Instructions
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Learning Objectives Upon completion of this course the participant should be able to: 1. Describe three ways gestational diabetes can be treated. 2. List at least two risks gestational diabetes presents for the baby. 3. List two things a pregnant woman can do pre-pregnancy to prevent gestational diabetes.
This course assumes you have a basic knowledge of gestational diabetes mellitus, or GDM--and some of the terms associated with it. But we will take a little time to review some background information to assure that the rest of the material is understood properly.
Let’s start with some background information, which will help to illustrate the importance of this topic in health care today. Gestational Diabetes Mellitus is characterized by a β (beta) cell dysfunction that cannot meet the body’s demand for insulin. The β cell defects in GDM result from the same causes that underlie diabetes: autoimmune disease, monogenic disease, and insulin resistance. GDM is usually diagnosed during the second or third trimester of pregnancy. First recognition of IGT during pregnancy has previously been the definition of GDM, but now only women who are diagnosed during the second or third trimester should be considered to have GDM. More women of childbearing age today have undiagnosed Type 2, so the American Diabetes Association has updated the definition of GDM. Women who are diagnosed in the first trimester would be considered to have Type 2.
Incidence of Gestational Diabetes
Gestational diabetes is fairly common. According to a 2014 retrospective analysis looking at 2010 data published in the CDC journal, “Preventing Chronic Disease”, nearly 9.2% of pregnant women develop gestational diabetes during pregnancy in the United States[1]. The majority of cases of diagnosed diabetes during pregnancy are gestational diabetes, and the trend is on the upswing as obesity rates rise.
What Happens During Normal Pregnancy?
Insulin resistance, know as IR, is a condition in which cells “resist” the action of insulin in facilitating the passage of glucose into cells. Insulin sensitivity in late normal pregnancy is 50-70% lower than that of normal non-pregnant women. The changes in insulin sensitivity are thought to be related to the fetoplacental unit and the hormones human chorionic somatomammotropin (or simply HCS), progesterone, cortisol, and prolactin. During the second half of the pregnancy high levels of human chorionic somatotropin (hcS) increase maternal insulin resistance to maintain glucose availability for the fetus. Human chorionic somatotropin promotes protein synthesis & the breakdown of fat for the mother’s energy use. The mother’s body is relying more on fat as a source of energy rather than glucose.
Why Does This Happen? In normal pregnancy: the β-cells of the pancreas secrete more insulin to compensate for the insulin resistance of pregnancy. This graph shows the increased insulin secretion as gestation progresses.
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These changes serve to shunt ingested nutrients
to the fetus
after eating
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Nutrients are first used to support:
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The mother’s nutritional needs for her health &
bodily
changes during pregnancy
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Then placental development
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Lastly nutrients become available to the fetus
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When the mother’s nutrient intake is less than
optimal then baby’s growth and development
suffer rather than the mother’s health.
These changes help the baby to get nutrients after the mother eats. When the mother eats, nutrients are first used for her body, then placental development, then for the fetus’s needs. Glucose is the fetus’ preferred fuel. It’s worth noting that due to this progression, if the mother doesn’t get adequate nutrition during pregnancy the baby will suffer the most.
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