National Birth Defects Prevention Study Finds Pre-pregnancy Diabetes Increases Risk for Multiple Types of Birth Defects
Study first to show range and severity of birth defects associated with Type 1 and Type 2 diabetes
For Immediate Release: July 30, 2008
Contact: CDC′s Division of Media Relations
Women who receive a diagnosis of diabetes before they become pregnant are three to four times more likely to have a child with one or even multiple birth defects than a mother who is not diabetic, according to a study by the Centers for Disease Control and Prevention (CDC), released in the American Journal of Obstetrics and Gynecology.
The article from the National Birth Defects Prevention Study (NBDPS), “Diabetes Mellitus and Birth Defects,” shows that pregnant women with pre-gestational diabetes mellitus (pre-pregnancy diagnosis of diabetes, such as type 1 or type 2 diabetes) are more likely than a mother with no diabetes or a mother with gestational diabetes mellitus (pregnancy-induced diabetes) to have a child with various types of individual or multiple birth defects. This includes heart defects, defects of the brain and spine, oral clefts, defects of the kidneys and gastrointestinal tract and limb deficiencies. This study is the first to show the broad range and severity of birth defects associated with type 1 and type 2 diabetes.
“The continued association of diabetes with a number of birth defects highlights the importance of increasing the number of women who receive the best possible preconception care, especially for those women diagnosed with diabetes,” says Adolfo Correa, M.D., M.P.H., Ph.D., lead author and epidemiologist at CDC’s National Center on Birth Defects and Developmental Disabilities. “Early and effective management of diabetes for pregnant women is critical in helping to not only prevent birth defects, but also to reduce the risk for other health complications for them and their children.”
Researchers also found that some of the pregnant women with gestational diabetes were more likely to have a child with birth defects. Because birth defects associated with diabetes are more likely to occur during the first trimester of pregnancy and before a diagnosis of gestational diabetes is made, the observed associations suggest that some of the mothers with it probably had undiagnosed diabetes before they became pregnant. However symptoms went unnoticed until pregnancy.
Further, the associations of gestational diabetes with various birth defects were noted primarily among women who had pre-pregnancy obesity, which is a known risk factor for both diabetes and birth defects. Preconception care also should be considered and promoted for women with pre-pregnancy obesity to prevent birth defects and reduce the risk for health complications.
The NBDPS is a population-based, case-control study that incorporates data from nine birth defect centers in the United States—Arkansas, California, Georgia, Iowa, Massachusetts, New York, North Carolina, Texas and Utah. These centers have been working on the largest study of birth defects causes ever undertaken in the United States. Researchers have gathered information from more than 30,000 participants and are using this information to look at key questions on potential causes of birth defects.
Birth defects affect one in 33 infants and are a leading cause of infant mortality. For some birth defects, some risk factors or causes have been identified; however, for the majority of birth defects the causes remain unknown.
In the United States, the prevalence of gestational diabetes has been increasing in recent years and currently affects about seven percent of all pregnancies, resulting in more than 200,000 cases annually. While it is usually resolved shortly after delivery, women who have had gestational diabetes are at increased risk of developing type 2 diabetes in the future.
For more information about birth defects, please visit http://www.cdc.gov/ncbddd/bd/facts.htm. For more information on diabetes, please visit http://www.cdc.gov/diabetes/, or call toll-free 1-800-CDC-INFO.
- Historical Document: July 30, 2008
- Content source: Office of the Associate Director for Communication
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