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American Journal of Clinical Nutrition, Vol. 87, No. 5, 1346-1355, May 2008
© 2008 American Society for Nutrition


ORIGINAL RESEARCH COMMUNICATION

Nutrient and food group intakes of women with and without bulimia nervosa and binge eating disorder during pregnancy1,2,3

Anna Maria Siega-Riz, Margaretha Haugen, Helle M Meltzer, Ann Von Holle, Robert Hamer, Leila Torgersen, Cecilie Knopf-Berg, Ted Reichborn-Kjennerud and Cynthia M Bulik

1 From the Departments of Epidemiology and Nutrition (AMS-R), the Department of Biostatistics (RH), and the Department of Nutrition (CMB), School of Public Health, University of North Carolina at Chapel Hill; the Division of Environmental Medicine (MH and HMM) and the Division of Mental Health (LT, CK-B, and TR-K), Norwegian Institute of Public Health, Oslo, Norway; the Department of Psychiatry, University of North Carolina at Chapel Hill (AVH, RH, and CMB); and the Institute of Psychiatry, University of Oslo, Oslo, Norway, and the Department of Epidemiology, Columbia University, New York, NY (CMB)

2 Supported by the National Institutes of Health (HD047186 to CMB) and the Clinical Nutrition Research Center (NIDDK56350 to AMS-R). The MoBa study is supported by the Norwegian Ministry of Health, NIH/NIEHS (N01-ES-85433), NIH/NINDS (1 UO1 NS 047537-01), and the Norwegian Research Council/FUGE (151918/S10).

3 Reprints not available. Address correspondence to AM Siega-Riz, Carolina Population Center, CB#8120 University Square, University of North Carolina at Chapel Hill, Chapel Hill, NC 27516-3997. E-mail: am_siegariz{at}unc.edu.


    ABSTRACT
 TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Background: Little is known concerning the dietary habits during pregnancy of women with eating disorders that may lie in the causal pathway of adverse birth outcomes.

Objective: We examined the nutrient and food group intakes of women with bulimia nervosa and binge-eating disorder during pregnancy and compared these with intakes of women with no eating disorders.

Design: Data on 30 040 mother-child pairs from the prospective Norwegian Mother and Child Cohort Study were used in cross-sectional analyses. Dietary information was collected by using a food-frequency questionnaire during the first half of pregnancy. Statistical testing by eating disorder categories with the non-eating-disorder category as the referent group was conducted by using log means adjusted for confounding and multiple comparisons. Food group differences were analyzed by using a Wilcoxon's two-sided normal approximation test that was also adjusted for multiple comparisons.

Results: Women with binge-eating disorder before and during pregnancy had higher intakes of total energy, total fat, monounsaturated fat, and saturated fat, and lower intakes of folate, potassium, and vitamin C than the referent (P < 0.02). Women with incident binge-eating disorder during pregnancy had higher intakes of total energy and saturated fat than the referent (P = 0.01). Several differences emerged in food group consumption between women with and without eating disorders, including intakes of artificial sweeteners, sweets, juice, fruit, and fats.

Conclusion: Women with bulimia nervosa before and during pregnancy and those with binge-eating disorder before pregnancy exhibit dietary patterns that differ from those in women without eating disorders, that are reflective of their symptomatology, and that may influence pregnancy outcomes.


    INTRODUCTION
 TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Eating disorders are prevalent in women of reproductive age, with {approx}1.5% of women reporting bulimia nervosa (BN) and 3.5% reporting binge-eating disorder (BED) (1). BN is characterized by eating an unusually large amount of food in a discrete period of time while feeling out of control (ie, binge eating) coupled with compensatory behaviors such as self-induced vomiting, laxative abuse, excessive exercise, or fasting. BED shares the symptoms of binge eating with BN, but in the absence of compensatory behaviors. Although the consequences of eating disorders for a woman's health are well-documented and potentially severe (2, 3), only a moderate amount of literature exists on their effect on the course of pregnancy and birth outcomes. The limited data show an increased risk of miscarriage, hyperemesis, preterm birth, lower birth weight, being small for gestational age, and smaller head circumferences (4-8).

The importance of nutrition during pregnancy has been well documented, with evidence suggesting a protective effect against various adverse birth outcomes for pregnant women following professional recommendations (9-11). For example, during pregnancy, women are encouraged to eat an additional 340 kcal/d starting in the second trimester and 452 kcal/d in the third trimester to meet the demands of the pregnancy state (12). The requirements for many micronutrients are increased as well, such as iron, folate, and vitamin C (13, 14). Given that BN and BED are characterized by erratic eating behaviors, and in BN purging and periods of restriction, one would predict high overall energy intake but low micronutrient intakes. However, there have been no prior prospective, population-based cohorts of pregnant women in which to study the impact of eating disorders on dietary intake during pregnancy. This analysis was carried out to fill this very important gap in the literature. Using data from the Norwegian Mother and Child Cohort (MoBa), we were able to examine the nutrient and food group intakes of women with BN and BED during pregnancy and compare these with intakes of women who were free of any eating disorder either before or during pregnancy.


    SUBJECTS AND METHODS
 TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Design
The data were collected as part of the MoBa Study at the Norwegian Institute of Public Health. This is a prospective pregnancy cohort that in the period from 1999 to spring 2007 included {approx}85 000 pregnancies and that aims to include 100 000 by 2008 (15). Pregnant women are recruited to the study by postal invitation after they have signed up for the routine ultrasound examination in their local hospital. Participants are asked to provide biological samples and to answer questionnaires covering a wide range of information, so far up to the age of 8 y for the child. The cohort database is linked to the Medical Birth Registry of Norway (16). Variables used to describe women in this analysis included maternal age, education, marital status, parity, and region of birth. The study was approved by the University of North Carolina, School of Medicine Institutional Review Board, the appropriate regional committees for ethics in medical research, and the Norwegian National Data Inspectorate.

Subjects
The number of records available for this analysis was initially 54 714. We excluded MoBa participants who had missing information in the Medical Birth Registry (n = 2464); had information from an early test version of questionnaire 1 (n = 2599); did not have valid values for self-reported age, weight, or height (n = 3078); had returned questionnaire 1 after delivery (n = 152); had multiple births (n = 1899); or had a stillbirth (n = 232). For those with more than one pregnancy in the study, we only included the first pregnancy. Of the 54 714 records available, 75.2% were available at the start for this analysis, in which each record represents one mother who had one child.

Information for the categorization of women into eating disorder subtypes came from questionnaire 1 and included items that were previously used for studies of eating disorders in the Norwegian Institute of Public Health Twin Panel (17-20) and were designed in accordance with the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (21). As previously published (22), diagnostic algorithms were constructed from the questionnaire items to define eating disorder subtypes: broadly defined anorexia nervosa (AN), defined as meeting the criteria for AN (with the exception of amenorrhea and also endorsing a body mass index < 19.0 at the time of low weight); broadly defined BN (endorsing at least weekly frequency of binge eating and purging and categorized as BN any type, BN purging type, BN nonpurging, type); broadly defined BED (at least weekly frequency of binge eating in the absence of compensatory behaviors); and eating disorders not otherwise specified with purging (purging at least weekly in the absence of binge eating). Questions for binge eating included both eating an unusually large amount of food and feeling out of control. AN was assessed before pregnancy only because of practical difficulties in determining low weight in the presence of pregnancy-related weight gain. BN, BED, and eating disorders not otherwise specified with purging were assessed for both 6 mo before pregnancy (retrospective assessment) and at the time of survey completion. The respondents were specifically asked to distinguish between pregnancy-related nausea and vomiting and self-induced vomiting as a purging method. Self-reported weight and height were used to calculate prepregnancy body mass index (in kg/m2) and body mass index at the time of assessment. Respondents completed questionnaire 1 at a median of 18.1 wk gestation (interquartile range: 16.7–20.1 wk).

We created categories of eating disorders that were mutually exclusive representing the status of the women both before and during pregnancy. If a woman was missing information on eating disorders either before or during pregnancy, she was excluded (n = 3983). We also excluded women with AN and eating disorders not otherwise specified with purging before pregnancy because of their small sample sizes, 30 and 38 respectively, and focused only on women with BN and BED (n = 37 106; Table 1Go, column 3). Women without eating disorders were those who did not report any eating disorder during either time period.


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TABLE 1. Categorization of eating disorders before and during pregnancy among women in the Norwegian Mother and Child Cohort (MoBa) Study

 
Assessment of the diet
Dietary intake was assessed by using a semiquantitative food-frequency questionnaire that included dietary supplements. The food-frequency questionnaire is extensively described in Meltzer et al (23), and its validation is described in Brantsæter et al (24-26). The MoBa food-frequency questionnaire was mailed to all participants at gestational weeks 15–22. The first version of the questionnaire asked women to reflect on their dietary habits before pregnancy; 7066 women in our analytic sample were under this protocol and thus were excluded from the analysis. This left 30 040 (81%) women with complete information on BN and BED and diet that reflected the time period from conception until midpregnancy (Table 1Go, column 4). Women answered 255 questions on specific foods, and the frequency of use was reported by selecting 1 out of 10 frequencies ranging from never to several times monthly, weekly, or daily. In addition, global questions were asked regarding hot meals and fruit and vegetables and these were used for scaling adjustments. Where portion sizes were not given in the questionnaire, consumption frequencies were converted into food amounts by use of standard Norwegian portion sizes for women. The questionnaires were optically scanned, and energy and nutrient intakes were calculated with FoodCalc (27) and the Norwegian food-composition table (28).

From the total number of food items on the questionnaire (n = 255), we aggregated the data into 20 food groups (see Appendix A). For example, all mixed-meat products, luncheon meats, liver pate, and organ meats were grouped into one food group called high-fat meats, and all diet drinks were grouped together. This allowed us to examine food group consumption that was nutritionally meaningful.

Statistics
Data from the MOBA cohort for these analyses were used in a cross-sectional manner. Descriptive statistics including means, medians, and SEs were calculated by eating disorder categories. Because the nutrient data were not normally distributed, we performed statistical testing by eating disorder categories with the non-eating-disorder category as the referent group in all comparisons by using a log transformation and adjusting for total energy, maternal education, age, income, and gestational age at the time the questionnaire was completed. For the food group data, certain groups were not commonly consumed by all women: 6 out of 20 food groups had >10% of the population with zero grams consumed. This required us to first estimate whether women with eating disorders were more likely to consume from that food group by calculating the odds and 95% CIs by using logistic regression. We then tested for differences in grams consumed by eating disorder groups among consumers similarly to the commonly eaten foods. For the other 14 food groups that were commonly consumed, we tested for food group differences in grams consumed by eating disorders by using a Wilcoxon's two-sided normal approximation test. We then performed single univariate tests controlling the False Discovery Rate with the Benjamini-Hochberg method (29) as a way to control the type I error inflation associated with the multiple testing. In this method of adjustment, there is control of the ratio of false rejections to the total number of rejected hypotheses. P values < 0.05 were considered statistically significant. We assessed the influence of outliers on the robustness of our findings by conducting the analysis both with and without the outliers using cutoffs of total energy equal to 1076 for the lower and 4777 kcal for the upper bounds (23). SAS software for WINDOWS and for SOLARIS (v9.1.3) was used for all analyses (SAS/STAT Software, version 9; SAS Institute, Inc, Cary, NC).


    RESULTS
 TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
The population represented in this analysis (n = 30 040) included pregnant women with a mean gestational age of 20.4 wk; 49.0% were primiparous, 49.7% reported being married, 95.1% spoke Norwegian, 57.4% had a combined minimum income of $33,000–$82 000 for the mother and father and 9% had a combined minimum income <$33 000, and 40% had less than or equal to a high school education, 41.4% had 13–16 y of education, and 18.6% had >16 y of education. Seventy-six percent reported being employed in either the private or the public sector, 9% considered themselves students, and only 6% reported being at home; 8% indicated "other." One-half of the women reported lifetime smoking, with 10.4% reporting smoking during pregnancy. By use of the World Health Organization guidelines for defining pregravid weight status (30), 3.0% of the women were classified as underweight, 64.3% as normal weight, 22.7% as overweight, and 10.0% as obese.

The distribution of nutrient intakes by eating disorder category is presented in Table 2Go, and percentage differences in means adjusted for maternal characteristics and energy intake are illustrated in Figure 1Go. Women with BED both before and during pregnancy and those with incident BED during pregnancy had higher total energy intakes than did women with no eating disorders (P < 0.05). Although there appeared to be many differences when we compared women with each of the eating disorders with women without eating disorders, after adjustment for total energy intake, maternal characteristics (age, education, and income), and gestational age at the time the questionnaire was completed as well as correction for multiple comparison testing, few statistically significant differences remained. These differences primarily occurred between women with BED both before and during pregnancy and non-eating-disordered women and included higher intakes of total, monosaturated, and saturated fat and lower intakes of folate, potassium, and vitamin C (P < 0.02). In addition, women who developed BED during pregnancy had significantly higher saturated fat intake than did women with no eating disorders (P = 0.01). No other significant differences were noted. In a sensitivity analysis, excluding women with outliers in energy intake, the results were unchanged with the exception of 2 additional significant results for women who developed BED during pregnancy with regard to vitamin C and vitamin B-6 intake (data not shown).


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TABLE 2. Distribution of nutrient intakes by bulimia nervosa (BN) and binge eating disorder (BED) of pregnant women in the Norwegian Mother and Child Cohort (MoBa) Study1

 

Figure 1
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FIGURE 1.. Percentage differences in mean log-transformed nutrient values by eating disorder subtype (before pregnancy/during pregnancy) with use of the "no eating disorders" category as the reference group. Adjusted for total energy, gestational age, mother's age, education, minimum combined income, and parity. BED, binge-eating disorder; BN, bulimia nervosa.

 
Food group intakes by eating disorder categories are presented in Table 3Go. For the food groups commonly consumed by all women (fish, high-fat meat, eggs, grains, vegetables, fruit, juice, yogurt and cheeses, milk desserts, cakes, sugar-sweetened beverages, and fats), there were no significant differences between women with BN before or BED during pregnancy and women without eating disorders. Women with BN before and during pregnancy had lower intakes of sweetened beverages and high-fat meats than did women with no eating disorders. Women with BN before pregnancy who remitted during pregnancy had higher intakes of fruit and lower intakes of fats, but these differences were of borderline significance (P = 0.05). Women with BED both before and during pregnancy had lower intakes of juice and fruit but higher intakes of candy, fats, and milk desserts than did women without eating disorders. Women with BED before pregnancy who remitted during pregnancy had lower intakes of yogurt and cheeses, fish, juices, grains and cakes, whereas women with incident BED during pregnancy had higher intakes of yogurt and cheeses, grains, fats, cakes, candy, and milk desserts and lower intakes of juices than did women with no eating disorders.


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TABLE 3. Distribution of food group consumption by bulimia nervosa (BN) and binge eating disorder (BED) categories for pregnant women in the Norwegian Mother and Child Cohort (MoBa) Study1

 
For the food groups not commonly consumed (ie, artificially sweetened beverages, coffee, tea, herbal teas, other categories of fish, and chicken), women with eating disorders, with the exception of those with BN who remitted during pregnancy, had a higher odds of consuming artificially sweetened beverages than did women with no eating disorders (data not shown). Among consumers of these food groups, women with any eating disorder reported higher intakes of artificially sweetened beverages. Women with BED during pregnancy reported higher coffee consumption, whereas women with BED who remitted during pregnancy reported lower coffee consumption than that of women with no eating disorders. Women with BED both before and during pregnancy also had a significantly lower intake of chicken items than did women with no eating disorders.

In sensitivity analysis, excluding the women with outliers in energy intake resulted in similar results with few exceptions. The finding related to higher consumption of artificially sweetened beverages among women with BN before and BED during pregnancy was no longer significant. The findings of higher fruit intake and lower fat intakes among women with BN before who remitted during pregnancy were also not significant. Last, the higher intakes of grains, yogurt and cheeses, and fats among women who developed BED during pregnancy were no longer significant.


    DISCUSSION
 TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
This study documents differences in nutrient and food group intakes during the first half of pregnancy among women with BN and BED in a large prospective cohort. Our results showed overall higher consumption of total energy, total fat, monounsaturated fat, and saturated fat and lower intakes of folate, potassium, and vitamin C among women with BED both before and during pregnancy than among women without eating disorders. This was reflected in the food group consumption comparison in that those women had higher intakes of fats (butter, margarines, oils, etc) and milk desserts and lower intakes of fruit and juices. Women who developed BED during pregnancy also had higher total energy and saturated fat intakes than did women with no eating disorders, and this was reflected in their higher consumption of cakes, yogurt and cheeses, milk desserts, and overall fats. No other statistically significant differences were noted for the nutrient comparisons. This lack of difference may have been due to our conservative approach of adjusting for covariates and multiple comparisons. The results presented in Table 2Go will allow for future comparisons with other studies that use a similar approach to assessing dietary intakes.

Compared with the recently published Nordic Nutrition Recommendations (14), the average intake of all nutrients in the eating disorder groups was sufficient, except for potassium and phosphorous being very high and iron and folate intakes being much lower than desired. However, the data do not include dietary supplements, which were reported to be taken by 80% of the women in MoBa (23). Thus, it is premature to determine whether the low dietary intakes are of concern.

The higher consumption of artificially sweetened beverages among all women with eating disorders is intriguing. Although high rates of use of artificial sweeteners have been reported in nonpregnant women with eating disorders (31), this is the first report of elevated use during pregnancy. This clearly demonstrates a behavior pattern of limiting intakes of added sugars by replacing diet drinks with other sweetened beverages. To date, there is little direct clinical evidence showing a negative long-term effect of the use of artificial sweeteners during pregnancy (32). Whether the observed differences are related to sweet taste preference is unclear; indeed, women with BN before and BED during pregnancy as well as those with BED both before and during also had higher intakes of sweetened beverages than did women with no eating disorders, though the differences were not statistically significant.

Other food group differences were noted for women who had BN before and during pregnancy. The higher intakes of yogurt and cheeses and lower intakes of high-fat meats and sweetened beverages were counter to what we would expect given the nature of eating disorders; however, because this represents their eating pattern during pregnancy it may well reflect the avoidance of "fattening" foods during an interval when purging episodes may be reduced. Indeed, a substantial number of women who reported BN before pregnancy resolved into BED during pregnancy. Subsequent data collection waves will allow us to determine whether the elimination of purging behavior was temporary or whether it returned after the birth of the child. Women with BED before who remitted during pregnancy also showed a behavioral pattern of limiting high-calorie foods by consuming lower amounts of cakes, yogurt and cheeses, fish, grains, and juices, as did women with BN before who remitted during pregnancy, who had lower intakes of fats and higher intakes of fruit. This difference could simply reflect the absence of binge eating episodes in these women, whose eating normalized during pregnancy. By contrast, women with BED both before and during pregnancy exhibited the opposite pattern by consuming higher amounts of candy and chocolates, fats, and milk desserts. Previous research showed that a high consumption of sweets early in pregnancy is associated with excessive gestational weight gains (33), and another study done among adolescents found that a high sugar consumption (>10th percentile) was associated with an increased risk of small-for-gestational age infants (34). Thus, further investigation of certain food group consumption on pregnancy outcomes is warranted.

Despite the many advantages that the use of the MoBa data provided us for examining nutrient and food group differences among women with eating disorders, we acknowledge several limitations. First, although the diagnostic questions used in the survey had been used in previous epidemiologic studies in Norway, they nonetheless were based on self-report and targeted broadly defined eating disorders. Second, dietary habits were assessed by using a semi-quantitative food-frequency questionnaire and are subject to the errors inherent in this mode of data collection. Third, the generalizability of the findings may be limited to higher educated women who are receiving prenatal care. When the sociodemographic characteristics of women who participated in MoBa were compared with all births, it was found that the MoBa participants were somewhat more educated than the general Norwegian population, with 58% attending some form of college compared with 46% of women between 25 and 29 y of age and 43% of women between 30 and 39 y of age reported to have higher education in 2005 by Statistics Norway (35). Last, because of the observational nature of our data, we cannot easily exclude the possibility that important confounders were omitted from the analysis or that adjustment for confounders was incomplete. Nonetheless, this study provides interesting information concerning the dietary habits of women with BN and BED both before and during pregnancy. Whether the observed differences influenced the course of pregnancy (ie, weight gain, gestational diabetes) and birth outcomes will be the topic of future analyses with this data set.


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APPENDIX A. Examples of foods in the 20 food groups

 

    ACKNOWLEDGMENTS
 
We gratefully acknowledge the participants of MoBa.

The contributions of the authors were as follows—all authors were involved in obtaining the funding for the analysis; AVH was responsible for the statistical analysis with guidance from AMS-R, CMB, and RH; AMS-R, HMM, and MH drafted the manuscript; and CMB, CK-B, LT, and TR-K provided critical and intellectual feedback. None of the authors had a conflict of interest to report.


    REFERENCES
 TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

  1. Hudson JI, Hiripi E, Pope HG, Kessler RC. The prevalence and correlates of eating disorders in the National Comorbidity Survey Replication. Biol Psychiatry 2007;61:348–58 (epub 2006 July 3).[Medline]
  2. Bulik C, Reichborn-Kjennerud T. Medical morbidity in binge eating disorder. Int J Eat Disord 2003;34:S39–46.[Medline]
  3. Berkman ND, Lohr KN, Bulik CM. Outcomes of eating disorders: a systematic review of the literature. Int J Eat Disord 2007;40:293–309.[Medline]
  4. Micali N, Simonoff E, Treasure J. Risk of major adverse perinatal outcomes in women with eating disorders. Br J Psychiatry 2007;190:255–9.[Abstract/Free Full Text]
  5. Morgan JF, Lacey JH, Chung E. Risk of postnatal depression, miscarriage and preterm birth in bulimia nervosa: retrospective controlled study. Psychosom Med 2006;68:487–92.[Abstract/Free Full Text]
  6. Kouba S, Hallstron T, Lindholm C, Hirschberg AL. Pregnancy and neonatal outcomes in women with eating disorders. Obstet Gynecol 2005;105:255–60.[Medline]
  7. Sollid CP, Wisborg K, Hjort J, Secher NJ. Eating disorder that was diagnosed before pregnancy and pregnancy outcome. Am J Obstet Gynecol 2004;190:206–10.[Medline]
  8. Abraham S. Sexuality and reproduction in bulimia nervosa patients over 10 years. J Psychosom Res 1998;44:491–502.[Medline]
  9. American Dietetic Association. Position of the American Dietetic Association: nutrition and lifestyle for a health pregnancy outcome. J Am Diet Assoc 2002;102:1479–90.[Medline]
  10. Nutrition during pregnancy. ACOG Technical Bulletin Number 179–April 1993. Int J Gynaecol Obstet 1993;43:67–74.[Medline]
  11. Institute of Medicine, Food and Nutrition Board. Nutrition during pregnancy. Part I. Weight gain. Part II. Nutrient supplements. Washington, DC: National Academy Press, 1990.
  12. Institute of Medicine, Food and Nutrition Board. Dietary reference intakes for energy, carbohydrates, fiber, fat, fatty acids, cholesterol, protein and amino acids. Washington, DC: National Academy Press, 2002.
  13. Institute of Medicine, Food and Nutrition Board. Dietary reference intakes for thiamin, riboflavin, niacin, vitamin B6, folate, vitamin B12, pantothenic acid, biotin, and choline. Washington, DC: National Academy Press, 1998.
  14. Nordic Nutrition Recommendations. Copenhagen, Norway: Nordic Council of Ministers, 2004.
  15. Magnus P, Irgens LM, Haug K, et al. Cohort profile: the Norwegian Mother and Child Cohort Study (MoBa). Int J Epidemiol 2006;35:146–50.
  16. Irgens LM. The Medical Birth Registry of Norway. Epidemiological research and surveillance throughout 30 years. Acta Obstet Gynecol Scand 2000;79:435–9.[Medline]
  17. Harris J, Magnus P, Tambs K. The Norwegian Institute of Public Health Twin Panel: a description of the sample and program of research. Twin Res 2002;5:415–23.[Medline]
  18. Reichborn-Kjennerud T, Bulik C, Kendler K, et al. Gender differences in binge-eating: a population-based twin study. Acta Psychiatr Scand 2003;108:196–202.[Medline]
  19. Reichborn-Kjennerud T, Bulik C, Kendler K, et al. Influence of weight on self-evaluation: a population-based study of gender differences. Int J Eat Disord 2004;35:123–32.[Medline]
  20. Reichborn-Kjennerud T, Bulik C, Tambs K, Harris J. Genetic and environmental influences on binge eating in the absence of compensatory behaviours: a population-based twin study. Int J Eat Disord 2004;36:307–14.[Medline]
  21. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4th ed. Washington, DC: American Psychiatric Association Press, 1994.
  22. Bulik C, Holle A, Hamer R, et al. Patterns of remission, continuation, and incidence of eating disorders during pregnancy in the Norwegian Mother and Child Cohort Study (MoBa). Psychol Med 2007;37:1109–18 (Epub 2007 May 10).[Medline]
  23. Meltzer HM, Brantsaeter AL, Ydersbond TA, Alexander J, Haugen M, Moba Dietary Support Group. Methodological challenges when monitoring the diet of pregnant women in a large cohort study: experiences from The Norwegian Mother and Child Cohort Study (MoBa). Matern Child Nutr 2008;4:14–27.[Medline]
  24. Brantsæter AL, Haugen M, Alexander J, Meltzer HM. Validity of a new Food Frequency Questionnaire for pregnant women in the Norwegian Mother and Child Cohort Study (MoBa). Matern Child Nutr 2008;4:28–43.[Medline]
  25. Brantsæter AL, Haugen M, Hagve T-A, et al. Self-reported dietary supplement use is confirmed by biological markers in the Norwegian Mother and Child Cohort Study (MoBa). Ann Nutr Metab 2007;51:146–54.[Medline]
  26. Brantsæter AL, Haugen M, Rasmussen SE, Alexander J, Samuelsen SO, Meltzer HM. Urine flavonoids and plasma carotenoids in the validation of fruit, vegetable and tea intake during pregnancy in the Norwegian Mother and Child Cohort Study (MoBa). Public Health Nutr 2007;10:274–83.
  27. Lauritsen J. FoodCalc. Version current 1 July 2005. Internet: http://www.ibt.ku.dk/jesper/foodcalc (accessed 5 July 2005).
  28. Rimestad AH, Borgejordet Å, Vesterhus KN, et al. Den store matvaretabellen/The Norwegian Food Composition Table. Oslo, Norway: Statens råd for ernæring og fysisk aktivitet, Statens næringsmiddeltilsyn, Institutt for ernæringsforskning, 2001.
  29. Benjamini Y, Hochberg Y. Controlling the false discovery rate: a practical and powerful approach to multiple testing. J R Stat Soc Ser B 1995;57:289–300.
  30. World Heath Organization. Obesity: preventing and managing the global epidemic. Geneva, Switzerland: World Health Organization; 2000. WHO technical report series 894.
  31. Klein DA, Boudreau GS, Devlin MJ, Walsh BT. Artificial sweetener use among individuals with eating disorders. Int J Eat Disord 2006;39:341–5.[Medline]
  32. American Dietetic Association. Position of the American Dietetic Association: use of nutritive and nonnutritive sweeteners. J Am Diet Assoc 2004;104:255–75.[Medline]
  33. Olafsdottir AS, Skuladottir GV, Thorsdottir A, Hauksson A, Steingrimsdottir L. Maternal diet in early and late pregnancy in relation to weight gain. Int J Obes 2006;30:492–9.[Medline]
  34. Lenders CM, Hediger ML, Scholl TO, Khoo CS, Slap GB, Stallings VA. Gestational age and infant size at birth are associated with dietary sugar intake among pregnant adolescents. J Nutr 1997;127:1113–7.[Abstract/Free Full Text]
  35. Statistics Norway. Internet: www.ssb.no. Accessed 6 March 2008 (in Norwegian).
Received for publication September 12, 2007. Accepted for publication December 5, 2007.





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