Postprandial dysmetabolism is a common entity of type 2 diabetes mellitus (T2DM) and may act as a daily stressor of the already dysfunctional diabetic platelets. This study aims to investigate whether oleocanthal-rich olive oils (OO), incorporated into a carbohydrate-rich meal, can affect postprandial dysmetabolism and platelet aggregation. Oleocanthal is a cyclooxygenase inhibitor with putative antiplatelet properties. In this randomized, single-blinded, crossover study, ten T2DM patients consumed five isocaloric meals containing 120 g white bread combined with: (i) 39 g butter, (ii) 39 g butter and 400 mg ibuprofen, (iii) 40 mL OO (phenolic content < 10 mg/Kg), (iv) 40 mL OO with 250 mg/Kg oleocanthal and (v) 40 mL OO with 500 mg/Kg oleocanthal. Metabolic markers along with ex vivo ADP- and thrombin receptor-activating peptide (TRAP)-induced platelet aggregation were measured before and for 4 h after the meals. The glycemic and lipidemic response was similar between meals. However, a sustained (90-240 min) dose-dependent reduction in platelets' sensitivity to both ADP (50-100%) and TRAP (20-50%) was observed after the oleocanthal meals in comparison to OO or butter meals. The antiplatelet effect of the OO containing 500 mg/Kg oleocanthal was comparable to that of the ibuprofen meal. In conclusion, the consumption of meals containing oleocanthal-rich OO can reduce platelet activity during the postprandial period, irrespective of postprandial hyperglycemia and lipidemia.

Nutrition therapy provides the foundation for treatment of gestational diabetes (GDM), and has historically been based on restricting carbohydrate (CHO) intake. In this paper, randomized controlled trials (RCTs) are reviewed to assess the effects of both low- and higher CHO nutrition approaches in GDM. The prevailing pattern across the evidence underscores that although CHO restriction improves glycemia at least in the short-term, similar outcomes could be achievable using less restrictive approaches that may not exacerbate IR. The quality of existing studies is limited, in part due to dietary non-adherence and confounding effects of treatment with insulin or oral medication. Recent evidence suggests that modified nutritional manipulation in GDM from usual intake, including but not limited to CHO restriction, improves maternal glucose and lowers infant birthweight. This creates a platform for future studies to further clarify the impact of multiple nutritional patterns in GDM on both maternal and infant outcomes.

Gestational diabetes mellitus (GDM) and large for gestational age (LGA) offspring are two common pregnancy complications. Connections also exist between the two conditions, including mutual maternal risk factors for the conditions and an increased prevalence of LGA offspring amongst pregnancies affected by GDM. Thus, it is important to elucidate potential shared underlying mechanisms of both LGA and GDM. One potential mechanistic link relates to macronutrient metabolism. Indeed, derangement of carbohydrate and lipid metabolism is present in GDM, and maternal biomarkers of glucose and lipid control are associated with LGA neonates in such pregnancies. The aim of this paper is therefore to reflect on the existing nutritional guidelines for GDM in light of our understanding of the pathophysiological mechanisms of GDM and LGA offspring. Lifestyle modification is first line treatment for GDM, and while there is some promise that nutritional interventions may favourably impact outcomes, there is a lack of definitive evidence that changing the macronutrient composition of the diet reduces the incidence of either GDM or LGA offspring. The quality of the available evidence is a major issue, and rigorous trials are needed to inform evidence-based treatment guidelines.

Gestational diabetes (GDM) is glucose intolerance, first recognised in pregnancy and usually resolving after birth. GDM is associated with both short- and long-term adverse effects for the mother and her infant. Lifestyle interventions are the primary therapeutic strategy for many women with GDM.

To evaluate the effects of combined lifestyle interventions with or without pharmacotherapy in treating women with gestational diabetes.

We searched the Pregnancy and Childbirth Group's Trials Register (14 May 2016), ClinicalTrials.gov, WHO International Clinical Trials Registry Platform (ICTRP) (14th May 2016) and reference lists of retrieved studies.

We included only randomised controlled trials comparing a lifestyle intervention with usual care or another intervention for the treatment of pregnant women with GDM. Quasi-randomised trials were excluded. Cross-over trials were not eligible for inclusion. Women with pre-existing type 1 or type 2 diabetes were excluded.

We used standard methodological procedures expected by the Cochrane Collaboration. All selection of studies, data extraction was conducted independently by two review authors.

Fifteen trials (in 45 reports) are included in this review (4501 women, 3768 infants). None of the trials were funded by a conditional grant from a pharmaceutical company. The lifestyle interventions included a wide variety of components such as education, diet, exercise and self-monitoring of blood glucose. The control group included usual antenatal care or diet alone. Using GRADE methodology, the quality of the evidence ranged from high to very low quality. The main reasons for downgrading evidence were inconsistency and risk of bias. We summarised the following data from the important outcomes of this review. Lifestyle intervention versus control groupFor the mother:There was no clear evidence of a difference between lifestyle intervention and control groups for the risk of hypertensive disorders of pregnancy (pre-eclampsia) (average risk ratio (RR) 0.70; 95% confidence interval (CI) 0.40 to 1.22; four trials, 2796 women; I2 = 79%, Tau2 = 0.23; low-quality evidence); caesarean section (average RR 0.90; 95% CI 0.78 to 1.05; 10 trials, 3545 women; I2 = 48%, Tau2 = 0.02; low-quality evidence); development of type 2 diabetes (up to a maximum of 10 years follow-up) (RR 0.98, 95% CI 0.54 to 1.76; two trials, 486 women; I2 = 16%; low-quality evidence); perineal trauma/tearing (RR 1.04, 95% CI 0.93 to 1.18; one trial, n = 1000 women; moderate-quality evidence) or induction of labour (average RR 1.20, 95% CI 0.99 to 1.46; four trials, n = 2699 women; I2 = 37%; high-quality evidence).More women in the lifestyle intervention group had met postpartum weight goals one year after birth than in the control group (RR 1.75, 95% CI 1.05 to 2.90; 156 women; one trial, low-quality evidence). Lifestyle interventions were associated with a decrease in the risk of postnatal depression compared with the control group (RR 0.49, 95% CI 0.31 to 0.78; one trial, n = 573 women; low-quality evidence).For the infant/child/adult:Lifestyle interventions were associated with a reduction in the risk of being born large-for-gestational age (LGA) (RR 0.60, 95% CI 0.50 to 0.71; six trials, 2994 infants; I2 = 4%; moderate-quality evidence). Birthweight and the incidence of macrosomia were lower in the lifestyle intervention group.Exposure to the lifestyle intervention was associated with decreased neonatal fat mass compared with the control group (mean difference (MD) -37.30 g, 95% CI -63.97 to -10.63; one trial, 958 infants; low-quality evidence). In childhood, there was no clear evidence of a difference between groups for body mass index (BMI) ≥ 85th percentile (RR 0.91, 95% CI 0.75 to 1.11; three trials, 767 children; I2 = 4%; moderate-quality evidence).There was no clear evidence of a difference between lifestyle intervention and control groups for the risk of perinatal death (RR 0.09, 95% CI 0.01 to 1.70; two trials, 1988 infants; low-quality evidence). Of 1988 infants, only five events were reported in total in the control group and there were no events in the lifestyle group. There was no clear evidence of a difference between lifestyle intervention and control groups for a composite of serious infant outcome/s (average RR 0.57, 95% CI 0.21 to 1.55; two trials, 1930 infants; I2 = 82%, Tau2 = 0.44; very low-quality evidence) or neonatal hypoglycaemia (average RR 0.99, 95% CI 0.65 to 1.52; six trials, 3000 infants; I2 = 48%, Tau2 = 0.12; moderate-quality evidence). Diabetes and adiposity in adulthood and neurosensory disability in later childhoodwere not prespecified or reported as outcomes for any of the trials included in this review.

Lifestyle interventions are the primary therapeutic strategy for women with GDM. Women receiving lifestyle interventions were less likely to have postnatal depression and were more likely to achieve postpartum weight goals. Exposure to lifestyle interventions was associated with a decreased risk of the baby being born LGA and decreased neonatal adiposity. Long-term maternal and childhood/adulthood outcomes were poorly reported.The value of lifestyle interventions in low-and middle-income countries or for different ethnicities remains unclear. The longer-term benefits or harms of lifestyle interventions remains unclear due to limited reporting.The contribution of individual components of lifestyle interventions could not be assessed. Ten per cent of participants also received some form of pharmacological therapy. Lifestyle interventions are useful as the primary therapeutic strategy and most commonly include healthy eating, physical activity and self-monitoring of blood glucose concentrations.Future research could focus on which specific interventions are most useful (as the sole intervention without pharmacological treatment), which health professionals should give them and the optimal format for providing the information. Evaluation of long-term outcomes for the mother and her child should be a priority when planning future trials. There has been no in-depth exploration of the costs 'saved' from reduction in risk of LGA/macrosomia and potential longer-term risks for the infants.

Dietary advice is the main strategy for managing gestational diabetes mellitus (GDM). It remains unclear what type of advice is best.

To assess the effects of different types of dietary advice for women with GDM for improving health outcomes for women and babies.

We searched Cochrane Pregnancy and Childbirth's Trials Register (8 March 2016), PSANZ's Trials Registry (22 March 2016) and reference lists of retrieved studies.

Randomised controlled trials comparing the effects of different types of dietary advice for women with GDM.

Two authors independently assessed study eligibility, risk of bias, and extracted data. Evidence quality for two comparisons was assessed using GRADE, for primary outcomes for the mother: hypertensive disorders of pregnancy; caesarean section; type 2 diabetes mellitus; and child: large-for-gestational age; perinatal mortality; neonatal mortality or morbidity composite; neurosensory disability; secondary outcomes for the mother: induction of labour; perineal trauma; postnatal depression; postnatal weight retention or return to pre-pregnancy weight; and child: hypoglycaemia; childhood/adulthood adiposity; childhood/adulthood type 2 diabetes mellitus.

In this update, we included 19 trials randomising 1398 women with GDM, at an overall unclear to moderate risk of bias (10 comparisons). For outcomes assessed using GRADE, downgrading was based on study limitations, imprecision and inconsistency. Where no findings are reported below for primary outcomes or pre-specified GRADE outcomes, no data were provided by included trials. Primary outcomes Low-moderate glycaemic index (GI) versus moderate-high GI diet (four trials): no clear differences observed for: large-for-gestational age (risk ratio (RR) 0.71, 95% confidence interval (CI) 0.22 to 2.34; two trials, 89 infants; low-quality evidence); severe hypertension or pre-eclampsia (RR 1.02, 95% CI 0.07 to 15.86; one trial, 95 women; very low-quality evidence); eclampsia (RR 0.34, 95% CI 0.01 to 8.14; one trial, 83 women; very low-quality evidence) or caesarean section (RR 0.66, 95% CI 0.29 to 1.47; one trial, 63 women; low-quality evidence). Energy-restricted versus no energy-restricted diet (three trials): no clear differences seen for: large-for-gestational age (RR 1.17, 95% CI 0.65 to 2.12; one trial, 123 infants; low-quality evidence); perinatal mortality (no events; two trials, 423 infants; low-quality evidence); pre-eclampsia (RR 1.00, 95% CI 0.51 to 1.97; one trial, 117 women; low-quality evidence); or caesarean section (RR 1.12, 95% CI 0.80 to 1.56; two trials, 420 women; low-quality evidence). DASH (Dietary Approaches to Stop Hypertension) diet versus control diet (three trials): no clear differences observed for: pre-eclampsia (RR 1.00, 95% CI 0.31 to 3.26; three trials, 136 women); however there were fewer caesarean sections in the DASH diet group (RR 0.53, 95% CI 0.37 to 0.76; two trials, 86 women). Low-carbohydrate versus high-carbohydrate diet (two trials): no clear differences seen for: large-for-gestational age (RR 0.51, 95% CI 0.13 to 1.95; one trial, 149 infants); perinatal mortality (RR 3.00, 95% CI 0.12 to 72.49; one trial, 150 infants); maternal hypertension (RR 0.40, 95% CI 0.13 to 1.22; one trial, 150 women); or caesarean section (RR 1.29, 95% CI 0.84 to 1.99; two trials, 179 women). High unsaturated fat versus low unsaturated fat diet (two trials): no clear differences observed for: large-for-gestational age (RR 0.54, 95% CI 0.21 to 1.37; one trial, 27 infants); pre-eclampsia (no cases; one trial, 27 women); hypertension in pregnancy (RR 0.54, 95% CI 0.06 to 5.26; one trial, 27 women); caesarean section (RR 1.08, 95% CI 0.07 to 15.50; one trial, 27 women); diabetes at one to two weeks (RR 2.00, 95% CI 0.45 to 8.94; one trial, 24 women) or four to 13 months postpartum (RR 1.00, 95% CI 0.10 to 9.61; one trial, six women). Low-GI versus high-fibre moderate-GI diet (one trial): no clear differences seen for: large-for-gestational age (RR 2.87, 95% CI 0.61 to 13.50; 92 infants); caesarean section (RR 1.91, 95% CI 0.91 to 4.03; 92 women); or type 2 diabetes at three months postpartum (RR 0.76, 95% CI 0.11 to 5.01; 58 women). Diet recommendation plus diet-related behavioural advice versus diet recommendation only (one trial): no clear differences observed for: large-for-gestational age (RR 0.73, 95% CI 0.25 to 2.14; 99 infants); or caesarean section (RR 0.78, 95% CI 0.38 to 1.62; 99 women). Soy protein-enriched versus no soy protein diet (one trial): no clear differences seen for: pre-eclampsia (RR 2.00, 95% CI 0.19 to 21.03; 68 women); or caesarean section (RR 1.00, 95% CI 0.57 to 1.77; 68 women). High-fibre versus standard-fibre diet (one trial): no primary outcomes reported. Ethnic-specific versus standard healthy diet (one trial): no clear differences observed for: large-for-gestational age (RR 0.14, 95% CI 0.01 to 2.45; 20 infants); neonatal composite adverse outcome (no events; 20 infants); gestational hypertension (RR 0.33, 95% CI 0.02 to 7.32; 20 women); or caesarean birth (RR 1.20, 95% CI 0.54 to 2.67; 20 women). Secondary outcomes For secondary outcomes assessed using GRADE no differences were observed: between a low-moderate and moderate-high GI diet for induction of labour (RR 0.88, 95% CI 0.33 to 2.34; one trial, 63 women; low-quality evidence); or an energy-restricted and no energy-restricted diet for induction of labour (RR 1.02, 95% CI 0.68 to 1.53; one trial, 114 women, low-quality evidence) and neonatal hypoglycaemia (average RR 1.06, 95% CI 0.48 to 2.32; two trials, 408 infants; very low-quality evidence).Few other clear differences were observed for reported outcomes. Longer-term health outcomes and health services use and costs were largely not reported.

Evidence from 19 trials assessing different types of dietary advice for women with GDM suggests no clear differences for primary outcomes and secondary outcomes assessed using GRADE, except for a possible reduction in caesarean section for women receiving a DASH diet compared with a control diet. Few differences were observed for secondary outcomes.Current evidence is limited by the small number of trials in each comparison, small sample sizes, and variable methodological quality. More evidence is needed to assess the effects of different types of dietary advice for women with GDM. Future trials should be adequately powered to evaluate short- and long-term outcomes.

IN BRIEF Restriction of dietary carbohydrate has been the cornerstone for treatment of gestational diabetes mellitus (GDM). However, there is evidence that a balanced liberalization of complex carbohydrate as part of an overall eating plan in GDM meets treatment goals and may mitigate maternal adipose tissue insulin resistance, both of which may promote optimal metabolic outcomes for mother and offspring.

Raman spectroscopy has previously been applied for studying lipid metabolism. In this study, a ball lens-installed hollow optical fiber Raman probe (BHRP) was used for the noninvasive measurement of skin lipids in hamsters. Our analysis suggested that multi-unsaturated lipids, once converted into a structure containing conjugated double bonds, were oxidized to form peroxides. These results were applied for analyzing lipid metabolism in adipose and skin tissues in hamsters fed tricaprin, saturated medium-chain triglyceride and trilinolein, unsaturated long-chain triglyceride fat diets. Unsaturated lipids formed conjugated structures in skin tissue but not in adipose tissue. Principal component analysis (PCA) revealed that the dietary fat intake correlated strongly with lipid composition in body and skin tissues. Hence, the present results successfully demonstrate that Raman spectroscopy with a BHRP can be a powerful tool for analyzing lipid metabolism.

Elucidating the optimal macronutrient composition for dietary management of gestational diabetes mellitus has enormous potential to improve perinatal outcomes. Diet therapy may result in significant cost savings if effective in deterring the need for expensive medical management within this growing population. In only 6 randomized controlled trials in 250 women, data suggest that a diet higher in complex carbohydrate and fiber, low in simple sugar, and lower in saturated fat may be effective in blunting postprandial hyperglycemia, preventing worsened insulin resistance and excess fetal growth. The use of diet in gestational diabetes mellitus remains an area in grave need for high-quality randomized controlled trials.

The conventional diet approach to gestational diabetes mellitus (GDM) advocates carbohydrate restriction, resulting in higher fat (HF), also a substrate for fetal fat accretion and associated with maternal insulin resistance. Consequently, there is no consensus about the ideal GDM diet. We hypothesized that, compared with a conventional, lower-carbohydrate/HF diet (40% carbohydrate/45% fat/15% protein), consumption of a higher-complex carbohydrate (HCC)/lower-fat (LF) Choosing Healthy Options in Carbohydrate Energy (CHOICE) diet (60/25/15%) would result in 24-h glucose area under the curve (AUC) profiles within therapeutic targets and lower postprandial lipids.

Using a randomized, crossover design, we provided 16 GDM women (BMI 34 ± 1 kg/m2) with two 3-day isocaloric diets at 31 ± 0.5 weeks (washout between diets) and performed continuous glucose monitoring. On day 4 of each diet, we determined postprandial (5 h) glucose, insulin, triglycerides (TGs), and free fatty acids (FFAs) following a controlled breakfast meal.

There were no between-diet differences for fasting or mean nocturnal glucose, but 24-h AUC was slightly higher (∼6%) on the HCC/LF CHOICE diet (P = 0.02). The continuous glucose monitoring system (CGMS) revealed modestly higher 1- and 2-h postprandial glucose on CHOICE (1 h, 115 ± 2 vs. 107 ± 3 mg/dL, P ≤ 0.01; 2 h, 106 ± 3 vs. 97 ± 3 mg/dL, P = 0.001) but well below current targets. After breakfast, 5-h glucose and insulin AUCs were slightly higher (P < 0.05), TG AUC was no different, but the FFA AUC was significantly lower (∼19%; P ≤ 0.01) on the CHOICE diet.

This highly controlled study randomizing isocaloric diets and using a CGMS is the first to show that liberalizing complex carbohydrates and reducing fat still achieved glycemia below current treatment targets and lower postprandial FFAs. This diet strategy may have important implications for preventing macrosomia.

Gestational diabetes mellitus (GDM) affects a significant number of women each year and is associated with a wide range of adverse outcomes for women and their babies. Dietary counselling is the main strategy in managing GDM, but it remains unclear which dietary therapy is best.

To assess the effects of different types of dietary advice for women with GDM on pregnancy outcomes.

We searched the Cochrane Pregnancy and Childbirth Group's Trials Register (17 May 2012) and the WOMBAT Perinatal Trials Registry (17 April 2012).

Randomised controlled trials (RCTs) and cluster-RCTs assessing the effects of different types of dietary advice for women with GDM on pregnancy outcomes.We intended to compare two or more forms of the same type of dietary advice against each other, i.e. standard dietary advice compared with individualised dietary advice, individual dietary education sessions compared with group dietary education sessions. We intended to compare different intensities of dietary intervention with each other, i.e. single dietary counselling session compared with multiple dietary counselling sessions.

Two review authors independently assessed study eligibility, extracted data and assessed risk of bias of included studies. Data were checked for accuracy.

We included nine trials; 429 women (436 babies) provided outcome data. All nine included trials had small sample sizes with variation in levels of risk of bias. A total of 11 different types of dietary advice were assessed under six different comparisons, including:low-moderate glycaemic index (GI) food versus high-moderate GI food, low-GI diet versus high-fibre moderate-GI diet, energy-restricted diet versus no energy restriction diet, low-carbohydrate diet (≤ 45% daily total energy intake from carbohydrate) versus high-carbohydrate diet (≥ 50% daily total energy intake from carbohydrate), high-monounsaturated fat diet (at least 20% total energy from monounsaturated fat) versus high-carbohydrate diet (at least 50% total energy from carbohydrate), standard-fibre diet (American Diabetes Association (ADA) diet) (20 grams fibre/day) versus fibre-enriched diet (80 grams fibre/day).In the low-moderate GI food versus moderate-high GI food comparison, no significant differences were seen for macrosomia or large-for-gestational age (LGA), (two trials, 89 babies) (risk ratio (RR) 0.45, 95% confidence interval (CI) 0.10 to 2.08), (RR 0.95, 95% CI 0.27 to 3.36), respectively; or caesarean section (RR 0.66, 95% CI 0.29 to 1.47, one trial, 63 women).In the low-GI diet versus high-fibre moderate-GI diet comparison, no significant differences were seen for macrosomia or LGA (one trial, 92 babies) (RR 0.32, 95% CI 0.03 to 2.96), (RR 2.87, 95% CI 0.61 to 13.50), respectively; or caesarean section (RR 1.80, 95% CI 0.66 to 4.94, one trial, 88 women).In the energy-restricted versus unrestricted diet comparison, no significant differences were seen for macrosomia (RR 1.56, 95% CI 0.61 to 3.94, one trial, 122 babies); LGA (RR 1.17, 95% CI 0.65 to 2.12, one trial, 123 babies); or caesarean section (RR 1.18, 95% CI 0.74 to 1.89, one trial, 121 women).In the low- versus high-carbohydrate diet comparison, none of the 30 babies in a single trial were macrosomic; and no significant differences in caesarean section rates were seen (RR 1.40, 95% CI 0.57 to 3.43, one trial, 30 women).In the high-monounsaturated fat versus high-carbohydrate diet comparison, neither macrosomia or LGA (one trial 27 babies) (RR 0.65, 95% CI 0.91 to 2.18), (RR 0.54 95% CI 0.21 to 1.37), respectively showed significant differences. Women having a high-monounsaturated fat diet had a significantly higher body mass index (BMI) at birth (mean difference (MD) 3.90 kg/m², 95% CI 2.41 to 5.39, one trial, 27 women) and at six to nine months postpartum (MD 4.10 kg/m², 95% CI 2.34 to 5.86, one trial, 27 women) when compared with those having a high-carbohydrate diet. However, these findings were based on a single, small RCT with baseline imbalance in maternal BMI.Perinatal mortality was reported in only trial which recorded no fetal deaths in either the energy- restricted or unrestricted diet group.A single trial comparing ADA diet (20 grams gram fibre/day) with fibre-enriched fibre enriched diet (80 grams gram fibre/day) did not report any of our prespecified primary outcomes.Very limited data were reported on the prespecified outcomes for each of the six comparisons. Only one trial reported on early postnatal outcomes. No trial reported long-term health outcomes for women and their babies. No data were reported on health service cost or women's quality of life.

Data for most comparisons were only available from single studies and they are too small for reliable conclusions about which types of dietary advice are the most suitable for women with GDM. Based on the current available evidence, we did not find any significant benefits of the diets investigated.Further larger trials with sufficient power to assess the effects of different diets for women with GDM on maternal and infant health outcomes are needed. Outcomes such as longer-term health outcomes for women and their babies, women's quality of life and health service cost should be included.

Gestational diabetes (GDM) affects 3% to 6% of all pregnancies. Women are often intensively managed with increased obstetric monitoring, dietary regulation, and insulin. However, there has been no sound evidence base to support intensive treatment. The key issue for clinicians and consumers is whether treatment of GDM improves perinatal outcome.

To compare the effect of alternative treatment policies for GDM on both maternal and infant outcomes.

We searched the Cochrane Pregnancy and Childbirth Group's Trials Register (January 2009) and bibliographies of relevant papers.

Randomised controlled trials comparing alternative management strategies for women with GDM and impaired glucose tolerance in pregnancy.

Two authors and a member of the Cochrane Pregnancy and Childbirth Group's editorial team extracted and checked data independently. Disagreements were resolved through discussion with the third author.

Eight randomised controlled trials (1418 women) were included.Caesarean section rate was not significantly different when comparing any specific treatment with routine antenatal care (ANC) including data from five trials with 1255 participants (risk ratio (RR) 0.94, 95% confidence interval (CI) 0.80 to 1.12). However, when comparing oral hypoglycaemics with insulin as treatment for GDM, there was a significant reduction (RR 0.46, 95% CI 0.27 to 0.77, two trials, 90 participants). There was a reduction in the risk of pre-eclampsia with intensive treatment (including dietary advice and insulin) compared to routine ANC (RR 0.65, 95% CI 0.48 to 0.88, one trial, 1000 participants). More women had their labours induced when given specific treatment compared to routine ANC (RR 1.33, 95% CI 1.13 to 1.57, two trials, 1068 participants). The composite outcome of perinatal morbidity (death, shoulder dystocia, bone fracture and nerve palsy) was significantly reduced for those receiving intensive treatment for mild GDM compared to routine ANC (RR 0.32, 95% CI 0.14 to 0.73, one trial, 1030 infants).There was a reduction in the proportion of infants weighing more than 4000 grams (RR 0.46, 95% CI 0.34 to 0.63, one trial, 1030 infants) and the proportion of infants weighing greater than the 90th birth centile (RR 0.55, 95% CI 0.30 to 0.99, three trials, 223 infants) of mothers receiving specific treatment for GDM compared to routine ANC. However, there was no statistically significant difference in this proportion between infants of mothers receiving oral drugs compared to insulin as treatment for GDM.

Specific treatment including dietary advice and insulin for mild GDM reduces the risk of maternal and perinatal morbidity. However, it is associated with higher risk of labour induction. More research is needed to assess the impact of different types of intensive treatment, including oral drugs and insulin, on individual short- and long-term infant outcomes.

The goals of medical nutrition therapy for gestational diabetes mellitus (GDM) are to meet the maternal and fetal nutritional needs, as well as to achieve and maintain optimal glycemic control. Nutrition requirements during pregnancy are similar for women with and without GDM. The American Diabetes Association and the American College of Obstetrics and Gynecology recommend nutrition therapy for GDM that emphasizes food choices to promote appropriate weight gain and normoglycemia without ketonuria, and moderate energy restriction for obese women. Current controversies in GDM nutrition therapy involve manipulation of dietary composition (amounts and types of carbohydrates and fats), gestational weight gain, and energy and carbohydrate restriction. Randomized controlled trials are needed to determine which dietary compositions and patterns promote normoglycemia as well as optimal maternal and infant outcomes. Until better evidence is available, nutrition therapy will remain a cornerstone of GDM management with potential benefits that cannot be fully realized in clinical practice.

Gestational diabetes (GD) develops because pregnancy increases requirements for insulin secretion while increasing insulin resistance. Women with GD often have impaired pancreatic beta-cell compensation for insulin resistance. The nature of GD is currently contentious, with debate about its existence, diagnosis and ramifications for both mother and offspring from pregnancy into later life. Also contentious are the outcomes of intervention with diet, insulin, glyburide (Glynase trade mark, Pharmacia Upjohn) and metformin (Glucophage trade mark, Bristol-Myers Squibb). There is consensus that women with unequivocal GD have a significant risk of adverse perinatal outcomes and increased risk of later type 2 diabetes mellitus. Foetuses from pregnancies with GD have a higher risk of macrosomia (associated with higher rate of birth injuries), asphyxia, and neonatal hypoglycaemia and hyperinsulinaemia. Uncontrolled GD predisposes foetuses to accelerated, excessive fat accumulation, insulin resistance, pancreatic exhaustion secondary to prenatal hyperglycaemia and possible higher risk of child and adult obesity and type 2 diabetes mellitus later in adult life. However, there is no consensus as to whether glucose intolerance of a severity below unequivocal GD is related to adverse maternal, fetal or perinatal outcomes, and whether this relationship is a continuous one. If dietary intervention is not sufficient in the treatment of GD, then, historically, insulin has been added. Recent studies suggest that glyburide may be efficaciously substituted for insulin. Preliminary studies suggest that metformin may have the unique potential to prevent the development of GD.

Gestational diabetes (GDM) is the commonest metabolic disorder of pregnancy. Most women with GDM are treated with nutritional management alone. There are conflicting guidelines surrounding its dietary management and this has resulted in a lack of conformity to the dietary advice currently prescribed. There is also conflicting opinions to the effectiveness of dietary management of GDM on pregnancy outcomes. The aim of this review was to examine the scientific evidence for the optimal nutritional management of GDM.

A Medline search of all English papers published between 1995 and 2001 that cross-referenced GDM with diet was under taken. Because of the poor quality of many of these papers, literature prior to 1995 known to the authors and considered relevant to the review were also included.

The evidence base in this area is of poor quality. One systematic review based on randomized control trials failed to show any benefit from dietary intervention in GDM. However, that review did not include informative clinical and observational studies that are not classified as randomized controlled trials. Overall current evidence points to the effectiveness of dietary advice as a means of improving maternal hyperglycaemia and reducing the risk of accelerated foetal growth. The evidence surrounding energy restriction, carbohydrate and fat manipulation in GDM remains controversial.

Current but limited evidence supports dietary alterations to reduce rates of accelerated foetal growth. There is a clear need for good quality randomized control trials in this area.