Gestational diabetes mellitus (GDM) is a serious complication from pregnancy, in which women without previously diagnosed diabetes develop chronically elevated blood sugar during gestation. While GDM usually resolves following delivery, it can have long-term health implications, including increased risk for type 2 diabetes (T2DM) and cardiovascular disease (CVD) in the mother, and future obesity, cardiovascular disease, T2DM, and GDM in the child. This contributes to a vicious intergenerational cycle of obesity and diabetes that impacts the health of the while populations.[2,3]
Risk factors of GDM include obesity, standard American diet, nutrient imbalances, a family history of insulin resistance or diabetes, excessive weight gain during gestation, ethnicity (more common in African American, indigenous Latin American, Indian population), advanced maternal age, intrauterine environment (low or high birth weight), family or personal history of GDM, and other diseases associated with insulin resistance such as polycystic ovarian syndrome (PCOS).
GDM is usually the result of pancreatic β-cell dysfunction induced by chronic insulin resistance during pregnancy. Both β-cell impairment and tissue insulin resistance represent critical components of its pathophysiology. In most cases, these impairments exist prior to pregnancy and can be progressive, indicating an increased risk of T2DM post-pregnancy.[2,3] Here are the key causes of GDM:
The primary function of pancreatic β-cells is to store and secrete insulin in response to a glucose load. When β-cells lose the ability to effectively sense blood glucose concentration or release sufficient insulin in response, this is defined as β-cell dysfunction.[1,2]
On the other hand, insulin resistance can occur when cells no longer adequately respond to insulin. At this molecular level, insulin resistance is usually a failure of insulin signaling to the cell insulin receptors, resulting in challenges to uptake glucose into the cells to produce energy. The rate of insulin-stimulated glucose uptake is reduced by 54% in GDM when compared with normal pregnancy.
Several other factors also play a role, including hormones such as adiponectin and leptin, adipose tissue, liver, gut microbiome, muscle, placenta transport, and oxidative stress in cells.
During pregnancy, the mother’s body undergoes a series of significant physiological changes to support the demands of the growing fetus. Among these changes, one crucial metabolic adaptation is insulin sensitivity. During gestation, insulin sensitivity shifts over time. In early pregnancy, insulin sensitivity increases, promoting glucose uptake into adipose stores for the upcoming energy demands of later pregnancy. However, as pregnancy progresses, a surge of local and placental hormones, including estrogen, progesterone, leptin, cortisol, placental lactogen, and placental growth hormone, promote a state of insulin resistance. As a result, blood glucose is mildly elevated and readily transported across the placenta to fuel the fetus's growth. This state of insulin resistance promotes endogenous glucose production and the breakdown of fat stores, resulting in a further increase in blood glucose and free fatty acid concentrations. This is why GDM is diagnosed most often in the 2nd or 3rd trimester of pregnancy.[2,3]
THE IMPACT of GDM to FETUS:
Extra glucose from the mother crosses the fetal placenta, and the fetus pancreas responds by releasing extra insulin to cope with the excess glucose. The excess glucose is then converted to fat, resulting in an increase in the baby’s size, possibly leading to cesarean delivery. After the birth, the extra glucose is no longer available. Until the baby’s pancreas can adjust, the baby may require extra glucose through intravenous feedings for a day or two to keep the baby’s blood glucose regular.
Considering fetal development and its contribution as one of the evolutionary origins of human diseases, it is imperative to improve pregnant women's glucose metabolism. Nutritional management is the primary therapy for GDM. It is estimated that 70-80% of the cases could only be controlled by changing lifestyles. Here are some of the dietary recommendations and considerations for GDM prevention and management:
The recommended daily energy intake of macronutrients is 33-40% complex carbohydrates, 35-40% fat, and 20% protein. Clinical studies show that this ratio improved insulin function and metabolism status in obese diabetic patients.
Glycemic Index (GI) & Glycemic Load (GL) of Carbohydrates:
Not all carbs are created equal! GI refers to blood sugar spikes following the intake of certain carbohydrate-containing foods. Foods low on the GI scale tend to release glucose slowly and steadily, and ones high on the scale release glucose rapidly.
GL is based on GI but represents both the quant