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A randomized trial of the effects of dietary counseling on gestational weight gain and glucose metabolism in obese pregnant women

International Journal of Obesity volume 32, pages 495501 (2008) | Download Citation




Can gestational weight gain in obese women be restricted by 10-h dietary consultations and does this restriction impact the pregnancy-induced changes in glucose metabolism?


A randomized controlled trial with or without restriction of gestational weight gain to 6–7 kg by ten 1-h dietary consultations.


Fifty nondiabetic nonsmoking Caucasian obese pregnant women were randomized into intervention group (n=23, 28±4 years, prepregnant body mass index (BMI) 35±4 kg m−2) or control group (n=27, 30±5 years, prepregnant BMI 35±3 kg m−2).


The weight development was measured at inclusion (15 weeks), at 27 weeks, and 36 weeks of gestation. The dietary intakes were reported in the respective weeks by three 7-day weighed food records and blood samples for analyses of fasting s-insulin, s-leptin, b-glucose, and 2-h b-glucose after an oral glucose tolerance test were collected.


The women in the intervention group successfully limited their energy intake, and restricted the gestational weight gain to 6.6 kg vs a gain of 13.3 kg in the control group (P=0.002, 95% confidence interval (CI): 2.6–10.8 kg). Both s-insulin and s-leptin were reduced by 20% in the intervention group compared to the control group at week 27, mean difference: −16 pmol l−1 (P=0.04, 95% CI: −32 to −1) for insulin and −23 ng ml−1 (P=0.004, 95% CI: −39 to −8) for leptin. At 36 weeks of gestation, the s-insulin was further reduced by 23%, −25 pmol l−1 (−47 to −4, P=0.022) and the fasting b-glucose were reduced by 8% compared with the control group (−0.3 mmol l−1, −0.6 to −0.0, P=0.03).


Restriction of gestational weight gain in obese women is achievable and reduces the deterioration in the glucose metabolism.


With the worldwide increasing prevalence of obesity, maternal obesity is now one of the most common high-risk obstetric conditions.1 Preconceptional obesity and excessive gestational weight gain are important preventable risk factors for maternal and neonatal morbidity and mortality. Maternal obesity is associated with higher risks of gestational diabetes mellitus (GDM),2, 3, 4, 5 preeclampsia and other hypertensive diseases,2, 3, 4, 5 late fetal death,5, 6, 7 macrosomia,4, 5, 8, 9 and cesarean delivery.2, 5, 8, 9 Whereas excessive gestational weight gain is an independent risk factor of high birth weight,2, 3, 10, 11 cesarean and operative deliveries,11 and postpartum maternal weight retention.12, 13, 14, 15, 16

Weight gain during pregnancy has generally been neglected in obesity research due to the relatively short period of gestation compared to total lifespan. With the worldwide increased prevalence of obesity and the high percentage of women with excessive gestational weight retention, the topic has become increasingly significant.17, 18, 19

The US Institute of Medicine (IOM) recommendations for gestational weight gain are based on observational studies in women delivering full-term babies weighing between 3 and 4 kg. The recommendations aim to balance the benefits of increased fetal growth with risks of complicated labor and delivery.10 However, due to a lack of studies that provide knowledge on gestational weight in obese women, IOM give no upper limit for obese women. As an aspect of public health concern, it is a high importance to encourage obese pregnant women only to gain the minimum amount needed, instead of building new depots and thereby further increasing their health risk. However, this recommendation has never been evaluated in randomized controlled trials.

An increase in serum insulin and development of insulin resistance is normal with advancing gestation because the maternal metabolism is directed towards supplying adequate nutrition for the fetus.20 However, obese women already have elevated serum insulin and leptin concentration in the nonpregnant state, and they may be more vulnerable to further elevations during pregnancy.21 The prevalence of GDM is rapidly increasing and recently reported numbers suggest that 5–6% of pregnancies are complicated by GDM.22 Recurrent GDM in a following pregnancy is seen among one-third of women who earlier experienced a pregnancy complicated by GDM.23, 24 Furthermore, offspring of obese mothers or mothers with GDM are at higher risk of being macrosomic or large-for-gestational-age at birth24, 25 and are at increased risk of childhood obesity15 and development of type 2 diabetes.26

New evidence suggests that the pregnancy-induced increases in leptin may trigger the development of macrosomia,27 preeclampsia,21 and GDM22 in women with elevated levels in early pregnancy. Leptin concentrations at delivery are positively associated with birth weight and cord leptin concentration is elevated in infants born to diabetic mothers.27

In nonpregnant state, weight loss is known to induce reductions in insulin and leptin concentrations, whereas weight gain increased the concentrations. Consequently, alterations in the metabolic control of blood glucose mediated though elevated insulin and leptin concentrations may be important predictors of high-risk obstetric complications.

In this study, we investigate whether restriction of gestational weight gain in obese women can be achieved by dietary counseling and whether this restriction could reduce the pregnancy-induced increases in insulin, leptin, and glucose.


Nondiabetic Caucasian obese pregnant women were enrolled in a randomized controlled intervention study, designed to restrict the gestational weight gain to 6–7 kg. The computerized randomization took place after the women had given written informed consent in accordance with the Helsinki II Declaration.

The intervention group received 10 consultations of 1 h each with a trained dietitian during the pregnancy. The women were instructed to eat a healthy diet according to the official Danish dietary recommendations (fat intake: max 30 energy percent (E%), protein intake: 15–20 E%, carbohydrate intake: 50–55 E%). The energy intake was restricted based on individually estimated energy requirements and estimated energetic cost of fetal growth (energy requirement=basal metabolic rate × 1.4 (physical activity level factor of 1.2+0.2 added to cover energetic cost of fetal growth)).

The control group had no consultations with the dietitian and had no restrictions on energy intake or gestational weight gain.

Seven-day weighed food records were obtained at inclusion, and at 27 and 36 weeks of gestation in both groups. Daily energy intake and diet composition were calculated using Dankost 3000 software (Danish Catering Center A/S). In the intervention group, the food records were used as a tool to identify unhealthy eating patterns and give individualized suggestions of improvements.

The weight (fasting with voided bladder and light clothing), height, blood pressure, and heart rate were measured at inclusion and at 27 and 36 weeks of gestation. Fasting blood samples for measurements of serum insulin, serum leptin, and blood glucose were also collected at these visits. Serum insulin was analyzed by AutoDelfia Insulin, Fluoroimmunoassay (PerkinElmer, Zaventem, Belgium) and serum leptin was analyzed by Biomol Leptin Sandwich ELISA kit (Biomol Research Laboratories Inc., Plymouth Meeting, Philadelphia, USA). Fasting blood glucose and blood glucose 2 h postprandial to an oral glucose tolerance test of a 50-g glucose load were analyzed by Hemocue B-Glucose Analyzer (HemoCue, Ägelholm, Sweden).

Dietary supplements were supplied to all participants to ensure a sufficient intake of vitamins and trace elements with special emphasis on iron and folic acid intake (BioVinci Female, Unikalk, PharmaVinci A/S; Iron, Matas A/S).

All participants followed the routine clinical schedule with additional ultrasound measurement of fetal growth at 30, 33, and 36 weeks of gestation. Duration of gestation was ascertained by ultrasound scanning of biparietal diameter. Birth weight, infant length at delivery, placental weight, Apgar score, head and abdominal circumference were obtained at delivery. The mothers' hospital journals were monitored for pregnancy and birth complications, and method of delivery. The physicians and midwives were blinded in regard to the treatment assignment, and the women were asked not to reveal the allocation by the randomization.

Prepregnancy weight, maternal weight development from 36 weeks of gestation until delivery, and 1st, 2nd, and 3rd week postpartum, was reported by self-administered questionnaires. Furthermore, the maternal body weight was measured at 4 weeks postpartum (28±9 days) at the department.

Total gestational weight gain was calculated as the difference between self-reported prepregnancy weight and weight just before delivery. Due to possible bias of self-reported prepregnancy weight, these data and inclusion data were collected before randomization, and possible effect of misreporting should thus be of the same size in both groups. Furthermore, to avoid a possible influence of bias, rate of weight gain was calculated as the difference between the measured weight at inclusion and 36 weeks of gestation divided by the number of weeks from inclusion to 36 weeks of gestation.


The study was performed in cooperation between the Department of Clinical Nutrition, Hvidovre Hospital and the Department of Obstetrics and Gynecology, Herlev Hospital. The local ethics committee of Frederiksberg and Copenhagen approved the research protocol (no. KF-01-102/01).

The pregnant obese women (body mass index (BMI) 30 kg m−2) were recruited in their early pregnancy (15±3 weeks of gestation) from the register of newly diagnosed pregnancies. Exclusion criteria were smoking, age below 18 or above 45 years, multiple pregnancy, and medical complications known to affect fetal growth adversely or to contraindicate limitation of weight gain.

Seventy-three pregnant women were recruited to the study, but seven women developed conditions that made them ineligible for continued participation; one women had a early spontaneous abortion, one discovered twin pregnancy, one continued smoking, two were bedridden from early pregnancy (one due to fibromyoma of the uterus and one due to pelvic pain), and two were diagnosed with GDM) at inclusion.

A flow chart of the 66 eligible pregnant women enrolled in the study is presented in Figure 1. Thirteen women dropped out early in the trial, mainly due to lack of time to participate in a time-consuming trial, or disappointment at being randomized to control group. The women, who dropped out, did not differ in characteristics from the participating women. Three women in the control group developed GDM during pregnancy and were offered dietary consultations following recommendation for gestational diabetic diet.19 Consequently, their data were excluded from statistical analyses, except for the reports on the incidence of GDM.

Figure 1
Figure 1

Flowchart of enrollment and randomization of eligible subjects. *Gestational diabetes mellitus (GDM).

Data at inclusion for the remaining 50 nondiabetic completers are shown in Table 1. There were no significant differences in baseline characteristics between the two groups.

Table 1: Data obtained at the inclusion visit and baseline measures of fasting s-insulin, s-leptin, and b-glucose, and b-glucose after a 2-h OGTT

Statistical methods

All statistical analyses were performed in SPSS for Windows (SPSS Inc., Chicago, IL, USA). For the descriptive analyses of differences between intervention and control group simple Student's t-test and 95% confidence intervals (CIs) were used. Dichotomous variables were tested using χ2 test.

Mean differences in weight development between the two groups and the changes in blood parameters were analyzed using analysis of covariance with maternal age and parity included as fixed factors, and height and weight at inclusion included as covariates in the model. For analyses of the blood parameters, the concentration at inclusion was added as covariate as well. The model was reduced by excluding factors with P>0.1. Ninety-five percentage CIs were calculated for mean differences.

Group effects on dietary intake were tested using repeated measurements including intake, weight, and height at inclusion as covariates and maternal age and parity included as fixed factors in the model.

Missing measurements and outlying values

Data and blood samples were collected at inclusion and 27 weeks of gestation for all 50 women, whereas three women missed their visit at 36 weeks of gestation: two due to early delivery and one because of vacation.

Maternal weight just before delivery, just after delivery, and 1, 2, and 3 weeks postpartum were only reported by 45, 36, 44, 45, and 42 of the 50 women, respectively. Fifteen women failed to have their weight measured within 3–7 weeks postpartum. Consequently, only 35 women were included in this measurement.

The analyses were subsequently controlled for impact of missing values by replacing these with average of the entire group to ensure that the statistical test did not differ, significantly. Two women had outlying values of insulin and leptin, the analyses were performed both with and without these values, but since they did not substantially impact the results, they were kept in the analyses.


Dietary intake and weight development

The women in the intervention group successfully limited their energy intake, and followed the dietary instructions for the recommended macronutrient composition of the diet (Table 2). The fat energy and carbohydrate percentages of the diet decreased, and the protein E% of the diet increased in the intervention group compared to the control group. There were no group differences in alcohol energy percentage or amount of food.

Table 2: Dietary intake during pregnancy in 50 obese pregnant women

Consequently, the intervention group restricted their total gestational weight gain to an average of 6.6±5.5 kg, compared to a gain of 13.3±7.5 kg in the control group (a mean difference of 6.7 kg; 95% CI of the difference: 2.6–10.8 kg, P=0.002) (Figure 2). The average weekly weight gain from inclusion to 36 weeks of gestation was significantly reduced by 0.18 kg week−1 (0.07–0.30, P=0.02) in the intervention group compared to the control group (0.26±0.15 vs 0.44±0.21 kg week−1). The weight gain until 36 weeks of gestation was highly correlated to total gestational weight gain (r2=0.73, P<0.001) and associated only by initial height and group allocation, which together explained 36% of the variation in weight gain (group: P=0.002, height: P=0.04). There were no group differences in weight gain from self-reported pregnancy weight to inclusion (0.6 vs 2.2 kg (95% CI of difference: −0.5 to 3.8, P=0.862)) or in the spontaneous weight loss by giving birth (6.7 vs 7.2 kg (95% CI of difference: −1.8 to 0.7, P=0.393)).

Figure 2
Figure 2

Weight development from prepregnancy weight to 4 weeks postpartum. Full-colored circles and squares symbolize intervention group, whereas open circles and squares represent the control group. Circles symbolize self-reported data and squares symbolize measured data. Data are presented as mean values+s.e.m. Stars indicate significant differences between the groups (**P=0.01). Tests not shown for weight just after delivery, and 1, 2, and 3 weeks post partum gain (all tests P=0.01).

The intervention group (n=16) retained 6.9 kg less weight than the control group (n=19) 4 weeks postpartum (−4.5 vs 2.4 kg, 95% CI of difference: 2.5–11.2, P=0.003) compared to the pregnancy weight (Figure 2).

Glucose metabolism

The restriction of the gestational weight gain in the intervention group reduced the increment in both s-insulin and s-leptin by 20% compared to the control group at 27 weeks of gestation, group difference: −16 pmol l−1 (−32 to −1, P=0.04) and −23 ng ml−1 (−39 to −8, P=0.004) (Figures 3 and 4). The s-insulin was further reduced by 23% at 36 weeks of gestation, −25 pmol l−1 (−47 to −4, P=0.022), whereas no significantly additional effect was obtained on the s-leptin concentration, −12 ng ml−1 (−31 to 7, P=0.201).

Figure 3
Figure 3

Changes in insulin concentration during pregnancy, intervention group (full-colored, n=23) vs controls (open squares, n=27). Data are presented as mean values+s.d. P-values represent test of group differences by reduced ANCOVA models at 27 and 36 weeks of gestation. ANCOVA, analysis of covariance.

Figure 4
Figure 4

Changes in leptin concentration during pregnancy, intervention group (full-colored, n=23) vs controls (open squares, n=27). Data are presented as mean values+s.d. P-values represent test of group differences by reduced ANCOVA models at 27 and 36 weeks of gestation. ANCOVA, analysis of covariance.

The fasting glucose concentration in the control group had a small decrease with advancing gestational age, −0.04 mmol l−1 (−0.2 to 0.2) at 27 weeks of gestation, and −0.1 mmol l−1 (−0.3 to 0.1) at week 36. The intervention showed no reduction of the fasting glucose at 27 weeks, but at 36 weeks the fasting glucose was significantly reduced by 8%, group difference −0.3 ng ml−1 (−0.6 to −0.0, P=0.03). No differences were obtained between intervention and control group in the 2-h glucose concentration after oral glucose tolerance test at 27 and 36 weeks of gestation, 0.1 ng ml−1 (−0.6 to 0.8, P=0.852) and 0.3 ng ml−1 (−0.4 to 1.0, P=0.406).

Birth outcomes

The birth outcomes and incidence of pregnancy and birth complications in the two groups is listed in Table 3.

Table 3: Birth outcomes and incidence of complications

It is beyond the scope of this study to investigate an impact of weight restriction on fetal growth. However, the intervention did not have any detectable adverse effects on fetal growth, and we observed fewer incidences of pregnancy and birth complications, although this requires further investigation in studies of larger sample size.


This study demonstrated that it is possible to restrict the gestational weight gain in obese women by a dietary intervention that aimed to restrict the energy intake and provide a macronutrient composition of the diet consistent with the official Danish dietary recommendations. The intervention resulted in a reduction of total gestational weight gain to half that of the control group. Furthermore, the results show that the restriction attenuated the increases in pregnancy-induced changes in fasting insulin, leptin, and glucose during pregnancy. We observed no adverse effects on fetal growth and incidences of pregnancy and birth complications, although this requires further investigation in studies of larger sample size.

Maternal obesity is the predominant risk factor for gestational diabetes and pregnancy-induced hypertensive disorders, and evidence suggests that the increased risk may be mediated through the metabolic changes in glucose, insulin, and leptin. A restriction of excessive gestational weight gain in obese women could play an import role in the prevention of these pregnancy complications by reduced concentrations of glucose, insulin, and leptin.

Pregnancy may be the phase in a woman's life when lifestyle interventions are likely to be successful, as they are highly motivated due to the possible positive impact for their child. However, to our knowledge no studies have previously investigated the metabolic impact of a restriction of the weight gain in obese women.

Qiu et al.22 found that elevated leptin concentrations in early pregnancy (13 weeks of gestation) were positively associated with the risk of development of GDM. The group of women with the highest tertile of leptin had a 4.9-fold increased risk of GDM compared to the lowest after adjustment of maternal prepregnant BMI. Each 10 ng ml−1 increase in leptin concentration was associated with a 20% increase in GDM risk. Ning et al.21 showed that the highest risk of development of preeclampsia was seen among overweight women with elevated leptin levels as compared to lean women with no leptin elevation. A 10 ng ml−1 increase in leptin concentration was associated with a 30% increased risk of preeclampsia, after adjusting for prepregnancy BMI maternal age, ethnicity, parity, and family history of hypertension.

Both studies suggest that elevated leptin concentrations in early pregnancy may be a strong predictor of common high-risk obstetric situations and that a positive linear association exists between increase in leptin and risk of GDM and preeclampsia. However, compared to our study on obese women, they also included normal weight women, and all participants in our study had leptin concentrations above 31.0 ng ml−1, which were the highest tertile in the study of Qiu et al.22 It would be of further interest to investigate whether this association is consistent among obese women and whether changes in leptin concentration altered by gestational weight gain could influence the relative risks of GDM and preeclampsia.

Strengths and limitations

An important strength of our study is the randomized design and intensive monitored weight development and repeated measures of insulin, leptin, and glucose. Time-integrated measures of the changes in the glucose metabolism could in a larger trial provide further information on how pregnancy and birth complications and are affected by alteration of the glucose metabolism. However, an important limitation for the generalization of the results from this study is the scientific settings of the trial with time-consuming extra ultrasound scans and blood samples that may also have increased the number of dropouts, favoring the recruitment of more motivated participants. Furthermore, the unrestricted control group knew they were participating in a study of maternal weight limitation. This may have influenced gestational weight gain in this group. However, this would only cause an underestimation of the effect of the intervention.

In this study, we excluded the three women who developed GDM in the control group, since these women received dietary counseling when diagnosed regardless of randomization. Inclusion of these subjects would probably have improved the effect of weight restriction. Repeating the study design in a larger group of women could provide information on whether the development of GDM and other pregnancy and birth complications as well as fetal growth could be affected by the intervention.


This study shows that prevention of excessive weight gain in obese women is achievable and can reduce the pregnancy-induced increases in fasting insulin, leptin, and glucose. Future studies should address whether prevention of excessive gestational weight gains in obese women decrease the risk for macrosomia, preeclampsia GDM and later type 2 diabetes.


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Dietitian Anna Marie Kjellingbro, study nurse Hanne Panduro, midwife Margit Holm, MSc Janne Lorentzen, and MSc Camilla Schou Larsen are acknowledged for the skilled and excellent contributions to this study.

Source of funding: Supported by the Desireé and Niels Yde Foundation. Pharma Vinci, Denmark provided vitamins.

Author information


  1. Department of Human Nutrition, Faculty of Life Science, Copenhagen University, Copenhagen, Denmark

    • S Wolff
    • , S Toubro
    •  & A Astrup
  2. Department of Obstetrics and Gynecology, Herlev Hospital, Copenhagen University, Copenhagen, Denmark

    • J Legarth
    •  & K Vangsgaard


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Correspondence to S Wolff.

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