Gestational Diabetes During and After Pregnancy

18. Nutrition and Weight Recommendations for Treating Gestational Diabetes Mellitus

Janet C. King  and David A. Sacks

(1)

Children’s Hospital Oakland Research Institute, Oakland, CA, USA

Janet C. King

Email: jking@chori.org

Abstract

With the rise in obesity among women of reproductive age, the prevalence of GDM has increased. When a woman is diagnosed with GDM, she is immediately scheduled for an appointment with a registered dietitian to develop an individualized food plan for achieving and maintaining control of her blood glucose concentrations. Thus, medical nutrition therapy (MNT) is the cornerstone for treating GDM; insulin and/or oral hypoglycemic therapy is initiated if MNT fails to establish good glycemic control. Although diet therapy is the basis of GDM treatment, specific dietary guidelines for managing the disease are lacking due to the absence of large-scale, randomized controlled trials of dietary patterns varying in energy and the amount and type of carbohydrate and fat. Observational studies suggest that a modest energy restriction (∼30% less than recommended levels, or about 1600-1800 kcal/d) along with a diet high in complex carbohydrates and polyunsaturated fatty acids may improve glucose tolerance. No weight gain standards have been proposed specifically for women with GDM. Instead, the women are advised to gain within the Institute of Medicine (IOM) ranges for their body mass index. Since glycemic control improves in nonpregnant individuals with weight loss, it has been suggested that weight maintenance or a modest loss may improve outcomes in obese women with GDM. Additional research on limited gestational weight change and glycemic control is needed. Presently, in the short-term, individualized dietary counseling aimed at following a healthy diet pattern based on cultural food preferences is the foundation for improving pregnancy outcome among women with GDM. Adopting a healthy diet also reduces prevalence of maternal and child co-morbidities in the long-term.

18.1 Introduction

The importance of nutrition in the treatment and management of gestational diabetes mellitus (GDM) is well established. Maternal and fetal needs for a healthy pregnancy outcome need to be met in the context of aberrant regulation of glucose metabolism, the primary fuel for the fetus. Nutrition of women with GDM poses a unique challenge. The primary objective of dietary advice for women with GDM is to maintain maternal normoglycemia while reducing accelerated fetal growth.1 Since excessive gestational weight gain, particularly fat gain, may exacerbate maternal insulin resistance,2 dietary recommendations for women with GDM should promote appropriate maternal weight gain. The overall objective of this chapter is to review past and current dietary recommendations for women with GDM and to integrate those recommendations with guidelines for healthy weight gains; complications of obesity during pregnancy are discussed in depth in another chapter in this book. It is important to recognize that the dietary principles promoted for women with GDM will have a lifelong positive impact on maternal health and decrease the risk for developing type 2 diabetes mellitus in the future.

18.2 Historical Evolution of Nutrition Recommendations for Treating GDM

Since the early days of treating women with diabetes during pregnancy, medical nutrition therapy (MNT) has been a cornerstone of management. The first reports of diet therapy for pregnant diabetic women come from Germany in the early twentieth century3 where diets high in protein and fat (85% of total energy) and, therefore, low in carbohydrate were applied. In severe cases, starvation diets were used. Subsequently, diabetic women at the Joslin Clinic in Boston were treated with a diet providing modest restrictions in energy, i.e., 30 kcal/kg body weight, 1 g protein/kg, and liberal amounts of carbohydrate (180–250 g).4 In 1951, Duncan modified the plan.5 Because many women were obese or had edema, he based energy and protein intakes on a proportion of the ideal body weight rather than actual body weight. At about the same time, Moss and Mulholland recommended using much higher protein intakes, 2 g protein/kg current body weight.6 However, they were the first to limit total weight gain to no more than 20 lb or 9.1 kg. In 1952, Reis introduced calorie restriction to keep hyperglycemia and glycosuria under control.7 Women doing light work were allowed 25 kcal/kg; those doing moderate work were allowed 30 kcal/kg. Based on the erroneous assumption that minimization of weight gain would reduce the incidence of edema, the latter being part of the definition of pre-eclampsia at that time, restrictions in energy intake and weight gain continued through the 1960s.

In 1970, the National Research Council of the National Academy of Sciences (NAS) published a landmark report demonstrating that fetal growth and development were adversely affected by maternal weight gain restriction.8This report recommended easing the weight gain restriction for pregnancy from 22 to 30 lb (10–13.6 kg). However, weight gain continued to be restricted for diabetic women to ≤15 lb (6.8 kg) until 1979. At that time, the American Diabetes Association in collaboration with the American Dietetic Association recommended that the NAS weight gain standards for non-diabetic pregnant women should also be applied to diabetic women.9 They recommended consuming moderate amounts of complex carbohydrates, no refined sugars, and to limit cholesterol and saturated fat intakes.9

Thus, since the early 1900s, MNT for pregnant women with diabetes has evolved from energy restricted diets, to moderate energy intakes with high amounts of protein with limited weight gain, to diets restricted in refined carbohydrates and limited amounts of fat. The research basis for these recommendations stems primarily from practical experiences and observations; the efficacy of these dietary regimens on maternal glycemic control and pregnancy outcome has not been studied systematically. Since 2000, individualized dietary prescriptions and exercise goals have been promoted to improve glycemic control, and gestational weight gain recommendations for normal pregnancy were also used for women with GDM.10,11 A review of the current recommendations and their evidence base follows.

18.3 Medical Nutrition Therapy for Gestational Diabetes Mellitus

18.3.1 Current Nutrition Recommendations for Women with GDM

The goals of MNT are to achieve and maintain normoglycemia, provide sufficient calories to promote appropriate weight gain, as recommended by the Institute of Medicine (IOM), to avoid maternal ketosis, and to provide adequate nutrients for maternal and fetal health.12 Upon diagnosis of GDM, the first course of action is to refer the patient to a dietitian for nutritional counseling and development of an individualized meal plan. Thus, MNT is the foundation for the management of GDM. Insulin therapy may be used concurrently with MNT if normoglycemia is not maintained consistently with diet alone. Although there are no universal specific guidelines for managing GDM, the American Diabetes Association, the American College of Obstetricians and Gynecologists, and the American Dietetic Association all recommend individualized counseling for developing a culturally-appropriate food plans emphasizing healthy food choices, portion control, and good cooking practices.1214 A modest energy restriction (30% of estimated energy needs) may be recommended for obese women with GDM to reduce blood glucose levels without elevating plasma free fatty acids or inducing ketonuria.15 However, there are no randomized controlled trials demonstrating which dietary compositions and patterns best promote normoglycemia and optimal maternal and fetal outcomes. Until those data are available, more specific recommendations cannot be made. A review of current information on the maternal diet and management of GDM or pregnancy outcome follows.

18.3.2 Energy Restriction for GDM

A common nutritional goal for all pregnant women is to provide adequate nourishment for the mother and fetus while limiting unnecessary maternal weight and fat gain. Thus, it is not surprising that the energy levels of diet patterns for women with GDM have received a lot of attention. Since 1985, seven studies have reported the effect of energy restricted diets on the outcomes of pregnancy in women who have GDM1622 (Table 18.1). Four of the studies were short-term,18,20,21,23 either 7 days or 4 weeks, making it impossible to determine the effect of maternal energy restriction on birth weight or other indicators of pregnancy outcome. Two short-term studies showed that a severe, 50%, energy restriction from 2,400 to 1,200 kcal/day for 7 days caused ketonemia and ketonuria to develop.20,23 However, 24-h mean glucose concentrations and fasting insulin levels declined. A more moderate energy restriction, 1,600–1,800 kcal/day, prevented ketonemia while improving glycemia.23

Table 18.1

Randomized controlled trials of energy restriction and pregnancy outcomes in women with gestational diabetes mellitusa

Year [reference] First Author

Study design

Study duration

Population and number [n]

Energy intake, kcal/day

Carbohydrate intake, g/day (as % of kcal)

Gestational weight gain, kg Mean ± SD

Effect on pregnancy outcome

Short-term studies

Maresh et al21

Randomized, cross-over of recently diagnosed GDM women at 28 weeks gestation

4 weeks

Diet Restr10

Diet Restr +Insulin10

1,500–1,800

1,800–2,100

120–150 (33)

150–180 (33)

0.7 kg/week

1.5 kg/week

Diet restriction + insulin reduced serum glucose to that of controls. Diet restriction with or without insulin caused ketonemia

Gillmer et al18

Randomized study of recently diagnosed GDM women

4 weeks

Diet Restr7

Diet Restr + Insulin8

1,500–1,800

2,100

120–150 g (∼33)

180 g (∼33)

−1.7 ± 2.6

+0.9 ± 2.4

Diet restriction with or without insulin caused ketonemia

Magee20

Randomized study of obese GDM women

1 week

Kcal Restr7

Control5

1,200

2,400

150 (50)

300 (50)

Not reported

Kcal restriction lower fasting insulin and 24-h mean glucose, but did not change OGTT results. Ketonemia and ketonuria occurred with kcal restriction

Knopp19

Randomized study of obese GDM women

1 week

Kcal Restr7

Control5

1,200

2,400

150 (50)

300 (50)

Not reported

Kcal restriction improved fasting and 24 h mean glucose by 22 and 10%. Ketonemia doubled in kcal/restricted group

with 33% kcal/restr (1,800 vs. 2,400), no marked ketonuria occurred

Longer-term studies

Algert16

Nonrandomized, observational

Diagnosis to delivery, 10–15 weeks

Obese GDM22

Lean GDM31

1,700–1,800

2,000–3,000

212–225 (50–60)

250–370

10.6 ± 7.7

13.3 ± 4.1

Moderate kcal restriction in obese GDM women reduced weight gain without causing ketonemia. Birth weight slightly higher – 3,922 vs. 3,544 g

Dornhorst17

Nonrandomized, observational

Diagnosis to delivery

GDM35

Non GDM [2337]

1,200–1,800

Not controlled

150–225 (50)

Not controlled

4.6 ± 4.9

9.7 ± 5.3

No difference in birth weights or incidence of macrosomia in comparison to a general prenatal non-GDM population

Rae, A.22

Stratified Randomized Controlled Trial

Diagnosis to delivery

GDM-kcal restr66

GDM-control58

1,590–1,776

2,010–2,220

210–244 (51)

240–274 (46)

11.6 ± 1.3

9.7 ± 1.5

Kcal restriction did not alter frequency of insulin therapy (17.5% vs. 16.9%), but it lowered the dose (23 vs. 60U). No difference in ketonemia, ketonuria, blood glucose, pregnancy complications, or birth weight

aAdapted from Gunderson92

Table 18.2

Dietary reference intakes (DRIs) for pregnancy that may be used for women with GDM42

Nutrient

DRI

Increase %

Rationale for increase

Comment

Energy (kcal/day)

2,855

19%

Maternal and fetal deposition

a

Carbohydrate (g/day)

175

35%

Fetal brain glucose utilization

 

Total fiber (g/day)

28

12%

Extrapolation based on increased energy intake

b

Protein (g/day)

71

54%

Maternal and fetal deposition

 

n-6 PUFA (g/day)

13

8%

Median linoleic acid intake from CSFII

c

n-3 PUFA (g/day)

1.4

27%

Median α-linolenic acid intake from CSFII

 

Calcium (mg/day)

1100

0%

Adequate adjustments in maternal homeostasis in pregnancy

d

Fluoride (mg/day)

3

0%

Limited data available to suggest increased need in pregnancy

d

Phosphorus (mg/day)

700

0%

Adequate adjustments in maternal homeostasis in pregnancy

 

Chloride (g/day)

2.3

0%

Limited data available to suggest increased need in pregnancy

d

Potassium (g/day)

4.7

0%

Daily accretion in pregnancy is small

b

Sodium (g/day)

1.5

0%

Daily accretion in pregnancy is small

d

Molybdenum (µg/day)

50

11%

Extrapolation based on average maternal weight gain

d

Selenium (µg/day)

60

9%

Fetal deposition

 

Zinc (mg/day)

11

38%

Maternal and fetal deposition

b

Choline (mg/day)

450

6%

Median intake from CSFII

d

Folate (µg/day)

600

50%

Maintain normal folate status

e

Niacin (mg/day)

18

29%

Maternal and fetal deposition plus increased energy utilization

 

Pantothenic acid (mg/day)

6

20%

Maternal and fetal deposition

 

Riboflavin (mg/day)

1.4

27%

Maternal and fetal deposition plus increased energy utilization

d

Thiamin (mg/day)

1.4

27%

Maternal and fetal deposition plus increased energy utilization

d

Vitamin A (µg/day)

770

10%

Fetal liver Vitamin A deposition

b

Vitamin B12 (µg/day)

2.6

8%

Fetal deposition and changes in maternal absorption

 

Vitamin B6 (mg/day)

1.9

46%

Maternal and fetal deposition

d

Vitamin C (mg/day)

85

13%

Amount needed to prevent scurvy in infant and estimated fetal transfer

d

Biotin (µg/day)

30

0%

Limited data available to suggest increased need in pregnancy

d

Vitamin D (µg/day)

5

0%

Daily accretion in pregnancy is small

 

Vitamin E (mg/day)

15

0%

Circulating concentrations normally increase in pregnancy; lack of clinical deficiency

 

Vitamin K (µg/day)

90

0%

Comparable concentrations in pregnancy; lack of clinical deficiency

 

aFor healthy moderately active individuals, third trimester; requirements for first trimester are not increased above non-pregnancy and requirements for second trimester are 2,708 kcal/d. Subtract 7 kcal/day for females for each year of age above 19 years.

bPercent increase for pregnant women 14–18 is slightly lower than for age 19–30 year.

cPercent increase for pregnant women 31–50 year is slightly higher than for age 19–30 year.

dPercent increase for pregnant women 14–18 year is slightly higher than for age 19–30 year.

eLow maternal folate status in very early pregnancy (before women typically know they have conceived) has been associated with the birth of offspring with a neural tube defect (NTD). Therefore, the non-pregnant DRI for women in their child-bearing years was formulated for preventing NTDs. In view of evidence linking the use of supplements containing folic acid before conception and during early pregnancy with reduced risk of NTDs in the fetus, it is recommended that all women capable of becoming pregnant take a supplement containing 400μg of folic acid every day, in addition to the amount of folate consumed in a healthy diet.

fAdapted from Ritchie and King.43

Three studies evaluated the effects of moderate energy restriction ranging from about 1,600–1,800 kcal/day from the time of diagnosis for GDM to term, or about 10–15 weeks.16,17,22 The studies were small and did not have sufficient power to determine the effects of energy restriction on birth weight. Nevertheless, none showed that a modest calorie reduction inhibited fetal growth. Furthermore, ketosis did not develop in any of the studies. One group assessed the impact of energy restriction on the need for insulin therapy in obese women with GDM.22 In both the energy restricted and control groups, about 17% of the women required insulin therapy, but there was a tendency in the restricted group toward initiating insulin therapy later in gestation and needing a lower maximum daily dosage. A larger trial with more subjects is needed to confirm this finding.

In sum, these studies of moderate energy restriction in GDM women show an improvement in glycemic control measured either by 24-h mean glucose levels, fasting insulin levels, or the amount of exogenous insulin required. The diets tended to reduce weight gain during the treatment period in the third trimester, the gestational age when fetal growth rate reaches a maximum. However, that reduction in maternal weight gain was not associated with a decrease in birth weight or an increase in the prevalence of macrosomic infants. Ketosis occurred only with a severe energy restriction to about 1,200 kcal/day; higher intakes ranging from 1,600 to 1,800 kcal/day did not produce ketosis. Since maternal body weight is a primary determinant of energy requirements, it is important to express moderate energy restriction in terms of kcal/kg rather than kcal/day. Algert et al16 showed that obese women with GDM do not develop ketosis or fetal growth retardation when consuming at least 25 kcal/kg/day. This led the fourth International Workshop-Conference on Gestational Diabetes Mellitus to support moderate calorie restriction for overweight women with GDM with prescriptions as low as “25 kcal/kg actual pregnant body weight.”24 Calorie recommendations for energy intake have not been established for normal weight women with GDM.

18.3.3 Sources and Amount of Dietary Carbohydrate

Glucose transfer occurs in a concentration-dependent manner across the placenta.1 Thus, maximal transfer across the maternal-fetal gradient occurs following meals when the maternal-fetal glucose gradient is greatest. It is thought, therefore, that accelerated fetal growth among progeny of diabetic women reflects accelerated glucose transfer due to their postprandial blood glucose levels being greater than that observed in non-diabetic women. A clear objective of dietary management for GDM women should therefore be to reduce postprandial glycemia. This can be achieved by either decreasing dietary carbohydrate at the expense of dietary fat, by increasing the proportion of carbohydrate from fiber or low glycemic sources, or both. Since fasting insulin resistance also occurs during pregnancy in normal women and women with GDM, higher fasting glucose levels may contribute to fetal overgrowth along with elevated levels postprandially. Elevated glucose concentrations in the fasting state are a particular problem among obese women.

To date, studies of the effect of the amount of dietary carbohydrate on pregnancy outcome in GDM women have been done only in women who were also consuming energy-restricted diets.25,26 As expected, the studies show that carbohydrate intake as percent of energy is positively correlated with the 1-h postprandial glucose response to a mixed meal.25,26 Likely because of the normal early morning increase in plasma cortisol (“dawn phenomenon”) the response following breakfast tended to be greater than that following lunch or dinner. This suggests the benefit of lower carbohydrate consumption at breakfast than at lunch and dinner. Major et al also demonstrated,25 that carbohydrate restriction along with a low calorie diet improves infant outcomes. In comparison with 21 women consuming between 45 and 50% of their energy as carbohydrate, women with less than 42% as carbohydrate had fewer large for gestational age (LGA) infants and less cesarean deliveries. This preliminary evidence is not sufficient to conclude that a low carbohydrate/low energy diet should be recommended for all GDM women. It suggests, however, that the benefits of an energy-restricted diet may be enhanced by a concurrent reduction in carbohydrate.

In contrast, Romon et al27 unexpectedly found that a high carbohydrate diet was associated with a decreased incidence of macrosomia in women with GDM. None of the women consuming more than 210 g carbohydrate/day gave birth to a LGA baby. This outcome is difficult to explain. It may reflect a decrease in lipolysis and circulating free fatty acids with higher amounts of dietary carbohydrate. Lower levels of free fatty acids may be associated with an improvement in insulin-stimulated glucose uptake.28 Thus, a higher intake of carbohydrate may reduce the rise in serum FFA and insulin resistance that in turn lowers the postprandial glycemic response and fetal overgrowth.

The postprandial blood glucose response is primarily determined by the rate of intestinal carbohydrate absorption, with the most rapidly absorbed refined sugars causing the highest response and the more complex, slowly absorbed carbohydrates causing the lowest response. Thus, shifting the source of carbohydrates to a higher proportion of complex, low glycemic foods may enable GDM women to maintain normoglycemia with higher carbohydrate intakes. Studies by both Fraser et al and Clapp et al showed that high fiber/low glycemic diets allowed non-diabetic pregnant women to sustain their pre-pregnancy postprandial glycemic response throughout gestation, whereas women consuming a lower fiber/high glycemic diet experienced a 190% increase in their postprandial response by late gestation.29,30 These findings suggest that the usual maternal insulin resistance and hyperglycemia observed in late pregnancy may reflect the intake of a Westernized, low fiber, high glycemic diet rather than being a normal metabolic response to pregnancy. A prospective, epidemiological cohort study confirmed that the source of dietary carbohydrate influences the risk of GDM. Among 13,110 women in the Nurses’ Health Study, high dietary fiber was strongly associated with a reduced GDM risk. Each 10 g/day increment in total fiber intake was associated with a 26% reduction in the risk for GDM. Conversely, a low cereal fiber/high glycemic load diet was associated with a 2.15-fold increased risk for GDM compared to the reciprocal diet.31 In 2008, a Cochrane review assessed the efficacy of either a high fiber or a low glycemic index diet for preventing GDM.32 Three trials (107 women) were included in the review,30,33,34 but the data were insufficient to determine if a diet rich in complex carbohydrates reduced the risk of GDM.

Recently, Moses et al evaluated the effect of a low glycemic diet on the need for insulin therapy in women with GDM. Sixty-three women with GDM were randomly assigned to a low glycemic index (GI) diet or a conventional high fiber, higher GI diet. The need for insulin therapy was significantly reduced in the low GI group, 29% vs. 59% (p = 0.023). Furthermore, 9 of the 19 women in the higher GI group were able to avoid the use of insulin by changing to the low GI diet. No differences in fetal growth or other pregnancy complications were observed between the two groups.

Currently, the American Diabetes Association recommends that dietary carbohydrate be limited to about 40–45% of the energy intake for women with GDM with a smaller proportion at breakfast than at lunch or dinner.3 In contrast, Felig and Naylor recommend greater than 45% of the total energy in the form of low glycemic carbohydrates.1 Based on the work of Fraser,30 it has also been suggested that carbohydrate intakes may be as high as 60% if they come primarily from complex sources. An adequately powered, randomized, controlled trial is needed to disentangle the relationship between pregnancy outcomes in GDM women with the amount of fiber and the amount and sources of carbohydrate they consume.

18.3.4 Sources or Types of Dietary Fat

To reduce the risk of dyslipidemia, non-pregnant, diabetic patients are advised to consume diets with less than 10% of the energy intake from saturated fats and less than 300 mg cholesterol/day.15 However, similar recommendations have not been made for women with GDM15 due to the lack of data showing a beneficial effect of dietary fat modifications on the metabolic adjustments of pregnancy in women with GDM. In a small study of women with GDM, Ilic et al35 found that the addition of fat to a test meal significantly lowered the glycemic and insulin response, presumably due to fat-induced slower gastric emptying and glucose absorption in the presence of more dietary fat. However, it is not prudent to recommend high fat intakes during gestation in order to improve glycemic control in a population at risk for future metabolic disorders, including cardiovascular disease.

To date, the effects of the degree of saturation of fatty acids on glucose tolerance during pregnancy has not been studied in a randomized controlled trial. However, evidence from several case control studies suggests that polyunsaturated fatty acids (PUFAs) may be protective against impaired glucose tolerance (IGT) or GDM whereas high intake of saturated fatty acids is detrimental.36,37 Bo et al36 found that a high intake of saturated fat, as a % of total fat, increased the risk of IGT/GDM twofold whereas the intake of PUFAs reduced the risk by 15% among 504 Italian women. Neither the total amount of dietary fat nor the amount of monounsaturated fatty acids was associated with risk for IGT/GDM. This finding was supported by a subsequent study of 1,698 pregnant women in North Carolina.38 When the diets of these women were modeled so that their intake of dietary fat was increased by 100 kcal while carbohydrate was reduced by 100 kcal, the risk of IGT and GDM increased by 12% and 9%, respectively. The types of dietary fat were not reported. However, since saturated fat intakes tend to be high in this region of the US, the increased risk of IGT/GDM with more dietary fat may reflect a higher intake of saturated fat and lower PUFAs, as observed in the study of Italian women.36 A study of 171 Chinese women37 also found that an increased intake of PUFAs (10.2 vs. 8.5% of total energy), and an associated reduction in saturated fat, lowered the incidence of GDM during pregnancy. It is not known which of the various PUFAs have the strongest impact on GDM risk. Among 1,733 first-trimester gravidas, Radesky and associates39 found that the intake of omega-3 fatty acids was associated with a small increased risk for GDM (11%), but not with IGT risk. Beneficial effects of omega-3 fatty acids on glucose tolerance have been reported in animal models, but there is no evidence that omega-3 fatty acids improve insulin action in humans.40

In addition to these nutrient-specific studies, a prospective cohort study of 13,110 women in the Nurses’ Health Study41 reported that a Western-type dietary pattern (i.e., high in red meat, refined sugars, and fried or snack foods) predicted a higher incidence of GDM compared to a prudent diet characterized by a high intake of fruit, green leafy vegetables, poultry and fish. Taken together, all of these data imply that pregnant women at risk for GDM may benefit from diets low in saturated fats and higher in PUFAs, but the findings are insufficient to determine the optimal dietary fatty acid composition for reducing IGT/GDM.

18.3.5 Micronutrient Intakes

An adequate intake of vitamins and minerals for maternal-fetal health is one of the GDM MNT goals.3 Since there is no evidence that the vitamin/mineral requirements of women with GDM differ from that of healthy pregnant women, the IOM Dietary Reference Intakes (DRIs) are appropriate for planning diets for women with GDM42 (Table 18.2). The MyPyramid (www.MyPyramid.gov) translates the DRIs into a food intake pattern. Using this pattern for pregnant women will assure that the recommended intakes of all micronutrients except iron and vitamin E will be adequate for pregnancy.43 The shortfall in iron and vitamin E can be provided easily by a vitamin-mineral supplement with at least 10 mg iron and 9 mg vitamin E.

Although there is no evidence that the dietary need for micronutrients differs between GDM and healthy women, there is evidence of an abnormal metabolism of some micronutrients in non-pregnant patients with type 2 diabetes.44 Urinary zinc excretion tends to be elevated in diabetic patients, possibly because zinc becomes chelated with glycosylated amino acids or peptides and excreted with those compounds. But, elevated urinary zinc is not always associated with reduced serum zinc concentrations in diabetic patients. Studies of diabetic pregnant rats suggest that zinc transport to the fetus is reduced, but there is no evidence that this occurs in humans. A study of 504 Italian pregnant women45 found that women with lower intakes and serum levels of zinc were more likely to be hyperglycemic. A similar inverse relationship was seen for selenium. There was no evidence, however, that the low intakes of zinc and selenium caused gestational hyperglycemia or that increased intakes of these trace elements lowers blood glucose levels.

Lower serum and urinary magnesium levels have been observed among women with type 1 diabetes or GDM.44 However, evidence that poor magnesium status increases the risk of hyperglycemia in non-pregnant or pregnant individuals is lacking. It is proposed that lower serum magnesium levels among diabetic patients reflect a positive effect of exogenous insulin on cellular magnesium uptake, leading to a decline in serum magnesium. No maternal or fetal health outcomes have been linked to low serum magnesium levels in women with GDM who are receiving exogenous insulin.

Since chromium is thought to be required for normal insulin function,41 the effects of supplemental chromium on glycemic control have been studied in healthy and GDM pregnant women. Jovanovic-Peterson and Peterson46found that chromium picolinate supplements (4 μg/kg/day) reduced hemoglobin A1c, glucose, and insulin levels compared with the patients’ baseline levels and improved glucose tolerance. However, other studies of chromium supplementation during pregnancy do not support those findings. In a prospective study of 425 women (396 healthy and 29 with GDM), serum chromium levels did not differ between the two groups of women when they enrolled for prenatal care or when they were screened for GDM in the second trimester.47 Gunton et al also reported that serum chromium concentrations were not related to glucose intolerance in late pregnancy.48 In addition, a meta-analysis of 15 RCTs concluded that the effects of supplemental chromium on glucose, insulin, or glycated hemoglobin in type 2 diabetic subjects were inclusive.49 Thus, there is no expectation that chromium supplementation would benefit women with GDM. Nor is there any evidence that poor chromium status increases the risk of GDM.

There is some evidence for an association between GDM and circulating maternal 25-hydroxy vitamin D (25(OH)D), a form of vitamin D. Zhang et al found plasma 25(OH)D at 16 weeks gestation to be significantly lower in women who subsequently developed GDM than in controls matched by season of conception, with the relation remaining significant after adjustment for maternal age, race, family history of diabetes, and pre-pregnancy BMI. There was a 1.29-fold increase in risk of GDM for every 12.5 nmol/L decrease in plasma 25(OH)D in non-Hispanic white subjects.50 Another study found a borderline significant inverse association between fasting plasma glucose and serum 25(OH)D at mid-gestation after adjusting for ethnicity, age, and BMI, but the odds ratio for GDM did not have any significance.51 This relationship between vitamin D status and GDM may be linked to maternal obesity since the incidence of both GDM and poor vitamin D status are associated with obesity.

In sum, at this time there is no evidence supporting an enhanced requirement for any micronutrient among GDM women.

18.4 Guidelines for Weight Gain During Pregnancy

The IOM recently published revised guidelines for weight gain during pregnancy for all pregnant women.2 Progressive decrements in total pregnancy weight gain were proposed for each of four categories of prepregnancy body mass index (BMI, in kg/m2) (Table 18.3). These guidelines were based on analyses of data demonstrating the amount of weight gain for women in each prepregnancy body mass index BMI category associated with delivery of a term baby weighing between 6.6 and 8.8 pounds. The only difference between these recommendations and those released in 199011 is that an upper level was established for obese women with BMIs greater than 30 kg/m2. In 1998, the National Heart, Lung and Blood Institute (NHLBI) published a similarly hierarchical set of criteria categorizing prepregnancy BMI.52 In addition to the four classes, the NHLBI created three subclasses of the heaviest (obese) group (Table 18.4). The NHLBI criteria were endorsed by the World Health Organization,53 and in 2002, the National Institutes of Health54 published guidelines for weight gain for each of the NHLBI categories of pre-pregnancy BMI.

Table 18.3

Institute of Medicine categories of prepregnancy bmi and weight gain recommendations for pregnancy for these categories3

Category

BMI (kg/m2)

Total weight gain

Rate of weight gain second and third trimester

   

In kg

In lbs

In kg/week

In lbs/week

Underweight

<18.5

12.5–18

28–40

0.44–0.58

1.0–1.3

Normal

18.5–24.9

11.5–16

25–35

0.35–0.50

0.8–1.0

Overweight

25–29.9

7.0–11.5

15–25

0.23–0.33

0.5–0.7

Obese

≥30

5.0–9.0

11–20

0.17–0.27

0.4–0.6

©2005 American Dietetic Association. Adapted with permission

Table 18.4

1998 National Heart, Lung, and Blood Institute and World Health Organization categories of pre-pregnancy BMI52 , 53 and 2002 National Institutes of Health weight gain recommendations for pregnancy for these categories54

Category

BMI (kg/m2)

Total weight gain

   

In kg

In lbs

Underweight

<18.5

12.2–18.1

27–40

Normal

18.5–24.9

11.3–15.9

25–35

Overweight

25–29.9

6.8–11.3

15–25

Obese

≥30

≤6.8

≤15

Class 1

30–34.9

   

Class 2

35–39.9

   

Class 3

≥40 or ≥35 with comorbidities

   

It is of great concern that over the past few decades there has been a marked increase in obesity. One third of all women in the US are obese. With the increase in obesity, there has been a concomitant decrease in small-for-dates neonates, and an increase in large-for-dates neonates.55 Furthermore, an increase in the proportion of pregnant women who gain more weight than is recommended for their pre-pregnancy BMI has been reported.56

Some medical societies concerned with women’s health are non-specific in their recommendations for weight gain by diabetic women during pregnancy, while others endorse the IOM, NHLBI, and NIH guidelines (Tables 18.3and 18.4). The American Diabetes Association recommends that all diabetic women follow a diet during pregnancy that provides adequate energy intake to maintain normoglycemia, appropriate weight gain, and avoidance of ketonemia. Weight reduction is discouraged, although a caloric reduction of 30% of daily energy needs for obese women who have GDM is permissible.57 The American Association of Clinical Endocrinologists advises only that weight gain should be monitored during pregnancy without commenting on caloric content.58 The American Dietetic Association recommends following the IOM guidelines for weight gain for women who have pregestational or GDM.59 While offering no guidelines for weight gain for women who have pregestational diabetes, the American College of Obstetricians and Gynecologists suggests adequate nutrients for appropriate weight gain, avoidance of ketosis, and a cautious caloric restriction of no more than 33% for obese women who have GDM.60 They recommend following the IOM guidelines for all obese pregnant women.61

Since studies of nonpregnant individuals have shown that even small reductions in body weight improve glycemic control,62 Artal et al63 initiated an intervention program to restrict weight gain in obese women with GDM. A total of 96 women were studied with 39 women in a kcal restricted diet plus exercise group and 57 women in a kcal restricted diet only group. The addition of exercise to a kcal restricted diet lowered weekly weight gain from 0.3 to 0.1 kg (p < 0.05). The incidence of LGA tended to be higher among the women who gained weight versus those who lost weight or had no weight change (10 vs. 1 macrosomic baby), but the difference did not reach statistical significance (p = 0.12). No adverse pregnancy outcomes were observed with weight maintenance or loss. It is unfortunate that the effect of weight loss or maintenance versus gain on glycemic control was not reported. However, the study suggests that prevention of excessive weight gain or, possibly, weight maintenance among high-risk, obese pregnant women may reduce the risk of fetal over-growth.

18.4.1 Rationale for Individualized Weight Gain Recommendations

That there is an association between maternal obesity during pregnancy and adverse maternal, fetal, neonatal, and childhood outcomes is of little dispute. Much of the research pertaining to the independent relationship between maternal weight gain and adverse outcomes has focused on weight gain in obese pregnant women. A number of studies of large patient populations have focused primarily on the relationships between weight gain during pregnancy and either pre-eclampsia, birth weight, or both. In studies of unselected populations of singleton births, controlling for such confounders as maternal age, ethnicity, and parity, an independent relationship has been reported between adverse outcomes and maternal weight gain exceeding 16 kg for all prepregnancy BMI groups,64 and maternal weight gain of 5–10 kg for women whose prepregnancy BMI is ≥30 kg/m2. 65 Similar findings have been reported for women whose pregnancy weight gain exceeded that recommended for BMI category by the IOM.66, 67, 68Some have,68 and some have not69 found the effects of pre-pregnancy BMI and pregnancy weight gain to be additive. Two population-based studies calculated the weight gain that was associated with the lowest incidence of a variety of adverse maternal and perinatal outcomes. One study found the optimal weight gain for obese women to be less than 13 pounds.70 The other study found the optimal weight change to be a gain of 10–25 pounds for class I and 0–9 pounds for class II, and a weight loss of 0–9 pounds for women with class III obesity.71

A study of an unselected population of pregnant women found that the average weekly weight gain before 16 weeks and between 28 and 32 weeks was significantly less than that of the respective succeeding 4 week periods.72 It appears that not only absolute weight gain but also the distribution of weight gain per trimester may be associated with the incidence of pregnancy complications. A study designed to look at the independent relationship of weight gain during each trimester and clinical outcomes analyzed data of patients who did not have diabetes or hypertension as well as those who were not obese.73 The mean weight gain was greatest in second trimester (7.7 kg) while that in first and third were respectively 2.1 kg and 6.6 kg. In multivariable analysis, weight gain in second trimester, either alone or in combination with weight gain in first and third trimester, was most strongly associated with birth weight.

After adjustment for confounders (e.g., maternal age, parity, prepregnancy BMI), studies of both gestational and pregestational diabetic women have shown independent positive relationships between maternal weight gain and adverse maternal and fetal outcomes. In women who have GDM, weight gains in excess of those recommended by the IOM were associated with an increased risk of LGA neonates and the need for augmenting diet therapy with insulin therapy to maintain acceptable levels of maternal glycemia.74 In another report,75 women who were screened for GDM with the 50-g glucose screening test and whose glucose results were <140 mg/dL and who gained ≤40 pounds during pregnancy had a significantly lower risk of having a macrosomic neonate within each of five incremental categories of the test results than did women who gained >40 pounds. Within the group found to have GDM, those who gained ≤40 pounds had a lower risk of a macrosomic neonate compared with women whose weight gain was >40 pounds (respectively 13.5% vs. 29.3%; p = 0.018). It appears that weight gain may be more influential than maternal glucose concentrations for developing fetal macrosomia since the risk of macrosomia was greater when a normal GST occurred with a weight gain of more than 40 pounds compared with that of women with one abnormal glucose tolerance test result and a weight gain of less than 40 pounds.74 Another study that combined the data of pregestational and gestational diabetic women reported positive independent relationships between LGA neonates and both prepregnancy BMI ≥30 and gestational weight gain.76 In contrast, among women with type 1 diabetes there was no relationship between gestational weight gain and the incidence of LGA neonates,77 but there was an independent relationship between LGA neonates and hemoglobin A1c concentrations during the second half of pregnancy. Finally, in another study that defined weight gain by subtracting the sum of maternal prepregnancy, neonatal, and placental weights from the maternal weight at term, there was no difference between weight gain and the incidence of LGA among women with either type 1, gestational, or no diabetes.78 The data from this study suggest that factors other than maternal weight gain, such as selective maternal-fetal transfer of energy, may influence fetal over-growth.

In summary, in the face of the burgeoning population of overweight and obese reproductive age women, analysis of contemporary data to establish ideal weight gain parameters for women who do and who do not have diabetes is indicated. In both diabetic and non-diabetic women, weight gains during pregnancy as well as maternal hyperglycemia appear to each have an independent relationship with adverse maternal and perinatal outcomes. The relative influence of each of these factors requires further exploration, however.

18.5 Effect of Cultural Beliefs and Practices on Dietary Practices

Many immigrants from developing economy nations are sustained by their indigenous cultural beliefs. Some also arrive bearing little formal education, poor language skills, little experience with and knowledge of the necessities of health care, and how to obtain them. Among immigrants from Mexico (and likely among those from other cultures) information about diet comes most often from family and friends. Thus, incorporating the spouses and members of these women’s social networks is an important component of education regarding a healthy diet during pregnancy.79

The so-called “Hispanic paradox” refers to the observation, primarily among Mexican immigrants, that despite having a number of demographic characteristics generally associated with adverse pregnancy outcomes (e.g., poverty, limited education, limited access to medical care) Mexican-American women have a lower incidence of low birth weight and prematurity than do Caucasians, Asians, and other people of color living in the USA.80,81 That these findings are more prevalent among first generation Mexican immigrant women than among those born in the U.S. may be more easily explained by elements of cultural background than by genetics.54 In one study,74 Mexico-born immigrant women were found to consume diets that contained significantly more calories, fiber, folate, vitamins A, C, and E, and zinc than did those of second generation women. When members of both groups who took diet supplements during pregnancy were compared, these differences remained significant except for the amounts of vitamin C consumed. Among the women born in Mexico, the longer they had lived in the USA, the lower their dietary content of calories, fiber, folate, vitamins A, C, and E, iron, and zinc.82

Some dietary beliefs and practices are shared by different Asian cultures. In Chinese, Korean, Vietnamese, and Asian subcontinent societies, a balance between the yin, or cool, female, soft, breath forces, and the yang, or hot, male, strong, blood forces, is thought to be necessary to achieve health and well-being for oneself and one’s baby. Pregnancy is a “hot” state. Thus, only cold foods are to be consumed. In contrast, the post-partum period is a “cold” period, and only hot foods such as hot water and tea, ginger, vinegar, pigs’ feet, and high protein meats are to be consumed. Red meats are an exception and are to be avoided because it is thought that they are slow healing. Brown seaweed soup is consumed during pregnancy and in the first 20 days following delivery. It is thought that brown seaweed soup benefits women postpartum because it cleanses the blood and increases milk production.83, 84 It is interesting that acculturation of Asian women may alter some less healthy dietary customs as well as healthy habits. For example, among Punjabi women living in Canada for 5 years or less, some requested a change from traditional high fat foods to foods with a lower fat content.85

In general, there has been little research into the effects of traditional Asian pregnancy diets and birth outcomes. One Australian study reported that there were no significant group differences in total energy intake, maternal weight gain, and birth weight between pregnant immigrants following a traditional Vietnamese diet and those consuming a non-traditional diet.86 Clearly, more research is needed on acculturation, nutrient intakes, and pregnancy outcomes. A list of beliefs and practices pertaining to pregnancy from several cultures is found in Table 18.5. Understanding these beliefs should help the health care provider to guide the pregnant immigrant to incorporate other healthy dietary practices into their traditional diets.

Table 18.5

Traditional cultural beliefs regarding diet during pregnancy and the puerperium

Mexico

Drinking milk during pregnancy causes large babies and difficult births

Ruda con chocolate (garden rue, an herb, with chocolate) speeds up labor, while chamomile tea is good for labor. Epizote (a Mexican herb) cleanses the stomach after delivery.

Because birth marks are the result of unsatisfied cravings (antojos), it is best to give in to these cravings.

China

See text re: “hot” and “cold” foods

Avoid shellfish because it may cause a rash on the baby ( www.hawcc.hawaii.edu/nursing/RNChinese02 )

Pineapple may cause miscarriages ( www.hawcc.hawaii.edu/nursing/RNChinese02 )

Squid and crab may cause the uterus to become sticky ( www.hawcc.hawaii.edu/nursing/RNChinese02 )

Coconut milk causes the baby to have good skin quality ( www.hawcc.hawaii.edu/nursing/RNChinese02 )

Soup of papaya, fish with papaya, and salty foods increase milk production ( www.hawcc.hawaii.edu/nursing/RNChinese02 )

Vietnam

See text re: “hot” and “cold” foods

Korea

See text re: “hot” and “cold” foods

See text re: brown seaweed soup (Park)

Food prohibitions including sources of protein: e.g., chicken, squid, pork, fish (Pritham)

Punjabi

Increased milk intake prevents chloasmae. (Grewal)

Soonf (fennel seeds) roasted in brown sugar induces labor (Grewal)

18.6 Lactation in Mothers Who Had GDM

There is no evidence that having had GDM interferes with initiating lactation. However, maternal obesity is a risk factor for lactation failure and, therefore, the prevalence of breast-feeding may be lower among obese women who had GDM. The reported associations between breastfeeding and a reduced risk of childhood obesity are compelling reasons to help obese mothers overcome lactation difficulties.87Because lactogenesis is promoted by maternal-fetal contact, one of the simplest ways to promote lactation among obese women is to limit maternal-newborn separation, and to assist the mother in finding comfortable ways to help the infant latch onto the breast. Obese women with larger breasts often have excess periareolar adipose tissue that flattens the areola and nipple making it more difficult for the infant to grasp the nipple.88

The energy and nutrient demands for lactating women exceed those of pregnancy.89 Given the elevated nutrient requirements of lactation, women need dietary counseling on how to plan meals that are nutrient-dense without exceeding their energy requirements. The MyPyramid food pattern developed for lactating women can assist the women in making wise food choices, http://www.mypyramid.gov/mypyramidmoms/index.html.

The postpartum period is also a good time to help obese women who had GDM lose weight and, therefore, reduce their risk for GDM in a subsequent pregnancy. A randomized intervention trial of breastfeeding overweight mothers found that those who reduced energy intake (−500 kcal/day) or who participated in aerobic exercise (45 min/4 days each week) had babies that grew similarly to those of women who were not on an energy-restricted diet or who did not exercise regularly.90 There is some evidence that energy restriction alone causes a greater loss of lean body mass compared to exercise in combination with energy restriction.91

18.7 Conclusions and Research Needed

GDM modifies the metabolism of carbohydrate and fat during pregnancy. Thus, medical nutritional therapy is the cornerstone for treating the disorder. Currently, the American Diabetic Association and the American Dietetic Association recommend developing individualized food plans for each patient that will achieve and maintain normal glycemia, provide sufficient energy to support an appropriate weight gain and avoid maternal ketosis, and supply adequate nutrients for maternal and fetal health. Specific dietary guidelines have not been established for accomplishing these goals. The limited studies of diet therapies for GDM women are observational case reports of a small number of women. Although varying degrees of energy restriction have been used for nearly 100 years to manage GDM, no large-scale, randomized, controlled trials have examined the appropriate energy need per kg body weight for improving glycemic control without ketosis and fetal growth restriction. There is some evidence that the efficacy of an energy-restricted diet is mediated by the amount and type of dietary carbohydrate. Further studies of this interaction between dietary energy and carbohydrate are needed in women who have GDM. Also, the efficacy of the amount and type of dietary carbohydrate and how it is distributed in the diet throughout the day on improving maternal glycemic control, the need for insulin therapy, and reducing fetal over-growth has not been determined independent of the amount of dietary energy. An assessment of the amount and type of dietary fat for healthy pregnancy outcomes in GDM women is also needed.

Since there is no evidence that the amount of weight gained by GDM women to support optimal fetal growth differs from that of healthy women, the American Diabetes Association recommends that the IOM guidelines for gestational weight gain in healthy women be used for women with GDM. Examination of the effect of restricting weight gain on maternal glycemic control pregnancy outcome is needed to determine if different standards should be established for overweight or obese women with GDM.

Finally, it is important to remember that GDM is a risk factor for future type 2 diabetes and cardiovascular disease. Thus, the dietary counseling provided to GDM women should be based on principles of good life-long dietary habits, and the recommended food patterns should consider the woman’s cultural background. This will enhance the likelihood of continuing the recommended food pattern into the postpartum period and, eventually, reducing the risk of GDM and associated morbidities in the mother and her child.

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