Our current knowledge about pregnancy and eating disorders comes primarily from clinical samples. These studies suggest that the impact of eating disorders on the pregnant woman and her unborn child can be significant–especially when the eating disorder is not detected or persists despite treatment (Abrams and Laros, 1986, van der Spuy et al., 1988, Stewart et al., 1987, Treasure and Russel, 1988, Brinch et al., 1988, Lacey and Smith, 1987, Conti et al., 1998). Increased complications from conception through the postpartum period have been described that adversely impact maternal and fetal well-being. Maternal complications that have been noted to occur at a higher prevalence in women with AN include miscarriages and cesarean deliveries (Bulik et al., 1999, Franko et al., 2001). High cesarean rates have also been reported in women with bulimia nervosa (BN) (Mitchell et al., 1991). Features that are characteristic of eating disorders such as low pre-pregnancy weight and low gestational weight gain are associated with adverse birth outcomes as well (Abrams and Newman, 1991, Siega-Riz et al., 1996) and a higher incidence of congenital malformations (van der Spuy et al., 1988). Poor birth outcomes that impact the infants of women with eating disorders include stillbirth, low birth weight, low Apgar scores, higher occurrence of breech presentation, and cleft lip and palate (Stewart et al., 1987, Treasure and Russel, 1988, Brinch et al., 1988, Lacey and Smith, 1987, Conti et al., 1998). Crow et al. (Crow et al., 2004) reported that bulimic symptoms tended to improve during pregnancy, pregnant women with past or active BN have been reported to be at greater risk for hyperemesis, and delivering infants with smaller head circumference, microcephaly, and who are small for gestational age, compared to healthy controls (Kouba et al., 2005). Less is known about the course and impact on pregnancy of eating disorders not otherwise specified (EDNOS). In this paper, we are particularly interested the impact of two forms of EDNOS, namely binge eating disorder (BED) and a clinical presentation marked by self-induced purging behavior in the absence of binge eating which we refer to as EDNOS-P. Although only recently the subject of scientific inquiry, this presentation has been described as a clinically significant phenomenon (Keel et al., 2005) and identified in a population-based sample of Australian twins (Wade, 2007).

Most studies of eating disorders and pregnancy have been retrospective reports on clinical samples. Some women with active eating disorders report a temporary or permanent improvement in eating disorders symptomatology during pregnancy (Lacey and Smith, 1987, Lemberg and Phillips, 1989, Morgan et al., 1999, Namir et al., 1986). However, the eating disorder, and a renewed obsession with slimness, may become acute in the postpartum period (Willis and Rand, 1988, Lacey and Smith, 1987, Lemberg and Phillips, 1989, Morgan et al., 1999). This may be offset by successful treatment, as we have previously found improved symptomatology in women with BN who became pregnant in the interval following treatment (Carter et al., in press).

Although the aforementioned studies are intriguing, they have important methodological limitations (e.g. clinical samples, retrospective data) and are therefore unable to shed adequate light on illness course during pregnancy. The present study advances this body of preliminary knowledge with information from the initial assessments in a prospective population-based birth cohort study. The Norwegian Mother and Child Cohort Study (MoBa) is designed to recruit a sample of 100,000 pregnant women between 1999 and 2008 or until the target is reached. This study collected information on eating disorders and eating disordered behavior of mothers assessed during pregnancy about their behavior both prior to and during pregnancy. We report the prevalence of eating disorders and disordered eating behavior prior to pregnancy as well as the patterns of remission, continuation, and incidence of eating disorders during pregnancy of 41,157 women entered into this cohort.

Our observed pre-pregnancy prevalence of AN is on the low end of that reported in epidemiologic investigations of women not selected on the basis of pregnancy (Hoek, 2006). This may reflect the fact that at least some individuals with AN have impaired fertility and/or social/interpersonal deficits decreasing their likelihood of becoming pregnant (Strimling, 1984, Weinfeld et al., 1977, Stewart et al., 1990), or alternatively, the stress of pregnancy in individuals with AN could make them less likely to agree to participate in a study such as MoBa.

Examining the course of eating disorders during pregnancy, we found the most common pattern for BN and EDNOS-P to be remission or partial remission of symptoms during pregnancy—with combined remission rates surpassing continuation rates for all types of BN and EDNOS-P. This suggests that for many, but clearly not all women, pregnancy is a powerful stimulus to decrease bulimic symptomatology. This can take the form of reductions in both binge eating and compensatory behavior, or in the case of those partially remitted women, elimination of compensatory behaviors only (which may be viewed as potentially more harmful to the fetus). This parallels similar observations of spontaneous quitting in pregnancy for both alcohol use and smoking (Bruce et al., 1993, Ockene et al., 2002, Kruse et al., 1986, Solomon and Quinn, 2004). Whether the observed decreases are limited to the period of pregnancy or are more lasting will be addressed in future waves of the MoBa study. In addition, although incident cases of BN during pregnancy were reported, they were rare.

Unexpectedly, we found the course of BED to be different than that of BN. For BED, continuation of symptoms during pregnancy was more common than remission. Most notably, new onsets of BED were much more common than the other eating disorders (1.12 per 1000 person-weeks) or 711 new cases in our sample. We are unaware of previous reports of incident BED during pregnancy and our finding raises the important issue of the validity of questions regarding binge eating during pregnancy. An important topic for further detailed investigation is whether the terms associated with the evaluation of binge eating (e.g. eating and unusually large amount of food, feeling out of control) are more likely to be endorsed by women who are experiencing appetite changes associated with pregnancy. The magnitude of our observed incident cases suggests that this is an important area of inquiry to determine the extent to which the reported behavior truly represents pathological eating behavior.

Although our analyses were unable to detect any demographic parameters associated with the course of BN except for smoking, for BED, new cases were associated with an array of variables reminiscent of the “matrix of disadvantage” (Mullen et al., 1993). Women with higher BMIs during pregnancy, more previous pregnancies, at least one abortion, lower income and education, greater smoking, and whose native language was not Norwegian were more likely to report developing BED during pregnancy. Although additional data are needed to characterize these individuals more fully, from this assessment it appears that general indices of economic and social disadvantage may be associated with the development of this symptom cluster during pregnancy.

Pregnancy is a powerful biopsychosocial event. For some, pregnancy appears to be a window of opportunity for discontinuing bulimic behaviors that could be harmful to both mother and child. For a smaller number of women, however, their bulimic behaviors (binge-eating and purging) persist during pregnancy. We will explore the impact of these persistent behaviors on pregnancy outcome and child development in future waves of data analysis in this cohort.

The somewhat surprising number of incident cases of BED during pregnancy raises several questions. For these women, rather than a window of opportunity, pregnancy appears to be a window of vulnerability. Several potential explanations for the emergence of BED during pregnancy emerge. Biologically, the myriad of adaptive neuroendocrine changes that occur in pregnancy that affect multiple brain functions influencing metabolism, appetite, and mood (Russell et al., 2001) may render pregnancy a high risk period for developing binge-eating. Behaviorally, women who fail to increase food intake according to the increased metabolic needs of pregnancy may experience unexpected and intense hunger which may lead to compensatory overeating and ultimately trigger a pattern of appetite dysregulation. This is perhaps less likely given that changes were seen relatively early in pregnancy prior to appreciable increases in metabolic requirements. Psychologically, especially given the pattern of social disadvantage associated with incident cases in this sample, the psychosocial stress of pregnancy may serve as an environmental trigger for binge eating.

These findings must be considered within the context of several limitations. First, although the diagnostic questions we used had been used in previous epidemiologic studies in Norway, they nonetheless were self-report questions and targeted broadly defined disorders. Direct diagnostic interviews may have yielded richer diagnostic information; however, given the magnitude of the sample, this was not practical. Second, although our frequency criteria for binge eating and purging differed from current DSM criteria, we emphasize that the established criteria have not been empirically supported (Sullivan et al., 1998). Third, women may have been hesitant to admit to eating disorders behaviors during pregnancy which would have led to an underestimation of continuation rates and an overestimation of remission. Fourth, BMI measures were self-report rather than measured—a common approach given the logistical complications and cost of measured weight in larges samples such as MoBa. Although there are no comparable data from Norway, data from other large samples suggest a correlation of 0.94 between measured and self-reported height and 0.98 between measured and self-reported weight for women (Bulik et al., 2001). Fifth, 42% of women invited agreed to participate in MoBa. Although this response rate is low, it is not uncommon to large epidemiologic studies and does not necessarily imply a biased sample (Hartge, 2006). The determination of bias is complex and would occur if and only if individuals who chose not to participate in this study differed markedly from those who did participate on the variables of interest. Initial comparisons of the MoBa cohort to the Norwegian population indicates lower rates of preterm birth (7.2% vs 7.7%) and low birth weight (< 2500g) (4.6 % vs 5.1%) possibly reflecting a socioeconomic gradient associated with participation (Magnus et al., 2006). Further exploration of this using education data suggests that the MoBa participants may be somewhat more educated than the general Norwegian population with 58% attending some form of college in comparison to 46% of women between 25-29 years and 43% of women between 30-39 years reported to have higher education in 2005 by Statistics Norway. Finally, our data reflect changes in eating disorders symptomatology in the early stages of pregnancy. It is possible that such changes may not reflect patterns of remission, continuation, and incidence across the entire gestational period.