Combined diet and exercise interventions for preventing gestational diabetes mellitus
Abstract
Background
Gestational diabetes mellitus (GDM) is associated with a wide range of adverse health consequences for women and their infants in the short and long term. With an increasing prevalence of GDM worldwide, there is an urgent need to assess strategies for GDM prevention, such as combined diet and exercise interventions. This is an update of a Cochrane review that was first published in 2015.
Objectives
To assess the effects of diet interventions in combination with exercise interventions for pregnant women for preventing GDM, and associated adverse health consequences for the mother and her infant/child.
Search methods
We searched the Cochrane Pregnancy and Childbirth Group's Trials Register (27 November 2016) and reference lists of retrieved studies.
Selection criteria
We included randomised controlled trials (RCTs) and cluster‐RCTs, comparing combined diet and exercise interventions with no intervention (i.e. standard care), that reported on GDM diagnosis as an outcome. Quasi‐RCTs were excluded. Cross‐over trials were not eligible for inclusion. We planned to include RCTs comparing two or more different diet/exercise interventions, however none were identified.
Data collection and analysis
Two review authors independently assessed study eligibility, extracted data, assessed the risk of bias of the included trials and assessed quality of evidence for selected maternal and infant/child outcomes using the GRADE approach. We checked data for accuracy.
Main results
In this update, we included 23 RCTs (involving 8918 women and 8709 infants) that compared combined diet and exercise interventions with no intervention (standard care). The studies varied in the diet and exercise programs evaluated and health outcomes reported. None reported receiving funding from a drug manufacturer or agency with interests in the results. Overall risk of bias was judged to be unclear due to the lack of methodological detail reported. Most studies were undertaken in high‐income countries.
For our primary review outcomes, there was a possible reduced risk of GDM in the diet and exercise intervention group compared with the standard care group (average risk ratio (RR) 0.85, 95% confidence interval (CI) 0.71 to 1.01; 6633 women; 19 RCTs; Tau² = 0.05; I² = 42%; P = 0.07; moderate‐quality evidence). There was also a possible reduced risk of caesarean section (RR 0.95, 95% CI 0.88 to 1.02; 6089 women; 14 RCTs; moderate‐quality evidence). No clear differences were seen between groups for pre‐eclampsia (RR 0.98, 95% CI 0.79 to 1.22; 5366 participants; 8 RCTs; low‐quality evidence), pregnancy‐induced hypertension and/or hypertension (average RR 0.78, 95% CI 0.47 to 1.27; 3073 participants; 6 RCTs; Tau² = 0.19; I² = 62%; very low‐quality evidence), perinatal mortality (RR 0.82, 95% CI 0.42 to 1.63; 3757 participants; 2 RCTs; low‐quality evidence) or large‐for‐gestational age (RR 0.93, 95% CI 0.81 to 1.07; 5353 participants; 11 RCTs; low‐quality evidence). No data were reported for infant mortality or morbidity composite.
Subgroup analyses (based on trial design, maternal body mass index (BMI) and ethnicity) revealed no clear differential treatment effects. We were unable to assess the impact of maternal age, parity and specific features of the diet and exercise interventions. Findings from sensitivity analyses (based on RCT quality) generally supported those observed in the main analyses. We were not able to perform subgroup analyses based on maternal age, parity or nature of the exercise/dietary interventions due to the paucity of information/data on these characteristics and the inability to meaningfully group intervention characteristics.
For most of the secondary review outcomes assessed using GRADE, there were no clear differences between groups, including for perineal trauma (RR 1.27, 95% CI 0.78 to 2.05; 2733 participants; 2 RCTs; moderate‐quality evidence), neonatal hypoglycaemia (average RR 1.42, 95% CI 0.67 to 2.98; 3653 participants; 2 RCTs; Tau² = 0.23; I² = 77%; low quality evidence); and childhood adiposity (BMI z score) (MD 0.05, 95% CI ‐0.29 to 0.40; 794 participants; 2 RCTs; Tau² = 0.04; I² = 59%; low‐quality evidence). However, there was evidence of less gestational weight gain in the diet and exercise intervention group compared with the control group (mean difference (MD) ‐0.89 kg, 95% CI ‐1.39 to ‐0.40; 5052 women; 16 RCTs; Tau² = 0.37; I² = 43%;moderate‐quality evidence). No data were reported for maternal postnatal depression or type 2 diabetes; childhood/adulthood type 2 diabetes, or neurosensory disability.
Authors' conclusions
Moderate‐quality evidence suggests reduced risks of GDM and caesarean section with combined diet and exercise interventions during pregnancy as well as reductions in gestational weight gain, compared with standard care. There were no clear differences in hypertensive disorders of pregnancy, perinatal mortality, large‐for‐gestational age, perineal trauma, neonatal hypoglycaemia, and childhood adiposity (moderate‐ tovery low‐quality evidence).
Using GRADE methodology, the evidence was assessed as moderate to very low quality. Downgrading decisions were predominantly due to design limitations (risk of bias), and imprecision (uncertain effect estimates, and at times, small sample sizes and low event rates), however two outcomes (pregnancy‐induced hypertension/hypertension and neonatal hypoglycaemia), were also downgraded for unexplained inconsistency (statistical heterogeneity).
Due to the variability of the diet and exercise components tested in the included studies, the evidence in this review has limited ability to inform practice. Future studies could describe the interventions used in more detail, if and how these influenced behaviour change and ideally be standardised between studies. Studies could also consider using existing core outcome sets to facilitate more standardised reporting.
PICOs
Plain language summary
Combined diet and exercise in pregnancy for preventing gestational diabetes mellitus
Review question
What are the effects of combined diet and exercise for preventing gestational diabetes mellitus (GDM), and related health problems for mothers and their babies? This is an update of a Cochrane review that was first published in 2015.
Background
GDM is high blood sugar (hyperglycaemia) during pregnancy. Up to a quarter of pregnant women develop GDM, with some at a higher risk than others (such as overweight or obese women, older women, and those of particular ethnicities). GDM can lead to significant health problems for women and their babies. In the short term, women with GDM may develop pre‐eclampsia (high blood pressure (hypertension) and protein in the urine), or give birth by caesarean section. Their babies may grow large for their gestational age, and, as a result, be injured at birth, and/or cause injury to their mothers during birth. Babies of mothers with GDM often have low blood glucose (hypoglycaemia) and are overweight. Later in life, health problems such as neurosensory disabilities and type 2 diabetes can develop in these babies. Eating well and exercising is known to prevent type 2 diabetes and may be effective for preventing GDM.
Study characteristics
We searched for evidence in November 2016 and included 23 randomised controlled trials (RCTs) (involving 8918 women and their 8709 babies). Most studies were undertaken in high‐income countries. All of the studies compared women receiving diet and exercise programs with women receiving standard care without diet and exercise programs. The studies varied in the diet and exercise programs evaluated and health outcomes reported. None reported receiving funding from a drug manufacturer or agency with interests in the results.
Key results
Findings from 19 studies (6633 women) showed a possible reduction in GDM in women who received diet and exercise programs compared with women who received standard care. Fourteen studies (6089 women) showed a possible reduction in caesarean birth (14 studies; 6089 women) and 16 studies (5052 women) showed lower weight gain during pregnancy in women who received exercise programs. We found no differences between groups in other health problems for: pre‐eclampsia (8 studies; 5366 women); high blood pressure (6 studies; 3073 women); a large for age baby at birth (11 studies; 5353 babies); and perineal trauma (2 studies; 2733 women). Death of babies around birth (2 studies; 3757 babies), the baby having low blood glucose after birth (2 studies; 3653 babies), and infants being overweight (2 studies; 794 infants) did not differ in the two groups. Effects on depression or type 2 diabetes for mothers, a combined outcome of death or ill‐health for babies, or type 2 diabetes or neurosensory disability for babies as children were not reported. Participant views of programs were examined.
The evidence suggests combined diet and exercise programs may be effective for preventing GDM though the optimum components of these programs are not yet clear. Future studies could describe the interventions used in more detail, if and how these influenced behaviour change and ideally be standardised between studies. Studies could also consider measuring similar maternal and infant outcomes and report them in a standardised way.
Quality of the evidence
The overall risk of bias was judged unclear due to lack of information on methods. We assessed evidence quality using GRADE considerations for selected key outcomes. Our assessments ranged from moderate to very low.
Authors' conclusions
Summary of findings
| Combined diet and exercise interventions for preventing GDM | ||||||
| Population: pregnant women, excluding women already diagnosed with GDM, type 1 or type 2 diabetes Setting: Australia (2 RCTs), Brazil (1 RCT), Canada (2 RCTs), China (2 RCTs), Denmark (1 RCT), Egypt (1 RCT), Finland (3 RCTs), Germany (1 RCT), Italy (2 RCTs), Norway (1 RCT), UK (2 RCTs), USA (5 RCTs) | ||||||
| Outcomes | Anticipated absolute effects* (95% CI) | Relative effect | № of participants | Quality of the evidence | Comments | |
| Risk with control | Risk with diet and exercise interventions | |||||
| GDM | Trial population | average RR 0.85 (0.71 to 1.01) | 6633 (19 RCTs) | ⊕⊕⊕⊝ MODERATE1,3 | ||
| 168 per 1000 | 143 per 1000 (119 to 170) | |||||
| Hypertensive disorders of pregnancy (pre‐eclampsia) | Trial population | RR 0.98 (0.79 to 1.22) | 5366 (8 RCTs) | ⊕⊕⊝⊝ LOW2,4 | Eclampsia was not reported by any trials (Sagedal 2017 reports combined severe pre‐eclampsia, HELLP and eclampsia) | |
| 57 per 1000 | 55 per 1000 (45 to 69) | |||||
| Hypertensive disorders of pregnancy (pregnancy‐induced hypertension/hypertension) | Trial population | average RR 0.78 | 3073 | ⊕⊝⊝⊝ VERY LOW2,5,6 | ||
| 103 per 1000 | 80 per 1000 (48 to 130) | |||||
| Caesarean section | Trial population | RR 0.95 (0.88 to 1.02) | 6089 (14 RCTs) | ⊕⊕⊕⊝ MODERATE7 | ||
| 299 per 1000 | 284 per 1000 (263 to 305) | |||||
| Perineal trauma | Trial population | RR 1.27 (0.78 to 2.05) | 2733 (2 RCTs) | ⊕⊕⊕⊝ MODERATE2 | ||
| 21 per 1000 | 27 per 1000 (17 to 44) | |||||
| Gestational weight gain (kg) | Trial population | MD ‐ 0.89 (‐1.39 to ‐ 0.40) | 5052 | ⊕⊕⊕⊝ MODERATE8,9 | ||
| The mean gestational weight gain in the intervention group was 0.89 kg less (1.39 kg less to 0.40 kg less) | ||||||
| Postnatal depression | Not estimable | (0 RCTs) | No data reported for postnatal depression in any of the included RCTs | |||
| Type 2 diabetes mellitus | Not estimable | (0 RCTs) | No data reported for type 2 diabetes mellitus in any of the included RCTs | |||
| *The risk in the intervention group (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 | ||||||
| 1Trial limitations (‐1): 19 RCTs, intervention unable to be blinded (not downgraded for this as outcome is objective); some RCTS with potentially serious design limitations (unclear randomisation, attrition bias) | ||||||
| Combined diet and exercise interventions for preventing GDM | ||||||
| Population: pregnant women, excluding women already diagnosed with GDM, type 1 or type 2 diabetes Setting: Australia (2 RCTs), Brazil (1 RCT), Canada (2 RCTs), China (2 RCTs), Denmark (1 RCT), Egypt (1 RCT), Finland (3 RCTs), Germany (1 RCT), Italy (2 RCTs), Norway (1 RCT), UK (2 RCTs), USA (5 RCTs) | ||||||
| Outcomes | Anticipated absolute effects* (95% CI) | Relative effect | № of participants | Quality of the evidence | Comments | |
| Risk with control | Risk with diet and exercise interventions | |||||
| Perinatal mortality | Trial population | RR 0.82 (0.42 to 1.63) | 3757 (2 RCTs) | ⊕⊕⊝⊝ LOW1 | ||
| 10 per 1000 | 8 per 1000 (4 to 16) | |||||
| Large‐for‐gestational age | Trial population | RR 0.93 (0.81 to 1.07) | 5353 (11 RCTs) | ⊕⊕⊝⊝ LOW2,3 | ||
| 135 per 1000 | 126 per 1000 (109 to 144) | |||||
| Mortality or morbidity composite | Not estimable | (0 RCTs) | No data reported for mortality or morbidity composite in any of the included RCTs | |||
| Neonatal hypoglycaemia | Trial population | average RR 1.42 (0.67 to 2.98) | 3653 (2 RCTs) | ⊕⊕⊝⊝ LOW3,4 | ||
| 63 per 1000 | 90 per 1000 (42 to 189) | |||||
| Childhood adiposity (latest time reported) (BMI z score) | Trial population | MD 0.05 (‐0.29 to 0.40) | 794 (2 RCTs) | ⊕⊕⊝⊝ LOW3,5,6 | Additional meta‐analyses presented in review for: abdominal circumference, subscapular skinfold thickness, triceps skinfold thickness and total body fat | |
| The mean BMI z score in the intervention group was 0.05 higher (0.29 lower to 0.40 higher) | ||||||
| Type 2 diabetes mellitus | Not estimable | (0 RCTs) | No data reported for type 2 diabetes mellitus in any of the included RCTs | |||
| Neurosensory disability | Not estimable | (0 RCTs) | No data reported for neurosensory disability in any of the included RCTs | |||
| *The risk in the intervention group (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 | ||||||
| 1Imprecision (‐2): confidence interval crossing the line of no effect and few events | ||||||
Background
Description of the condition
Introduction and definition
Gestational diabetes mellitus (GDM) is defined as carbohydrate intolerance resulting in hyperglycaemia (abnormally high blood sugar) of variable severity with onset or first recognition during pregnancy (WHO 1999). GDM defined in this way includes women with undiagnosed pre‐existing diabetes, as well as those for whom the first onset is during pregnancy (especially during the third trimester of pregnancy).
Pathophysiology and symptoms
In normal pregnancy, relative maternal insulin resistance develops, beginning in the second trimester, with a progressive decline in insulin sensitivity until term. This physiological change facilitates the transport of glucose across the placenta to stimulate normal fetal growth and development. For women with GDM, a greater degree of maternal insulin resistance may lead to maternal hyperglycaemia, increased glucose transport across the placenta, fetal hyperinsulinaemia and accelerated growth in the fetus (Setji 2005). Usually, pregnancy‐induced maternal insulin resistance resolves promptly after the baby is born. While many women are asymptomatic, symptoms and signs associated with hyperglycaemia, such as polyuria (increased urinary frequency), polydipsia (increased thirst), blurred vision and fatigue, may be seen where GDM is undetected or poorly controlled (Kjos 1999).
Risk factors for GDM
Observational studies have helped to identify a multitude of potential risk factors for GDM; these include increasing maternal body mass index (BMI), physical inactivity (Chasan‐Taber 2008), advancing maternal age (Morisset 2010), increasing parity, and certain ethnicities. Diets low in fibre, with a high glycaemic load have been shown to increase the risk of GDM (Zhang 2006). Women who have had a previous macrosomic baby (birthweight 4000 g or more), have had previous GDM (Petry 2010), have a family history or first‐degree relative with diabetes, or have polycystic ovarian syndrome (Reece 2010) are also at an increased risk of GDM. High weight gain during pregnancy for women who are overweight or obese has been shown to correlate with GDM risk (Hedderson 2010; Morisset 2010).
Investigations
The prevalence of GDM is increasing worldwide in parallel with increasing rates of type 2 diabetes mellitus and maternal obesity (Bottalico 2007; Dabelea 2005). Depending on the population sampled, screening procedures and diagnostic criteria used, reported prevalences range up to 28% (Jiwani 2012). Screening procedures vary internationally, with inconsistencies between and within countries, ranging from universal or routine screening, to testing on a case‐by‐case basis (i.e. risk factor screening), according to clinician or patient decisions (Buckley 2012). Diagnostic criteria similarly vary worldwide.
The Hyperglycaemia and Adverse Pregnancy Outcome (HAPO) study was designed to clarify risks of adverse outcomes associated with degrees of maternal glucose intolerance (Coustan 2010). Given the lack of consistency internationally in regards to diagnostic criteria for GDM, following this study, a task force of the International Association of Diabetes in Pregnancy Study Group (IADPSG) recommended new criteria for the diagnosis of GDM ‐ with revised (lower) cut‐off values of thresholds representing an odds ratio for adverse pregnancy outcomes of 1.75 for women with GDM, compared with women without GDM (IADPSG Consensus Panel 2010). These criteria diagnose GDM if any of the following three 75 g oral glucose tolerance test (OGTT) thresholds are met or exceeded: fasting plasma glucose: 5.1 mmol/L (92 mg/dL), one‐hour plasma glucose: 10.0 mmol/L (180 mg/dL) or two‐hour plasma glucose: 8.5 mmol/L (153 mg/dL) (IADPSG Consensus Panel 2010). While studies have generally revealed a higher GDM prevalence when using the IADPSG compared with other criteria, some (Duran 2014; Hung 2015), but not all (Gerome 2017), have found an improvement in pregnancy outcomes with their use. Debate and controversy surrounding the risks, costs and benefits of use of these diagnostic criteria is ongoing (Farrar 2016; Langer 2013).
Health consequences of GDM
GDM is associated with an increased occurrence of a number of complications during pregnancy including pre‐eclampsia, and the requirement for induction of labour or caesarean section (Reece 2010). Fetal consequences may include macrosomia, which in turn may be associated with adverse maternal outcomes such as uterine rupture, and perineal trauma (Reece 2010). Women who develop GDM have a significantly increased risk of developing type 2 diabetes later in life (Bellamy 2009); they are also at an increased risk of developing GDM in future pregnancies (Bottalico 2007).
For the infant, GDM is associated with a range of complications. Babies born to mothers with GDM are more likely to be macrosomic or large‐for‐gestational age (Reece 2009; Reece 2010). Large‐for‐gestational‐age infants are at increased risk of birth injury, including shoulder dystocia, bone fractures and nerve palsies (Henriksen 2008; Reece 2010). These infants are at increased risk of developing type 2 diabetes, hypertension, obesity and metabolic syndrome later in life (Reece 2010; Whincup 2008). In addition, babies born to mothers with GDM are at increased risk of neonatal hypoglycaemia, respiratory distress syndrome, polycythaemia (raised red blood cell count), hyperbilirubinaemia, and being born preterm (Reece 2009; Reece 2010). Such health consequences together contribute to a need for enhanced neonatal care.
In randomised controlled trials, the treatment of women with GDM (dietary intervention, self‐monitoring of blood glucose and insulin therapy if needed) has been shown to significantly reduce the risk of a number of associated complications (Crowther 2005; Landon 2009). The importance of management for women with GDM is now widely accepted (Alwan 2009; Crowther 2005; Landon 2009) and is the subject of several Cochrane reviews, assessing different aspects of management, including lifestyle interventions (Brown 2017a), insulin (Brown 2016a), oral anti‐diabetic therapies (Brown 2017b), exercise (Ceysens 2016), dietary supplementation with myo‐inositol (Brown 2016b), and different intensities of glycaemic control (Martis 2016).
Description of the intervention
Dietary interventions
The aim of dietary advice or related interventions in pregnancy is to optimise health outcomes, which might include controlling excessive gestational weight gain or glycaemic control. While observational evidence indicates a relationship between GDM and high consumption of processed meats, snacks and fast foods and low consumption of vegetables before or during pregnancy (Lamyian 2017; Schoenaker 2015), evidence from intervention studies about the influence of diet on preventing GDM is sparse.
Exercise interventions
Benefits of exercise during pregnancy are now recognised, and thus women are generally encouraged to engage in 'moderate' exercise in the absence of any known pregnancy or medical complications (ACOG 2015; NICE 2017). Women often reduce their levels of physical activity during pregnancy (Pereira 2007), many due to a perceived risk to maternal or fetal health (Clarke 2004) and the impact of early pregnancy symptoms such as nausea and fatigue (Pereira 2007).
Regular aerobic exercise may lead to lower fasting and postprandial blood glucose concentrations in previously sedentary individuals. Exercise may decrease circulating glucose and insulin during, and for a period of time after, an exercise session (Clapp 1991; Clapp 1998). It has been shown outside of pregnancy that exercise can reduce the risk and delay the onset of the development of type 2 diabetes mellitus (Jeon 2007). Exercise has been shown to reduce insulin resistance in men and non‐pregnant women, leading to effective prevention and management of type 2 diabetes (Clapp 2006; Knowler 2002; Redden 2011).
Suggested benefits of exercise during pregnancy include a reduction in lower back pain, fluid retention and cardiovascular stress (Schlüssel 2008). Exercise is believed to play a role in reducing the risk of complications such as preterm birth and pre‐eclampsia (Dempsey 2005; Schlüssel 2008), and may help prevent excess pregnancy weight gain and postpartum weight retention (Schlüssel 2008). There is increasing evidence from observational studies indicating that pre‐pregnancy exercise and exercise in early pregnancy is associated with a reduction in insulin resistance (Reece 2009), and consequently a reduced risk of developing GDM (Jeon 2007; Redden 2011).
How the intervention might work
Combined diet and exercise interventions
While diet and exercise interventions alone and separately for the prevention of type 2 diabetes and GDM have been widely assessed, more recently there has been a shift towards combining such interventions in what may be regarded as 'lifestyle' interventions.
Several randomised controlled trials have established that the progression to type 2 diabetes can be prevented or postponed with lifestyle interventions in individuals with impaired glucose tolerance in the general population ('high‐risk' individuals) (Knowler 2002; Li 2008; Ratner 2008; Tuomilehto 2001). Such studies have focused strongly on combining increased physical activity and dietary modification, along with weight reduction for overweight participants. Long‐term follow‐up studies of such lifestyle interventions (that lasted for a limited time), have shown sustained beneficial effects on risk factors and diabetes incidence (Tuomilehto 2011). It has been suggested that a key factor in the success of such interventions is the comprehensive approach, addressing and working to correct several lifestyle‐related risk factors simultaneously (Tuomilehto 2011).
As it is accepted that a multitude of risk factors may increase the risk of type 2 diabetes, these randomised trials focused on a number of lifestyle‐related factors concurrently. In a Finnish Diabetes Prevention Study, five lifestyle targets were predefined, including: weight loss greater than 5%, intake of fat lower than 30% energy, intake of saturated fats lower than 10% energy, intake of dietary fibre greater than 15 g/1000 kcal, and an increase of physical activity to at least four hours per week (Tuomilehto 2001). These targets were perceived as relatively modest, and it was believed that such lifestyle changes would be feasible to maintain in the long term (Tuomilehto 2011). No 'high‐risk' individual with impaired glucose tolerance developed diabetes during the trial if they achieved at least four of the five lifestyle targets (Tuomilehto 2001). This trial was the first of a number to show that type 2 diabetes may be prevented with lifestyle interventions, and highlighted the importance of addressing multiple lifestyle‐related risk factors for optimal benefit (Knowler 2002; Li 2008; Tuomilehto 2001).
Whilst such trials considered type 2 diabetes and did not focus on pregnant women, they do offer some support for the use of lifestyle interventions in pregnant women for the prevention of GDM. To date, the Cochrane reviews assessing dietary advice alone and exercise interventions alone, for GDM prevention, have revealed inconclusive findings (Han 2012; Tieu 2017). The review 'Dietary advice in pregnancy for preventing gestational diabetes mellitus' (Tieu 2017) included 11 trials, and concluded that while very low‐quality evidence suggests a possible reduction in GDM risk for women receiving dietary advice versus standard care, further high‐quality evidence is needed to determine the effects of dietary advice interventions in pregnancy (Tieu 2017). The review 'Exercise for pregnant women for preventing gestational diabetes mellitus' (Han 2012), included five trials, and concluded that there was no clear evidence to support a reduction in GDM risk for women receiving an exercise intervention versus standard care, and highlighted a need for further high‐quality evidence (Han 2012).
As it is widely acknowledged that many factors are associated with GDM risk, it is considered plausible that lifestyle interventions, aimed at addressing lifestyle‐related risk factors, may be effective in preventing GDM. Such lifestyle interventions may combine diet interventions with exercise interventions.
Why it is important to do this review
GDM is associated with a wide range of adverse health consequences for women and their babies in the short and long term. Effective strategies are thus required to prevent GDM and the associated complications. This review will complement the existing reviews titled 'Dietary advice in pregnancy for preventing gestational diabetes mellitus' (Tieu 2017) and 'Exercise for pregnant women for preventing gestational diabetes mellitus' (Han 2012), and will assess combined diet and exercise interventions for preventing GDM. This is an update of the review which was first published in 2015 (Bain 2015).
Objectives
To assess the effects of diet interventions in combination with exercise interventions for pregnant women for preventing gestational diabetes mellitus (GDM), and associated adverse health consequences for the mother and her infant/child.
Methods
Criteria for considering studies for this review
Types of studies
We included all published randomised controlled trials assessing the effects of combined diet and exercise interventions for preventing gestational diabetes mellitus (GDM). We included cluster‐randomised trials, and trials published as abstracts only. We excluded quasi‐randomised controlled trials. Cross‐over trials were not eligible for inclusion.
Types of participants
We included trials of pregnant women regardless of age, gestation, parity or plurality. We excluded trials involving women with pre‐existing GDM, type 1 or type 2 diabetes.
Types of interventions
We included interventions that incorporated any type of diet intervention with any type of exercise intervention. We included trials where such interventions were compared with no intervention (i.e. standard care), and planned to include where they were compared with a different diet and exercise intervention.
Types of outcome measures
For this update, we used the standard outcomes agreed by consensus between review authors of Cochrane Pregnancy and Childbirth systematic reviews for prevention and treatment of GDM and pre‐existing diabetes.
Primary outcomes
Mother
-
GDM (diagnostic criteria as defined in individual trials)
-
Hypertensive disorders of pregnancy (e.g. pre‐eclampsia, pregnancy‐induced hypertension, eclampsia)
-
Caesarean section
Child
-
Perinatal mortality (stillbirth or neonatal mortality)
-
Large‐for‐gestational age
-
Mortality or morbidity composite (e.g. death, shoulder dystocia, bone fracture or nerve palsy)
Secondary outcomes
Mother
Perinatal outcomes
-
Operative vaginal birth
-
Induction of labour
-
Perineal trauma
-
Placental abruption
-
Postpartum haemorrhage
-
Postpartum infection
-
Gestational weight gain
-
Adherence to the intervention
-
Behaviour changes associated with the intervention
-
Relevant biomarker changes associated with the intervention
-
Sense of well‐being and quality of life
-
Views of intervention
-
Breastfeeding (e.g. at discharge, six weeks postpartum)
Long‐term maternal outcomes
-
Postnatal depression
-
Postnatal weight retention or return to pre‐pregnancy weight
-
Body mass index (BMI)
-
GDM in subsequent pregnancy
-
Type 1 diabetes mellitus
-
Type 2 diabetes mellitus
-
Impaired glucose tolerance
-
Cardiovascular health (e.g. blood pressure, hypertension, cardiovascular disease, metabolic syndrome)
Child
Fetal/neonatal outcomes
-
Stillbirth
-
Neonatal mortality
-
Gestational age at birth
-
Preterm birth (before 37 weeks gestation; before 34 weeks gestation)
-
Apgar score less than seven at five minutes
-
Macrosomia
-
Small‐for‐gestational age
-
Birthweight and z score
-
Head circumference and z score
-
Length and z score
-
Ponderal index
-
Adiposity (e.g. as measured by BMI, skinfold thickness)
-
Shoulder dystocia
-
Nerve palsy
-
Bone fracture
-
Respiratory distress syndrome
-
Hypoglycaemia
-
Hyperbilirubinaemia
Childhood/adulthood outcomes
-
Weight and z scores
-
Height and z scores
-
Head circumference and z scores
-
Adiposity (e.g. as measured by BMI, skinfold thickness)
-
Cardiovascular health (e.g. blood pressure, hypertension, cardiovascular disease, metabolic syndrome)
-
Employment, education and social status/achievement
-
Type 1 diabetes mellitus
-
Type 2 diabetes mellitus
-
Impaired glucose tolerance
-
Neurosensory disability
Health services
-
Number of hospital or health professional visits (e.g. midwife, obstetrician, physician, dietitian, diabetic nurse)
-
Number of antenatal visits or admissions
-
Length of antenatal stay
-
Neonatal intensive care unit admission
-
Length of postnatal stay (mother)
-
Length of postnatal stay (baby)
-
Costs to families associated with the management provided
-
Costs associated with the intervention
-
Cost of maternal care
-
Cost of infant care
To be included, trials had to report on our primary outcome, GDM. Trials that appeared to meet other criteria for inclusion in this review that did not report on GDM have been included as 'Awaiting classification' (pending the availability/reporting of GDM outcome data), and will be re‐considered in future updates of this review.
Search methods for identification of studies
The following methods section of this review is based on a standard template used by Cochrane Pregnancy and Childbirth.
Electronic searches
We searched Cochrane Pregnancy and Childbirth’s Trials Register by contacting their Information Specialist (27 November 2016).
The Register is a database containing over 22,000 reports of controlled trials in the field of pregnancy and childbirth. For full search methods used to populate Pregnancy and Childbirth’s Trials Register including the detailed search strategies for CENTRAL, MEDLINE, Embase and CINAHL; the list of handsearched journals and conference proceedings, and the list of journals reviewed via the current awareness service, please follow this link to the editorial information about the Cochrane Pregnancy and Childbirth in the Cochrane Library and select the ‘Specialized Register ’ section from the options on the left side of the screen.
Briefly, Cochrane Pregnancy and Childbirth’s Trials Register is maintained by their Information Specialist and contains trials identified from:
-
monthly searches of the Cochrane Central Register of Controlled Trials (CENTRAL);
-
weekly searches of MEDLINE (Ovid);
-
weekly searches of Embase (Ovid);
-
monthly searches of CINAHL (EBSCO);
-
handsearches of 30 journals and the proceedings of major conferences;
-
weekly current awareness alerts for a further 44 journals plus monthly BioMed Central email alerts.
-
scoping searches of ClinicalTrials.gov and the WHO International Clinical Trials Registry Platform (ICTRP).
Search results are screened by two people and the full text of all relevant trial reports identified through the searching activities described above is reviewed. Based on the intervention described, each trial report is assigned a number that corresponds to a specific Pregnancy and Childbirth review topic (or topics), and is then added to the Register. The Information Specialist searches the Register for each review using this topic number rather than keywords. This results in a more specific search set which has been fully accounted for in the relevant review sections (Included studies; Excluded studies; Studies awaiting classification; Ongoing studies).
Searching other resources
We searched the reference lists of retrieved trials.
We did not apply any language or date restrictions.
Data collection and analysis
The following methods section of this review is based on a standard template used by Cochrane Pregnancy and Childbirth.
Selection of studies
Two review authors independently assessed for inclusion all the potential studies we identified as a result of the search strategy. We resolved any disagreement through discussion or, if required, we consulted a third review author.
Data extraction and management
We designed a form to extract data. For eligible trials, two review authors extracted the data using the agreed form. We resolved discrepancies through discussion or, if required, we consulted a third review author. We entered data into Review Manager software (RevMan 2014) and checked for accuracy.
When information regarding any of the above was unclear, we attempted to contact authors of the original reports to provide further details.
Assessment of risk of bias in included studies
Two review authors independently assessed risk of bias for each trial using the criteria outlined in the Cochrane Handbook for Systematic Reviews of Interventions (Higgins 2011). We resolved any disagreement by discussion or by involving a third assessor.
(1) Random sequence generation (checking for possible selection bias)
We described for each included trial 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:
-
low risk of bias (any truly random process, e.g. random number table; computer random number generator);
-
high risk of bias (any non‐random process, e.g. odd or even date of birth; hospital or clinic record number);
-
unclear risk of bias.
(2) Allocation concealment (checking for possible selection bias)
We described for each included trial 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:
-
low risk of bias (e.g. telephone or central randomisation; consecutively numbered sealed opaque envelopes);
-
high risk of bias (open random allocation; unsealed or non‐opaque envelopes, alternation; date of birth);
-
unclear risk of bias.
(3.1) Blinding of participants and personnel (checking for possible performance bias)
We described for each included trial the methods used, if any, to blind trial participants and personnel from knowledge of which intervention a participant received. We considered trials to be at low risk of bias if they were blinded, or if we judged that the lack of blinding would be unlikely to affect results. We assessed blinding separately for different outcomes or classes of outcomes.
We assessed the methods as:
-
low, high or unclear risk of bias for participants;
-
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 trial 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:
-
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 trial, and for each outcome or class of outcomes, the completeness of data including attrition and exclusions from the analysis. We have 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.
We assessed methods as:
-
low risk of bias (e.g. no missing outcome data; missing outcome data balanced across groups);
-
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);
-
unclear risk of bias.
(5) Selective reporting (checking for reporting bias)
We described for each included trial how we investigated the possibility of selective outcome reporting bias and what we found.
We assessed the methods as:
-
low risk of bias (where it was clear that all of the trial’s pre‐specified outcomes and all expected outcomes of interest to the review were reported);
-
high risk of bias (where not all the trial’s pre‐specified outcomes were reported; one or more reported primary outcomes were not pre‐specified; outcomes of interest were reported incompletely and so could not be used; trial failed to include results of a key outcome that would have been expected to have been reported);
-
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 trial any important concerns we had about other possible sources of bias.
We assessed whether each trial was free of other problems that could put it at risk of bias:
-
low risk of other bias;
-
high risk of other bias;
-
unclear whether there was risk of other bias.
(7) Overall risk of bias
We made explicit judgements about whether trials were at high risk of bias, according to the criteria given in the Cochrane Handbook for Systematic Reviews of Interventions (Higgins 2011). With reference to (1) to (6) above, we assessed the likely magnitude and direction of the bias and whether we considered it was likely to impact on the findings. We explored the impact of the level of bias through undertaking sensitivity analyses ‐ seeSensitivity analysis.
Assessment of the quality of the evidence using the GRADE approach
For this update, we evaluated the quality of the evidence for the below outcomes using the GRADE approach as outlined in the GRADE handbook. The GRADE approach uses five considerations (trial limitations, consistency of effect, imprecision, indirectness and publication bias) to assess the quality of the body of evidence for specific outcomes. The evidence can be downgraded 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, inconsistency, imprecision of effect estimates or publication bias.
Mother
Perinatal outcomes
-
GDM
-
Hypertensive disorders of pregnancy (e.g. pre‐eclampsia, pregnancy‐induced hypertension, eclampsia)
-
Caesarean section
-
Perineal trauma
-
Gestational weight gain
Long‐term maternal outcomes
-
Postnatal depression
-
Type 2 diabetes mellitus
Child
Fetal/neonatal outcomes
-
Perinatal mortality (stillbirth or neonatal mortality)
-
Large‐for‐gestational age
-
Mortality or morbidity composite (e.g. death, shoulder dystocia, bone fracture or nerve palsy)
-
Hypoglycaemia
Childhood/adulthood outcomes
-
Adiposity (e.g. as measured by BMI, skinfold thickness)
-
Type 2 diabetes mellitus
-
Neurosensory disability
'Summary of findings' table
We used GRADEpro Guideline Development Tool to import data from Review Manager 5.3 (RevMan 2014) in order to create 'Summary of findings’ tables for maternal and child outcomes. Summaries of the intervention effect and measures of quality according to the GRADE approach are presented in the 'Summary of findings' tables.
Measures of treatment effect
Dichotomous data
For dichotomous data, we have presented results as summary risk ratio with 95% confidence intervals.
Continuous data
For continuous data, we have used the mean difference where outcomes were measured in the same way between trials. In future updates, we plan to use the standardised mean difference to combine trials that measure the same outcome, but use different methods.
Unit of analysis issues
Cluster‐randomised trials
We included cluster‐randomised trials in the analyses along with individually‐randomised trials. We adjusted their sample sizes and event rates using the methods described in the Cochrane Handbook for Systematic Reviews of Interventions (Higgins 2011), using an estimate of the intracluster correlation co‐efficient (ICC) of 0.12 derived from an included trial (Luoto 2011). We considered it reasonable to combine the results from the cluster‐randomised trials and the individually‐randomised trials as there was little heterogeneity between the trial designs and the interaction between the effect of intervention and the choice of randomisation unit was considered to be unlikely.
We acknowledged heterogeneity in the randomisation unit and performed a subgroup analysis to investigate the effects of the randomisation unit.
Cross‐over trials
We considered cross‐over designs inappropriate for this research question.
Multi‐arm trials
In future updates of this review, if we include multi‐arm trials, we plan to use methods as described in the Cochrane Handbook for Systematic Reviews of Interventions (Higgins 2011) to overcome possible unit‐of analysis errors, by combining groups to make a single pair‐wise comparison (where appropriate), or by splitting the 'shared' group into two (or more) groups with smaller sample sizes, and including the two (or more) comparisons.
Dealing with missing data
For included trials, we noted levels of attrition. In future updates, we plan to explore the impact of including trials with high levels of missing data in the overall assessment of treatment effect by using sensitivity analyses.
For all outcomes, we carried out analyses, as far as possible, on an intention‐to‐treat basis, i.e. we attempted to include all participants randomised to each group in the analyses, and all participants were analysed in the group to which they were allocated, regardless of whether or not they received the allocated intervention. 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 T², I² and Chi² statistics. We regarded heterogeneity as substantial where the I² was greater than 30% and either the T² was greater than zero, or there was a low P value (less than 0.10) in the Chi² test for heterogeneity.
Assessment of reporting biases
Where there were 10 or more trials in a meta‐analysis, we investigated reporting biases (such as publication bias) using funnel plots. We assessed funnel plot asymmetry visually. In future updates of this review, if asymmetry is suggested by a visual assessment, we plan to perform exploratory analyses to investigate it.
Data synthesis
We carried out statistical analysis using Review Manager software (RevMan 2014). We used fixed‐effect meta‐analysis for combining data where it was reasonable to assume that trials were estimating the same underlying treatment effect: i.e. where trials were examining the same intervention, and the trials’ populations and methods were judged sufficiently similar. Where there was clinical heterogeneity sufficient to expect that the underlying treatment effects differed between trials, or where substantial statistical heterogeneity was detected, 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 have discussed the clinical implications of treatment effects differing between trials. If the average treatment effect was not clinically meaningful, we would not have combined trials.
Where we have used random‐effects analyses, the results have been presented as the average treatment effect with 95% confidence intervals, and the estimates of Tau² and I².
Subgroup analysis and investigation of heterogeneity
Had we identified substantial heterogeneity, we planned to investigate it using subgroup analyses and sensitivity analyses. We planned to consider whether an overall summary was meaningful, and if it was, use random‐effects analysis to produce it.
Maternal characteristics, and characteristics of the diet and exercise interventions assessed were considered likely to affect outcomes.
We planned to carry out the following subgroup analyses.
-
Maternal age (35 years of age or more versus less than 35 years of age).
-
Maternal BMI (at or before trial entry) (BMI of less than 18.5 kg/m² versus BMI of 18.5 to 24.9 kg/m² versus BMI of 25 to 29.9 kg/m² versus BMI of 30 kg/m² to 39.9 kg/m² and versus BMI of 40 kg/m² or more).
-
Ethnicity (ethnic groups at high risk for GDM versus ethnic groups for lower risk of GDM).
-
Parity (parity of zero versus one to two and versus three or more).
-
Nature of the exercise intervention (e.g. frequent versus infrequent advice/sessions; short versus long duration of advice/sessions; high‐intensity verus low‐intensity of advice/sessions; advice only versus interactive sessions).
-
Nature of the dietary intervention (e.g. frequent versus infrequent intervention; short versus long duration of intervention; advice only versus more intensive support).
We were not able to perform subgroup analyses based on maternal age, parity or nature of the exercise/dietary interventions due to the paucity of information/data on these characteristics and the inability to meaningfully group intervention characteristics.
Formation of subgroups for maternal BMI and ethnicity was restricted by reporting in the included trials. Our analyses based on maternal BMI thus included the following subgroups: BMI less than 25 kg/m² versus BMI or 25 kg/m² or more versus BMI of 30 kg/m² or more versus any BMI; our analyses based on ethnicity included the following subgroups: majority 'low risk' ethnicities versus majority 'high risk' ethnicities versus mixed ethnicities versus unclear ethnicities.
We also performed a subgroup analysis on unit of randomisation ‐ cluster‐randomised versus individually‐randomised trials.
We used only primary outcomes in subgroup analyses.
We assessed subgroup differences by interaction tests available within RevMan (RevMan 2014). We reported the results of subgroup analyses quoting the Chi² statistic and P value, and the interaction test I² value.
Sensitivity analysis
We carried out sensitivity analyses to explore the effects of trial quality assessed by sequence generation and allocation concealment, by omitting trials rated as 'high risk of bias' or 'unclear risk of bias' for these components. We restricted this to the primary outcomes.
Results
Description of studies
Results of the search
In the previous version of the review we identified 79 records relating to 41 studies. We included 13 trials, excluded 11, 16 were ongoing, and one was awaiting further classification. See Figure 1.
Updated searches of the Cochrane Pregnancy and Childbirth's Trials Register in February 2015 (28 records) and November 2016 (72 records) identified 100 new records; and additional searching identified 23 records. Therefore we assessed 123 new records.
We included 10 new trials (Bruno 2016; Hawkins 2014; Herring 2016; Hoirisch‐Clapauch 2016; Hui 2014; Jing 2015; Koivusalo 2016; Poston 2015; Sagedal 2017; Wang 2015), excluded nine studies (Barakat 2006; Bo 2014; Crowther 2012; McGowan 2013; Parat 2015; Peacock 2014; Simmons 2015; Sun 2016; Youngwanichsetha 2014), identified eight ongoing studies (Chasan‐Taber 2015; Clements 2016; Farajzadegan 2013; Garmendia 2015; Kennelly 2016; Rauh 2014; Spieker 2015; Vesco 2012), and eight await further classification (Asci 2016; Kieffer 2014; Kim 2015; Marcinkevage 2013; Mujsindi 2014; Santos‐Rocha 2015; Skouteris 2016; Torres 2016). We also identified additional records relating to nine of the trials included in the previous version of this review. See Figure 2.
Update study flow diagram.
Where required, we also re‐classified some of the studies/records which were listed as excluded, ongoing or awaiting classification in the previous version of the review.
Overall, therefore, we have included 23 trials (Asbee 2009; Bruno 2016; Dodd 2014; El Beltagy 2013; Harrison 2013; Hawkins 2014; Herring 2016; Hoirisch‐Clapauch 2016; Hui 2012; Hui 2014; Jing 2015; Koivusalo 2016; Korpi‐Hyovalti 2011; Luoto 2011; Petrella 2013; Phelan 2011; Polley 2002; Poston 2013; Poston 2015; Rauh 2013; Sagedal 2017; Vinter 2011; Wang 2015), excluded 15 studies (Barakat 2006; Bo 2014; Clapp 1997; Crowther 2012; Luoto 2010; McGowan 2013; Nascimento 2012; NCT00924599; Parat 2015; Peacock 2014; Quinlivan 2011; Ruchat 2012; Simmons 2015; Sun 2016; Youngwanichsetha 2014), 14 are ongoing (Chasan‐Taber 2015; Clements 2016; Farajzadegan 2013; Garmendia 2015; Jelsma 2013; Kennelly 2016; Nagle 2013; NCT01643356; NCT01693510; NCT01719406; NCT01782105; Rauh 2014; Spieker 2015; Vesco 2012), and 10 await further classification, pending the availability of data on GDM (Althuizen 2013; Asci 2016; Kieffer 2014; Kim 2015; Marcinkevage 2013; Mujsindi 2014; Santos‐Rocha 2015; Skouteris 2016; Torres 2016; Wilkinson 2012).
Included studies
Following application of eligibility criteria 23 randomised controlled trials were included in this review (Asbee 2009; Bruno 2016; Dodd 2014; El Beltagy 2013; Harrison 2013; Hawkins 2014; Herring 2016; Hoirisch‐Clapauch 2016; Hui 2012; Hui 2014; Jing 2015; Koivusalo 2016; Korpi‐Hyovalti 2011; Luoto 2011; Petrella 2013; Phelan 2011; Polley 2002; Poston 2013; Poston 2015; Rauh 2013; Sagedal 2017; Vinter 2011; Wang 2015). Two trials (Luoto 2011; Rauh 2013) were cluster‐randomised and the other 21 were individually‐randomised.
A total of 8918 women and 8709 infants were involved in the included trials. Dodd 2014 was the largest trial, randomising 2212 women, followed by Poston 2015, randomising 1280 women. Korpi‐Hyovalti 2011, Petrella 2013, Herring 2016 and Hawkins 2014 were the smallest trials randomising 60, 63, 66 and 68 women, respectively. For the majority of included trials, fewer women were included in the analyses than were randomised, with a maximum of 6633 women and 5763 infants included in review meta‐analyses.
Settings
The majority of the trials were conducted in upper‐middle and high‐income countries. Five trials were conducted in the USA (Asbee 2009; Hawkins 2014; Herring 2016; Phelan 2011; Polley 2002); three in Finland (Koivusalo 2016; Korpi‐Hyovalti 2011; Luoto 2011); two in Australia (Dodd 2014; Harrison 2013); two in the UK (Poston 2013; Poston 2015); two in Canada (Hui 2012; Hui 2014); two in Italy (Bruno 2016; Petrella 2013); two in China (Jing 2015; Wang 2015); and one each in Brazil (Hoirisch‐Clapauch 2016); Denmark (Vinter 2011); Egypt (El Beltagy 2013); Germany (Rauh 2013); and Norway (Sagedal 2017).
Participants
All participants were pregnant women. Where reported, the mean (standard deviation (SD)) ages of women ranged from 25.5 (4.8) years in Polley 2002 to 32.3 (4.9) (diet and exercise intervention) and 32.6 (4.5) (standard care) years in Koivusalo 2016. In eight of the trials (Bruno 2016; Harrison 2013; Koivusalo 2016; Petrella 2013; Poston 2013; Poston 2015; Rauh 2013; Wang 2015), the mean ages of women in both the diet and exercise intervention and standard care groups were at least 30 years. Maternal age across the trials is further summarised in Table 1.
| Study ID | Diet and exercise intervention | Control |
| Mean (SD): 26.7 (6.0) | Mean (SD): 26.4 (5.0) | |
| Mean (SD): 31.5 (5) | Mean (SD): 30.8 (5.5) | |
| Mean (SD): 29.3 (5.4) | Mean (SD): 29.6 (5.6) | |
| Not reported | Not reported | |
| Mean (SD): 32.4 (4.6) | Mean (SD): 31.7 (4.5) | |
| N (%) | N (%) | |
| Mean (SD): 25.9 (4.9) | Mean (SD): 25.0 (5.7) | |
| Not reported | Not reported | |
| Mean (SD): 30.1 (5.2) | Mean (SD): 28.7 (5.9) | |
| Mean (SD) BMI ≤ 24.9 kg/m²: 31 (3) BMI ≥ 25 kg/m²: 31 (4) | Mean (SD) BMI ≤ 24.9 kg/m²: 29 (6) BMI ≥ 25 kg/m²: 32 (5) | |
| Mean (SD): 29.57 (4.13) | Mean (SD): 29.89 (3.86) | |
| Mean (SD): 32.3 (4.9) | Mean (SD): 32.6 (4.5) | |
| Mean (SD): 29.1 (5.4) | Mean (SD): 29.8 (5.4) | |
| Mean (SD): 29.5 (4.8) | Mean (SD): 30.0 (4.7) | |
| Mean (SD): 31.5 (4.2) | Mean (SD): 32.4 (5.9) | |
| Mean (SD): 28.6 (5.2) | Mean (SD): 28.8 (5.2) | |
| Mean (SD): 25.5 (4.8) | ||
| Mean (SD): 30.4 (5.7) | Mean (SD): 30.7 (4.9) | |
| Mean (SD): 30.5 (5.5) | Mean (SD): 30.4 (5.6) | |
| Mean (SD): 32.2 (4.4) | Mean (SD): 30.8 (4.9) | |
| Mean (SD): 27.9 (4.2) | Mean (SD): 28.1 (4.5) | |
| Median (IQR): 29 (27 ‐ 32) | Median (IQR): 29 (26 ‐ 31) | |
| Mean (SD): 31.0 (3.8) | Mean (SD): 30.27 (3.64) | |
Abbreviations: BMI: body mass index; IQR: interquartile range; N: number; SD: standard deviation
In regards to body mass index (BMI), 13 of the trials (Asbee 2009; Hoirisch‐Clapauch 2016; Hui 2012; Hui 2014; Jing 2015; Koivusalo 2016; Korpi‐Hyovalti 2011; Luoto 2011; Phelan 2011; Polley 2002; Rauh 2013; Sagedal 2017; Wang 2015) generally included all women regardless of their BMI, though some had restrictions: four had a specific lower acceptable BMI (ranging from 18 kg/m² to 19.8 kg/m²) (Phelan 2011; Polley 2002; Rauh 2013; Sagedal 2017); and three had a specific upper acceptable BMI (of 25 kg/m²) (Wang 2015), (or 40 kg/m²) (Asbee 2009; Phelan 2011). The remaining 10 trials only included women who were overweight or obese (six trials: Bruno 2016; Dodd 2014; Harrison 2013; Hawkins 2014; Herring 2016; Petrella 2013); or obese (four trials: El Beltagy 2013; Poston 2013; Poston 2015; Vinter 2011). The BMI eligibility criteria are reflected in the mean (SD) or median (interquartile range (IQR)) BMI of women pre‐pregnancy or at baseline, which was reported in all except for two trials (El Beltagy 2013; Hoirisch‐Clapauch 2016), and is summarised in Table 2.
| Study ID | Diet and exercise intervention | Control |
| Mean (SD): 25.5 (6.0) [pre‐pregnancy] | Mean (SD): 25.6 (5.1) [pre‐pregnancy] | |
| Mean (SD): 33.3 (6) [pre‐pregnancy] Mean (SD): 34.5 (6.8) [baseline] | Mean (SD): 33.4 (5.5) [pre‐pregnancy] Mean (SD): 33.9 (5.7) [baseline] | |
| Median (IQR): 31.0 (28.1‐35.9) [baseline] | Median (IQR): 31.1 (27.7‐35.6) [baseline] | |
| Not reported (all women were obese) | Not reported (all women were obese) | |
| Mean (SD): 30.4 (5.6) [baseline] | Mean (SD): 30.3 (5.9) [baseline] | |
| N (%) [pre‐pregnancy] | N (%) [pre‐pregnancy] | |
| Mean (SD): 33.5 (5.8) [early pregnancy] | Mean (SD): 32.2 (5.4) [early pregnancy] | |
| Not reported | Not reported | |
| Mean (SD): 25.7 (5.1) [pre‐pregnancy] | Mean (SD): 24.9 (5.4) [pre‐pregnancy] | |
| Mean (SD) [pre‐pregnancy] BMI ≤ 24.9 kg/m²: 21.6 (2.2) BMI ≥ 25 kg/m²: 29.5 (5.1) | Mean (SD) [pre‐pregnancy] BMI ≤ 24.9 kg/m²: 22.6 (1.9) BMI ≥ 25 kg/m²: 29.7 (1.3) | |
| Mean (SD): 20.44 (2.54) [pre‐pregnancy] | Mean (SD): 20.44 (2.54); 20.74 (2.43) [pre‐pregnancy] | |
| Mean (SD): 31.5 (6.0) [pre‐pregnancy] Mean (SD): 32.2 (5.9) [baseline] | Mean (SD): 32.0 (5.5) [pre‐pregnancy] Mean (SD): 32.3 (5.4) [baseline] | |
| Mean (SD): 27.3 (6.0) [baseline] | Mean (SD): 25.5 (3.4) [baseline] | |
| Mean (SD): 26.3 (4.9) [pre‐pregnancy] | Mean (SD): 26.4 (4.3) [pre‐pregnancy] | |
| Mean (SD): 32.1 (5) [baseline] | Mean (SD): 32.9 (6.2) [baseline] | |
| Mean (SD): 26.32 (5.6) [baseline] | Mean (SD): 26.48 (5.9) [baseline] | |
| Mean (SD) [pre‐pregnancy] Normal weight: 22.8 (1.9) Overweight: 31.4 (6.0) | Mean (SD) [pre‐pregnancy] Normal weight: 22.5 (2.0) Overweight: 34.1 (7.2) | |
| Mean (SD): 36.5 (4.7) [baseline] | Mean (SD): 36.1 (4.8) [baseline] | |
| Mean (SD): 36.3 (5.0) [baseline] | Mean (SD): 36.3 (4.6) [baseline] | |
| Median (IQR): 21.7 (19.9 ‐ 23.7) [pre‐pregnancy] Median (IQR): 22.2 (20.7 ‐ 24.3) [booking] | Median (IQR): 22.8 (20.6 ‐ 26.6) [pre‐pregnancy] Median (IQR): 23.3 (21.2 ‐ 26.8) [booking] | |
| Mean (SD): 23.8 (4.1) [pre‐pregnancy] | Mean (SD): 23.5 (3.7) [pre‐pregnancy] | |
| Median (IQR): 33.4 (31.7 ‐ 36.5) | Median (IQR): 33.3 (31.7 ‐ 36.9) | |
| Mean (SD): 22.95 (3.65) [pre‐pregnancy] | Mean (SD): 23.06 (3.63) [pre‐pregnancy] |
Abbreviations: BMI: body mass index; IQR: interquartile range; N: number; SD: standard deviation
Considering ethnicity, three trials included women predominately of ethnicities regarded to be at high risk for GDM (Asbee 2009: more than 75% of women were Hispanic or African American; Hawkins 2014: all women were Hispanic; Herring 2016: all women were African American), while five trials included women predominately of ethnicities at lower risk of GDM (Bruno 2016: more than 80% of women were Caucasian; Dodd 2014: more than 90% of women were Caucasian; Petrella 2013: more than 75% were Caucasian; Phelan 2011: more than 68% of women were non‐Hispanic white; Vinter 2011: all women were Caucasian). In seven trials ethnicity was considered 'mixed' or there was insufficient information to confidently determine ethnicity (Harrison 2013 reported only on country of birth (Australia, Southeast Asia, Southern/Central Asia, other); Hui 2012 and Hui 2014 reported only that approximately 20% of women were First Nations (Canadian Aboriginal people with First Nations status); Polley 2002, Poston 2013 and Poston 2015 only reported on the proportion of women who were 'Black' or 'White' (or 'Asian', or 'Other'); and Rauh 2013 only reported that over 80% of women were born in Germany). In eight trials, no baseline information related to the ethnicity/race/country of birth of women was reported (El Beltagy 2013; Hoirisch‐Clapauch 2016; Jing 2015; Koivusalo 2016; Korpi‐Hyovalti 2011; Luoto 2011; Sagedal 2017; Wang 2015). Information related to ethnicity is further summarised in Table 3.
| Study ID | Diet and exercise intervention | Control |
| N (%) | N (%) | |
| N (%) Caucasian: 79 (82.3) | N (%) Caucasian: 78 (82.1) | |
| N (%) | N (%) White: 998 (91.0) | |
| Not reported (conducted in Egypt) | Not reported (conducted in Egypt) | |
| Country of birth, N (%) | Country of birth, N (%) | |
| N (%) Hispanic: 33 (100) | N (%) Hispanic: 35 (100) | |
| N (%) African American: 33 (100) | N (%) African American: 33 (100) | |
| Not reported | Not reported | |
| N (%) | N (%) | |
| First Nations (Canadian Aboriginals with First Nations status), N (%) BMI ≤ 24.9 kg/m²: 2 (6.7) BMI ≥ 25 kg/m²: 3 (11.1) | First Nations (Canadian Aboriginals with First Nations status), N (%) BMI ≤ 24.9 kg/m²: 1 (3.7) BMI ≥ 25 kg/m²: 4 (13.8) | |
| Not reported (conducted in China) | Not reported (conducted in China) | |
| Not reported (conducted in Finland) | Not reported (conducted in Finland) | |
| Not reported (conducted in Norway) | Not reported (conducted in Norway) | |
| Not reported (conducted in Finland) | Not reported (conducted in Finland) | |
| N (%) Caucasian: 28 (84.9) Maghreb: 4 (12.1) Other: 1 (3.0) | Caucasian: 20 (66.7) Maghreb: 6 (20) Other: 4 (13.3) | |
| N (%) Non‐Hispanic White: 138 (68.7) Latina and Hispanic: 39 (19.6) Non‐Hispanic African American: 14 (7.1) Other: 9 (4.6) | N (%) Latina and Hispanic: 39 (19.6) Non‐Hispanic African American: 19 (9.6) Other: 7 (3.3) | |
| N (%) Black: 47 (39) White 73 (61) | ||
| N (%) White: 52 (55) Black: 38 (40) Asian: 2 (2) Other: 2 (2) | N (%) White: 51 (57) Black: 32 (26) Asian: 1 (1) Other: 5 (6) | |
| N (%) White: 490 (63) Black: 202 (26) Asian: 47 (6) Other: 44 (6) | N (%) Black: 200 (26) Asian: 48 (6) Other: 41 (5) | |
| Country of birth, N (%) Germany: 140 (83.8) Others: 27 (16.2) | Country of birth, N (%) Germany: 68 (81.9) Others: 15 (18.1) | |
| Not reported (conducted in Norway) | Not reported (conducted in Norway) | |
| N (%) | N (%) Caucasian: 154 (100) | |
| Not reported (conducted in China) | Not reported (conducted in China) | |
Abbreviations: N: number
Only one trial (Sagedal 2017) reported eligibility criteria relating to parity ‐ including only nulliparous women. Both nulliparous and multiparous women were included in the remaining trials (Asbee 2009; Bruno 2016; Dodd 2014; Harrison 2013; Hawkins 2014; Herring 2016; Koivusalo 2016; Korpi‐Hyovalti 2011; Luoto 2011; Petrella 2013; Phelan 2011; Polley 2002; Poston 2013; Poston 2015; Rauh 2013; Vinter 2011), though six trials did not report clearly report baseline information related to parity (El Beltagy 2013; Hoirisch‐Clapauch 2016; Hui 2012; Hui 2014; Jing 2015; Wang 2015). Detailed information relating to parity is reported in Table 4.
| Study ID | Diet and exercise intervention | Control |
| N (%) | N (%) | |
| N (%) 0: 53 (55.2) | N (%) 0: 59 (62.1) | |
| N (%) 0: 441 (40.2) | N (%) 0: 441 (40.2) | |
| Not reported | Not reported | |
| N (%) | N (%) | |
| N (%) | N (%) | |
| N (%): 0: 9 (27) | N (%): 0: 10 (30) | |
| Not reported | Not reported | |
| Not reported | Not reported | |
| Not reported | Not reported | |
| Not reported | Not reported | |
| Previous deliveries, N (%) | Previous deliveries, N (%) | |
| N (%) 0: 13 (50) | N (%) 0: 17 (63) | |
| N (%) 0: 103 (47.0) | N (%) 0: 73 (40.6) | |
| N (%) 0: 13 (39.4) | N (%) 0: 13 (43.3) | |
| N (%) 0: 153 (76.3) ≥ 1: 48 (23.7) | N (%) 0: 153 (76.6) ≥ 1: 47 (23.4) | |
| N (%) First pregnancy: 56 (47) Second pregnancy: 36 (30) Third pregnancy: 20 (17) > third pregnancy: 7 (6) | ||
| N (%) 0: 42 (45) 1: 29 (31) ≥ 2: 23 (24) | N (%) 0: 38 (43) 1: 36 (40) ≥ 2: 15 (17) | |
| N (%) 0: 336 (43) ≥ 1: 447 (57) | N (%) 0: 338 (44) ≥ 1: 434 (56) | |
| N (%) 0: 110 (65.9) 1: 50 (29.9) ≥ 2: 7 (4.2) | N (%) 0: 53 (63.9) 1: 23 (27.7) ≥ 2: 7 (8.4) | |
| N (%) 0: 303 (100) | N (%) 0: 303 (100) | |
| N (%) 0: 79 (52.7) | N (%) 0: 84 (54.6) | |
| Not reported | Not reported | |
Abbreviations: N: number
Interventions
Each of the 23 included trials assessed an intervention that included both diet and exercise components compared with standard/routine antenatal care and reported on GDM. However, the primary focus of many of the included trials was on limiting gestational weight gain. The interventions assessed varied greatly, as can be seen below.
-
Asbee 2009: an intensive‐lifestyle intervention consisting of an initial standardised counselling session delivered one‐on‐one in person by a dietitian in which women were provided with dietary advice, instructed to engage in moderate‐intensity exercise at least three times a week and educated about the Institute of Medicine (IOM) guidelines for gestational weight gain, supported by personalised monitoring and feedback at follow‐up at routine visits.
-
Bruno 2016: diet and exercise counselling provided in one one‐on‐one session by a dietitian at baseline (a hypocaloric, low‐glycaemic, low‐saturated fat diet and 30 minutes of moderate‐intensity exercise at least three times a week were recommended) with monitoring of progress on lifestyle changes and further individually‐tailored lifestyle advice by the dietitian and gynaecologist at routine antenatal appointments (16th, 20th, 25th and 36th weeks of pregnancy).
-
Dodd 2014: a comprehensive individually‐tailored lifestyle intervention that included a combination of diet and exercise advice and behavioural change strategies, delivered by a research dietitian and trained research assistants in three one‐on‐one face‐to‐face sessions (at entry, 28 and 36 weeks), and three phone sessions (at 22, 24 and 32 weeks).
-
El Beltagy 2013: a 12‐week mild exercise and diet control program (no further details provided in the conference abstract of this trial).
-
Harrison 2013: a personalised intervention delivered by a health coach (exercise physiologist) in four one‐on‐one sessions scheduled at the same time as routine visits (in which women were provided with individually‐tailored advice about diet and encouraged to increase exercise frequency) plus strategies to support behaviour change including self‐monitoring (pedometers provided).
-
Hawkins 2014: an intensive, personalised intervention tailored for Hispanic women consisting of six one‐on‐one face‐to‐face counselling sessions (individually‐tailored advice about diet provided and women advised to undertake at least 30 minutes of moderate‐intensity activity most days of the week to achieve the American College of Obstetricians and Gynecologists guidelines for gestational weight gain) and strategies to support adherence and behaviour change (including five telephone "booster" counselling sessions, pedometers and a exercise log books).
-
Herring 2016: a technology‐based intervention delivered via Facebook, telephone and text messaging and one one‐to‐one consultation (at baseline) tailored for African American women living in low‐income settings consisting of diet and exercise advice (including the recommendation that women increase activity to walking 5000 steps daily), distribution of digital scales for weighing food at home, strategies to support adherence (pedometers and a DVD walking video), and ongoing support via telephone and other technology platforms.
-
Hoirisch‐Clapauch 2016: diet and exercise advice (women were instructed to walk briskly for at least 40 minutes seven days a week, to avoid high‐carbohydrate index meals, e.g. such as snacks, candies, fibre‐free juices or sugar‐sweetened beverages, and to eat two daily servings of meat, poultry, fish or other protein‐rich food, starting when they decided to get pregnant and continuing until birth).
-
Hui 2012 and Hui 2014: an intensive lifestyle intervention consisting of mild to moderate exercise three to five times a week (group sessions in community centres or if not feasible, at home supported by a DVD) plus one‐on‐one diet counselling sessions (two, with a registered dietitian, providing individually‐tailored diet advice) and self‐monitoring of gestational weight gain goals.
-
Jing 2015: a moderate‐intensity intervention consisting of two one‐on‐one in person counselling sessions (with a trained graduate student) on a healthy diet and exercise regimen to follow during pregnancy, education about the benefits of a healthy lifestyle and harms of GDM (materials written by trial staff provided) as well as ongoing communication and support for behaviour change (provided through telephone or Tencent instant messenger).
-
Koivusalo 2016: an intensive lifestyle‐counselling intervention delivered via an initial two‐hour group counselling session (at enrolment) followed by three one‐to‐one in person counselling sessions delivered by trained trial nurses and dietitians supplemented by various strategies to support adherence to the diet and exercise recommendations and weight gain goals including self‐monitoring of behaviour (including via food diaries, activity log books and pedometers) and provision of free access to swimming pools and exercise classes of local municipalities.
-
Korpi‐Hyovalti 2011: an intensive lifestyle‐counselling intervention that included six one‐to‐one sessions with a nurse in which women were provided with personalised diet advice to follow during their pregnancy, as well as six sessions with a physiotherapist (in which women were encouraged to exercise 30 minutes daily if they had previously exercised less than two and a half hours per week, and 45 minutes if they had already engaged in two and a half hours per week).
-
Luoto 2011: an intensive lifestyle counselling delivered by nurses in five face‐to‐face, one‐on‐one counselling sessions (in session one gestational goals were set, women were provided with a notebook for monitoring and exercise recommendations were introduced, including participation in a monthly group exercise class, in the second session the healthy diet was introduced, sessions three reinforced the messages and focused on monitoring).
-
Petrella 2013: a Therapeutic Lifestyle Changes (TLC) program including a diet of 1700 kcal/day for overweight women and 1800 kcal/day for obese women and mild exercise (30 min/day, three times/week), introduced at randomisation by both a gynaecologist and a dietitian, and further detailed at a subsequent one‐hour appointment, with pedometers to support adherence.
-
Phelan 2011: an intensive individually‐tailored intervention consisting of one face‐to‐face visit during the first trimester delivered by a dietitian (focused on appropriate gestational weight gain, what constitutes a healthy diet during pregnancy. the benefits of walking 30 minutes walking most days of the week during pregnancy and the importance of daily self‐monitoring of eating, exercise, and weight gain) followed by three phone calls from the dietitian to support adherence and provide further tailored advice (women who were over or under weight gain guidelines during any one month interval received additional phone calls that provided structured meal plans, and specific goals).
-
Polley 2002: a lifestyle intervention consisting of education about appropriate gestational weight gain (as per the IOM guidelines), personalised advice about diet and exercise, as well as weight monitoring, delivered at regularly schedule clinic visits by masters and doctoral level staff with training in nutrition or clinical psychology and bi‐weekly provision of written education materials/reminders.
-
Poston 2013 and Poston 2015: a comprehensive intensive lifestyle change intervention that delivered via a one‐to‐one appointment with a"Health Trainer" (no specific health professional qualification, but experience in behaviour modification and conducting group sessions) and weekly group sessions for eight consecutive weeks from 19 weeks gestation (for women unable to attend, the session content was delivered by phone or email) which included diet advice (focus on substituting high‐ with low‐GI foods), exercise advice (women encouraged to undertake frequent walking at moderate intensity) as well as goal setting for diet and exercise and strategies to support achieving them (e.g. self‐monitoring through use of a pedometer and log‐book and provision of a DVD of a specifically devised pregnancy exercise regimen).
-
Rauh 2013: the Feasibility of a Lifestyle Intervention in Pregnancy to Optimise maternal weight development (FeLIPO) intervention consisting of two one‐to‐one lifestyle‐counselling sessions with trained researchers (in which women were educated about healthy gestational weight gain as per IOM guidelines, given diet and exercise advice to follow to achieve weight gain goals, including the recommendation of engaging in at least 30 minutes moderate‐intensity exercise most days of the week, and were provided with a list of suitable local prenatal exercise programs to attend) plus strategies to support behaviour change (including self‐monitoring through use of charts).
-
Sagedal 2017: the Norwegian Fit for Delivery (NFFD) intervention consisting of an intensive exercise program that included participation in group‐based exercise classes (moderate‐intensity exercise) twice a week and additional moderate‐intensity exercise three days of the week, diet advice (delivered via telephone by experienced clinical dietitians or graduate students), education focused on the IOM guidelines for gestational weight gain and strategies to support adherence to the lifestyle recommendations (including written materials reinforcing the recommendations, an invitation to one cooking class and one evening meeting).
-
Vinter 2011: intensive individually‐tailored intervention (women in the intervention group received a free six‐month gym membership and pedometer, were encouraged to attend exercise classes with a physiotherapist weekly and four to six group coaching sessions, plus individually‐tailored diet counselling with trained dietitians on four occasions, at 15, 20, 28, and 35 weeks gestation).
-
Wang 2015: a standardised group‐based lifestyle intervention that included three education sessions of 40 to 60 minutes on "a balanced diet" during pregnancy, the benefits of proper exercise (women were encouraged to walk at least 30 minutes walking after a meal at least once a day) and appropriate gestational weight gain (defined according to the IOM recommendations).
For additional details on the diet and exercise interventions (and controls) and how they varied across the trials see Characteristics of included studies.
Outcomes
For the primary outcomes for the mother, data in a format suitable for meta‐analysis were reported for GDM by 19 trials (Bruno 2016; Dodd 2014; Harrison 2013; Herring 2016; Hui 2012; Hui 2014; Jing 2015; Koivusalo 2016; Korpi‐Hyovalti 2011; Luoto 2011; Petrella 2013; Phelan 2011; Polley 2002; Poston 2013; Poston 2015; Rauh 2013; Sagedal 2017; Vinter 2011; Wang 2015), pre‐eclampsia by eight trials (Dodd 2014; Koivusalo 2016; Luoto 2011; Phelan 2011; Polley 2002; Poston 2015; Sagedal 2017; Vinter 2011), hypertension by six trials (Bruno 2016; Dodd 2014; Koivusalo 2016; Petrella 2013; Phelan 2011; Polley 2002), and caesarean section by 14 trials (Asbee 2009; Bruno 2016; Dodd 2014; Herring 2016; Hui 2012; Hui 2014; Koivusalo 2016; Petrella 2013; Phelan 2011; Polley 2002; Poston 2015; Rauh 2013; Sagedal 2017; Vinter 2011). For the primary outcomes for the child, data were reported in a format suitable for meta‐analysis by two trials for perinatal mortality (Dodd 2014; Poston 2015) and 11 trials for large‐for‐gestational age (Bruno 2016; Dodd 2014; Herring 2016; Hui 2012; Hui 2014; Luoto 2011; Poston 2013; Poston 2015; Rauh 2013; Sagedal 2017; Vinter 2011); no trial reported on mortality or morbidity composite (e.g. death, shoulder dystocia, bone fracture or nerve palsy).
Some data were reported for all secondary outcomes for the mother in the perinatal period, with between one and 17 included trials reporting data suitable for meta‐analyses or other data tables for these outcomes. However in regards to long‐term outcomes for the mother, data were only available for postnatal weight retention or return to pre‐pregnancy weight, BMI and cardiovascular health (blood pressure); no data were reported by the included trials for postnatal depression; GDM in a subsequent pregnancy; type 1 diabetes mellitus; type 2 diabetes mellitus or impaired glucose tolerance. Similarly, some data were reported for all secondary outcomes for the child in the fetal/neonatal period, with one, up to 13 included trials reporting data suitable for meta‐analyses for these outcomes. However in regards to childhood/adulthood outcomes, data were only available for weight, height, head circumference, adiposity and cardiovascular health; no data were reported by the included trials for employment, education and social status/achievement; type 1 diabetes mellitus; type 2 diabetes mellitus; impaired glucose tolerance; or neurosensory disability. Secondary outcomes related to health services were generally reported by only one to four included trials for included in meta‐analyses; no trial reported data for the outcome number of hospital or health professional visits.
Funding
Funding sources were reported by 18 included trials (Asbee 2009; Bruno 2016; Dodd 2014; Harrison 2013; Hawkins 2014; Herring 2016; Hui 2012; Hui 2014; Koivusalo 2016; Korpi‐Hyovalti 2011; Luoto 2011; Phelan 2011; Polley 2002; Poston 2013; Poston 2015; Rauh 2013; Sagedal 2017; Vinter 2011); funding bodies listed by the trials were all non‐commercial organisations (e.g. government funding bodies, health services, and other not‐for‐profit foundations). Five trials did not describe sources of funding (if any) (El Beltagy 2013; Hoirisch‐Clapauch 2016; Jing 2015; Petrella 2013; Wang 2015).
Declarations of interest
Sixteen of the trials (Asbee 2009; Bruno 2016; Dodd 2014; Harrison 2013; Hawkins 2014; Hui 2012; Hui 2014; Jing 2015; Koivusalo 2016; Korpi‐Hyovalti 2011; Luoto 2011; Petrella 2013; Phelan 2011; Poston 2013; Rauh 2013; Vinter 2011) reported that there were no conflicts of interests for any of the authors. Four trials (El Beltagy 2013; Hoirisch‐Clapauch 2016; Polley 2002; Wang 2015) did not report any information regarding declarations of interest. The remaining three trials (Herring 2016; Poston 2015; Sagedal 2017) reported information related to potential conflicts of interest for the trial authors, primarily related to income received from pharmaceutical companies/other commercial organisations. For further detail of these reported declarations, see Characteristics of included studies.
Excluded studies
We excluded 15 studies (Barakat 2006; Bo 2014; Clapp 1997; Crowther 2012; Luoto 2010; McGowan 2013; Nascimento 2012; NCT00924599; Parat 2015; Peacock 2014; Quinlivan 2011; Ruchat 2012; Simmons 2015; Sun 2016; Youngwanichsetha 2014). Seven trials assessed the effects of diet (Clapp 1997; McGowan 2013; Parat 2015; Quinlivan 2011) or exercise (Barakat 2006; Nascimento 2012; Ruchat 2012) interventions (not combined diet and exercise interventions), and one compared a diet and exercise intervention with a diet alone intervention and an exercise alone intervention (Simmons 2015). In five trials, the participants were women preconception (NCT00924599), or women with GDM (Bo 2014; Peacock 2014; Youngwanichsetha 2014) or borderline GDM (Crowther 2012). One trial was non‐randomised (Luoto 2011) and one was quasi‐randomised (Sun 2016).
Risk of bias in included studies
For a summary of the risk of bias across the included trials, see Figure 3 and Figure 4. Primarily due to lack of reporting, the overall risk of bias was judged to be unclear.
'Risk of bias' graph: review authors' judgements about each risk of bias item presented as percentages across all included trials.
'Risk of bias' summary: review authors' judgements about each risk of bias item for each included trial.
Allocation
Methods to generate the random sequence were judged to be adequate in 17 of the 23 included trials (Asbee 2009; Bruno 2016; Dodd 2014; Harrison 2013; Herring 2016; Hui 2012; Hui 2014; Jing 2015; Korpi‐Hyovalti 2011; Luoto 2011; Petrella 2013; Phelan 2011; Poston 2013; Poston 2015; Rauh 2013; Sagedal 2017; Vinter 2011), all using computer‐generated random number lists/tables. In the remaining six trials (El Beltagy 2013; Hawkins 2014; Hoirisch‐Clapauch 2016; Koivusalo 2016; Polley 2002; Wang 2015), the risk of selection bias associated with sequence generation was judged to be unclear, with insufficient information provided.
Thirteen trials (Asbee 2009; Bruno 2016; Dodd 2014; Harrison 2013; Herring 2016; Hui 2012; Hui 2014; Koivusalo 2016; Petrella 2013; Phelan 2011; Poston 2013; Poston 2015; Vinter 2011) were judged to have used adequate methods for allocation concealment. Of these, 10 (Asbee 2009; Bruno 2016; Harrison 2013; Herring 2016; Hui 2012; Hui 2014; Koivusalo 2016; Petrella 2013; Phelan 2011; Vinter 2011;) reported using sealed envelopes (with varying detail provided regarding these envelopes being consecutively numbered, opaque etc.) and three (Dodd 2014; Poston 2013; Poston 2015) used centralised phone or online randomisation services. For the remaining 10 trials (El Beltagy 2013; Hawkins 2014; Hoirisch‐Clapauch 2016; Jing 2015; Korpi‐Hyovalti 2011; Luoto 2011; Polley 2002; Rauh 2013; Sagedal 2017; Wang 2015), the risk of selection bias was judged to be unclear, with no methods detailed, or the reported methods lacking sufficient detail.
Blinding
In all 23 trials Asbee 2009; Bruno 2016; Dodd 2014; El Beltagy 2013; Harrison 2013; Hawkins 2014; Herring 2016; Hoirisch‐Clapauch 2016; Hui 2012; Hui 2014; Jing 2015; Koivusalo 2016; Korpi‐Hyovalti 2011; Luoto 2011; Petrella 2013; Phelan 2011; Polley 2002; Poston 2013; Poston 2015; Rauh 2013; Sagedal 2017; Vinter 2011; Wang 2015), the risk of performance bias, due to inadequate blinding of women and/or trial personnel, was judged to be high. While for some trials, lack of blinding was specifically stated, for others, no information was provided. While some of the trials suggested that women and/or trial personnel were blinded, in view of the interventions assessed, it was considered unlikely that this would have been successfully achieved.
Considering blinding of outcome assessors, only eight trials (Bruno 2016; Dodd 2014; Harrison 2013; Hawkins 2014; Hui 2014; Koivusalo 2016; Phelan 2011; Sagedal 2017) clearly indicated that blinded trial personnel were involved in outcome assessment or data collection, and were judged to be at low risk of detection bias. For the remaining 15 trials, the risk of detection bias was judged to be unclear (Asbee 2009; El Beltagy 2013; Herring 2016; Hoirisch‐Clapauch 2016; Hui 2012; Jing 2015; Korpi‐Hyovalti 2011; Luoto 2011; Petrella 2013; Polley 2002; Poston 2013; Poston 2015; Rauh 2013; Vinter 2011; Wang 2015), with many of the trials not clearly detailing whether it was possible to blind outcome assessors.
Incomplete outcome data
Twelve trials (Dodd 2014; Harrison 2013; Hawkins 2014; Hui 2014; Koivusalo 2016; Petrella 2013; Phelan 2011; Polley 2002; Poston 2013; Rauh 2013; Sagedal 2017; Wang 2015) were judged to be at a low risk of attrition bias, with minimal losses to follow‐up, and similar numbers/reasons for losses between groups. For four trials (Asbee 2009; Bruno 2016; Hoirisch‐Clapauch 2016; Luoto 2011), the risk of bias due to incomplete outcome data was judged to be high. In Asbee 2009, of the 144 women randomised, 100 (69%) were included in the analyses; further, the number of women excluded from each group was not reported; in Bruno 2016, of the 191 women randomised, 131 (69%) were included in the analyses; women lost to follow‐up differed from those included in the analyses on a number of characteristics; in Hoirisch‐Clapauch 2016, of the 480 women randomised, 319 (66%) completed the trial; and in Luoto 2011, of the 634 women who agreed to participate, 399 (63%) were followed up (and, for a number of outcomes "number missing" is reported in the manuscript tables, however it was not clear from which groups the data were missing).
The remaining seven trials (El Beltagy 2013; Herring 2016; Hui 2012; Jing 2015; Korpi‐Hyovalti 2011; Poston 2015; Vinter 2011) were judged to be at an unclear risk of attrition bias. In two of the trials (Herring 2016; Korpi‐Hyovalti 2011), losses/exclusions of approximately 10% were considered relatively high in small samples (66 and 60, respectively); in one trial (Vinter 2011), of 360 women randomised, a maximum of 304 (84%) were included in the analyses; in three trials (Hui 2012; Jing 2015; Poston 2015) there was some concern regarding differential losses/exclusions between groups; the final trial (El Beltagy 2013), was reported in abstract form only, with insufficient information to determine losses/exclusions.
Judgements regarding risk of attrition bias were primarily made considering the main trial period and the assessment of perinatal and fetal/neonatal clinical outcomes (not longer‐term maternal or child follow‐up, where reported).
Selective reporting
Only three trials (Dodd 2014; Poston 2015; Sagedal 2017) were judged to be at low risk of reporting bias, providing data for pre‐specified and/or expected outcomes (including from the published protocols). Fifteen trials were judged to be at an unclear risk of reporting bias (El Beltagy 2013; Harrison 2013; Herring 2016; Hoirisch‐Clapauch 2016; Hui 2012; Hui 2014; Jing 2015; Koivusalo 2016; Luoto 2011; Phelan 2011; Polley 2002; Poston 2013; Rauh 2013; Vinter 2011; Wang 2015). For the majority of these trials, there was insufficient information to confidently assess selective reporting (i.e. no access to a published trial protocol).
The remaining five trials (Asbee 2009; Bruno 2016; Hawkins 2014; Korpi‐Hyovalti 2011; Petrella 2013) were judged to be at a high risk of reporting bias. Outcomes in Asbee 2009 were not clearly pre‐specified in the methods; while the results section detailed a number of outcomes, no outcome data were reported: "no statistically significant differences were noted between the groups". In Bruno 2016, for a number of outcomes, it was only reported that there "were very few and did not differ between groups".Hawkins 2014 reported very limited clinical data and reported GDM incompletely in the text, providing only the number of cases across both groups. Korpi‐Hyovalti 2011 reported P values for baseline characteristics, and a number of outcomes only as "NS", and for some outcomes, made statements made such as "There was no statistically significant difference between the randomised groups in terms of pre‐eclampsia, induction of labor, lacerations, Cesarean deliveries (data not shown)".Petrella 2013 reported a number of outcomes incompletely in the text as "similar" or described "no statistically significant differences" between groups.
Other potential sources of bias
Sixteen trials (Asbee 2009; Bruno 2016; Dodd 2014; Harrison 2013; Hawkins 2014; Herring 2016; Hui 2012; Hui 2014; Jing 2015; Koivusalo 2016; Petrella 2013; Phelan 2011; Polley 2002; Poston 2013; Poston 2015; Sagedal 2017) were judged to be at a low risk of potential sources of other bias. In one trial (Rauh 2013), significant baseline imbalance between groups existed in maternal pre‐pregnancy weight, pre‐pregnancy BMI and maternal median weight at the first antenatal appointment. In the same trial (Rauh 2013), the authors also reported that it was easier to recruit women for the diet and exercise intervention group than for the standard care group (and accordingly, the group numbers are imbalanced in a 2:1 ratio); thus, this trial (Rauh 2013) was judged to be at high risk of other bias. For the remaining six trials (El Beltagy 2013; Hoirisch‐Clapauch 2016; Korpi‐Hyovalti 2011; Luoto 2011; Vinter 2011; Wang 2015), the risk of other bias was judged to be unclear, due to, for example, possible baseline imbalances between groups (Korpi‐Hyovalti 2011; Luoto 2011; Vinter 2011), or insufficient methodological information available to confidently assess other sources of bias (El Beltagy 2013; Hoirisch‐Clapauch 2016; Wang 2015).
Effects of interventions
See: Summary of findings for the main comparison Combined diet and exercise interventions versus standard care (mother); Summary of findings 2 Combined diet and exercise interventions versus standard care (child)
Combined diet and exercise interventions versus standard care
Primary outcomes
Mother
GDM
There was a possible reduced risk of gestational diabetes mellitus (GDM) in the diet and exercise intervention group compared with the standard care group (average risk ratio (RR) 0.85, 95% confidence interval (CI) 0.71 to 1.01; 6633 participants; 19 trials; Tau² = 0.05; I² = 42%; P = 0.07; moderate‐quality evidence) (Analysis 1.1). The screening/diagnostic tests and criteria used across the 19 trials are reported in Table 5. Three of the trials (Harrison 2013; Luoto 2011; Vinter 2011) reported data for GDM according to additional diagnostic criteria (see Table 5). While we have included the data from the main/pre‐specified criteria reported by the trials in the meta‐analysis, when we substituted results for the additional criteria provided into the meta‐analysis for this outcome, the overall result remained largely unchanged. No obvious asymmetry was observed on visual assessment of a funnel plot for this outcome (Figure 5).
Funnel plot of comparison: 1 Diet and exercise interventions versus control, outcome: 1.1 Gestational diabetes.
| Study ID | Timing | Screening/diagnosis test(s) and glucose threshold(s) used for diagnosis | Reference(s) | Notes |
| Not reported | Not reported | Not provided | Data not provided in format suitable for meta‐analysis | |
| 16th to 18th weeks; repeated in 24th to 28th weeks for women negative at first test | 75 g 2‐hour OGTT Thresholds: fasting ≥ 5.1 mmol/L and/or 1‐hour ≥ 10.0 mmol/L and/or 2‐hour ≥ 8.5 mmol/L | "IADPSG criteria" (no reference provided) | ||
| Not reported | "all women were encouraged to undergo screening" 75 g 2‐hour OGTT Thresholds: fasting ≥ 5.5 mmol/L or 2‐hour ≥ 7.8 mmol/L | South Australian Perinatal Practice Guidelines 2013 (South Australian Perinatal Practice Guidelines: diabetes mellitus and abnormal glucose tolerance Government of Australia, SA Health, 2013. www.health.sa.gov.au/ppg/Default. | ||
| 24 to 28 weeks | "All women underwent routine GDM screening" | Not provided | Data not provided in format suitable for meta‐analysis | |
| 28 weeks | 2‐hour OGTT Thresholds: fasting ≥ 5.5 mmol/L and/or 2‐hour ≥ 8.0 mmol/L OR Thresholds: fasting ≥ 5.1 mmol/L and/or 1‐hour ≥ 10.0 mmol/L and/or 2‐hour ≥ 8.5 mmol/L | ADIPS 1998 (Hoffmann L, Nolan C, Wilson JD, Oats JJN, Simmons D. Gestational diabetes mellitus: management guidelines. MJA 1998;169:93–7.) OR IADPSG 2010 (Metzger BE, Gabbe SG, Persson B, et al. International association of diabetes and pregnancy study groups recommendations on the diagnosis and classification of hyperglycaemia in pregnancy. Diabetes Care 2010;33:676–82.) | Data in meta‐analysis according to IADPSG 2010 criteria [groups Ns not reported for ADIPS 1998 criteria] | |
| 24 to 28 weeks gestation | 50 g 1‐hour OGTT Thresholds: 1‐hour > 7.493 mmol/L 100 g 3‐hour OGTT Thresholds: not reported | American Diabetes Association 2012 (American Diabetes Association. Standards of medical care in diabetes–2012. Diabetes Care 2012; 35(Suppl. 1): S11–63.) | Data not provided in format suitable for meta‐analysis | |
| Not reported | Not reported | Not provided | ||
| Not reported | Not reported | Not provided | Data not provided in format suitable for meta‐analysis | |
| Not reported | Not reported | Canadian Diabetes Association 2008 (Canadian Diabetes Association. 2008 Clinical practice guidelines for the prevention and management of diabetes in Canada. Can J Diabetes 2008;32:S168–80.) | ||
| Not reported | Not reported | Canadian Diabetes Association 2008 (Canadian Diabetes Association, Clinical Practice Guidelines Committee, Canadian Diabetes Association: 2008 Clinical Practice Guidelines for the Prevention and Management of Diabetes in Canada. Can J Diabetes Care 2008, 32:S1:171.) | ||
| Not reported | Not reported | Not provided | ||
| 24 to 28 weeks | 75 g 2‐hour OGTT Thresholds: fasting ≥ 5.3 mmol/L and/or 1‐hour ≥ 10.0 mmol/L and/or 2‐hour ≥ 8.6 mmol/L | American Diabetes Association 2008 (Holcomb SS; American Diabetes Association. Update: standards of medical care in diabetes. Nurse Pract 2008;33:12–5.) | ||
| 26 to 28 weeks | 75 g 2‐hour OGTT Thresholds: fasting ≥ 5.6 mmol/L or 2‐hour ≥ 7.8 mmol/L | Modified from the World Health Organization 1998 (Alberti KG, Zimmet PZ: Definition, diagnosis and classification of diabetes mellitus and its complications. Part 1: diagnosis and classification of diabetes mellitus: provisional report of WHO consultation. Diabet Med 1998, 15:539‐53.) | All women also underwent 75 g 2 hour OGTT at 8 to 12 weeks; those diagnosed with GDM were excluded from the trial | |
| 26 to 28 weeks | 2‐hour OGTT Thresholds: fasting ≥ 5.3 mmol/L and/or 1‐hour > 10.0 mmol/L and/or 2‐hour > 8.6 mmol/L OR 1) Any of the above thresholds or newborn birthweight ≥ 4500 g or use of insulin or other diabetic medication 2) Any of the above thresholds or newborn birthweight ≥ 4000 g or use of insulin or other diabetic medication 3) Any of the above thresholds or use of insulin or other diabetic medication | American Diabetes Association 2010 ((2010) Diagnosis and classification of diabetes mellitus. Diabetes Care 33: S62–9.) | Data in meta‐analysis according to American Diabetes Association 2010 criteria [use of data according to other criteria did not change results] | |
| 16th to 18th week or 24th to 28th week "as recommend" | 75 g 2‐hour OGTT Thresholds: not reported | American Diabetes Association 2011 (American Diabetes Association. Standards of medical care in diabetes‐2011. Diabetes Care 2011;34:S11–61.) | ||
| Not reported | Not reported | Not provided | ||
| Not reported | Not reported | Not provided | ||
| 27 + 0 to 28 + 6 weeks | 75 g 2‐hour OGTT Thresholds: fasting ≥ 5.1 mmol/L and/or 1‐hour ≥ 10.0 mmol/L and/or 2‐hour ≥ 8.5 mmol/L | IADPSG 2010 (Metzger B, Gabbe SG, Persson B, Buchanan TA, Catalano PA, Damm P, Dyer AR, Leiva A, Hod M, Kitzmiler JL, Lowe LP, McIntyre HD, Oats JJ, Omori Y, Schmidt MI: International association of diabetes and pregnancy study groups recommendations on the diagnosis and classification of hyperglycaemia in pregnancy. Diabetes Care 2010, 33:676–82.) | ||
| 27 + 0 to 28 + 6 weeks | 75 g 2‐hour OGTT Thresholds: fasting ≥ 5.1 mmol/L and/or 1‐hour ≥ 10.0 mmol/L and/or 2‐hour ≥ 8.5 mmol/L | IADPSG 2010 (Metzger BE, Gabbe SG, Persson B, et al. International Association of Diabetes and Pregnancy Study Groups recommendations on the diagnosis and classification of hyperglycaemia in pregnancy. Diabetes Care 2010; 33: 676–82.) | ||
| 24th to 28th week | 2‐hour OGTT Thresholds: not reported | German Society of Gynecology and Obstetrics 2010 (Deutsche Gesellschaft für Gynäkologie und Geburtshilfe e.V.: Diagnostik und Therapie des Gestationsdiabetes. [http://www.dggg.de/leitlinien/].) | ||
| 30 weeks | 75 g 2‐hour OGTT Thresholds: 2‐hour ≥ 7.8 mmol/L | Norway national criteria 2008 (Tore HH, Torun C. Veileder i Fødselshjelp 2008 In) NGFNSfGaO, editor. Veileder i Fødselshjelp 2008; 2008. p. 112.); World Health Organization 2006 (World Health Organization. Definition and Diagnosis of Diabetes Mellitus and Intermediate Hyperglycaemia: Report of a WHO/IDF Consultation. Geneva, Switzerland: World Health Organization, 2006.) | ||
| 28 to 30 weeks and 34 to 36 weeks | 75 g 2‐hour OGTT Thresholds: 2‐hour ≥ 9 mmol/L OR Thresholds: 2‐hour ≥ 8.5 mmol/L | "Danish national recommendations" (no reference provided) OR IADPSG 2010 (Metzger BE, Gabbe SG, Persson B, Buchanan TA, Catalano PA, Damm P et al. International Association of Diabetes and Pregnancy Study Group’s recommendations on the diagnosis and classification of hyperglycaemia in pregnancy. Diabetes Care 2010; 33: 676–82.) | All women also underwent an OGTT at baseline (12 to 15 weeks); those diagnosed with GDM were excluded from the trial Data in meta‐analysis according to Danish national recommendations [use of data according to IADPSG 2010 criteria did not change results] | |
| 24 to 28 weeks | 75 g OGTT | "The International Association of Diabetes and Pregnancy Study Groups (IADPSG) criterion was used" (no reference provided) |
Abbreviations: ADIPS: Australasian Diabetes in Pregnancy Society; g: gram; GDM: gestational diabetes mellitus; IADPSG: International Association of the Diabetes and Pregnancy Study Group; OGTT: oral glucose tolerance test;
Four trials presented data for GDM that could not be included in the above meta‐analysis: Asbee 2009 reported "No statistically significant differences were noted between the groups in... gestational diabetes mellitus";El Beltagy 2013 reported "obese women enrolled in mild physical activity program and diet plan (48 women) had a lower incidence to develop GDM than those participated in neither intervention (48 women) (OR 0.91, 95% CI 0.06‐1.02)";Hawkins 2014 reported "When we repeated the above analyses excluding women with gestational diabetes (n = 7), the findings were virtually unchanged;"Hoirisch‐Clapauch 2016 reported "Protocol W + D… helped prevent gestational diabetes (OR, 0.1; 95% CI, 0.02–0.57);" and "W&D... reduced the risk of gestational diabetes (2% vs. 11%)".
Hypertensive disorders of pregnancy
There was no evidence of a difference in the risk of pre‐eclampsia between the diet and exercise and standard care groups (RR 0.98, 95% CI 0.79 to 1.22; 5366 participants; 8 trials; low‐quality evidence); nor in the risk of severe pre‐eclampsia, eclampsia or HELLP (Haemolysis, Elevated Liver enzymes and Low Platelet count) syndrome (RR 0.72, 95% CI 0.35 to 1.46; 2088 participants; 2 trials) (Analysis 1.2); pregnancy‐induced hypertension and/or hypertension (average RR 0.78, 95% CI 0.47 to 1.27; 3073 participants; 6 trials; Tau² = 0.19; I² = 62%; very low‐quality evidence); pregnancy‐induced hypertension (average RR 0.46, 95% CI 0.16 to 1.29; 810 participants; 4 trials; Tau² = 0.72; I² = 69%) or hypertension (RR 1.07, 95% CI 0.84 to 1.38; 2532 participants; 3 trials) (Analysis 1.3).
Three trials presented data for pre‐eclampsia that could not be included in the above meta‐analysis: Asbee 2009 reported that "No statistically significant differences were noted between the groups in... preeclampsia";Korpi‐Hyovalti 2011 reported "There was no statistically significant difference between the randomised groups in terms of pre‐eclampsia;" and Hoirisch‐Clapauch 2016 reported "W&D... reduced the risk of... preeclampsia (5% vs. 13%)".
Caesarean section
There was a possible reduction in the risk of caesarean birth between the diet and exercise and standard care groups (RR 0.95, 95% CI 0.88 to 1.02; 6089 participants; 14 trials; moderate‐quality evidence) (Analysis 1.4). No obvious asymmetry was observed on visual assessment of a funnel plot for this outcome (Figure 6).
Funnel plot of comparison: 1 Diet and exercise interventions versus control, outcome: 1.4 Caesarean section.
Korpi‐Hyovalti 2011 reported "There was no statistically significant difference between the randomised groups in terms of...Cesarean deliveries (data not shown)".
Child
Perinatal mortality
Only Dodd 2014 and Poston 2015 reported on perinatal mortality, and there was no evidence of a difference in the risk observed between the diet and exercise and standard care groups (RR 0.82, 95% CI 0.42 to 1.63; 3757 participants; 2 trials; low‐quality evidence) (Analysis 1.5).
Hoirisch‐Clapauch 2016 reported "Protocol W + D… increased the rate of take‐home (OR, 6.9; 95% CI, 3.93–12.3)… babies;" and "W&D increased the rate of take‐home (88% vs. 52%)... babies".
Large‐for‐gestational age
There was no evidence of a difference in the risk of large‐for‐gestational age between the diet and exercise and standard care groups (RR 0.93, 95% CI 0.81 to 1.07; 5353 participants; 11 trials; low‐quality evidence) (Analysis 1.6). No obvious asymmetry was observed on visual assessment of a funnel plot for this outcome (Figure 7).
Funnel plot of comparison: 1 Diet and exercise interventions versus control, outcome: 1.6 Large‐for‐gestational age.
Two trials presented data for large‐for‐gestational age that could not be included in the above meta‐analysis: Hoirisch‐Clapauch 2016 reported "Protocol W + D… increased the rate of… appropriate‐for gestational‐age babies (OR, 7.5, 95% CI, 3.56–15.8);" and "W&D increased the rate of... appropriate‐for‐gestational‐age babies (respectively 90% vs. 63% and 92% vs. 61% of all live‐born babies)"; and Petrella 2013 reported "Large for gestational age babies were similar among groups".
Mortality or morbidity composite
A mortality or morbidity composite was not reported by any of the included trials.
Secondary outcomes
Mother
Perinatal outcomes
Operative vaginal birth
There was no evidence of a difference in the risk of operative vaginal birth between the diet and exercise intervention and standard care groups (RR 1.07, 95% CI 0.86 to 1.34; 2164 participants; 3 trials) (Analysis 1.7).
Asbee 2009 reported "No statistically significant differences were noted between the groups....[in] rate of ... operative vaginal delivery".
Induction of labour
There was no evidence of a difference in the risk of induction of labour between the diet and exercise intervention and standard care groups (average RR 0.92, 95% CI 0.79 to 1.06; 3907 participants; 5 trials; Tau² = 0.01; I² = 39%) (Analysis 1.8).
Korpi‐Hyovalti 2011 reported "There was no statistically significant difference between the randomised groups in terms of... induction of labor".
Perineal trauma
Only Dodd 2014 and Sagedal 2017 reported on perineal trauma, and there was no evidence of a difference in the risk between the diet and exercise intervention and standard care groups (RR 1.27, 95% CI 0.78 to 2.05; 2733 participants; 2 trials; moderate‐quality evidence) (Analysis 1.9).
Three trials presented data for perineal trauma that could be included in the above meta‐analysis: Asbee 2009 reported"No statistically significant differences were noted between the groups in...vaginal lacerations;"Korpi‐Hyovalti 2011 reported"There was no statistically significant difference between the randomised groups in terms of... lacerations;" and Petrella 2013 reported"No statistically significant differences were found in maternal morbidity (...perineal tears) at delivery".
Placental abruption
Only Poston 2015 reported on placental abruption and observed no evidence of a difference in the risk between the diet and exercise intervention and standard care groups (RR 2.96, 95% CI 0.12 to 72.50; 1555 participants; 1 trial) (Analysis 1.10).
Postpartum haemorrhage
There was no evidence of a difference in the risk of postpartum haemorrhage between the diet and exercise intervention and standard care groups (RR 1.03, 95% CI 0.89 to 1.18; 4235 participants; 3 trials) (Analysis 1.11).
Petrella 2013 reported"No statistically significant differences were found in maternal morbidity (post‐partum hemorrhage ...) at delivery".
Postpartum infection
Dodd 2014 and Poston 2015 were the only trials to report data on outcomes relating to postpartum infection, and observed no evidence of a difference in the risk between the diet and exercise intervention and standard care groups for endometritis (RR 1.19, 95% CI 0.52 to 2.74; 2142 participants; 1 trial), wound infection (RR 1.06, 95% CI 0.65 to 1.73; 2142 participants; 1 trial), postpartum antibiotic use (RR 1.00, 95% CI 0.77 to 1.31; 2142 participants; 1 trial), and postpartum sepsis (RR 0.33, 95% CI 0.01 to 8.06; 1555 participants; 1 trial) (Analysis 1.12).
Gestational weight gain
There was evidence of less total gestational weight gain in the diet and exercise intervention group compared with the standard care group (mean difference (MD) ‐0.89 kg, 95% CI ‐1.39 to ‐0.40; 5052 participants; 16 trials; Tau² = 0.37; I² = 43%;moderate‐quality evidence) (Analysis 1.13). Some asymmetry was observed on visual assessment of a funnel plot for this outcome, possibly indicating a lack of small negative studies (Figure 8).
Funnel plot of comparison: 1 Diet and exercise interventions versus control, outcome: 1.13 Gestational weight gain (kg).
Four additional trials that did not report on total gestational weight gain, reported on weight gain at various time points during pregnancy; there was no evidence of a difference in gestational weight gain during the first (MD ‐0.03 kg, 95% CI ‐0.62 to 0.56; 272 participants; 1 trial), second (MD ‐0.38 kg, 95% CI ‐0.77 to 0.02; 541 participants; 2 trials) or third trimesters (MD ‐0.10 kg, 95% CI ‐1.17 to 0.97; 269 participants; 1 trial), or specifically at 20 to 24 weeks gestation (MD ‐0.45 kg, 95% CI ‐1.48 to 0.58; 221 participants; 1 trial); however, there was evidence of less weight gain at 26 to 28 weeks (MD ‐0.90 kg, 95% CI ‐1.75 to ‐0.05; 203 participants; 1 trial) (Analysis 1.14).
Three further trials presented data on gestational weight gain that could not be included in the above meta‐analysis: El Beltagy 2013 reported "weight gain per week was significantly lower in the diet and exercise group than the other group (p<0.001)";Hoirisch‐Clapauch 2016 reported "Protocol W + D… also helped prevent… excessive weight gain in term pregnancies (10 ± 2 versus 17 ± 9 kg);" and Poston 2013 reported "There was also no significant difference in gestational weight gain between control and intervention arms (secondary outcome)".
There was evidence of less gestational weight gain per week in the diet and exercise intervention group compared with the standard care group (MD ‐0.03 kg, 95% CI ‐0.06 to ‐0.00; 2772 participants; 4 trials; Tau² = 0.00; I² = 64%) (Analysis 1.15).
There was also evidence of a reduction in gestational weight gain above IOM recommendations in the diet and exercise intervention group compared with the standard care group (average RR 0.87, 95% CI 0.79 to 0.96; 4556 participants; 11 trials; Tau² = 0.01; I² = 50%) (Analysis 1.16). No obvious asymmetry was observed on visual assessment of a funnel plot for this outcome (Figure 9).
Funnel plot of comparison: 1 Diet and exercise interventions versus control, outcome: 1.16 Gestational weight gain (above IOM recommendations).
Harrison 2013 reported "The proportion of women exceeding Institute of Medicine recommendations for gestational weight gain was significantly reduced in the intervention group compared to controls, with results most marked in overweight women (17% vs 55%)".
There was, however, no evidence of a difference in gestational weight gain within (RR 1.02, 95% CI 0.93 to 1.11; 3730 participants; 9 trials) (Analysis 1.17) or below (RR 1.10, 95% CI 0.98 to 1.24; 3499 participants; 7 trials) (Analysis 1.18) IOM recommendations between the diet and exercise intervention and standard care groups.
Adherence to the intervention
The following trials provided information relating to adherence to the intervention, which was not considered suitable for meta‐analysis.
-
Harrison 2013: "Of the women allocated to the intervention, 95% attended session two, 89% session three and 93% session four".
-
Hawkins 2014: "In the lifestyle intervention group, 100% of the first and 96.9% of the second counselling sessions were completed. Rates were 93.5% for the third session and declined to 76.9% for session 4, 87.5% for session 5 and 85.7% for session 6. Overall, the women completed a mean ± SD of 4 ± 1.45 sessions".
-
Herring 2016: "The mean frequency of self‐monitoring response texts per intervention participant was 65.2 ± 29.4 (expected texts = 114), with the majority of participants (70%) responding to ≥ 50% of the self‐monitoring text prompts... Intervention participants also completed an average of 4 ± 1.5 coaching calls (expected calls = 7) during the first 12 program weeks and an average of 1 ± 0.5 additional calls until delivery... More than 90% of calls were attempted. While few participants (11%) commented or "liked" posts on Facebook, average number of weekly coach posts was 1.7 ± 0.9, which waned over time".
-
Hui 2014: "All participants in the intervention group met with the dietitian at baseline and at 2 months after. These women attended the group exercise and exercise regularly at home according to the protocol".
-
Luoto 2011: "The timing of the counseling sessions was as intended: The mean weeks gestation at the primary session was 9 (range 6 to 13), at the first booster session 17 (range 8‐25), at the second booster session 23 (range 19 to 29), at the third booster session 33 (range 30 to 37) and at the final booster session 37 (range 34 to 40). The mean duration of the primary counseling session on PA was 21 min (range 5 to 55) and the duration of subsequent booster sessions 10 (range 0 to 30), 11 (range 2 to 32), 10 (range 0 to 56) and 6 min (range 2 to 20). Two participants missed the second booster session at 22‐24 weeks gestation and three participants the last booster at 36‐37 weeks gestation. The average attendance at the monthly thematic meetings with group exercise was 33% ranging from 20% to 52% in the municipalities. On average, only 6% (municipality‐specific range 0% to 15%) of the participants attended all thematic meetings and 33% (municipality‐ specific range 10% to 67%) at least 3 of the meetings during their pregnancy".
-
Poston 2013: "Of the 94 women randomised to the intervention, 82 (88%) attended at least one group session, and 60 (64%) attended 4 or more. A total of 42 women (45%) received material from all eight sessions, 6 by full attendance (6%) and the remainder when partly/wholly covered by subsequent phone contact. For all women, 6.1 (SD 2.6) sessions were attended or partly/wholly covered".
-
Poston 2015: "On average, women who were assigned the intervention attended seven (SD 3) of eight health trainer‐led sessions, including four in person, and a further three by telephone or email. For sessions attended in person, 30% of women attended only one session, and 46% attended fewer than four. For sessions delivered by any method, 10% of women received only one session and 17% had fewer than four".
-
Sagedal 2017: "Among women in the intervention arm, 259 (87.5%) received both dietary consultations, 28 (9.5%) received one, and nine (3%) received none. All received access to physical fitness classes and 274 (92.6%) attended at least one class. The number of classes attended varied between 0 and 38, with a median of 14;" and at 12‐month follow‐up "Among intervention participants in the present analysis, 115 (56.7%) were defined as compliant and 88 (43.3%) non‐compliant with the intervention".
-
Vinter 2011: "92% of the women completed all four dietetic counseling sessions and 98% completed at least three sessions… The mean attendance for the 20 aerobic classes was 10.4 h, and 56% of women in the intervention group attended the aerobic classes for at least half of the lessons".
Behaviour changes associated with the intervention
Seventeen of the included trials (Bruno 2016; Dodd 2014; Harrison 2013; Hawkins 2014; Hui 2012; Hui 2014; Jing 2015; Koivusalo 2016; Luoto 2011; Petrella 2013; Phelan 2011; Polley 2002; Poston 2013; Poston 2015; Rauh 2013; Sagedal 2017; Vinter 2011) provided information relating to diet and/or exercise changes, which (given the substantial variation in reporting) was not considered suitable for meta‐analysis. We have summarised the findings from the trials in Analysis 1.19. The majority of these trials (Bruno 2016; Dodd 2014; Harrison 2013; Hawkins 2014; Hui 2012; Hui 2014; Jing 2015; Koivusalo 2016; Luoto 2011; Poston 2013; Poston 2015; Rauh 2013; Sagedal 2017; Vinter 2011) observed some evidence of benefit(s) in favour of the diet and exercise interventions; while one trial (Polley 2002) observed no evidence of difference between the diet and exercise interventions and control, and one trial (Bruno 2016) observed some evidence of benefit in favour of the control for exercise. Petrella 2013 did not report group differences.
Relevant biomarker changes associated with the intervention
Six of the included trials (Hawkins 2014; Koivusalo 2016; Korpi‐Hyovalti 2011; Luoto 2011; Poston 2015; Vinter 2011) provided information related to biomarker changes, which (given the substantial variation in reporting) was not considered suitable for meta‐analysis. We have summarised the findings from the trials in Analysis 1.20, Two of the trials (Koivusalo 2016; Vinter 2011) reported some evidence of benefit(s) in favour of the diet and exercise interventions for these changes; while the other four trials (Hawkins 2014; Korpi‐Hyovalti 2011; Luoto 2011; Poston 2015) observed no evidence of difference between the diet and exercise interventions and control.
Sense of well‐being and quality of life
Four of the included trials (Dodd 2014; Luoto 2011; Phelan 2011; Poston 2013) provided information related to sense of well‐being and/or quality of life, which (given the substantial variation in reporting) was not considered suitable for meta‐analysis. We have summarised the findings from the trials in Analysis 1.21. One of the trials (Dodd 2014) observed some evidence of benefit in favour of the diet and exercise intervention; while two of the trials (Luoto 2011; Poston 2013) observed no evidence of difference between the diet and exercise interventions and control, and one trial (Phelan 2011) observed some evidence of benefit in favour of the control.
Views of intervention
The following trials provided information relating to views of the intervention, which was not suitable for meta‐analysis.
-
Dodd 2014: "Although there were no significant differences in the proportion of women who indicated that they would participate in the study again [Lifestyle Advice 433 (74.4%) vs. Standard Care 467 (74.8%); p = 0.7222] or recommend participation to a friend [Lifestyle Advice 484 (82.7%) vs. Standard Care 492 (78.8%); p = 0.2302], women who received the intervention were more likely to be satisfied with their group allocation [Lifestyle Advice 506 (87.5%) vs. Standard Care 439 (70.6%); p < 0.0001]".
-
Hawkins 2014: "The majority of the participants were satisfied with the amount of information received (83.9%) and the amount of time spent on the study (88.7%), and found the written materials sometimes or always useful (80.6%). Finally, 91.9% of the women reported that they would definitely or possibly participate in a similar study in the future".
-
Herring 2016: "Among intervention participants who completed the treatment acceptability questionnaire (n= 22; 81%), 96% reported that the skills they learned in the program were extremely helpful (at least an 8 on a 10‐point scale); 96% found the text messages and 82% found the coach calls extremely useful; and 87% reported the program was extremely successful in changing eating habits. Qualitative feedback included: (i) "I believe without this program my weight gain would have been out of control" and (ii) "I’m [now] watching what I eat and drink as well as monitoring my kids diets so we can stay healthy and fit throughout our lives".
-
Poston 2013: "Women in both arms of the trial found the research processes acceptable, and felt supported by the study midwives. Women in the intervention group were generally willing, in principle, to attend the eight health trainer sessions, and most women who attended valued the group approach, citing opportunities to raise questions and discuss each other's experiences. Some were surprised at the extent of the intervention, having anticipated a less intensive, more advice‐based approach...Some women found the information contained in the handbook new, whilst for others it was too basic. The pedometers and step goals were generally well received. Setting and reflecting on weekly goals was motivational for most, but could also invoke feelings of guilt, or a sense of being observed and judges. Women reported having watched the DVD, but few used it regularly".
Breastfeeding
There was no evidence of a difference in exclusive breastfeeding at three days (RR 1.02, 95% CI 0.91 to 1.15; 695 participants; 1 trial), six weeks (RR 0.93, 95% CI 0.76 to 1.13; 202 participants; 1 trial) or six months (RR 0.91, 95% CI 0.61 to 1.36; 921 participants; 2 trials) postpartum (Analysis 1.22); or in partial breastfeeding at three days (RR 0.51, 95% CI 0.40 to 0.66; 695 participants; 1 trial), six weeks (RR 1.44, 95% CI 0.80 to 2.60; 202 participants; 1 trial) or six months postpartum (RR 0.98, 95% CI 0.82 to 1.18; 921 participants; 2 trials) (Analysis 1.23).
Three trials presented data on breastfeeding that could not be included in the above meta‐analysis: Rauh 2013 reported only group means, with no measures of variance, and found no difference between groups in exclusive and total breastfeeding durations (Analysis 1.24); Phelan 2011 reported"The intervention did not target breastfeeding and had no significant effect on breastfeeding rates, which were low in both the intervention and standard‐care groups (10.4% and 8.3%, respectively, at 6 mo and 3.4% and 4.6%, respectively, at 12 mo)";Sagedal 2017 reported "There was no significant difference in duration of breastfeeding between women compliant with the intervention and those in the control group (37.3 versus 34.2 weeks, mean difference 3.0 weeks, 95% CI ‐1.3, 7.5; P = 0.294)".
Long‐term maternal outcomes
Postnatal depression
Postnatal depression was not reported by the included trials.
Postnatal weight retention or return to pre‐pregnancy weight
There was evidence of less postnatal weight retention at latest time reported (from six weeks to 12 months postpartum) in the diet and exercise intervention group compared with the standard care group (MD ‐0.94 kg, 95% CI ‐1.52 to ‐0.37; 1673 participants; 6 trials) (Analysis 1.25).
There was also evidence of an increased chance of returning to pre‐pregnancy weight at latest time reported (from six to 12 months postpartum) in the diet and exercise intervention group compared with the standard care group (RR 1.25, 95% CI 1.08 to 1.45; 960 participants; 3 trials) (Analysis 1.26).
Postnatal BMI
Harrison 2013 and Poston 2015 reported on postnatal BMI (at six weeks and six months postpartum respectively), and there was no evidence of a difference between the diet and exercise intervention and standard care groups (MD ‐0.15 kg/m², 95% CI ‐0.85 to 0.55; 902 participants; 2 trials). Harrison 2013, however, observed evidence of a smaller change in BMI from baseline to six weeks postpartum in the diet and exercise group compared with the standard care group (MD ‐0.56 kg/m², 95% CI ‐1.12 to ‐0.00; 202 participants; 1 trial) (Analysis 1.27).
GDM in subsequent pregnancy
GDM in subsequent pregnancies was not reported by the included trials.
Type 1 diabetes mellitus
Type 1 diabetes mellitus was not reported by the included trials.
Type 2 diabetes mellitus
Type 2 diabetes mellitus was not reported by the included trials.
Impaired glucose tolerance
Impaired glucose tolerance was not reported by the included trials.
Cardiovascular health
Vinter 2011 observed no evidence of a difference in median systolic or diastolic blood pressure between the diet and exercise intervention and standard care groups at six months postpartum (Analysis 1.28).
Child
Fetal/neonatal outcomes
Stillbirth
There was no evidence of a difference in risk of stillbirth between the diet and exercise intervention and standard care groups (RR 0.69, 95% CI 0.35 to 1.36; 4783 participants; 5 trials) (Analysis 1.29).
Vinter 2011 presented data related to stillbirth, however it was unclear whether one of the three stillbirths occurred in the intervention or standard care group; and it was additionally unclear as to whether the three stillbirths discussed were the only deaths that occurred: "One woman had an unexplained stillbirth after induction of labor in GA 42. Two additional women had a preterm delivery with stillborn infants in second trimester of pregnancy, one from each randomization group".
Neonatal mortality
Only Dodd 2014 and Poston 2015 reported on neonatal mortality, and there was no evidence of a difference in risk between the diet and exercise intervention and standard care groups overall (RR 2.31, 95% CI 0.60 to 8.90; 3756 participants; 2 trials), or in Dodd 2014 when mortality associated with no lethal anomalies (RR 0.99, 95% CI 0.06 to 15.85; 2202 participants; 1 trial) and mortality due to lethal anomalies (RR 6.95, 95% CI 0.36 to 134.38; 2202 participants; 1 trial) were considered separately (Analysis 1.30).
Gestational age at birth
There was no evidence of a difference in gestational age at birth between the diet and exercise intervention and standard care groups (MD 0.05 weeks, 95% CI ‐0.05 to 0.15; 5658 participants; 11 trials) (Analysis 1.31). No obvious asymmetry was observed on visual assessment of a funnel plot for this outcome (Figure 10).
Funnel plot of comparison: 1 Diet and exercise interventions versus control, outcome: 1.31 Gestational age at birth (weeks).
Four trials presented data on gestational age at birth that could not be included in the above meta‐analysis: Polley 2002 reported only the mean values by group, and Vinter 2011 reported median values and interquartile ranges by group; neither trial observed evidence of a difference between groups (Analysis 1.32); Hoirisch‐Clapauch 2016 reported "Protocol W + D… increased the rate of … full‐term (OR, 12.2; 95% CI, 5.96–25.2)… babies";Korpi‐Hyovalti 2011 reported "There was no statistically significant difference between the randomized groups in terms of gestational age... (data not shown)".
Preterm birth
There was evidence of a reduction in preterm birth in the diet and exercise intervention group compared with the standard care group (RR 0.80, 95% CI 0.65 to 0.98; 5398 participants; 11 trials) (Analysis 1.33). No obvious asymmetry was observed on visual assessment of a funnel plot for this outcome (Figure 11).
Funnel plot of comparison: 1 Diet and exercise interventions versus control, outcome: 1.33 Preterm birth.
Apgar score less than seven at five minutes
There was no evidence of a difference in risk of Apgar score less than seven at five minutes between the diet and exercise intervention and standard care groups (RR 0.80, 95% CI 0.48 to 1.32; 2864 participants; 3 trials) (Analysis 1.34).
Petrella 2013 reported "Low 5‐min Apgar... [was] equally distributed among groups".
Macrosomia
There was evidence of a reduction in macrosomia, defined as birthweight less than 4000 g (RR 0.89, 95% CI 0.78 to 1.01; 5368 participants; 9 trials; P = 0.06) and evidence of a reduction in macrosomia, defined as birthweight less than 4500 g (RR 0.63, 95% CI 0.42 to 0.94; 3061 participants; 4 trials) in the diet and exercise intervention group compared with the standard care group (Analysis 1.35). No obvious asymmetry was observed on visual assessment of a funnel plot for this outcome (Figure 12).
Funnel plot of comparison: 1 Diet and exercise interventions versus control, outcome: 1.35 Macrosomia.
Korpi‐Hyovalti 2011 reported "There was no difference in macrosomia (p = 0.480, adjusted by the prepregnancy weight of the women) between the groups".
Small‐for‐gestational age
There was a possible increase in the risk of small‐for‐gestational age between the diet and exercise intervention and standard care groups (RR 1.20, 95% CI 0.95 to 1.52; 2434 participants; 6 trials) (Analysis 1.36).
Birthweight and z score
There was no evidence of a difference in birthweight (MD ‐17.67 g, 95% CI ‐46.28 to 10.94; 5763 participants; 13 trials) (Analysis 1.37), or birthweight z score (MD ‐0.05, 95% CI ‐0.13 to 0.03; 2661 participants; 4 trials) (Analysis 1.39) between the diet and exercise intervention and standard care groups. No obvious asymmetry was observed on visual assessment of a funnel plot for this outcome (Figure 13).
Funnel plot of comparison: 1 Diet and exercise interventions versus control, outcome: 1.37 Birthweight (g).
Three trials presented data on birthweight that could not be included in the above meta‐analysis: Herring 2016 and Polley 2002 reported only the mean values by group; Vinter 2011 reported median values and interquartile ranges by group. While Herring 2016 and Polley 2002 observed no evidence of a difference in birthweight between the two groups, Vinter 2011 reported a higher birthweight in the diet and exercise intervention group compared with the standard care group (Analysis 1.38).
Head circumference and z score
There was no evidence of a difference in head circumference (MD ‐0.01 cm, 95% CI ‐0.11 to 0.10; 4229 participants; 4 trials) (Analysis 1.40), or head circumference z score (reported by Dodd 2014 only) (MD ‐0.05, 95% CI ‐0.14 to 0.04; 2142 participants; 1 trial) (Analysis 1.41) between the diet and exercise intervention and standard care groups.
Length and z score
There was no evidence of a difference in length between the diet and exercise intervention and standard care groups (MD ‐0.09 cm, 95% CI ‐0.26 to 0.09; 3303 participants; 6 trials) (Analysis 1.42). There was evidence of a lower length z score in the diet and exercise intervention group compared with the standard care group (reported by Dodd 2014 and Luoto 2011 only) (MD ‐0.08, 95% CI ‐0.15 to ‐0.02; 2235 participants; 2 trials) (Analysis 1.43).
Ponderal index
There was no evidence of a difference in ponderal index between the diet and exercise intervention and standard care groups (MD 0.04 kg/m3, 95% CI ‐0.16 to 0.25; 2826 participants; 3 trials) (Analysis 1.44).
Adiposity
Dodd 2014; and Poston 2015 reported on adiposity at birth, and there was no evidence of a difference in sum of skinfold thickness (MD 0.09 mm, 95% CI ‐0.33 to 0.50; 1472 participants; 2 trials) (Analysis 1.45) or abdominal circumference (MD ‐0.01 cm, 95% CI ‐0.23 to 0.22; 1566 participants; 2 trials) (Analysis 1.46) between the diet and exercise intervention and standard care groups.
Dodd 2014 and Poston 2015 provided additional information related to adiposity at birth, which (given the substantial variation in reporting) was not considered suitable for meta‐analysis. We have summarised the findings from the trials in Analysis 1.47. Neither trial observed evidence of a difference between the diet and exercise intervention and standard care groups for measures of adiposity.
Shoulder dystocia
Only Dodd 2014 and Sagedal 2017 reported on shoulder dystocia, and there was no evidence of a difference in risk between the diet and exercise intervention and standard care groups (RR 1.20, 95% CI 0.79 to 1.83; 2733 participants; 2 trials) (Analysis 1.48).
Nerve palsy
Dodd 2014 observed no evidence of a difference in risk of nerve palsy between the diet and exercise intervention and standard care groups (RR 1.99, 95% CI 0.36 to 10.82; 2142 participants; 1 trial) (Analysis 1.49).
Bone fracture
Dodd 2014 observed no evidence of a difference in risk of bone fracture between the diet and exercise intervention and standard care groups (RR 1.99, 95% CI 0.36 to 10.82; 2142 participants; 1 trial) (Analysis 1.50).
Respiratory distress syndrome
Only Dodd 2014 and Koivusalo 2016 reported on respiratory distress syndrome, and there was evidence of a reduction in the risk in the diet and exercise intervention group compared with the standard care group (RR 0.56, 95% CI 0.33 to 0.97; 2411 participants; 2 trials) (Analysis 1.51).
Korpi‐Hyovalti 2011 reported "There was no statistically significant difference between the randomized groups in terms of... respiratory distress (data not shown)".
Hypoglycaemia
Only Dodd 2014 and Poston 2015 reported on neonatal hypoglycaemia, and there was no evidence of a difference in risk between the diet and exercise intervention and standard care groups (average RR 1.42, 95% CI 0.67 to 2.98; 3653 participants; 2 trials; Tau² = 0.23; Chi² = 4.39, P = 0.04; I² = 77%; low‐quality evidence) (Analysis 1.52).
Hoirisch‐Clapauch 2016 reported "Protocol W + D… also helped prevent… neonatal hypoglycemia (2% versus 17%, OR, 0.1; 95% CI, 0.03–0.46);" and "W&D... reduced the risk of... neonatal hypoglycaemia (2% vs. 16%)".
Hyperbilirubinaemia
Dodd 2014 observed no evidence of a difference in risk of neonatal hyperbilirubinaemia between the diet and exercise intervention and standard care groups (RR 0.82, 95% CI 0.61 to 1.11; 2142 participants; 1 trial) (Analysis 1.53).
Korpi‐Hyovalti 2011 reported "There was no statistically significant difference between the randomized groups in terms of... jaundice requiring phototherapy... (data not shown)".
Childhood/adulthood outcomes
Weight and z scores
Poston 2015, Rauh 2013 and Vinter 2011 reported on childhood weight (at six months, 10‐12 months and 2.8 years respectively), and there was no evidence of a difference between the diet and exercise intervention and standard care groups. (MD ‐0.05 kg, 95% CI ‐0.33 to 0.22; 882 participants; 3 trials; Tau² = 0.03; Chi² = 3.20, P = 0.20; I² = 37%) (Analysis 1.54). Poston 2015 also observed no difference in childhood weight z score at six months between the diet and exercise intervention and standard care groups (MD ‐0.09, 95% CI ‐0.26 to 0.08; 643 participants; 1 trial) (Analysis 1.55).
Height and z scores
Poston 2015 and Vinter 2011 reported on childhood height (at six months, and 2.8 years respectively), and there was no evidence of a difference between the diet and exercise intervention and standard care groups (MD 0.33 cm, 95% CI ‐0.58 to 1.25; 816 participants; 2 trials) (Analysis 1.56). Poston 2015 also observed no difference in childhood height z score at six months between the diet and exercise intervention and standard care groups (MD ‐0.02, 95% CI ‐0.31 to 0.27; 622 participants; 1 trial) (Analysis 1.57).
Head circumference and z scores
Poston 2015 observed no difference in childhood head circumference at six months between the diet and exercise intervention and standard care groups (MD ‐0.12 cm, 95% CI ‐0.70 to 0.46; 670 participants; 1 trial) (Analysis 1.58).
Adiposity
Poston 2015 and Vinter 2011 reported on childhood adiposity (at six months, and 2.8 years, respectively), and there was no evidence of a difference between the diet and exercise intervention and standard care groups, as measured by: BMI z score (MD 0.05, 95% CI ‐0.29 to 0.40; 794 participants; 2 trials; Tau² = 0.04; I² = 59%; low‐quality evidence) (Analysis 1.59), abdominal circumference (MD 0.26 cm, 95% CI ‐0.37 to 0.90; 833 participants; 2 trials) (Analysis 1.60), subscapular skinfold thickness (MD ‐0.17 mm, 95% CI ‐0.66 to 0.32; 705 participants; 2 trials; Tau² = 0.09; I² = 70%) (Analysis 1.61), triceps skinfold thickness (MD ‐0.12 mm, 95% CI ‐0.48 to 0.23; 784 participants; 2 trials) (Analysis 1.62) and total body fat (MD ‐0.74 %, 95% CI ‐1.56 to 0.07; 614 participants; 2 trials) (Analysis 1.63).
Poston 2015 and Vinter 2011 provided additional information related to childhood adiposity (at six months, and 2.8 years, respectively), which (given the substantial variation in reporting) was not considered suitable for meta‐analysis. We have summarised the findings from the trials in Analysis 1.64. Neither trial observed evidence of a difference between the diet and exercise intervention and standard care groups for measures of adiposity, except for in Poston 2015, who observed evidence of a lower subscapular skinfold thickness z score at six months for the diet and exercise intervention group compared with the standard care group.
Cardiovascular health
Vinter 2011 provided information related to various measures of childhood cardiovascular health at 2.8 years; we have summarised the findings in Analysis 1.65. Vinter 2011 observed no evidence of differences between the diet and exercise intervention and standard care groups for these measures.
Employment, education and social status/achievement
Employment, education and social status/achievement were not reported by the included trials.
Type 1 diabetes mellitus
Type 1 diabetes mellitus was not reported by the included trials.
Type 2 diabetes mellitus
Type 2 diabetes mellitus was not reported by the included trials.
Impaired glucose tolerance
Impaired glucose tolerance was not reported by the included trials.
Neurosensory disability
Neurosensory disability was not reported by the included trials.
Health services
Number of hospital or health professional visits
Numbers of hospital or health professional visits were not reported by the included trials.
Number of antenatal visits or admissions
Koivusalo 2016 observed no evidence of a difference in the number of antenatal clinic visits before the second‐trimester oral glucose tolerance test (OGTT) between the diet and exercise intervention and standard care groups (MD 0.00 visits, 95% CI ‐0.36 to 0.36; 269 participants; 1 trial) (Analysis 1.66).
Dodd 2014 observed no evidence of a difference in the risk of antenatal hospital admission between the diet and exercise intervention and standard care groups (RR 0.86, 95% CI 0.71 to 1.04; 2153 participants; 1 trial) (Analysis 1.67).
Length of antenatal stay
Dodd 2014 observed evidence of a reduction in length of antenatal stay for the diet and exercise intervention group compared with the standard care group (MD ‐0.27 days, 95% CI ‐0.49 to ‐0.05; 2153 participants; 1 trial); Poston 2015, however, observed no evidence of a difference in number of antenatal inpatient nights (for those women admitted antenatally) (MD 0.00 nights, 95% CI ‐1.00 to 1.00; 139 participants; 1 trial) (Analysis 1.68).
Neonatal intensive care unit admission
There was no evidence of a difference in risk of neonatal intensive care unit admission between the diet and exercise intervention and standard care groups (RR 1.03, 95% CI 0.93 to 1.14; 4549 participants; 4 trials) (Analysis 1.69).
Three trials presented data on neonatal intensive care unit admission that could not be included in the above meta‐analysis: Bruno 2016 reported "Newborns... admitted to the NICU (3) were very few and did not differ between the groups";Korpi‐Hyovalti 2011 reported "There was no statistically significant difference between the randomized groups in terms of... admissions to neonatal intensive care unit... (data not shown);" and Petrella 2013 reported "Neonatal Intensive Care Unit admission [was] equally distributed among groups".
Length of postnatal stay (mother)
Dodd 2014 and Poston 2015 reported on length of postnatal stay (mother) (in Poston 2015 postnatal inpatient nights were reported), and there was no evidence of a difference between the diet and exercise intervention and standard care groups (MD 0.01 days, 95% CI ‐0.14 to 0.17; 3511 participants; 2 trials; Tau² = 0.01; I² = 47%) (Analysis 1.70).
Length of postnatal stay (baby)
Dodd 2014 and Poston 2015 reported on length of postnatal stay (baby), and there was no evidence of a difference between the diet and exercise intervention and standard care groups (MD ‐0.35 days, 95% CI ‐0.90 to 0.20; 3618 participants; 2 trials) (Analysis 1.71).
Costs to families associated with the management provided
Luoto 2011 observed no evidence of a difference in costs to families associated with the management provided between the diet and exercise intervention and standard care groups, as measured by: delivery costs to the patient (MD 3.00 €, 95% CI ‐10.82 to 16.82; 93 participants; 1 trial) and neonatal care costs to the patient (MD 3.00 €, 95% CI ‐13.67 to 19.67; 93 participants; 1 trial) (Analysis 1.72). In Luoto 2011, unit costs were entered at the price level for 2009.
Costs associated with the intervention
Luoto 2011 reported that the supplemental public‐health nurse’s and physiotherapist’s work contributions per person were €118 and €23, respectively for the diet and exercise intervention group. Luoto 2011 observed no evidence of a difference in costs associated with the intervention between the diet and exercise intervention and standard care groups, as measured by: total costs (MD 769.00 €, 95% CI ‐1032.23 to 2570.23; 93 participants; 1 trial) (Analysis 1.73). In Luoto 2011 unit costs were entered at the price level for 2009.
Luoto 2011 also reported that "The study indicated that intensive lifestyle counselling among GDM‐risk groups was not significantly cost‐effective as compared to the usual care for birth weight... quality of life in a 15‐dimension questionnaire... or VAS".
Cost of maternal care
Luoto 2011 observed no evidence of a difference in costs of maternal care between the diet and exercise intervention and standard care groups, as measured by: costs of visits for primary health care (MD ‐43.00 €, 95% CI ‐127.61 to 41.61; 93 participants; 1 trial), costs of visits for specialist health care (MD ‐47.00 €, 95% CI ‐195.33 to 101.33; 93 participants; 1 trial), costs of visits to a diabetes nurse (MD 6.00 €, 95% CI ‐7.02 to 19.02; 93 participants; 1 trial), costs of visits to a dietitian (not estimable), costs of use of insulin/other diabetes medications (MD ‐1.00 €, 95% CI ‐7.83 to 5.83; 93 participants; 1 trial), costs of hospital days before and after delivery (MD 101.00 €, 95% CI ‐206.71 to 408.71; 93 participants; 1 trial), delivery cost to the municipality (MD 22.00 €, 95% CI ‐234.43 to 278.43; 93 participants; 1 trial), costs of absence from work (MD 128.00 €, 95% CI ‐1295.58 to 1551.58; 93 participants; 1 trial) (Analysis 1.74). In Luoto 2011 unit costs were entered at the price level for 2009.
Cost of infant care
Luoto 2011 observed no evidence of a difference in costs of infant care between the diet and exercise intervention and standard care groups, as measured by: neonatal care cost to municipality (MD 453.00 €, 95% CI ‐298.20 to 1204.20; 93 participants; 1 trial) (Analysis 1.75). In Luoto 2011 unit costs were entered at the price level for 2009.
Subgroup analyses
Trial design
Analyses based on trial design used (individually‐randomised versus cluster‐randomised), revealed no clear subgroup differences for the primary outcomes, GDM (Chi² = 0.22; P = 0.64; I² = 0%) (Analysis 2.1), pre‐eclampsia (Chi² = 0.07; P = 0.79; I² = 0%) (Analysis 2.2), caesarean birth (Chi² = 0.52; P = 0.47; I² = 0%) (Analysis 2.3), and large‐for‐gestational age (Chi² = 1.09; P = 0.30; I² = 8.3%) (Analysis 2.4), suggesting no clear differences in treatment effect for these outcomes according to the randomisation unit. We did not perform subgroup analyses based on trial design for perinatal mortality and pregnancy‐induced hypertension, as only individually‐randomised trials reported on these outcomes.
Maternal BMI (at or before trial entry)
Analyses were performed based on maternal BMI at or before trial entry (considering normal weight women (BMI < 25 kg/m²) versus overweight or obese women (BMI ≥ 25 kg/m²) versus obese women (BMI ≥ 30 kg/m²) versus any women (a mixed subgroup which included normal weight, overweight and obese women)). No clear subgroup differences were revealed for the primary outcomes, GDM (Chi² = 1.73, P = 0.63, I² = 0%) (Analysis 3.1), pre‐eclampsia (Chi² = 3.45, P = 0.33, I² = 13.1%) (Analysis 3.2), pregnancy‐induced hypertension or hypertension (Chi² = 2.29, P = 0.32, I² = 12.9 %) (Analysis 3.3), caesarean section (Chi² = 0.95, P = 0.81, I² = 0%) (Analysis 3.4), perinatal mortality (Chi² = 0.17, P = 0.68, I² = 0%) (Analysis 3.5) or large‐for‐gestational age (Chi² = 5.46, P = 0.14, I² = 45.0%) (Analysis 3.6), suggesting no clear differences in treatment effect for these outcomes based on maternal BMI. Due to the difficulty in interpreting the results associated with the 'any women' (mixed) subgroup, we also conducted these analyses excluding this subgroup; similarly no clear subgroup differences were observed. Further, when we conducted these analyses combining the 'overweight or obese women' and 'obese women' subgroups, no clear subgroup differences were observed.
Ethnicity
Analyses were performed based on ethnicity (considering majority 'low‐risk' ethnicities versus majority 'high‐risk' ethnicities versus mixed ethnicities versus unclear). No clear subgroup differences were observed for the primary outcomes, GDM (Chi² = 0.22, P = 0.97, I² = 0%) (Analysis 4.1), pre‐eclampsia (Chi² = 0.04, P = 0.98, I² = 0%) (Analysis 4.2), pregnancy‐induced hypertension or hypertension (Chi² = 2.71, P = 0.10, I² = 63.0%) (Analysis 4.3), caesarean birth (Chi² = 1.75, P = 0.63, I² = 0%) (Analysis 4.4), perinatal mortality (Chi² = 0.17, P = 0.68, I² = 0%) (Analysis 4.5), or large‐for‐gestational age (Chi² = 2.76, P = 0.43, I² = 0%) (Analysis 4.6), suggesting no clear differences in treatment effect for these outcomes based on ethnicity. Due to the difficulty in interpreting the results associated with the 'mixed ethnicities' and 'unclear' subgroups, we also conducted these analyses excluding these two subgroups; similarly no clear subgroup differences were observed.
Sensitivity analyses
The 12 trials (Asbee 2009; Bruno 2016; Dodd 2014; Harrison 2013; Herring 2016; Hui 2012; Hui 2014; Petrella 2013; Phelan 2011; Poston 2013; Poston 2015; Vinter 2011) considered to be at low risk of selection bias were included in sensitivity analyses. There was still a possibly reduced risk of GDM between the diet and exercise intervention and standard care groups(though with a widening of the confidence intervals) (average RR 0.86, 95% CI 0.68 to 1.09; 5019 participants; 11 trials; Tau² = 0.06; Chi² = 21.30, P = 0.02; I² = 53%) (Analysis 5.1). pre‐eclampsia (RR 0.99, 95% CI 0.78 to 1.26; 4311 participants; 4 trials) (Analysis 5.2), pregnancy‐induced hypertension or hypertension (average RR 0.58, 95% CI 0.27 to 1.25; 2694 participants; 4 trials; Tau² = 0.36; Chi² = 11.71, P = 0.008; I² = 74%) (Analysis 5.3), caesarean birth (RR 0.94, 95% CI 0.87 to 1.02; 4968 participants; 10 trials) (Analysis 5.4), perinatal mortality (RR 0.82, 95% CI 0.42 to 1.63; 3757 participants; 2 trials; identical to main analysis) (Analysis 5.5), or large‐for‐gestational age (RR 0.95, 95% CI 0.83 to 1.09; 4618 participants; 8 trials) (Analysis 5.6). These findings supported those observed in the main analysis.
Discussion
Summary of main results
in this updated Cochrane review we included 23 randomised controlled trials (involving 8918 women and their 8709 infants) that compared combined diet and exercise interventions with no intervention (standard care).
For our primary review outcomes, there was a possible reduced risk of gestational diabetes mellitus (GDM) and caesarean section for women receiving diet and exercise interventions compared with standard care (both moderate‐quality evidence). Of the 3353 women receiving diet and exercise interventions, 525 (16%) were diagnosed with GDM, compared with 551 (17%) of the 3280 women receiving standard care (an absolute risk reduction of approximately 1%). These data supported rates of GDM of 168 per 1000 for the standard care group, and 143 per 1000 (95% CI 119 to 170) for the diet and exercise intervention group. There were no clear differences between groups for pre‐eclampsia (low‐quality evidence), pregnancy‐induced hypertension/hypertension (very low‐quality evidence), perinatal mortality (low‐quality evidence) or large‐for‐gestational age low‐quality evidence). No data were reported from any of the included trials for infant mortality or morbidity composite.
Subgroup analyses (based on trial design, maternal body mass index (BMI) and ethnicity) for our primary outcomes revealed no clear differential treatment effects according to the characteristics assessed. The impact of maternal age, parity and specific features of the diet and exercise interventions could not be assessed, due to the paucity of information/data and the inability to meaningfully group intervention characteristics. Sensitivity analyses (restricted to the trials at low risk of selection bias) supported findings observed in the main analyses.
Similarly, for most of the secondary outcomes assessed using GRADE, there were no clear differences between groups, including for perineal trauma (moderate‐quality evidence), neonatal hypoglycaemia (low‐quality evidence), and childhood adiposity (BMI z score) (low‐quality evidence). However, there was evidence of less gestational weight gain for women receiving diet and exercise interventions compared with standard care (moderate‐quality evidence). On average, women receiving the diet and exercise interventions gained 0.89 kg less (95% CI 1.39 kg to 0.40 kg less) than women receiving standard care. No data were reported by the included trials for maternal postnatal depression or type 2 diabetes mellitus, or for childhood/adulthood type 2 diabetes mellitus or neurosensory disability.
For the majority of other secondary outcomes (not assessed using GRADE), we did not observe clear differences between groups. However, we did observe additional benefits in relation to gestational weight gain (less gestational weight gain per week; and a lower chance of having gestational weight gain above Institute of Medicine (IOM) recommendations) for women receiving diet and exercise interventions compared with standard care. Further, postnatally, women receiving diet and exercise interventions had less weight retention and a higher chance of returning to their pre‐pregnancy weight compared with those receiving standard care. There were also reductions in preterm birth, macrosomia (defined as birthweight less than 4500 g) and respiratory distress syndrome observed among infants born to mothers receiving diet and exercise interventions, compared with those born to mothers receiving standard care. We did not conduct meta‐analyses for secondary outcomes relating to adherence to the intervention, behaviour changes associated with the intervention, relevant biomarker changes associated with the intervention, sense of well‐being and quality of life, or views of the intervention, as data were not considered suitable, often due to substantial variation in reporting. Generally, good adherence and positive views were reported among women in the diet and exercise intervention groups. While findings related to biomarker changes and sense of well‐being and quality of life were mixed, the majority of trials demonstrated some benefits in regards to diet and/or exercise behaviour changes for women receiving the diet and exercise interventions compared with those receiving standard care.
Overall completeness and applicability of evidence
The evidence for combined diet and exercise interventions during pregnancy for GDM prevention is incomplete. Though we were able to include 23 trials involving almost 9000 women, assessing a wide range of combined diet and exercise interventions, many of these trials reported on few review outcomes. All included trials compared the interventions with standard or routine care, and thus we were not able to consider comparisons of different types of combined diet and exercise interventions.
In regards to review outcomes selected for quality assessment using GRADE, while 19, 16 and 14 trials, respectively provided data for meta‐analyses of GDM, gestational weight gain and caesarean section, less than half of the included trials contributed data for meta‐analyses for large‐for‐gestational age (11 trials), pre‐eclampsia (eight trials), pregnancy‐induced hypertension/hypertension (six trials), perineal trauma (two trials), perinatal mortality (two trials), neonatal hypoglycaemia (two trials), and childhood adiposity (two trials). For the remaining outcomes selected for quality assessment using GRADE (maternal depression and type 2 diabetes; infant mortality or morbidity composite; childhood/adulthood type 2 diabetes and neurosensory disability), no included trials provided data.
For many of our other secondary review outcomes (including outcomes in childhood and those related to the use and costs of healthcare services), evidence was limited to data from one or two trials. Though included trials have now provided some (limited) data on childhood health and maternal health in the postpartum period, for the majority of review outcomes relating to long‐term health for the mothers and their infants in childhood and adulthood, there were no data. Thus, there remains a paucity of evidence regarding the effects of these interventions during pregnancy on longer‐term health. Further, there were limited data provided from included trials in regards to adherence, women's sense of well‐being, quality of life and their views. Reporting of outcomes such as relevant biomarkers and behaviour changes associated with the intervention was not standardised (and varied greatly) in included trials, restricting our ability to combine data.
The ability to draw firm conclusions was further limited, particularly, by notable variations in the characteristics of the interventions assessed (considering the features of both the diet and exercise components) and women included in the trials. While we chose to combine trials in one comparison, and attempted to explore variation through subgroup analyses, the ability to do this was limited by the difficulty in meaningfully grouping trials according to important characteristics. In regards to applicability, of the 23 included trials, all except one were conducted in upper‐middle or high‐income countries. This likely limits the generalisability of the findings to other countries, particularly low‐resource settings. Further, the included trials used specific and varying screening/diagnostic tests, diagnostic criteria, and subsequent management strategies for GDM, which may limit both the interpretation of data, and also, the applicability of the results for countries/settings using different approaches, and with varying practicability and feasibility considerations.
Quality of the evidence
Risk of bias of the 23 included trials was mixed. Dodd 2014, the largest trial (involving 2212 women and their infants) was considered to be at low risk of bias overall. Across the included trials, there was a general lack of methodological detail provided to assess specific aspects of risk of bias, leading to many 'unclear' judgements. We were able to include 12 of the 23 trials, judged to be at low risk of selection bias, in sensitivity analyses, which largely supported findings from the main analyses (with Dodd 2014 contributing between approximately 20% and 66% of the weight to the meta‐analyses).
For outcomes assessed using GRADE, evidence was determined to be moderate quality (GDM, caesarean section, gestational weight gain and perineal trauma), low quality (pre‐eclampsia, perinatal mortality, large‐for‐gestational age, neonatal hypoglycaemia and childhood adiposity), or very low quality (pregnancy‐induced hypertension/hypertension). Evidence was predominantly downgraded due to design limitations (risk of bias), and imprecision (uncertain effect estimates, and at times, small sample sizes and low event rates), however two outcomes (pregnancy‐induced hypertension/hypertension and neonatal hypoglycaemia), were also downgraded for unexplained inconsistency (statistical heterogeneity).
Potential biases in the review process
The search for trials in this area was performed using Cochrane Pregnancy and Childbirth’s Trials Register. It is unlikely that trials that have been conducted have been missed, however unpublished trials, or ongoing trials not registered in clinical trial registries could be missing. Should such trials be identified, we will include them in future updates of the review.
We explored the potential for publication bias using funnel plots for outcomes with 10 or more trials included in meta‐analyses (GDM, caesarean section, large‐for‐gestational age, gestational weight gain, gestational weight gain above the IOM recommendations, gestational age at birth, preterm birth, macrosomia, and birthweight), and there was no clear indication of asymmetry except in the case of gestational weight gain.
We aimed to reduce bias wherever possible by having at least two review authors independently working on trial selection, data extraction, risk of bias judgements, and GRADE assessments.
Agreements and disagreements with other studies or reviews
Two Cochrane reviews have assessed diet interventions (Tieu 2017) and exercise interventions (Han 2012) for GDM prevention. Tieu 2017 included 11 trials involving 2786 women and their infants, six of which compared diet interventions with standard care. Similar to our review, a reduction in GDM was observed for women receiving diet interventions compared with standard care (very low‐quality evidence), however unlike our review, a subgroup analysis suggested a greater treatment effect for overweight and obese women (Tieu 2017). Tieu 2017 also found less gestational weight gain among women who received diet interventions compared with standard care (low‐quality evidence). Han 2012 included five trials involving 1115 women and their infants, assessing exercise intervention compared with standard care. Unlike our review, no clear impact of exercise interventions on GDM was shown (quality of evidence not assessed) (Han 2012). Both reviews concluded that additional high‐quality evidence is required (Han 2012; Tieu 2017).
A further Cochrane review has assessed diet interventions, exercise interventions, or combined diet and exercise interventions for preventing excessive gestational weight gain in pregnancy (Muktabhant 2015). Muktabhant 2015 included 65 trials, of which 49 involving 11,444 women and their infants contributed data, most of which compared such interventions with standard care. As in our review, diet or exercise, or both, interventions were shown to reduce excessive gestational weight gain (high‐quality evidence), and lead to lower gestational weight gain compared with standard care (moderate‐quality evidence) (Muktabhant 2015). Unlike our review, a reduction in maternal hypertension (low‐quality evidence) was observed, and no clear differences in preterm birth (moderate‐quality evidence) or macrosomia (high‐quality evidence) were observed, as were seen in our review. In a subgroup analysis by risk, however, high‐risk women who received combined diet and exercise interventions had a lower risk of macrosomia (moderate‐quality evidence), and their infants had a lower risk of respiratory distress syndrome (moderate‐quality evidence) (Muktabhant 2015), as we observed. Muktabhant 2015 did not assess the impact of such interventions on GDM (as it is the focus of our review).
Numerous other systematic and non‐systematic reviews have assessed diet and/or exercise interventions for reducing adverse pregnancy outcomes, including GDM. The reviews continue to reveal inconsistent findings in regards to benefit, however much of this variation is likely attributable to differences in groups of women and types of interventions (and thus trials) included and assessed. For example, in regards to variations in types of interventions, recently, Song 2016 conducted a systematic review and meta‐analysis assessing the effects of diet and/or exercise interventions on the risk of GDM. The review included 29 trials involving 11,487 women and overall showed a reduction in GDM (Song 2016). Song 2016 thus concluded that lifestyle modification during pregnancy can reduce the risk of GDM. However, when combined diet and exercise (14 trials), diet alone (five trials), and exercise alone (10 trials) interventions were considered separately, the observed reductions in GDM were no longer 'statistically significant', although the direction of effect for each type of intervention did suggest benefit (Song 2016). In regards to assessments of interventions in different groups of women, O'Brien 2016, for example, showed no clear impact of diet and/or lifestyle interventions on GDM specifically in women with a normal BMI; while Madhuvrata 2015 showed a reduction in GDM with diet interventions (but not exercise interventions or combined diet and exercise interventions) specifically in women with risk factors for GDM.
A recent individual participant data (IPD) analysis of antenatal diet and exercise interventions (Rogozińska 2017) showed some similarities and some differences with our findings. In the overall IPD, there were 36 studies with 12,343 women (last searched in March 2015), covering diet alone, exercise alone and mixed diet and exercise interventions compared with standard care. The IPD found no overall difference for GDM or preterm birth, in contrast to our finding of a reduction in these two outcomes. However, both our review and the IPD found reductions in gestational weight gain and caesarean section with lifestyle interventions. The IPD included 16 mixed diet and exercise studies but noted that 10 other mixed diet and exercise studies were not included, which may explain differences in findings (our review included 23 studies).
Although evidence appears to be accumulating in favour of diet and combined diet and exercise interventions for the prevention of GDM, uncertainty remains, and further work is required to disentangle specific effects in different groups of women, and with different diet and exercise intervention characteristics.
Update study flow diagram.
'Risk of bias' graph: review authors' judgements about each risk of bias item presented as percentages across all included trials.
'Risk of bias' summary: review authors' judgements about each risk of bias item for each included trial.
Funnel plot of comparison: 1 Diet and exercise interventions versus control, outcome: 1.1 Gestational diabetes.
Funnel plot of comparison: 1 Diet and exercise interventions versus control, outcome: 1.4 Caesarean section.
Funnel plot of comparison: 1 Diet and exercise interventions versus control, outcome: 1.6 Large‐for‐gestational age.
Funnel plot of comparison: 1 Diet and exercise interventions versus control, outcome: 1.13 Gestational weight gain (kg).
Funnel plot of comparison: 1 Diet and exercise interventions versus control, outcome: 1.16 Gestational weight gain (above IOM recommendations).
Funnel plot of comparison: 1 Diet and exercise interventions versus control, outcome: 1.31 Gestational age at birth (weeks).
Funnel plot of comparison: 1 Diet and exercise interventions versus control, outcome: 1.33 Preterm birth.
Funnel plot of comparison: 1 Diet and exercise interventions versus control, outcome: 1.35 Macrosomia.
Funnel plot of comparison: 1 Diet and exercise interventions versus control, outcome: 1.37 Birthweight (g).
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 1 Gestational diabetes.
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 2 Pre‐eclampsia.
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 3 Pregnancy‐induced hypertension and/or hypertension.
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 4 Caesarean section.
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 5 Perinatal mortality.
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 6 Large‐for‐gestational age.
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 7 Operative vaginal birth.
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 8 Induction of labour.
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 9 Perineal trauma.
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 10 Placental abruption.
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 11 Postpartum haemorrhage.
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 12 Postpartum infection.
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 13 Gestational weight gain (kg).
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 14 Gestational weight gain (various times reported) (kg).
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 15 Gestational weight gain (kg/week).
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 16 Gestational weight gain (above IOM recommendations).
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 17 Gestational weight gain (within IOM recommendations).
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 18 Gestational weight gain (below IOM recommendations).
| Study | Diet | Exercise | Benefit in favour of intervention | Benefit in favour of control |
| Bruno 2016 | Higher proportion of women in intervention group, compared with the control group, with Food Frequency Questionnaire score ≥ 2 at 36th week (P = 0.028). No clear difference between groups in ≥ 2 servings of vegetables/day (P = 0.400) or ≤ 3 times/week of food rich in saturated fat; higher proportion of women in intervention group, compared with the control group, having ≤ 30 g sugar/day (P = 0.026). | No clear difference between groups in number of steps/day or duration of physical activity in minutes at the 20th week. Women in the intervention group, compared with the control group, were less active at the 36th week (fewer steps/day (P = 0.016) and had a shorter duration of physical activity (P = 0.039)). | Some (diet) | Some (exercise) |
| Dodd 2014 | Macronutrient consumption and food groups Micronutrient consumption Healthy Eating Index (HEI) Glycaemic index and glycaemic load No clear difference between groups (from trial entry to 28 weeks, 36 weeks, 4 months) in glycaemic load (P = 0.15) or glycaemic index (P = 0.10). Changes in diet and knowledge of healthy food choices "women receiving lifestyle advice were more likely to indicate that the approach to participate in the trial prompted changes to... their diet [... p < 0.0001]... Women who received the intervention indicated greater knowledge about healthy food choices [... p < 0.0001]... compared with women who received Standard Care." | Physical activity Women in the intervention group, compared with the control group (from trial entry, to 28 weeks, 36 weeks, 4 months) had an increase in total activity (P = 0.01); and specifically an increase in household activity (P = 0.01). No clear differences between groups for commuting activity (P = 0.55), leisure activity (P = 0.06) or work activity (P = 0.52). Changes in lifestyle and knowledge of healthy exercise during pregnancy "women receiving lifestyle advice were more likely to indicate that the approach to participate in the trial prompted changes to... their lifestyle [...p < 0.0001]. Women who received the intervention indicated greater knowledge about... exercise during pregnancy [... p < 0.0001] compared with women who received Standard Care." | Some (diet and exercise) | No |
| Harrison 2013 | Not reported | The intervention group had higher steps/day at 28 weeks gestation compared with the control group (P < 0.05); no clear difference between groups in MET minutes‐1/day estimated by the The International Physical Activity Questionnaire (P value not reported). No clear difference between groups at 6 weeks postpartum in physical activity (steps/day) (P = 0.6). | Some (exercise) | No |
| Hawkins 2014 | No clear differences between groups in change from baseline to mid‐pregnancy and baseline to postpartum for total caloric intake (P = 0.78; P = 0.44), calories from fat (%) (P = 0.66; P = 0.14), and fibre (g) (P = 0.20; P = 0.23). | No clear differences between groups in change from baseline to mid‐pregnancy and baseline to postpartum for moderate‐intensity (P = 0.17; P = 0.78), moderate and vigorous‐intensity (P = 0.80; P = 0.82), or sports/exercise (P = 0.72; P = 0.63) physical activity; though significant increase in vigorous‐intensity physical activity in the intervention compared with control group (P = 0.04; P = 0.046) (MET hours/week). | No (diet) Some (exercise) | No |
| Hui 2012 | At 2 months after enrolment, the intervention group, compared with the control group, had lower daily intakes of total calories (P = 0.002*), carbohydrate (g) (P = 0.04), fat (g) (P = 0.0001*), saturated fat (g) (P = 0.00004*), cholesterol (mg) (P = P = 0.001*) and fat ratio (%) (P = 0.001*); and higher carbohydrate ratio (%) (P = 0.02) and protein ratio (%) (P = 0.04); no clear differences between groups for intakes of protein (g) (P = 0.11), and fibre (g) (P = 0.63). At 2 months after enrolment, the intervention group, compared with the control group, had lower daily servings of medium‐fat meat (P = 0.01), 1‐2% fat milk (P = 0.02) and oil and fats (P = 0.02), and higher daily servings of skim milk (P = 0.02); no clear differences between groups for starch (P = 0.66), very lean meat (P = 0.66), lean meat (P = 0.17), high‐fat meat (P = 0.50), vegetables (P = 0.43), fruits (P = 0.39), or whole fat milk (P = 0.15). *P values with statistical significance after Bonferroni | At 2 months after enrolment, the physical activity index was higher in the intervention group compared with the control group (P = 0.00002). | Some (diet) Yes (exercise) | No |
| Hui 2014 | Pre‐pregnancy BMI < 25 At 2 months after the onset of the intervention, women in the intervention group compared with the control group had lower intakes of total calorie (P = 0.01), carbohydrate (g) (P = 0.03), total fat (g) (P = 0.008), saturated fat (g) (P = 0.008), and cholesterol (mg) (P = 0.02); no clear difference between groups for intake of protein (g) (P = 0.36). Pre‐pregnancy BMI ≥ 25 At 2 months after the onset of the intervention, women in the intervention group compared with the control group had lower intakes of total calorie (P = 0.05), total fat (g) (P = 0.02), saturated fat (g) (P = 0.01), and cholesterol (mg) (P = 0.03); no clear differences between groups for intakes of carbohydrate (g) (P = 0.44) or protein (g) (P = 0.17). | Pre‐pregnancy BMI < 25 At 2 months after the onset of the intervention, women in the intervention group compared with the control group had higher physical activity index (units) (P < 0.01). Pre‐pregnancy BMI ≥ 25 At 2 months after the onset of the intervention, no clear difference between groups for physical activity index (units) (P value not reported) | Some (diet and exercise) | No |
| Jing 2015 | No clear differences between groups at 20‐24 weeks gestation for intake of carbohydrate (g) (P = 0.058), fat (g) (P = 0.216), meat (g) (P = 0.235), vegetables (g) (P = 0.637), eggs (g) (P = 0.962), milk (g) (P = 0.060), beans (g) (P = 0.982). Higher intake of energy (kcal) (P = 0.024), protein (g) (P = 0.003), grain (g) (P = 0.013), fruit (g) (P = 0.048), seafood (P = 0.031), and nuts (P = 0.036) for women in intervention group compared with control group. | No clear difference between groups at 20‐24 weeks for time spent (hours/day) doing moderate activity (P = 0.824) [and no clear difference between groups for time spent (hours/day) on intensities A, B, C, E, F, G, H]. Less time spent resting (P = 0.033) and more time doing mild activity (P = 0.016) among women in the intervention group compared with control group [and more time spent (hours/day) on intensity D]. | Some (diet and exercise) | No |
| Koivusalo 2016 | The dietary index score improved more among women in the intervention group, compared with the control group (P = 0.16 unadjusted, P = 0.037 adjusted). No clear differences between groups in changes in food intake from the first to second trimester for low‐fat milk (times/day) (P = 0.726), whole‐grain cereal (times/day) (P = 0.182), fruits and berries (times/day) (P = 0.865), vegetables and legumes (times/day) (P = 0.419), animal protein (times/day) (P = 0.658), snacks (times/week) (P = 0.112), sugar sweetened beverages (times/week) (P = 0.750), fast food (times/week) (P = 0.731), spread fat (score) (P = 0.103), cooking fat (score) (P = 0.937). Intakes of low‐fat cheese (P = 0.040) and fish (P = 0.011) increased in the intervention group compared with the control group. | Women in the intervention group increased their median weekly leisure time physical activity while the physical activities of women in the control group remained unchanged (P = 0.17 unadjusted, P = 0.029 adjusted). No clear difference between groups in proportion of women meeting the physical activity goal (150 minutes/week in the second trimester). | Some (diet and exercise) | No |
| Luoto 2011 | Dietary changes Compared with the control group, from baseline to 26‐28 weeks, the intervention group reduced their intake of saccharose (E%) (P = 0.04), and saturated fatty acids (E%) (P = 0.005); no clear differences between groups seen for intakes of total energy (MJ/day) (P = 0.97), total energy (kcal/day) (P = 0.97), protein (E%) (P = 0.094), carbohydrates (E%) (P = 0.76), dietary fibre (g/day) (P = 0.44), total fat (E%) (P = 0.15), trans fatty acids (E%) (P = 0.65), mono saturated fatty acids (E%) (P = 0.99), or polyunsaturated fatty acids (E%) (P = 0.21). Compared with the control group, from baseline to 36‐37 weeks, the intervention group reduced their intake of saccharose (E%) (P = 0.023) and saturated fatty acids (E%) (P = 0.01) and increased their intake of dietary fibre (g/day) (P = 0.019) and polyunsaturated fatty acids (E%) (P < 0.001); no clear differences between groups seen for intakes of total energy (MJ/day) (P = 0.90), total energy (kcal/day) (P = 0.90), protein (E%) (P = 0.29), carbohydrates (E%) (P = 0.60), total fat (E%) (P = 0.86), trans fatty acids (E%) (P = 0.30), or mono saturated fatty acids (E%) (P = 0.51). Food habits related to the objectives of dietary counselling From baseline to 26‐28 weeks, the intervention group, compared with the control group, increased their proportion of high‐fibre bread (% of all bread) (P = 0.001) and vegetable fats (% of all dietary fat) (P = 0.001), while the control group decreased their proportion of low‐fat cheeses (% of all cheese) (P = 0.001), and increased intake of snacks high in sugar and/or fat (g/day) (P = 0.022); no clear differences between groups in intake of vegetables, fruits and berries (g/day) (P = 0.117), fat‐free or low‐fat milk (% of all milk) (P = 0.093), frequency of eating fish (per week) (P = 0.120), or high‐fat foods (g/day) (0.664). From baseline to 36‐37 weeks, the intervention group, compared with the control group, increased their intake of vegetables, fruits and berries (g/day) (P = 0.001), proportion of high‐fibre bread (% of all bread) (P = 0.003) and vegetable fats (% of all dietary fat) (P = 0.003), while the control group decreased their proportion of low‐fat cheeses (% of all cheese) (P = 0.009); no clear differences between groups in proportion of fat‐free or low‐fat milk (% of all milk) (P = 0.630), frequency of eating fish (per week) (P = 0.068), intake of high‐fat foods (g/day) (0.108), or snacks high in sugar and/or fat (g/day) (P = 0.551). Consumption of the main food groups and foods From baseline to 26‐28 weeks gestation, the intervention group, compared with the control group, increased total intake of milk (P = 0.025), fish (P = 0.041), vegetable oils (P = 0.002) and oil based salad dressings (P = 0.002); while the control group, compared with the intervention group, increased consumption of porridge and breakfast cereals (P = 0.003) and candies and chocolates (P = 0.008) (all g/day); no clear differences between groups for intake of fruits and berries (P = 0.575), cooked potato or in dishes (P = 0.686), french fries, chips and other fatty potato products (P = 0.995), total bread (P = 0.459), rice and pasta (P = 0.118), total cheese (P = 0.318), red meat and game (P = 0.851), poultry (P = 0.252), sausages (P = 0.896), vegetable spreads (P = 0.071), butter and butter mixtures (P = 0.128), solid baking margarines (P = 0.194), sweet pastries and other sugary food items (P = 0.055), pizza and hamburgers (P = 0.703), tea (P = 0.464), coffee (P = 0.976), sugary soft drinks (P = 0.088) or juice (P = 0.096) (all g/day). From baseline to 36‐37 weeks gestation, the intervention group, compared with the control group, increased total intake of fish (P = 0.044), vegetable oils (P = 0.002) and oil based salad dressings (P = 0.010); while the control group, compared with the intervention group, decreased consumption of vegetables (P = 0.005); no clear differences between groups for intake of fruits and berries (P = 0.134), cooked potato or in dishes (P = 0.157), french fries, chips and other fatty potato products (P = 0.388), total bread (P = 0.175), porridge and breakfast cereals (P = 0.811), rice and pasta (P = 0.187), total milk (P = 0.878), total cheese (P = 0.364), red meat and game (P = 0.806), poultry (P = 0.482), sausages (P = 0.444), vegetable spreads (P = 0.215), butter and butter mixtures (P = 0.417), solid baking margarines (P = 0.208), candies and chocolates (P = 0.133), sweet pastries and other sugary food items (P = 0.104), pizza and hamburgers (P = 0.755), tea (P = 0.235), coffee (P = 0.481), sugary soft drinks (P = 0.730) or juice (P = 0.094) (all g/day). | Physical activity changes No clear differences between baseline to 26‐28 weeks or baseline to 36‐37 weeks for total MET minutes/week (P = 0.36; P = 0.63), MET minutes/week for at least moderate activity (P = 0.17; P = 0.82), MET minutes/week for light activity (P = 0.57; P = 0.17), or ≥ 800 MET minutes/week (%) (P = 0.27; P = 0.51). At 26‐28 weeks, the decreases in total leisure‐time physical activity (LTPA) (days/week) and moderate‐to‐vigorous LTPA (days/week) were smaller in the intervention group compared with the control group (P = 0.040; P = 0.016); though no clear differences between group/days in total LTPA (minutes/week) (P = 0.58), moderate‐to‐vigorous LTPA (minutes/week) (P = 0.11), light LTPA (days/week) (P = 0.80), light LTPA (minutes/week) (P = 0.65), or meeting physical activity recommendations for health (%) (P = 0.060) were observed. No clear differences between groups from baseline to 36‐37 weeks in total LTPA (days/week: P = 0.80; minutes/week: P = 0.60), moderate‐to‐vigorous LTPA (days/week: P = 0.16; minutes/week: P = 0.96), or light LTPA (days/week: P = 0.21; minutes/week: P = 0.75), or meeting physical activity recommendations for health (%: P = 0.70). "From 26‐28 weeks’ gestation to 36‐37 weeks’ gestation the number of weekly days with light‐intensity LTPA decreased significantly less in INT than in UC (0.1 vs. 0.6 days, p = 0.05, not shown in Table 4)." | Some (diet and exercise) | No |
| Petrella 2013 | "Significant changes in eating habits occurred in the Therapeutic Lifestyle Changes group, increasing the number of snacks/day, the consumption of vegetables and fruits. Moreover, intervention also decreased the consumption of sugar. No differences in the number of daily spoons of oil, red meat and complex carbohydrates intake were found." | "The step numbers for each walking session was constant during pregnancy (3267 ± 1683 at 36th week and 3755 ± 1816 at 28th week)." | Not applicable (only reported for intervention group) | Not applicable (only reported for intervention group) |
| Phelan 2011 | "No significant treatment... interaction effects over time were observed... for dietary factors." Repeated‐measures ANOVA of time (early pregnancy, late pregnancy, 6 months postpartum, 12 months postpartum) x treatment group interactions for dietary changes in calorie intake, percentage of calories from fat, percentage of calories from carbohydrate, percentage of calories from protein, percentage of calories from sweets, daily calories from soft drinks, daily saturated fat (g), daily servings of vegetables, daily servings of fruit and fruit juices, daily servings of bread, cereals, rice, pasta, daily servings of milk, yogurt, cheese, daily frequency of fats and oils, sweets, sodas, weekly fast food, daily iron from food (mg), daily calcium from food (mg), total daily dietary fibre (g), daily vitamin D from food (IU), daily folate from food (μg): P values all "NS." | "A trend was observed for an effect of the intervention on physical activity... which suggested a small intervention‐related increase in calories expended in physical activity during the postpartum period." Repeated‐measures ANOVA of time (early pregnancy, late pregnancy, 6 months postpartum, 12 months postpartum) x treatment group interaction for kcal (F = 2.5, P = 0.06, hp2 = 0.02). | No (diet) Yes (exercise) | No |
| Polley 2002 | "All groups decreased their fat consumption from these foods from baseline to 30 weeks, except normal‐weight women in the control condition. There was no effect of treatment on changes in fat intake from these foods from recruitment to 30 weeks (P>0.2)." | "Changes in exercise level from recruitment to 30 weeks (P>0.8) were not related to treatment condition." | No | No |
| Poston 2013 | At 28 weeks gestation, the intervention group had lower intakes of total energy (MJ/day) (P = 0.016), dietary glycaemic load (g/day) (P = < 0.001), glycaemic load (%E) (P = 0.013), total fat (%E) (P = 0.010) and saturated fatty acids (%E) (P = 0.015), and higher protein (%E) (P = 0.034), and fibre (non‐starch polysaccharides) (g) (P = 0.040) compared with the control group; no clear differences between groups for dietary glycaemic index (%) (P = 0.054), carbohydrate (%E) (P = 0.207), protein (g) (P = 0.204), monounsaturated fatty acids (%E) (P = 0.088), polyunsaturated fatty acids (%E) (P = 0.075), or polyunsaturated fatty acid, saturated fatty acid ratio (P = 0.075). "A principal component analysis (PCA) of Food Frequency Questionnaire (FFQ) data from the UPBEAT pilot study database was performed to derive three diet patterns: two with high coefficients for high‐sugar and/or highfat food groups defined as ‘Western’ and ‘Healthy‐unhealthy choices’ and a ‘traditional’ African or African‐Caribbean diet pattern…. The ‘Western’ and ‘Healthy‐unhealthy choices’ patterns scores were reduced in those who received the intervention." | At 28 weeks gestation, no clear differences between groups for physical activity, as measured by accelerometer (minutes/day of sedentary, active, light, moderate to vigorous activity) (P values not reported; mean differences with 95% confidence intervals indicate no clear differences), and Recent Physical Activity Questionnaire (minutes/day of sedentary, activity, light activity); self‐reported moderate to vigorous activity (minutes/day) was higher in the intervention group compared with the control group (P value not reported; mean difference with 95% confidence interval indicates difference), and women in the intervention group self‐reported walking (minutes/day) for leisure more than those in the control group (P = 0.003). | Some (diet and exercise) | No |
| Poston 2015 | At 27‐28 weeks and 6 days, women in the intervention group, compared with the control group, had lower mean total energy (MJ/day) (P < 0.0001), glycaemic index (0‐100) (P < 0.0001), glycaemic load per day (P < 0.0001), and intake carbohydrate (% energy) (P = 0.0011), total fat (% energy) (P = 0.0011), saturated fat (g/day) (P < 0.0001) and saturated fat (% energy) (P < 0.0001); and higher intake of protein (% energy) (P < 0.0001), and fibre (g/day) (P = 0.013). At 6 months postpartum, women in the intervention group, compared with the control group, had lower glycaemic load per day (P < 0.001), glycaemic index (0‐100) (P < 0.001), intakes of total energy (kcal per day) (P < 0.001), saturated fat (% energy) (P < 0.001), and total fat (% energy) (P < 0.001), and higher intake of protein (% energy) (P < 0.001); no clear differences between groups for intakes of carbohydrates (% energy) (P = 0.835) and fibre (g/day) (P = 0.873). | At 27‐28 weeks and 6 days, women in the intervention group, compared with the control group, were more physically active: MET (minutes/week) (P = 0.0015); attributed to more time spent walking (minutes/week) (P = 0.0018), with no clear difference seen between groups for moderate or vigorous activity (minutes/week) (P > 0.99). At 6 months postpartum, no clear differences between groups for measures of physical activity: MET (minutes/week) (P = 0.607), moderate or vigorous activity (minutes/week) (P = 0.681), or walking (minutes/week) (P = 1.00). | Some (diet and exercise) | No |
| Rauh 2013 | The intervention group had a lower change from baseline to 36‐38th week gestation energy intake compared with the control group (kcal/day) (P = 0.035). | No clear difference between groups in change from baseline to 36‐38th week gestation total activity (MET‐min/week) (P = 0.425). | Yes (diet) No (exercise) | No |
| Sagedal 2017 | At 36 weeks gestation the intervention group had a higher (more favourable) diet score compared with the control group (P = 0.013); dietary differences favouring the intervention group were identified in 7 domains: ‘drinking water when thirsty’ (P = 0.002), ‘vegetables with dinner’ (P = 0.027), ‘fruits and vegetables for between‐meal snacks’ (P = 0.023), ‘package size of unhealthy foods’ (P = 0.010), ‘added sugar' (P = 0.005), ‘eating beyond satiety’ (P = 0.009) and ‘food labels’ (P = 0.011); no clear differences between groups for 'meal regularity' (P = 0.176), 'eating sweets or snacks without appreciation' (P = 0.446), 'added salt' (P = 0.680). | At 36 weeks gestation the intervention group compared with the control group had higher weekly energy expenditure (MET‐minutes/week) (P = 0.009), and according to the International Physical Activity Questionnaire, fewer had 'low activity', and more had 'moderate activity' and 'high activity' (P = 0.013). | Some (diet) Yes (exercise) | No |
| Vinter 2011 | "When asked at 35 weeks’ gestation whether participation in the LiP study had resulted in more healthy eating habits, 85% of women in the intervention group responded affirmatively. In addition, 21% of women in the control group thought that their dietary habits in pregnancy were positively influenced by their participation." At 35 weeks' gestation, women in the intervention group had higher self‐reported physical activity levels compared with those in the control group (physical activity ≥ 2 hours/week (P = 0.001); physical activity making them sweaty or short of breath ≥ 2 hours/week (P < 0.001)); no clear differences between groups at 6 months postpartum (physical activity ≥ 2 hours/week (P = 0.620); physical activity making them sweaty or short of breath ≥ 2 hours/week (P = 0.961)). | "Among women in the intervention group, 77.5% undertook leisure time sporting activities in addition to the aerobic classes. In addition, 65% of women in the control group engaged in some type of leisure time sporting activities during pregnancy (P = 0.016)." At 35 weeks' gestation, women in the intervention group had improved eating habits compared with those in the control group (considered themselves as in the most healthy eating habit groups (P = 0.003)); no clear differences between groups at 6 months postpartum (considered themselves as in the most healthy eating habit groups (P = 0.609)). | Some (diet and exercise) | No |
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 19 Behaviour changes associated with the intervention.
| Study | Results | Benefit in favour of intervention | Benefit in favour of control |
| Hawkins 2014 | No clear differences between groups in change in biomarkers of insulin resistance from baseline to mid‐pregnancy: glucose (mmol/L) (P = 0.63); insulin (pmol/L) (P = 0.39); leptin (pmol/L) (P = 0.73); adiponectin (nmol/L) (P = 0.51); resistin (nmol/L) (P = 0.19); tumour necrosis factor‐alpha (pmol/L) (P = 0.11); c‐reactive protein (nmol/L) (P = 0.19). | No | No |
| Koivusalo 2016 | Women in the intervention group compared with the control group had a greater change (reduction) in fasting plasma glucose from baseline to the third trimester (P = 0.026 unadjusted; P = 0.011 adjusted). No clear difference between groups in change (increase) in 2‐hour glucose from baseline to second trimester (P = 0.92 unadjusted, P = 0.42 adjusted). | Some | No |
| Korpi‐Hyovalti 2011 | No clear difference between groups in fasting glucose (mmol/L), OGTT 1‐hour glucose (mmol/L), OGTT 2‐hour glucose (mmol/L), or area under the curve (mmol/L/2 hour) (all reported to be P = NS) at weeks 26‐28. | No | No |
| Luoto 2011 | There were no clear differences between groups in glucose intolerance measurements at 26‐28 weeks (glucose concentrations in 2‐hour OGTT (mg/L): fasting (P = 0.44), 1‐hour (P = 0.23), 2‐hour (P = 0.99); insulin (P = 0.10), or HOMA‐IR (P = 0.13)); or in the change from baseline (8‐12 weeks) to 26‐28 week values for insulin (P = 0.23), or HOMA‐IR (P = 0.24). | No | No |
| Poston 2015 | At 27‐28 weeks and 6 days gestation, no clear differences between groups in fasting blood glucose (mmol/L) (P = 0.49), 1‐hour blood glucose (mmol/L) (P = 0.43), 2‐hour blood glucose (mmol/L) (P = 0.81), plasma fasting insulin (mU/L) (P = 0.57), HOMA‐IR (units) (P = 0.60), plasma triglycerides (mmol/L) (P = 0.39), plasma LDL cholesterol (mmol/L) (P = 0.27), plasma HDL cholesterol (mmol/L) (0.93), plasma VLDL (mmol/L) (P = 0.39). | No | No |
| Vinter 2011 | Glucose metabolism and insulin sensitivity No clear differences between groups in fasting plasma glucose (mmol/L) at 28‐30 weeks (P = 0.060) or 34‐36 weeks (P = 0.431). No clear differences between groups in 2‐hour oral glucose tolerance test (mmol/L) at 28‐30 weeks (P = 0.459) or 34‐36 weeks (P = 0.723). No clear differences between groups in fasting insulin (mU/L) at 34‐36 weeks (P = 0.065) or change from baseline to 34‐36 weeks fasting insulin (P = 0.063); women in the intervention group had lower fasting insulin at 28‐30 weeks (P = 0.040), and lower change from baseline to 28‐30 weeks fasting insulin (P = 0.015). No clear differences between groups in HOMA‐IR at 34‐36 weeks (P = 0.062) or change from baseline to 34‐36 weeks fasting insulin (P = 0.079); women in the intervention group had lower fasting insulin at 28‐30 weeks (P = 0.032), and lower change from baseline to 28‐30 weeks fasting insulin (P = 0.022). No clear differences between groups at 28‐30 weeks or 34‐36 weeks for fasting cholesterol (mmol/L) (P = 0.332; P = 0.484), fasting HDL (mmol/L) (P = 0.781; P = 0.871), fasting LDL (mmol/L) (P = 0.148; P = 0.183), or fasting triglycerides (mmol/L) (P = 0.385; P = 0.399). | Some | No |
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 20 Relevant biomarker changes associated with the intervention.
| Study | Results | Benefits in favour of intervention | Benefits in favour of control |
| Dodd 2014 | There were no clear differences between groups (from trial entry, to 28 weeks, 36 weeks and 4 months postpartum) in mean depressive scores (Edinburgh Postnatal Depression Scale (EPDS) mean scores) (adjusted P = 0.25), risk of depression (EPDS score > 12, %) (adjusted P = 0.95), symptoms of anxiety (Spielberger State‐Trait Anxiety Inventory (STAI) mean scores) (adjusted P = 0.51), or risk of high level anxiety (STAI score ≥ 15, %) (adjusted P = 0.31). There were no clear differences between groups for any of the domains assessing health related quality of life (from trial entry, to 28 weeks, 36 weeks and 4 months postpartum) (mean scores: physical functioning adjusted P = 0.53; physical role adjusted P = 0.59; bodily pain adjusted P = 0.27; general health adjusted P = 1.00; vitality adjusted P = 0.48; social functioning adjusted P = 0.52; emotional role adjusted P > 0.11; mental health adjusted P = 0.07; physical component adjusted P = 0.47; mental component adjusted P = 0.36). For emotional role and mental health domains there were significant interactions between treatment group and time point (P = 0.03; P = 0.007); although there were no significant differences between treatment groups at any individual time point, the pattern of change over pregnancy differed according to treatment group. "All women reported a high degree of satisfaction with their pregnancy... p = 0.8722... and with birth... p = 0.9235... Most women agreed or strongly agreed that they felt in control during their pregnancy... p = 0.9945... and birth... p = 0.4510... and they liked their care providers... p = 0.1530... There were no differences with regard to the proportion of women who felt healthy during pregnancy... p = 0.3517... women who received the intervention were more likely to feel reassured about their own health... p = 0.0112... and that of their baby... p = 0.0143... In the postpartum period, most women felt healthy... p = 0.5942... and were not concerned about their future health... p = 0.9444... or the future health of their baby or child... p = 0.9467" | Some (reassurance about own health and health of baby) | No |
| Luoto 2011 | No clear difference between groups from 8‐13 weeks to 36‐37 weeks in change in health related quality of life (15D questionnaire) (P = 0.24), or perceived health (VAS scale of 0–10 cm) (P = 0.061). | No | No |
| Phelan 2011 | "The intervention group... had a significantly greater increase in scores on the Edinburgh Depression Scale during the postpartum period than did the standard‐care group (F = 23.2, P = 0.0001, hp2 = 0.094); however, multiple logistic regression analyses indicated no significant effects of the intervention compared with standard care on the prevalence of depression (defined as a score ≥13) at 30 wk of gestation (6.4% compared with 7.2%, respectively), 6 mo (3.4% compared with 3.6%, respectively), or 12 mo (5.2% compared with 6.3%, respectively) postpartum. Both groups reported very low depression scores overall... No significant treatment... interaction effects over time were observed for dietary disinhibition, stress or sleep." Repeated‐measures ANOVA of time (early pregnancy, late pregnancy, 6 months postpartum, 12 months postpartum) x treatment group interactions for disinhibition, stress, and sleep score: P values all reported to be "NS." | No | Some (Edinburgh Depression Scale scores) |
| Poston 2013 | At 28 weeks gestation, there was no clear difference between groups in the numbers of women reporting problems in each of the EuroQol quality of life (EQ‐5D) questionnaire domains: mobility, self‐care, usual activities, pain and discomfort, anxiety and depression; or in the time trade‐off health state rating and visual analogue scale of health related quality of life (0 to 100) (P values not reported, however treatment effects indicate no clear differences). At 28 weeks gestation there were also no clear differences between groups in Edinburgh Postnatal Depression Score total, total score > 9, and total score > 12 (P values not reported, however treatment effects indicate no clear differences). | No | No |
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 21 Sense of well‐being and quality of life.
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 22 Breastfeeding (exclusive).
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 23 Breastfeeding (partial).
| Study | Diet and exercise | Control | P value |
| Rauh 2013 | Mean (SD not reported) (N = 148, unadjusted) Exclusive breastfeeding duration (days): 130.7 Total breastfeeding duration (days): 232.1 | Mean (SD not reported) (N = 65, unadjusted) Exclusive breastfeeding duration (days): 116.3 Total breastfeeding duration (days): 219.4 | P = 0.180 P = 0.465 |
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 24 Breastfeeding.
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 25 Postnatal weight retention (latest time reported) (kg).
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 26 Return to pre‐pregnancy weight (latest time reported).
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 27 Postnatal BMI (latest time reported).
| Study | Intervention | Control | P value |
| Vinter 2011 | 6 months postpartum (median (IQR)) (N = 123) Systolic blood pressure (mm Hg): 122 (116–129) Diastolic blood pressure (mm Hg): 83.5 (78–88) | 6 months postpartum (median (IQR)) (N = 115) Systolic blood pressure (mm Hg): 122 (115–128) Diastolic blood pressure (mm Hg): 82 (78–88) | 0.770 0.733 |
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 28 Maternal cardiovascular health (latest time reported).
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 29 Stillbirth.
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 30 Neonatal mortality.
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 31 Gestational age at birth (weeks).
| Study | Intervention group | Control group | P value |
| Polley 2002 | Mean (SD not reported) Normal weight women (N = 30) 39.1 weeks Overweight women (N = 27) 39.4 weeks | Mean (SD not reported) Normal weight women (N = 31) 39.5 weeks Overweight women (N = 22) 39.1 weeks | Not reported |
| Vinter 2011 | Median (IQR) (N = 150) 283 days (273‐290) | Median (IQR) (n = 154) 283 days (274‐289) | 0.952 |
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 32 Gestational age at birth (days or weeks).
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 33 Preterm birth.
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 34 Apgar score less than seven at five minutes.
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 35 Macrosomia.
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 36 Small‐for‐gestational age.
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 37 Birthweight (g).
| Study | Intervention group | Control group | P value |
| Herring 2016 | Mean (SD not reported) (N = 27) 3147 | Mean (SD not reported) (N = 29) 3361 | Mean difference: ‐213 (95% CI: ‐431 to 3.7) |
| Polley 2002 | Mean (SD not reported) Born to normal weight women (N = 30) 3133.0 Born to overweight women (N = 27) 3282.8 | Mean (SD not reported) Born to normal weight women (N = 31) 3226.4 Born to overweight women (N = 22) 3349.0 | Not reported |
| Vinter 2011 | Median (IQR) (N = 150) 3742 (3464‐4070) | Median (IQR) (N = 154) 3593 (3335‐3930) | 0.039 |
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 38 Birthweight (g).
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 39 Birthweight z score.
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 40 Head circumference (cm).
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 41 Head circumference z score.
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 42 Length (cm).
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 43 Length z score.
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 44 Ponderal index (kg/m3).
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 45 Adiposity (sum of skinfold thickness) (mm).
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 46 Adiposity (abdominal circumference) (cm).
| Study | Intervention | Control | P value |
| Dodd 2014 | Neonatal anthropometric measures Mean (SD) (N = 488) Chest circumference Arm circumference Biceps SFTM (mm): 4.37 (1.12) Triceps SFTM (mm): 5.45 (1.30) Subscapular SFTM (mm): 5.15 (1.30) Suprailiac SFTM (mm): 5.76 (1.83) Abdominal SFTM (mm): 3.85 (1.02) Thigh SFTM (mm): 6.99 (1.85) Abdominal circumference to length ratio: 0.65 (0.04) Fat mass (g): 522.72 (180.70) Fat‐free mass (g): 3026.64 (339.96) Percentage body fat: 14.41 (3.39) Percentage fat‐free mass: 85.59 (3.39) (N = 215) Fat‐free mass R0 (g): 3096.62 (320.97) Percentage fat‐free mass R0: 88.98 (2.98) | Neonatal anthropometric measures Mean (SD) (N = 482) Chest circumference Arm circumference Biceps SFTM (mm): 4.31 (1.13) Triceps SFTM (mm): 5.41 (1.44) Subscapular SFTM (mm): 5.11 (1.21) Suprailiac SFTM (mm): 5.75 (1.92) Abdominal SFTM (mm): 3.82 (1.06) Thigh SFTM (mm): 7.02 (1.90) Abdominal circumference to length ratio: 0.65 (0.04) Fat mass (g): 523.48 (189.05) Fat‐free mass (g): 3030.07 (362.54) Percentage body fat: 14.37 (3.44) Percentage fat‐free mass: 85.63 (3.44) (N = 179) Fat‐free mass R0 (g): 3133.15 (348.92) Percentage fat‐free mass R0: 89.10 (3.40) | "Average body circumferences, SFTM and calculated body fat measures were similar between the treatment groups, with no statistically significant differences identified... There were also no statistically significant differences identified between the two groups, with regard to fat‐free mass (R0) and percentage fat‐free mass (R0) obtained using bio‐impedance analysis" (P value: 0.94; 0.60; 0.45; 0.85; 0.90; 0.97; 0.85; 0.74; 0.90; 0.94; 0.97; 0.91; 0.91; 0.56; 0.79) |
| Poston 2015 | Mean (SD) (N = 249) Triceps SFTM (mm): 5.3 (1.4) (N = 244) Subscapular SFTM (mm): 5.7 (1.4) | Mean (SD) (N = 268) Triceps SFTM (mm): 5.3 (1.6) (N = 258) Subscapular SFTM (mm): 5.6 (1.4) | "Neonatal anthropometric measures were evaluated in a subgroup of infants and did not differ between groups" (P values: 0.72; 0.66) |
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 47 Adiposity.
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 48 Shoulder dystocia.
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 49 Nerve palsy.
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 50 Bone fracture.
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 51 Respiratory distress syndrome.
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 52 Hypoglycaemia.
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 53 Hyperbilirubinaemia.
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 54 Childhood weight (latest time reported) (kg).
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 55 Childhood weight z score (latest time reported).
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 56 Childhood height (latest time reported) (cm).
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 57 Childhood height z score (latest time reported).
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 58 Childhood head circumference (latest time reported) (cm).
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 59 Childhood adiposity (latest time reported) (BMI z score).
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 60 Childhood adiposity (latest time reported) (abdominal circumference) (cm).
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 61 Childhood adiposity (latest time reported) (subscapular skinfold thickness) (mm).
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 62 Childhood adiposity (latest time reported) (triceps skinfold thickness) (mm).
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 63 Childhood adiposity (latest time reported) (total body fat) (%).
| Study | Intervention | Control | P value |
| Poston 2015 | Anthropometric measures at 6 months Mean (SD) (N = 267) Subscapular SFTM z score: 0.08 (1.37) (N = 296) Triceps SFTM z score: 0.10 (1.56) (N = 267) Sum of SFTM (mm): 17.08 (3.93) (N = 267) Subscapular triceps ratio: 0.83 (0.22) (N = 315) Waist length ratio: 0.64 (0.08) (N = 314) Weight for length z score: ‐0.08 (1.79) (N = 329) Mid upper arm circumference (cm): 15.30 (1.49) | Anthropometric measures at 6 months Mean (SD) (N = 280) Subscapular SFTM z score: 0.36 (1.37) (N = 298) Triceps SFTM z score: 0.24 (1.43) (N = 280) Sum of SFTM (mm): 17.71 (3.97) (N = 280) Subscapular triceps ratio: 0.85 (0.23) (N = 328) Waist length ratio: 0.64 (0.10) (N = 324) Weight for length z score: 0.08 (1.63) (N = 347) Mid upper arm circumference (cm): 15.39 (2.08) | "There was no statistical difference in triceps skinfold thickness... but subscapular skinfold thickness z‐score was... lower in the intervention arm... The infant sum of skinfold thickness... did not reach statistical significance... There were no differences... in other anthropometric measures between the two arms" (P values: 0.021; 0.246; 0.058; 0.423; 0.928; 0.184; 0.511) |
| Vinter 2011 | Anthropometric measures at 2.8 years Mean (95% CI) or N (%) (N = 82) Overweight or obese: 9 (10.9%) BMI (kg/m²): 16.4 (16.1; 16.7) Hip (cm): 50.8 (50.1; 51.5) Abdominal circumference/hip ratio: 0.97 (0.95; 0.97) Dual Energy X‐ray scan results at 2.8 years Mean (95% CI) (N = 37) Total fat (g): 2463 (2147; 2779) Lean body mass (g): 11,336 (10,942; 11,730) | Anthropometric measures at 2.8 years Mean (95% CI) or N (%) (N = 75) Overweight or obese: 5 (6.7%) BMI (kg/m²): 16.1 (15.8; 16.4) Hip (cm): 50.2 (49.4; 51.0) Abdominal circumference/hip ratio: 0.96 (0.95; 0.97) Dual Energy X‐ray scan results at 2.8 years Mean (95% CI) (N = 30) Total fat (g): 2442 (2189; 2696) Lean body mass (g): 11,236 (10,797; 11,675) | "At a significance level of 0.05 (two‐sided), there were no statistically significant differences in any variables between the LiP intervention and control groups." (Individual P values not reported) |
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 64 Childhood adiposity (latest time reported).
| Study | Intervention | Control | P value |
| Vinter 2011 | Metabolic risk factors at 2.8 years Mean (95% CI) or N (%) (N = 63) Systolic blood pressure (mm Hg): 98.3 (93.7–105.3) Systolic blood pressure ≥ 90th percentile: 16 (25.4) Diastolic blood pressure (mm Hg): 64.3 (61.0–67.3) Diastolic blood pressure ≥ 90th percentile: 16 (25.4) (N = 59) Fasting plasma glucose (mmol/L): 5.2 (4.6 –5.6) Fasting plasma glucose ≥ 5.6 mmol/L: 16 (20.8) (N = 39) Fasting insulin (pmol/L): 16 (8–33) Fasting insulin ≥ 55 pmol/L: 3 (7.7) Fasting HDL (mmol/L): 1.2 (1.1–1.4) Fasting HDL ≥ 1.03 mmol/L: 6 (17.1) Fasting triglycerides (mmol/L): 0.7 (0.6 –1.1) Fasting triglycerides ≥ 1.7 mmol/L: 1 (2.9) Metabolic syndrome (a high abdominal circumference plus 2 or more of the following: low HDL, high triglycerides, high fasting glucose, and high systolic and/or diastolic blood pressure): 0 (0) | Metabolic risk factors at 2.8 years Mean (95% CI) or N (%) (N = 54) Systolic blood pressure (mm Hg): 97.3 (94.3–101.3) Systolic blood pressure ≥ 90th percentile: 12 (22.0) Diastolic blood pressure (mm Hg): 62.0 (60.3– 65.3) Diastolic blood pressure ≥ 90th percentile: 12 (22.0) (N = 59) Fasting plasma glucose (mmol/L): 5.1 (4.7–5.5) Fasting plasma glucose ≥ 5.6 mmol/L: 13 (18.1) (N = 51) Fasting insulin (pmol/L): 12 (8–18) Fasting insulin ≥ 55 pmol/L: 3 (5.9) Fasting HDL (mmol/L): 1.3 (1.1–1.5) Fasting HDL ≥ 1.03 mmol/L: 6 (12.2) Fasting triglycerides (mmol/L): 0.9 (0.6 –1.0) Fasting triglycerides ≥ 1.7 mmol/L: 3 (6.1) Metabolic syndrome (a high abdominal circumference plus 2 or more of the following: low HDL, high triglycerides, high fasting glucose, and high systolic and/or diastolic blood pressure): 0 (0) | "At a significance level of .05 (two‐sided), there were no statistically |
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 65 Childhood cardiovascular health (latest time reported).
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 66 Antenatal visits.
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 67 Antenatal admissions.
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 68 Length of antenatal stay (days).
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 69 Neonatal intensive care unit admission.
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 70 Length of postnatal stay (mother) (days).
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 71 Length of postnatal stay (baby) (days).
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 72 Costs to families associated with the management provided (unit cost, €).
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 73 Costs associated with the intervention (unit cost, €).
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 74 Cost of maternal care (unit cost, €).
Comparison 1 Combined diet and exercise interventions versus standard care, Outcome 75 Cost of infant care (unit cost, €).
Comparison 2 Combined diet and exercise interventions versus standard care: subgroups based on study design, Outcome 1 Gestational diabetes.
Comparison 2 Combined diet and exercise interventions versus standard care: subgroups based on study design, Outcome 2 Pre‐eclampsia.
Comparison 2 Combined diet and exercise interventions versus standard care: subgroups based on study design, Outcome 3 Caesarean section.
Comparison 2 Combined diet and exercise interventions versus standard care: subgroups based on study design, Outcome 4 Large‐for‐gestational age.
Comparison 3 Combined diet and exercise interventions versus standard care: subgroups based on maternal BMI, Outcome 1 Gestational diabetes.
Comparison 3 Combined diet and exercise interventions versus standard care: subgroups based on maternal BMI, Outcome 2 Pre‐eclampsia.
Comparison 3 Combined diet and exercise interventions versus standard care: subgroups based on maternal BMI, Outcome 3 Pregnancy‐induced hypertension or hypertension.
Comparison 3 Combined diet and exercise interventions versus standard care: subgroups based on maternal BMI, Outcome 4 Caesarean section.
Comparison 3 Combined diet and exercise interventions versus standard care: subgroups based on maternal BMI, Outcome 5 Perinatal mortality.
Comparison 3 Combined diet and exercise interventions versus standard care: subgroups based on maternal BMI, Outcome 6 Large‐for‐gestational age.
Comparison 4 Combined diet and exercise interventions versus standard care: subgroups based on ethnicity, Outcome 1 Gestational diabetes.
Comparison 4 Combined diet and exercise interventions versus standard care: subgroups based on ethnicity, Outcome 2 Pre‐eclampsia.
Comparison 4 Combined diet and exercise interventions versus standard care: subgroups based on ethnicity, Outcome 3 Pregnancy‐induced hypertension or hypertension.
Comparison 4 Combined diet and exercise interventions versus standard care: subgroups based on ethnicity, Outcome 4 Caesarean section.
Comparison 4 Combined diet and exercise interventions versus standard care: subgroups based on ethnicity, Outcome 5 Perinatal mortality.
Comparison 4 Combined diet and exercise interventions versus standard care: subgroups based on ethnicity, Outcome 6 Large‐for‐gestational age.
Comparison 5 Combined diet and exercise interventions versus standard care: sensitivity analyses, Outcome 1 Gestational diabetes.
Comparison 5 Combined diet and exercise interventions versus standard care: sensitivity analyses, Outcome 2 Pre‐eclampsia.
Comparison 5 Combined diet and exercise interventions versus standard care: sensitivity analyses, Outcome 3 Pregnancy‐induced hypertension.
Comparison 5 Combined diet and exercise interventions versus standard care: sensitivity analyses, Outcome 4 Caesarean section.
Comparison 5 Combined diet and exercise interventions versus standard care: sensitivity analyses, Outcome 5 Perinatal mortality.
Comparison 5 Combined diet and exercise interventions versus standard care: sensitivity analyses, Outcome 6 Large‐for‐gestational age.
| Combined diet and exercise interventions for preventing GDM | ||||||
| Population: pregnant women, excluding women already diagnosed with GDM, type 1 or type 2 diabetes Setting: Australia (2 RCTs), Brazil (1 RCT), Canada (2 RCTs), China (2 RCTs), Denmark (1 RCT), Egypt (1 RCT), Finland (3 RCTs), Germany (1 RCT), Italy (2 RCTs), Norway (1 RCT), UK (2 RCTs), USA (5 RCTs) | ||||||
| Outcomes | Anticipated absolute effects* (95% CI) | Relative effect | № of participants | Quality of the evidence | Comments | |
| Risk with control | Risk with diet and exercise interventions | |||||
| GDM | Trial population | average RR 0.85 (0.71 to 1.01) | 6633 (19 RCTs) | ⊕⊕⊕⊝ MODERATE1,3 | ||
| 168 per 1000 | 143 per 1000 (119 to 170) | |||||
| Hypertensive disorders of pregnancy (pre‐eclampsia) | Trial population | RR 0.98 (0.79 to 1.22) | 5366 (8 RCTs) | ⊕⊕⊝⊝ LOW2,4 | Eclampsia was not reported by any trials (Sagedal 2017 reports combined severe pre‐eclampsia, HELLP and eclampsia) | |
| 57 per 1000 | 55 per 1000 (45 to 69) | |||||
| Hypertensive disorders of pregnancy (pregnancy‐induced hypertension/hypertension) | Trial population | average RR 0.78 | 3073 | ⊕⊝⊝⊝ VERY LOW2,5,6 | ||
| 103 per 1000 | 80 per 1000 (48 to 130) | |||||
| Caesarean section | Trial population | RR 0.95 (0.88 to 1.02) | 6089 (14 RCTs) | ⊕⊕⊕⊝ MODERATE7 | ||
| 299 per 1000 | 284 per 1000 (263 to 305) | |||||
| Perineal trauma | Trial population | RR 1.27 (0.78 to 2.05) | 2733 (2 RCTs) | ⊕⊕⊕⊝ MODERATE2 | ||
| 21 per 1000 | 27 per 1000 (17 to 44) | |||||
| Gestational weight gain (kg) | Trial population | MD ‐ 0.89 (‐1.39 to ‐ 0.40) | 5052 | ⊕⊕⊕⊝ MODERATE8,9 | ||
| The mean gestational weight gain in the intervention group was 0.89 kg less (1.39 kg less to 0.40 kg less) | ||||||
| Postnatal depression | Not estimable | (0 RCTs) | No data reported for postnatal depression in any of the included RCTs | |||
| Type 2 diabetes mellitus | Not estimable | (0 RCTs) | No data reported for type 2 diabetes mellitus in any of the included RCTs | |||
| *The risk in the intervention group (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 | ||||||
| 1Trial limitations (‐1): 19 RCTs, intervention unable to be blinded (not downgraded for this as outcome is objective); some RCTS with potentially serious design limitations (unclear randomisation, attrition bias) | ||||||
| Combined diet and exercise interventions for preventing GDM | ||||||
| Population: pregnant women, excluding women already diagnosed with GDM, type 1 or type 2 diabetes Setting: Australia (2 RCTs), Brazil (1 RCT), Canada (2 RCTs), China (2 RCTs), Denmark (1 RCT), Egypt (1 RCT), Finland (3 RCTs), Germany (1 RCT), Italy (2 RCTs), Norway (1 RCT), UK (2 RCTs), USA (5 RCTs) | ||||||
| Outcomes | Anticipated absolute effects* (95% CI) | Relative effect | № of participants | Quality of the evidence | Comments | |
| Risk with control | Risk with diet and exercise interventions | |||||
| Perinatal mortality | Trial population | RR 0.82 (0.42 to 1.63) | 3757 (2 RCTs) | ⊕⊕⊝⊝ LOW1 | ||
| 10 per 1000 | 8 per 1000 (4 to 16) | |||||
| Large‐for‐gestational age | Trial population | RR 0.93 (0.81 to 1.07) | 5353 (11 RCTs) | ⊕⊕⊝⊝ LOW2,3 | ||
| 135 per 1000 | 126 per 1000 (109 to 144) | |||||
| Mortality or morbidity composite | Not estimable | (0 RCTs) | No data reported for mortality or morbidity composite in any of the included RCTs | |||
| Neonatal hypoglycaemia | Trial population | average RR 1.42 (0.67 to 2.98) | 3653 (2 RCTs) | ⊕⊕⊝⊝ LOW3,4 | ||
| 63 per 1000 | 90 per 1000 (42 to 189) | |||||
| Childhood adiposity (latest time reported) (BMI z score) | Trial population | MD 0.05 (‐0.29 to 0.40) | 794 (2 RCTs) | ⊕⊕⊝⊝ LOW3,5,6 | Additional meta‐analyses presented in review for: abdominal circumference, subscapular skinfold thickness, triceps skinfold thickness and total body fat | |
| The mean BMI z score in the intervention group was 0.05 higher (0.29 lower to 0.40 higher) | ||||||
| Type 2 diabetes mellitus | Not estimable | (0 RCTs) | No data reported for type 2 diabetes mellitus in any of the included RCTs | |||
| Neurosensory disability | Not estimable | (0 RCTs) | No data reported for neurosensory disability in any of the included RCTs | |||
| *The risk in the intervention group (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 | ||||||
| 1Imprecision (‐2): confidence interval crossing the line of no effect and few events | ||||||
| Study ID | Diet and exercise intervention | Control |
| Mean (SD): 26.7 (6.0) | Mean (SD): 26.4 (5.0) | |
| Mean (SD): 31.5 (5) | Mean (SD): 30.8 (5.5) | |
| Mean (SD): 29.3 (5.4) | Mean (SD): 29.6 (5.6) | |
| Not reported | Not reported | |
| Mean (SD): 32.4 (4.6) | Mean (SD): 31.7 (4.5) | |
| N (%) | N (%) | |
| Mean (SD): 25.9 (4.9) | Mean (SD): 25.0 (5.7) | |
| Not reported | Not reported | |
| Mean (SD): 30.1 (5.2) | Mean (SD): 28.7 (5.9) | |
| Mean (SD) BMI ≤ 24.9 kg/m²: 31 (3) BMI ≥ 25 kg/m²: 31 (4) | Mean (SD) BMI ≤ 24.9 kg/m²: 29 (6) BMI ≥ 25 kg/m²: 32 (5) | |
| Mean (SD): 29.57 (4.13) | Mean (SD): 29.89 (3.86) | |
| Mean (SD): 32.3 (4.9) | Mean (SD): 32.6 (4.5) | |
| Mean (SD): 29.1 (5.4) | Mean (SD): 29.8 (5.4) | |
| Mean (SD): 29.5 (4.8) | Mean (SD): 30.0 (4.7) | |
| Mean (SD): 31.5 (4.2) | Mean (SD): 32.4 (5.9) | |
| Mean (SD): 28.6 (5.2) | Mean (SD): 28.8 (5.2) | |
| Mean (SD): 25.5 (4.8) | ||
| Mean (SD): 30.4 (5.7) | Mean (SD): 30.7 (4.9) | |
| Mean (SD): 30.5 (5.5) | Mean (SD): 30.4 (5.6) | |
| Mean (SD): 32.2 (4.4) | Mean (SD): 30.8 (4.9) | |
| Mean (SD): 27.9 (4.2) | Mean (SD): 28.1 (4.5) | |
| Median (IQR): 29 (27 ‐ 32) | Median (IQR): 29 (26 ‐ 31) | |
| Mean (SD): 31.0 (3.8) | Mean (SD): 30.27 (3.64) | |
| Abbreviations: BMI: body mass index; IQR: interquartile range; N: number; SD: standard deviation | ||
| Study ID | Diet and exercise intervention | Control |
| Mean (SD): 25.5 (6.0) [pre‐pregnancy] | Mean (SD): 25.6 (5.1) [pre‐pregnancy] | |
| Mean (SD): 33.3 (6) [pre‐pregnancy] Mean (SD): 34.5 (6.8) [baseline] | Mean (SD): 33.4 (5.5) [pre‐pregnancy] Mean (SD): 33.9 (5.7) [baseline] | |
| Median (IQR): 31.0 (28.1‐35.9) [baseline] | Median (IQR): 31.1 (27.7‐35.6) [baseline] | |
| Not reported (all women were obese) | Not reported (all women were obese) | |
| Mean (SD): 30.4 (5.6) [baseline] | Mean (SD): 30.3 (5.9) [baseline] | |
| N (%) [pre‐pregnancy] | N (%) [pre‐pregnancy] | |
| Mean (SD): 33.5 (5.8) [early pregnancy] | Mean (SD): 32.2 (5.4) [early pregnancy] | |
| Not reported | Not reported | |
| Mean (SD): 25.7 (5.1) [pre‐pregnancy] | Mean (SD): 24.9 (5.4) [pre‐pregnancy] | |
| Mean (SD) [pre‐pregnancy] BMI ≤ 24.9 kg/m²: 21.6 (2.2) BMI ≥ 25 kg/m²: 29.5 (5.1) | Mean (SD) [pre‐pregnancy] BMI ≤ 24.9 kg/m²: 22.6 (1.9) BMI ≥ 25 kg/m²: 29.7 (1.3) | |
| Mean (SD): 20.44 (2.54) [pre‐pregnancy] | Mean (SD): 20.44 (2.54); 20.74 (2.43) [pre‐pregnancy] | |
| Mean (SD): 31.5 (6.0) [pre‐pregnancy] Mean (SD): 32.2 (5.9) [baseline] | Mean (SD): 32.0 (5.5) [pre‐pregnancy] Mean (SD): 32.3 (5.4) [baseline] | |
| Mean (SD): 27.3 (6.0) [baseline] | Mean (SD): 25.5 (3.4) [baseline] | |
| Mean (SD): 26.3 (4.9) [pre‐pregnancy] | Mean (SD): 26.4 (4.3) [pre‐pregnancy] | |
| Mean (SD): 32.1 (5) [baseline] | Mean (SD): 32.9 (6.2) [baseline] | |
| Mean (SD): 26.32 (5.6) [baseline] | Mean (SD): 26.48 (5.9) [baseline] | |
| Mean (SD) [pre‐pregnancy] Normal weight: 22.8 (1.9) Overweight: 31.4 (6.0) | Mean (SD) [pre‐pregnancy] Normal weight: 22.5 (2.0) Overweight: 34.1 (7.2) | |
| Mean (SD): 36.5 (4.7) [baseline] | Mean (SD): 36.1 (4.8) [baseline] | |
| Mean (SD): 36.3 (5.0) [baseline] | Mean (SD): 36.3 (4.6) [baseline] | |
| Median (IQR): 21.7 (19.9 ‐ 23.7) [pre‐pregnancy] Median (IQR): 22.2 (20.7 ‐ 24.3) [booking] | Median (IQR): 22.8 (20.6 ‐ 26.6) [pre‐pregnancy] Median (IQR): 23.3 (21.2 ‐ 26.8) [booking] | |
| Mean (SD): 23.8 (4.1) [pre‐pregnancy] | Mean (SD): 23.5 (3.7) [pre‐pregnancy] | |
| Median (IQR): 33.4 (31.7 ‐ 36.5) | Median (IQR): 33.3 (31.7 ‐ 36.9) | |
| Mean (SD): 22.95 (3.65) [pre‐pregnancy] | Mean (SD): 23.06 (3.63) [pre‐pregnancy] | |
| Abbreviations: BMI: body mass index; IQR: interquartile range; N: number; SD: standard deviation | ||
| Study ID | Diet and exercise intervention | Control |
| N (%) | N (%) | |
| N (%) Caucasian: 79 (82.3) | N (%) Caucasian: 78 (82.1) | |
| N (%) | N (%) White: 998 (91.0) | |
| Not reported (conducted in Egypt) | Not reported (conducted in Egypt) | |
| Country of birth, N (%) | Country of birth, N (%) | |
| N (%) Hispanic: 33 (100) | N (%) Hispanic: 35 (100) | |
| N (%) African American: 33 (100) | N (%) African American: 33 (100) | |
| Not reported | Not reported | |
| N (%) | N (%) | |
| First Nations (Canadian Aboriginals with First Nations status), N (%) BMI ≤ 24.9 kg/m²: 2 (6.7) BMI ≥ 25 kg/m²: 3 (11.1) | First Nations (Canadian Aboriginals with First Nations status), N (%) BMI ≤ 24.9 kg/m²: 1 (3.7) BMI ≥ 25 kg/m²: 4 (13.8) | |
| Not reported (conducted in China) | Not reported (conducted in China) | |
| Not reported (conducted in Finland) | Not reported (conducted in Finland) | |
| Not reported (conducted in Norway) | Not reported (conducted in Norway) | |
| Not reported (conducted in Finland) | Not reported (conducted in Finland) | |
| N (%) Caucasian: 28 (84.9) Maghreb: 4 (12.1) Other: 1 (3.0) | Caucasian: 20 (66.7) Maghreb: 6 (20) Other: 4 (13.3) | |
| N (%) Non‐Hispanic White: 138 (68.7) Latina and Hispanic: 39 (19.6) Non‐Hispanic African American: 14 (7.1) Other: 9 (4.6) | N (%) Latina and Hispanic: 39 (19.6) Non‐Hispanic African American: 19 (9.6) Other: 7 (3.3) | |
| N (%) Black: 47 (39) White 73 (61) | ||
| N (%) White: 52 (55) Black: 38 (40) Asian: 2 (2) Other: 2 (2) | N (%) White: 51 (57) Black: 32 (26) Asian: 1 (1) Other: 5 (6) | |
| N (%) White: 490 (63) Black: 202 (26) Asian: 47 (6) Other: 44 (6) | N (%) Black: 200 (26) Asian: 48 (6) Other: 41 (5) | |
| Country of birth, N (%) Germany: 140 (83.8) Others: 27 (16.2) | Country of birth, N (%) Germany: 68 (81.9) Others: 15 (18.1) | |
| Not reported (conducted in Norway) | Not reported (conducted in Norway) | |
| N (%) | N (%) Caucasian: 154 (100) | |
| Not reported (conducted in China) | Not reported (conducted in China) | |
| Abbreviations: N: number | ||
| Study ID | Diet and exercise intervention | Control |
| N (%) | N (%) | |
| N (%) 0: 53 (55.2) | N (%) 0: 59 (62.1) | |
| N (%) 0: 441 (40.2) | N (%) 0: 441 (40.2) | |
| Not reported | Not reported | |
| N (%) | N (%) | |
| N (%) | N (%) | |
| N (%): 0: 9 (27) | N (%): 0: 10 (30) | |
| Not reported | Not reported | |
| Not reported | Not reported | |
| Not reported | Not reported | |
| Not reported | Not reported | |
| Previous deliveries, N (%) | Previous deliveries, N (%) | |
| N (%) 0: 13 (50) | N (%) 0: 17 (63) | |
| N (%) 0: 103 (47.0) | N (%) 0: 73 (40.6) | |
| N (%) 0: 13 (39.4) | N (%) 0: 13 (43.3) | |
| N (%) 0: 153 (76.3) ≥ 1: 48 (23.7) | N (%) 0: 153 (76.6) ≥ 1: 47 (23.4) | |
| N (%) First pregnancy: 56 (47) Second pregnancy: 36 (30) Third pregnancy: 20 (17) > third pregnancy: 7 (6) | ||
| N (%) 0: 42 (45) 1: 29 (31) ≥ 2: 23 (24) | N (%) 0: 38 (43) 1: 36 (40) ≥ 2: 15 (17) | |
| N (%) 0: 336 (43) ≥ 1: 447 (57) | N (%) 0: 338 (44) ≥ 1: 434 (56) | |
| N (%) 0: 110 (65.9) 1: 50 (29.9) ≥ 2: 7 (4.2) | N (%) 0: 53 (63.9) 1: 23 (27.7) ≥ 2: 7 (8.4) | |
| N (%) 0: 303 (100) | N (%) 0: 303 (100) | |
| N (%) 0: 79 (52.7) | N (%) 0: 84 (54.6) | |
| Not reported | Not reported | |
| Abbreviations: N: number | ||
| Study ID | Timing | Screening/diagnosis test(s) and glucose threshold(s) used for diagnosis | Reference(s) | Notes |
| Not reported | Not reported | Not provided | Data not provided in format suitable for meta‐analysis | |
| 16th to 18th weeks; repeated in 24th to 28th weeks for women negative at first test | 75 g 2‐hour OGTT Thresholds: fasting ≥ 5.1 mmol/L and/or 1‐hour ≥ 10.0 mmol/L and/or 2‐hour ≥ 8.5 mmol/L | "IADPSG criteria" (no reference provided) | ||
| Not reported | "all women were encouraged to undergo screening" 75 g 2‐hour OGTT Thresholds: fasting ≥ 5.5 mmol/L or 2‐hour ≥ 7.8 mmol/L | South Australian Perinatal Practice Guidelines 2013 (South Australian Perinatal Practice Guidelines: diabetes mellitus and abnormal glucose tolerance Government of Australia, SA Health, 2013. www.health.sa.gov.au/ppg/Default. | ||
| 24 to 28 weeks | "All women underwent routine GDM screening" | Not provided | Data not provided in format suitable for meta‐analysis | |
| 28 weeks | 2‐hour OGTT Thresholds: fasting ≥ 5.5 mmol/L and/or 2‐hour ≥ 8.0 mmol/L OR Thresholds: fasting ≥ 5.1 mmol/L and/or 1‐hour ≥ 10.0 mmol/L and/or 2‐hour ≥ 8.5 mmol/L | ADIPS 1998 (Hoffmann L, Nolan C, Wilson JD, Oats JJN, Simmons D. Gestational diabetes mellitus: management guidelines. MJA 1998;169:93–7.) OR IADPSG 2010 (Metzger BE, Gabbe SG, Persson B, et al. International association of diabetes and pregnancy study groups recommendations on the diagnosis and classification of hyperglycaemia in pregnancy. Diabetes Care 2010;33:676–82.) | Data in meta‐analysis according to IADPSG 2010 criteria [groups Ns not reported for ADIPS 1998 criteria] | |
| 24 to 28 weeks gestation | 50 g 1‐hour OGTT Thresholds: 1‐hour > 7.493 mmol/L 100 g 3‐hour OGTT Thresholds: not reported | American Diabetes Association 2012 (American Diabetes Association. Standards of medical care in diabetes–2012. Diabetes Care 2012; 35(Suppl. 1): S11–63.) | Data not provided in format suitable for meta‐analysis | |
| Not reported | Not reported | Not provided | ||
| Not reported | Not reported | Not provided | Data not provided in format suitable for meta‐analysis | |
| Not reported | Not reported | Canadian Diabetes Association 2008 (Canadian Diabetes Association. 2008 Clinical practice guidelines for the prevention and management of diabetes in Canada. Can J Diabetes 2008;32:S168–80.) | ||
| Not reported | Not reported | Canadian Diabetes Association 2008 (Canadian Diabetes Association, Clinical Practice Guidelines Committee, Canadian Diabetes Association: 2008 Clinical Practice Guidelines for the Prevention and Management of Diabetes in Canada. Can J Diabetes Care 2008, 32:S1:171.) | ||
| Not reported | Not reported | Not provided | ||
| 24 to 28 weeks | 75 g 2‐hour OGTT Thresholds: fasting ≥ 5.3 mmol/L and/or 1‐hour ≥ 10.0 mmol/L and/or 2‐hour ≥ 8.6 mmol/L | American Diabetes Association 2008 (Holcomb SS; American Diabetes Association. Update: standards of medical care in diabetes. Nurse Pract 2008;33:12–5.) | ||
| 26 to 28 weeks | 75 g 2‐hour OGTT Thresholds: fasting ≥ 5.6 mmol/L or 2‐hour ≥ 7.8 mmol/L | Modified from the World Health Organization 1998 (Alberti KG, Zimmet PZ: Definition, diagnosis and classification of diabetes mellitus and its complications. Part 1: diagnosis and classification of diabetes mellitus: provisional report of WHO consultation. Diabet Med 1998, 15:539‐53.) | All women also underwent 75 g 2 hour OGTT at 8 to 12 weeks; those diagnosed with GDM were excluded from the trial | |
| 26 to 28 weeks | 2‐hour OGTT Thresholds: fasting ≥ 5.3 mmol/L and/or 1‐hour > 10.0 mmol/L and/or 2‐hour > 8.6 mmol/L OR 1) Any of the above thresholds or newborn birthweight ≥ 4500 g or use of insulin or other diabetic medication 2) Any of the above thresholds or newborn birthweight ≥ 4000 g or use of insulin or other diabetic medication 3) Any of the above thresholds or use of insulin or other diabetic medication | American Diabetes Association 2010 ((2010) Diagnosis and classification of diabetes mellitus. Diabetes Care 33: S62–9.) | Data in meta‐analysis according to American Diabetes Association 2010 criteria [use of data according to other criteria did not change results] | |
| 16th to 18th week or 24th to 28th week "as recommend" | 75 g 2‐hour OGTT Thresholds: not reported | American Diabetes Association 2011 (American Diabetes Association. Standards of medical care in diabetes‐2011. Diabetes Care 2011;34:S11–61.) | ||
| Not reported | Not reported | Not provided | ||
| Not reported | Not reported | Not provided | ||
| 27 + 0 to 28 + 6 weeks | 75 g 2‐hour OGTT Thresholds: fasting ≥ 5.1 mmol/L and/or 1‐hour ≥ 10.0 mmol/L and/or 2‐hour ≥ 8.5 mmol/L | IADPSG 2010 (Metzger B, Gabbe SG, Persson B, Buchanan TA, Catalano PA, Damm P, Dyer AR, Leiva A, Hod M, Kitzmiler JL, Lowe LP, McIntyre HD, Oats JJ, Omori Y, Schmidt MI: International association of diabetes and pregnancy study groups recommendations on the diagnosis and classification of hyperglycaemia in pregnancy. Diabetes Care 2010, 33:676–82.) | ||
| 27 + 0 to 28 + 6 weeks | 75 g 2‐hour OGTT Thresholds: fasting ≥ 5.1 mmol/L and/or 1‐hour ≥ 10.0 mmol/L and/or 2‐hour ≥ 8.5 mmol/L | IADPSG 2010 (Metzger BE, Gabbe SG, Persson B, et al. International Association of Diabetes and Pregnancy Study Groups recommendations on the diagnosis and classification of hyperglycaemia in pregnancy. Diabetes Care 2010; 33: 676–82.) | ||
| 24th to 28th week | 2‐hour OGTT Thresholds: not reported | German Society of Gynecology and Obstetrics 2010 (Deutsche Gesellschaft für Gynäkologie und Geburtshilfe e.V.: Diagnostik und Therapie des Gestationsdiabetes. [http://www.dggg.de/leitlinien/].) | ||
| 30 weeks | 75 g 2‐hour OGTT Thresholds: 2‐hour ≥ 7.8 mmol/L | Norway national criteria 2008 (Tore HH, Torun C. Veileder i Fødselshjelp 2008 In) NGFNSfGaO, editor. Veileder i Fødselshjelp 2008; 2008. p. 112.); World Health Organization 2006 (World Health Organization. Definition and Diagnosis of Diabetes Mellitus and Intermediate Hyperglycaemia: Report of a WHO/IDF Consultation. Geneva, Switzerland: World Health Organization, 2006.) | ||
| 28 to 30 weeks and 34 to 36 weeks | 75 g 2‐hour OGTT Thresholds: 2‐hour ≥ 9 mmol/L OR Thresholds: 2‐hour ≥ 8.5 mmol/L | "Danish national recommendations" (no reference provided) OR IADPSG 2010 (Metzger BE, Gabbe SG, Persson B, Buchanan TA, Catalano PA, Damm P et al. International Association of Diabetes and Pregnancy Study Group’s recommendations on the diagnosis and classification of hyperglycaemia in pregnancy. Diabetes Care 2010; 33: 676–82.) | All women also underwent an OGTT at baseline (12 to 15 weeks); those diagnosed with GDM were excluded from the trial Data in meta‐analysis according to Danish national recommendations [use of data according to IADPSG 2010 criteria did not change results] | |
| 24 to 28 weeks | 75 g OGTT | "The International Association of Diabetes and Pregnancy Study Groups (IADPSG) criterion was used" (no reference provided) | ||
| Abbreviations: ADIPS: Australasian Diabetes in Pregnancy Society; g: gram; GDM: gestational diabetes mellitus; IADPSG: International Association of the Diabetes and Pregnancy Study Group; OGTT: oral glucose tolerance test; | ||||
| Outcome or subgroup title | No. of studies | No. of participants | Statistical method | Effect size |
| 1 Gestational diabetes Show forest plot | 19 | 6633 | Risk Ratio (M‐H, Random, 95% CI) | 0.85 [0.71, 1.01] |
| 2 Pre‐eclampsia Show forest plot | 8 | Risk Ratio (M‐H, Fixed, 95% CI) | Subtotals only | |
| 2.1 Pre‐eclampsia | 8 | 5366 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.98 [0.79, 1.22] |
| 2.2 Severe pre‐eclampsia/HELLP/eclampsia | 2 | 2088 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.72 [0.35, 1.46] |
| 3 Pregnancy‐induced hypertension and/or hypertension Show forest plot | 6 | Risk Ratio (M‐H, Random, 95% CI) | Subtotals only | |
| 3.1 Pregnancy‐induced hypertension and/or hypertension | 6 | 3073 | Risk Ratio (M‐H, Random, 95% CI) | 0.78 [0.47, 1.27] |
| 3.2 Pregnancy‐induced hypertension | 4 | 810 | Risk Ratio (M‐H, Random, 95% CI) | 0.46 [0.16, 1.29] |
| 3.3 Hypertension | 3 | 2532 | Risk Ratio (M‐H, Random, 95% CI) | 1.07 [0.84, 1.38] |
| 4 Caesarean section Show forest plot | 14 | 6089 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.95 [0.88, 1.02] |
| 5 Perinatal mortality Show forest plot | 2 | 3757 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.82 [0.42, 1.63] |
| 6 Large‐for‐gestational age Show forest plot | 11 | 5353 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.93 [0.81, 1.07] |
| 7 Operative vaginal birth Show forest plot | 3 | 2164 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.07 [0.86, 1.34] |
| 8 Induction of labour Show forest plot | 5 | 3907 | Risk Ratio (M‐H, Random, 95% CI) | 0.92 [0.79, 1.06] |
| 9 Perineal trauma Show forest plot | 2 | 2733 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.27 [0.78, 2.05] |
| 10 Placental abruption Show forest plot | 1 | 1555 | Risk Ratio (M‐H, Fixed, 95% CI) | 2.96 [0.12, 72.50] |
| 11 Postpartum haemorrhage Show forest plot | 3 | 4235 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.03 [0.89, 1.18] |
| 12 Postpartum infection Show forest plot | 2 | Risk Ratio (M‐H, Fixed, 95% CI) | Subtotals only | |
| 12.1 Endometritis | 1 | 2142 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.19 [0.52, 2.74] |
| 12.2 Wound infection | 1 | 2142 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.06 [0.65, 1.73] |
| 12.3 Postpartum antibiotics | 1 | 2142 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.00 [0.77, 1.31] |
| 12.4 Postpartum sepsis | 1 | 1555 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.33 [0.01, 8.06] |
| 13 Gestational weight gain (kg) Show forest plot | 16 | 5052 | Mean Difference (IV, Random, 95% CI) | ‐0.89 [‐1.39, ‐0.40] |
| 14 Gestational weight gain (various times reported) (kg) Show forest plot | 4 | Mean Difference (IV, Fixed, 95% CI) | Subtotals only | |
| 14.1 First trimester | 1 | 272 | Mean Difference (IV, Fixed, 95% CI) | ‐0.03 [‐0.62, 0.56] |
| 14.2 Second trimester | 2 | 541 | Mean Difference (IV, Fixed, 95% CI) | ‐0.38 [‐0.77, 0.02] |
| 14.3 Third trimester | 1 | 269 | Mean Difference (IV, Fixed, 95% CI) | ‐0.10 [‐1.17, 0.97] |
| 14.4 At 20‐24 weeks gestation | 1 | 221 | Mean Difference (IV, Fixed, 95% CI) | ‐0.45 [‐1.48, 0.58] |
| 14.5 At 26‐28 weeks gestation | 1 | 203 | Mean Difference (IV, Fixed, 95% CI) | ‐0.90 [‐1.75, ‐0.05] |
| 15 Gestational weight gain (kg/week) Show forest plot | 4 | 2772 | Mean Difference (IV, Random, 95% CI) | ‐0.03 [‐0.06, ‐0.00] |
| 16 Gestational weight gain (above IOM recommendations) Show forest plot | 11 | 4556 | Risk Ratio (M‐H, Random, 95% CI) | 0.87 [0.79, 0.96] |
| 17 Gestational weight gain (within IOM recommendations) Show forest plot | 9 | 3730 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.02 [0.93, 1.11] |
| 18 Gestational weight gain (below IOM recommendations) Show forest plot | 7 | 3499 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.10 [0.98, 1.24] |
| 19 Behaviour changes associated with the intervention Show forest plot | Other data | No numeric data | ||
| 20 Relevant biomarker changes associated with the intervention Show forest plot | Other data | No numeric data | ||
| 21 Sense of well‐being and quality of life Show forest plot | Other data | No numeric data | ||
| 22 Breastfeeding (exclusive) Show forest plot | 3 | Risk Ratio (M‐H, Fixed, 95% CI) | Subtotals only | |
| 22.1 3 days postpartum | 1 | 695 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.02 [0.91, 1.15] |
| 22.2 6 weeks postpartum | 1 | 202 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.93 [0.76, 1.13] |
| 22.3 6 months postpartum | 2 | 921 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.91 [0.61, 1.36] |
| 23 Breastfeeding (partial) Show forest plot | 3 | Risk Ratio (M‐H, Fixed, 95% CI) | Subtotals only | |
| 23.1 3 days postpartum | 1 | 695 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.51 [0.40, 0.66] |
| 23.2 6 weeks postpartum | 1 | 202 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.44 [0.80, 2.60] |
| 23.3 6 months postpartum | 2 | 921 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.98 [0.82, 1.18] |
| 24 Breastfeeding Show forest plot | Other data | No numeric data | ||
| 25 Postnatal weight retention (latest time reported) (kg) Show forest plot | 6 | 1673 | Mean Difference (IV, Fixed, 95% CI) | ‐0.94 [‐1.52, ‐0.37] |
| 26 Return to pre‐pregnancy weight (latest time reported) Show forest plot | 3 | 960 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.25 [1.08, 1.45] |
| 27 Postnatal BMI (latest time reported) Show forest plot | 2 | Mean Difference (IV, Fixed, 95% CI) | Subtotals only | |
| 27.1 BMI | 2 | 902 | Mean Difference (IV, Fixed, 95% CI) | ‐0.15 [‐0.85, 0.55] |
| 27.2 BMI change from baseline to 6 weeks postpartum | 1 | 202 | Mean Difference (IV, Fixed, 95% CI) | ‐0.56 [‐1.12, ‐0.00] |
| 28 Maternal cardiovascular health (latest time reported) Show forest plot | Other data | No numeric data | ||
| 29 Stillbirth Show forest plot | 5 | 4783 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.69 [0.35, 1.36] |
| 30 Neonatal mortality Show forest plot | 2 | Risk Ratio (M‐H, Fixed, 95% CI) | Subtotals only | |
| 30.1 Total | 2 | 3756 | Risk Ratio (M‐H, Fixed, 95% CI) | 2.31 [0.60, 8.90] |
| 30.2 No lethal anomalies | 1 | 2202 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.99 [0.06, 15.85] |
| 30.3 Lethal anomalies | 1 | 2202 | Risk Ratio (M‐H, Fixed, 95% CI) | 6.95 [0.36, 134.38] |
| 31 Gestational age at birth (weeks) Show forest plot | 11 | 5658 | Mean Difference (IV, Fixed, 95% CI) | 0.05 [‐0.05, 0.15] |
| 32 Gestational age at birth (days or weeks) Show forest plot | Other data | No numeric data | ||
| 33 Preterm birth Show forest plot | 11 | 5398 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.80 [0.65, 0.98] |
| 34 Apgar score less than seven at five minutes Show forest plot | 3 | 2864 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.80 [0.48, 1.32] |
| 35 Macrosomia Show forest plot | 10 | Risk Ratio (M‐H, Fixed, 95% CI) | Subtotals only | |
| 35.1 > 4000 g | 9 | 5368 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.89 [0.78, 1.01] |
| 35.2 > 4500 g | 4 | 3061 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.63 [0.42, 0.94] |
| 36 Small‐for‐gestational age Show forest plot | 6 | 2434 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.20 [0.95, 1.52] |
| 37 Birthweight (g) Show forest plot | 13 | 5763 | Mean Difference (IV, Fixed, 95% CI) | ‐17.67 [‐46.28, 10.94] |
| 38 Birthweight (g) Show forest plot | Other data | No numeric data | ||
| 39 Birthweight z score Show forest plot | 4 | 2661 | Mean Difference (IV, Fixed, 95% CI) | ‐0.05 [‐0.13, 0.03] |
| 40 Head circumference (cm) Show forest plot | 4 | 4229 | Mean Difference (IV, Fixed, 95% CI) | ‐0.01 [‐0.11, 0.10] |
| 41 Head circumference z score Show forest plot | 1 | 2142 | Mean Difference (IV, Fixed, 95% CI) | ‐0.05 [‐0.14, 0.04] |
| 42 Length (cm) Show forest plot | 6 | 3303 | Mean Difference (IV, Fixed, 95% CI) | ‐0.09 [‐0.26, 0.09] |
| 43 Length z score Show forest plot | 2 | 2235 | Mean Difference (IV, Fixed, 95% CI) | ‐0.08 [‐0.15, ‐0.02] |
| 44 Ponderal index (kg/m3) Show forest plot | 3 | 2826 | Mean Difference (IV, Fixed, 95% CI) | 0.04 [‐0.16, 0.25] |
| 45 Adiposity (sum of skinfold thickness) (mm) Show forest plot | 2 | 1472 | Mean Difference (IV, Fixed, 95% CI) | 0.09 [‐0.33, 0.50] |
| 45.1 Sum of biceps, triceps, subscapular, suprailiac, abdominal and thigh skinfold thickness | 1 | 970 | Mean Difference (IV, Fixed, 95% CI) | 0.03 [‐0.86, 0.92] |
| 45.2 Sum of triceps and subscapular skinfold thickness (mm) | 1 | 502 | Mean Difference (IV, Fixed, 95% CI) | 0.10 [‐0.36, 0.56] |
| 46 Adiposity (abdominal circumference) (cm) Show forest plot | 2 | 1566 | Mean Difference (IV, Fixed, 95% CI) | ‐0.01 [‐0.23, 0.22] |
| 47 Adiposity Show forest plot | Other data | No numeric data | ||
| 48 Shoulder dystocia Show forest plot | 2 | 2733 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.20 [0.79, 1.83] |
| 49 Nerve palsy Show forest plot | 1 | 2142 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.99 [0.36, 10.82] |
| 50 Bone fracture Show forest plot | 1 | 2142 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.99 [0.36, 10.82] |
| 51 Respiratory distress syndrome Show forest plot | 2 | 2411 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.56 [0.33, 0.97] |
| 52 Hypoglycaemia Show forest plot | 2 | 3653 | Risk Ratio (M‐H, Random, 95% CI) | 1.42 [0.67, 2.98] |
| 53 Hyperbilirubinaemia Show forest plot | 1 | 2142 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.82 [0.61, 1.11] |
| 54 Childhood weight (latest time reported) (kg) Show forest plot | 3 | 882 | Mean Difference (IV, Random, 95% CI) | ‐0.05 [‐0.33, 0.22] |
| 54.1 6 months | 1 | 677 | Mean Difference (IV, Random, 95% CI) | ‐0.10 [‐0.26, 0.06] |
| 54.2 10‐12 months | 1 | 48 | Mean Difference (IV, Random, 95% CI) | ‐0.36 [‐0.96, 0.24] |
| 54.3 2.8 years | 1 | 157 | Mean Difference (IV, Random, 95% CI) | 0.30 [‐0.19, 0.79] |
| 55 Childhood weight z score (latest time reported) Show forest plot | 1 | 643 | Mean Difference (IV, Fixed, 95% CI) | ‐0.09 [‐0.26, 0.08] |
| 56 Childhood height (latest time reported) (cm) Show forest plot | 2 | 816 | Mean Difference (IV, Fixed, 95% CI) | 0.33 [‐0.58, 1.25] |
| 56.1 6 months | 1 | 659 | Mean Difference (IV, Fixed, 95% CI) | 1.04 [‐0.58, 2.66] |
| 56.2 2.8 years | 1 | 157 | Mean Difference (IV, Fixed, 95% CI) | 0.0 [‐1.11, 1.11] |
| 57 Childhood height z score (latest time reported) Show forest plot | 1 | 622 | Mean Difference (IV, Fixed, 95% CI) | ‐0.02 [‐0.31, 0.27] |
| 58 Childhood head circumference (latest time reported) (cm) Show forest plot | 1 | 670 | Mean Difference (IV, Fixed, 95% CI) | ‐0.12 [‐0.70, 0.46] |
| 59 Childhood adiposity (latest time reported) (BMI z score) Show forest plot | 2 | 794 | Mean Difference (IV, Random, 95% CI) | 0.05 [‐0.29, 0.40] |
| 59.1 6 months | 1 | 637 | Mean Difference (IV, Random, 95% CI) | ‐0.11 [‐0.39, 0.17] |
| 59.2 2.8 years | 1 | 157 | Mean Difference (IV, Random, 95% CI) | 0.24 [‐0.10, 0.58] |
| 60 Childhood adiposity (latest time reported) (abdominal circumference) (cm) Show forest plot | 2 | 833 | Mean Difference (IV, Fixed, 95% CI) | 0.26 [‐0.37, 0.90] |
| 60.1 6 months | 1 | 676 | Mean Difference (IV, Fixed, 95% CI) | 0.02 [‐0.81, 0.85] |
| 60.2 2.8 years | 1 | 157 | Mean Difference (IV, Fixed, 95% CI) | 0.60 [‐0.38, 1.58] |
| 61 Childhood adiposity (latest time reported) (subscapular skinfold thickness) (mm) Show forest plot | 2 | 705 | Mean Difference (IV, Random, 95% CI) | ‐0.17 [‐0.66, 0.32] |
| 61.1 6 months | 1 | 548 | Mean Difference (IV, Random, 95% CI) | ‐0.40 [‐0.73, ‐0.07] |
| 61.2 2.8 years | 1 | 157 | Mean Difference (IV, Random, 95% CI) | 0.10 [‐0.33, 0.53] |
| 62 Childhood adiposity (latest time reported) (triceps skinfold thickness) (mm) Show forest plot | 2 | 784 | Mean Difference (IV, Fixed, 95% CI) | ‐0.12 [‐0.48, 0.23] |
| 62.1 6 months | 1 | 627 | Mean Difference (IV, Fixed, 95% CI) | ‐0.18 [‐0.61, 0.25] |
| 62.2 2.8 years | 1 | 157 | Mean Difference (IV, Fixed, 95% CI) | 0.0 [‐0.63, 0.63] |
| 63 Childhood adiposity (latest time reported) (total body fat) (%) Show forest plot | 2 | 614 | Mean Difference (IV, Fixed, 95% CI) | ‐0.74 [‐1.56, 0.07] |
| 63.1 6 months | 1 | 547 | Mean Difference (IV, Fixed, 95% CI) | ‐0.80 [‐1.64, 0.04] |
| 63.2 2.8 years | 1 | 67 | Mean Difference (IV, Fixed, 95% CI) | 0.0 [‐3.03, 3.03] |
| 64 Childhood adiposity (latest time reported) Show forest plot | Other data | No numeric data | ||
| 65 Childhood cardiovascular health (latest time reported) Show forest plot | Other data | No numeric data | ||
| 66 Antenatal visits Show forest plot | 1 | 269 | Mean Difference (IV, Fixed, 95% CI) | 0.0 [‐0.36, 0.36] |
| 67 Antenatal admissions Show forest plot | 1 | 2153 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.86 [0.71, 1.04] |
| 68 Length of antenatal stay (days) Show forest plot | 2 | Mean Difference (IV, Fixed, 95% CI) | Subtotals only | |
| 68.1 Antenatal stay (days) | 1 | 2153 | Mean Difference (IV, Fixed, 95% CI) | ‐0.27 [‐0.49, ‐0.05] |
| 68.2 Antenatal inpatient stay (nights), if admitted | 1 | 139 | Mean Difference (IV, Fixed, 95% CI) | 0.0 [‐1.00, 1.00] |
| 69 Neonatal intensive care unit admission Show forest plot | 4 | 4549 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.03 [0.93, 1.14] |
| 70 Length of postnatal stay (mother) (days) Show forest plot | 2 | 3511 | Mean Difference (IV, Random, 95% CI) | 0.01 [‐0.14, 0.17] |
| 71 Length of postnatal stay (baby) (days) Show forest plot | 2 | 3618 | Mean Difference (IV, Fixed, 95% CI) | ‐0.35 [‐0.90, 0.20] |
| 72 Costs to families associated with the management provided (unit cost, €) Show forest plot | 1 | Mean Difference (IV, Fixed, 95% CI) | Subtotals only | |
| 72.1 Delivery cost to the patient | 1 | 93 | Mean Difference (IV, Fixed, 95% CI) | 3.0 [‐10.82, 16.82] |
| 72.2 Neonatal care cost to the patient | 1 | 93 | Mean Difference (IV, Fixed, 95% CI) | 3.00 [‐13.67, 19.67] |
| 73 Costs associated with the intervention (unit cost, €) Show forest plot | 1 | 93 | Mean Difference (IV, Fixed, 95% CI) | 769.0 [‐1032.23, 2570.23] |
| 73.1 Total costs | 1 | 93 | Mean Difference (IV, Fixed, 95% CI) | 769.0 [‐1032.23, 2570.23] |
| 74 Cost of maternal care (unit cost, €) Show forest plot | 1 | Mean Difference (IV, Fixed, 95% CI) | Subtotals only | |
| 74.1 Visits for primary health care | 1 | 93 | Mean Difference (IV, Fixed, 95% CI) | ‐43.0 [‐127.61, 41.61] |
| 74.2 Visits for specialist health care | 1 | 93 | Mean Difference (IV, Fixed, 95% CI) | ‐47.0 [‐195.33, 101.33] |
| 74.3 Visits to a diabetes nurse | 1 | 93 | Mean Difference (IV, Fixed, 95% CI) | 6.00 [‐7.02, 19.02] |
| 74.4 Visits to a dietitian | 1 | 93 | Mean Difference (IV, Fixed, 95% CI) | 0.0 [0.0, 0.0] |
| 74.5 Use of insulin/other diabetes medication | 1 | 93 | Mean Difference (IV, Fixed, 95% CI) | ‐1.0 [‐7.83, 5.83] |
| 74.6 Hospital days before and after delivery | 1 | 93 | Mean Difference (IV, Fixed, 95% CI) | 101.00 [‐206.71, 408.71] |
| 74.7 Delivery cost to the municipality | 1 | 93 | Mean Difference (IV, Fixed, 95% CI) | 22.0 [‐234.43, 278.43] |
| 74.8 Absence from work | 1 | 93 | Mean Difference (IV, Fixed, 95% CI) | 128.0 [‐1295.58, 1551.58] |
| 75 Cost of infant care (unit cost, €) Show forest plot | 1 | 93 | Mean Difference (IV, Fixed, 95% CI) | 453.0 [‐298.20, 1204.20] |
| 75.1 Neonatal care cost to municipality | 1 | 93 | Mean Difference (IV, Fixed, 95% CI) | 453.0 [‐298.20, 1204.20] |
| Outcome or subgroup title | No. of studies | No. of participants | Statistical method | Effect size |
| 1 Gestational diabetes Show forest plot | 19 | 6633 | Risk Ratio (M‐H, Random, 95% CI) | 0.85 [0.71, 1.01] |
| 1.1 Individually‐randomised | 17 | 6492 | Risk Ratio (M‐H, Random, 95% CI) | 0.84 [0.70, 1.01] |
| 1.2 Cluster‐randomised | 2 | 141 | Risk Ratio (M‐H, Random, 95% CI) | 1.05 [0.42, 2.60] |
| 2 Pre‐eclampsia Show forest plot | 8 | 5366 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.98 [0.79, 1.22] |
| 2.1 Individually‐randomised | 7 | 5273 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.97 [0.78, 1.21] |
| 2.2 Cluster‐randomised | 1 | 93 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.24 [0.22, 7.05] |
| 3 Caesarean section Show forest plot | 14 | 6089 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.95 [0.88, 1.02] |
| 3.1 Individually‐randomised | 13 | 6038 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.95 [0.88, 1.02] |
| 3.2 Cluster‐randomised | 1 | 51 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.71 [0.33, 1.54] |
| 4 Large‐for‐gestational age Show forest plot | 11 | 5353 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.93 [0.81, 1.07] |
| 4.1 Individually‐randomised | 9 | 5209 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.94 [0.82, 1.08] |
| 4.2 Cluster‐randomised | 2 | 144 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.59 [0.25, 1.40] |
| Outcome or subgroup title | No. of studies | No. of participants | Statistical method | Effect size |
| 1 Gestational diabetes Show forest plot | 19 | 6633 | Risk Ratio (M‐H, Random, 95% CI) | 0.86 [0.72, 1.02] |
| 1.1 Normal weight women (BMI < 25 kg/m²) | 3 | 300 | Risk Ratio (M‐H, Random, 95% CI) | 0.91 [0.19, 4.24] |
| 1.2 Overweight or obese women (BMI ≥ 25kg/m²) | 8 | 2901 | Risk Ratio (M‐H, Random, 95% CI) | 0.77 [0.50, 1.20] |
| 1.3 Obese women (BMI ≥ 30kg/m²) | 3 | 1738 | Risk Ratio (M‐H, Random, 95% CI) | 0.96 [0.81, 1.13] |
| 1.4 Any women | 8 | 1694 | Risk Ratio (M‐H, Random, 95% CI) | 0.80 [0.63, 1.03] |
| 2 Pre‐eclampsia Show forest plot | 8 | 5366 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.98 [0.79, 1.21] |
| 2.1 Normal weight women (BMI < 25 kg/m²) | 2 | 243 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.34 [0.10, 1.22] |
| 2.2 Overweight or obese women (BMI ≥ 25kg/m²) | 3 | 2369 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.12 [0.82, 1.54] |
| 2.3 Obese women (BMI ≥ 30kg/m²) | 2 | 1809 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.92 [0.64, 1.32] |
| 2.4 Any women | 3 | 945 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.94 [0.51, 1.73] |
| 3 Pregnancy‐induced hypertension or hypertension Show forest plot | 6 | 3073 | Risk Ratio (M‐H, Random, 95% CI) | 0.71 [0.41, 1.25] |
| 3.1 Underweight women | 1 | 110 | Risk Ratio (M‐H, Random, 95% CI) | 0.70 [0.26, 1.88] |
| 3.2 Normal weight women (BMI < 25 kg/m²) | 1 | 182 | Risk Ratio (M‐H, Random, 95% CI) | 0.28 [0.08, 0.97] |
| 3.3 Overweight or obese women (BMI ≥ 25kg/m²) | 5 | 2781 | Risk Ratio (M‐H, Random, 95% CI) | 0.82 [0.43, 1.58] |
| 4 Caesarean section Show forest plot | 14 | 6089 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.95 [0.88, 1.02] |
| 4.1 Normal weight women (BMI < 25 kg/m²) | 3 | 300 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.92 [0.58, 1.45] |
| 4.2 Overweight or obese women (BMI ≥ 25kg/m²) | 7 | 2662 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.91 [0.83, 1.01] |
| 4.3 Obese women (BMI ≥ 30kg/m²) | 2 | 1826 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.99 [0.87, 1.12] |
| 4.4 Any women | 5 | 1301 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.98 [0.75, 1.28] |
| 5 Perinatal mortality Show forest plot | 2 | 3757 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.82 [0.42, 1.63] |
| 5.1 Overweight or obese women (BMI ≥ 25kg/m²) | 1 | 2202 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.99 [0.32, 3.07] |
| 5.2 Obese women (BMI ≥ 30 kg/m²) | 1 | 1555 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.74 [0.31, 1.74] |
| 6 Large‐for‐gestational age Show forest plot | 11 | 5353 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.93 [0.81, 1.07] |
| 6.1 Normal weight women (BMI < 25 kg/m²) | 1 | 57 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.6 [0.11, 3.32] |
| 6.2 Overweight or obese women (BMI ≥ 25kg/m²) | 4 | 2385 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.89 [0.76, 1.06] |
| 6.3 Obese women (BMI ≥ 30kg/m²) | 3 | 1986 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.17 [0.89, 1.54] |
| 6.4 Any women | 4 | 925 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.64 [0.40, 1.03] |
| Outcome or subgroup title | No. of studies | No. of participants | Statistical method | Effect size |
| 1 Gestational diabetes Show forest plot | 19 | 6633 | Risk Ratio (M‐H, Random, 95% CI) | 0.85 [0.71, 1.01] |
| 1.1 Majority 'low risk' ethnicities | 5 | 2998 | Risk Ratio (M‐H, Random, 95% CI) | 0.85 [0.50, 1.43] |
| 1.2 Majority 'high risk' ethnicities | 1 | 56 | Risk Ratio (M‐H, Random, 95% CI) | 1.07 [0.07, 16.33] |
| 1.3 Mixed ethnicities | 7 | 2123 | Risk Ratio (M‐H, Random, 95% CI) | 0.89 [0.76, 1.05] |
| 1.4 Unclear | 6 | 1456 | Risk Ratio (M‐H, Random, 95% CI) | 0.83 [0.61, 1.12] |
| 2 Pre‐eclampsia Show forest plot | 8 | 5366 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.98 [0.79, 1.22] |
| 2.1 Majority 'low risk' ethnicities | 3 | 2806 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.99 [0.76, 1.29] |
| 2.2 Mixed ethnicities | 2 | 1615 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.96 [0.58, 1.58] |
| 2.3 Unclear | 3 | 945 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.94 [0.51, 1.73] |
| 3 Pregnancy‐induced hypertension or hypertension Show forest plot | 6 | 3073 | Risk Ratio (M‐H, Random, 95% CI) | 0.78 [0.47, 1.27] |
| 3.1 Majority 'low risk' ethnicities | 5 | 2804 | Risk Ratio (M‐H, Random, 95% CI) | 0.64 [0.34, 1.17] |
| 3.2 Unclear | 1 | 269 | Risk Ratio (M‐H, Random, 95% CI) | 1.37 [0.70, 2.72] |
| 4 Caesarean section Show forest plot | 14 | 6089 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.95 [0.88, 1.02] |
| 4.1 Majority 'low risk' ethnicities | 5 | 2987 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.93 [0.84, 1.03] |
| 4.2 Majority 'high risk' ethnicities | 2 | 156 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.87 [0.54, 1.42] |
| 4.3 Mixed ethnicities | 5 | 1986 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.94 [0.82, 1.07] |
| 4.4 Unclear | 2 | 960 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.15 [0.84, 1.56] |
| 5 Perinatal mortality Show forest plot | 2 | 3757 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.82 [0.42, 1.63] |
| 5.1 Majority 'low risk' ethnicities | 1 | 2202 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.99 [0.32, 3.07] |
| 5.2 Mixed ethnicities | 1 | 1555 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.74 [0.31, 1.74] |
| 6 Large‐for‐gestational age Show forest plot | 11 | 5353 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.93 [0.81, 1.07] |
| 6.1 Majority 'low risk' ethnicities | 3 | 2577 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.91 [0.77, 1.07] |
| 6.2 Majority 'high risk' ethnicities | 1 | 56 | Risk Ratio (M‐H, Fixed, 95% CI) | 3.21 [0.14, 75.68] |
| 6.3 Mixed ethnicities | 5 | 2036 | Risk Ratio (M‐H, Fixed, 95% CI) | 1.05 [0.80, 1.38] |
| 6.4 Unclear | 2 | 684 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.63 [0.32, 1.23] |
| Outcome or subgroup title | No. of studies | No. of participants | Statistical method | Effect size |
| 1 Gestational diabetes Show forest plot | 11 | 5019 | Risk Ratio (M‐H, Random, 95% CI) | 0.86 [0.68, 1.09] |
| 2 Pre‐eclampsia Show forest plot | 4 | 4311 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.99 [0.78, 1.26] |
| 3 Pregnancy‐induced hypertension Show forest plot | 4 | 2694 | Risk Ratio (M‐H, Random, 95% CI) | 0.58 [0.27, 1.25] |
| 4 Caesarean section Show forest plot | 10 | 4968 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.94 [0.87, 1.02] |
| 5 Perinatal mortality Show forest plot | 2 | 3757 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.82 [0.42, 1.63] |
| 6 Large‐for‐gestational age Show forest plot | 8 | 4618 | Risk Ratio (M‐H, Fixed, 95% CI) | 0.95 [0.83, 1.09] |
