Gestational Diabetes — Causes, Symptoms & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Gestational diabetes mellitus (GDM) is defined as glucose intolerance first diagnosed or first onset during pregnancy, typically detected at 24–28 weeks of gestation. It affects approximately 14% of pregnancies worldwide — approximately 21 million births annually — and is rising in prevalence parallel to global obesity rates. GDM results from insulin resistance induced by placental hormones (human placental lactogen, progesterone, cortisol), which cannot be compensated by increased pancreatic insulin secretion in susceptible women. Unlike pre-existing type 1 or type 2 diabetes, GDM resolves after delivery in most women. However, it is associated with significant risks during pregnancy (preeclampsia, macrosomia, Caesarean section) and long-term risks — 50% of women with GDM develop type 2 diabetes within 10 years. Neonates born to mothers with GDM are at increased risk of neonatal hypoglycaemia, macrosomia, shoulder dystocia, respiratory distress, and polycythaemia, making optimal glucose control during pregnancy essential for both maternal and fetal health.

GDM develops when the normal insulin resistance of mid-to-late pregnancy (driven by placental hormones — human placental lactogen, progesterone, oestrogen, and cortisol) cannot be overcome by compensatory insulin secretion. Women with underlying insulin resistance are most susceptible. Major risk factors: pre-pregnancy overweight or obesity (BMI ≥25 — most significant risk factor, 2–4 fold increased risk); age >35; family history of type 2 diabetes (first-degree relative); prior GDM in a previous pregnancy (50% recurrence risk); previous macrosomic baby (>4 kg); polycystic ovary syndrome (PCOS); ethnicity (South Asian, Middle Eastern, Black African, Hispanic, and Pacific Islander — 2–3 times higher risk compared to White European); glucocorticoid therapy during pregnancy; and sedentary lifestyle. Lean women without these risk factors can still develop GDM.

Most women with GDM are asymptomatic — it is a laboratory diagnosis identified through universal or risk-based screening at 24–28 weeks. When blood glucose is very high, symptoms may include: increased thirst (polydipsia), frequent urination (polyuria — difficult to distinguish from normal pregnancy symptoms), unusual fatigue, and blurred vision. These are often absent or attributed to pregnancy. GDM is therefore predominantly a condition that must be actively sought through screening rather than clinical presentation. Obstetric clues suggesting uncontrolled GDM: polyhydramnios (excess amniotic fluid) on ultrasound, macrosomia (large-for-dates fetus on growth scans), and glycosuria on urine dipstick (though glycosuria is common in normal pregnancy due to reduced renal glucose threshold).

NICE guideline (UK): women with ≥1 risk factor are offered a 75 g oral glucose tolerance test (OGTT) at 24–28 weeks. GDM diagnosed if fasting glucose ≥5.6 mmol/L (100 mg/dL) or 2-hour glucose ≥7.8 mmol/L (140 mg/dL). Women with prior GDM or BMI ≥40 are offered earlier OGTT at 16–18 weeks. WHO diagnostic criteria (used internationally): fasting ≥5.1 mmol/L (92 mg/dL) or 1-hour ≥10.0 mmol/L (180 mg/dL) or 2-hour ≥8.5 mmol/L (153 mg/dL). OGTT diagnostic thresholds vary by country and guideline — clinicians should apply local criteria. HbA1c is not reliable for GDM diagnosis due to haemodilution and increased red cell turnover in pregnancy. A fasting glucose ≥7.0 mmol/L or random ≥11.1 mmol/L with symptoms indicates pre-existing diabetes requiring immediate referral.

Medical nutrition therapy (MNT) is the cornerstone: carbohydrate-controlled diet (40–45% of calories from low-glycaemic index carbohydrates), distributing carbohydrates across 3 meals and 2–3 snacks, with increased protein and healthy fat. A registered dietitian is essential. Physical activity — 30 minutes of moderate exercise (walking, swimming) on most days — improves insulin sensitivity. Self-monitoring blood glucose (SMBG): fasting target <5.3 mmol/L (95 mg/dL); 1-hour post-meal <7.8 mmol/L (140 mg/dL); 2-hour post-meal <6.7 mmol/L (120 mg/dL). If glucose targets are not met with lifestyle changes after 1–2 weeks: pharmacological therapy. Metformin is used widely for GDM (off-label but NICE-recommended as first-line oral option — MFMU network study showed non-inferiority to insulin; however, 50% of women still require supplemental insulin). Insulin therapy: NPH insulin (intermediate-acting) or insulin detemir for fasting hyperglycaemia; rapid-acting insulin (aspart, lispro — safe in pregnancy) for post-meal spikes. Glibenclamide (glyburide) is an alternative but has higher neonatal hypoglycaemia risk. Obstetric monitoring: growth scans every 4 weeks, fetal wellbeing assessment (CTG from 36–38 weeks in well-controlled GDM).

Macrosomia (fetal birthweight above 4 kg or above the 90th centile for gestational age) is the primary fetal complication of poorly controlled GDM — occurring in 15–45% of GDM pregnancies versus 10% in euglycaemic controls. Macrosomia causes obstetric complications: shoulder dystocia (head delivers but shoulders are impacted — emergency requiring specific manoeuvres; risk of brachial plexus injury and hypoxic brain injury), Erb's palsy, clavicle and humerus fractures, fetal distress, and perinatal asphyxia. Neonatal hypoglycaemia (blood glucose below 2.6 mmol/L) in the first hours after birth from fetal hyperinsulinism (the fetus adapts to maternal hyperglycaemia by producing excess insulin — which persists briefly after delivery when the glucose supply stops) requires immediate feeding and monitoring in neonatal units; severe neonatal hypoglycaemia causes permanent neurological damage. Preeclampsia affects 10–15% of GDM pregnancies versus 5% in the general obstetric population — a twofold increased risk. Caesarean section rates are significantly elevated in GDM from macrosomia and fetal distress. Stillbirth risk is elevated in severe, poorly controlled GDM. Maternal long-term complications: GDM confers a 7-fold lifetime increased risk of type 2 diabetes (50% cumulative risk at 10 years); recurrence risk in subsequent pregnancies is 30–70%; cardiovascular disease risk is increased 2-fold. Offspring of mothers with GDM have significantly increased risk of childhood obesity, metabolic syndrome, and type 2 diabetes — representing intergenerational transmission of metabolic risk.

Pre-conception: achieve and maintain healthy BMI before pregnancy — a 5–10% weight reduction in overweight women significantly reduces GDM risk. Regular physical activity before and during pregnancy is protective. Mediterranean and low-glycaemic-index diets before pregnancy reduce GDM risk. During pregnancy: consume a balanced, low-glycaemic diet with moderate carbohydrate restriction. Moderate-intensity exercise (walking, swimming, yoga) most days of the week reduces GDM incidence by 30–35% in high-risk women. Inositol supplements (myo-inositol) have shown modest benefit in reducing GDM incidence in PCOS patients. After delivery: all women with GDM should have a fasting glucose or 75g OGTT at 6–12 weeks postpartum to detect persistent diabetes; annual HbA1c thereafter — 50% develop type 2 diabetes within 10 years without lifestyle intervention. Breastfeeding reduces both maternal and offspring diabetes risk.

Seek urgent obstetric care if during pregnancy you experience: severe headache with visual disturbances (preeclampsia signs — GDM increases preeclampsia risk 2–3 fold), sudden facial or leg swelling, reduced fetal movements, or symptoms of hypoglycaemia (shakiness, sweating, confusion — especially if you take insulin). Contact your diabetes midwife or antenatal team same-day if: your blood glucose readings are consistently above target despite diet changes; you are not sure how to use your glucose monitor; or you develop severe nausea/vomiting preventing food intake (hypoglycaemia risk if taking insulin). All pregnant women at risk should attend their 24–28 week OGTT appointment — early diagnosis and treatment significantly reduces complications for mother and baby.