Understanding gestational diabetes: causes and care

Gestational diabetes is a form of diabetes mellitus that appears for the first time in the 2nd or 3rd trimester of pregnancy [1]. Your body produces insulin, but the hormones secreted by the placenta partially block its action. When your pancreas cannot produce enough insulin to compensate for this increased resistance, your blood glucose rises above normal values [2].

The process develops gradually, as the placenta grows and releases ever larger amounts of diabetogenic hormones, that is, hormones that raise blood glucose [1]. Factors such as excess weight before pregnancy, being over 35 years of age, and a family history of type 2 diabetes increase the risk of developing this condition. However, gestational diabetes can also occur in women without obvious risk factors.

Gestational diabetes differs fundamentally from the other types through its temporary cause, which is specific to pregnancy [2]. In type 1 diabetes, the immune system destroys the insulin-producing cells, and this destruction is permanent. In type 2 diabetes, the body becomes resistant to insulin over several years because of lifestyle and genetic predisposition.

In gestational diabetes, insulin resistance is caused by placental hormones and usually disappears after birth [1]. It is not an autoimmune disease, nor does it involve the destruction of the pancreatic beta cells, that is, the cells in the pancreas that produce insulin. Treatment is generally needed only during pregnancy, although the risk of later developing type 2 diabetes remains increased, as the figure below shows [3].

Before pregnancy, your pancreas produced enough insulin for your body's needs. There were no placental hormones interfering with the action of insulin. Your body maintained a balance between insulin production and the glucose requirements of your cells [4].

Pregnancy asks your body for more energy and changes the way your body uses glucose. Placental hormones progressively increase insulin resistance, and the pancreas must double or even triple its insulin production [1]. If this adaptive capacity is exceeded, hyperglycemia appears, that is, gestational diabetes.

Gestational diabetes is by definition a temporary condition, which resolves in most cases after birth [2]. When the placenta is delivered, the hormones responsible for insulin resistance disappear rapidly [1]. Blood glucose usually returns to normal values within the first hours or days after birth.

However, temporary does not mean without long-term consequences. Women with a history of gestational diabetes remain at risk of type 2 diabetes. Between 30% and 50% of them develop type 2 diabetes within the next 15-20 years, and the lifetime risk can reach up to 60% [3]. That is why blood glucose monitoring after birth and adopting a healthy lifestyle are essential for preventing type 2 diabetes.

Gestational diabetes most often appears in the second trimester, usually between weeks 24 and 28 of pregnancy [2]. This is the period when the placenta reaches a size large enough to produce significant amounts of diabetogenic hormones. That is precisely why the glucose tolerance test (OGTT) is carried out in this interval [3].

In the third trimester, insulin resistance continues to rise, at a slower pace, and reaches its peak in weeks 32-36 [1]. Some cases of gestational diabetes are diagnosed later, if the standard screening was negative but the risk factors persist and express themselves later on. A blood glucose level in the diabetes range, found as early as the first trimester, in most cases means pre-existing diabetes that went undetected before pregnancy, not one brought on by the pregnancy.

Gestational diabetes affects between 10% and 14% of pregnancies worldwide, with variations depending on the population studied and the diagnostic criteria used [5]. Prevalence varies significantly between regions, being higher in the Middle East, North Africa, and Southeast Asia [2]. For you, this figure means that the glucose tolerance test in weeks 24-28 is part of routine pregnancy care, not a measure reserved for women at risk.

Over recent decades, the incidence of gestational diabetes has risen steadily, in parallel with the global obesity epidemic [2]. Lifestyle changes, more advanced maternal age, and the rising prevalence of obesity all contribute to this trend. The standardization of the diagnostic criteria proposed by the IADPSG (an international group of experts in diabetes and pregnancy) has allowed a more accurate global estimate of this condition [5].

Several hormones secreted by the placenta interfere with the action of insulin [4]. Human placental lactogen (hPL) plays the leading role: it increases insulin resistance because it activates lipolysis, that is, the breakdown of stored fat, and sends free fatty acids into the bloodstream [1]. Progesterone and estrogen also contribute to reducing the tissues' sensitivity to insulin.

Cortisol, the hormone produced by the adrenal glands, also rises in pregnancy and amplifies insulin resistance by acting on the glucocorticoid receptors, that is, the sites on cells through which it exerts its effect [6]. Placental growth hormone and leptin round out this complex hormonal picture, which puts pressure on the pancreas's capacity to secrete insulin [4].

Yes, gestational diabetes can theoretically occur in any pregnancy, including in women without apparent risk factors. However, the risk is significantly higher if you had gestational diabetes in a previous pregnancy [7]. Between 30% and 50% of affected women will develop gestational diabetes again in a later pregnancy, with higher rates in high-risk populations [8].

Other factors that increase the likelihood include excess weight, being over 35 years of age, a family history of type 2 diabetes, and polycystic ovary syndrome [3]. The fact that you had a pregnancy without gestational diabetes does not guarantee that the next pregnancies will be the same. Each pregnancy must be monitored individually, and blood glucose testing remains mandatory.

The placenta influences glucose metabolism in order to ensure a continuous supply of nutrients to the fetus [6]. The fetus depends exclusively on maternal glucose for its growth and development, as it cannot produce what it needs on its own. By increasing the mother's insulin resistance, the placenta directs more glucose toward the fetal circulation [4].

This mechanism is an evolutionary adaptation that works well as long as the maternal pancreas is able to compensate [6]. The placenta acts as a complex endocrine organ, secreting hormones that reconfigure the mother's metabolism. When this reconfiguration exceeds the mother's adaptive capacity, the result is gestational diabetes [1].

After the placenta is delivered, the hormones responsible for insulin resistance disappear rapidly from the circulation [1]. In most cases blood glucose returns to normal within the first hours or days after birth. Treatment with insulin or oral antidiabetic medication is usually stopped immediately after birth; the timing and the decision, though, rest with your medical team, which continues to monitor your blood glucose [2].

However, it is essential to undergo a glucose tolerance test 4-12 weeks after birth, to confirm that the problem has resolved [3]. The risk of developing type 2 diabetes remains increased over the long term, which is why a long-term annual check-up is recommended. Breastfeeding, maintaining a normal weight, and regular physical activity can significantly reduce the risk of developing type 2 diabetes in a mother with a history of gestational diabetes [9].