Gestational Diabetes — Symptoms, Causes & Treatment | MyMedicPlus

Gestational diabetes mellitus (GDM) is a form of glucose intolerance first recognised or diagnosed during pregnancy, resulting from inadequate pancreatic beta-cell compensation for the physiological insulin resistance induced by placental hormones (human placental lactogen, progesterone, cortisol, and growth hormone). GDM affects approximately 7–14% of pregnancies globally — equivalent to 18 million pregnancies annually — with prevalence rising in parallel with the global obesity epidemic and increasing maternal age. Using the WHO 2013 diagnostic criteria (fasting glucose at or above 5.1 mmol/L or 2-hour post-OGTT glucose at or above 8.5 mmol/L), prevalence reaches 25% in some high-risk populations. GDM typically manifests in the second or third trimester and resolves after delivery in the majority of women, but carries significant risks for both mother and baby if poorly controlled — including macrosomia, birth trauma, neonatal hypoglycaemia, and preeclampsia. Critically, GDM is a powerful metabolic marker: affected women have a 7-fold increased lifetime risk of developing type 2 diabetes (50% cumulative risk over 10 years), and their offspring have increased risk of childhood obesity and metabolic syndrome.

During normal pregnancy, placental hormones — human placental lactogen (hPL), progesterone, cortisol, and placental growth hormone — progressively induce physiological insulin resistance in peripheral tissues (muscle, adipose) to ensure a constant glucose supply to the fetus across the placenta. The magnitude of this insulin resistance increases exponentially in the second and third trimesters. In the majority of pregnant women, the pancreatic beta cells compensate by increasing insulin secretion 2–3-fold. In women with pre-existing marginal beta-cell reserve (from prior subclinical beta-cell loss, genetic polymorphisms in KCNJ11, TCF7L2, or other type 2 diabetes risk genes, or chronic low-grade inflammation from obesity), this compensatory response is insufficient and hyperglycaemia ensues. Obesity (BMI above 25 kg/m²) is the single strongest modifiable risk factor — present in 50–70% of GDM cases; visceral adiposity drives insulin resistance through elevated free fatty acid levels and adipokine dysregulation. Additional risk factors: advanced maternal age (above 35 years — progressive beta-cell function decline); family history of type 2 diabetes (first-degree relative — 2–4-fold increased risk); prior GDM (recurrence risk 30–70% in subsequent pregnancies); prior macrosomic infant (birthweight above 4 kg or above 4.5 kg); polycystic ovary syndrome (PCOS — characterised by hyperinsulinaemia and insulin resistance — 3-fold elevated GDM risk); South Asian, Middle Eastern, Hispanic, or Afro-Caribbean ethnic origin (elevated type 2 diabetes susceptibility); and multiple gestation (higher placental mass means greater placental hormone output). Glucocorticoid therapy during pregnancy (e.g., for asthma or threatened preterm labour) markedly aggravates insulin resistance and may precipitate or worsen GDM.

Gestational diabetes mellitus (GDM) is characteristically asymptomatic in the mother — maternal glycaemia at the levels meeting GDM diagnostic thresholds rarely causes the classic osmotic symptoms of established diabetes. This is why universal screening with oral glucose tolerance testing at 24–28 weeks is essential rather than symptom-driven testing. When maternal hyperglycaemia is more severe (fasting glucose above 7.0 mmol/L or post-challenge glucose above 11.1 mmol/L, approaching the diagnostic threshold for pre-existing type 2 diabetes diagnosed in pregnancy), symptoms may occasionally be present: polydipsia (increased thirst from osmotic fluid shift); polyuria (increased urination from glucosuria when renal glucose threshold is exceeded); and fatigue (from impaired glucose utilisation). Clinical and ultrasound findings rather than maternal symptoms often alert clinicians: fetal macrosomia (estimated fetal weight above 90th centile for gestational age on third trimester ultrasound biometry — abdominal circumference above the 90th percentile is the most sensitive sign of fetal overgrowth); polyhydramnios (excessive amniotic fluid — amniotic fluid index above 25 cm — from fetal polyuria in response to hyperglycaemia and fetal hyperinsulinaemia, increasing perinatal morbidity from cord prolapse and preterm labour). Neonatal signs of untreated GDM: neonatal hypoglycaemia (within 2 hours of delivery, from neonatal hyperinsulinaemia persisting after cord cutting — glucose below 2.6 mmol/L requiring dextrose feeds or IV glucose); macrosomia and cushingoid features (fat accumulation from fetal hyperinsulinaemia); polycythaemia; respiratory distress syndrome (surfactant production impaired by insulin); and neonatal jaundice.

Universal screening with oral glucose tolerance testing (OGTT) is recommended between 24–28 weeks gestation in all pregnant women not previously diagnosed with diabetes — this timing reflects the peak of placental insulin-antagonist hormone production. The standard 75-gram OGTT protocol: the patient consumes 75 g of anhydrous glucose dissolved in 200–300 mL water after an overnight fast (minimum 8 hours); venous plasma glucose is measured fasting, at 1 hour, and at 2 hours. WHO 2013 / IADPSG diagnostic thresholds (adopted by the NHS, Australia, most of Europe, and Asia): GDM is diagnosed if any single value meets or exceeds: fasting glucose at or above 5.1 mmol/L (92 mg/dL) — note that this threshold is lower than the normal non-pregnant fasting glucose threshold of 6.1 mmol/L; 1-hour glucose at or above 10.0 mmol/L (180 mg/dL); 2-hour glucose at or above 8.5 mmol/L (153 mg/dL). A fasting venous plasma glucose at or above 7.0 mmol/L on any occasion during pregnancy (or random glucose above 11.1 mmol/L with symptoms) indicates pre-existing (overt) diabetes diagnosed in pregnancy rather than GDM — these women require more intensive management. High-risk women (previous GDM, BMI above 30, prior macrosomic infant, ethnic high-risk groups, first-degree family history) should have early glucose testing (OGTT or fasting glucose) at the first antenatal booking appointment (typically 8–12 weeks) to detect undiagnosed pre-existing type 2 diabetes; if negative, they repeat the OGTT at 24–28 weeks. HbA1c in early pregnancy (above 48 mmol/mol/6.5% — overt diabetes; 39–47 mmol/mol — pre-diabetes; below 39 mmol/mol — reassuring but does not exclude GDM developing later) is used alongside fasting glucose for early risk stratification. Continuous glucose monitoring (CGM) is increasingly used in GDM management — the target time in range (70–140 mg/dL / 3.9–7.8 mmol/L) above 70% correlates with reduced macrosomia risk.

First-line treatment is structured medical nutrition therapy (MNT) guided by a registered dietitian: total daily carbohydrate intake controlled at 175 g/day (the minimum required to prevent ketosis during pregnancy), distributed across 3 main meals and 2–3 snacks; emphasising low glycaemic index (GI) complex carbohydrates (oats, legumes, sweet potato, wholegrain bread), lean protein, and monounsaturated fats; eliminating concentrated sugars (fruit juices, confectionery, white bread, processed breakfast cereals); and ensuring adequate fibre intake. Regular moderate physical activity (30 minutes brisk walking or other aerobic activity daily, unless obstetric contraindication) enhances insulin sensitivity and reduces post-prandial glucose peaks by 2–3 mmol/L. Capillary blood glucose self-monitoring (SMBG) guides management: targets are fasting capillary glucose below 5.3 mmol/L (95 mg/dL) and 1-hour post-meal below 7.8 mmol/L (140 mg/dL), or 2-hour post-meal below 6.7 mmol/L (120 mg/dL). Pharmacotherapy is initiated when blood glucose targets are not achieved within 1–2 weeks of MNT (approximately 30–40% of GDM patients require pharmacotherapy): Metformin (1,000–2,500 mg/day in divided doses with meals): first-line oral agent — reduces hepatic glucose production and improves peripheral insulin sensitivity; crosses the placenta (long-term offspring follow-up ongoing); avoids injections; reduces the dose of insulin required if combination therapy is needed. Insulin therapy: the most effective pharmacological treatment and the only option when glucose is markedly elevated at diagnosis; intermediate-acting insulin (NPH — isophane) at bedtime for fasting hyperglycaemia; rapid-acting insulin analogs (insulin aspart/Novorapid — the only rapid-acting insulin approved for use in pregnancy) at meal-time for post-prandial spikes; total daily insulin dose typically 0.5–1.0 units/kg body weight in the third trimester. Glibenclamide (glyburide) is used in some countries (USA, Australia) but is not recommended by NICE or the UK due to concerns regarding neonatal hypoglycaemia and inadequate glycaemic control compared to insulin.

Maternal complications include preeclampsia, cesarean section (due to macrosomia and labor complications), and 50% lifetime risk of type 2 diabetes. Fetal complications include macrosomia (birth weight over 4 kg), shoulder dystocia, birth trauma, and neonatal hypoglycemia requiring immediate monitoring and feeding in the newborn. Intrauterine fetal demise risk is elevated in severe, poorly controlled GDM. Long-term, children of mothers with GDM have increased risk of obesity and type 2 diabetes in childhood and adult life, reflecting in utero metabolic programming.

Achieve a healthy pre-pregnancy weight — each 5 kg/m² increase in BMI increases GDM risk by approximately 60%. Regular physical activity before and during pregnancy reduces GDM incidence. Limit weight gain in pregnancy to within IOM guidelines (11–16 kg for normal weight women). All women with a history of GDM should have a 75g OGTT at 6–12 weeks postpartum to screen for type 2 diabetes, then fasting glucose or HbA1c annually. Breastfeeding reduces both maternal and child risk of future type 2 diabetes. Metformin may reduce GDM recurrence in high-risk women in subsequent pregnancies.

Pregnant women should be screened for gestational diabetes at 24-28 weeks via the oral glucose tolerance test (OGTT) if they have any risk factors: BMI above 30, previous GDM, previous macrosomic baby (above 4.5 kg), family history of type 2 diabetes, or South Asian, Black, Middle Eastern, or minority ethnic background. Contact your midwife or obstetric team promptly for: blood glucose readings consistently above target despite dietary modification; difficulty understanding or performing blood glucose monitoring; or feeling unwell while managing GDM. Seek emergency obstetric care for: significantly elevated blood glucose (above 15-20 mmol/L) with symptoms of nausea, vomiting, and abdominal pain (possible diabetic ketoacidosis — rare but life-threatening in pregnancy); and reduced foetal movements after 28 weeks (contact maternity triage immediately). All women with GDM should have a 75g OGTT at 6-13 weeks postnatal to screen for persistent type 2 diabetes — as GDM confers 7-fold increased lifetime risk of type 2 diabetes.