Gestational diabetes mellitus is chronically high blood sugar (hyperglycemia) that starts in or is first diagnosed during pregnancy. Like other forms of glucose (blood sugar) intolerance, gestational diabetes is characterized by pancreatic β-cell dysfunction, which produces insufficient insulin to meet the body’s needs.
Usually there are no signs or symptoms with gestational diabetes, but when present, they are generally mild and include fatigue, increased urination, excessive thirst, blurred vision, and slight weight loss; and there is a higher risk of skin, bladder and vaginal infections. Blood sugar regulation usually returns to normal after delivery of the baby.
Available evidence suggests that β-cell defects in gestational diabetes result from the same spectrum of causes that underlie hyperglycemia in general, such as genetic issues, insulin resistance, pancreatic injury due to toxicity and autoimmune disease.
Gestational diabetes occurs in 3-10% of pregnant women. The vast majority (roughly 90%) of gestational diabetes cases are not considered a result of autoimmune complications. Instead, in these cases, pregnancy hormones increase insulin resistance (an effect seen, to a lesser extent, in normal pregnancies as well), which inhibits the transfer of glucose from the bloodstream into cells. Gestational diabetes is typically only present during pregnancy (resolves once the baby is born), though it can increase risk for type-1 or type-2 diabetes onset later in life.
Gestational diabetes, like type-2 diabetes, occurs more often in African Americans, American Indians, Hispanic Americans, and among women with a family history of diabetes. Women are at higher risk if they have delivered a baby who weighed more than 9 pounds in the past, have high blood pressure, or were overweight going into the pregnancy, among other risk factors. Women who have had gestational diabetes have a 20 to 50 percent chance of developing type-2 diabetes within 5 to 10 years.
Latent autoimmune diabetes of adults (LADA), which some endocrinologists refer to as “type-1.5 diabetes”, is a term used to describe a slowly developing autoimmune variant of type-1 diabetes in adults, that has clinical features resembling those of type-2 diabetes. (Most cases of type-1 diabetes are diagnosed during childhood, and alternately referred to as “juvenile-onset diabetes”). LADA is an inherited condition where the body mistakes the pancreatic tissues as foreign and responds by targeting the insulin producing β-cells for destruction. Unfortunately, those with LADA are often first misdiagnosed with type-2 diabetes, based on demographics such as age and ethnicity rather than the potential cause, which is quite different than with type-2 disease. In addition, LADA can be difficult to distinguish from adult-onset type-1 diabetes. As a result of this confusion, gestational diabetes that has not resolved within 6-8 weeks post-delivery may be mischaracterized as type-2 (formerly “adult onset”) diabetes instead of type-1.5, potentially impacting treatment.
About the Author
Dr. Rothbard is a professional medical writer and consultant based in New York City, specializing in medical education articles targeted at a variety of audiences, from children through clinicians. After leaving medicine, he worked as a biology and medical science educator for several years, before deciding to pursue writing full-time. He may be reached at [email protected].
This blog post was originally published by AutoimmuneMom.com, written by Dr. Rothbard, and first published on Sep 15, 2012.