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Medical Nutrition Therapy for Gestational Diabetes Mellitus

Medical Nutrition Therapy for Gestational Diabetes Mellitus. Michelle Synhorst Concordia College 2009 Moorhead, MN. Objectives. Identify risks factors of GDM. Understand the diagnosis and etiology of GDM. Be familiar with maternal and fetal complications due to GDM.

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Medical Nutrition Therapy for Gestational Diabetes Mellitus

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  1. Medical Nutrition Therapy for Gestational Diabetes Mellitus Michelle Synhorst Concordia College 2009 Moorhead, MN

  2. Objectives • Identify risks factors of GDM. • Understand the diagnosis and etiology of GDM. • Be familiar with maternal and fetal complications due to GDM. • Gain an understanding on medical nutrition therapy for GDM. • Identify ethical issues of GDM.

  3. Background Information • Defined as any degree of glucose intolerance during pregnancy • Affects approximately 7% pregnant woman • 200,000 cases are diagnosed each year • Women who have had GDM have a 20% to 50% chance of developing Type 2 diabetes in the next 5 to 10 years American Diabetes Association. Position Statement. (2004). Gestational diabetes mellitus.Diabetes Care, 27, S88-S90. Long,S., Nelms, M., & Sucher, K. (2007). Nutrition therapy and pathophysiology. Belmont, CA: Thomas Wadsworth.

  4. Risk Factors • Obesity (BMI > 30) • Personal History of GDM • Glycosuria • Strong family history of diabetes (1st degree relative) • Prior poor obstetrical outcome • Stillbirth • Birth Defects • Baby >9lbs • Member of high-risk ethnic group • Hispanic, African American, South or East Asian, Pacific Islander Long,S., Nelms, M., & Sucher, K. (2007). Nutrition therapy and pathophysiology. Belmont, CA: Thomas Wadsworth.

  5. Low Risk Factors • Age <25 years • Weight normal before pregnancy • Member of an ethnic group with low prevalence of GDM • No known diabetes in first-degree relatives • No history of abnormal glucose tolerance • No history of poor obstetric outcome Brown, J. (2008). Nutrition through the life cycle. Belmont, CA: Thomson Wadsworth.

  6. Diagnosis • Woman of high risk should be checked at initial visit • Women of “average risk” should be checked between 24 and 28 weeks of pregnancy • Glucose screens are not recommended for women at low risk • 50-gram oral glucose challenge test (GCT) • Test can be performed without fasting • Blood is collected 1 hour after glucose load is consumed • If blood glucose ≥130 mg/dl oral glucose tolerance test is performed American Diabetes Association. (2004). Diagnosis and classification of diabetes mellitus. Diabetes Care, 27, S5-S10.

  7. Diagnosis • Oral glucose tolerance test (OGTT) • Basis for the diagnosis of GDM • 100-gram glucose; 3-hour test • Diagnosis of GDM made when two or more levels exceed: • Overnight fast 95 mg/dl • One hour after glucose load 180 mg/dl • Two hours after glucose load 155 mg/dl • Three hours after glucose load 140 mg/dl American Diabetes Association. (2004). Diagnosis and classification of diabetes mellitus. Diabetes Care, 27, S5-S10.

  8. Diagnosis

  9. Etiology • Physiological alterations affect glucose, amino acid, and lipid metabolism and insulin secretion • Normal Pregnancy • During first trimester hormones human placental lactogen (hPL) and cortisol increase • Elevation of hPL and cortisol decreases maternal glucose levels • Increase in serum estrogen and progesterone levels stimulates production and secretion of additional insulin • Also increases insulin sensitivity • Result is a decresase in maternal fasting and postprandial glucose levels in first 12 weeks of gestation Gutierrez, Y.M., & Thomas, A.M. (2005). American diabetes guide to gestational diabetes mellitus. Library of Congress Cataloging-in-Publication Data.

  10. Etiology • Normal Pregnancy cont. • Maternal insulin resistance continues through third trimester • Placenta • Regulates maternal and fetal transfer of nutrients • Glucose is transferred to fetus through facilitated diffusion • Fetal glucose levels are 10 to 20mg/dL lower than maternal concentration • GLUT transporters • Insulin-dependent glucose transport molecules • Assist in transport of glucose across placenta • Alterations in the rate of GLUT transporters will affect circulating glucose concentration Gutierrez, Y.M., & Thomas, A.M. (2005). American diabetes guide to gestational diabetes mellitus. Library of Congress Cataloging-in-Publication Data. Illsley, N.P. (2000). Placental glucose transport in diabetic pregnancy. Clinical Obstet Gynecol, 43, 116-126.

  11. Etiology • Normal Pregnancy cont. • During second trimester levels of estrogen, progesterone, and placental hormones (hPL, prolactin, and cortisol) increase • Increase in insulin resistance; decrease in insulin sensitivity • Higher fasting and postprandial blood glucose levels • Lactogen is main contributor to reduced insulin sensitivity and impaired glucose tolerance • Increased hPL inhibits uptake of glucose in peripheral tissues and stimulates fetal pancreatic insulin secretion • Prolactin blocks insulin action • Cortisol increases hepatic production of glucose Gutierrez, Y.M., & Thomas, A.M. (2005). American diabetes guide to gestational diabetes mellitus. Library of Congress Cataloging-in-Publication Data.

  12. Etiology • Normal Pregnancy cont. • After eating, glycemic levels will rise • Pancreas secretes additional insulin • Returns glucose levels to normal and adequately supplies fetus • Hypoglycemia tends to occur between meals and during the night due to constant need for glucose by fetus • Mother’s body compensates by an enhanced capacity for nutrient storage during feeding • Insulin responsible for storing excess calories to lipid and tissue sites Gutierrez, Y.M., & Thomas, A.M. (2005). American diabetes guide to gestational diabetes mellitus. Library of Congress Cataloging-in-Publication Data.

  13. Pathophysiology • Pathophysiologically similar to Type 2 diabetes • Islet cell function abnormalities or peripheral insulin resistance at the receptor level • Inability of pancreatic -cells to increase insulin secretion • Exact cause of GDM is not known • Increasing insulin resistance and increase liver production of glucose • -cells are not able to produce enough insulin to compensate for increased insulin resistance Jansen, C. Greenspoon, J.S., & Palmer, S.M. (2003). Diabetes mellitus and pregnancy. In DeCherney, A.H., Nathan, L., eds. Current Obstetric and Gynecologic Diagnosis and Treatment. New York, NY: Lange Medical Books/McGraw-Hill.

  14. Risk Factors for Mother • Cesarean delivery to prevent shoulder dystocia • Increased risk for preeclampsia during pregnancy • Polyhydramnios • excessive accumulation of amniotic fluid • Preterm delivery (before 38 weeks gestation) • Increased risk of type 2 diabetes, hypertension, and obesity later in life • Increased risk for gestational diabetes in a subsequent pregnancy Berkowitz, K.M. (1998). Insulin resistance. Clinical Perinatol, 25, 873-85. Butte, N.F. (2000). Carbohydrate and lipid metabolism in pregnancy: normal compared with gestational diabetes mellitus. Am J Clin Nurtirion, 71, 1256S-61S.

  15. Risk Factors for Fetus • Stillbirth • Spontaneous abortion • Congenital anomalies • Macrosomia (>10 lb or 4500g) • Respiratory distress syndrome • Hypocalcemia, hyperbilirubinemia, & polycythemia • Neonatal hypoglycemia, death • Increased risk of insulin resistance, type 2 diabetes, high blood pressure, and obesity later in life Berkowitz, K.M. (1998). Insulin resistance. Clinical Perinatol, 25, 873-85. Butte, N.F. (2000). Carbohydrate and lipid metabolism in pregnancy: normal compared with gestational diabetes mellitus. Am J Clin Nurtirion, 71, 1256S-61S.

  16. Macrosomia (2009) Retrieved from www.get-discount-medical-supplies.com.

  17. Medical Nutrition Therapy • According to the ADA nutrition practice guidelines there are three clinical goals for treatment: • To achieve and maintain normoglycemia • To consume adequate energy to promote appropriate gestational weight gain and avoid maternal ketosis • To consume food-providing nutrients necessary for maternal and fetal health • Health care team includes an obstetrician, registered dietitian who is also a certified diabetes educator, a nurse educator, and an endocrinologist • Primary approach is to normalize blood glucose levels through diet and exercise Gutierrez, Y.M., & Thomas, A.M. (2005). American diabetes guide to gestational diabetes mellitus. Library of Congress Cataloging-in-Publication Data.

  18. Medical Nutrition Therapy • Weight Gain • Weight gain goals based on woman’s BMI Gutierrez, Y.M., & Thomas, A.M. (2005). American diabetes guide to gestational diabetes mellitus. Library of Congress Cataloging-in-Publication Data.

  19. Medical Nutrition Therapy • Energy Needs • First calculate estimated energy requirement (EER) • EER = 354 - (6.91 x A) + Pa x (9.36 x Wt +726 x Ht) • Formulas for calculating energy requirements for normal weight • First Trimester • Adult EER + 0 • Second Trimester • Adult EER + 160 kcal + 180 kcal • Third Trimester • Adult EER + 272 kcal + 180 kcal • Use an adjusted body weight with the Harris-Benedict for overweight or obese individuals • (ABW - IDBW) x 0.25 + IDBW = Weight used to calculate energy needs • No formula supported by research to determine energy needs during pregnancy Gutierrez, Y.M., & Thomas, A.M. (2005). American diabetes guide to gestational diabetes mellitus. Library of Congress Cataloging-in-Publication Data.

  20. Medical Nutrition Therapy • Carbohydrate Intake • Ideal amount is unknown • Should be about 40% to 45% of total daily energy intake • RDA is 175g for pregnant woman; 40% would give 200g • Distributed throughout the day into three-moderate size meals and two to four snacks • Breakfast-2 carbohydrate choices • Morning, afternoon, and evening snacks-2 carbohydrate choices • Lunch-4 carbohydrate choices • Dinner-4 carbohydrate choices Gutierrez, Y.M., & Thomas, A.M. (2005). American diabetes guide to gestational diabetes mellitus. Library of Congress Cataloging-in-Publication Data.

  21. Medical Nutrition Therapy • Protein Intake • For the first trimester intake should be about 46g/day or .8g protein/kg/day • For the second and third trimester protein needs increase by 25g/day or 1.1g protein/kg • Maternal protein synthesis increases to support the expansion of the blood volume, uterus, and breasts Gutierrez, Y.M., & Thomas, A.M. (2005). American diabetes guide to gestational diabetes mellitus. Library of Congress Cataloging-in-Publication Data.

  22. Medical Nutrition Therapy • Dietary Fat Intake • 30-40% of calories from fat • Limit intake of saturated and trans fatty acids • Limit foods high in cholesterol • Adequate intake of EPA (eicosapentaenoic acid) and DHA (doceosahexaenoic acid) of 300 mg/day • EPA reduces inflammation, dilates blood vessels, and reduces blood clotting • DHA is a major structural component of phospholipids in cell membranes in central nervous system Brown, J. (2008). Nutrition through the life cycle. Belmont, CA: Thomson Wadsworth.

  23. Medical Nutrition Therapy • Folate • Involved in cell multiplication and DNA synthesis • Requirement of 600µg/day during pregnancy • Deficiency may result in: • Neural tube defects • Down syndrome • Preterm delivery • Elevated serum homocysteine levels • Vollset et al performed a study to determine the effect of plasma homocysteine levels on pregnancy • Compared upper to lower quartiles in 14,492 pregnancies in 5,883 Norwegian women Brown, J. (2008). Nutrition through the life cycle. Belmont, CA: Thomson Wadsworth. Vollset, S.E., Refsum, H., Irgens, L.M. Emblem, B.M., Tverdal, A., Gjessing, H.K., Monsen, A.L., & Ueland, P.M. (2000). Plasma total homocysteine, pregnancy complications, and adverse pregnancy outcomes: the Hordaland Homocysteine study. Am J Clin Nutr, 71, 962-968.

  24. Medical Nutrition Therapy • Calcium • 1,300 mg for ages 14 to 18 • 1,000 mg for ages 19 to 50 • Iron • Need about an additional 1,000 mg during pregnancy • Approximately 3 mg/day • Recommendation of an iron supplement of 30mg ferrous iron in the second and third trimester • Pros and Cons about supplementation • Screen women for iron status before pregnancy Allen, L.H. (2001). Biological mechanisms that might underlie iron’s effects on fetal growth and preterm birth. J Nutrition, 131, 581S-9S. Brown, J. (2008). Nutrition through the life cycle. Belmont, CA: Thomson Wadsworth.

  25. Blood Glucose Monitoring • Blood glucose levels should be checked regularly • Fasting plasma glucose • ≤150 mg/dl • One hour postprandial plasma glucose • ≤155 mg/dl • Two hour postprandial plasma glucose • ≤130 mg/dl • When MNT cannot maintain blood glucose levels insulin will be initiated Gutierrez, Y.M., & Thomas, A.M. (2005). American diabetes guide to gestational diabetes mellitus. Library of Congress Cataloging-in-Publication Data.

  26. Insulin • Four types of insulin • Rapid acting • Short-acting • Intermediate-acting • Long-acting • Oral Insulin • Glyburide • Second-generation sulfonylurea • Minimally transported across the placenta • Acts to improve glycemic control by stimulating pancreas to increase insulin secretion Gutierrez, Y.M., & Thomas, A.M. (2005). American diabetes guide to gestational diabetes mellitus. Library of Congress Cataloging-in-Publication Data.

  27. Ethical Dilemmas • Debate over universal screening • Who and when should they be tested? • Lack of data from well-controlled studies to determine ideal screening criteria • Iron supplementation • Supplement providing 60 mg or more regularly expose intestinal mucosa to free iron radicals • Oxidizing effects cause inflammation and mitochondrial damage in cells • Use of oral medications • Glyburide • Randomized controlled study by Langer et al showed no differences in incidence of preeclampsia, cesarean deliveries, or macrosomia • Can be safely used Casanueve, E. et al. (2003). Iron and oxidative stress in pregnancy. J Nutirtion, 133, 1700S-1708S. Gutierrez, Y.M., & Thomas, A.M. (2005). American diabetes guide to gestational diabetes mellitus. Library of Congress Cataloging-in-Publication Data. Langer, O., Yogev, Y., Xenakis, E.M., & Rosenn, B. (2005). Inuslin and glyburide therapy: dosage, severity level of gestational diabetes, and pregnancy outcome. Am J Obstet Gynecol., 192, 134-139.

  28. Bibliography • (2009) Retrieved from www.get-discount-medical-supplies.com. • American Diabetes Association. (2004). Diagnosis and classification of diabetes mellitus. Diabetes Care, 27, S5-S10. • American Diabetes Association. Position Statement. (2004). Gestational diabetes mellitus.Diabetes Care, 27, S88-S90. • Berkowitz, K.M. (1998). Insulin resistance. Clinical Perinatol, 25, 873-85. • Brown, J. (2008). Nutrition through the life cycle. Belmont, CA: Thomson Wadsworth • Brown, J. (2008). Nutrition through the life cycle. Belmont, CA: Thomson Wadsworth. • Butte, N.F. (2000). Carbohydrate and lipid metabolism in pregnancy: normal compared with gestational diabetes mellitus. Am J Clin Nurtirion, 71, 1256S-61S. • Casanueve, E. et al. (2003). Iron and oxidative stress in pregnancy. J Nutirtion, 133, 1700S- 1708S. • Gutierrez, Y.M., & Thomas, A.M. (2005). American diabetes guide to gestational diabetes mellitus. Library of Congress Cataloging-in-Publication Data. • Illsley, N.P. (2000). Placental glucose transport in diabetic pregnancy. Clinical Obstet Gynecol, 43, 116-126.

  29. Bibliography • Jansen, C. Greenspoon, J.S., & Palmer, S.M. (2003). Diabetes mellitus and pregnancy. In DeCherney, A.H., Nathan, L., eds. Current Obstetric and Gynecologic Diagnosis and Treatment. New York, NY: Lange Medical Books/McGraw-Hill. • Langer, O., Yogev, Y., Xenakis, E.M., & Rosenn, B. (2005). Insulin and glyburide therapy: dosage, severity level of gestational diabetes, and pregnancy outcome. Am J Obstet Gynecol., 192, 134-139. • Long,S., Nelms, M., & Sucher, K. (2007). Nutrition therapy and pathophysiology. Belmont, CA: Thomas Wadsworth. • Vollset, S.E., Refsum, H., Irgens, L.M. Emblem, B.M., Tverdal, A., Gjessing, H.K., Monsen, A.L., & Ueland, P.M. (2000). Plasma total homocysteine, pregnancy complications, and adverse pregnancy outcomes: the Hordaland Homocysteine study. Am J Clin Nutr, 71, 962-968.

  30. Questions?

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