Dietary advice interventions in pregnancy for preventing gestational diabetes mellitus

Summary of findings for the main comparison. Dietary advice interventions versus standard care (maternal outcomes)

Dietary advice interventions versus standard care (maternal outcomes)
Population: pregnant women Setting: 6 studies carried out in Australia, the USA, Brazil, Denmark, Ireland and Finland Intervention: dietary advice interventions Comparison: standard care
Outcomes	*Anticipated absolute effects^ (95% CI)**		Relative effect (95% CI)	№ of participants (studies)	Quality of the evidence (GRADE)	Comments
	Risk with standard care	Risk with dietary advice interventions
Gestational diabetes	Study population		RR 0.60 (0.35 to 1.04)	1279 (5 RCTs)	⊕⊝⊝⊝ VERY LOW ^1,2,3
	126 per 1000	76 per 1000 (44 to 131)
Hypertensive disorders of pregnancy (pregnancy‐induced hypertension)	Study population		RR 0.30 (0.10 to 0.88)	282 (2 RCTs)	⊕⊕⊝⊝ LOW ^1,4	Anticipated absolute effects based on only 2 trials contributing data
	98 per 1000	29 per 1000 (10 to 86)
Hypertensive disorders of pregnancy (pre‐eclampsia)	Study population		RR 0.61 (0.25 to 1.46)	282 (2 RCTs)	⊕⊕⊝⊝ LOW ^1,5	Anticipated absolute effects based on only 2 trials contributing data
	84 per 1000	51 per 1000 (21 to 123)
Caesarean section	Study population		RR 0.98 (0.78 to 1.24)	1194 (4 RCTs)	⊕⊕⊝⊝ LOW ^1,3
	300 per 1000	294 per 1000 (234 to 372)
Perineal trauma (anal sphincter injury)	Study population		RR 0.83 (0.23 to 3.08)	759 (1 RCT)	⊕⊝⊝⊝ VERY LOW ^6,7	Anticipated absolute effect based on findings from a single study
	13 per 1000	11 per 1000 (3 to 40)
Gestational weight gain (kg)	The mean gestational weight gain in the intervention group was 4.7 kg less (8.07 kg less to 1.34 kg less)		MD ‐4.70 (‐8.07 to ‐1.34)	1336 (5 RCTs)	⊕⊕⊝⊝ LOW ^1,8	There was high heterogeneity for this outcome
Postnatal depression			Not estimable	(0 studies)		No data reported for postnatal depression in any of the included studies
*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). CI: confidence interval; kg: kilogram; MD: mean difference; RCT: randomised controlled trial; RR: risk ratio
GRADE Working Group grades of evidence High quality: We are very confident that the true effect lies close to that of the estimate of the effect Moderate quality: We are moderately confident in the effect estimate: The true effect is likely to be close to the estimate of the effect, but there is a possibility that it is substantially different Low quality: Our confidence in the effect estimate is limited: The true effect may be substantially different from the estimate of the effect Very low quality: We have very little confidence in the effect estimate: The true effect is likely to be substantially different from the estimate of effect
¹The studies contributing data had design limitations ²There was considerable variation in the size of the effect in different studies ³Wide 95% CI crossing the line of no effect ⁴Estimate based on studies with small sample sizes ⁵Estimate based on studies with small sample sizes, low event rates and 95% CI crossing the line of no effect ⁶Single study with design limitations ⁷Single study contributing data, low event rate and wide 95% CI crossing the line of no effect ⁸Very substantial heterogeneity (I² = 96%)

Summary of findings 2. Dietary advice interventions versus standard care (child outcomes)

Dietary advice interventions versus standard care (child outcomes)
Population: pregnant women Setting: 6 studies carried out in Australia, the USA, Brazil, Denmark, Ireland and Finland Intervention: dietary advice interventions Comparison: standard care
Outcomes	*Anticipated absolute effects^ (95% CI)**		Relative effect (95% CI)	№ of participants (studies)	Quality of the evidence (GRADE)	Comments
	Risk with standard care	Risk with dietary advice interventions
Perinatal mortality	Study population		Not estimable	159 (1 RCT)	⊕⊝⊝⊝ VERY LOW ^1,2	Effect not estimable. Outcome reported in a single study with no events
	0 per 1000	0 per 1000 (0 to 0)
Large‐for‐gestational age			Not estimable	(0 studies)		No data reported for large‐for‐gestational age in any of the included studies
Mortality or morbidity composite outcome			Not estimable	(0 studies)		No data reported for mortality or morbidity composite in any of the included studies
Neonatal hypoglycaemia			Not estimable	(0 studies)		No data reported for neonatal hypoglycaemia in any of the included studies
Childhood/adulthood adiposity: skinfold thickness at 6 months (mm)	The mean skinfold thickness in the intervention group was 0.1 mm less (0.71 less to 0.51 more)		MD ‐0.10 (‐0.71 to 0.51)	132 (1 RCT)	⊕⊕⊝⊝ LOW ^1,3	Estimate based on findings from a single study
Chilhood/adulthood type 2 diabetes mellitus			Not estimable	(0 studies)		No data reported for childhood/adulthood type 2 diabetes in any of the included studies
Childhood/adulthood neurosensory disability			Not estimable	(0 studies)		No data reported for childhood/adulthood neurosensory disability in any of the included studies
*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). CI: confidence interval; MD: mean difference; mm: millimetre; RCT: randomised controlled trial; RR: risk ratio; SD: standard deviation
GRADE Working Group grades of evidence High quality: We are very confident that the true effect lies close to that of the estimate of the effect Moderate quality: We are moderately confident in the effect estimate: The true effect is likely to be close to the estimate of the effect, but there is a possibility that it is substantially different Low quality: Our confidence in the effect estimate is limited: The true effect may be substantially different from the estimate of the effect Very low quality: We have very little confidence in the effect estimate: The true effect is likely to be substantially different from the estimate of effect
¹Single study with design limitations contributing data ²Single study with small sample size and no events ³Estimate based on single study with small sample size and wide 95% CI crossing the line of no effect

Summary of findings 3. Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice (maternal outcomes)

Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice (maternal outcomes)
Population: pregnant women Setting: 4 studies carried out in Australia (3) and the USA (1) Intervention: low‐GI dietary advice Comparison: moderate‐ to high‐GI dietary advice
Outcomes	*Anticipated absolute effects^ (95% CI)**		Relative effect (95% CI)	№ of participants (studies)	Quality of the evidence (GRADE)	Comments
	Risk with moderate‐ to high‐GI dietary advice	Risk with low‐ GI dietary advice
Gestational diabetes	Study population		RR 0.91 (0.63 to 1.31)	912 (4 RCTs)	⊕⊕⊝⊝ LOW ^1,2
	110 per 1000	100 per 1000 (70 to 145)
Hypertensive disorders of pregnancy			Not estimable	(0 studies)		No data reported for hypertensive disorders of pregnancy in any of the included studies
Caesarean birth	Study population		RR 1.27 (0.79 to 2.04)	201 (2 RCTs)	⊕⊝⊝⊝ VERY LOW ^3,4
	227 per 1000	288 per 1000 (179 to 463)
Perineal trauma			Not estimable	(0 studies)		No data reported for perineal trauma in any of the included studies
Gestational weight gain (kg)	The mean gestational weight gain in the intervention group was 1.23 kg less than in the control group (4.08 kg less to 1.61 more)		MD ‐1.23 (‐4.08 to 1.61)	787 (4 RCTs)	⊕⊝⊝⊝ VERY LOW ^2,3,5
Postnatal depression			Not estimable	(0 studies)		No data reported for postnatal depression in any of the included studies
Type 2 diabetes mellitus			Not estimable	(0 studies)		No data reported for type 2 diabetes in any of the included studies
*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). CI: confidence interval; kg: kilogram; MD: mean difference; RCT: randomised controlled trial; RR: risk ratio
GRADE Working Group grades of evidence High quality: We are very confident that the true effect lies close to that of the estimate of the effect Moderate quality: We are moderately confident in the effect estimate: The true effect is likely to be close to the estimate of the effect, but there is a possibility that it is substantially different Low quality: Our confidence in the effect estimate is limited: The true effect may be substantially different from the estimate of the effect Very low quality: We have very little confidence in the effect estimate: The true effect is likely to be substantially different from the estimate of effect
¹Studies contributing data had design limitations ²Wide 95% CI crossing the line of no effect ³Studies contributing data had serious or very serious design limitations ⁴Estimate based on studies with small sample sizes, and wide 95% CI crossing the line of no effect ⁵Substantial heterogeneity (I² = 90%)

See: Summary of findings for the main comparison Dietary advice interventions versus standard care (maternal outcomes); Summary of findings 2 Dietary advice interventions versus standard care (child outcomes); Summary of findings 3 Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice (maternal outcomes); Summary of findings 4 Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice (child outcomes)

Summary of findings 4. Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice (child outcomes)

Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice (child outcomes)
Population: pregnant women Setting: 4 studies carried out in Australia (3) and the USA (1) Intervention: low‐GI dietary advice Comparison: moderate‐ to high‐GI dietary advice
Outcomes	*Anticipated absolute effects^ (95% CI)**		Relative effect (95% CI)	№ of participants (studies)	Quality of the evidence (GRADE)	Comments
	Risk with moderate‐ to high‐GI dietary advice	Risk with low‐GI dietary advice
Perinatal mortality			Not estimable	(0 studies)		No data reported for perinatal mortality in any of the included studies
Large‐for‐gestational age	Study population		RR 0.60 (0.19 to 1.86)	777 (3 RCTs)	⊕⊝⊝⊝ VERY LOW ^1,2,3
	114 per 1000	68 per 1000 (22 to 212)
Mortality or morbidity composite outcome			Not estimable	(0 studies)		No data reported for mortality or morbidity composite in any of the included studies
Neonatal hypoglycaemia			Not estimable	(0 studies)		No data reported for neonatal hypoglycaemia in any of the included studies
Childhood/adulthood adiposity			Not estimable	(0 studies)		No data reported for childhood/adulthood adiposity in any of the included studies
Chilhood/adulthood type 2 diabetes mellitus			Not estimable	(0 studies)		No data reported for childhood/adulthood type 2 diabetes in any of the included studies
Childhood/adulthood neurosensory disability			Not estimable	(0 studies)		No data reported for childhood/adulthood neurosensory disability in any of the included studies
*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). CI: confidence interval; RCT: randomised controlled trial; RR: risk ratio
GRADE Working Group grades of evidence High quality: We are very confident that the true effect lies close to that of the estimate of the effect Moderate quality: We are moderately confident in the effect estimate: The true effect is likely to be close to the estimate of the effect, but there is a possibility that it is substantially different Low quality: Our confidence in the effect estimate is limited: The true effect may be substantially different from the estimate of the effect Very low quality: We have very little confidence in the effect estimate: The true effect is likely to be substantially different from the estimate of effect
¹Studies contributing data had serious or very serious design limitations ²Substantial heterogeneity (I² = 62%) ³Wide 95% CI crossing the line of no effect

Background

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Description of the condition

Gestational diabetes mellitus

Gestational diabetes mellitus (GDM) is defined as glucose intolerance or hyperglycaemia (high blood glucose concentration) that begins or is first detected during pregnancy (WHO 1999). In pregnancy, placental hormones (including oestrogen, progesterone, cortisol, placental lactogen, prolactin and growth hormone), create an insulin‐resistant state in order to direct sufficient nutrition to the fetus (Setji 2005). For women with GDM, increased insulin resistance accompanied by an insufficient compensatory insulin release limits glucose transport into cells, resulting in maternal hyperglycaemia (Setji 2005). This in turn can result in fetal hyperglycaemia, which stimulates insulin production, thus allowing increased glucose and amino acid entry into cells, increasing metabolism and, ultimately, over‐nourishing the fetus (Setji 2005).

A variety of risk factors for the development of GDM have been identified. These include non‐modifiable risk factors, such as ethnicity (e.g. African, Hispanic, South or East Asian, Native American and Pacific Islander), advanced maternal age, maternal high or low birthweight, high parity (Petry 2010), polycystic ovarian syndrome (Toulis 2009), a past history of a macrosomic (large) baby or a stillbirth (Petry 2010), a past history of GDM (Kim 2007), and family history of first‐degree relatives with GDM or type 2 diabetes (Petry 2010). Risk factors considered modifiable include maternal overweight or obesity (body mass index (BMI) equal to or greater than 25 kg/m² or 30 kg/m², respectively) (Morisset 2010; Torloni 2009), certain dietary factors (Morisset 2010; Zhang 2011; discussed further below), physical inactivity before or in early pregnancy (Tobias 2011), and weight gain during pregnancy (Morisset 2010), including for those women who are overweight or obese.

Selective (risk factor) or universal screening for GDM is usually performed between 24 and 28 weeks' gestation, with the use of a 50 g oral glucose challenge test (OGCT). Diagnosis is then made following a 75 g two‐hour or 100 g three‐hour oral glucose tolerance test (OGTT). Alternatively, a diagnostic OGTT may be used without prior OGCT. Diagnostic criteria for GDM have changed over time, and vary nationally and internationally (ACOG 2013; ADA 2013; IADPSG 2010; Nankervis 2014; New Zealand Ministry of Health 2014; NICE 2015; WHO 1999). Accordingly, GDM prevalence estimates vary depending on both the diagnostic criteria used, and the population(s) assessed; for example, a recent study identified GDM prevalence estimates to range from less than 1% to 28% (with data derived from expert estimates, single/multi‐site and national prevalence assessments across 30 countries) (Jiwani 2012). Despite variation in diagnostic criteria, there is widespread agreement that the prevalence of diabetes, including GDM, is increasing across the world, in line with the escalating prevalence of obesity. A recent estimate of the global prevalence of hyperglycaemia in pregnancy (including GDM and 'total diabetes' (known/unknown pre‐existing diabetes) was 17% (Guariguata 2014).

GDM is associated with adverse consequences for women and their babies, in the short and long term. Babies of women with GDM are more likely to be macrosomic (with a birthweight exceeding 4000 g or 4500 g), or be born large for their gestational age (Reece 2009; Reece 2010). These babies are thus at an increased risk of injury at the time of birth, including birth asphyxia, shoulder dystocia, bone fracture or nerve palsy (Reece 2009; Reece 2010). Additional risks for babies in the short term include respiratory distress syndrome, hypoglycaemia, hyperbilirubinaemia, hypocalcaemia, hypomagnesaemia, and polycythaemia (Reece 2009; Reece 2010); such health consequences together contribute to an increased risk of admission to the neonatal nursery, and perinatal mortality. There is increasing evidence to suggest that infants born to women with GDM are at risk of being obese in childhood or adulthood, and at increased risk of developing metabolic syndrome, and type 2 diabetes later in life (Reece 2009; Reece 2010). Women with GDM are at additional risk in the short term of developing pre‐eclampsia, having a caesarean section birth (including due to their babies being large‐for‐gestational age) and perineal trauma; in the longer term, women are at increased risk of developing GDM in a subsequent pregnancy, and of developing later cardiovascular disease, metabolic syndrome and type 2 diabetes (Reece 2009; Reece 2010).

Description of the intervention

Dietary advice in pregnancy for preventing gestational diabetes mellitus

Dietary interventions in pregnancy to prevent GDM may incorporate varied advice, based on addressing potential risk factors, with the aim of preventing maternal hyperglycaemia. Dietary interventions to treat pregnancy hyperglycaemia have a similar aim of optimising glycaemic control, and thus improving outcomes for women and their babies, and are widely used as a primary management strategy. Three Cochrane reviews have assessed such interventions (incorporating dietary advice), in pregnancy for the treatment of hyperglycaemia (Han 2012b) or GDM (Alwan 2009; Han 2013), and have showed some benefits. Han 2012b included four trials (involving 543 women and their babies) assessing dietary advice and blood glucose concentration monitoring for women with pregnancy hyperglycaemia not meeting GDM and type 2 diagnostic criteria. The review revealed a reduced risk of babies being born large‐for‐gestational age and macrosomic with such interventions; however Han 2012b highlighted that the results were based on small, low‐quality randomised trials and thus recognised a need for further research (Han 2012b). Alwan 2009 included eight randomised trials (involving 1418 women and their babies) assessing a range of interventions for treating GDM, with five incorporating dietary advice. This review revealed that these interventions, incorporating dietary advice (and insulin therapy, where indicated), reduced the risk of adverse consequences for women and their babies (including pre‐eclampsia, a composite outcome of perinatal death, shoulder dystocia, bone fracture and nerve palsy, macrosomia and large‐for‐gestational age), and concluded that further research should focus on the impact of different types of intensive treatment on short‐ and long‐term outcomes (Alwan 2009). Han 2013 was specifically conducted to assess the effects of different types of dietary advice for women with GDM, and identified nine randomised trials (involving 437 women and their babies). These trials compared dietary advice focused on: low‐ to moderate‐GI food versus high‐ to moderate‐GI food; low‐GI diet versus high‐fibre moderate‐GI diet; energy‐restricted diet versus no energy restriction diet; low‐carbohydrate diet versus high‐carbohydrate diet; high‐monounsaturated fat diet versus high‐carbohydrate diet; and standard‐fibre diet versus fibre‐enriched diet. The types of dietary advice that are most effective for women with GDM remains uncertain (Han 2013).

Two further Cochrane reviews have assessed the effects of dietary advice interventions (Nield 2008), and combined dietary advice and exercise advice interventions (Orozco 2008) for preventing type 2 diabetes in adults. Nield 2008 included two randomised trials involving 328 people. A 33% reduction (P < 0.03) in the incidence of diabetes with dietary advice in one trial at six‐year follow‐up and beneficial effects on markers of metabolic control (reductions in insulin resistance, fasting insulin and blood glucose) in the other included trial at one‐year follow‐up were shown. Nield 2008 recognised that "more well‐designed, long‐term studies, providing well‐reported, high‐quality data are required before proper conclusions can be made into the best dietary advice for the prevention of diabetes mellitus in adults" (Nield 2008). The Nield 2008 review has been withdrawn as it will be superseded by a new review, with broader scope, focused on ‘Diet, physical activity or both for the prevention or delay of type 2 diabetes mellitus and its associated complications in persons at increased risk' (Nield 2016). Orozco 2008 included eight trials (involving 5956 people) assessing exercise plus diet interventions for prevention of type 2 diabetes, and overall showed a reduction in the risk of diabetes with such interventions (risk ratio (RR) 0.63, 95% confidence interval (CI) 0.49 to 0.79). The authors of the review concluded benefit for the high‐risk groups assessed (people with impaired glucose tolerance or the metabolic syndrome), and highlighted a need for further research assessing impact on other outcomes including quality of life, morbidity and mortality, with a special focus on cardiovascular outcomes (Orozco 2008).

While the benefits of dietary advice intervention have been observed in randomised trials and systematic reviews for women with GDM (Alwan 2009), in relation to improved outcomes for women and their babies, and for adults at risk of type 2 diabetes (Nield 2008; Orozco 2008), in regards to prevention of diabetes development, to date, the effects of such interventions for pregnant women for the prevention of GDM are unclear.

How the intervention might work

Dietary advice in pregnancy for preventing gestational diabetes mellitus

A large and increasing number of observational studies have suggested various components of women's diets or dietary patterns before and during pregnancy which may influence GDM risk (Zhang 2011). Some of the most recent published evidence relates to the Nurses' Health Study II, a longitudinal cohort of 116,000 nurses between the ages of 25 and 42 in the USA followed since 1989. Studies from this cohort indicate that pre‐pregnancy, higher consumption of sugar‐sweetened cola (Chen 2009); frequent fried food consumption, particularly away from home (Bao 2014); higher levels of potato consumption (Bao 2016); higher intakes of animal fat and dietary cholesterol (Bowers 2012); a high‐glycaemic load and low‐cereal fibre diet (Zhang 2006b); higher intake of dietary heme iron (Bowers 2011); higher intake of animal protein, in particular red and processed meat (Zhang 2006); and a low‐carbohydrate dietary pattern with high protein and fat from animal‐food sources (Bao 2014b) are associated with a higher risk of GDM (Bao 2013). Conversely, pre‐pregnancy, a high‐fibre diet (Zhang 2006b); higher intake of vegetable protein (specifically nuts); the substitution of red meat with poultry, fish, nuts or legumes (Bao 2013); the substitution of potatoes with other vegetables, legumes or whole grain foods (Bao 2016); and adherence to "healthful" dietary patterns (alternate Mediterranean (aMED), Dietary Approaches to Stop Hypertension (DASH), and the alternate Healthy Eating Index (aHEI) dietary patterns) (Tobias 2012) are associated with a lower risk of GDM.

Additional observational studies have shown numerous, and often similar, findings; with high egg and cholesterol intakes before and during pregnancy (Qiu 2011b); high levels of dietary heme iron intake before and during early pregnancy (Qiu 2011); a 'Meats, snacks and sweets' dietary pattern before pregnancy (Schoenaker 2015); lower carbohydrate and higher total fat intakes as a percentage of energy in pregnancy (Ley 2011); and high consumption of refined grains, fat, added sugars and low intake of fruits and vegetables during pregnancy (Shin 2015) shown to be associated with a higher risk of GDM. A 'Mediterranean‐style' dietary pattern before pregnancy (Schoenaker 2015); a healthy "prudent" dietary pattern (with high intakes of seafood, eggs, vegetables, fruits and berries, vegetable oils, nuts and seeds, pasta, breakfast cereals; and low intakes of soft drinks and French fries) during pregnancy especially among women who were overweight or obese (Tryggvadottir 2016); and improved quality of dietary fat incorporating increased n‐3 polyunsaturated fatty acid intake during pregnancy (Barbieiri 2015) have been associated with a lower risk of GDM.

Thus, as a number of dietary components/patterns have been shown to influence GDM risk, specific dietary advice interventions aimed at preventing GDM may be varied, and as such, may influence maternal glycaemic control through multiple mechanisms.

Advice can focus on both the quantity and type of carbohydrates consumed, with carbohydrates being the main nutrient affecting post‐prandial glucose concentration (Reader 2007). Dietary GI can be used to characterise the capability of carbohydrate‐based foods to induce post‐prandial glycaemia (Jenkins 1981); foods with a low GI (such as whole‐grain foods and many fruits and vegetables) produce a lower post‐prandial glucose elevation, while foods with a high GI (highly processed foods such as white bread and some breakfast cereals) produce a rapid increase in post‐prandial blood glucose concentration (Jenkins 1981). Dietary fibre may influence glucose homeostasis through a number of mechanisms (Zhang 2006b). For example, a high‐fibre diet may reduce appetite and lower total energy intake, thus reducing adiposity and improving insulin sensitivity, or increased fibre may delay gastric emptying and slow digestion, subsequently reducing glucose absorption and insulin secretion (Zhang 2006b). Red and processed meat intake is postulated to influence glycaemic control through a variety of pathways (Zhang 2006), including through the adverse effects of components including saturated fat and cholesterol, and nitrites, used as a preservative agent, influencing insulin sensitivity and/or pancreatic beta‐cell function, or through the toxic effects of advanced glycation end products (AGEs), which can be formed in meat following heating and processing (Zhang 2006). Restricting calorie intake could also influence glycaemic status and insulin sensitivity, through promoting weight loss and reduced fat mass (Knopp 1991). Excessive calorie restriction can however lead to ketonuria and ketonaemia through ketosis by accelerated fat catabolism, which has been associated with adverse psychomotor development for the child (Rizzo 1995).

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. With potential for adverse consequences, and the increasing prevalence worldwide, there is an urgent need for effective strategies to prevent GDM.

This review will complement the existing reviews assessing interventions for preventing GDM, including: 'Diet and exercise interventions for preventing gestational diabetes mellitus' (Bain 2015); 'Exercise for pregnant women for preventing gestational diabetes mellitus' (Han 2012); 'Antenatal dietary supplementation with myo‐inositol in women during pregnancy for preventing gestational diabetes' (Crawford 2015); and 'Probiotics for preventing gestational diabetes' (Barrett 2014); and will assess dietary advice interventions for preventing GDM.

Objectives

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To assess the effects of dietary advice interventions for preventing gestational diabetes mellitus (GDM) and associated adverse health outcomes for women and their babies (as neonates, infants, children and adults).

Methods

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Criteria for considering studies for this review

Types of studies

We included all randomised and quasi‐randomised controlled trials assessing the effects of dietary advice interventions for preventing gestational diabetes mellitus (GDM). We planned to include cluster‐randomised trials, and we excluded cross‐over trials.

We did not include trials presented only as abstracts (unless sufficient information was available to assess risk of bias and obtain data on primary/secondary outcomes); we plan to reconsider such trials for inclusion once they are published in full‐text manuscript format.

Types of participants

We included studies involving pregnant women regardless of age, gestation, parity or plurality. We excluded studies involving women with pre‐existing type 1 or type 2 diabetes.

Types of interventions

We included interventions that assessed any type of dietary advice before testing for GDM. We included studies where such interventions were compared with no dietary advice intervention (i.e. standard care), and to different types of dietary advice.

We did not include interventions assessing combined dietary advice and exercise interventions, as these are assessed in the Bain 2015 Cochrane review.

Types of outcome measures

Primary outcomes

For this update, we used the core outcome set agreed by consensus between review authors of Cochrane Pregnancy and Childbirth systematic reviews for prevention and treatment of gestational diabetes mellitus (GDM) and pre‐existing diabetes.

Perinatal outcomes

GDM
Hypertensive disorders of pregnancy (e.g. pre‐eclampsia, pregnancy‐induced hypertension, eclampsia)

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)

Secondary outcomes

For the mother

Perinatal outcomes

Caesarean section birth
Operative vaginal birth
Induction of labour
Perineal trauma
Placental abruption
Postpartum haemorrhage
Postpartum infection
Breastfeeding (e.g. at discharge, six weeks postpartum)
Gestational weight gain
Adherence with the intervention
Behaviour changes associated with the dietary intervention
Relevant biomarker changes associated with the intervention
Sense of well‐being and quality of life
Views of the intervention

Longer‐term maternal outcomes

Postnatal depression
GDM in a subsequent pregnancy
Type 1 diabetes mellitus
Type 2 diabetes mellitus
Impaired glucose tolerance
Postnatal weight retention or return to pre‐pregnancy weight
Body mass index (BMI)
Cardiovascular health (e.g. blood pressure, hypertension, cardiovascular disease, metabolic syndrome)

For the child

Fetal/neonatal outcomes

Stillbirth
Neonatal mortality
Preterm birth (before 37 weeks' gestation; before 34 weeks' gestation)
Apgar score less than seven at five minutes
Macrosomia
Small‐for‐gestational age
Shoulder dystocia
Nerve palsy
Bone fracture
Respiratory distress syndrome
Hypoglycaemia
Hyperbilirubinemia
Gestational age at birth
Birthweight and z score
Head circumference and z score
Length and z score
Ponderal index
Adiposity (e.g. as measured by BMI or skinfold thickness)

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

Use of 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

Search methods for identification of studies

The following methods section of this review is based on a standard template used by the Cochrane Pregnancy and Childbirth Group.

Electronic searches

We searched Cochrane Pregnancy and Childbirth’s Trials Register by contacting their Information Specialist (3 January 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.

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 reference lists of retrieved articles. We did not apply any language or date restrictions.

Data collection and analysis

For methods used in the previous version of this review, seeTieu 2008.

For this update, the following methods were used for assessing the reports that were identified as a result of the updated search. Where required, information pertaining to the previously included studies was updated according to methods outlined in the Cochrane Handbook for Systematic Reviews of Interventions (Higgins 2011).

Selection of studies

Two review authors independently assessed for inclusion all the potential studies identified as a result of the search strategy. We resolved any disagreement through discussion or, if required, we consulted the third review author.

Data extraction and management

At least two review authors extracted the data using the agreed form. We resolved discrepancies through discussion or, if required, we consulted the third review author. Data were entered into Review Manager software (RevMan 2014) and checked for accuracy.

When information regarding any of the above was unclear, we contacted 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 study using the criteria outlined in the Cochrane Handbook for Systematic Reviews of Interventions (Higgins 2011). Any disagreement was resolved by discussion or by involving a third assessor.

(1) Random sequence generation (checking for possible selection bias)

We described for each included study the method used to generate the allocation sequence in sufficient detail to allow an assessment of whether it should produce comparable groups.

We assessed the method as:

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 study the method used to conceal allocation to interventions prior to assignment and assessed whether intervention allocation could have been foreseen in advance of, or during recruitment, or changed after assignment.

We assessed the methods as:

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 study the methods used, if any, to blind study participants and personnel from knowledge of which intervention a participant received. We considered that studies were at low risk of bias if they were blinded, or if we judged that the lack of blinding was unlikely to affect results. We assessed blinding separately for different outcomes or classes of outcomes.

We have 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 study the methods used, if any, to blind outcome assessors from knowledge of which intervention a participant received. We assessed blinding separately for different outcomes or classes of outcomes.

We have 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 study, and for each outcome or class of outcomes, the completeness of data including attrition and exclusions from the analysis. We stated whether attrition and exclusions were reported and the numbers included in the analysis at each stage (compared with the total randomised participants), reasons for attrition or exclusion where reported, and whether missing data were balanced across groups or were related to outcomes. Where sufficient information was reported, or could be supplied by the study authors, we planned to re‐include missing data in the analyses which we undertook.

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 study 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 study’s pre‐specified outcomes and all expected outcomes of interest to the review were reported);
high risk of bias (where not all the study’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; study 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 (6) above)

We described for each included study any important concerns we had about other possible sources of bias.

(7) Overall risk of bias

We made explicit judgements about whether studies were at high risk of bias, according to the criteria given in the Handbook (Higgins 2011). With reference to (1) to (6) above, we 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 two of our three comparisons using the GRADE approach as outlined in the GRADE handbook. The GRADE approach uses five considerations (study 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. In this review we planned to use the GRADE approach to assess the primary outcomes, as follows. We used the Cochrane Pregnancy and Childbirth GRADE core outcome set for reviews of prevention and treatment of gestational diabetes mellitus (GDM) and pre‐existing diabetes in pregnancy.

For the mother

Perinatal outcomes

GDM
Hypertensive disorders of pregnancy (e.g. pre‐eclampsia, pregnancy‐induced hypertension, eclampsia)
Caesarean section birth
Perineal trauma
Gestational weight gain

Longer‐term maternal outcomes

Postnatal depression
Type 2 diabetes mellitus

For the 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)
Neonatal hypoglycaemia

Childhood/adulthood outcomes

Childhood/adulthood adiposity (e.g. as measured by BMI, skinfold thickness)
Childhood/adulthood type 2 diabetes mellitus
Childhood/adulthood 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 two of the three comparisons in this review: dietary advice versus standard care, and low‐GI dietary advice versus moderate‐ to high‐GI dietary advice. We produced separate 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 presented results as summary risk ratio with 95% confidence intervals.

Continuous data

For continuous data, we used the mean difference. We planned to use the standardised mean difference to combine trials that measured the same outcome, but used different methods.

Unit of analysis issues

Cluster‐randomised trials

We did not identify any cluster‐randomised trials for inclusion in this review.

If cluster‐randomised trials are included in future reviews, we plan to include these trials in the analyses along with individually‐randomised trials. Their sample sizes will be adjusted using the methods described in the Handbook (Higgins 2011) using an estimate of the intra‐cluster correlation co‐efficient (ICC) derived from the trial (if possible), or from another source. If ICCs from other sources are used, we will report this and conduct sensitivity analyses to investigate the effect of variation in the ICC. If we identify both cluster‐randomised trials and individually‐randomised trials, we plan to synthesise the relevant information. We consider it reasonable to combine the results from both types of studies if there is little heterogeneity between the study designs and the interaction between the effect of intervention and the choice of randomisation unit is considered to be unlikely. We plan also to acknowledge heterogeneity in the randomisation unit and perform a sensitivity analysis to investigate the effects of the randomisation units.

Other unit of analysis issues

Cross‐over trials

We excluded trials with cross‐over designs.

Multiple pregnancies

We did not identify any eligible studies that included a notable proportion of multiple pregnancies. Laitinen 2009 reported one twin pregnancy in the dietary advice intervention group (any twin pairs were excluded from growth follow‐up in this study). If studies with multiple pregnancies are included in trials included in future updates of this review, we will adjust for clustering in the analyses wherever possible, and use the inverse variance method for adjusted analyses, as described in the Cochrane Handbook for Systematic Reviews of Interventions (Higgins 2011) and in Yelland 2011.

Multi‐armed trials

We included one multi‐armed trial (Laitinen 2009). We created a single pair‐wise comparison, by including only the two treatment groups relevant to this review.

Dealing with missing data

For included studies, we noted levels of attrition. In future updates, if more eligible studies are included, the impact of including studies with high levels of missing data in the overall assessment of treatment effect will be explored by using sensitivity analyses.

For all outcomes, analyses were carried out, 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. The denominator for each outcome in each trial was the number randomised minus any participants whose outcomes were known to be missing.

Assessment of heterogeneity

We assessed statistical heterogeneity in each meta‐analysis using the Tau², I² and Chi² statistics. We regarded heterogeneity as substantial if an I² was greater than 30% and either the Tau² was greater than zero, or there was a low P value (less than 0.10) in the Chi² test for heterogeneity. Where we identified substantial heterogeneity (above 30%), we aimed to explore it using pre‐specified subgroup analyses.

Assessment of reporting biases

Had there been 10 or more studies in a meta‐analysis, we planned to investigate reporting biases (such as publication bias) using funnel plots. We planned to assess funnel plot asymmetry visually. If asymmetry was suggested by a visual assessment, we planned to perform exploratory analyses to investigate it.

Data synthesis

We carried out statistical analysis using the Review Manager software (RevMan 2014). We used fixed‐effect meta‐analysis for combining data where it was reasonable to assume that studies were estimating the same underlying treatment effect: i.e. where studies were examining the same intervention, and the studies' 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 has been 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 did not combine trials. Where we 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.

We performed separate comparisons for different types of interventions. We planned to consider separately, where possible: studies comparing dietary advice interventions with no dietary advice (i.e. standard care); and those studies comparing two different types of dietary advice interventions.

Subgroup analysis and investigation of heterogeneity

Where we identified substantial heterogeneity, we planned to investigate it using subgroup and sensitivity analyses. We planned to consider whether an overall summary was meaningful, and if it was, we used random‐effects analysis to produce it.

Maternal characteristics, and characteristics of the dietary advice interventions are likely to affect health outcomes.

Therefore, we planned to carry out the following subgroup analyses for our primary outcomes.

Maternal characteristics

Age at or before trial entry (e.g. < 35 years versus ≥ 35 years of age).
BMI at or before trial entry (e.g. < 25 kg/m² versus ≥ 25 to < 30 kg/m² versus ≥ 30 kg/m²).
Ethnicity (high‐risk ethnicity versus low‐risk ethnicity).

Characteristics of the interventions

Frequency (e.g. frequent versus infrequent intervention).
Duration (e.g. short versus long duration of intervention).
Intensity (e.g. advice only versus more intensive support).

We planned to assess subgroup differences by interaction tests available within RevMan (RevMan 2014), and to report the results of subgroup analyses quoting the Chi² statistic and P value, and the interaction test I² value.

However, due to the paucity of data in this review, across three comparisons (only two with data for some of the primary outcomes), we were unable to conduct the majority of planned subgroup analyses in this version of the review, except for 'according to BMI at or before trial entry' for Comparison 1, where three of the six included trials included only overweight or obese women.

Sensitivity analysis

We carried out sensitivity analyses to explore the effects of trial quality assessed by sequence generation and allocation concealment, by omitting studies 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 (Tieu 2008), 15 reports, relating to nine studies were identified. We included three trials (eight reports) (Clapp 1998; Fraser 1983; Moses 2006), excluded one study (two reports) (Fraser 1988), one study (one report) was awaiting further classification, and four studies (four reports) were ongoing.

The updated search of Cochrane Pregnancy and Childbirth's Trials Register in January 2016 identified a further 108 reports, and we identified a further three reports by contacting trial authors, and accessing reports cited on trial registrations web sites.

In total, we included 11 trials (54 records) in this update (Clapp 1998; Fraser 1983; Laitinen 2009; Markovic 2016; Moses 2006; Moses 2014; Quinlivan 2011; Thornton 2009; Vitolo 2011; Walsh 2012; Wolff 2008), and excluded 31 studies (62 records) (Althuizen 2013; Asbee 2009; Asemi 2013; Brand‐Miller 2007; Dodd 2014; Facchinetti 2013; Fraser 1988; Hui 2006; King 2013; Korpi‐Hyovalti 2012; Krummel 2009; Laitinen 2015; Lesser 2015; Lindsay 2014; Liu 2013; Luoto 2011; Maitland 2014; Matarrelli 2013; Mike O'Callaghan Federal Hospital 2011; Min 2014; Hellenes 2015; Moses 2009; Phelan 2011; Phelan 2016; Poston 2015; Reyes‐Munoz 2014; Rhodes 2010; Taghizadeh 2014; Vesco 2014; Yap 2014; Zhou 2011).

Four studies (five records) are awaiting further classification (Angel 2011; Parat 2015; Simmons 2015; Zhang 2015), and five studies (five records) were identified as ongoing (NCT01056406; NCT01105455; NCT01628835; NCT01894139; NCT02218931).

The four studies awaiting classification have been published in abstract format only, with limited information regarding methods, intervention and outcomes provided to date; they assessed: a low glycaemic load diet versus a low fat diet in 64 overweight and obese pregnancy women in the USA (Angel 2011); individual and group dietary counselling sessions versus standard care in 268 overweight and obese pregnancy women in France (Parat 2015); face‐to‐face and telephone coaching sessions focused on healthy eating (versus coaching sessions focused on physical activity or both healthy eating and physical activity) in 146 women at risk of gestational diabetes mellitus (GDM) in Europe (Simmons 2015); and 'medical nutrition guidance' in 261 pregnant women (country not reported) (Zhang 2015).

The five ongoing studies are being undertaken in the USA (NCT01056406), Canada (NCT01105455), China (NCT01628835), Denmark (NCT01894139) and the UK (NCT02218931), with interventions being assessed including:

twice‐monthly interaction with a registered dietitian from six to 16 weeks' gestation until six months postpartum versus no intervention (NCT01056406);
group nutrition classes supplemented by handouts and provision of key study foods versus a leaflet with advice regarding a high‐fibre diet (NCT01105455);
four diet sessions at baseline, the end of the first trimester, the second trimester and the third trimester, including dietary assessments and consultations specifically recommending a low glycaemic index (GI) diet versus routine dietary advice (NCT01628835);
a dietary and advice intervention recommending a high protein, especially marine and dairy protein and low‐GI diet versus a diet according to the Nordic Nutritional Recommendations (NCT01894139);
targeted advice intervention based on Mediterranean dietary pattern, including structured meal plans and grocery lists, recipes for healthy diet and appropriate choices at restaurants versus usual antenatal dietary advice (NCT02218931).

For further details see Figure 1; Characteristics of included studies; Characteristics of excluded studies; Characteristics of ongoing studies; and Characteristics of studies awaiting classification for further details.

Figure 1

Study flow diagram.

Included studies

The 11 trials in this review involved a total of 2786 women and their babies, ranging from Clapp 1998 and Fraser 1983, with only 20 and 25 women respectively, to Moses 2014 and Walsh 2012 with 691 and 800 women respectively. These 11 trials were conducted across a variety of countries including four in Australia (Markovic 2016; Moses 2006; Moses 2014; Quinlivan 2011), two in the USA (Clapp 1998; Thornton 2009), and one each in Brazil (Vitolo 2011), Denmark (Wolff 2008), Finland (Laitinen 2009), Ireland (Walsh 2012), and the UK (Fraser 1983).

The included trials compared a variety of dietary interventions, and thus have been organised into three comparison: dietary advice interventions versus standard care; low‐GI dietary advice versus moderate‐ to high‐GI dietary advice; and high‐fibre dietary advice versus standard dietary advice. Six trials compared a dietary advice intervention with standard care (Laitinen 2009; Quinlivan 2011; Thornton 2009; Vitolo 2011; Walsh 2012; Wolff 2008); four trials compared low‐ and moderate‐ to high‐GI dietary advice (Clapp 1998; Markovic 2016; Moses 2006; Moses 2014); and one trial compared specific dietary advice (high‐fibre focused) and standard dietary advice (Fraser 1983).

1) Dietary advice interventions versus standard care

As mentioned above, six trials were included in this arm of the review (Laitinen 2009; Quinlivan 2011; Thornton 2009; Vitolo 2011; Walsh 2012; Wolff 2008).

Participants

Three of the six trials included women who were overweight or obese: Quinlivan 2011 included women with a singleton pregnancy, who were overweight (body mass index (BMI) 25 to 29.9) or obese (BMI > 29.9); Thornton 2009 included 257 women (BMI ≥ 30). Women with pre‐existing diabetes, hypertension, or chronic renal disease) with a singleton fetus between 12 and 28 weeks' gestation who were obese were excluded. Wolff 2008 included 73 women with a singleton pregnancy, early in their pregnancy (mean: 15 + 3 weeks' gestation), who were obese (BMI ≥ 30), and excluded women who smoked or had any medical complications known to affect fetal growth adversely or to indicate limitation of weight gain.

The other three trials had varying inclusion criteria: Laitinen 2009 included 256 women with singleton or twin pregnancies at less than 17 weeks' gestation with no metabolic or chronic diseases; Vitolo 2011 included 315 women between 10 and 29 weeks' gestation (excluding those who had previously been diagnosed with diabetes, who had hypertension, anaemia or other conditions requiring a special diet); and the ROLO trial (Walsh 2012) included 800 women, who were secunda gravida with singleton pregnancies less than 18 weeks' gestation, with first infants weighing more than 4000 g at birth, and excluded women with any underlying medical disorders or history of GDM.

Interventions

Although all six trials compared dietary advice with standard care, a range of specific dietary interventions were assessed. In general, women were counselled with regards to common healthy eating strategies, though resources used and protocols followed by each trial varied.

Women in the dietary advice intervention group of Wolff 2008 received a total of 10, one‐hour consultations with a dietitian. Advice was based on Danish dietary recommendations (fat intake: max 30 energy percent (E%), protein intake: 15 to 20 E%, carbohydrate intake: 50 to 55 E%), and individualised intake restrictions were based on each woman's energy requirements and the estimated energetic cost of fetal growth.

In Laitinen 2009, women in the dietary advice intervention group received counselling by a dietitian at each study visit, which occurred three times during pregnancy (mean of 13, 24 and 34 weeks' gestation) and at one, six and 12 months postpartum, which aimed to modify dietary intake to confirm with Nordic Nutrition Recommendations (with a particular focus on quality of dietary fat: saturated fatty acids providing 10% or less of energy intake, monounsaturated 10% to 15% and polyunsaturated fatty acids 5% to 10%). Women in the dietary advice intervention group were also provided with food products of favourable fat composition and fibre contents.

Women in the dietary advice intervention group of Walsh 2012 attended a two‐hour group dietary session (mean: 15.7 weeks' gestation) in groups of two to six with a research dietitian, where women received advice on general healthy eating guidelines for pregnancy; with women encouraged to choose as many low‐GI foods as possible, but not to reduce their total caloric intake. Women then received two further dietary intervention sessions with the research dietitian at 28 and 34 weeks' gestation who reinforced the low‐GI diet, and answered any questions.

Quinlivan 2011 used Australian guidelines from the National Health and Medical Research Council for healthy eating as the basis of the dietary advice intervention which utilised a ‘four‐step multidisciplinary approach.’ For women in the dietary advice intervention group, this approach, at a study‐specific antenatal clinic, included 1) continuity of care by a single maternity provider; 2) assessment of weight gain at each antenatal visit; 3) a brief intervention (five minutes) by a food technologist before each visit; 4) an assessment by a clinical psychologist with intervention if required.

In Thornton 2009, women in the dietary advice intervention group were 'nutritionally monitored'. They were prescribed a nutritionally balanced diet based on their weight at study entry and were asked to record all food and drink consumed each day in a food diary and these records were reviewed at each antenatal visit by the physician. Women in both groups were counselled at least once by a dietitian regarding conventional nutrition guidelines, however the intervention group received more detailed intake advice (recommendations: 18 to 24 kcal/kg (at least 2000 calories) consisting of 40% carbohydrates, 30% protein and 30% fat).

Women in the dietary advice intervention group in Vitolo 2011 received dietary counselling according to their baseline nutritional status (assessed to be low weight, eutrophic or overweight), at an initial session, with reinforcement once a month thereafter. Advice in this trial aimed to improve the quality of food consumed in addition to augmenting the speed of weight gain during pregnancy.

The control groups in the trials received standard care without additional dietary advice at the hospital/clinic they attended (Quinlivan 2011; Laitinen 2009; Vitolo 2011; Walsh 2012; Wolff 2008). In Laitinen 2009"All women attended communal dietary counselling provided by welfare clinics according to a national program, which consists of information of dietary guidelines through conversations and written material mediated by educated nurses;" and in Thornton 2009, all women in the standard care group were counselled at least once by a registered dietitian regarding conventional nutrition guidelines. Three of the trials (Laitinen 2009, Walsh 2012; Wolff 2008) asked women in both dietary advice intervention and standard care groups to provide information on their dietary intake through food diaries/records including at baseline, and in the second and/or third trimesters.

Both dietary advice intervention and standard care groups in Wolff 2008 were given supplements to ensure adequate vitamin and trace element intake, particularly iron and folic acid.

Laitinen 2009 also assessed the effects of probiotics, necessitating a third study group, not included in this review, who received dietary counselling in addition to a probiotic. Women in both the dietary advice and standard care groups of Laitinen 2009, included in this review, received placebo capsules (containing microcrystalline cellulose and dextrose anhydrate), from their first study visit until the end of exclusive breastfeeding.

GDM diagnosis

In Laitinen 2009, a 75 g oral glucose tolerance test (OGTT) was used, and the diagnosis of GDM was based on modified criteria of the Fourth International Workshop Conference on Gestational Diabetes Mellitus. Specifically, GDM was diagnosed when one plasma glucose concentration exceeded ≥ 4.8 mmol/L at baseline, ≥ 10.0 mmol/L at one hour or ≥ 8.7 mmol/L at two hours.

Quinlivan 2011 similarly used a 75 g OGTT, with the diagnosis of GDM based on World Health Organization Criteria; specifically, GDM was diagnosed when the two‐hour plasma glucose concentration was > 7.7 mmol/L.

In Walsh 2012, a 50 g oral glucose challenge test (OGCT) was used at 28 weeks' gestation, and women with a one‐hour blood glucose concentration ≥ 8.3 mmol/L underwent an OGTT; GDM was diagnosed if two or more abnormal results were observed during a three‐hour, 100 g OGTT diagnosed according to the Carpenter and Coustan criteria (fasting ≥ 5.3 mmol/L, one‐hour ≥ 10.0 mmol/L, two‐hour ≥ 8.6 mmol/L, three‐hour ≥ 7.8 mmol/L). Walsh 2012 reported GDM diagnosed according American Diabetes Association criteria (GDM diagnosed when any one of the following plasma glucose concentrations were exceeded: fasting ≥ 5.1 mmol/L, one‐hour ≥ 10.0 mmol/L, two‐hour ≥ 8.5 mmol/L).

Wolff 2008 reported that "Fasting blood glucose and blood glucose 2 h postprandial to an oral glucose tolerance test of a 50‐g glucose load were analyzed", however did not report specific criteria for GDM diagnosis.

Thornton 2009 did not report on the criteria used for GDM diagnosis, only detailing: "Antepartum and intrapartum complications such as development of gestational diabetes, ketonuria, preeclampsia, and shoulder dystocia were identified from the medical record after the patient delivered".

Similarly, Vitolo 2011 did not report on the criteria for GDM diagnosis, rather reporting only on a composite outcome 'clinical complications' (which included GDM, pre‐eclampsia, low birthweight, prematurity).

2) Low GI‐dietary advice versus moderate‐ to high‐GI dietary advice

Four trials, involving 928 women and their babies were included in this comparison of the review (Clapp 1998; Markovic 2016; Moses 2006; Moses 2014). All trials were conducted in hospital settings, three in Australia (Markovic 2016; Moses 2006; Moses 2014), and one in the USA (Clapp 1998).

Participants

Clapp 1998 included 20 healthy women preconception,"who eventually completed an uncomplicated pregnancy", who commenced a regular, supervised exercise and weight‐maintaining diet of predominantly carbohydrates until they were randomised at eight weeks' gestation. Moses 2006 included 70 healthy "white" pregnant women with a singleton pregnancy at 12 to 16 weeks' gestation (and specifically excluded women with any problems that may have been associated with glucose metabolism or insulin resistance or could interfere with their ability to follow dietary instructions). The PREGGIO trial (Moses 2014) included 691 women with a singleton pregnancy at less than 20 weeks' gestation and excluded women with known diabetes or previous GDM, special dietary needs or any medical conditions that may affect metabolic status or use of medication likely to affect body weight.

The GI Baby 3 trial (Markovic 2016), however, included 147 women, between 12 and 20 weeks' gestation, specifically at high risk of GDM (with at least one of the risk factors: aged older than 35 years; first degree relative with type 2 diabetes; pre‐pregnancy BMI 30 or over; past history of GDM or glucose intolerance; history of a previous baby with birthweight over 4000 g; high‐risk ethnic group), with an otherwise healthy singleton pregnancy.

Interventions

Women in Clapp 1998 were randomised at eight weeks' gestation, to either a high‐GI/cafeteria diet (with carbohydrates from highly processed grains, root vegetables, and simple sugars) or a low‐GI/Aboriginal diet (with carbohydrates from unprocessed whole grains, fruits, beans and vegetables, and dairy products).

Women in both groups of Clapp 1998 were recommended diets with a composition of 17% to 19% protein, 20% to 25% fat and 55% to 60% carbohydrate, with a total intake of 35 to 45 kcal/kg of lean body mass. Adherence was assessed by random, twice weekly 24‐hour dietary recalls by a dietitian.

In Markovic 2016, women in the low‐GI dietary advice group had a target GI of 50 or less, while those in the high‐fibre, moderate‐GI dietary advice group had a target GI of 60; though all women were recommended a similar macronutrient composition, of 15% to 25% protein, 25% to 39% fat, and 40% to 45% carbohydrate. All women attended a total of five individual dietary consultations with a dietitian (at 14 to 20, 18 to 24, 22 to 28, 26 to 32, and 34 to 36 weeks' gestation); with visit one using a three‐day food record as the basis of dietary counselling, and written information regarding low‐GI/high‐fibre foods and pregnancy nutrition provided; and visits two to four using four‐stage multiple‐pass 24‐hour recalls, and suitable alternative foods encouraged for non‐compliant women. All women in Markovic 2016 were also provided with food samples (supplementary baskets) containing key foods for their assigned diet at all five consultations.

Women in both groups of Moses 2006 were also seen by a dietitian five times during their pregnancy (who was also available for telephone queries outside of scheduled visits); at visit one, a three‐day food record and diet history was taken; at visit two (a week later), women received dietary education for either a low‐GI diet (verified low‐GI foods including pasta, brand‐name breads and breakfast cereals with high‐fibre content) or a moderate‐ to high‐GI diet (high fibre, low sugar foods including potatoes, wheat‐meal bread, and specific high‐fibre breakfast cereals with moderate‐ to high‐GI); at visits three (22 weeks' gestation) and four (30 weeks' gestation), 24‐hour diet recalls were taken, and at visit five (36 weeks) a further three day food record and diet history were taken. All women in Moses 2006 were advised to maintain a diet of 33% fat and 55% carbohydrate (with only the recommended choice of carbohydrate foods varying), were provided with a booklet that outlined the carbohydrate choices and the food amounts that constituted one serving, and were provided key foods in a monthly hamper.

In Moses 2014, all women received a set of booklets; for women in the low‐GI dietary advice group, counselling focused on choices for and serving sizes of carbohydrate‐rich foods, with specific information provided on low‐GI alternatives for relevant food groups; while for women in the healthy eating dietary advice group, counselling focused on a conventional healthy diet with recommended foods and serving sizes as noted in the Australian Guide to Healthy Eating and no specific guidance on GI was given. There was no intended difference between groups in the macronutrient distribution of the diet, and for all women in Moses 2014 there were four contact points; at the first, a three‐day food record was reviewed, and diet education was given specific to the assigned group by the dietitian; at the second, a phone call was made (four weeks after the first visit), to ensure adherence to the diet and goals set and identify any barriers or concerns; at the third, a dietitian reviewed the women face‐to‐face (at 28 weeks) before their obstetric appointment to monitor progress; at the fourth (as late as possible, and at a minimum of 34 weeks' gestation), the dietitian collected and reviewed the final three‐day food records. For all women in Moses 2014, the research dietitian was available for telephone queries outside of scheduled visits, and an email with nutrition tips and recipes was sent monthly (five in total) to all women with content dependent on group.

GDM diagnosis

Clapp 1998 focused on biochemical outcomes (including glucose and insulin responses), and reported data relating to GDM as a result of "glucose screens, which were conducted as part of their clinical care at approximately 28 weeks’ gestation" (OGCT). No further information regarding GDM diagnosis criteria was provided.

In Markovic 2016, GDM diagnosis was based on modified Australasian Diabetes in Pregnancy Society 1998 criteria: following a 75 g OGTT, at either study entry (between 14 and 20 weeks' gestation) or at 26 to 28 weeks' gestation, with GDM diagnosed where fasting blood glucose was ≥ 5.5 mmol/L, one‐hour ≥ 10.0 mmol/L, or two‐hour ≥ 8.0 mmol/L.

Moses 2006 reported that a routine OGTT was performed at 28 weeks' gestation. Specific diagnostic criteria used were not provided (no further information regarding GDM diagnosis criteria were provided).

In Moses 2014, all women were tested for GDM between 24 and 28 weeks' gestation; at the beginning of the study, the test was based on the Australasian Diabetes in Pregnancy Society criteria (with GDM diagnosed following a 75 g OGTT if: fasting plasma glucose ≥ 5.5 mmol/L, or two‐hour ≥ 8.0 mmol/L); and, later, was based on new International Association of Diabetes in Pregnancy Study Group criteria (with GDM diagnosed following a 75 g OGTT if any of: fasting plasma glucose ≥ 5.1 mmol/L, one‐hour ≥ 10.0 mmol/L, or two‐hour ≥ 8.5 mmol/L). Women diagnosed with GDM in Moses 2014 were "withdrawn from the study and treated conventionally"; we have however included data on these women in the relevant meta‐analysis for GDM.

3) High‐fibre dietary advice versus "standard" dietary advice

One trial was included in this comparison (Fraser 1983).

Participants

Fraser 1983 was a trial (conducted in a hospital in Sheffield, UK) of 25 primigravid European women in their second half of pregnancy, of 'normal' weight, and with no family history of diabetes; thus considered to be at low risk for GDM.

Interventions

Women in the intervention (high‐dietary fibre) group of Fraser 1983 saw a dietitian at 27 weeks' gestation, and were advised to reduce intake of sucrose and white flour, and to make as many high‐fibre substitutions as possible; aiming for a calorie intake of 2400. Women were also given diet and recipe sheets, and tokens for free wholemeal bread. Women in the control (standard dietary advice) group of Fraser 1983 were given "standard" advice at an interview with a dietitian at 27 weeks' gestation, with a suggested calorie intake of 2400 (no further details were provided regarding the "standard" dietary advice). Women in both groups were seen by the dietitian at each of their antenatal attendances.

GDM diagnosis

Fraser 1983 focused on biochemical outcomes (including glucose and insulin profiles), and thus reported only a limited number of review outcomes, including results of a 75 g OGTT at 35 weeks; however, GDM diagnosis was not reported.

Excluded studies

We excluded 31 studies from this review (Althuizen 2013; Asbee 2009; Asemi 2013; Brand‐Miller 2007; Dodd 2014; Facchinetti 2013; Fraser 1988; Hui 2006; King 2013; Korpi‐Hyovalti 2012; Krummel 2009; Laitinen 2015; Lesser 2015; Lindsay 2014; Liu 2013; Luoto 2011; Maitland 2014; Matarrelli 2013; Mike O'Callaghan Federal Hospital 2011; Min 2014; Hellenes 2015; Moses 2009; Phelan 2011; Phelan 2016; Poston 2015; Reyes‐Munoz 2014; Rhodes 2010; Taghizadeh 2014; Vesco 2014; Yap 2014; Zhou 2011).

Ten trials were excluded as they assessed a combined diet and exercise intervention for preventing GDM (Althuizen 2013; Asbee 2009; Dodd 2014; Hui 2006; Korpi‐Hyovalti 2012; Luoto 2011; Phelan 2011; Phelan 2016; Poston 2015; Vesco 2014), which is the focus of another Cochrane review (Bain 2015), and one trial assessed diet interventions in overweight and obese women and did not report on GDM (Rhodes 2010) (it is included in another Cochrane review (Muktabhant 2015)). Three trials were excluded for assessing a probiotic intervention (Asemi 2013; Laitinen 2015; Taghizadeh 2014), which is the focus of another Cochrane review (Barrett 2014); three for assessing myo‐inositol (Facchinetti 2013; Lindsay 2014; Matarrelli 2013), which is the focus of another Cochrane review (Brown 2015); and three for assessing docosahexaenoic acid (DHA) (Min 2014; Krummel 2009; Zhou 2011), which is the focus of another Cochrane review (Makrides 2006). One trial each was excluded for assessing an exercise intervention (Hellenes 2015), which is the focus of another Cochrane review (Han 2012), magnesium supplementation (Liu 2013), which is the focus of another Cochrane review (Makrides 2014); metformin (Reyes‐Munoz 2014); and vitamin D (Yap 2014).

One trial was excluded as the participants were women with GDM (Moses 2009). Four studies were excluded as they were cross‐over trials (Fraser 1988; King 2013; Lesser 2015; Maitland 2014), and two were excluded as they were not conducted (one did not proceed due to lack of funding [personal correspondence] (Brand‐Miller 2007); and one, designed to assess folic acid for prevention of GDM, appeared to have been withdrawn prior to enrolment (Mike O'Callaghan Federal Hospital 2011)).

For further details see Characteristics of excluded studies.

Risk of bias in included studies

Overall, the risk of bias was judged to be unclear to moderate ‐ see Characteristics of included studies and Figure 2 and Figure 3 for further details.

Figure 2

'Risk of bias' graph: review authors' judgements about each risk of bias item presented as percentages across all included studies.

Figure 3

'Risk of bias' summary: review authors' judgements about each risk of bias item for each included study.

Allocation

Four trials were judged to be at a low risk of selection bias, with adequate methods for both random sequence generation and allocation concealment (Laitinen 2009; Quinlivan 2011; Thornton 2009; Walsh 2012). In three of these trials a computer‐generated random number sequence was used (Laitinen 2009; Quinlivan 2011; Walsh 2012), and in the fourth one a random number table was used (Thornton 2009); and in each of the four trials, consecutively numbered, sealed, (opaque) envelopes were used. In three trials (Markovic 2016; Moses 2014; Wolff 2008), though adequate methods were reported for sequence generation (computer‐generated random number sequences were used), methods for concealing allocation were not clearly specified.

For three trials (Clapp 1998; Fraser 1983; Vitolo 2011) the risk of selection bias was unclear; in Clapp 1998 no details regarding sequence generation or allocation concealment were provided, and in Fraser 1983 it was detailed only that sealed envelopes were opened after women had agreed to participate, however no detail of whether the envelopes were consecutively numbered or opaque was provided. In Vitolo 2011 (from the translation available) women "were randomized by means of a dark pouch with two equal sized cubes containing the term intervention in one and control in the other".

The final trial, Moses 2006, was judged to be at a high risk of selection bias, as the trial was quasi‐randomised (with allocation by alternation).

Blinding

All 11 trials (Clapp 1998; Fraser 1983; Laitinen 2009; Markovic 2016; Moses 2006; Moses 2014; Quinlivan 2011; Thornton 2009; Vitolo 2011; Walsh 2012; Wolff 2008) were judged to be at a high risk of performance bias. While for a number of trials details on blinding were not explicit, due to the nature of the interventions it was presumed that is was unfeasible to blind participants and/or study personnel.

Two trials were judged to be low risk of detection bias (Markovic 2016; Quinlivan 2011). Markovic 2016 reported that "Apart from the study dietitian… who provided dietary education, all study personnel were blinded to dietary assignment;" and "A biostatistician blinded to the dietary allocation performed the statistical analysis". In Quinlivan 2011 it was reported that outcome data for the mother and infant were 'audited' by a nurse, independent of clinical care, and blind to group allocation.

Nine of the 11 trials (Clapp 1998; Fraser 1983; Laitinen 2009; Moses 2006; Moses 2014; Thornton 2009; Vitolo 2011; Walsh 2012; Wolff 2008) were judged to be at an unclear risk of detection bias; while blinding of women and personnel was not possible due to the nature of the interventions, it was unclear in six studies as to whether it had been possible to blind outcome assessment (Clapp 1998; Fraser 1983; Moses 2006; Moses 2014; Thornton 2009; Vitolo 2011). In Laitinen 2009, all personnel who handled or analysed blood samples were blind to the intervention, however no detail of whether other outcomes were assessed blinded was provided. Wolff 2008, reported that while women and dietitians were not blinded, women were asked not to reveal their group assignment to physicians and midwives, however it is unclear as to whether blinding of outcomes assessors would have been successfully achieved; and in Walsh 2012 it was reported only that "blinded sonographers made ultrasound measurements," with no detail of blinding for other outcomes.

Incomplete outcome data

Five trials were judged to be at low risk of attrition bias (Clapp 1998; Laitinen 2009; Markovic 2016; Quinlivan 2011; Walsh 2012). In Clapp 1998, there were no losses to follow‐up and all women were analysed according to the group they were randomised, while in Quinlivan 2011, only four of 132 women withdrew from the study, and no other losses, attritions or exclusions were detailed. In Markovic 2016, only eight of the 147 women were excluded from the analyses (four in each group, for similar reasons), and in Walsh 2012, 41 of 800 women were excluded from the final analyses (with numbers and reasons for loss to follow‐up/exclusions similar between groups). In Laitinen 2009, of the 256 mothers participating in the trial, 208 completed the one‐year follow‐up with reasons for discontinuation similar across the three groups.

Five trials were judged to be at unclear risk of attrition bias (Fraser 1983; Moses 2006; Moses 2014; Thornton 2009; Vitolo 2011), with no data provided regarding losses, or with unbalanced numbers/reasons for losses across groups. For example, Fraser 1983 did not report clearly on whether there were any missing data/losses; Thornton 2009 reported that 25 of 257 women were lost to follow‐up, and there was some indication of higher loss in the control group (8/124 in the intervention group and 17/133 in the control group); and in Moses 2006, while data were provided for the 62/70 women who completed the study 19/62 women (30%) did not wish to participate in follow‐up (those women had a similar BMI and age, but a higher parity than the 43 women who agreed to participate).

One trial, Wolff 2008, was judged to be at a high risk of attrition bias; of the 73 women"recruited to the study", 50 (68%) were followed to birth, however additional data were missing for outcomes including weight measurement, without comment.

Selective reporting

Only two of the 11 trials were judged to be at low risk of reporting bias (Markovic 2016; Walsh 2012), with no obvious risk of selective reporting.

For eight of the trials (Clapp 1998; Laitinen 2009; Moses 2006; Moses 2014; Quinlivan 2011; Thornton 2009; Vitolo 2011; Wolff 2008), the risk of reporting bias was judged to be unclear, largely due to insufficient information (such as access to trial registrations and/or trial protocols) available to confidently assess risk of selective reporting. In Clapp 1998, many results (such as for GDM and large‐for‐gestational age were reported only narratively in text). It is not clear which outcomes were pre‐specified In Laitinen 2009, a number of outcomes not pre‐specified in the manuscript methods were reported, such as breastfeeding and Apgar score at five minutes, and it is difficult to interpret and use infant data for outcomes such as birthweight, gestation, birth height, head circumference and Apgar at five minutes, as these data have been reported with 'ranges' of infants. In Moses 2006, some results were reported incompletely, quote:"The analysis of the diet histories produced similar findings (data not shown)".Moses 2014 included discrepancies between trial registration and published manuscript, with development of GDM listed as a primary outcome in the trial registration, but not reported as such in the manuscript. In Quinlivan 2011, data for all pre‐specified outcomes (in the trial manuscript methods) were provided, however only three outcomes were pre‐specified, and additional outcomes including changes in diet and serious adverse events were reported but not pre‐specified in the methods. Thornton 2009 reported results for the majority of pre‐specified outcomes, though there was no access to a trial protocol to assess selective reporting. In Vitolo 2011, the manuscript methods specify that data were obtained for outcomes such as newborn weight, length, gestational age, cephalic perimeter, Apgar scores at one and five minutes, mode of birth, gestational complications, diabetes and gestational hypertension; from the translation, data for these outcomes were not clearly reported. Wolff 2008 reported results for the majority of pre‐specified outcomes in the trial manuscript methods, though no trial protocol or registration was available to assess selective reporting. Data were not provided for Apgar scores or ‘methods of delivery’ (data for caesarean birth were only reported).

One trial, Fraser 1983, was judged to be at high risk of reporting bias, with a general statement in text made for a number of outcomes and no data provided for these important outcomes; quote: "results of the antenatal monitoring (including maternal weight gain and serum ferritin) and fetal anthropometry showed no significant differences between the groups".

Other potential sources of bias

Six trials were judged to be at a low risk of other bias, with no other obvious sources of bias identified (Laitinen 2009; Moses 2014; Quinlivan 2011; Thornton 2009; Walsh 2012; Wolff 2008).

The other five trials were judged to be at unclear risk of other sources of bias (Clapp 1998; Fraser 1983; Markovic 2016; Moses 2006; Vitolo 2011). Clapp 1998 and Fraser 1983 provided limited methodological details to confidently assess other sources of bias, and Vitolo 2011 was assessed using a partial translation of the manuscript, making assessment of other sources of bias difficult; Markovic 2016 reported that while the majority of baseline characteristics were balanced across groups, family history of type 2 diabetes was more common in the low‐GI group; in Moses 2006, it was reported that "Women who were assigned to the HGI diet group had a slightly higher BMI (P = 0.04) and higher HOMA2‐ cell function (P = 0.07) than did women in the LGI diet group".

Effects of interventions

Comparison 1: Dietary advice interventions versus standard care

Six trials were included in this comparison (Laitinen 2009; Quinlivan 2011; Thornton 2009; Vitolo 2011; Walsh 2012; Wolff 2008).

Primary outcomes

Gestational diabetes (GDM)

Overall, a trend towards a reduction in GDM was observed for women receiving dietary advice interventions compared with those receiving standard care (average risk ratio (RR) 0.60, 95% confidence interval (CI) 0.35 to 1.04; five trials, 1279 women; P = 0.07; GRADE: very low‐quality evidence) (Analysis 1.1). As there was substantial heterogeneity identified for this outcome (Tau² = 0.20; I² = 56%), a random‐effects meta‐analysis was used.

Walsh 2012 reported on GDM according to two criteria (the Carpenter and Coustan criteria, and American Diabetes Association criteria). We have included the diagnoses according to the American Diabetes Association in this meta‐analysis. Replacing these data with those relating to diagnoses according to the Carpenter and Coustan criteria (7/350 in the dietary advice intervention group and 9/371 in the standard care group) did not impact on the overall result.

Hypertensive disorders of pregnancy

A reduction in pregnancy‐induced hypertension was observed for women receiving dietary advice interventions compared with those receiving standard care (RR 0.30, 95% CI 0.10 to 0.88; two trials, 282 women; GRADE: low‐quality evidence) (Analysis 1.2). No clear difference between groups was however observed for the risk of pre‐eclampsia (RR 0.61, 95% CI 0.25 to 1.46; two trials, 282 women; GRADE: low‐quality evidence) (Analysis 1.3).

Perinatal mortality (stillbirth or neonatal mortality)

Only one trial (Laitinen 2009) reported on perinatal mortality, and there were no perinatal deaths in either the dietary advice interventions or standard care groups (GRADE: very low‐quality evidence) (Analysis 1.4).

Large‐for‐gestational age

None of the six trials in this comparison reported on the primary outcome: large‐for‐gestational age.

Neonatal mortality or morbidity composite

None of the six trials in this comparison reported on the primary outcome: mortality or morbidity composite.

Secondary outcomes

For the mother

Perinatal outcomes

No clear differences between the dietary advice interventions and standard care groups were seen for the following secondary outcomes: caesarean section (average RR 0.98, 95% CI 0.78 to 1.24; four trials, 1194; Tau² = 0.02; I² = 36%; GRADE: low‐quality evidence) (Analysis 1.5); induction of labour (average RR 1.10, 95% CI 0.48 to 2.51; two trials, 991 women; Tau² = 0.31; I² = 87%) (Analysis 1.6); perineal trauma (RR 0.83, 95% CI 0.23 to 3.08; one trial, 759 women; GRADE: very low‐quality evidence) (Analysis 1.7); postpartum haemorrhage (RR 0.71, 95% CI 0.28 to 1.86; two trials, 991 women) (Analysis 1.8); postpartum infection (RR 0.83, 95% CI 0.26 to 2.65; one trial, 232 women) (Analysis 1.9); breastfeeding at three months (RR 1.02, 95% CI 0.89 to 1.17; one trial, 452 women) (Analysis 1.10); or six months (RR 0.99, 95% CI 0.82 to 1.19; one trial, 146 women) (Analysis 1.11). Considerable statistical heterogeneity was observed in the meta‐analysis for induction of labour, and thus the pooled result should be interpreted with some caution.

A reduction in gestational weight gain, was observed for women who received the dietary advice interventions (mean difference (MD) ‐4.70 kg, 95% CI ‐8.07 to ‐1.34; five trials, 1336 women; Tau² = 13.64; I² = 96%; GRADE: low‐quality evidence) (Analysis 1.12). Considerable statistical heterogeneity was observed in the meta‐analysis for gestational weight gain, and thus the pooled result should be interpreted with some caution. Vitolo 2011 also reported on weekly gestational weight gain, however separately for women who were of 'low weight', were 'eutrophic' or were of 'excess weight.' Women of 'excess weight' in the dietary advice group had less weekly gestational weight gain, compared with women in the standard care group (P = 0.01); no clear differences between groups were seen for the 'low weight' or 'eutrophic' women (Analysis 1.13). As the numbers in each group were not clearly reported, these data have not been included in the meta‐analysis.

Few behaviour changes were observed at three months postpartum for women in the dietary advice intervention group of one trial (Walsh 2012); more women were likely to be consuming a low‐GI diet (RR 5.37, 95% CI 1.93 to 14.89; 197 women), and were reading food labels (RR 1.11, 95% CI 1.01 to 1.23; 453 women), specifically the nutrients (RR 1.21, 95% CI 1.03 to 1.41; 453 women) (Analysis 1.14). At three months postpartum, there were no clear differences between groups, however, for having a weight reducing diet (RR 0.95, 95% CI 0.66 to 1.38; 458 women), taking supplements (RR 1.12, 95% CI 0.98 to 1.28; 459 women), having made dietary changes since the study (RR 1.12, 95% CI 0.98 to 1.29; 420 women), and reading ingredients (RR 1.12, 95% CI 0.91 to 1.37; 453 women), calories (RR 1.08, 95% CI 0.89 to 1.31; 453 women), food weight (RR 1.51, 95% CI 0.90 to 2.54; 453 women), additives (RR 1.33, 95% CI 0.99 to 1.79; 453 women), or serving size (RR 1.39, 95% CI 0.83 to 2.34; 453 women), or in attending the gym (RR 0.98, 95% CI 0.65 to 1.49; 440 women) (Analysis 1.14).

A second trial (Quinlivan 2011) also reported on changes in diet associated with the intervention for the dietary advice intervention group only: "the intervention was associated with changes in diet, as recorded by the food technologist at every visit where women were asked to itemise their food consumption of the previous day... The intervention resulted in increased consumption of water, fresh fruit and vegetables and home‐cooked meals. It was associated with a reduction in consumption of carbonated ‘fizzy’ drinks and juices and fast foods (frozen and fresh)".

While in one trial, no clear difference in fasting blood glucose concentrations (MD ‐0.06 mmol/L, 95% CI ‐0.13 to 0.01; 759 women) (Analysis 1.15) including fasting hyperglycaemia (≥ 5.1 mmol/L) (RR 0.64, 95% CI 0.40 to 1.04; 673 women) (Analysis 1.16), and blood glucose concentrations following OGCT at 28 weeks' gestation were observed (MD ‐0.20 mmol/L, 95% CI ‐0.42 to 0.02; 759 women) (Analysis 1.17), there were fewer women with a OGCT > 7.8 mmol/L (RR 0.72, 95% CI 0.53 to 0.99; 721 women) (Analysis 1.18), and fewer with a fasting glucose concentration ≥ 5.1 mmol/L or OGCT > 7.8 mmol/L at 28 weeks' gestation (RR 0.74, 95% CI 0.56 to 0.97; 672 women) (Analysis 1.19) in the same trial.

Wolff 2008 also reported that "The fasting glucose concentration in the control group had a small decrease with advancing gestational age, ‐0.04mmol‐1 (‐0.2 to 0.2) at 27 weeks of gestation, and ‐0.1mmol‐1 (‐0.3 to 0.1) at week 36. The intervention showed no reduction of the fasting glucose at 27 weeks, but at 36 weeks the fasting glucose was significantly reduced by 8%, group difference ‐0.3 ng ml‐1 (‐0.6 to ‐0.0, P=0.03). No differences were obtained between intervention and control group in the 2‐h glucose concentration after oral glucose tolerance test at 27 and 36 weeks of gestation, 0.1 ng ml‐1 (‐0.6 to 0.8, P=0.852) and 0.3 ng ml‐1 (‐0.4 to 1.0, P=0.406)".

In one trial, well‐being was assessed using the World Health Organization well‐being index (expressed as a percentage score), a five‐item scale used to rate quality of life and psychological well‐being, giving an overall score of nought to 25 which is converted to a percentage well‐being score (Walsh 2012). Women in the dietary advice intervention group had a lower sense of well‐being score, assessed by questionnaire between 14 and 28 weeks' gestation (MD ‐3.60, 95% CI ‐5.98 to ‐1.22; 618 women) (Analysis 1.20).

In regards to adherence with the intervention:

Laitinen 2009 reported for the dietary advice intervention group "According to the interviews, the proportion of women who consumed the food products provided for each 12‐week period between study visits ranged from 68% to 100% depending on the product...However, as assessed by 3‐day food records filled in immediately before the study visits, fewer women (39–81%) had, except for spreads, consumed the provided food products".

Thornton 2009 reported that 77.6% (90/116) of women in the dietary advice intervention group were adherent with the prescribed nutritional regimen.

Walsh 2012 reported that "Almost 80% (n=294) of the intervention arm reported following the low glycaemic index dietary advice either all or most of the time on the adherence questionnaire".

Walsh 2012 reported on women's views, for women in the dietary advice intervention group: "Results from the compliance and acceptability questionnaires showed that 68% of women either agreed or strongly agreed that the diet was easy to follow. Sixty five percent of women agreed that they enjoyed making the changes to their diets, 72% of women reported that their family were happy with the changes they made to their diets, and 78% of women agreed/strongly agreed that they had enough energy while on the diet. Finally, over 80% of women reportedly enjoyed a wide variety of foods while following the diet".

The trials in this comparison did not report on the outcomes: operative vaginal birth; placental abruption.

Longer‐term maternal outcomes

While in three trials, no clear differences were seen for postpartum weight loss at six weeks (MD ‐0.90 kg, 95% CI ‐3.67 to 1.87; one trial, 232 women) (Analysis 1.21), change in weight from late pregnancy to three months postpartum (MD ‐0.35 kg, 95% CI ‐1.84 to 1.14; one trial, 165 women) (Analysis 1.22), and postpartum BMI (reported as mean and range in Laitinen 2009: Analysis 1.24), in one of the trials, women in the dietary intervention group had a greater reduction in weight from baseline to three months postpartum (MD ‐1.43 kg, 95% CI ‐2.66 to ‐0.20; 414 women) (Analysis 1.23). Of interest, in Thornton 2009 the reported standard deviation for the standard care group for postpartum weight loss at six weeks (Analysis 1.21) was notably higher (14.84 kg versus 3.27 kg), indicating weight loss was more variable in the standard care compared with the dietary intervention group. Wolff 2008 also reported that "The intervention group (n=16) retained 6.9 kg less weight than the control group (n=19) 4 weeks postpartum (‐4.5 vs 2.4 kg, 95% CI of difference: 2.5–11.2, P=0.003) compared to the pregnancy weight".

The trials in this comparison did not report on the outcomes: postnatal depression; GDM in a subsequent pregnancy; type 1 diabetes mellitus; type 2 diabetes mellitus; impaired glucose tolerance; cardiovascular health (e.g. blood pressure, hypertension, cardiovascular disease, metabolic syndrome).

For the child

Fetal/neonatal outcomes

Only two trials reported on stillbirth; in one trial there were no stillborn babies, and in the other, there was one stillbirth in the dietary intervention group (associated with trisomy 21) (RR 3.09, 95% CI 0.13 to 75.65; two trials, 959 babies) (Analysis 1.25). Only one of these trials reported on neonatal deaths, and none occurred in either group (Analysis 1.26).

There were no clear differences between the dietary advice intervention and standard care groups for the following outcomes: preterm birth (less than 37 weeks) (RR 0.51, 95% CI 0.21 to 1.25; three trials, 1149 babies) (Analysis 1.27); preterm birth (less than 32 weeks) (RR 1.70, 95% CI 0.23 to 12.88; two trials, 917 babies) (Analysis 1.28); Apgar score less than seven at five minutes (RR 3.00, 95% CI 0.12 to 72.89; one trial, 232 babies) (Analysis 1.29); macrosomia (< 4000 g) (RR 0.99, 95% CI 0.86 to 1.14; one trial, 759 babies) (Analysis 1.30) and macrosomia (< 4500 g) (RR 2.25, 95% CI 0.71 to 7.10; one trial, 232 babies) (Analysis 1.31); shoulder dystocia (RR 0.52, 95% CI 0.10 to 2.82; one trial, 759 babies) (Analysis 1.32); gestational age at birth (MD 0.05 weeks, 95% CI ‐0.31 to 0.40; four trials, 1195 babies; Tau² = 0.05; I² = 34%) (Analysis 1.33); birthweight (MD 5.94 g, 95% CI ‐51.11 to 62.99; five trials, 1324 babies) (Analysis 1.34); head circumference at birth (MD ‐0.21 cm, 95% CI ‐0.67 to 0.25; three trials, 968 babies; Tau² = 0.11; I² = 72%) (Analysis 1.35); length at birth (MD 0.16 cm, 95% CI ‐0.28 to 0.60; three trials, 968 babies; Tau² = 0.05; I² = 33%) (Analysis 1.36); ponderal index at birth (MD 0.01, 95% CI ‐0.38 to 0.40; one trial, 759 babies) (Analysis 1.37); or adiposity (skin‐fold thickness at birth) (MD ‐1.60 mm, 95% CI ‐4.77 to 1.57; one trial, 219 babies) (Analysis 1.38). In Walsh 2012 the reported standard deviation for the dietary intervention group for ponderal index at birth (Analysis 1.37) was considerably higher (3.8 versus 0.33), suggesting ponderal indices were more variable in the dietary intervention compared with the standard care group. Substantial statistical heterogeneity was observed in the meta‐analysis for head circumference at birth, and thus the pooled result should be interpreted with some caution.

The trials in this comparison did not report on the outcomes: small‐for‐gestational age; nerve palsy; bone fracture; respiratory distress syndrome; hypoglycaemia; hyperbilirubinaemia.

Childhood/adulthood outcomes

There was no difference between the dietary advice intervention and standard care groups in Walsh 2012 for weight at three months (MD 0.23 kg, 95% CI ‐0.37 to 0.83; one trial, 422 children) (Analysis 1.39). In Walsh 2012, the reported standard deviation for the dietary intervention group for weight at three months (Analysis 1.39) was notably higher (4.36 kg versus 0.98 kg), indicating ponderal indices were more variable in the dietary intervention compared with the standard care group.

Similarly, there were no clear differences between the dietary advice intervention and standard care groups in Laitinen 2009 for the following outcomes: weight at six months (MD ‐0.03 kg, 95% CI ‐0.35 to 0.29; one trial, 143 children) (Analysis 1.40); length at six months (MD 0.00 cm, 95% CI ‐1.06 to 1.06; one trial, 143 children) (Analysis 1.41); head circumference at six months (MD ‐0.20 cm, 95% CI ‐0.61 to 0.21; one trial, 132 children) (Analysis 1.42); adiposity (skin‐fold thickness at six months) (MD ‐0.10 mm, 95% CI ‐0.71 to 0.51; one trial, 132 children; GRADE: low‐quality evidence) (Analysis 1.43); systolic (MD ‐1.00 mmHg, 95% CI ‐4.53 to 2.53; one trial, 113 children) (Analysis 1.44), diastolic (MD ‐1.00 mmHg, 95% CI ‐3.77 to 1.77; one trial, 113 children) (Analysis 1.45), or mean blood pressure (MD ‐1.00 mmHg, 95% CI ‐3.77 to 1.77; one trial, 113 children) at six months (Analysis 1.46); or heart rate at six months (MD 2.00 bpm, 95% CI ‐2.89 to 6.89; one trial, 113 children) (Analysis 1.47).

Laitinen 2009 also reported no clear differences in growth at follow up between groups: "Weight gain and growth in length during the periods 0–6 months, 6–12 months and 12–24 months showed no statistically significant differences between the diet/probiotics, diet/placebo and control groups. The respective mean weight gains (g/month) over 0–6 months were 759 (SD 160), 762 (SD 165) and 756 (SD 148); over 6–12 months were 323 (SD 80), 296 (SD 99) and 315 (SD 91); over 12–24 months were 211 (SD 76), 230 (SD 61) and 218 (SD 52) (P=0·983 for group effect; P<0·001 for time effect; P=0·520 for group X time interaction; ANOVA for repeated measurements). The mean growths in length (cm/month) in the respective periods were 2·84 (SD 0·35), 2·89 (SD 0·29) and 2·93 (SD 0·35); 1·40 (SD 0·19), 1·38 (SD 0·21) and 1·36 (SD 0·24); 0·95 (SD 0·14), 0·94 (SD 0·15) and 0·93 (SD 0·12) in the diet/probiotics, diet/placebo and control groups, respectively (P=0·872 for group effect; P<0·001 for time effect; P=0·325 for group X time interaction; ANOVA for repeated measurements)". We have not included these data in the meta‐analyses as the N values for the two relevant groups (diet/placebo and control groups) were not clearly reported.

The trials in this comparison did not report on the outcomes: employment, education and social status/achievement; type 1 diabetes mellitus; type 2 diabetes mellitus; impaired glucose tolerance; neurosensory disability.

Use of health services

The trials in this comparison did not report on any of the secondary outcomes relating to the use of health services.

Non pre‐specified review outcomes

Vitolo 2011 reported on a composite outcome 'clinical complications' (GDM, pre‐eclampsia, low birthweight, prematurity), and showed a reduction in this outcome for women who received the dietary advice intervention (RR 0.37, 95% CI 0.21 to 0.66; 305 women/babies) (Analysis 1.48).

Comparison 2: Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice

Four trials were included in this arm of the review (Clapp 1998; Markovic 2016; Moses 2006; Moses 2014).

Primary outcomes

Gestational diabetes (GDM)

No clear difference was shown in the risk of GDM between women in the low‐GI dietary advice group and moderate‐ to high‐GI dietary advice group (RR 0.91, 95% CI 0.63 to 1.31; four trials, 912 women; GRADE: low‐quality evidence) (Analysis 2.1).

Hypertensive disorders of pregnancy

None of the four trials in this comparison reported on the primary outcome: hypertensive disorders of pregnancy.

Perinatal mortality (stillbirth or neonatal mortality)

None of the four trials in this comparison reported on the primary outcome: perinatal mortality.

Large‐for‐gestational age

There was no clear difference in the risk of babies being born large‐for‐gestational age between the low‐GI dietary advice and moderate‐ to high‐GI dietary advice groups (average RR 0.60, 95% CI 0.19 to 1.86; three trials, 777 babies; Tau² = 0.61; P = 0.07; I² = 62%; GRADE: very low‐quality evidence) (Analysis 2.2).

Clapp 1998 reported that "The women who ate the low‐glycemic diets were delivered of normal sized infants whose measurements fell between the 25th and 75th centiles. Those born of women eating the high‐glycemic diet were symmetrically overgrown with average birth weights, crown‐heel lengths, ponderal indices and lean body masses >90th centile without an excessive increase in either fat mass or the feto‐placental weight ratio"; however these data were not able to be included in the above meta‐analysis.

Neonatal mortality or morbidity composite

None of the four trials in this comparison reported on the primary outcome: mortality or morbidity composite.

Secondary outcomes

For the mother

Perinatal outcomes

No clear differences were shown between the low‐GI dietary advice and moderate‐ to high‐GI dietary advice groups for the secondary outcomes: caesarean birth (RR 1.27, 95% CI 0.79 to 2.04; two trials, 201 women; GRADE: very low‐quality evidence) (Analysis 2.3); operative vaginal birth (RR 1.25, 95% CI 0.49 to 3.18; one trial, 62 women) (Analysis 2.4); and gestational weight gain (MD ‐1.23 kg, 95% CI ‐4.08 to 1.61; four trials, 787 women; Tau² = 7.31; I² = 90%; GRADE: very low‐quality evidence) (Analysis 2.5). Considerable statistical heterogeneity was observed in the meta‐analysis for gestational weight gain, and thus the pooled result should be interpreted with some caution.

In regards to adherence to the intervention, two trials (Moses 2006; Moses 2014) asked women to respond to the statement 'I adhered well to the dietary instructions' using a five‐point Likert scale (with one being 'all of the time' and five being 'none of the time'). No clear difference between the low GI‐dietary advice and moderate‐ to high‐GI dietary advice groups was seen in regards to adherence (MD 0.03, 95% CI ‐0.07 to 0.13; two trials, 636 women) (Analysis 2.6).

While no clear difference was seen between the low‐GI dietary advice and moderate‐ to high‐GI dietary advice groups for fasting blood glucose at 24 to 28 weeks in one trial (MD ‐0.17 mmol/L, 95% CI ‐0.57 to 0.23; 20 women) (Analysis 2.7); at 32 to 36 weeks, the low‐GI dietary advice group in two trials had a significantly lower fasting blood glucose concentration (MD ‐0.27 mmol/L, 95% CI ‐0.52 to ‐0.03; 82 women) (Analysis 2.8).

In two trials (Moses 2006; Moses 2014), women were asked to respond to a number of statements relating to their views of the intervention, using a five‐point Likert scale (with one being 'strongly agree' and five being 'strongly disagree'). No clear difference between the low‐GI dietary advice and moderate‐ to high‐GI dietary advice groups were seen for the following statements: 'It was easy to follow the diet recommended during this study' (MD ‐0.09, 95% CI ‐0.45 to 0.27; two trials, 636 women; Tau² = 0.06; I² = 82%); 'I enjoyed the dietary changes that I made' (MD ‐0.09, 95% CI ‐0.22 to 0.03; two trials, 636 women); 'The changes recommended were affordable' (MD 0.04, 95% CI ‐0.08 to 0.16; two trials, 636 women); 'My family was accepting of the changes made to my eating habits' (MD ‐0.02, 95% CI ‐0.15 to 0.10; two trials, 636 women); 'The study diet helped me meet the physical challenges of pregnancy' (MD 0.10, 95% CI ‐0.03 to 0.22; two trials, 636 women); and 'I enjoyed a wide variety of foods in my eating plan' (MD ‐0.05, 95% CI ‐0.15 to 0.05; two trials, 636 women) (Analysis 2.9).

The trials in this comparison did not report on the outcomes: induction of labour; perineal trauma; placental abruption; postpartum haemorrhage; postpartum infection; breastfeeding; behaviour changes associated with the intervention; sense of well‐being and quality of life.

Longer‐term maternal outcomes

The trials in this comparison did not report on any of the secondary longer‐term maternal outcomes.

For the child

Fetal/neonatal outcomes

No clear differences were shown between the low‐GI dietary advice and moderate‐ to high‐GI dietary advice groups for the secondary outcomes: Apgar score less than seven at five minutes (RR 2.82, 95% CI 0.12 to 66.62; one trial, 62 babies) (Analysis 2.10); macrosomia (> 4000 g) (RR 0.73, 95% CI 0.49 to 1.09; two trials, 715 babies) (Analysis 2.11) and macrosomia (> 4500 g) (RR 0.32, 95% CI 0.06 to 1.55; one trial, 576 babies) (Analysis 2.12); small‐for‐gestational age (RR 0.88, 95% CI 0.53 to 1.45; three trials, 777 babies) (Analysis 2.13); gestational age at birth (MD 0.11 weeks, 95% CI ‐0.11 to 0.33; three trials, 777 babies) (Analysis 2.14); birthweight (MD ‐217.97 g, 95% CI ‐483.96 to 48.02; four trials, 797 babies; Tau² = 62689.88; I² = 90%) (Analysis 2.15); birthweight z score (MD 0.07, 95% CI ‐0.26 to 0.40; one trial, 139 babies) (Analysis 2.16); head circumference at birth (MD ‐1.20 cm, 95% CI ‐2.75 to 0.36; two trials, 82 babies; Tau² = 0.99; I² = 78%) (Analysis 2.17); length at birth (MD ‐0.77 cm, 95% CI ‐1.98 to 0.45; three trials, 658 babies; Tau² = 0.89; I² = 81%) (Analysis 2.18); ponderal index at birth (MD ‐0.06, 95% CI ‐0.16 to 0.04; four trials, 797 babies; Tau² = 0.01; I² = 80%) (Analysis 2.19); or adiposity at birth (% body fat) (MD 0.02, 95% CI ‐1.43 to 1.47; two trials, 108 babies) (Analysis 2.20). Considerable statistical heterogeneity was observed in the meta‐analyses for birthweight, head circumference, length at birth and ponderal index at birth, and thus the pooled results should be interpreted with some caution.

The trials in this comparison did not report on the secondary outcomes: stillbirth; neonatal mortality; preterm birth; shoulder dystocia; nerve palsy; bone fracture; respiratory distress syndrome; hypoglycaemia; hyperbilirubinaemia.

Childhood/adulthood outcomes

Markovic 2016 reported that "At 3 months of age, there were no significant differences between diet groups in growth parameters or body composition".

The four trials in this comparison did not report any other data regarding the secondary childhood/adulthood outcomes.

Use of health services

No clear difference was shown between the low‐GI dietary advice and moderate‐ to high‐GI dietary advice groups for neonatal intensive care unit admission (RR 0.37, 95% CI 0.12 to 1.11; one trial, 138 babies) (Analysis 2.21).

The trials in this comparison did not report on any of the other secondary outcomes relating to the use of health services.

Comparison 3: High‐fibre dietary advice versus 'standard' dietary advice

One trial was included in this comparison (Fraser 1983).

Primary outcomes

Fraser 1983 did not report on any of the primary outcomes: GDM; hypertensive disorders of pregnancy; perinatal mortality (stillbirth or neonatal mortality); large‐for‐gestational age; neonatal mortality or morbidity composite.

Secondary outcomes

For the mother

Perinatal outcomes

Fraser 1983 reported on mean blood glucose concentrations following an OGTT at 35 weeks, and showed no clear difference between the high‐fibre dietary advice and standard dietary advice groups (MD ‐0.36 mmol/L, 95% CI ‐0.90 to 0.18; 25 women) (Analysis 3.1). Fraser 1983 also reported that "Results of the antenatal monitoring (including maternal weight gain)... showed no significant differences between the groups".

Fraser 1983 did not report on any of the other secondary perinatal outcomes.

Longer‐term maternal outcomes

Fraser 1983 did not report on any of the secondary longer‐term maternal outcomes.

For the child

Fetal/neonatal outcomes

Fraser 1983 reported on birthweight centile, and showed no clear difference between the high‐fibre dietary advice and standard dietary advice groups (MD ‐0.30, 95% CI ‐5.40 to 4.80; 25 babies) (Analysis 3.2). Fraser 1983 also reported that "Results of... fetal anthropometry showed no significant differences between the groups".

Fraser 1983 did not report on any of the other secondary fetal/neonatal outcomes.

Childhood/adulthood outcomes

Fraser 1983 did not report on any of the secondary childhood/adulthood outcomes.

Use of health services

Fraser 1983 did not report on any of the secondary outcomes relating to the use of health services.

Subgroup analyses

For Comparison 1: Dietary advice interventions versus standard care, we conducted a subgroup analysis for our primary outcome, GDM, based on BMI at trial entry. The test for subgroup differences was significant (Chi² = 4.57, P = 0.03, I² = 78.1%), indicating a possible difference in treatment effect based on BMI (Analysis 1.1). In particular, this subgroup analysis suggested a greater treatment effect (reduction in GDM risk for women who received dietary advice interventions) among trials that recruited overweight and/or obese women (BMI > 25). We were not able to perform subgroup analyses based on BMI at trial entry for the other primary outcomes in this comparison, with only two trials (both recruiting overweight/obese women) reporting on hypertensive disorders of pregnancy, and only one trial reporting on perinatal mortality.

We were not able to perform the other pre‐specified subgroup analyses in this version of the review, due to the paucity of data across the three comparisons.

Sensitivity analyses

For Comparison 1: Dietary advice interventions versus standard care, we conducted sensitivity analyses for our primary outcomes with reported data, exploring the effects of trial quality assessed by sequence generation and allocation concealment by omitting studies rated as 'high risk of bias' or 'unclear risk of bias' for these components. As Wolff 2008 was the only trial to have an 'unclear risk of bias' rating for allocation concealment, this was the only trial excluded from the GDM meta‐analysis. Excluding this trial from the meta‐analysis did not greatly impact the overall effect observed for this outcome (RR 0.63, 95% CI 0.36 to 1.10; four trials, 1266 women) (Analysis 1.1). When we excluded data from Wolff 2008 from the meta‐analysis for pregnancy‐induced hypertension, only data from Thornton 2009 remained, which showed no clear difference between groups (different to in the main analysis) (RR 0.30, 95% CI 0.08 to 1.06; one trial, 232 women) (Analysis 1.2). Similarly, when data from Wolff 2008 were excluded from the meta‐analysis for pre‐eclampsia, only data from Thornton 2009 remained, with no clear difference between groups (as in the main analysis) (RR 0.64, 95% CI 0.26 to 1.58; one trial, 232 women) (Analysis 1.3). Only Laitinen 2009 reported on perinatal mortality (with no deaths observed in this trial) (Analysis 1.4), and thus no sensitivity analysis was performed for this outcome.

For Comparison 2: Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice, we planned to conduct sensitivity analyses for our primary outcomes with reported data (GDM and large‐for‐gestational age). However, as all of the four trials contributing data to these meta‐analyses had an 'unclear risk of bias' or 'high risk of bias' for at least one of the two domains (sequence generation or allocation concealment), we did not perform these analyses.

No sensitivity analyses were performed for Comparison 3: High‐fibre dietary advice versus standard dietary advice, given that only one trial was included (Fraser 1983), and this trial did not report on the primary outcomes.

Discussion

available in

Summary of main results

Eleven trials (involving 2786 women and their babies) met the inclusion criteria for the review. Six trials compared dietary advice interventions with standard care (Laitinen 2009; Quinlivan 2011; Thornton 2009; Vitolo 2011; Walsh 2012; Wolff 2008); four compared low glycaemic index (GI) with moderate‐ to high‐GI dietary advice interventions (Clapp 1998; Markovic 2016; Moses 2006; Moses 2014); and one compared specific (high‐fibre focused) with standard dietary advice (Fraser 1983).

Meta‐analysis of trials comparing dietary advice interventions with standard care demonstrated a trend towards a reduction in the risk of gestational diabetes mellitus (GDM) (8.60% versus 12.60%, in five trials) (P = 0.07). The subgroup analysis based on body mass index (BMI) at trial entry, suggested a possible differential treatment effect for this outcome based on trial entry BMI, with a greater effect on GDM incidence observed in overweight and/or obese women receiving dietary advice. No clear differences were observed for the other reported primary outcomes pre‐eclampsia and perinatal mortality; these findings remained unchanged in the sensitivity analyses involving trials with a low risk of bias in the domains of sequence generation and allocation concealment.

Similarly, we found no clear differences in these trials for the majority of reported secondary outcomes for the mother and the child. In these trials, reductions in pregnancy‐induced hypertension (2.88% versus 9.79%, across two trials) and gestational weight gain (on average 4.70 kg less, across five trials) were observed, along with greater weight loss at three months postpartum (on average 1.43 kg more, in one trial) for women who received the dietary advice interventions. Well‐being (assessed using the WHO well‐being index) at 14 to 28 weeks' gestation, was found to be lower in the dietary intervention group (a percentage score 3.60 lower, in one trial). Diet‐related behaviour changes were mixed at three months postpartum (one trial). Over‐interpretation of these findings is cautioned in view of the small sample sizes and limited high‐quality evidence.

In the trials comparing low‐GI with moderate‐ to high‐GI dietary advice interventions, no clear differences were seen for the reported primary outcomes: GDM and large‐for‐gestational age; or for the majority of reported secondary outcomes for the mother and the child. While no difference was shown for fasting glucose at 24 to 28 weeks (one trial), women receiving low‐GI dietary advice had a marginally lower fasting blood glucose at 32 to 36 weeks (0.27 mmol/L lower, in two trials).

In the trial comparing high‐fibre dietary advice with standard dietary advice, no clear differences were seen for the two reported secondary outcomes: blood glucose following an oral glucose tolerance test (OGTT) at 35 weeks; and birthweight centile.

Overall completeness and applicability of evidence

The trials in this review were conducted with healthy women and those considered at high risk of developing GDM, including overweight/obese women. These trials recruited pregnant women from hospitals in Australia (Markovic 2016; Moses 2006; Moses 2014; Quinlivan 2011), the USA (Clapp 1998; Thornton 2009), Brazil (Vitolo 2011), Denmark (Wolff 2008), Finland (Laitinen 2009), Ireland (Walsh 2012), and the UK (Fraser 1983); and thus, the results may not be applicable to all settings or countries worldwide.

Four of the included trials (Clapp 1998; Fraser 1983; Moses 2006; Wolff 2008) included 73 women or fewer, five trials included 315 women or fewer (Markovic 2016; Quinlivan 2011; Thornton 2009; Vitolo 2011). The two largest trials were in 691 and 800 women (Moses 2014; Walsh 2012). Thus, largely the included trials were far too small to show differences in important but rare outcomes, such as perinatal mortality, and even in more common outcomes, such as GDM.

Though there were a total of 2786 women and their babies across the included trials, for the majority of outcomes, only one or two trials reported data, further limiting the statistical power of the meta‐analyses and the precision of the estimates of treatment effects. Lack of uniformity in reporting outcomes including diagnostic criteria limits the interpretation of data. Many important outcomes for women and their babies were not reported across the comparisons.

The six trials assessing dietary advice interventions versus standard care (Laitinen 2009; Quinlivan 2011; Thornton 2009; Vitolo 2011; Walsh 2012; Wolff 2008), did not report on the primary outcomes included in this review: large‐for‐gestational age and neonatal mortality and morbidity composite; and the trials did not report on a number of secondary outcomes, particularly long‐term outcomes for the mother and child, and health services outcomes.
The four trials comparing low‐GI dietary advice with moderate‐ to high‐GI dietary advice (Clapp 1998; Markovic 2016; Moses 2006; Moses 2014), did not report on the primary outcomes of this review: hypertensive disorders of pregnancy, perinatal mortality, and neonatal mortality and morbidity composite; and similarly did not report the majority of secondary outcomes, including long‐term outcomes for the mother and child, and health services outcomes.
The one trial comparing high‐fibre dietary advice with "standard advice" (Fraser 1983) did not report on any primary outcomes, and reported on only two secondary outcomes.

This may reflect multiple factors influencing outcome data collection and reporting, including evolving recognition of important outcome measures and changes in diagnostic parameters, particularly affecting older trials, the selective reporting of outcome data by trials where no differences were observed, or limitations at manuscript publication. The limited data regarding longer‐term health of women and their children reported to date from the included trials, could reflect a 'lag' time between recognition by trialists of the importance of such outcomes, and the subsequent collection and reporting of these outcome data (Bain 2016). While long‐term follow‐up of trials assessing perinatal interventions is widely regarded as important, it has been recognised that only a minority of trials are able to do so; often due to the time‐consuming and expensive nature of follow‐up, commonly falling outside of the funding period, or interest of the trialists (Teune 2013).

While the often 'negative' results from included trials to date may reflect lack of statistical power, the absence of observed clear differences could also be partially attributable to lack of intervention uptake (Halperin 2014). The efficacy of dietary intervention is likely to be influenced by many factors, including background dietary habits and barriers such as affordability, satisfaction with changes and convenience. It is noteworthy that in one small trial, low‐GI diet was associated with a poorer sense of well‐being, which is likely to influence intervention adherence. In the included trials, information regarding adherence, but particularly women's views, has to date been limited. As noted by Halperin 2014 in a recent narrative review of the role of lifestyle interventions for GDM prevention, in addition to being powered to detect reductions in GDM, future trials should be designed to monitor lifestyle changes closely, and may include a psychological component as part of the intervention, such as in Quinlivan 2011.

Earlier trials, such as Clapp 1998 and Moses 2006 compared low‐GI with high or moderate‐ to high‐GI dietary advice, including to test the hypothesis that a woman's dietary carbohydrate mix modifies glucose and insulin responses (Clapp 1998). In recognition that current best practice for GDM prevention, and indeed management, focuses on optimising glycaemic control, it is unlikely that further trials specifically assessing high‐GI diets will be conducted. More recent trials, such as Markovic 2016 and Moses 2014, have instead focused on comparisons of low‐GI specific dietary advice with 'standard' healthy eating advice (including for a moderate‐GI diet), or on comparing more general 'healthy eating' advice (including in combination with a multi‐disciplinary approach (Quinlivan 2011), or with an additional focus on low‐GI foods (Walsh 2012)) with standard care.

Quality of the evidence

Overall, the 11 included trials were judged to be at unclear to moderate risk of bias. Often there was insufficient information provided to enable a judgement of risk, particularly with regard to sequence generation and allocation concealment, blinding of outcome assessment, and selective reporting. Only four trials (Laitinen 2009; Quinlivan 2011; Thornton 2009; Walsh 2012) were considered to be at low risk of selection bias (with methods considered to be adequate for both sequence generation and allocation concealment); where possible, these trials were included in sensitivity analyses for primary outcomes in the first comparison.

We used GRADE profiler to assess the quality of the evidence for the two comparisons 'Dietary advice interventions versus standard care', summary of findings Table for the main comparison; summary of findings Table 2, and 'Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice' summary of findings Table 3; summary of findings Table 4. Several maternal and child outcomes were assessed for their quality of evidence.

For the first comparison, the evidence was of low quality (assessed using the GRADE system) for the following outcomes: hypertensive disorders of pregnancy (pre‐eclampsia; pregnancy‐induced hypertension), caesarean section, gestational weight gain, and childhood adult adiposity (skin‐fold thickness at six months). The evidence for the outcomes: GDM, perineal trauma and perinatal mortality was very low quality.

For the second comparison, the evidence for GDM was assessed of being low quality, while the evidence for the outcomes: caesarean section, gestational weight gain, and large‐for‐gestational age, was assessed as being very low quality.

Evidence downgrading was based on study limitations (risk of bias), imprecision (largely the presence of wide confidence intervals crossing the line of no effect), and inconsistency.

Potential biases in the review process

To reduce the potential for publication bias, a detailed, systematic search process was conducted by the Information Specialist of the Cochrane Pregnancy and Childbirth Group, without language or publication status restrictions. It is possible that additional trials assessing dietary advice intervention in pregnancy have been published but not identified; and/or that further trials have been conducted but are not yet published. Should any such studies be identified, we will include them in future updates of this review.

In order to minimise bias throughout the review process, two review authors independently assessed eligibility for inclusion, extracted data and assessed risk of bias.

Agreements and disagreements with other studies or reviews

Two Cochrane systematic reviews have assessed exercise alone (Han 2012) and combined diet and exercise interventions (Bain 2015) for preventing GDM. In Han 2012, five randomised trials (involving 1115 women and their babies) assessing exercise interventions were included. Han 2012 found no clear difference between women who received exercise interventions during pregnancy and those who received standard care for the risk of GDM, nor for any of the other primary or secondary outcomes for women and their babies reported by the included trials (Han 2012). Bain 2015 included 13 randomised trials (involving 4983 women and their babies) assessing combined diet and exercise interventions. In this review no clear difference between groups was shown for the risk of GDM, nor for the majority of other primary and secondary outcomes reported by the included trials (Bain 2015). The review did show a possible reduction in preterm birth for women receiving diet and exercise interventions (risk ratio (RR) 0.71, 95% confidence interval (CI) 0.55 to 0.93; five trials, 2713 infants) (Bain 2015) (a difference not observed in this review), however the review authors suggested caution in interpretation of these results due to clinical and statistical heterogeneity of the trials combined in the meta‐analysis. In Bain 2015, similar to our review, a possible benefit in relation to less weight gain during pregnancy was observed for women receiving combined diet and exercise interventions. On average, women receiving diet and exercise interventions gained 0.76 kg less than women in the control group (mean difference (MD) ‐0.76 kg, 95% CI ‐1.55 to 0.03; eight trials, 2707 women) (Bain 2015). These reviews have largely been limited by quality of evidence, heterogeneity in trial methodologies and outcome reporting, similar to this review.

An additional Cochrane review (Muktabhant 2015) has assessed diet or exercise, or both, interventions for preventing excessive weight gain during pregnancy, and associated complications. This review included 65 randomised trials (49 involving 11,444 women with data in the meta‐analyses) (Muktabhant 2015). Similar to in our review, a benefit in relation to less weight gain during pregnancy was observed ‐ women receiving diet or exercise, or both interventions (including interventions involving low glycaemic load diets, supervised or unsupervised exercise only, or diet and exercise combined) were less likely to gain excessive gestational weight gain (RR 0.80, 95% CI 0.73 to 0.87; 24 trials, 7096 women) (Muktabhant 2015). Also similar to our review, while no clear difference was seen in the risk of pre‐eclampsia, a possible reduction in maternal hypertension was observed for women receiving diet or exercise, or both interventions (RR 0.70, 95% CI 0.51 to 0.96; 11 trials, 5162 women) (Muktabhant 2015).

A number of additional non‐Cochrane systematic reviews have recently assessed a range of interventions, such as dietary advice, exercise, metformin, self‐monitoring of weight gain, and probiotics for preventing GDM (Oostdam 2011), behaviour‐modification interventions for preventing GDM (Skouteris 2014), lifestyle interventions for overweight and obese pregnant women for improving pregnancy outcomes, including GDM (Oteng‐Ntim 2012), and 'nutritional manipulation in pregnancy' for preventing GDM (Rogozińska 2015). The methods of these reviews, and particularly their inclusion/exclusion criteria, differed to those employed in our review, and thus they have revealed some similar, and some contrasting findings.

For example, the Rogozińska 2015 review (which included 20 randomised trials) assessed diet‐based, mixed approach (diet and lifestyle) interventions, and nutritional supplements (myo‐inositol and probiotics) and did not find a clear difference in GDM risk overall (RR 0.67, 95% CI 0.39 to 1.15; six trials, 1479 women). With the same three trials included in our overweight and/or obese subgroup, the review similarly showed a reduced risk of GDM in overweight or obese women with diet‐based interventions (RR 0.40, 95% CI 0.18 to 0.86; three trials, 455 women). The Oteng‐Ntim 2012 review (which included 13 randomised and six non‐randomised trials, all in overweight and/or obese women), found that dietary and lifestyle interventions in pregnancy could reduce gestational weight gain (MD ‐2.21, 95% CI ‐2.86 to 1.59; 10 trials, 1228 women); this review also reported a trend towards a reduction in GDM risk (OR 0.80, 95% CI 0.58 to 1.10, six trials, 1011 women) (Oteng‐Ntim 2012) specifically for overweight and/or obese women, as was seen in our review.

Skouteris 2014 (which included nine trials), did not pool data from individual studies in meta‐analyses. Skouteris 2014 did however similarly conclude that the majority of trials incorporating 'behaviour change techniques' designed to prevent GDM as a primary or secondary outcome have not demonstrated clear effectiveness. Skouteris 2014) highlighted the need for further research to inform the combination of information delivery and behaviour‐modification techniques used to prevent GDM. Oostdam 2011 (including 19 studies assessing a variety of interventions for GDM prevention) reported that dietary counselling reduced GDM compared with standard care (risk difference (RD) ‐0.05, 95% CI ‐0.10 to ‐0.01, seven trials, 813 women). Of note, the relevant meta‐analysis in the Oostdam 2011 review, included data from some trials which were included in the Bain 2015 Cochrane review (where exercise advice or sessions were provided in addition to dietary advice). Further, the Oostdam 2011 review did not include a number of trials which have been included in our review (reported after its publication), and included data from the two intervention arms of Laitinen 2009 (one of which assessed dietary advice and a probiotic; and thus this arm was excluded from our review).

Figure 1

Study flow diagram.

Figure 2

'Risk of bias' graph: review authors' judgements about each risk of bias item presented as percentages across all included studies.

Figure 3

'Risk of bias' summary: review authors' judgements about each risk of bias item for each included study.

Analysis 1.1

Comparison 1 Dietary advice interventions versus standard care, Outcome 1 Gestational diabetes.

Analysis 1.2

Comparison 1 Dietary advice interventions versus standard care, Outcome 2 Hypertensive disorders of pregnancy (pregnancy‐induced hypertension).

Analysis 1.3

Comparison 1 Dietary advice interventions versus standard care, Outcome 3 Hypertensive disorders of pregnancy (pre‐eclampsia).

Analysis 1.4

Comparison 1 Dietary advice interventions versus standard care, Outcome 4 Perinatal mortality.

Analysis 1.5

Comparison 1 Dietary advice interventions versus standard care, Outcome 5 Caesarean section.

Analysis 1.6

Comparison 1 Dietary advice interventions versus standard care, Outcome 6 Induction of labour.

Analysis 1.7

Comparison 1 Dietary advice interventions versus standard care, Outcome 7 Perineal trauma (anal sphincter injury).

Analysis 1.8

Comparison 1 Dietary advice interventions versus standard care, Outcome 8 Postpartum haemorrhage.

Analysis 1.9

Comparison 1 Dietary advice interventions versus standard care, Outcome 9 Postpartum infection.

Analysis 1.10

Comparison 1 Dietary advice interventions versus standard care, Outcome 10 Breastfeeding (at 3 months).

Analysis 1.11

Comparison 1 Dietary advice interventions versus standard care, Outcome 11 Breastfeeding (at 6 months).

Analysis 1.12

Comparison 1 Dietary advice interventions versus standard care, Outcome 12 Gestational weight gain (kg).

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Study

Dietary advice intervention

Standard care

P value

Vitolo 2011

Weekly average weight gain

Low weight: Mean: 507.8, standard deviation: 496.1; N=unclear

Eutrophic: Mean: 460.1, standard deviation: 135.2; N=unclear

Excess weight: Mean: 342.2, standard deviation: 143.6; N=unclear

Weekly average weight gain

Low weight: Mean: 496.1, standard deviation: 177.0; N=unclear

Eutrophic: Mean: 492.2, standard deviation: 222.1; N=unclear

Excess weight: Mean: 143.6, standard deviation: 185.4; N=unclear

Low weight: 0.8

Eutrophic: 0.2

Excess weight: 0.01

Analysis 1.13

Comparison 1 Dietary advice interventions versus standard care, Outcome 13 Gestational weight gain (g/week).

Analysis 1.14

Comparison 1 Dietary advice interventions versus standard care, Outcome 14 Behaviour changes associated with the intervention: health behaviours at 3 months postpartum.

Analysis 1.15

Comparison 1 Dietary advice interventions versus standard care, Outcome 15 Fasting glucose at 28 weeks (mmol/L).

Analysis 1.16

Comparison 1 Dietary advice interventions versus standard care, Outcome 16 Fasting glucose at 28 weeks ≥ 5.1 mmol/L.

Analysis 1.17

Comparison 1 Dietary advice interventions versus standard care, Outcome 17 OGCT at 28 weeks (mmol/L).

Analysis 1.18

Comparison 1 Dietary advice interventions versus standard care, Outcome 18 OGCT at 28 weeks > 7.8 mmol/L.

Analysis 1.19

Comparison 1 Dietary advice interventions versus standard care, Outcome 19 Fasting glucose at 28 weeks ≥ 5.1 mmol/L or OGCT at 28 week s> 7.8 mmol/L.

Analysis 1.20

Comparison 1 Dietary advice interventions versus standard care, Outcome 20 Sense of well‐being: score (% score between 14 to 28 weeks).

Analysis 1.21

Comparison 1 Dietary advice interventions versus standard care, Outcome 21 Postpartum weight loss at 6 weeks (kg).

Analysis 1.22

Comparison 1 Dietary advice interventions versus standard care, Outcome 22 Postnatal weight retention: change in weight from late pregnancy to 3 months postpartum (kg).

Analysis 1.23

Comparison 1 Dietary advice interventions versus standard care, Outcome 23 Return to pre‐pregnancy weight: change in weight from baseline to 3 months postpartum (kg).

Navigate to figure in Review


Study	Dietary advice intervention	Standard care
Laitinen 2009	Mean: 25.9; range: 19.5‐35.8; N=85 (Vahamiko 2013)	Mean: 25.4; range: 18.6‐35.9; N=84 (Vahamiko 2013)

Analysis 1.24

Comparison 1 Dietary advice interventions versus standard care, Outcome 24 Postpartum BMI.

Analysis 1.25

Comparison 1 Dietary advice interventions versus standard care, Outcome 25 Stillbirth.

Analysis 1.26

Comparison 1 Dietary advice interventions versus standard care, Outcome 26 Neonatal mortality.

Analysis 1.27

Comparison 1 Dietary advice interventions versus standard care, Outcome 27 Preterm birth (less than 37 weeks' gestation).

Analysis 1.28

Comparison 1 Dietary advice interventions versus standard care, Outcome 28 Preterm birth (less than 32 weeks' gestation).

Analysis 1.29

Comparison 1 Dietary advice interventions versus standard care, Outcome 29 Apgar score less than 7 at 5 minutes.

Analysis 1.30

Comparison 1 Dietary advice interventions versus standard care, Outcome 30 Macrosomia (> 4000 g).

Analysis 1.31

Comparison 1 Dietary advice interventions versus standard care, Outcome 31 Macrosomia (> 4500 g).

Analysis 1.32

Comparison 1 Dietary advice interventions versus standard care, Outcome 32 Shoulder dystocia.

Analysis 1.33

Comparison 1 Dietary advice interventions versus standard care, Outcome 33 Gestational age at birth (weeks).

Analysis 1.34

Comparison 1 Dietary advice interventions versus standard care, Outcome 34 Birthweight (g).

Analysis 1.35

Comparison 1 Dietary advice interventions versus standard care, Outcome 35 Head circumference at birth (cm).

Analysis 1.36

Comparison 1 Dietary advice interventions versus standard care, Outcome 36 Length at birth (cm).

Analysis 1.37

Comparison 1 Dietary advice interventions versus standard care, Outcome 37 Ponderal index at birth.

Analysis 1.38

Comparison 1 Dietary advice interventions versus standard care, Outcome 38 Adiposity at birth: skin‐fold thickness (mm).

Analysis 1.39

Comparison 1 Dietary advice interventions versus standard care, Outcome 39 Weight at 3 months (kg).

Analysis 1.40

Comparison 1 Dietary advice interventions versus standard care, Outcome 40 Weight at 6 months (kg).

Analysis 1.41

Comparison 1 Dietary advice interventions versus standard care, Outcome 41 Length at 6 months (cm).

Analysis 1.42

Comparison 1 Dietary advice interventions versus standard care, Outcome 42 Head circumference at 6 months (cm).

Analysis 1.43

Comparison 1 Dietary advice interventions versus standard care, Outcome 43 Skinfold thickness at 6 months (mm).

Analysis 1.44

Comparison 1 Dietary advice interventions versus standard care, Outcome 44 Systolic blood pressure at 6 months (mmHg).

Analysis 1.45

Comparison 1 Dietary advice interventions versus standard care, Outcome 45 Diastolic blood pressure at 6 months (mmHg).

Analysis 1.46

Comparison 1 Dietary advice interventions versus standard care, Outcome 46 Mean blood pressure at 6 months (mmHg).

Analysis 1.47

Comparison 1 Dietary advice interventions versus standard care, Outcome 47 Heart rate at 6 months (bpm).

Analysis 1.48

Comparison 1 Dietary advice interventions versus standard care, Outcome 48 Clinical complications (gestational diabetes, pre‐eclampsia, low birthweight, prematurity).

Analysis 2.1

Comparison 2 Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice, Outcome 1 Gestational diabetes.

Analysis 2.2

Comparison 2 Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice, Outcome 2 Large‐for‐gestational age.

Analysis 2.3

Comparison 2 Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice, Outcome 3 Caesarean birth.

Analysis 2.4

Comparison 2 Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice, Outcome 4 Operative vaginal birth.

Analysis 2.5

Comparison 2 Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice, Outcome 5 Gestational weight gain (kg).

Analysis 2.6

Comparison 2 Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice, Outcome 6 Adherence to the intervention.

Analysis 2.7

Comparison 2 Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice, Outcome 7 Fasting glucose at 24‐28 weeks (mmol/L).

Analysis 2.8

Comparison 2 Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice, Outcome 8 Fasting glucose at 32‐36 weeks (mmol/L).

Analysis 2.9

Comparison 2 Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice, Outcome 9 Views of the intervention.

Analysis 2.10

Comparison 2 Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice, Outcome 10 Apgar score less than 7 at 5 minutes.

Analysis 2.11

Comparison 2 Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice, Outcome 11 Macrosomia (> 4000 g).

Analysis 2.12

Comparison 2 Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice, Outcome 12 Macrosomia (> 4500 g).

Analysis 2.13

Comparison 2 Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice, Outcome 13 Small‐for‐gestational age.

Analysis 2.14

Comparison 2 Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice, Outcome 14 Gestational age at birth (weeks).

Analysis 2.15

Comparison 2 Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice, Outcome 15 Birthweight (g).

Analysis 2.16

Comparison 2 Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice, Outcome 16 Birthweight (z score).

Analysis 2.17

Comparison 2 Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice, Outcome 17 Head circumference at birth (cm).

Analysis 2.18

Comparison 2 Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice, Outcome 18 Length at birth (cm).

Analysis 2.19

Comparison 2 Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice, Outcome 19 Ponderal index at birth.

Analysis 2.20

Comparison 2 Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice, Outcome 20 Adiposity at birth: % body fat.

Analysis 2.21

Comparison 2 Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice, Outcome 21 Neonatal intensive care unit admission.

Analysis 3.1

Comparison 3 High‐fibre dietary advice versus ‘standard’ dietary advice, Outcome 1 OGTT at 35 weeks (mmol/L).

Analysis 3.2

Comparison 3 High‐fibre dietary advice versus ‘standard’ dietary advice, Outcome 2 Birthweight centile.

Summary of findings for the main comparison. Dietary advice interventions versus standard care (maternal outcomes)

Dietary advice interventions versus standard care (maternal outcomes)
Population: pregnant women Setting: 6 studies carried out in Australia, the USA, Brazil, Denmark, Ireland and Finland Intervention: dietary advice interventions Comparison: standard care
Outcomes	*Anticipated absolute effects^ (95% CI)**		Relative effect (95% CI)	№ of participants (studies)	Quality of the evidence (GRADE)	Comments
	Risk with standard care	Risk with dietary advice interventions
Gestational diabetes	Study population		RR 0.60 (0.35 to 1.04)	1279 (5 RCTs)	⊕⊝⊝⊝ VERY LOW ^1,2,3
	126 per 1000	76 per 1000 (44 to 131)
Hypertensive disorders of pregnancy (pregnancy‐induced hypertension)	Study population		RR 0.30 (0.10 to 0.88)	282 (2 RCTs)	⊕⊕⊝⊝ LOW ^1,4	Anticipated absolute effects based on only 2 trials contributing data
	98 per 1000	29 per 1000 (10 to 86)
Hypertensive disorders of pregnancy (pre‐eclampsia)	Study population		RR 0.61 (0.25 to 1.46)	282 (2 RCTs)	⊕⊕⊝⊝ LOW ^1,5	Anticipated absolute effects based on only 2 trials contributing data
	84 per 1000	51 per 1000 (21 to 123)
Caesarean section	Study population		RR 0.98 (0.78 to 1.24)	1194 (4 RCTs)	⊕⊕⊝⊝ LOW ^1,3
	300 per 1000	294 per 1000 (234 to 372)
Perineal trauma (anal sphincter injury)	Study population		RR 0.83 (0.23 to 3.08)	759 (1 RCT)	⊕⊝⊝⊝ VERY LOW ^6,7	Anticipated absolute effect based on findings from a single study
	13 per 1000	11 per 1000 (3 to 40)
Gestational weight gain (kg)	The mean gestational weight gain in the intervention group was 4.7 kg less (8.07 kg less to 1.34 kg less)		MD ‐4.70 (‐8.07 to ‐1.34)	1336 (5 RCTs)	⊕⊕⊝⊝ LOW ^1,8	There was high heterogeneity for this outcome
Postnatal depression			Not estimable	(0 studies)		No data reported for postnatal depression in any of the included studies
*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). CI: confidence interval; kg: kilogram; MD: mean difference; RCT: randomised controlled trial; RR: risk ratio
GRADE Working Group grades of evidence High quality: We are very confident that the true effect lies close to that of the estimate of the effect Moderate quality: We are moderately confident in the effect estimate: The true effect is likely to be close to the estimate of the effect, but there is a possibility that it is substantially different Low quality: Our confidence in the effect estimate is limited: The true effect may be substantially different from the estimate of the effect Very low quality: We have very little confidence in the effect estimate: The true effect is likely to be substantially different from the estimate of effect
¹The studies contributing data had design limitations ²There was considerable variation in the size of the effect in different studies ³Wide 95% CI crossing the line of no effect ⁴Estimate based on studies with small sample sizes ⁵Estimate based on studies with small sample sizes, low event rates and 95% CI crossing the line of no effect ⁶Single study with design limitations ⁷Single study contributing data, low event rate and wide 95% CI crossing the line of no effect ⁸Very substantial heterogeneity (I² = 96%)

Summary of findings for the main comparison. Dietary advice interventions versus standard care (maternal outcomes)

Summary of findings 2. Dietary advice interventions versus standard care (child outcomes)

Dietary advice interventions versus standard care (child outcomes)
Population: pregnant women Setting: 6 studies carried out in Australia, the USA, Brazil, Denmark, Ireland and Finland Intervention: dietary advice interventions Comparison: standard care
Outcomes	*Anticipated absolute effects^ (95% CI)**		Relative effect (95% CI)	№ of participants (studies)	Quality of the evidence (GRADE)	Comments
	Risk with standard care	Risk with dietary advice interventions
Perinatal mortality	Study population		Not estimable	159 (1 RCT)	⊕⊝⊝⊝ VERY LOW ^1,2	Effect not estimable. Outcome reported in a single study with no events
	0 per 1000	0 per 1000 (0 to 0)
Large‐for‐gestational age			Not estimable	(0 studies)		No data reported for large‐for‐gestational age in any of the included studies
Mortality or morbidity composite outcome			Not estimable	(0 studies)		No data reported for mortality or morbidity composite in any of the included studies
Neonatal hypoglycaemia			Not estimable	(0 studies)		No data reported for neonatal hypoglycaemia in any of the included studies
Childhood/adulthood adiposity: skinfold thickness at 6 months (mm)	The mean skinfold thickness in the intervention group was 0.1 mm less (0.71 less to 0.51 more)		MD ‐0.10 (‐0.71 to 0.51)	132 (1 RCT)	⊕⊕⊝⊝ LOW ^1,3	Estimate based on findings from a single study
Chilhood/adulthood type 2 diabetes mellitus			Not estimable	(0 studies)		No data reported for childhood/adulthood type 2 diabetes in any of the included studies
Childhood/adulthood neurosensory disability			Not estimable	(0 studies)		No data reported for childhood/adulthood neurosensory disability in any of the included studies
*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). CI: confidence interval; MD: mean difference; mm: millimetre; RCT: randomised controlled trial; RR: risk ratio; SD: standard deviation
GRADE Working Group grades of evidence High quality: We are very confident that the true effect lies close to that of the estimate of the effect Moderate quality: We are moderately confident in the effect estimate: The true effect is likely to be close to the estimate of the effect, but there is a possibility that it is substantially different Low quality: Our confidence in the effect estimate is limited: The true effect may be substantially different from the estimate of the effect Very low quality: We have very little confidence in the effect estimate: The true effect is likely to be substantially different from the estimate of effect
¹Single study with design limitations contributing data ²Single study with small sample size and no events ³Estimate based on single study with small sample size and wide 95% CI crossing the line of no effect

Summary of findings 2. Dietary advice interventions versus standard care (child outcomes)

Summary of findings 3. Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice (maternal outcomes)

Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice (maternal outcomes)
Population: pregnant women Setting: 4 studies carried out in Australia (3) and the USA (1) Intervention: low‐GI dietary advice Comparison: moderate‐ to high‐GI dietary advice
Outcomes	*Anticipated absolute effects^ (95% CI)**		Relative effect (95% CI)	№ of participants (studies)	Quality of the evidence (GRADE)	Comments
	Risk with moderate‐ to high‐GI dietary advice	Risk with low‐ GI dietary advice
Gestational diabetes	Study population		RR 0.91 (0.63 to 1.31)	912 (4 RCTs)	⊕⊕⊝⊝ LOW ^1,2
	110 per 1000	100 per 1000 (70 to 145)
Hypertensive disorders of pregnancy			Not estimable	(0 studies)		No data reported for hypertensive disorders of pregnancy in any of the included studies
Caesarean birth	Study population		RR 1.27 (0.79 to 2.04)	201 (2 RCTs)	⊕⊝⊝⊝ VERY LOW ^3,4
	227 per 1000	288 per 1000 (179 to 463)
Perineal trauma			Not estimable	(0 studies)		No data reported for perineal trauma in any of the included studies
Gestational weight gain (kg)	The mean gestational weight gain in the intervention group was 1.23 kg less than in the control group (4.08 kg less to 1.61 more)		MD ‐1.23 (‐4.08 to 1.61)	787 (4 RCTs)	⊕⊝⊝⊝ VERY LOW ^2,3,5
Postnatal depression			Not estimable	(0 studies)		No data reported for postnatal depression in any of the included studies
Type 2 diabetes mellitus			Not estimable	(0 studies)		No data reported for type 2 diabetes in any of the included studies
*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). CI: confidence interval; kg: kilogram; MD: mean difference; RCT: randomised controlled trial; RR: risk ratio
GRADE Working Group grades of evidence High quality: We are very confident that the true effect lies close to that of the estimate of the effect Moderate quality: We are moderately confident in the effect estimate: The true effect is likely to be close to the estimate of the effect, but there is a possibility that it is substantially different Low quality: Our confidence in the effect estimate is limited: The true effect may be substantially different from the estimate of the effect Very low quality: We have very little confidence in the effect estimate: The true effect is likely to be substantially different from the estimate of effect
¹Studies contributing data had design limitations ²Wide 95% CI crossing the line of no effect ³Studies contributing data had serious or very serious design limitations ⁴Estimate based on studies with small sample sizes, and wide 95% CI crossing the line of no effect ⁵Substantial heterogeneity (I² = 90%)

Summary of findings 3. Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice (maternal outcomes)

Summary of findings 4. Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice (child outcomes)

Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice (child outcomes)
Population: pregnant women Setting: 4 studies carried out in Australia (3) and the USA (1) Intervention: low‐GI dietary advice Comparison: moderate‐ to high‐GI dietary advice
Outcomes	*Anticipated absolute effects^ (95% CI)**		Relative effect (95% CI)	№ of participants (studies)	Quality of the evidence (GRADE)	Comments
	Risk with moderate‐ to high‐GI dietary advice	Risk with low‐GI dietary advice
Perinatal mortality			Not estimable	(0 studies)		No data reported for perinatal mortality in any of the included studies
Large‐for‐gestational age	Study population		RR 0.60 (0.19 to 1.86)	777 (3 RCTs)	⊕⊝⊝⊝ VERY LOW ^1,2,3
	114 per 1000	68 per 1000 (22 to 212)
Mortality or morbidity composite outcome			Not estimable	(0 studies)		No data reported for mortality or morbidity composite in any of the included studies
Neonatal hypoglycaemia			Not estimable	(0 studies)		No data reported for neonatal hypoglycaemia in any of the included studies
Childhood/adulthood adiposity			Not estimable	(0 studies)		No data reported for childhood/adulthood adiposity in any of the included studies
Chilhood/adulthood type 2 diabetes mellitus			Not estimable	(0 studies)		No data reported for childhood/adulthood type 2 diabetes in any of the included studies
Childhood/adulthood neurosensory disability			Not estimable	(0 studies)		No data reported for childhood/adulthood neurosensory disability in any of the included studies
*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). CI: confidence interval; RCT: randomised controlled trial; RR: risk ratio
GRADE Working Group grades of evidence High quality: We are very confident that the true effect lies close to that of the estimate of the effect Moderate quality: We are moderately confident in the effect estimate: The true effect is likely to be close to the estimate of the effect, but there is a possibility that it is substantially different Low quality: Our confidence in the effect estimate is limited: The true effect may be substantially different from the estimate of the effect Very low quality: We have very little confidence in the effect estimate: The true effect is likely to be substantially different from the estimate of effect
¹Studies contributing data had serious or very serious design limitations ²Substantial heterogeneity (I² = 62%) ³Wide 95% CI crossing the line of no effect

Summary of findings 4. Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice (child outcomes)

Comparison 1. Dietary advice interventions versus standard care

Outcome or subgroup title	No. of studies	No. of participants	Statistical method	Effect size
1 Gestational diabetes Show forest plot	5	1279	Risk Ratio (M‐H, Random, 95% CI)	0.60 [0.35, 1.04]

1.1 All women	2	870	Risk Ratio (M‐H, Random, 95% CI)	0.93 [0.64, 1.36]
1.2 Overweight or obese women (BMI > 25)	3	409	Risk Ratio (M‐H, Random, 95% CI)	0.39 [0.19, 0.79]
2 Hypertensive disorders of pregnancy (pregnancy‐induced hypertension) Show forest plot	2	282	Risk Ratio (M‐H, Fixed, 95% CI)	0.30 [0.10, 0.88]

3 Hypertensive disorders of pregnancy (pre‐eclampsia) Show forest plot	2	282	Risk Ratio (M‐H, Fixed, 95% CI)	0.61 [0.25, 1.46]

4 Perinatal mortality Show forest plot	1	159	Risk Ratio (M‐H, Fixed, 95% CI)	0.0 [0.0, 0.0]

5 Caesarean section Show forest plot	4	1194	Risk Ratio (M‐H, Random, 95% CI)	0.98 [0.78, 1.24]

6 Induction of labour Show forest plot	2	991	Risk Ratio (M‐H, Random, 95% CI)	1.10 [0.48, 2.51]

7 Perineal trauma (anal sphincter injury) Show forest plot	1	759	Risk Ratio (M‐H, Fixed, 95% CI)	0.83 [0.23, 3.08]

8 Postpartum haemorrhage Show forest plot	2	991	Risk Ratio (M‐H, Fixed, 95% CI)	0.71 [0.28, 1.86]

9 Postpartum infection Show forest plot	1	232	Risk Ratio (M‐H, Fixed, 95% CI)	0.83 [0.26, 2.65]

10 Breastfeeding (at 3 months) Show forest plot	1	452	Risk Ratio (M‐H, Fixed, 95% CI)	1.02 [0.89, 1.17]

11 Breastfeeding (at 6 months) Show forest plot	1	146	Risk Ratio (M‐H, Fixed, 95% CI)	0.99 [0.82, 1.19]

12 Gestational weight gain (kg) Show forest plot	5	1336	Mean Difference (IV, Random, 95% CI)	‐4.70 [‐8.07, ‐1.34]

13 Gestational weight gain (g/week) Show forest plot			Other data	No numeric data

14 Behaviour changes associated with the intervention: health behaviours at 3 months postpartum Show forest plot	1		Risk Ratio (M‐H, Fixed, 95% CI)	Subtotals only

14.1 Weight reducing diet at 3 months postpartum	1	458	Risk Ratio (M‐H, Fixed, 95% CI)	0.95 [0.66, 1.38]
14.2 Supplements at 3 months postpartum	1	459	Risk Ratio (M‐H, Fixed, 95% CI)	1.12 [0.98, 1.28]
14.3 Made dietary changes since ROLO study	1	420	Risk Ratio (M‐H, Fixed, 95% CI)	1.12 [0.98, 1.29]
14.4 Low GI diet at 3 months postpartum	1	197	Risk Ratio (M‐H, Fixed, 95% CI)	5.37 [1.93, 14.89]
14.5 Reading food labels at 3 months postpartum	1	453	Risk Ratio (M‐H, Fixed, 95% CI)	1.11 [1.01, 1.23]
14.6 Reading ingredients at 3 months postpartum	1	453	Risk Ratio (M‐H, Fixed, 95% CI)	1.12 [0.91, 1.37]
14.7 Reading nutrients at 3 months postpartum	1	453	Risk Ratio (M‐H, Fixed, 95% CI)	1.21 [1.03, 1.41]
14.8 Reading calories at 3 months postpartum	1	453	Risk Ratio (M‐H, Fixed, 95% CI)	1.08 [0.89, 1.31]
14.9 Reading food weight at 3 months postpartum	1	453	Risk Ratio (M‐H, Fixed, 95% CI)	1.51 [0.90, 2.54]
14.10 Reading additives at 3 months postpartum	1	453	Risk Ratio (M‐H, Fixed, 95% CI)	1.33 [0.99, 1.79]
14.11 Reading serving size at 3 months postpartum	1	453	Risk Ratio (M‐H, Fixed, 95% CI)	1.39 [0.83, 2.34]
14.12 Attending gym at 3 months postpartum	1	440	Risk Ratio (M‐H, Fixed, 95% CI)	0.98 [0.65, 1.49]
15 Fasting glucose at 28 weeks (mmol/L) Show forest plot	1	759	Mean Difference (IV, Fixed, 95% CI)	‐0.06 [‐0.13, 0.01]

16 Fasting glucose at 28 weeks ≥ 5.1 mmol/L Show forest plot	1	673	Risk Ratio (M‐H, Fixed, 95% CI)	0.64 [0.40, 1.04]

17 OGCT at 28 weeks (mmol/L) Show forest plot	1	759	Mean Difference (IV, Fixed, 95% CI)	‐0.20 [‐0.42, 0.02]

18 OGCT at 28 weeks > 7.8 mmol/L Show forest plot	1	721	Risk Ratio (M‐H, Fixed, 95% CI)	0.72 [0.53, 0.99]

19 Fasting glucose at 28 weeks ≥ 5.1 mmol/L or OGCT at 28 week s> 7.8 mmol/L Show forest plot	1	672	Risk Ratio (M‐H, Fixed, 95% CI)	0.74 [0.56, 0.97]

20 Sense of well‐being: score (% score between 14 to 28 weeks) Show forest plot	1	618	Mean Difference (IV, Fixed, 95% CI)	‐3.60 [‐5.98, ‐1.22]

21 Postpartum weight loss at 6 weeks (kg) Show forest plot	1	232	Mean Difference (IV, Fixed, 95% CI)	‐0.90 [‐3.67, 1.87]

22 Postnatal weight retention: change in weight from late pregnancy to 3 months postpartum (kg) Show forest plot	1	165	Mean Difference (IV, Fixed, 95% CI)	‐0.35 [‐1.84, 1.14]

23 Return to pre‐pregnancy weight: change in weight from baseline to 3 months postpartum (kg) Show forest plot	1	414	Mean Difference (IV, Fixed, 95% CI)	‐1.43 [‐2.66, ‐0.20]

24 Postpartum BMI Show forest plot			Other data	No numeric data

25 Stillbirth Show forest plot	2	959	Risk Ratio (M‐H, Fixed, 95% CI)	3.09 [0.13, 75.65]

26 Neonatal mortality Show forest plot	1	159	Risk Ratio (M‐H, Fixed, 95% CI)	0.0 [0.0, 0.0]

27 Preterm birth (less than 37 weeks' gestation) Show forest plot	3	1149	Risk Ratio (M‐H, Fixed, 95% CI)	0.51 [0.21, 1.25]

28 Preterm birth (less than 32 weeks' gestation) Show forest plot	2	917	Risk Ratio (M‐H, Fixed, 95% CI)	1.70 [0.23, 12.88]

29 Apgar score less than 7 at 5 minutes Show forest plot	1	232	Risk Ratio (M‐H, Fixed, 95% CI)	3.0 [0.12, 72.89]

30 Macrosomia (> 4000 g) Show forest plot	1	759	Risk Ratio (M‐H, Fixed, 95% CI)	0.99 [0.86, 1.14]

31 Macrosomia (> 4500 g) Show forest plot	1	232	Risk Ratio (M‐H, Fixed, 95% CI)	2.25 [0.71, 7.10]

32 Shoulder dystocia Show forest plot	1	759	Risk Ratio (M‐H, Fixed, 95% CI)	0.52 [0.10, 2.82]

33 Gestational age at birth (weeks) Show forest plot	4	1195	Mean Difference (IV, Random, 95% CI)	0.05 [‐0.31, 0.40]

34 Birthweight (g) Show forest plot	5	1324	Mean Difference (IV, Fixed, 95% CI)	5.94 [‐51.11, 62.99]

35 Head circumference at birth (cm) Show forest plot	3	968	Mean Difference (IV, Random, 95% CI)	‐0.21 [‐0.67, 0.25]

36 Length at birth (cm) Show forest plot	3	968	Mean Difference (IV, Random, 95% CI)	0.16 [‐0.28, 0.60]

37 Ponderal index at birth Show forest plot	1	759	Mean Difference (IV, Fixed, 95% CI)	0.01 [‐0.38, 0.40]

38 Adiposity at birth: skin‐fold thickness (mm) Show forest plot	1		Mean Difference (IV, Fixed, 95% CI)	Subtotals only

38.1 Subscapular skin‐fold (mm)	1	219	Mean Difference (IV, Fixed, 95% CI)	‐0.04 [‐0.45, 0.37]
38.2 Triceps skin‐fold (mm)	1	219	Mean Difference (IV, Fixed, 95% CI)	‐0.18 [‐0.58, 0.22]
38.3 Biceps skin‐fold (mm)	1	219	Mean Difference (IV, Fixed, 95% CI)	‐0.10 [‐0.50, 0.30]
38.4 Leg skin‐fold (mm)	1	219	Mean Difference (IV, Fixed, 95% CI)	0.06 [‐0.42, 0.54]
38.5 Sum of skin‐folds (mm)	1	219	Mean Difference (IV, Fixed, 95% CI)	‐1.60 [‐4.77, 1.57]
39 Weight at 3 months (kg) Show forest plot	1	422	Mean Difference (IV, Fixed, 95% CI)	0.23 [‐0.37, 0.83]

40 Weight at 6 months (kg) Show forest plot	1	143	Mean Difference (IV, Fixed, 95% CI)	‐0.03 [‐0.35, 0.29]

41 Length at 6 months (cm) Show forest plot	1	143	Mean Difference (IV, Fixed, 95% CI)	0.0 [‐1.06, 1.06]

42 Head circumference at 6 months (cm) Show forest plot	1	132	Mean Difference (IV, Fixed, 95% CI)	‐0.20 [‐0.61, 0.21]

43 Skinfold thickness at 6 months (mm) Show forest plot	1	132	Mean Difference (IV, Fixed, 95% CI)	‐0.10 [‐0.71, 0.51]

44 Systolic blood pressure at 6 months (mmHg) Show forest plot	1	113	Mean Difference (IV, Fixed, 95% CI)	‐1.0 [‐4.53, 2.53]

45 Diastolic blood pressure at 6 months (mmHg) Show forest plot	1	113	Mean Difference (IV, Fixed, 95% CI)	‐1.0 [‐3.77, 1.77]

46 Mean blood pressure at 6 months (mmHg) Show forest plot	1	113	Mean Difference (IV, Fixed, 95% CI)	‐1.0 [‐3.77, 1.77]

47 Heart rate at 6 months (bpm) Show forest plot	1	113	Mean Difference (IV, Fixed, 95% CI)	2.0 [‐2.89, 6.89]

48 Clinical complications (gestational diabetes, pre‐eclampsia, low birthweight, prematurity) Show forest plot	1	305	Risk Ratio (M‐H, Fixed, 95% CI)	0.37 [0.21, 0.66]

Comparison 1. Dietary advice interventions versus standard care

Comparison 2. Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice

Outcome or subgroup title	No. of studies	No. of participants	Statistical method	Effect size
1 Gestational diabetes Show forest plot	4	912	Risk Ratio (M‐H, Fixed, 95% CI)	0.91 [0.63, 1.31]

2 Large‐for‐gestational age Show forest plot	3	777	Risk Ratio (M‐H, Random, 95% CI)	0.60 [0.19, 1.86]

3 Caesarean birth Show forest plot	2	201	Risk Ratio (M‐H, Fixed, 95% CI)	1.27 [0.79, 2.04]

4 Operative vaginal birth Show forest plot	1	62	Risk Ratio (M‐H, Fixed, 95% CI)	1.25 [0.49, 3.18]

5 Gestational weight gain (kg) Show forest plot	4	787	Mean Difference (IV, Random, 95% CI)	‐1.23 [‐4.08, 1.61]

6 Adherence to the intervention Show forest plot	2	636	Mean Difference (IV, Fixed, 95% CI)	0.03 [‐0.07, 0.13]

6.1 I adhered well to the dietary instructions	2	636	Mean Difference (IV, Fixed, 95% CI)	0.03 [‐0.07, 0.13]
7 Fasting glucose at 24‐28 weeks (mmol/L) Show forest plot	1	20	Mean Difference (IV, Fixed, 95% CI)	‐0.17 [‐0.57, 0.23]

8 Fasting glucose at 32‐36 weeks (mmol/L) Show forest plot	2	82	Mean Difference (IV, Fixed, 95% CI)	‐0.27 [‐0.52, ‐0.03]

9 Views of the intervention Show forest plot	2		Mean Difference (IV, Random, 95% CI)	Subtotals only

9.1 It was easy to follow the diet recommended during this study	2	636	Mean Difference (IV, Random, 95% CI)	‐0.09 [‐0.45, 0.27]
9.2 I enjoyed the dietary changes that I made	2	636	Mean Difference (IV, Random, 95% CI)	‐0.09 [‐0.22, 0.03]
9.3 The changes recommended were affordable	2	636	Mean Difference (IV, Random, 95% CI)	0.04 [‐0.08, 0.16]
9.4 My family was accepting of the changes made to my eating habits	2	636	Mean Difference (IV, Random, 95% CI)	‐0.02 [‐0.15, 0.10]
9.5 The study diet helped me meet the physical challenges of pregnancy	2	636	Mean Difference (IV, Random, 95% CI)	0.10 [‐0.03, 0.22]
9.6 I enjoyed a wide variety of foods in my eating plan	2	636	Mean Difference (IV, Random, 95% CI)	‐0.05 [‐0.15, 0.05]
10 Apgar score less than 7 at 5 minutes Show forest plot	1	62	Risk Ratio (M‐H, Fixed, 95% CI)	2.82 [0.12, 66.62]

11 Macrosomia (> 4000 g) Show forest plot	2	715	Risk Ratio (M‐H, Fixed, 95% CI)	0.73 [0.49, 1.09]

12 Macrosomia (> 4500 g) Show forest plot	1	576	Risk Ratio (M‐H, Fixed, 95% CI)	0.32 [0.06, 1.55]

13 Small‐for‐gestational age Show forest plot	3	777	Risk Ratio (M‐H, Fixed, 95% CI)	0.88 [0.53, 1.45]

14 Gestational age at birth (weeks) Show forest plot	3	777	Mean Difference (IV, Fixed, 95% CI)	0.11 [‐0.11, 0.33]

15 Birthweight (g) Show forest plot	4	797	Mean Difference (IV, Random, 95% CI)	‐217.97 [‐483.96, 48.02]

16 Birthweight (z score) Show forest plot	1	139	Mean Difference (IV, Fixed, 95% CI)	0.07 [‐0.26, 0.40]

17 Head circumference at birth (cm) Show forest plot	2	82	Mean Difference (IV, Random, 95% CI)	‐1.20 [‐2.75, 0.36]

18 Length at birth (cm) Show forest plot	3	658	Mean Difference (IV, Random, 95% CI)	‐0.77 [‐1.98, 0.45]

19 Ponderal index at birth Show forest plot	4	797	Mean Difference (IV, Random, 95% CI)	‐0.06 [‐0.16, 0.04]

20 Adiposity at birth: % body fat Show forest plot	2	108	Mean Difference (IV, Fixed, 95% CI)	0.02 [‐1.43, 1.47]

21 Neonatal intensive care unit admission Show forest plot	1	138	Risk Ratio (M‐H, Fixed, 95% CI)	0.37 [0.12, 1.11]

Comparison 2. Low‐GI dietary advice versus moderate‐ to high‐GI dietary advice

Comparison 3. High‐fibre dietary advice versus ‘standard’ dietary advice

Outcome or subgroup title	No. of studies	No. of participants	Statistical method	Effect size
1 OGTT at 35 weeks (mmol/L) Show forest plot	1	25	Mean Difference (IV, Fixed, 95% CI)	‐0.36 [‐0.90, 0.18]

2 Birthweight centile Show forest plot	1	25	Mean Difference (IV, Fixed, 95% CI)	‐0.30 [‐5.40, 4.80]

Comparison 3. High‐fibre dietary advice versus ‘standard’ dietary advice