidence as moderate quality due to imprecision.
1,22 Neonatal hyperbilirubinaemia
There was no statistically significant difference between intervention and control groups (average RR 0.83, 95% CI 0.62 to 1.10; participants = 2256; studies = two; I² = 0%, Analysis 1.22). Both included studies (Dodd 2014; Vesco 2013) were diet and exercise counselling interventions and were conducted in high‐risk populations.
Quality of the evidence
We graded this evidence as moderate quality due to indirectness (may not apply to all types of interventions).
1.23 Neonatal respiratory distress syndrome
Infants in the intervention group had a significantly reduced risk of experiencing respiratory distress than infants in the control group (average RR 0.47, 95% CI 0.26 to 0.85; participants = 2256; studies = two; I² = 0%; Analysis 1.23). Both included studies (Dodd 2014; Vesco 2013) were diet and exercise counselling interventions and were conducted in high‐risk populations.
Quality of the evidence
We graded this evidence as moderate quality due to indirectness (may not apply to all types of interventions).
1.24 Postpartum haemorrhage
There was no difference in this outcome between intervention and control groups (average RR 0.94, 95% CI 0.78 to 1.14; participants = 2901; studies = two; I² = 0%; Analysis 1.24).
Quality of the evidence
We graded this evidence as high quality.
2. Diet interventions (low glycaemic load (GL) diet) versus routine care
A maximum of five studies contributed data to this comparison (Clapp 2002a; Louie 2011; Moses 2014; Rhodes 2010; ROLO 2012).
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Excessive GWG: Low GL dietary interventions significantly reduced the risk of excessive GWG in the intervention group compared with the control group (RR 0.74, 95% CI 0.55 to 0.99; participants = 833; studies = two; I² = 46%; Analysis 2.1). The test for subgroup differences was not significant (Chi² = 1.30, df = 1 (P = 0.25), I² = 22.9%).
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Mean GWG: Due to substantial heterogeneity, we did not pool these data.
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Low GWG: Only one study contributed data (Louie 2011) and found no statistically significant difference between intervention and control arms (Analysis 2.3).
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Preterm birth: One study contributed data to two subgroups in this analysis. There was no statistically significant difference between intervention and control groups (average RR 0.33, 95% CI 0.11 to 1.02; participants = 804; studies = two; I² = 0%; Analysis 2.4; Test for subgroup differences: Chi² = 0.21, df = 1 (P = 0.65), I² = 0%).
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Caesarean delivery: Two studies contributed data to the high‐risk subgroup. There was no statistically significant difference between the intervention and control groups (average RR 0.99, 95% CI 0.33 to 3.01; participants = 133; studies = two; I² = 65%; Analysis 2.5).
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Infant birthweight greater than 4000 g: There was no statistically significant difference between the intervention and control groups (average RR 0.96, 95% CI 0.77 to 1.20; participants = 1472; studies = four; I² = 14%; Analysis 2.6; however, the test for subgroup differences suggested that subgroup results may differ in respect to this outcome, with more macrosomia babies born to high‐risk women in the intervention group (Chi² = 2.12, df = 1 (P = 0.15), I² = 52.9%).
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Pre‐eclampsia: no data available.
We graded the evidence relating to excessive GWG as moderate quality, and for the other outcomes analysed as low quality due to heterogeneity or imprecision and sparse data, therefore it is likely that further research may change these effect estimates.
3. Diet and exercise counselling versus routine care
A maximum of 13 studies contributed data to these meta‐analyses. To avoid duplication of data from Althuizen 2013 we did not combine subgroup data.
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Excessive GWG: Interventions reduced the incidence of excessive GWG in low‐risk participants (average RR 0.72, 95% CI 0.55 to 0.95; participants = 247; studies = 2; I² = 0%) and there was a trend towards a reduction in excessive GWG in the high‐risk subgroup (RR 0.85, 95% CI 0.71 to 1.02; participants = 2725; studies = nine; I² = 69%; Analysis 3.1; Test for subgroup differences: Chi² = 3.51, df = 2 (P = 0.17), I² = 43.0%). We downgraded this evidence to moderate due to heterogeneity.
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Mean GWG: Mean GWG in kg was reduced with the intervention for the mixed‐risk subgroup (MD ‐1.80, 95% CI ‐3.36 to ‐0.24; participants = 444; studies = three; I² = 76%) and the high‐risk subgroup (MD ‐0.71, 95% CI ‐1.34 to ‐0.08; participants = 2741; studies = 11; I² = 57%) but heterogeneity was high (Analysis 3.2). In the latter, this could be explained by the timing of the measurements, and when two studies that measured weight gain at less than 34 weeks were excluded, data were homogeneous and favoured no clear difference between the intervention and control groups (MD ‐0.15, 95% CI ‐0.44 to 0.15; participants = 2424; studies = nine; I² = 0%; Test for subgroup differences suggested a difference in effect between subgroups: Chi² = 5.44, df = 2 (P = 0.07), I² = 63.2%).
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Low GWG: There was no significant difference in low GWG on average overall (RR 1.23, 95% CI 0.89 to 1.72; participants = 2552; studies = five; I² = 49%; Analysis 3.3; Test for subgroup differences: Chi² = 0.07, df = 1 (P = 0.79), I² = 0%) or for subgroups; however the overall trend favoured the control group.
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Preterm birth: There was no significant difference in preterm birth on average overall (RR 0.94, 95% CI 0.57 to 1.55; participants = 3170; studies = seven; I² = 52%; Analysis 3.4) or for subgroups; Test for subgroup differences: Chi² = 0.32, df = 1 (P = 0.57), I² = 0%). We downgraded this evidence to low due to imprecision and heterogeneity.
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Pre‐eclampsia: There was no significant difference in pre‐eclampsia on average between intervention and control groups for the high‐risk population (average RR 1.06, 95% CI 0.79 to 1.43; participants = 2896; studies = seven; I² = 0%; Analysis 3.5). Only one study contributed events to the low‐risk subgroup.
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Caesarean delivery: Interventions reduced the incidence of caesarean section on average (RR 0.89, 95% CI 0.80 to 1.00; participants = 3406; studies = nine; I² = 3%; Analysis 3.6; P = 0.05; borderline statistical significance). This trend was consistent across risk subgroups; Test for subgroup differences: Chi² = 1.53, df = 2 (P = 0.46), I² = 0%.
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Infant birthweight greater than 4000 g: There was no statistically significant difference in macrosomia on average between intervention and control groups overall (RR 0.92, 95% CI 0.77 to 1.11; participants = 3705; studies = 10; I² = 7%; Analysis 3.7). or for the low‐risk or mixed‐risk subgroups. However, in the high‐risk subgroup an effect in favour of a reduction in macrosomia was of borderline statistical significance (average RR 0.85, 95% CI 0.73 to 1.00; participants = 3252; studies = nine; I² = 0%; P = 0.05) and the test for subgroup differences was statistically significant (Chi² = 3.86, df = 1 (P = 0.05), I² = 74.1%).
We graded the evidence for diet and exercise counselling interventions as moderate quality, except for the outcome preterm birth which we graded as low quality.
4. Exercise interventions versus routine care
A maximum of 13 studies contributed data to these analyses. Three studies (Kong 2014; Renault 2014; Ronnberg 2014) involved unsupervised (as opposed to supervised) exercise interventions and we performed sensitivity analyses to determine whether including unsupervised exercise intervention studies had an impact on the results. To avoid duplication of data, where individual studies contributed data to both risk subgroups (Ronnberg 2014; Ruiz 2013), we did not combine subgroup data.
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Excessive GWG: Exercise interventions significantly reduced this outcome consistently across risk subgroups with point estimates for low, mixed and high risk subgroups of 0.69, 0.77, and 0,84 respectively(Analysis 4.1). Test for subgroup differences were not significant: Chi² = 1.36, df = 2 (P = 0.51), I² = 0%.
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Mean GWG: When one study at a high risk of bias (Price 2012) was excluded from the mixed‐risk subgroup, the intervention was associated with a statistically significant reduction in mean weight gain in kg compared with the control in the mixed‐risk subgroup (MD ‐1.35, 95% CI ‐1.80 to ‐0.89; participants = 1134; studies = three; I² = 0%), and low risk subgroup (one study only), but not the high‐risk subgroup (MD ‐0.32, 95% CI ‐1.15 to 0.50; participants = 476; studies = four; I² = 0%); Analysis 4.2. Test for subgroup differences suggested a difference in effect between subgroups: Chi² = 5.78, df = 2 (P = 0.06), I² = 65.4%.
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Low GWG: There was an increase in low GWG of borderline statistical significance between intervention and control groups for the mixed risk subgroup (average RR 1.20, 95% CI 1.00 to 1.43; participants = 1336; studies = two; I² = 0%; P = 0.05) and low risk subgroup (one study only) but not the high‐risk subgroup (average RR 1.03, 95% CI 0.66 to 1.60; participants = 504; studies = three; I² = 0%; Analysis 4.3). Test for subgroup differences were not significant: Chi² = 0.98, df = 2 (P = 0.61), I² = 0%.
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Preterm birth: There was no statistically significant difference in preterm birth on average between intervention and control groups for the low risk (one study only), mixed risk (average RR 1.92, 95% CI 0.75 to 4.93; participants = 1129; studies = three; I² = 0%) or the high‐risk subgroup (average RR 1.34, 95% CI 0.51 to 3.55; participants = 504; studies = three; I² = 0%; Analysis 4.4); however the trend consistently favoured the control group. The test for subgroup differences was not significant: Chi² = 0.27, df = 1 (P = 0.60), I² = 0%.
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Pre‐eclampsia: There was no statistically significant difference in pre‐eclampsia overall between intervention and control groups (average RR 0.99, 95% CI 0.58 to 1.66; participants = 1253; studies = four; I² = 0%; Analysis 4.5) and subgroup findings were similar: Test for subgroup differences: Chi² = 0.51, df = 1 (P = 0.48), I² = 0%.
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Caesarean delivery: There was no statistically significant difference in caesarean delivery between intervention and control groups for low risk (one study only), mixed risk (average RR 0.96, 95% CI 0.76 to 1.22; participants = 2263; studies = six; I² = 24%) or the high‐risk subgroup (average RR 0.98, 95% CI 0.81 to 1.20; participants = 645; studies = five; I² = 0%; Analysis 4.6); . Test for subgroup differences: Chi² = 0.37, df = 2 (P = 0.83), I² = 0%.
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Infant birthweight greater than 4000 g: There was no statistically significant difference in macrosomia between intervention and control groups for the low‐risk (one study only), mixed‐risk (average RR 0.81, 95% CI 0.64 to 1.02; participants = 2445; studies = seven; I² = 0%) or the high‐risk subgroups (RR 0.65, 95% CI 0.22 to 1.91; participants = 504; studies = three; I² = 74%; Analysis 4.7 Test for subgroup differences: Chi² = 0.14, df = 1 (P = 0.71), I² = 0%. However, the trend across subgroups consistently favoured the intervention, and the effect for the mixed‐risk subgroup was of borderline statistical significance.(P = 0.07) Furthermore, when three studies with risk of bias concerns were excluded (Cordero 2014; Murtezani 2014; Stafne 2012), the RR for the mixed‐risk population clearly favoured the intervention group (average RR 0.56, 95% CI 0.36 to 0.88; participants = 1274; studies = eight; I² = 0%).
As the number of studies included in most analyses were few, we did not assess funnel plots. Including studies of unsupervised exercise did not have a significant impact on the results. We graded this evidence as moderate quality overall, except for the evidence on preterm birth (low quality) which was very imprecise and potentially subject to a serious risk of attrition and/or reporting bias.
5. Diet and supervised exercise interventions versus routine care
A maximum of five studies contributed data to these analyses; two studies contributed data to each of the mixed‐ and high‐risk subgroups, one study (Hui 2014) reported results separately for both subgroups, therefore we were able to pool these data.
-
Excessive GWG: Combined exercise and diet interventions significantly reduced excessive weight gain (average RR 0.75, 95% CI 0.61 to 0.92; participants = 689; studies = five; I² = 18%, Analysis 5.1; When one study at high risk of bias was excluded (Ruchat 2012), the test for subgroup differences suggested that there might be a difference in effect according to risk, with a smaller effect in the high‐risk subgroup: Test for subgroup differences: Chi² = 4.54, df = 2 (P = 0.10), I² = 55.9%.
-
Mean GWG: The interventions reduced mean GWG compared with controls (average MD ‐1.31, 95% CI ‐3.00 to 0.37; participants = 348; studies = three; I² = 43%; borderline significance, Analysis 5.2). However, the test for subgroup differences suggested that there might be a difference in effect according to risk,with a smaller effect in the high‐risk subgroup :Test for subgroup differences: Chi² = 4.90, df = 2 (P = 0.09), I² = 59.2%.
-
Low GWG: Only one study showing no difference contributed data to this outcome (Analysis 5.3).
-
Preterm birth: No data available
-
Pre‐eclampsia: Only one study showing no difference contributed data to this outcome (Analysis 5.4).
-
Caesarean delivery: There was no statistically significant difference in the risk of caesarean delivery between intervention and control groups (average RR 1.00, 95% CI 0.69 to 1.45; participants = 607; studies = three; I² = 0%; Analysis 5.5; Test for subgroup differences: Chi² = 0.29, df = 1 (P = 0.59), I² = 0%.
-
Infant birthweight greater than 4000 g: There was no statistically significant difference between groups for this outcome (RR 1.02, 95% CI 0.71 to 1.46; participants = 398; studies = three; I² = 0%; Analysis 5.6; Test for subgroup differences: Chi² = 0.33, df = 1 (P = 0.56), I² = 0%.
We graded this evidence from analyses as low‐to‐moderate quality due to imprecision (sparse data) and some inconsistencies.
6. Diet counselling only versus routine care
A maximum of seven heterogeneous studies contributed data to these analyses (Di Carlo 2014; Jeffries 2009; Laitinen 2009; Quinlivan 2011; Rae 2000; Thornton 2009; Wolff 2008).
-
Excessive GWG: We did not combine subgroup data for this analysis as one study contributed data to both subgroups. There was no statistically significant difference between intervention and control arms (Analysis 6.1). The test for subgroup differences showed that subgroup results were similar: Chi² = 0.49, df = 1 (P = 0.48), I² = 0%.
-
Mean GWG: Data for this outcome were very heterogeneous (I² greater than 90%) with four out of seven studies finding a difference in mean GWG of greater than 4 kg, with the other three studies finding little difference; therefore, we did not combine these data (Analysis 6.2).
-
Low GWG: Only one study contributed data (Laitinen 2009), which found that significantly more women in the intervention arm had low GWG compared with the control arm (Analysis 6.3).
-
Preterm birth: There was no statistically significant difference in the risk of preterm birth between intervention and control groups (average RR 0.67, 95% CI 0.26 to 1.73; participants = 591; studies = three; I² = 0%,Analysis 6.4); Test for subgroup differences: Chi² = 0.00, df = 1 (P = 0.99), I² = 0%.
-
Pre‐eclampsia: There was no statistically significant difference in the risk of pre‐eclampsia between intervention and control groups (RR 0.90, 95% CI 0.54 to 1.48; participants = 634; studies = four; I² = 0%; Analysis 6.5; Test for subgroup differences: Chi² = 2.05, df = 1 (P = 0.15), I² = 51.2%.
-
Caesarean section: There was no statistically significant difference in the risk of caesarean delivery between intervention and control groups (average RR 1.06, 95% CI 0.93 to 1.21; participants = 754; studies = five I² = 2%; Analysis 6.6; Test for subgroup differences: Chi² = 0.30, df = 1 (P = 0.59), I² = 0%).
-
Infant birthweight greater than 4000 g: There was no statistically significant difference in the risk of macrosomia between intervention and control groups when data from two studies conducted in high‐risk women were pooled (RR 1.81, 95% CI 0.88 to 3.72; participants = 349; studies = two; I² = 0%, Analysis 6.7).
We graded the evidence relating to these interventions as low quality overall due to heterogeneity and risk of bias concerns. As the number of studies included in most analyses were few, we did not assess funnel plots.
Discussion
Summary of main results
This updated review included 65 randomised controlled trials (RCTs) in total with 49 RCTs involving at least 11,444 participants contributing data to quantitative synthesis. Twenty RCTs were considered to be at moderate‐to‐high risk of bias. Where these studies contributed data (14 studies), we performed sensitivity analysis to determine how including these data impacted on the results. Diet interventions most commonly involved a low GL, diabetic, calorie‐controlled or low fat diet; exercise interventions were most commonly of moderate intensity involving walking, dance, or aerobic classes. Most included studies were conducted in developed countries. Overall findings are summarised in summary of findings Table for the main comparison. Diet or exercise,or both, interventions reduced the risk of excessive gestational weight gain (GWG) by an average of 20% (95% CI, 13 to 27%) overall. Data were moderately heterogeneous; however this overall effect was robust to sensitivity analysis and consistent across the different types of interventions, therefore we graded this evidence as high quality. The greatest effect on excessive GWG was noted for combined diet plus supervised exercise interventions.
Data for mean GWG were too heterogenous to pool and were inconsistent between, and frequently within, the different types of intervention groups, therefore, we did not pool these data. However, for subgroup analyses according to the risk of weight‐related complications, we pooled data if heterogeneity was mild or moderate, and downgraded the evidence accordingly. Limited evidence from diet and exercise counselling interventions, exercise only interventions, and diet and supervised exercise interventions suggested that there might be a difference in effect on mean weight gain according to risk, with a smaller effect in the high‐risk subgroups (low quality evidence).
Women receiving diet or exercise, or both interventions were more likely to experience low GWG than controls (average risk ratio (RR) 1.14, 95% confidence interval (CI) 1.02 to 1.27; participants = 4422; studies = 11; I² = 3; moderate‐quality evidence). We found no difference between intervention and control groups with regard to pre‐eclampsia ((RR 0.95, 95% CI 0.77 to 1.16; participants = 5330; studies = 15; I² = 0%; high‐quality evidence); however, maternal hypertension (not a pre‐specified outcome) was reduced in the intervention group compared with the control group overall (average RR 0.70, 95% CI 0.51 to 0.96; participants = 5162; studies = 11; I² = 43%; low‐quality evidence).
There was no clear difference between groups with regard to caesarean delivery overall (RR 0.95, 95% CI 0.88 to 1.03; participants = 7534; studies = 28; I² = 9%; high‐quality evidence); although the effect estimate suggested a small difference (5%) in favour of the interventions. In addition, for combined diet and exercise counselling interventions there was a 13% (‐1% to 25%) reduction in this outcome (borderline statistical significance).
We found no difference between groups with regard to preterm birth overall (average RR 0.91, 95% CI 0.68 to 1.22; participants = 5923; studies = 16; I² = 16%; moderate‐quality evidence); however limited evidence suggested that these effect estimates may differ according to the types of interventions, with a trend towards an increased risk for exercise‐only interventions.
We found no clear difference between intervention and control groups with regard to infant macrosomia overall (average RR 0.93, 95% CI 0.86 to 1.02; participants = 8598; studies = 27; I² = 0%; high‐quality evidence), although the effect estimate suggested a small difference (7% reduction) in favour of the intervention group. The largest effect size occurred in the supervised exercise‐only intervention group (RR 0.81, 95% CI 0.64 to 1.02; participants = 2445; studies = seven; I² = 0%), which approached statistical significance (P = 0.07). Furthermore, in subgroup analysis by risk, high‐risk women receiving combined diet and exercise counselling interventions experienced a 15% reduced risk of infant macrosomia (average RR 0.85, 95% CI 0.73 to 1.00; participants = 3252; studies = nine; I² = 0; P = 0.05; moderate‐quality evidence).
There were no differences in the risk of poor neonatal outcomes including shoulder dystocia, neonatal hypoglycaemia, hyperbilirubinaemia, or birth trauma (all moderate‐quality evidence) between intervention and control groups; however, infants of high‐risk women had a reduced risk of respiratory distress syndrome if their mothers were in the intervention group (RR 0.47, 95% CI 0.26 to 0.85; participants = 2256; studies = two; I² = 0%; moderate‐quality evidence).
The effect on behaviour modification outcomes, i.e. dietary and physical activity outcomes, in general, favoured the intervention groups; however, these outcomes were at high risk of bias and mainly reflected whether the implementation of the interventions was successful. Low‐quality evidence suggested that the beneficial effects of interventions on weight control during pregnancy may be sustained postpartum. For certain outcomes, e.g. childhood weight, we found no data for meta‐analysis.
For a brief summary of the effects of the different types of interventions on the main outcomes, see summary of findings Table 2.
Overall completeness and applicability of evidence
There is a growing body of evidence to support the use of diet or exercise, or both, interventions to reduce excessive GWG in pregnancy. We found high‐quality evidence of other related health benefits for women and newborns, applicable to most pregnant women who are otherwise healthy, irrespective of their prepregnancy weight. Exercise appears to be an important component of weight reduction interventions; however the evidence with regard to the effect of exercise on the risk of preterm birth is of a moderate quality and this outcome should be rigorously evaluated in future studies to enable the establishment of appropriate guidelines.The evidence is not applicable to women with specific contraindications to exercise in pregnancy or pre‐existing medical conditions. Although we included four studies conducted in women with gestational diabetes, data were sparse and it is not clear whether the review findings apply to women with this condition. More research (qualitative and quantitative) to improve outcomes in this high risk group is needed.
Most included studies were carried out in developed countries and it is not clear whether these results are widely applicable to lower income settings with fewer human and financial resources. More research is needed in these less developed settings, where obesity is increasingly a major health issue. Innovative interventions utilising mobile‐phone technology (e.g. Pollak 2014) are of interest and further developments in this area are anticipated.
Quality of the evidence
Using the GRADE approach, we considered the quality of the evidence relating to excessive GWG as high quality. Although moderate heterogeneity was present, we upgraded our assessment of evidence quality from moderate‐to‐high quality as findings were precise and robust to sensitivity analysis. We graded the evidence with regard to the risk of low GWG as high quality as these estimates were consistent and precise across included studies. We downgraded the evidence with regard to preterm birth (no statistically significant difference) to moderate due to risk of bias concerns from attrition and under‐reporting. We graded the quality of the evidence for pre‐eclampsia, caesarean delivery and macrosomia as high quality and most other outcomes, as moderate quality.
We downgraded some evidence due to heterogeneity. Many factors might have contributed to this heterogeneity including obvious and subtle differences in the types of interventions, types of participants (e.g. BMIs, parity, age), delivery of the intervention (e.g. whether the intervention was incorporated into antenatal visits or delivered separately by a dietician), timing of the measurements (e.g. weight gain assessed at 34 versus 38 weeks), timing of commencement of the intervention (e.g. first, second or third trimester), sample sizes, etc. An in‐depth evaluation of individual interventions was beyond the scope of this review; however, our impression was that the more intensely monitored/supervised the intervention, the better the study results.
Potential biases in the review process
We took a number of steps to minimise bias in the review process by including all relevant RCTs, with two review authors independently classifying them, extracting data, and resolving disagreements by discussion with the other authors. Where expected outcome data were missing we made an effort to contact the study investigators, and we included adjusted data from cluster‐RCTs where possible. In the previous version of this review we included two quasi‐RCTs (Bechtel‐Blackwell 2002; Moses 2006), which we excluded for this update after deciding to limit the review to RCTs. Due to issues of scope and relevance, we also excluded two early studies of appetite suppressant drugs that had been included in the original review (Boileau 1968; Silverman 1971).
We considered it clinically meaningful to produce overall estimates of average effects across all studies where possible, organised by the type of intervention, using random effects methods. Interventions were often multifaceted and were quite heterogeneous in approach, for example, in the timing, duration, intensity, content and delivery. Some studies evaluated more than one type of intervention. Dodd 2014, for example, was mainly a diet and exercise counselling intervention study and we included it as such; however, 26% of participants in the intervention arm underwent a supervised walking exercise as part of a nested RCT. Where possible, when heterogeneity existed between studies evaluating apparently similar interventions, which could not be explained by our 'Risk of bias' assessment, we attempted to identify the possible reasons for it. In addition, although we made distinctions between types of diet and exercise interventions according to whether the exercise component was supervised or not, the results were robust on exploratory analyses when all combined diet and exercise intervention data for the main outcomes were pooled.
Two studies compared higher impact interventions with lower impact interventions (Ruchat 2012; Thornton 2009), and several studies of low GL diets compared the intervention with an alternative (low‐fat, moderate/high GL or conventional healthy eating) diet (Rhodes 2010; Louie 2011; Moses 2009; Moses 2014). For these studies, we pooled the data of the alternative intervention with the control group which, in most other studies, comprised routine care. This may have contributed to heterogeneity in the meta‐analyses and might have led to an underestimation of the summary effect of the intervention. Clapp 2002b compared different exercise intensities at different stages of pregnancy (before versus after 20 weeks' gestation) and found that low‐intensity exercise in early pregnancy moving on to higher‐intensity exercise after 20 weeks was associated with a lower pregnancy weight gain than either high‐ followed by low‐intensity exercise or moderate‐intensity exercise throughout. We did not explore the impact of higher‐ versus lower‐intensity interventions, which may have provided important information for exercise interventions and certain outcomes, such as preterm birth. This was largely due to a sparseness of data and time constraints.
Several studies reported maternal 'hypertension', and not pre‐eclampsia, and we extracted and analysed these data. This was not prespecified in the protocol (see Differences between protocol and review); however, we made every effort to minimise bias in this process, and consider the pooled findings to be of value, albeit low‐quality evidence. The effect estimates for hypertension differed from those for pre‐eclampsia with a consistent trend towards a reduction in hypertension, but not pre‐eclampsia, in intervention arms.
We did not perform meta‐analyses according to BMI classification of degree of obesity, although several studies stratified results by BMI (overweight or obese or morbidly obese). In one study that reported these BMI categories separately (Kong 2014), we combined these data for use in our meta‐analysis. For studies of high‐risk women that reported combined and separate results for overweight and obese categories (Harrison 2013; Petrella 2013; Nascimento 2012), we extracted all data but used the combined data only in our meta‐analyses. It is possible that certain types of interventions may be more effective for different high‐risk BMI categories and we may try to address this in future versions of this review.
Behaviour modification outcomes may have been subject to potential reviewer bias. Multiple and varied behaviour modification outcomes were reported by the various investigators and we pre‐specified only three outcomes (energy intake, fibre intake and a physical activity measure) for inclusion in the review. In addition, numerous different scales and time points were reported by study investigators, a narrative discussion of which is beyond the scope of this review. However, in many respects, behaviour outcome measures are measures of the intervention rather than the effect of the intervention and we consider this outcome to be a poor (indirect) measure of effectiveness of an intervention. In addition, these outcomes were subject to other serious risk of bias concerns, including detection (often self‐reported) and attrition bias.
Agreements and disagreements with other studies or reviews
A 2012 UK Health Technology Assessment review (Thangaratinam 2012) included 30 RCTs in a meta‐analysis of GWG and reported an overall reduction (± 1 kg) in mean GWG in the intervention group compared with controls.Two other systematic reviews (Ronnberg 2010; Skouteris 2010) that included RCTs and non‐randomised studies also reported GWG outcomes in favour of the interventions. Thangaratinam 2012 reported that the largest weight reduction occurred with dietary interventions (a mean reduction of 3.36 kg), which were also effective at reducing gestational hypertension, pre‐eclampsia, preterm birth and shoulder dystocia. Due to substantial heterogeneity, we did not pool mean weight gain data and our review does not agree with these findings. Thangaratinam 2012 utilised data from non‐randomised studies to provide evidence on adverse effects; however, most of these data were derived from studies on extreme diet and famine and therefore have limited applicability. Randomised controlled trial data on adverse effects remain sparse and we were unable to provide additional evidence in this regard.
We were unable to show a reduced risk of macrosomia overall, as was shown in Thangaratinam 2012, although our findings did not exclude a small reduction in risk. In addition, our findings suggested greater reductions may be achieved for high‐risk women who received combined diet and exercise interventions, and women receiving supervised exercise‐only interventions. Dodd 2014, the largest study included in this review additionally reported the rate of very high birthweight babies (greater than 4500 g), finding a significant reduction in this outcome in the intervention arm; however, we did not include this outcome.
We found limited evidence that certain interventions were somewhat less effective in reducing GWG in high‐risk women compared with the lower‐risk group. To our knowledge this has not been previously shown and requires further investigation. Several of our included studies reported gestational diabetes as an outcome and exploratory analysis suggested that the effect of diet and exercise interventions on this outcome might be significant. We did not modify our protocol to include this important outcome as a separate Cochrane review on the topic is in progress (Crane 2013).
Methodological quality summary: review authors' judgements about each methodological quality item for each included study.
Methodological quality graph: review authors' judgements about each methodological quality item presented as percentages across all included studies.
Comparison 1 All diet and/or exercise interventions vs standard/other care, Outcome 1 Excessive weight gain.
Comparison 1 All diet and/or exercise interventions vs standard/other care, Outcome 2 Weight gain (kg).
Comparison 1 All diet and/or exercise interventions vs standard/other care, Outcome 3 Low weight gain.
Comparison 1 All diet and/or exercise interventions vs standard/other care, Outcome 4 Preterm birth.
Comparison 1 All diet and/or exercise interventions vs standard/other care, Outcome 5 Pre‐eclampsia.
Comparison 1 All diet and/or exercise interventions vs standard/other care, Outcome 6 Hypertension (not prespecified).
Comparison 1 All diet and/or exercise interventions vs standard/other care, Outcome 7 Induction of labour.
Comparison 1 All diet and/or exercise interventions vs standard/other care, Outcome 8 Caesarean delivery.
Comparison 1 All diet and/or exercise interventions vs standard/other care, Outcome 9 Postpartum weight retention (kg).
Comparison 1 All diet and/or exercise interventions vs standard/other care, Outcome 10 Postpartum weight retention (n/N; investigator defined time frame).
Comparison 1 All diet and/or exercise interventions vs standard/other care, Outcome 11 Energy intake (kj).
Comparison 1 All diet and/or exercise interventions vs standard/other care, Outcome 12 Fibre intake (g).
Comparison 1 All diet and/or exercise interventions vs standard/other care, Outcome 13 Physical activity score (26‐29 weeks).
Comparison 1 All diet and/or exercise interventions vs standard/other care, Outcome 14 Macrosomia Infant birthweight > 4000 g.
Comparison 1 All diet and/or exercise interventions vs standard/other care, Outcome 15 Infant birthweight > 90th centile.
Comparison 1 All diet and/or exercise interventions vs standard/other care, Outcome 16 Birthweight (g) (not prespecified).
Comparison 1 All diet and/or exercise interventions vs standard/other care, Outcome 17 Infant birthweight < 2500 g.
Comparison 1 All diet and/or exercise interventions vs standard/other care, Outcome 18 Infant birthweight < 10th centile.
Comparison 1 All diet and/or exercise interventions vs standard/other care, Outcome 19 Shoulder dystocia.
Comparison 1 All diet and/or exercise interventions vs standard/other care, Outcome 20 Neonatal hypoglycaemia.
Comparison 1 All diet and/or exercise interventions vs standard/other care, Outcome 21 Birth trauma.
Comparison 1 All diet and/or exercise interventions vs standard/other care, Outcome 22 Neonatal hyperbilirubinaemia.
Comparison 1 All diet and/or exercise interventions vs standard/other care, Outcome 23 Neonatal respiratory distress syndrome.
Comparison 1 All diet and/or exercise interventions vs standard/other care, Outcome 24 Postpartum hemorrhage.
Comparison 2 Diet intervention (low GI diet) vs standard/other care, Outcome 1 Excessive weight gain.
Comparison 2 Diet intervention (low GI diet) vs standard/other care, Outcome 2 Weight gain (kg).
Comparison 2 Diet intervention (low GI diet) vs standard/other care, Outcome 3 Low weight gain.
Comparison 2 Diet intervention (low GI diet) vs standard/other care, Outcome 4 Preterm birth.
Comparison 2 Diet intervention (low GI diet) vs standard/other care, Outcome 5 Caesarean delivery.
Comparison 2 Diet intervention (low GI diet) vs standard/other care, Outcome 6 Macrosomia (Infant birthweight > 4000 g).
Comparison 3 Diet and exercise counselling vs standard/other care, Outcome 1 Excessive weight gain.
Comparison 3 Diet and exercise counselling vs standard/other care, Outcome 2 Weight gain (kg).
Comparison 3 Diet and exercise counselling vs standard/other care, Outcome 3 Low weight gain.
Comparison 3 Diet and exercise counselling vs standard/other care, Outcome 4 Preterm birth.
Comparison 3 Diet and exercise counselling vs standard/other care, Outcome 5 Pre‐eclampsia.
Comparison 3 Diet and exercise counselling vs standard/other care, Outcome 6 Caesarean delivery.
Comparison 3 Diet and exercise counselling vs standard/other care, Outcome 7 Macrosomia (Infant birthweight > 4000 g).
Comparison 4 Exercise vs standard/other care, Outcome 1 Excessive weight gain.
Comparison 4 Exercise vs standard/other care, Outcome 2 Weight gain (kg).
Comparison 4 Exercise vs standard/other care, Outcome 3 Low weight gain.
Comparison 4 Exercise vs standard/other care, Outcome 4 Preterm birth.
Comparison 4 Exercise vs standard/other care, Outcome 5 Pre‐eclampsia.
Comparison 4 Exercise vs standard/other care, Outcome 6 Caesarean delivery.
Comparison 4 Exercise vs standard/other care, Outcome 7 Macrosomia (Infant birthweight > 4000 g).
Comparison 5 Diet and supervised exercise vs standard/other care, Outcome 1 Excessive weight gain.
Comparison 5 Diet and supervised exercise vs standard/other care, Outcome 2 Weight gain (kg).
Comparison 5 Diet and supervised exercise vs standard/other care, Outcome 3 Low weight gain.
Comparison 5 Diet and supervised exercise vs standard/other care, Outcome 4 Pre‐eclampsia.
Comparison 5 Diet and supervised exercise vs standard/other care, Outcome 5 Caesarean delivery.
Comparison 5 Diet and supervised exercise vs standard/other care, Outcome 6 Macrosomia (Infant birthweight > 4000 g).
Comparison 6 Diet counselling/other vs standard/other care, Outcome 1 Excessive weight gain.
Comparison 6 Diet counselling/other vs standard/other care, Outcome 2 Weight gain (kg).
Comparison 6 Diet counselling/other vs standard/other care, Outcome 3 Low weight gain.
Comparison 6 Diet counselling/other vs standard/other care, Outcome 4 Preterm birth.
Comparison 6 Diet counselling/other vs standard/other care, Outcome 5 Pre‐eclampsia.
Comparison 6 Diet counselling/other vs standard/other care, Outcome 6 Caesarean delivery.
Comparison 6 Diet counselling/other vs standard/other care, Outcome 7 Macrosomia (Infant birthweight > 4000 g).
| All diet and/or exercise interventions compared to standard/other care for preventing excessive weight gain in pregnancy | ||||||
| Patient or population: pregnant women | ||||||
| Outcomes | Illustrative comparative risks* (95% CI) | Relative effect | No of Participants | Quality of the evidence | Comments | |
| Assumed risk | Corresponding risk | |||||
| Standard/other care | All diet and/or exercise interventions | |||||
| Excessive weight gain | Study population | RR 0.80 | 7096 | ⊕⊕⊕⊕ | ||
| 453 per 1000 | 362 per 1000 | |||||
| Mean GWG (kg) | Mean difference not estimated | Due to substantial heterogeneity among studies, we did not consider the pooled estimate to be meaningful. Limited subgroup analyses suggested that effect estimates might differ according to risk group. | ||||
| Low weight gain | Study population | RR 1.14 | 4422 | ⊕⊕⊕⊝ MODERATE2 | ||
| 227 per 1000 | 259 per 1000 | |||||
| Preterm birth | Study population | RR 0.91 | 5923 | ⊕⊕⊕⊝ | ||
| 57 per 1000 | 52 per 1000 | |||||
| Pre‐eclampsia | Study population | RR 0.95 | 5330 | ⊕⊕⊕⊕ | ||
| 66 per 1000 | 62 per 1000 | |||||
| Caesarean delivery | Study population | RR 0.95 | 7534 | ⊕⊕⊕⊕ | ||
| 288 per 1000 | 274 per 1000 | |||||
| Macrosomia Infant birthweight > 4000 g | Study population | RR 0.93 | 8598 | ⊕⊕⊕⊕ | ||
| 178 per 1000 | 166 per 1000 | |||||
| *The basis for the assumed risk was the median control group risk across studies. The corresponding risk (and its 95% confidence interval) is based on the assumed risk in the comparison group and the relative effect of the intervention (and its 95% CI). | ||||||
| GRADE Working Group grades of evidence | ||||||
| 1Although heterogeneity was moderate‐to‐high (I² = 52%), the RR was robust to sensitivity analysis, which was associated with less heterogeneity (I² ‐ 40%), therefore we did not downgrade this evidence 2Downgraded due to imprecision of results according to types of intervention (‐1) 3Downgraded due to risk of bias concerns and concerns that data could not be included in the analysis due to studies excluding women with or at risk of preterm birth post‐randomisation from analysis (Cordero 2014; Di Carlo 2014; Murtezani 2014; Rauh 2013). This omission might have led to publication bias in the review's 'preterm birth' outcome (‐1) | ||||||
| Intervention type | Risk group | EGWG | Mean GWG | Low GWG | Preterm birth | Caesarean | Pre‐eclampsia | Macrosomia |
| All interventions (max 36 studies) | Overall | 20% reduction (13 to 27%) | Not estimated | 14% increase (2% to 27%) | NS | NS | NS | BS (7% reduction, ‐2% to 14%) |
| Low GL diet (max 5 studies) | Overall | 23% reduction (9% to 33%) | Not estimated | NS | BS in favour of the intervention | NS | NA | NS |
| Low | 40% reduction (6% to 52%) | NS | NS | NS | NS | NA | NA | |
| Mixed | 21% reduction (1 study) | NS | NA | NS | NS | NA | NS | |
| High | NS | NS | NS | NS | NS | NA | NS | |
| Diet and exercise counselling (max 13 studies) | Overall | 14% reduction (2% to 25%) | Not estimated | NS | NS | BS (13% reduction; ‐1% to 25%) | NS | NS |
| Low | 28% reduction (5% to 45%) | NS | NS | NS | NS | NS | NS | |
| Mixed | NS | 1.80 kg reduction (0.24 to 3.36 kg) | NA | NS | BS (34% reduction; ‐5% to 59%) | NA | NS | |
| High | NS | 0.71 kg reduction (0.08 to 1.34) | NS | NS | BS (11% reduction; ‐4 to 24%) | NS | 15% reduction (0% to 27%) | |
| Exercise (supervised or unsupervised) only (max 10 studies) | Overall | 21% reduction (11% to 30%) | Not estimated | BS (19% increase; 0% to 41%) | NS | NS | NS | NS |
| Low | BS (31%; ‐2 to 53%) | 1.50 kg reduction (0,92 to 2.08 kg; one study only) | 29% increase; 6% to 42%) | BS (one study) | NS | NA | ||
| Mixed | 23% reduction (12% to 34%) | 1.35 kg reduction (0.89 to 1.80) | NS | NS | NS | NS | BS* (19% reduction; ‐2% to 36%) | |
| High | 16% reduction (5% to 27%) | NS | NS | NS | NS | NS | NS | |
| Unsupervised exercise only (max 3 studies) | Overall | 17% reduction (3% to 29%) | Not estimated | NS | NS | NS | NS | NS |
| Supervised exercise only (max 7 studies) | Overall | 25% reduction (11% to 37%) | Not estimated | BS (21% increase; ‐1% to 52%) | NS (trend in favour of control) | NS | NS | BS (19% reduction;‐2% to 36%) |
| Diet and supervised exercise (max 5 studies) | Overall | 29% reduction (15% to 41%) | NS | NS | NA | NS | NS | NS |
| Low | NS | 3.33 kg reduction (1,21 to 5.45; one study only) | NA | NA | Not estimable | NA | NA | |
| Mixed | 36% reduction (16% to 52%) | 1.69 kg reduction (0.11 to 3.48) | NS | NA | NS | NA | NS | |
| High | NS | NS | NA | NA | NS | NA | NS | |
| Diet counselling/other (max 7 studies) | Overall | NS | Not estimated | NS | NS | NS | NS | NS |
| Mixed | NS | NA | NA | NS | NS | NS | NA | |
| High | NS | NA | NA | NS | NS | NS | NS | |
| Finding are presented with reference to the intervention group * Sensitivity analysis suggested that there may be a statistically significant difference in favour of the intervention for the mixed‐risk subgroup. Abbreviations: NA = not available; NS = not statistically significant (P ≥ 0.05); BS = borderline significance | ||||||||
| Number | Study ID | Experimental intervention (unless otherwise stated, the control intervention was routine care) | Participants analysed | Contributed data | ||
| Low risk | Mixed risk | High risk | ||||
| Diet counselling/other | ||||||
| 1 | The intervention involved a supervised personalised diet plan meeting both personal preferences and specific gestational needs with the average caloric intake being 1916 kcal. The only fat allowed was olive oil. Participants in the intervention group underwent monthly follow‐up appointments with a dietician who monitored their weight gain and discussed issues. Control group received standard brochure on healthy eating. | 120 | / | |||
| 2. | Women were given a personalised weight measurement card, advised of their optimal gestational weight gain based on their BMI at the time of recruitment and the United States IOM guidelines, and instructed to record their weight at 16, 20, 24, 28, 30, 32 and 34 weeks' gestation. | 236 | / | / | ||
| 3. | Dietary counselling was given by a dietitian at each study visit and aimed to modify dietary intake to conform with that currently recommended, particular attention being paid to the quality of dietary fat. Study visits took place 3 times during pregnancy and at 1, 6 and 12 months postpartum. | 171 | / | |||
| 4. | This was a multi‐faceted intervention that included weighing on arrival and a brief dietary intervention by a food technologist at every antenatal visit. Other aspects of the intervention involved continuity of care provider and psychological assessment. | 124 | / | |||
| 5. | The intervention comprised instruction in a moderately energy restricted diabetic diet providing between 1590‐1776 kcal (70% RDA). | 117 | / | |||
| 6. | Participants were counselled in nutrition and monitored by a registered dietitian and given a detailed nutrition program similar to a diabetic diet. | 232 | / | |||
| 7. | Intervention comprise a healthy diet according to the official Danish dietary recommendations (% fat, protein, CHO, 30%, 15%‐20%, 50%‐55%). The energy intake was restricted based on individually estimated energy requirements and estimated energetic cost of fetal growth. | 50 | / | |||
| Low GL diet | ||||||
| 8. | Participants were randomised to either a low‐glycaemic diet (aboriginal diet) or high‐glycaemic diet (cafeteria diet). | 20 | / | |||
| 9. | Intervention was a healthy low‐GL diet of protein (15%‐25%), fat (25%‐30%) and carbohydrate (40%‐45%) (versus healthy high‐fibre diet with moderate GL, similar to population average). Participants attended at least 3 face‐to‐face visits with the study dietician for monitoring adherence and encouragement. Intervention began after 29th week. | 92 | / | |||
| 10. | Low‐GL diet versus high‐GL diet. The dietary advice by dietitian was individualised with specific mention of the energy and nutrient balance to achieve normal weight gain during the 3rd trimester. | 63 | / | |||
| 11. | The intervention involved a low glycaemic diet from 12 to 16 weeks' gestation for the remainder of pregnancy (compared with conventional healthy eating). Women received a detailed dietary education tailored for the group assignment at baseline ‐ there were no difference in the macronutrient distribution in the diets, only the substitution of carbohydrate‐rich foods with low GL alternatives in the experimental group. Information booklets were provided. 4 contact points with a research dietician were planned (first visit, phone call, midway and final visits) to collect data and ensure adherence. | 576 | / | |||
| 12. | Nutrition education, dietary counselling, and a low‐GL diet (vs a low‐fat diet). | 50 | / | |||
| 13. | Low‐GL dietary intervention given by a dietitian involving 1 dietary education session lasting 2 hours in groups of 2 ‐6 women at baseline. Follow‐up reinforcement sessions were held at 28 and 34 weeks' gestation. Women also received written resources about low‐GL foods. | 759 | / | / | / | |
| Diet and exercise counselling | ||||||
| 14. | The intervention involved counselling by members of the research team consisting of 5 x 15 minute sessions on weight, physical activity and diet. Interventions were face‐to‐face at 18, 22, 30, and 36 weeks' gestation, with a telephone session at 8 weeks postpartum. Counsellors discussed how to control weight gain during and after pregnancy, and how to maintain a healthy lifestyle. | 219 | / | / | ||
| 15 | At the initial visit, participants met with a registered dietician to receive a standardised counselling session, including information on pregnancy‐specific dietary and lifestyle choices. Participants were instructed to engage in moderate‐intensity exercise at least 3 times per week and preferably 5 times per week. Weight gain was reviewed at each routine antenatal visit. | 100 | / | |||
| 16. | Comprehensive dietary and lifestyle intervention (counselling) (n = 1108) Intervention involved meetings and home visits with advice on dietary, exercise, and behavioural strategies delivered by a dietician and trained research assistants. Exercise advice primarily encouraged women to increase their amount of walking and incidental activity. | 2212 | / | |||
| 17. | Lifestyle intervention involved 3 in‐person sessions and up to 15 telephone calls with counselling re diet, physical activity and breast‐feeding up to 12 months postpartum. The intervention was delivered by 2 dietitians. Participants were encouraged to engage in moderate‐intensity physical activity for 150 minutes per week and received written materials about food size, foods with low GL or low fat, and how to read food labels were discussed, | 197 | / | |||
| 18. | 2 intervention arms: 1 involved a brochure only, the other involved a brochure and counselling by a trained nutritionist in 3 group sessions. A maximum of 5 women were brought together in these 1‐hour sessions, which were scheduled at 15, 20, and 32 weeks of pregnancy. The sessions provided participants with recommendations on a balanced, healthy diet, and physical activity specifically designed for the study to limit weight gain. | 124 | / | |||
| 19. | Intervention provided dietary advice, simple healthy eating, and "physical activity messages" and weight gain self‐monitoring. Also included "regular self‐weighing as a key behavioural strategy". | 203 | / | |||
| 20. | A lifestyle intervention consisting of a culturally and linguistically modified, motivationally targeted, individually tailored 6‐month prenatal programme. Educators encouraged women to achieve guidelines for physical activity, decrease saturated fat and increase dietary fibre. The intervention consisted of 6 monthly in‐person behavioural counselling sessions and 5 telephone booster sessions with follow‐up to 6 weeks postpartum. Women were encourage to achieve ≥ 30 minutes of moderate‐intensity activity on most days of the week through walking and developing a more active lifestyle. | 68 | / | |||
| 21. | The intervention was delivered at regularly scheduled clinic visits by nurses with training in nutrition and physical fitness. The nurse discussed with each participant how to design an individualised diet and physical activity plan. The intervention consisted of 6 1‐to‐1 counselling sessions: 1 primary session (about 30–40 minutes) at the 16‐week gestation visit, and 5 1‐to‐1 booster sessions (at 28 gestational weeks, 36–38 gestational weeks, before hospital discharge after a 3 to 7‐day stay, 6 weeks' postpartum and 3 months postpartum). After each clinic visit, women in the experimental groups were sent a personalised graph of their weight changes. At the 1st session, the experimental groups also received a researcher‐prepared brochure that provided detailed information on weight management goals during pregnancy and postpartum. | 160 | / | |||
| 22. | Individual dietary advice tailored to each participant at 6 visits to include a low fat diet rich in vegetables, fruit and berries. Moderate‐intensity physical exercise was encouraged at 6 exercise counselling sessions. | 60 | / | |||
| 23. | Individual counselling on physical activity and diet and weight gain. At the first visit the recommendations for gestational weight gain were discussed and an appropriate weight gain graph was selected to guide the participant in monitoring her weight gain. Physical activity counselling was implemented at 8–12 weeks' gestation and the dietary counselling session occurred at 16–18 weeks' gestation. Physical activity counselling was enhanced at 4, and diet counselling at 3 subsequent visits. | 399 | / | |||
| 24. | Lifestyle intervention involving a caloric restricted diet (1500 kcal/day) and mild exercise 30 minutes/day, 3 times per week monitored by a pedometer. | 63 | / | |||
| 25. | The Fit for Delivery intervention included a face‐to‐face visit with an interventionist at the onset of treatment who discussed appropriate weight gains during pregnancy, physical activity (30 minutes of walking most days of the week), and calorie goals (20 kcal/kg). Emphasis was placed on decreasing high fat foods, increasing physical activity, and daily self‐monitoring. Women also received personalised weight graphs after each clinic visit, automated supportive postcards and 3 supportive phone calls. | 401 | / | / | ||
| 26. | Intervention conducted at routine clinic visits by staff with training in nutrition or psychology involved education about weight gain, healthy eating, and exercise, and individual graphs of their weight gain. After each clinic visit, women were sent a personalised graph of their weight gain. | 110 | / | / | ||
| 27. | A lifestyle intervention (diet plus exercise) involving 1 1‐to‐1 counselling session with a health trainer and then weekly group sessions for 8 consecutive weeks from 19 weeks' gestation. Sessions delivered by health trainers involved diet and exercise advice informed by psychological models of health behaviour. Dietary advice focused on increased consumption of foods with a low‐dietary GL, and reduction of saturated fats. Physical activity advice encouraged women to increase daily walking activity at moderate‐intensity level, setting goals monitored by a pedometer. Women also received a DVD of a pregnancy specific exercise regimen. | 154 | / | |||
| 28. | A 3‐arm study with 2 intervention groups. 1 intervention involved unsupervised exercise only (women were given a pedometer), the other involved diet and exercise counselling only. The diet and exercise intervention included follow‐up on a hypocaloric Mediterranean‐style diet. Instruction was given by a dietician every 2 weeks with alternating outpatient visits and phone calls, including weight measurement, encouragement and correcting advice on exercise and diet. | 389 | / | |||
| 29. | Intervention involved a 45‐minute diet consultation with an individualised caloric goal, a second individualised session, weekly group meetings with weigh ins, food/activity logs. Women are encouraged to accumulate at least 30 minutes of moderate‐intensity activity per day. Pedometers recorded steps with a target of 10,000 steps daily and were only provided to the intervention group. | 114 | / | |||
| Unsupervised exercise intervention | ||||||
| 30. | Unsupervised exercise intervention involved a walking program on treadmill or other setting for a minimum of 150 min/week. Women were loaned treadmills for the study and steps monitored. | 42 | / | |||
| 31. | A 3‐arm study with 2 intervention groups. 1 intervention involved unsupervised exercise only (women were given a pedometer), the other involved diet and exercise counselling. The physical activity intervention included encouragement or increase physical activity, aiming at a daily step count of 11,000, monitored by pedometer assessment on 7 consecutive days, every 4 weeks. | 389 | / | |||
| 32. | Intervention involved prescribed exercise to be at a "moderate level of exertion for approximately 30 min/day". | 374 | / | / | / | |
| Supervised exercise intervention | ||||||
| 33. | Intervention involved 35‐ to 45‐minute exercise sessions 3 times per week from the start of the pregnancy (weeks 6‐9) to the end of the 3rd trimester (weeks 38‐39) ‐ an average of 85 training sessions. Exercise intensity was light‐to‐moderate and was supervised by a fitness specialist in groups of 10‐12 women. | 80 | / | |||
| 34. | A supervised exercise program consisting of aerobic and toning exercises for 3 sessions per week. 2 weekly sessions were performed on land (60 minutes) and 1 session was aquatic based (50 minutes). Program commenced from 10‐14 weeks to the end of the third trimester. Sessions were supervised by a qualified fitness specialist and an obstetrician. | 257 | / | |||
| 35. | Supervised moderate‐intensity exercise (initiated at 13 weeks or 20 weeks) vs control . Sessions consisted of warming up and stretching exercises, followed by supervised walking 3 times a week in the open air. Supervised by physical education professionals and medical, physiotherapy and nursing students. | 187 | / | |||
| 36. | Exercise (60 minutes supervised aerobic dance at least twice a week for a minimum of 12 weeks) (n = 52). Women in the exercise group were advised to have moderate, self‐imposed physical activity on the remaining weekdays. | 105 | / | |||
| 37. | The exercise training program started in the second trimester and was continued until the end of pregnancy. Each session consisted of 40‐45 minutes of aerobic and strength exercise. Individuals were supervised by certified aerobic‐instructors, and each session included a maximum of 10 participants. Intensity was moderate‐to‐vigorous; supine postures and Valsalva manoeuvres were avoided. | 63 | / | |||
| 38. | Intervention consisted of a supervised exercise program guided by a trained physical therapist in weekly classes with light‐to‐moderate‐intensity exercise for 40 minutes. It also included home exercise counselling which was to be performed 5 times per week (consisting of a sequence of 22 exercises or walking). | 82 | / | |||
| 39. | A supervised exercise intervention comprising 2 sessions of aerobic and strengthening exercises per week; each exercise session lasted for 60 minutes from 20 weeks' gestation. | 101 | / | |||
| 40. | Intervention group received supervised resistance exercise twice a week, with light barbells and weight plates in a group setting, performed at an activity level equivalent to within moderate–to‐vigorous between weeks 14 to 25 gestation, and was self‐adjusted. In addition, walking, cycling, water‐gymnastics, Pilates, yoga and home exercises that included pelvic floor training were recommended. | 72 | / | |||
| 41. | Intervention involved a program of supervised aerobic training of 45‐60 minutes, 4 days per week. | 62 | / | |||
| 42. | Intervention involved light‐to moderate‐intensity supervised aerobic and resistance exercises (including pelvic floor exercises) performed 3 days a week (50‐55 minutes per session) from 9 weeks to weeks 38‐39. Exercise sessions involved 8‐10 participants. | 962 | / | / | / | |
| 43 | The intervention consisted of a program of supervised physical exercise of 60 minutes duration, performed 3 times per week for 12 weeks. | 72 | / | |||
| 44. | intervention comprised a 12‐week regular standardised exercise program including aerobic activity, strength training, and balance exercises. The exercise program followed standard recommendations and included moderate‐intensity to high‐intensity activity 3 or more days per week. Physiotherapist‐supervised training sessions of 60 minutes in groups of 8‐15 women were offered once per week. | 702 | / | |||
| Supervised exercise and diet intervention | ||||||
| 45. | Exercise intervention involved a weekly supervised group session including floor aerobics, stretching and strength exercises, and similar home‐based exercise 3‐5 times/week for 30‐45 minutes per session. A video was provided to participants to assist with home‐based exercise. Diet intervention involved a computer‐assisted food choice map interview and a personalised plan by a dietician. | 46 | / | |||
| 46. | Exercise intervention involved an exercise regimen comprising 3 to 5 times per week, including a weekly supervised community‐based session and multiple home sessions, of mild‐to‐moderate exercise for 30 to 45 minutes. Program started between 20‐26 weeks. Group exercise sessions including aerobics were held in community centres and instructors were licensed fitness trainers. 2 dietary interviews with counselling were provided. | 190 | / | |||
| 47. | Lifestyle intervention (diet counselling and a supervised exercise program) vs control. Intervention included "a community‐based exercise program specifically designed for pregnant women was provided". An exercise regimen, 3 to 5 times per week including a weekly exercise session and home sessions with DVD instruction of mild‐to‐moderate aerobic exercise for 30 to 45 minutes was recommended. Program started between 20‐26 weeks and continued to 36 weeks. Group exercise sessions including aerobics were held in community centres and instructors were licensed fitness trainers. 2 dietary interviews with dietician counselling using a Food Choice Map were provided (baseline and 2 months later). Control group received standard care. | 113 | / | / | ||
| 48. | Moderate‐intensity exercise 3‐4 times per week, including 1 supervised session (versus low‐intensity exercise in the form of a walking program 3‐4 times per week). All participants received a diet plan based on a modified diabetic diet. | 49 | / | |||
| 49. | A lifestyle intervention consisting of dietary counselling and exercise. The intervention involved dietary advise on 4 occasions (15, 20, 28 and 35 weeks) by a dietician. Energy requirements were personalised for each participant. Exercise intervention included a pedometer and free gym membership for 6 months. Participants were encouraged to do 30‐60 minutes moderate‐physical activity daily. In addition, at the gym they had 1 supervised aerobic class with a physiotherapist for 1 hour each week. | 304 | / | |||
| BMI: body mass index | ||||||
| Outcome or subgroup title | No. of studies | No. of participants | Statistical method | Effect size |
| 1 Excessive weight gain Show forest plot | 24 | 7096 | Risk Ratio (M‐H, Random, 95% CI) | 0.80 [0.73, 0.87] |
| 1.1 Diet intervention (low GI diet) | 2 | 835 | Risk Ratio (M‐H, Random, 95% CI) | 0.77 [0.66, 0.91] |
| 1.2 Diet and exercise counselling | 9 | 3144 | Risk Ratio (M‐H, Random, 95% CI) | 0.86 [0.75, 0.98] |
| 1.3 Unsupervised exercise | 3 | 603 | Risk Ratio (M‐H, Random, 95% CI) | 0.83 [0.71, 0.97] |
| 1.4 Supervised exercise | 3 | 1298 | Risk Ratio (M‐H, Random, 95% CI) | 0.75 [0.63, 0.89] |
| 1.5 Supervised exercise and diet | 5 | 689 | Risk Ratio (M‐H, Random, 95% CI) | 0.71 [0.59, 0.85] |
| 1.6 Diet counselling/other | 3 | 527 | Risk Ratio (M‐H, Random, 95% CI) | 0.46 [0.17, 1.23] |
| 2 Weight gain (kg) Show forest plot | 36 | Mean Difference (IV, Random, 95% CI) | Totals not selected | |
| 2.1 Diet intervention (low GI diet) | 5 | Mean Difference (IV, Random, 95% CI) | 0.0 [0.0, 0.0] | |
| 2.2 Diet and exercise counselling | 13 | Mean Difference (IV, Random, 95% CI) | 0.0 [0.0, 0.0] | |
| 2.3 Unsupervised exercise | 1 | Mean Difference (IV, Random, 95% CI) | 0.0 [0.0, 0.0] | |
| 2.4 Supervised exercise intervention | 7 | Mean Difference (IV, Random, 95% CI) | 0.0 [0.0, 0.0] | |
| 2.5 Supervised exercise plus diet intervention | 3 | Mean Difference (IV, Random, 95% CI) | 0.0 [0.0, 0.0] | |
| 2.6 Diet counselling/other | 7 | Mean Difference (IV, Random, 95% CI) | 0.0 [0.0, 0.0] | |
| 3 Low weight gain Show forest plot | 11 | 4422 | Risk Ratio (M‐H, Random, 95% CI) | 1.14 [1.02, 1.27] |
| 3.1 Diet intervention (low GI diet) | 1 | 87 | Risk Ratio (M‐H, Random, 95% CI) | 1.24 [0.64, 2.43] |
| 3.2 Diet and exercise counselling | 5 | 2552 | Risk Ratio (M‐H, Random, 95% CI) | 1.25 [0.90, 1.75] |
| 3.3 Unsupervised exercise | 3 | 603 | Risk Ratio (M‐H, Random, 95% CI) | 1.13 [0.80, 1.60] |
| 3.4 Supervised exercise | 1 | 962 | Risk Ratio (M‐H, Random, 95% CI) | 1.21 [0.99, 1.48] |
| 3.5 Supervised exercise plus diet | 1 | 49 | Risk Ratio (M‐H, Random, 95% CI) | 1.47 [0.40, 5.50] |
| 3.6 Diet counselling/other | 1 | 169 | Risk Ratio (M‐H, Random, 95% CI) | 1.21 [0.80, 1.82] |
| 4 Preterm birth Show forest plot | 16 | 5923 | Risk Ratio (M‐H, Random, 95% CI) | 0.91 [0.68, 1.22] |
| 4.1 Diet intervention (low GI diet) | 2 | 804 | Risk Ratio (M‐H, Random, 95% CI) | 0.33 [0.11, 1.02] |
| 4.2 Diet and exercise counselling | 7 | 3170 | Risk Ratio (M‐H, Random, 95% CI) | 0.95 [0.60, 1.51] |
| 4.3 Unsupervised exercise | 2 | 229 | Risk Ratio (M‐H, Random, 95% CI) | 1.17 [0.35, 3.85] |
| 4.4 Supervised exercise | 3 | 1129 | Risk Ratio (M‐H, Random, 95% CI) | 1.92 [0.75, 4.93] |
| 4.5 Diet counselling/other | 3 | 591 | Risk Ratio (M‐H, Random, 95% CI) | 0.67 [0.26, 1.73] |
| 5 Pre‐eclampsia Show forest plot | 15 | 5330 | Risk Ratio (M‐H, Random, 95% CI) | 0.95 [0.77, 1.16] |
| 5.1 Diet and exercise counselling | 7 | 3139 | Risk Ratio (M‐H, Random, 95% CI) | 0.99 [0.74, 1.31] |
| 5.2 Supervised exercise | 2 | 1024 | Risk Ratio (M‐H, Random, 95% CI) | 0.91 [0.52, 1.60] |
| 5.3 Unsupervised exercise | 2 | 229 | Risk Ratio (M‐H, Random, 95% CI) | 1.60 [0.38, 6.73] |
| 5.4 Supervised exercise plus diet | 1 | 304 | Risk Ratio (M‐H, Random, 95% CI) | 0.84 [0.51, 1.40] |
| 5.5 Diet counselling/other | 4 | 634 | Risk Ratio (M‐H, Random, 95% CI) | 0.90 [0.54, 1.48] |
| 6 Hypertension (not prespecified) Show forest plot | 11 | 5162 | Risk Ratio (M‐H, Random, 95% CI) | 0.70 [0.51, 0.96] |
| 6.1 Diet and exercise counselling | 5 | 2648 | Risk Ratio (M‐H, Random, 95% CI) | 0.84 [0.54, 1.29] |
| 6.2 Unsupervised exercise | 2 | 229 | Risk Ratio (M‐H, Random, 95% CI) | 0.43 [0.12, 1.54] |
| 6.3 Supervised exercise | 3 | 1749 | Risk Ratio (M‐H, Random, 95% CI) | 0.55 [0.29, 1.03] |
| 6.4 Supervised exercise plus diet | 1 | 304 | Risk Ratio (M‐H, Random, 95% CI) | 0.84 [0.51, 1.40] |
| 6.5 Diet counselling/other | 1 | 232 | Risk Ratio (M‐H, Random, 95% CI) | 0.30 [0.08, 1.06] |
| 7 Induction of labour Show forest plot | 8 | 3832 | Risk Ratio (M‐H, Random, 95% CI) | 1.06 [0.94, 1.19] |
| 7.1 Diet intervention (low GI diet) | 1 | 734 | Risk Ratio (M‐H, Random, 95% CI) | 1.64 [1.14, 2.36] |
| 7.2 Diet and exercise counselling | 4 | 2522 | Risk Ratio (M‐H, Random, 95% CI) | 1.03 [0.93, 1.14] |
| 7.3 Unsupervised exercise | 1 | 192 | Risk Ratio (M‐H, Random, 95% CI) | 0.98 [0.65, 1.48] |
| 7.4 Supervised exercise | 1 | 35 | Risk Ratio (M‐H, Random, 95% CI) | 0.32 [0.01, 7.26] |
| 7.5 Diet counselling/other | 2 | 349 | Risk Ratio (M‐H, Random, 95% CI) | 0.89 [0.59, 1.35] |
| 8 Caesarean delivery Show forest plot | 28 | 7534 | Risk Ratio (M‐H, Random, 95% CI) | 0.95 [0.88, 1.03] |
| 8.1 Diet intervention (low GI diet) | 2 | 133 | Risk Ratio (M‐H, Random, 95% CI) | 0.99 [0.33, 3.01] |
| 8.2 Diet and exercise counselling | 9 | 3406 | Risk Ratio (M‐H, Random, 95% CI) | 0.87 [0.75, 1.01] |
| 8.3 Unsupervised exercise intervention | 2 | 229 | Risk Ratio (M‐H, Random, 95% CI) | 0.91 [0.53, 1.59] |
| 8.4 Supervised exercise | 8 | 2405 | Risk Ratio (M‐H, Random, 95% CI) | 0.96 [0.82, 1.11] |
| 8.5 Supervised exercise plus diet | 3 | 607 | Risk Ratio (M‐H, Random, 95% CI) | 1.00 [0.69, 1.45] |
| 8.6 Diet counselling/other | 5 | 754 | Risk Ratio (M‐H, Random, 95% CI) | 1.06 [0.93, 1.21] |
| 9 Postpartum weight retention (kg) Show forest plot | 7 | 818 | Mean Difference (IV, Random, 95% CI) | ‐1.12 [‐2.49, 0.25] |
| 9.1 Diet intervention (low GI diet) | 1 | 414 | Mean Difference (IV, Random, 95% CI) | ‐1.40 [‐2.63, ‐0.17] |
| 9.2 Diet and exercise counselling | 2 | 188 | Mean Difference (IV, Random, 95% CI) | ‐1.13 [‐4.88, 2.61] |
| 9.3 Supervised exercise | 2 | 132 | Mean Difference (IV, Random, 95% CI) | 0.17 [‐1.61, 1.96] |
| 9.4 Supervised exercise plus diet | 1 | 49 | Mean Difference (IV, Random, 95% CI) | ‐0.80 [‐2.84, 1.24] |
| 9.5 Diet counselling/other | 1 | 35 | Mean Difference (IV, Random, 95% CI) | ‐6.9 [‐15.28, 1.48] |
| 10 Postpartum weight retention (n/N; investigator defined time frame) Show forest plot | 5 | 902 | Risk Ratio (M‐H, Random, 95% CI) | 0.78 [0.63, 0.97] |
| 10.1 Diet and exercise counselling | 3 | 615 | Risk Ratio (M‐H, Random, 95% CI) | 0.72 [0.51, 1.01] |
| 10.2 Supervised exercise plus diet intervention | 2 | 287 | Risk Ratio (M‐H, Random, 95% CI) | 0.85 [0.66, 1.10] |
| 11 Energy intake (kj) Show forest plot | 12 | 4065 | Mean Difference (IV, Random, 95% CI) | ‐570.77 [‐894.28, ‐247.26] |
| 11.1 Diet intervention (low GI diet) | 4 | 1462 | Mean Difference (IV, Random, 95% CI) | ‐297.26 [‐562.80, ‐31.72] |
| 11.2 Diet and exercise counselling | 4 | 2190 | Mean Difference (IV, Random, 95% CI) | ‐897.66 [‐1763.09, ‐32.23] |
| 11.3 Supervised exercise plus diet intervention | 3 | 274 | Mean Difference (IV, Random, 95% CI) | ‐1090.80 [‐2263.86, 82.26] |
| 11.4 Diet counselling/other | 1 | 139 | Mean Difference (IV, Random, 95% CI) | ‐172.0 [‐686.85, 342.85] |
| 12 Fibre intake (g) Show forest plot | 8 | 3466 | Mean Difference (IV, Random, 95% CI) | 1.53 [0.94, 2.12] |
| 12.1 Diet intervention (low GI diet) | 4 | 1223 | Mean Difference (IV, Random, 95% CI) | 1.35 [0.55, 2.15] |
| 12.2 Diet and exercise counselling | 2 | 1996 | Mean Difference (IV, Random, 95% CI) | 1.97 [0.95, 2.99] |
| 12.3 Supervised exercise plus diet intervention | 1 | 112 | Mean Difference (IV, Random, 95% CI) | 1.0 [‐3.06, 5.06] |
| 12.4 Diet counselling//other | 1 | 135 | Mean Difference (IV, Random, 95% CI) | 1.10 [‐0.91, 3.11] |
| 13 Physical activity score (26‐29 weeks) Show forest plot | 9 | 2851 | Std. Mean Difference (IV, Random, 95% CI) | 0.40 [0.18, 0.61] |
| 13.1 Diet and exercise counselling | 5 | 2395 | Std. Mean Difference (IV, Random, 95% CI) | 0.27 [0.03, 0.51] |
| 13.2 Supervised exercise intervention | 2 | 232 | Std. Mean Difference (IV, Random, 95% CI) | 0.43 [0.06, 0.79] |
| 13.3 Supervised exercise plus diet intervention | 2 | 224 | Std. Mean Difference (IV, Random, 95% CI) | 0.73 [0.46, 1.00] |
| 14 Macrosomia Infant birthweight > 4000 g Show forest plot | 27 | 8598 | Risk Ratio (M‐H, Random, 95% CI) | 0.93 [0.86, 1.02] |
| 14.1 Diet intervention (low GI diet) | 4 | 1472 | Risk Ratio (M‐H, Random, 95% CI) | 0.96 [0.84, 1.10] |
| 14.2 Diet and exercise counselling | 10 | 3705 | Risk Ratio (M‐H, Random, 95% CI) | 0.93 [0.77, 1.12] |
| 14.3 Unsupervised exercise | 2 | 229 | Risk Ratio (M‐H, Random, 95% CI) | 1.16 [0.74, 1.81] |
| 14.4 Supervised exercise intervention | 7 | 2445 | Risk Ratio (M‐H, Random, 95% CI) | 0.81 [0.64, 1.02] |
| 14.5 Supervised exercise plus diet intervention | 3 | 398 | Risk Ratio (M‐H, Random, 95% CI) | 1.02 [0.71, 1.46] |
| 14.6 Diet counselling/other | 2 | 349 | Risk Ratio (M‐H, Random, 95% CI) | 1.81 [0.88, 3.72] |
| 15 Infant birthweight > 90th centile Show forest plot | 18 | 4525 | Risk Ratio (M‐H, Random, 95% CI) | 0.92 [0.80, 1.05] |
| 15.1 Diet and exercise counselling | 6 | 2777 | Risk Ratio (M‐H, Random, 95% CI) | 0.87 [0.74, 1.02] |
| 15.2 Unsupervised exercise | 1 | 192 | Risk Ratio (M‐H, Random, 95% CI) | 1.07 [0.34, 3.43] |
| 15.3 Supervised exercise intervention | 4 | 397 | Risk Ratio (M‐H, Random, 95% CI) | 1.09 [0.59, 2.00] |
| 15.4 Supervised exercise plus diet intervention | 3 | 607 | Risk Ratio (M‐H, Random, 95% CI) | 1.06 [0.67, 1.66] |
| 15.5 Diet intervention (low GI diet) | 3 | 200 | Risk Ratio (M‐H, Random, 95% CI) | 1.25 [0.50, 3.11] |
| 15.6 Diet counselling/other | 2 | 352 | Risk Ratio (M‐H, Random, 95% CI) | 0.95 [0.54, 1.69] |
| 16 Birthweight (g) (not prespecified) Show forest plot | 29 | 8350 | Mean Difference (IV, Random, 95% CI) | 12.20 [‐15.26, 39.65] |
| 16.1 Diet intervention (low GI diet) | 4 | 1447 | Mean Difference (IV, Random, 95% CI) | ‐0.84 [‐1.16, ‐0.52] |
| 16.2 Diet and exercise counselling | 9 | 3516 | Mean Difference (IV, Random, 95% CI) | 52.33 [‐33.23, 137.89] |
| 16.3 Unsupervised exercise | 1 | 37 | Mean Difference (IV, Random, 95% CI) | ‐124.21 [‐435.86, 187.44] |
| 16.4 Supervised exercise | 11 | 2714 | Mean Difference (IV, Random, 95% CI) | 16.27 [‐38.56, 71.11] |
| 16.5 Supervised exercise and diet | 1 | 49 | Mean Difference (IV, Random, 95% CI) | ‐107.0 [‐343.33, 129.33] |
| 16.6 Diet counselling/other | 3 | 587 | Mean Difference (IV, Random, 95% CI) | 1.40 [‐78.04, 80.84] |
| 17 Infant birthweight < 2500 g Show forest plot | 12 | 4834 | Risk Ratio (M‐H, Random, 95% CI) | 0.88 [0.67, 1.14] |
| 17.1 Exercise and diet counselling | 5 | 2934 | Risk Ratio (M‐H, Random, 95% CI) | 0.84 [0.60, 1.17] |
| 17.2 Unsupervised exercise | 2 | 229 | Risk Ratio (M‐H, Random, 95% CI) | 2.14 [0.24, 18.80] |
| 17.3 Supervised exercise | 4 | 1387 | Risk Ratio (M‐H, Random, 95% CI) | 0.99 [0.61, 1.63] |
| 17.4 Supervised exercise plus diet | 1 | 49 | Risk Ratio (M‐H, Random, 95% CI) | 2.67 [0.11, 62.42] |
| 17.5 Diet counselling/other | 1 | 235 | Risk Ratio (M‐H, Random, 95% CI) | 0.67 [0.29, 1.53] |
| 18 Infant birthweight < 10th centile Show forest plot | 7 | 662 | Risk Ratio (M‐H, Random, 95% CI) | 1.09 [0.61, 1.94] |
| 18.1 Diet intervention (low GI diet) | 2 | 155 | Risk Ratio (M‐H, Random, 95% CI) | 1.49 [0.47, 4.71] |
| 18.2 Diet and exercise counselling | 2 | 207 | Risk Ratio (M‐H, Random, 95% CI) | 0.95 [0.28, 3.29] |
| 18.3 Supervised exercise | 3 | 300 | Risk Ratio (M‐H, Random, 95% CI) | 0.99 [0.45, 2.19] |
| 19 Shoulder dystocia Show forest plot | 4 | 3253 | Risk Ratio (M‐H, Random, 95% CI) | 1.02 [0.57, 1.83] |
| 19.1 Diet intervention (low GI diet) | 1 | 759 | Risk Ratio (M‐H, Random, 95% CI) | 0.52 [0.10, 2.82] |
| 19.2 Diet and exercise counselling | 1 | 2142 | Risk Ratio (M‐H, Random, 95% CI) | 1.25 [0.81, 1.93] |
| 19.3 Diet counselling/other | 2 | 352 | Risk Ratio (M‐H, Random, 95% CI) | 0.35 [0.05, 2.64] |
| 20 Neonatal hypoglycaemia Show forest plot | 4 | 2601 | Risk Ratio (M‐H, Random, 95% CI) | 0.95 [0.76, 1.18] |
| 20.1 Diet and exercise counselling | 2 | 2256 | Risk Ratio (M‐H, Random, 95% CI) | 1.02 [0.79, 1.32] |
| 20.2 Diet counselling/other | 2 | 345 | Risk Ratio (M‐H, Random, 95% CI) | 0.88 [0.36, 2.15] |
| 21 Birth trauma Show forest plot | 2 | 2256 | Risk Ratio (M‐H, Random, 95% CI) | 0.89 [0.35, 2.30] |
| 21.1 Diet and exercise counselling | 2 | 2256 | Risk Ratio (M‐H, Random, 95% CI) | 0.89 [0.35, 2.30] |
| 22 Neonatal hyperbilirubinaemia Show forest plot | 2 | 2256 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.83 [0.62, 1.10] |
| 22.1 Diet and exercise counselling | 2 | 2256 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.83 [0.62, 1.10] |
| 23 Neonatal respiratory distress syndrome Show forest plot | 2 | 2256 | Risk Ratio (M‐H, Random, 95% CI) | 0.47 [0.26, 0.85] |
| 23.1 Diet and exercise counselling | 2 | 2256 | Risk Ratio (M‐H, Random, 95% CI) | 0.47 [0.26, 0.85] |
| 24 Postpartum hemorrhage Show forest plot | 2 | 2901 | Risk Ratio (M‐H, Random, 95% CI) | 0.94 [0.78, 1.14] |
| 24.1 Diet intervention (low GL diet) | 1 | 759 | Risk Ratio (M‐H, Random, 95% CI) | 0.83 [0.23, 3.08] |
| 24.2 Diet and exercise counselling | 1 | 2142 | Risk Ratio (M‐H, Random, 95% CI) | 0.94 [0.78, 1.14] |
| Outcome or subgroup title | No. of studies | No. of participants | Statistical method | Effect size |
| 1 Excessive weight gain Show forest plot | 2 | 833 | Risk Ratio (M‐H, Random, 95% CI) | 0.74 [0.55, 0.99] |
| 1.1 Low risk population | 1 | 317 | Risk Ratio (M‐H, Random, 95% CI) | 0.60 [0.38, 0.94] |
| 1.2 High risk population | 2 | 516 | Risk Ratio (M‐H, Random, 95% CI) | 0.81 [0.61, 1.08] |
| 2 Weight gain (kg) Show forest plot | 5 | Mean Difference (IV, Random, 95% CI) | Totals not selected | |
| 2.1 Mixed risk population | 3 | Mean Difference (IV, Random, 95% CI) | 0.0 [0.0, 0.0] | |
| 2.2 High risk population | 2 | Mean Difference (IV, Random, 95% CI) | 0.0 [0.0, 0.0] | |
| 3 Low weight gain Show forest plot | 1 | Risk Ratio (M‐H, Random, 95% CI) | Totals not selected | |
| 3.1 High risk population | 1 | Risk Ratio (M‐H, Random, 95% CI) | 0.0 [0.0, 0.0] | |
| 4 Preterm birth Show forest plot | 2 | 804 | Risk Ratio (M‐H, Random, 95% CI) | 0.33 [0.11, 1.02] |
| 4.1 Mixed risk population | 1 | 759 | Risk Ratio (M‐H, Random, 95% CI) | 0.39 [0.10, 1.46] |
| 4.2 High risk population | 1 | 45 | Risk Ratio (M‐H, Random, 95% CI) | 0.22 [0.03, 1.81] |
| 5 Caesarean delivery Show forest plot | 2 | 133 | Risk Ratio (M‐H, Random, 95% CI) | 0.99 [0.33, 3.01] |
| 5.1 High risk population | 2 | 133 | Risk Ratio (M‐H, Random, 95% CI) | 0.99 [0.33, 3.01] |
| 6 Macrosomia (Infant birthweight > 4000 g) Show forest plot | 4 | 1472 | Risk Ratio (M‐H, Random, 95% CI) | 0.96 [0.77, 1.20] |
| 6.1 Mixed risk population | 2 | 1335 | Risk Ratio (M‐H, Random, 95% CI) | 0.93 [0.75, 1.17] |
| 6.2 High risk population | 2 | 137 | Risk Ratio (M‐H, Random, 95% CI) | 2.47 [0.68, 8.95] |
| Outcome or subgroup title | No. of studies | No. of participants | Statistical method | Effect size |
| 1 Excessive weight gain Show forest plot | 9 | Risk Ratio (M‐H, Random, 95% CI) | Subtotals only | |
| 1.1 Low risk population | 2 | 247 | Risk Ratio (M‐H, Random, 95% CI) | 0.72 [0.55, 0.95] |
| 1.2 Mixed risk population | 1 | 219 | Risk Ratio (M‐H, Random, 95% CI) | 0.98 [0.83, 1.15] |
| 1.3 High risk women | 9 | 2725 | Risk Ratio (M‐H, Random, 95% CI) | 0.85 [0.71, 1.02] |
| 2 Weight gain (kg) Show forest plot | 13 | Mean Difference (IV, Random, 95% CI) | Subtotals only | |
| 2.1 Low risk population | 2 | 241 | Mean Difference (IV, Random, 95% CI) | ‐0.92 [‐2.12, 0.29] |
| 2.2 Mixed risk population | 3 | 444 | Mean Difference (IV, Random, 95% CI) | ‐1.80 [‐3.36, ‐0.24] |
| 2.3 High risk women | 11 | 2741 | Mean Difference (IV, Random, 95% CI) | ‐0.71 [‐1.34, ‐0.08] |
| 3 Low weight gain Show forest plot | 5 | 2552 | Risk Ratio (M‐H, Random, 95% CI) | 1.23 [0.89, 1.72] |
| 3.1 Low risk population | 2 | 247 | Risk Ratio (M‐H, Random, 95% CI) | 1.34 [0.74, 2.39] |
| 3.2 High risk women | 5 | 2305 | Risk Ratio (M‐H, Random, 95% CI) | 1.21 [0.79, 1.85] |
| 4 Preterm birth Show forest plot | 7 | 3170 | Risk Ratio (M‐H, Random, 95% CI) | 0.94 [0.57, 1.55] |
| 4.1 Low risk population | 2 | 243 | Risk Ratio (M‐H, Random, 95% CI) | 0.98 [0.19, 5.09] |
| 4.2 Mixed risk population | 1 | 197 | Risk Ratio (M‐H, Random, 95% CI) | 1.63 [0.84, 3.18] |
| 4.3 High risk population | 6 | 2730 | Risk Ratio (M‐H, Random, 95% CI) | 0.83 [0.43, 1.60] |
| 5 Pre‐eclampsia Show forest plot | 7 | 3139 | Risk Ratio (M‐H, Random, 95% CI) | 1.00 [0.75, 1.34] |
| 5.1 Low risk population | 2 | 243 | Risk Ratio (M‐H, Random, 95% CI) | 0.34 [0.10, 1.22] |
| 5.2 High risk women | 7 | 2896 | Risk Ratio (M‐H, Random, 95% CI) | 1.06 [0.79, 1.43] |
| 6 Caesarean delivery Show forest plot | 9 | 3406 | Risk Ratio (M‐H, Random, 95% CI) | 0.89 [0.80, 1.00] |
| 6.1 Low risk population | 2 | 243 | Risk Ratio (M‐H, Random, 95% CI) | 0.93 [0.59, 1.48] |
| 6.2 Mixed risk population | 2 | 310 | Risk Ratio (M‐H, Random, 95% CI) | 0.66 [0.41, 1.05] |
| 6.3 High risk women | 7 | 2853 | Risk Ratio (M‐H, Random, 95% CI) | 0.89 [0.76, 1.04] |
| 7 Macrosomia (Infant birthweight > 4000 g) Show forest plot | 10 | 3705 | Risk Ratio (M‐H, Random, 95% CI) | 0.92 [0.77, 1.11] |
| 7.1 Low risk population | 2 | 243 | Risk Ratio (M‐H, Random, 95% CI) | 2.18 [0.63, 7.58] |
| 7.2 Mixed risk population | 1 | 210 | Risk Ratio (M‐H, Random, 95% CI) | 1.39 [0.75, 2.56] |
| 7.3 High risk women | 9 | 3252 | Risk Ratio (M‐H, Random, 95% CI) | 0.85 [0.73, 1.00] |
| Outcome or subgroup title | No. of studies | No. of participants | Statistical method | Effect size |
| 1 Excessive weight gain Show forest plot | 6 | Risk Ratio (M‐H, Random, 95% CI) | Subtotals only | |
| 1.1 Low risk population | 2 | 953 | Risk Ratio (M‐H, Random, 95% CI) | 0.69 [0.47, 1.02] |
| 1.2 Mixed risk population | 3 | 1592 | Risk Ratio (M‐H, Random, 95% CI) | 0.77 [0.66, 0.88] |
| 1.3 High risk population | 5 | 690 | Risk Ratio (M‐H, Random, 95% CI) | 0.84 [0.73, 0.95] |
| 2 Weight gain (kg) Show forest plot | 8 | Mean Difference (IV, Random, 95% CI) | Subtotals only | |
| 2.1 Low risk population | 1 | 687 | Mean Difference (IV, Random, 95% CI) | ‐1.5 [‐2.08, ‐0.92] |
| 2.2 Mixed risk population | 4 | 1196 | Mean Difference (IV, Random, 95% CI) | ‐1.00 [‐2.01, 0.01] |
| 2.3 High risk women | 5 | 548 | Mean Difference (IV, Random, 95% CI) | ‐0.34 [‐1.15, 0.47] |
| 3 Low weight gain Show forest plot | 4 | Risk Ratio (M‐H, Random, 95% CI) | Subtotals only | |
| 3.1 Low risk population | 1 | 687 | Risk Ratio (M‐H, Random, 95% CI) | 1.29 [1.06, 1.58] |
| 3.2 Mixed risk population | 2 | 1336 | Risk Ratio (M‐H, Random, 95% CI) | 1.20 [1.00, 1.43] |
| 3.3 High risk population | 3 | 504 | Risk Ratio (M‐H, Random, 95% CI) | 1.03 [0.66, 1.60] |
| 4 Preterm birth Show forest plot | 5 | Risk Ratio (M‐H, Random, 95% CI) | Subtotals only | |
| 4.1 Low risk population | 1 | 687 | Risk Ratio (M‐H, Random, 95% CI) | 4.20 [0.90, 19.65] |
| 4.2 Mixed risk population | 3 | 1129 | Risk Ratio (M‐H, Random, 95% CI) | 1.92 [0.75, 4.93] |
| 4.3 High risk population | 3 | 504 | Risk Ratio (M‐H, Random, 95% CI) | 1.34 [0.51, 3.55] |
| 5 Pre‐eclampsia Show forest plot | 4 | 1253 | Risk Ratio (M‐H, Random, 95% CI) | 0.99 [0.58, 1.66] |
| 5.1 Mixed risk population | 2 | 1024 | Risk Ratio (M‐H, Random, 95% CI) | 0.91 [0.52, 1.60] |
| 5.2 High risk population | 2 | 229 | Risk Ratio (M‐H, Random, 95% CI) | 1.60 [0.38, 6.73] |
| 6 Caesarean delivery Show forest plot | 10 | Risk Ratio (M‐H, Random, 95% CI) | Subtotals only | |
| 6.1 Low risk population | 1 | 687 | Risk Ratio (M‐H, Random, 95% CI) | 0.88 [0.63, 1.21] |
| 6.2 Mixed risk population | 6 | 2263 | Risk Ratio (M‐H, Random, 95% CI) | 0.96 [0.76, 1.22] |
| 6.3 High risk population | 5 | 645 | Risk Ratio (M‐H, Random, 95% CI) | 0.98 [0.81, 1.20] |
| 7 Macrosomia (Infant birthweight > 4000 g) Show forest plot | 9 | Risk Ratio (M‐H, Random, 95% CI) | Subtotals only | |
| 7.1 Low risk population | 1 | 687 | Risk Ratio (M‐H, Random, 95% CI) | 0.60 [0.26, 1.41] |
| 7.2 Mixed risk population | 7 | 2445 | Risk Ratio (M‐H, Random, 95% CI) | 0.81 [0.64, 1.02] |
| 7.3 High risk population | 3 | 504 | Risk Ratio (M‐H, Random, 95% CI) | 0.65 [0.22, 1.91] |
| Outcome or subgroup title | No. of studies | No. of participants | Statistical method | Effect size |
| 1 Excessive weight gain Show forest plot | 5 | 689 | Risk Ratio (M‐H, Random, 95% CI) | 0.75 [0.61, 0.92] |
| 1.1 Low risk population | 2 | 106 | Risk Ratio (M‐H, Random, 95% CI) | 0.53 [0.16, 1.71] |
| 1.2 Mixed risk population | 2 | 235 | Risk Ratio (M‐H, Random, 95% CI) | 0.64 [0.47, 0.88] |
| 1.3 High risk women | 2 | 348 | Risk Ratio (M‐H, Random, 95% CI) | 0.83 [0.66, 1.06] |
| 2 Weight gain (kg) Show forest plot | 3 | 348 | Mean Difference (IV, Random, 95% CI) | ‐1.31 [‐1.00, 0.37] |
| 2.1 Low risk population | 1 | 57 | Mean Difference (IV, Random, 95% CI) | ‐3.33 [‐5.45, ‐1.21] |
| 2.2 Mixed risk population | 2 | 235 | Mean Difference (IV, Random, 95% CI) | ‐0.88 [‐2.40, 0.64] |
| 2.3 High risk women | 1 | 56 | Mean Difference (IV, Random, 95% CI) | 0.82 [‐1.00, 4.64] |
| 3 Low weight gain Show forest plot | 1 | Risk Ratio (M‐H, Random, 95% CI) | Subtotals only | |
| 3.1 Mixed risk population | 1 | 49 | Risk Ratio (M‐H, Random, 95% CI) | 1.47 [0.40, 5.50] |
| 4 Pre‐eclampsia Show forest plot | 1 | Risk Ratio (M‐H, Random, 95% CI) | Subtotals only | |
| 4.1 High risk women | 1 | 304 | Risk Ratio (M‐H, Random, 95% CI) | 0.84 [0.51, 1.40] |
| 5 Caesarean delivery Show forest plot | 3 | 607 | Risk Ratio (M‐H, Random, 95% CI) | 1.00 [0.69, 1.45] |
| 5.1 Low risk | 1 | 57 | Risk Ratio (M‐H, Random, 95% CI) | 0.0 [0.0, 0.0] |
| 5.2 Mixed risk population | 1 | 190 | Risk Ratio (M‐H, Random, 95% CI) | 0.58 [0.10, 3.36] |
| 5.3 High risk women | 2 | 360 | Risk Ratio (M‐H, Random, 95% CI) | 0.97 [0.48, 1.96] |
| 6 Macrosomia (Infant birthweight > 4000 g) Show forest plot | 3 | 398 | Risk Ratio (M‐H, Random, 95% CI) | 1.02 [0.71, 1.46] |
| 6.1 Mixed risk population | 2 | 94 | Risk Ratio (M‐H, Random, 95% CI) | 0.74 [0.23, 2.35] |
| 6.2 High risk women | 1 | 304 | Risk Ratio (M‐H, Random, 95% CI) | 1.05 [0.72, 1.54] |
| Outcome or subgroup title | No. of studies | No. of participants | Statistical method | Effect size |
| 1 Excessive weight gain Show forest plot | 3 | Risk Ratio (M‐H, Random, 95% CI) | Subtotals only | |
| 1.1 Mixed risk population | 3 | 443 | Risk Ratio (M‐H, Random, 95% CI) | 0.47 [0.08, 2.85] |
| 1.2 High risk population | 1 | 84 | Risk Ratio (M‐H, Random, 95% CI) | 0.92 [0.53, 1.62] |
| 2 Weight gain (kg) Show forest plot | 7 | Mean Difference (IV, Random, 95% CI) | Totals not selected | |
| 2.1 Mixed risk population | 3 | Mean Difference (IV, Random, 95% CI) | 0.0 [0.0, 0.0] | |
| 2.2 High risk population | 5 | Mean Difference (IV, Random, 95% CI) | 0.0 [0.0, 0.0] | |
| 3 Low weight gain Show forest plot | 1 | Risk Ratio (M‐H, Fixed, 95% CI) | Totals not selected | |
| 3.1 Mixed risk population | 1 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.0 [0.0, 0.0] | |
| 4 Preterm birth Show forest plot | 3 | 591 | Risk Ratio (M‐H, Random, 95% CI) | 0.67 [0.26, 1.73] |
| 4.1 Mixed risk population | 1 | 235 | Risk Ratio (M‐H, Random, 95% CI) | 0.67 [0.15, 2.93] |
| 4.2 High risk population | 2 | 356 | Risk Ratio (M‐H, Random, 95% CI) | 0.66 [0.19, 2.32] |
| 5 Pre‐eclampsia Show forest plot | 4 | 634 | Risk Ratio (M‐H, Random, 95% CI) | 0.90 [0.54, 1.48] |
| 5.1 Mixed risk population | 1 | 235 | Risk Ratio (M‐H, Random, 95% CI) | 2.69 [0.55, 13.03] |
| 5.2 High risk population | 3 | 399 | Risk Ratio (M‐H, Random, 95% CI) | 0.80 [0.47, 1.35] |
| 6 Caesarean delivery Show forest plot | 5 | 754 | Risk Ratio (M‐H, Random, 95% CI) | 1.06 [0.93, 1.21] |
| 6.1 Mixed risk population | 2 | 355 | Risk Ratio (M‐H, Random, 95% CI) | 0.96 [0.60, 1.54] |
| 6.2 High risk population | 3 | 399 | Risk Ratio (M‐H, Random, 95% CI) | 1.10 [0.96, 1.27] |
| 7 Macrosomia (Infant birthweight > 4000 g) Show forest plot | 2 | 349 | Risk Ratio (M‐H, Random, 95% CI) | 1.81 [0.88, 3.72] |
| 7.1 High risk population | 2 | 349 | Risk Ratio (M‐H, Random, 95% CI) | 1.81 [0.88, 3.72] |
