Gestational diabetes mellitus, commonly abbreviated GDM, is diabetes or clinically significant hyperglycaemia first recognised during pregnancy that does not clearly represent overt diabetes existing before pregnancy. It occurs because pregnancy naturally increases insulin resistance, particularly as placental hormones alter maternal metabolism to support fetal nutrient supply. Most pregnant people compensate by increasing insulin production, but some cannot produce enough insulin to meet the increased requirement. Blood glucose then rises.
GDM is most common during the second and third trimesters, although abnormal glucose metabolism can be detected earlier. It is distinct from pre-existing type 1 or type 2 diabetes that happens to be present during pregnancy. The NHS describes GDM as high blood glucose developing during pregnancy and notes that it usually disappears after birth.
Pregnancy causes progressive physiological changes in glucose metabolism. Placental hormones, including human placental lactogen and other endocrine signals, contribute to increased maternal insulin resistance. This adaptation helps ensure an adequate nutrient supply for the developing fetus, but it also increases the workload placed on pancreatic beta cells. If insulin secretion cannot increase sufficiently, maternal glucose rises. This is therefore not simply a condition caused by eating sugary foods during pregnancy.
Dietary quality and physical activity influence glucose control, but the fundamental mechanism is pregnancy-induced insulin resistance combined with inadequate beta-cell compensation. Risk factors include previous gestational diabetes, obesity, older maternal age, a previous large baby and a close family history of diabetes. Some people without obvious risk factors nevertheless develop GDM, which is why screening strategies are used.
Gestational diabetes can affect both the pregnant person and fetus because maternal glucose crosses the placenta while maternal insulin does not cross it in the same way. When maternal glucose is elevated, more glucose reaches the fetus, stimulating fetal pancreatic insulin production. Fetal hyperinsulinaemia promotes growth and can contribute to a larger-than-average baby, known as macrosomia. Increased fetal size can complicate labour and increase the likelihood of assisted delivery, induction or caesarean birth.
GDM is also associated with maternal complications such as pre-eclampsia and with neonatal problems including hypoglycaemia after birth. The degree of risk increases with maternal glycaemia, and the large HAPO study demonstrated continuous relationships between maternal glucose and several adverse pregnancy and neonatal outcomes. Appropriate diagnosis and management therefore aim to reduce exposure to excessive maternal glucose rather than merely treat symptoms.
Screening for gestational diabetes varies internationally because different professional bodies use different diagnostic strategies. Current ADA guidance recommends screening for GDM at 24–28 weeks of gestation in people not previously found to have diabetes or high-risk abnormal glucose metabolism. One recognised strategy uses a 75-g oral glucose tolerance test with fasting, one-hour and two-hour plasma glucose measurements.
Under the one-step criteria cited by the ADA, GDM is diagnosed when any of the following is met or exceeded: fasting 5.1 mmol/L, one-hour 10.0 mmol/L or two-hour 8.5 mmol/L. A two-step strategy begins with a non-fasting 50-g glucose challenge and, if positive, proceeds to a fasting 100-g oral glucose tolerance test; criteria such as the Carpenter-Coustan thresholds may then require two abnormal values. Differences between criteria mean that prevalence estimates can vary according to the diagnostic system used.
Treatment aims to keep maternal glucose within pregnancy-specific targets while supporting normal fetal growth and maternal health. Initial management commonly involves dietary advice, appropriate physical activity and self-monitoring of blood glucose. The NHS recommends regular meals, emphasis on healthier carbohydrate choices, vegetables and other nutritious foods, and avoidance of sugary drinks, while physical activity can improve glucose control when medically appropriate. If glucose remains above target despite these measures, medication may be required.
Depending on clinical circumstances and local practice, this can include metformin or insulin. Pregnancy alters insulin requirements over time, so treatment may need adjustment as gestation progresses. The NHS notes that people receiving insulin may require increasing doses as pregnancy advances because blood glucose can rise with increasing insulin resistance.
Pregnancy-specific glucose targets are generally stricter than ordinary diabetes targets because maternal hyperglycaemia has consequences for fetal development and neonatal health. ADA guidance gives goals for diabetes in pregnancy of fasting glucose 3.9–5.3 mmol/L, one-hour post-meal glucose 6.1–7.8 mmol/L and two-hour post-meal glucose 5.6–6.7 mmol/L for type 1 or type 2 diabetes and insulin-treated GDM, with corresponding upper limits for GDM not treated with insulin.
Exact targets can differ according to guideline and clinical circumstances, and the aim is to achieve them without significant hypoglycaemia. People with GDM are commonly given a glucose meter and instructed to test at specified times, often before breakfast and after meals. Continuous glucose monitoring may be appropriate in selected pregnancies, particularly for people using insulin or with type 1 diabetes.
Gestational diabetes usually improves rapidly after delivery because the placenta, which produces many of the hormones driving pregnancy-related insulin resistance, is no longer present. Nevertheless, it is not equivalent to having no future metabolic risk. People who have had GDM have a substantially increased risk of developing type 2 diabetes later and are also more likely to experience GDM in a future pregnancy.
The NHS recommends a blood test approximately 6–13 weeks after birth and, if that result is normal, annual diabetes testing. This follow-up matters because persistent hyperglycaemia after pregnancy may indicate previously unrecognised type 2 diabetes or another form of diabetes rather than resolved GDM. Children of people who have had GDM may also have increased long-term metabolic risk.
Gestational diabetes should be distinguished from ordinary temporary glucose changes during pregnancy and from overt diabetes diagnosed during pregnancy. Pregnancy itself changes glucose metabolism, but clinically significant abnormalities are assessed using defined laboratory thresholds. If a pregnant person meets standard diagnostic criteria for overt diabetes early in pregnancy, the condition is generally classified as diabetes complicating pregnancy rather than ordinary GDM.
This distinction matters because established type 1 or type 2 diabetes may require treatment immediately and carries different pre-pregnancy and pregnancy-management considerations. GDM also should not be interpreted as a moral or behavioural failure. Its development reflects a combination of placental physiology, pancreatic reserve, genetics, previous metabolic status and risk factors. Appropriate management can substantially reduce pregnancy complications, and most people with GDM have healthy pregnancies and babies when glucose and obstetric care are appropriately monitored.
