Nutritional Management of Gestational Diabetes and Nutritional Management of Women With a History of Gestational Diabetes: Two Different Therapies or the Same?
Deborah Thomas-Dobersen, RD, MS, CDE
Gestational diabetes mellitus (GDM) is defined as carbohydrate intolerance of varying degrees of severity with onset or first recognition during pregnancy. This definition applies regardless of whether insulin is used for treatment or the condition persists after pregnancy. It does not exclude the possibility that unrecognized glucose intolerance may have antedated the pregnancy.1
GDM is the most common medical complication of pregnancy,2 occurring in 4% of all pregnancies in the United States (all ethnicities),3 or approximately 100,000 pregnant women annually. In addition, it is increasing in prevalence globally.3
The incidence of this metabolic complication of pregnancy will also notably increase if the new diagnostic criteria extrapolated from the O'Sullivan and Mahan data by Carpenter and Coustan as suggested by the 4th International Workshop-Conference on GDM are accepted and widely used.4 The new diagnostic criteria are suggested in part because of the thought that intervention at a lower level of blood glucose will help prevent the major complication of GDM, macrosomia of the infant.
Currently, the American Diabetes Association is sponsoring the writing of a technical paper that will assess the scientific evidence on which the proposal to change the new diagnostic standard is based. This technical paper should be finished this fall, and its conclusions are anticipated to be included as a Clinical Practice Recommendation at the earliest in the spring of 2000. (personal communication, Gwen Twillman, Manager of Clinical Affairs, American Diabetes Association).
Although there is still considerable controversy regarding the clinical importance of GDM and its significance to mothers and offspring, increased screening, identification, and intensive treatment appear to decrease the morbidity in infants of mothers with GDM. The major cause of morbidity in infants attributable to GDM is macrosomia (birth weight >4,000 g), with its attendant higher rates of cesarean sections and birth trauma. Other causes of neonatal morbidity include hypoglycemia, hypocalcemia, hyperbilirubinemia, and polycythemia.4
Women with GDM have a significant risk of developing GDM with a subsequent pregnancy, with recurrence rates ranging from 3050%5 to 65%.6 In addition, women with GDM have a significant risk of developing type 2 diabetes later in life. Studies show that 2230% of women with GDM develop type 2 diabetes mellitus 710 years postpartum,7,8 and 5060% will develop type 2 diabetes during their lifetime.8 The diagnosis of GDM appears to unmask those women with inadequate -cell reserve who are at substantial risk of developing type 2 diabetes. This ability to predict who may go on to develop type 2 diabetes gives a window of time for any prevention techniques, an idea that has been used in the Diabetes Prevention Program of the National Institutes of Health.9
Of even greater potential significance are the potential influences that GDM may have on the future health of the offspring. Long-term follow-up studies show an increased risk for obesity and glucose intolerance in offspring of mothers with diabetes, including GDM, present during the index pregnancy.10,11
Given the newer understanding of the importance of GDM, it is unfortunate that nutritional management, the cornerstone of treatment, is understudied. There are no randomized, controlled studies specifically looking at optimal medical nutritional therapy for GDM, lean or obese. Yet there are published reports of clinic programs that were able to get good infant and maternal outcomes by intensive monitoring of women with GDM using a wide range of nutritional practices (Langer, 55% carbohydrate, 20% fat, and Jovanovic, 40% carbohydrate, 40% fat).12,13 This article offers practical pointers that seem to make sense until the supporting framework of nutritional research is provided.
The Diabetes Care and Education (DCE) Practice Group of the American Dietetic Association is currently recruiting sites for a multicenter, randomized, controlled study in an attempt to answer the question, "What is the optimal medical nutrition therapy for GDM?" The DCE will verify through field testing the resulting nutrition practice guidelines for GDM. Information on the results of this study may be obtained after January 2000 on the American Dietetic Association's web site: http://www.eatright.org.
Nutrition Therapy for GDM
In 1990, the Institute of Medicine released recommendations for pregnancy weight gain contingent upon pre-pregnancy weight status (Table 1).15 The total amount of weight gain is not as important as the weekly rate of gain. Most women are diagnosed with GDM during the second or third trimester, when the rate of weight gain is normally approximately 3/41 lb/week. Many women are gaining almost 2 lb/week when they are diagnosed with GDM. Slowing down the rate of weight gain to 1 lb/week often restores blood glucose levels to normal.
A weight gain graph is a helpful tool to share with women with GDM. A curve approximating the desired rate of weight gain starting from where the woman is on the graph can be given as a take-home chart (Figure 1).
Often after being diagnosed with GDM, a woman's weight gain may cease for a period to 12 weeks. This seems to be common and harmless in the absence of small to moderate ketones. Sweets often add as many as 25% of kcal to the diet, and when restricted may lead to the flattening of the weight gain curve. A change in body composition may also be to blame when the percentage of macronutrients in the diet is changed. If weight gain is not resumed after 2 weeks, a thorough assessment of the diet and urinary ketones should be done.
In the long run, this lack of consensus on calorie level should not be a problem. The initial calorie level, used as a starting point, can easily be adjusted as a woman adopts the nutritional modifications and monitors her weight gain, appetite, and urinary ketones. Inadequate weight gain needs more calories in the face of small to moderate ketones. Excessive weight gain requires fewer calories. A detailed diet history before initiating meal plans can give a practiced eye advance notice if the calorie level proposed is workable. When a woman is eating a well-balanced diet without excessive fat and sugar, with meals and snacks spaced frequently and is getting regular exercise, her appetite should be a good guideline for adequate calories.
For the majority of women with GDM, a calorie level of 2,2002,400 kcal is a good starting point. Having women keep food records helps both as a behavioral change tool and as a source of information for the health care provider on subsequent visits. For obese women with GDM, severe calorie restriction, 50% of normal, leads to ketonuria and ketonemia and is not recommended.16 Moderate calorie restrictions (33% of normal calories), approximately 1,800 calories, has been shown to reduce macrosomia without neonatal morbidity or maternal ketonemia.17 However, some risk to the fetus may occur in calorie restriction during pregnancy, even in obese women, and caution should be exercised.
Carbohydrate Content of Meal Plan
The last goal in Table 2 is predicated on the assumption that most patients with GDM will not typically be seen postpartum for medical nutrition therapy. Therefore, the impression that they get when they last see the doctor before delivery (perhaps that they should restrict carbohydrate and liberalize fat) is likely to be the impression that they are left with until they are again diagnosed with GDM or diagnosed with type 2 diabetes later.
To date, three different approaches to maternal euglycemia in GDM are emerging. Central to all is the agreement that increasing maternal glucose level is the gold standard for monitoring pregnancies complicated with GDM, and that increasing maternal hyperglycemia leads to increasing neonatal morbidity. One approach uses a higher-carbohydrate/lower-fat diet, of 55% carbohydrate, 25% protein, and 20% fat, and a larger percentage of women on insulin to achieve these goals.12 The second approach advocates use of carbohydrate restriction and a higher-fat diet (3540% carbohydrate, 2025% protein, 3540% fat) to achieve maternal euglycemia with fewer women on insulin.13 The third approach, by Clapp, has yet to be tested on GDM. This approach uses low-glycemic-index carbohydrates, higher carbohydrates, and lower fats (5560% carbohydrate, 1719% protein, 2025% fat) rather than higher-glycemic-index foods to achieve lower postprandial blood glucose values. Clapp also notes that exercise proves a useful adjunct to treatment, consistent with what others have found.18
Of concern when restricting carbohydrates is:
1. Does 35% of total energy from cabohydrate distort the diet, making the diet deficient in micronutrients? Nutritionists are not naive enough to suggest that we have put all necessary vitamins/minerals into a prenatal supplement.
2. Is keeping carbohydrates as low as 35% of total calories really preferable to starting insulin? As the per centage of carbohydrates in the diet is decreased, the percentage of fats increases. Therefore, whenever carbohydrate restriction is used, a high er-fat diet is employed.
3. Does a diet with 40% of calories from fat give a woman at risk of cardiovascular disease and type 2 diabetes as well as obesity a head start on developing more insulin resistance?
Perhaps, instead of restricting carbohydrates (<45% of total energy), the use of high-glycemic-index foods and more consistent (daily) exercise would obviate the need to have two diets (one prenatal and one postpartum) and the concern regarding inadequate micro- nutrients. Certainly more research is needed to answer these questions.
There are those who argue that carbohydrate restriction to prevent the use of insulin is more cost-effective19 and that the medical nutrition therapy for GDM is not intended to address the issue of long-term diabetes prevention (see Table 3). They need to show 1) that these women are not staying on high-fat diets (>38% of calories) postpartum and 2) that their rate of conversion to type 2 diabetes is not accelerated by this higher-fat diet. Certainly the cost-effectiveness of delaying the onset of type 2 diabetes is greater than that of not using insulin during pregnancy. Gregory showed theoretical savings of more than $71 million in health care dollars assuming a 10% reduction in such conversion could be achieved.20
In addition to the amount of carbohydrate, the timing and distribution of carbohydrate intake is also important. Many women are more insulin resistant in the early morning and can tolerate less carbohydrate at breakfast. The division of calories into three meals and three or four snacks is commonly used.
of Blood Glucose
SMBG empowers women with GDM, allowing them to become active participants in achieving euglycemia. Monitoring will give these women immediate feedback about portion size, particular foods that cause hyperglycemia, stable temporal patterns of elevated blood glucose levels, and where in the day exercise is most likely to help keep blood glucose in the target range. With this information, women are free to make choices and to see the effects of those choices in a timely manner. Studies have shown that SMBG helps with adherence to the goals of treatment in addition to reassuring women without causing undue stress and potentially saving the expense of neonatal intensive care.23 Patients are more likely to believe the advice they receive when they can see high blood glucose levels 2 hours after a known indiscretion or when they can see blood glucose levels come down with walking. SMBG allows adjustments to be made to the meal plan/exercise program to normalize blood glucose levels. Without SMBG, the meal plan, solely a starting point, cannot be individualized to the different responses that many women have. And lastly, SMBG allows the earlier introduction of insulin, which likely is important in preventing macrosomia.
The number of blood glucose readings to obtain daily can be anywhere from 4 to 7. Postprandial glucose levels are more closely related to fetal risks than are fasting levels. Therefore, in addition to fasting levels, postprandial blood glucose readings are recommended. There is no consensus on whether a 1-hour or a 2-hour postprandial reading is best.4
Three days of food records before the first visit with a dietitian or whomever is instructing on the meal plan will give good data regarding the appropriate kcal level and particular food habits to discuss. Food records after education on the meal plan will help practitioners assess patients' ability to follow the plan, acceptance of kcal level, and understanding of teaching performed.
Anytime blood glucose levels are outside of the target level, women should be instructed to write down what they ate at the last meal. Luckily for most of us, remembering a meal eaten 2 hours ago is within our grasp. This information proves helpful in trying to assess whether the high blood glucose seen is due to dietary indiscretion, to a particular food or food portion, or to inadequate insulin production.
The American College of Obstetrics and Gynecology has published guidelines for safe exercise during pregnancy and also gives guidelines for which women should not be encouraged to exercise.27 In general, for a healthy pregnancy, moderate regular exercise of a nonstanding nature (cycling, swimming) that does not require a lot of balance, when well-hydrated and well-nourished, is encouraged. Hypertensive women, however, should not exercise, as this may lead to preeclampsia.
Brisk walking, cycling, and swimming are often done safely by pregnant women. Communities often have prenatal exercise programs in pools or gyms. Exercising for 1520 minutes after a meal may help to keep blood glucose levels within the target range for women with GDM.
It All Together
SMBG and food records are analyzed to fine-tune the meal plan. For example, some women can tolerate more carbohydrate at breakfast, but fast-food dinners lead to hyperglycemia. Records of rate of weight gain, food intake, and ketonuria are also used to fine-tune the meal plan. For example, a very obese woman with no weight gain over a 1-month period but whose records show at least 2,200 calories of good nutrient composition, with no ketonuria, is less worrisome. Many very obese women have weight gains and rates of weight gains much lower than recommended, but still deliver healthy infants of good birth weight.
Telephone/fax management can be a cost-effective means of using these tools to make course corrections in therapy. In many programs, women with GDM are asked to call/fax records in weekly. A health care practitioner (RD, CDE) skilled in working with these women can use the records to reinforce the initial concepts taught, answer questions that come up as a woman works with the program, and monitor records for those who are in need of extra help (i.e., insulin).
If a woman receives a call from the program asking for her SMBG, ketonuria, and food records, it reinforces the expectation that this is important. This type of program also catches the high blood glucose levels that are not necessarily brought to the attention of the physician. Many times when blood glucose is elevated, a patient who has been instructed to call will not do so, whether from fear or denial. A weekly call-or-get-called program will not let this continue for 2 weeks or possibly a month until the next physician appointment.
My particular bias is for telephone management, rather than fax management, because a therapeutic bond is formed between patient and health practitioner that is more personal by telephone than by fax.
Women With a History of Gestational Diabetes Mellitus
The 4th International Workshop-Conference on Gestational Diabetes Mellitus included more emphasis on the importance of postpartum education for women with GDM. All women with a history of GDM should be screened annually for diabetes and heart disease risk factors. Such women should know that any subsequent pregnancy should be planned (i.e., that they should know 3 months before conception that their glucose tolerance is normal). A woman who enters pregnancy with undiagnosed type 2 diabetes, usually asymptomatic, would put her fetus at risk for congenital malformations. The risk of subsequent pregnancy complicated by GDM is approximately 65%.Therefore, the doctor should know of any past history of GDM.
Factors that influence whether a woman is more likely to develop type 2 diabetes in the future are listed in Table 4. All women with GDM history should be counseled on the modifiable risk factors, such as the importance of healthy weight maintenance and daily exercise and the risk of postpartum weight gain to the development of subsequent GDM and type 2 diabetes. In addition, such women should receive medical nutritional therapy to decrease dietary fat. If they can achieve a 10-lb weight loss postpartum, they can decrease the risk of subsequent diabetes by one-half.32
Factors Influencing Recurrence of GDM and Progression to Type 2 Diabetes
Evidence from animal and epidemiological studies increasingly support the hypothesis that high-fat, low-carbohydrate diets contribute to excess obesity and a high prevalence of type 2 diabetes.34 Salmeron and associates showed that a diet with a high glycemic index and a low fiber content increased the relative risk of developing type 2 diabetes.35 Marshall and associates followed for 8 years 1,069 people in San Luis Valley, Colo., who had no glucose intolerance. As the amount of total fat and saturated fat in the diet increased, irrespective of total calorie intake or weight, the risk of developing diabetes, as measured by increasing fasting insulin, increased.36
In another study, a high fat intake and low carbohydrate, low fiber intake increased the risk of developing glucose intolerance and type 2 diabetes independent of age, sex, ethnicity, and calorie intake. Again, the difference in fat intake between groups was small (approximately 3 g/day).37 Studies of subjects with impaired glucose tolerance showed a higher fat intake as a percentage of total calories in individuals who converted to type 2 diabetes compared with those who reverted to normal glucose tolerance (43.9 vs. 38.9%).34
Mechanisms relating dietary fat to the etiology of type 2 diabetes are unknown. Possible explanations include the relationship of dietary fat to obesity and altered distribution of body fat, the elevation of free fatty acids levels promoting insulin resistance, or alterations in cell membrane composition, which could alter subsequent insulin action.37
As not all women with GDM respond the same to carbohydrate loads, try a modest carbohydrate level (not <50% of calories) distributed among 3 meals and 3 snacks first. A percentage of women will not keep blood glucose levels within target range on this amount. It may help to decrease to 45% of calories. Use a daily exercise program as an adjunct to treatment if possible to help attain maternal euglycemia. If blood glucose cannot be kept within target range, insulin may be added. If the practitioner chooses to use a lower carbohydrate level (<45% of kcal), be sure to educate and evaluate postpartum whether this woman has switched to a low-fat ( <30% of calories) diet and maintains that low-fat diet on yearly revisits.
1Metzger BE, Organizing Committee: Summary and recommendations of the Third International Workshop-Conference on Gestational Diabetes Mellitus. Diabetes 40 (Suppl 2):197-201, 1991.
2Carr DB, Gabbe S: Gestational diabetes: detection, management, and implications. Clin Diabetes 16:4-11, 1998.
3King H: Epidemiology of glucose intolerance and gestational diabetes in women of childbearing age. Diabetes Care 21(Suppl 2):B9-13, 1998.
4Metzger BE, Coustan DR, Organizing Committee: Summary and recommendations of the Fourth International Workshop-Conference on Gestational Diabetes Mellitus. Diabetes Care 21 (Suppl. 2):B161-67, 1998.
5Moses RG: The recurrence rate of gestational diabetes in subsequent pregnancies. Diabetes Care 19:1349-56, 1996.
6Philipson EH, Super DM: Gestational diabetes mellitus: does it recur in subsequent pregnancy? Am J Obstet Gynecol 160:1324-31, 1989.
7Coustan DR, Carpenter WE, O'Sullivan PS, Carr SR: Gestational diabetes mellitus: predictors of subsequent disordered glucose metabolism. Am J Obstet Gynecol 168:1139-45, 1993.
8O'Sullivan JB, Mahan CM: Criteria for the oral glucose tolerance test in pregnancy. Diabetes 13:278-85, 1964.
9Diabetes Prevention Program Research Group: The Diabetes Prevention Program (DDP) (Abstract). Diabetes 46 (Suppl 1):138A, 1977.
10Silverman BL, Metzger BE, Cho NH, Loeb CA: Impaired glucose tolerance in adolescent offspring of diabetic mothers. Diabetes Care 18:611-17, 1995.
11Silverman BL, Rizzo T, Green OC, Cho NH, Winter RJ, Ogata ES: Long-term prospective evaluation of offspring of diabetic mother. Diabetes 40:121-25, 1991.
12Langer O, Hod M: Management of gestational diabetes mellitus. Obstet Gynecol Clin North Am 23:137-59, 1996.
13Jovanovic-Peterson L, Peterson CM: Dietary manipulation as a primary treatment strategy for pregnancies complicated by diabetes. J Am Coll Nutr 9:320-25, 1990.
14Brown JE, Kahn ESB: Maternal nutrition and the outcome of pregnancy: a renaissance in research. Clin Perinatol July 1997.
15Brown JE: Nutrition and Pregnancy: A Complete Guide From Preconception to Postdelivery. Los Angeles, Lowell House, 1998, p. 96. As adapted from the Institute of Medicine, National Academy of Sciences: Nutrition During Pregnancy. Washington, D.C., National Academy of Sciences Press, 1990.
16Magee MS, Knopp RH, Benedetti TJ: Metabolic effects of 1200-kcal diet in obese pregnant women with gestational diabetes. Diabetes 39:234-40, 1990.
17Knopp RH, Magee MS, Raisys V: Hypocaloric diets and ketogenesis in the management of obese gestational diabetic women. J Am Coll Nutr 10:649-67, 1991.
18Clapp JF: Effect of dietary carbohydrate on the glucose and insulin response to mixed caloric intake and exercise in both nonpregnant and pregnant women. Diabetes Care 21 (Suppl 2):B107-12, 1998.
19Gunderson EP: Intensive nutrition therapy for gestational diabetes. Diabetes Care 20:221-26, 1997.
20Gregory KD, Kjos SL, Peters RK: Cost of non-insulin-dependent diabetes in women with a history of gestational diabetes: implications for prevention. Obstet Gynecol 81:782-86, 1993.
21Langer O, Mazzee R: The relationship between large-for-gestational-age infants and glycemic control in women with gestational diabetes. Am J Obstet Gyneol 159:1478-83, 1988.
22Langer O, Langer N, Piper JM, Elliott B, Anyaebunam A: Cultural diversity as a factor in self-monitoring blood glucose in gestational diabetes. J Assoc Acad Min Phys 6:73-77, 1995.
23Homko CJ, Sivan E, Reece EA: Is self-monitoring of blood glucose necessary in the management of gestational diabetes mellitus? Diabetes Care 21 (Suppl 2):B118-22, 1998.
24Jovanovic-Peterson L, Durak EP, Peterson CM: Randomized trial of diet versus diet plus cardiovascular conditioning on glucose levels in gestational diabetes. Am J Obstet Gynecol 161:415-19, 1989.
25Bung P, Artal R: Gestational diabetes and exercise: A survey. Sem Perinatol 20:328-33, 1996.
26Artal R: The Role of Exercise in the Treatment of Hyperglycemia in Pregnancy. Presentation at the American Diabetes Association 59th Scientific Sessions, San Diego, Calif., June 1999.
27ACOG technical bulletin #189, Febr. 1994.
28Work Group on Breastfeeding, American Academy of Pediatrics: Breastfeeding and the use of human milk. Pediatrics 100:1035-39, 1997.
29Kjos SL, Henry O, Lee RM, Buchanon TA, Mishell DR: The effect of lactation on glucose and lipid metabolism in women with recent gestational diabetes. Obstet Gynecol 82:451-55, 1993.
30Dornhorst A, Rossi M: Risk and prevention of type 2 diabetes in women with gestational diabetes. Diabetes Care 21 (Suppl 2):B43-49, 1998.
31Oats JJN: Fourth International Workshop-Conference on Gestational Diabetes Mellitus: overview and commentary on first session. Diabetes Care 21 (Suppl 2):B58-59, 1998.
32Peters RK, Kjos SL, Xiang A, Buchanon TA: Long-term diabetogenic effect of single pregnancy in women with previous GDM. Lancet 347:227-30, 1996.
33Moses RG, Shand JL, Tapsell LC: The recurrence of gestational diabetes: could dietary differences in fat intake be an explanation? Diabetes Care 20:1647-50, 1997.
34Marshall JA, Hoag S, Shetterly S, Hamman RF: Dietary fat predicts conversion from impaired glucose tolerance to NIDDM. Diabetes Care 17:50-55, 1994.
35Salmeron J, Manson JE, Stampfer MJ, Colditz GA, Wing AL, Willett WC: Dietary fiber, glycemic load, and risk of non-insulin-dependent diabetes mellitus in women. JAMA 277:472-77, 1997.
36Marshall JA, Bessesen DH, Hamman RF: High saturated fat and low starch and fibre are associated with hyperinsulinaemia in a non-diabetic population: The San Luis Valley Diabetes Study. Diabetologia 40:430-38, 1997.
37Marshall JA, Hamman RF, Baxter J: High-fat, low-carbohydrate diet and the etiology of non-insulin-dependent diabetes mellitus: The San Luis Valley diabetes study. Am J Epidem 134:590-602, 1991.
Deborah Thomas-Dobersen, RD, MS, CDE, is in private practice in Littleton, Colo.
Guidelines for Women
Eat 3 meals and 3 snacks daily.
Omit foods high in sugar and concentrated sweets.
Omit juices, but instead use whole pieces of fruit (apples instead of applesauce).
Spread carbohydrates out throughout the day.
Choose foods high in fiber: whole grains, whole fruits and vegetables, beans and legumes, oats.
Choose foods low in fat and avoid adding extra fat, such as oil, margarine, or butter. Choose low-fat meat selections, such as lean cuts of beef, pork, and lamb. Emphasize more fish and poultry (without the skin). Choose:
Limit foods from fast-food restaurants. Ask for nutritional information on menu selections, and choose foods that are low in fat. For many women, a burger and fries or more than 2 pieces of pizza will cause high blood glucose levels.
Be careful to gain at least 1/2 lb/week. Cutting back too much on calories and weight gain can increase your risk of a low-birth-weight infant.
Adapted from Understanding Gestational Diabetes: A Practical Guide to a Healthy Pregnancy. Bethesda, Md., National Institutes of Health, National Institutes of Child Health and Human Development. (NIH Publication No. 93-2788), 1993 .
Copyright © 1999 American Diabetes
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