Table 7.2 The 1990 guidelines of the United States Institute of Medicine on maternal weight gain targets according to pre-pregnancy BMI
Underweight Normal weight Overweight <19.8 kg/m2 19.8, 26 kg/m2 >26 kg/m2
Weight gain term target 12.5, 18 kg 11.5, 16 kg 7.0, 11.5 kg
96 NUTRITIONAL MANAGEMENT OF DIABETES MELLITUS
environmental conditions maternal adipose deposition is limited, and diet- induced thermogenesis can fall which, when combined with a small decrease in physical activity, can conserve sufficient energy for foetal development (29,31,32).
With extreme calorie restriction in the first half of pregnancy, maternal basal metabolic rate can also fall (30).
The energy requirements of pregnancy are seldom, if ever, met by increased dietary intake as shown by cross-sectional and longitudinal nutritional studies (30).
Well-nourished women only obtain 20% of their pregnancy energy requirement from increased dietary intake (29).
In fact no increase in maternal energy intake is required providing maternal physical activity falls by 20% during pregnancy (27).
In women with high physical energy expenditures before pregnancy decreases in physical activity contribute significantly to the overall energy costs of the pregnancy (29,33).
Despite these observational studies many of the dietary recommendations for pregnancy are based on providing the total energy costs of pregnancy from increased energy intake (34).
METABOLIC CHANGES IN NON-DIABETIC PREGNANCY
Metabolic changes occur throughout pregnancy to ensure optimal foetal growth.
Maternal glucose is the primary foetal oxidative substrate (35) and by late pregnancy 17, 26 g glucose is metabolised per day (36).
The maternal respiratory quotient rises during pregnancy as foetal carbohydrate metabolism increases (29).
Metabolic changes occur to maximise the maternal, foetal transfer of glucose.
Several placental hormones are lipolytic and increase maternal circulating free fatty acids that increase maternal peripheral insulin resistance (37).
This increase in maternal insulin resistance diverts glucose away from maternal peripheral tissues to the foetus (35,38,39,40).
Post-prandial glucose and insulin concentrations rise during pregnancy in women consuming a typical Western diet.
The ability to remain glucose-tolerant while pregnant requires a trebling of insulin secretion by the end of pregnancy to counter this increase in insulin resistance (41).
Observational studies suggest that habitual diet and lifestyle factors can influence maternal glucose tolerance and insulin sensitivity in pregnancy (42).
Active women consuming low glycaemic index diets have significantly lower post-prandial glucose and insulin levels in pregnancy than women consuming high glycaemic index diets (43,44).
The higher post-prandial insulin levels encountered in pregnancy facilitate maternal fat deposition (45,46), which in well-nourished women approximates to a minimum of 4 kg of adipose tissue (46) and in undernourished women to 2 kg (32).
A fall in fatty acid oxidation in late pregnancy also contributes to adipose deposition (29).
THE DIETARY MANAGEMENT OF DIABETIC PREGNANCIES 97
Other maternal metabolic changes occur to ensure a steady supply of glucose to the foetus.
Lipolytic placental hormones increase maternal lipolysis during the post-absorbative periods, generating sufficient gluconeogenic substrates in the form of ketone bodies and glycerol to provide the necessary glucose for foetal use (45).
An increase in maternal hepatic glucose output ensures a necessary glucose supply to the foetus during fasting (48,49).
Although ketone bodies can cross the placenta and be used as foetal fuels, non-esterified acids cannot.
SPECIFIC METABOLIC CHANGES ASSOCIATED WITH TYPE 1 DIABETES
Dietary factors, insulin adjustments and blood glucose values are so interdependent in women with Type 1 diabetes that one should not consider any one in isolation.
Women with Type 1 diabetes have an absolute deficiency of insulin and their glycaemic control is totally dependent on exogenous insulin and dietary intake.
The metabolic and physiological changes occurring in early pregnancy make these women especially vulnerable to hypoglycaemia, and this is further compounded if food intake falls due to pregnancy-induced nausea or vomiting.
In later pregnancy, due to the increase in maternal lipolysis during the post-absorbative and fasting periods, ketoacidosis may develop rapidly.
To minimise metabolic complications one needs to continually match and adjust the insulin doses to the carbohydrate intake.
Maternal ketosis, as assessed by urine strips, is usually an indication for an increase in both dietary carbohydrate and insulin treatment.
Diets need to be individual and flexible enough to adjust to any of the numerous co-morbidities encountered in pregnancy, such as hyperemesis gravidarum or gastroparesis.
If nausea is a problem in early pregnancy the use of liquid meals should be considered, as these are often better tolerated than solids.
Going without regular food and insulin in this group is not an option.
SPECIFIC METABOLIC CHANGES ASSOCIATED WITH TYPE 2 DIABETES
Women with Type 2 diabetes have a relative rather than an absolute deficiency of insulin.
These women are already insulin-resistant and with the physio- logical increase in insulin resistance that occurs in pregnancy their insulin deficiency is further compromised.
Very large doses of exogenous insulin are often required to obtain the necessary blood glucose target values.
Avoiding excessive weight gain in these obese women being treated with large insulin doses requires considerable dietary education and intervention early in
98 NUTRITIONAL MANAGEMENT OF DIABETES MELLITUS
pregnancy. The use of low-calorie foods and snacks should be encouraged. Appropriate weight targets should be set and a degree of energy restriction considered, see below.
SPECIFIC METABOLIC CHANGES ASSOCIATED WITH GESTATIONAL DIABETES
A degree of b-cell dysfunction is universal in women with GDM, both during and following pregnancy (50, 52).
Women who develop GDM not only have insufficient b-cell reserve to remain glucose-tolerant in pregnancy, but higher peripheral and hepatic insulin resistance than glucose-tolerant women (53).
The b-cell defect is more apparent in the non-obese than obese GDM women in whom insulin resistance is often a greater contributing factor (54).
These metabolic defects result in abnormalities of post-prandial lipoprotein metabolism (55) that can further reduce insulin sensitivity and compromise b-cell function (37,56).
The diet should be aimed at lessening these metabolic abnormalities.
As with the Type 2 diabetic women, most of the women who develop GDM are obese and weight gain targets should be set and a degree of energy restriction considered, see below.
However, unlike the Type 2 diabetic women most can achieve adequate glycaemic control with diet alone.
For this reason the dietary recommendations for GDM will be considered in further detail below.
GENERAL DIETARY RECOMMENDATIONS FOR GDM
A dogmatic approach to the dietary advice for GDM should be avoided as only four randomised trials of primary dietary management of GDM against no treatment were considered to be of sufficient standard to include in a recent Cochrane systematic review (57).
This pooled data analysis of 612 women failed to show any benefit of dietary intervention on final birthweight, risk of LGA infants and/or Caesarean deliveries (57).
However, ignoring all clinical and observational nutritional studies that have no non-intervention arm is probably unwise, and until definitively controlled studies are done each available study should be considered on its own merit.
The objectives in the dietary management of GDM include glycaemic control, balancing adequate nourishment for the mother and foetus, while limiting excessive weight gain, and establishing healthy eating habits that will continue beyond the pregnancy.
Lifestyle changes encompassing diet and exercise should be started during the pregnancy itself, when access to a qualified dietitian is likely to be greater than at any future time.
THE DIETARY MANAGEMENT OF DIABETIC PREGNANCIES 99
It is important that women with gestational diabetes understand why dietary intervention during the pregnancy is so important to obstetric care.
It is worth stressing that adherence to a diet in pregnancy can in most women improve glycaemic control.
Understanding that a diet will reduce her risk of having a very large baby and the need for insulin therapy in pregnancy will help compliance.
The importance of avoiding unnecessary weight gain needs to be emphasised, and women need to know that too much weight gain increases the risk of delivering an LGA infant and increased obesity post partum (58).
Unnecessary weight gain will also increase the future risk of developing GDM in a subsequent pregnancy (59), and diabetes in later life (60).
CALCULATING TOTAL ENERGY FOR THE DIET AND SETTING SAFE WEIGHT GAIN TARGETS
In our practice we calculate an individual’s energy requirement using the pre- pregnancy weight to calculate resting energy expenditure, using Schofield’s formula (61), and a physical activity ratio of 1.6.
To this we add 200 kcal for the energy requirements for the third trimester.
If we wish to induce a mild degree of negative energy balance we subtract 500 kcal from this calculated daily energy requirement to provide the total energy for the diet.
The American Diabetic Association (ADA) have endorsed dietary guidelines for diabetes in pregnancy (62) that are based on pre-pregnancy weights, see Table 7.3.
As previously mentioned, current American guidelines recommend a minimum weight gain of 7.0 kg for all obese (BMI>29 kg/m2) women, both diabetic (63) and non-diabetic (24).
No equivalent weight or daily calorie guidelines exist for the UK.
Our own unit limits weight gains in diabetic pregnancies to the bottom rather than the top of those recommended for average, overweight and obese women.
For Type 2 diabetic women and those with GDM if the BMI is >34 kg/m2 we set no minimum weight gain.
Ideally we like to achieve no overall weight gain in the overweight woman post partum and weight loss in the morbidly obese woman.
Table 7.3
Pre-pregnancy weight (% ideal body weight) Daily calorie intake (kcal/kg)
<90% 36, 40 90, 120% 30 121, 150% 24 >150% 12, 18