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. Author manuscript; available in PMC: 2024 May 9.
Published in final edited form as: Appetite. 2023 May 4;187:106589. doi: 10.1016/j.appet.2023.106589

Food addiction and dietary restraint in postpartum women: The role of childhood trauma exposure and postpartum depression

Sara F Stein a,b,*, Julia M Rios c, Ashley N Gearhardt c, Amy K Nuttall d, Hurley O Riley a, Niko Kaciroti e, Katherine L Rosenblum g, Julie C Lumeng f, Alison L Miller a
PMCID: PMC11079996  NIHMSID: NIHMS1932987  PMID: 37146651

Abstract

The early postpartum period is a sensitive time for understanding women’s high-risk eating (i.e., eating behavior associated with negative health outcomes) given potential long-term eating behavior implications for infants. Food addiction and dietary restraint are two high-risk eating phenotypes associated with long-term negative health outcomes that have been theoretically linked. Yet, no research has considered how much these constructs overlap during the early postpartum period. The present study sought to characterize these two high-risk eating phenotypes in postpartum women to examine whether these are distinct constructs with specific etiologies and to inform future targets of intervention. Women (N = 277) in the early postpartum period reported on high-risk eating, childhood trauma exposure, depression symptoms, and pre-pregnancy weight. Women’s height was measured and pre-pregnancy BMI was calculated. We conducted bivariate correlations and path analysis to characterize the relationship between food addiction and dietary restraint, controlling for pre-pregnancy BMI. Results showed that food addiction and dietary restraint were not significantly associated and that women’s childhood trauma exposure and postpartum depression were associated with food addiction but not dietary restraint. Sequential mediation revealed that higher levels of childhood trauma exposure were associated with worse postpartum depression and, in turn, greater food addiction during the early postpartum period. Findings suggest that food addiction and dietary restraint have distinct psychosocial predictors and etiological pathways, which suggests important construct validity differences between the two high-risk eating phenotypes. Interventions seeking to address food addiction in postpartum women and mitigate the impact of this high-risk eating phenotype on the next generation may benefit from treating postpartum depression, especially in women with histories of childhood trauma exposure.

Keywords: Postpartum women, Food addiction, Dietary restraint, Childhood trauma exposure, Postpartum depression

High-risk eating phenotypes are eating behaviors associated with long-term, negative health consequences such as obesity and diet-related disease (Gearhardt & Schulte, 2021). The early postpartum period is a sensitive time for maternal high-risk eating behaviors given women’s recent body and eating changes during pregnancy (Brown & Toma, 1986; Faas et al., 2010; Kazma et al., 2020; Orloff & Hormes, 2014) and postpartum body demand (e.g. breastfeeding, limited sleep) and changes (e.g. altered food tastes) (Cho et al., 2011; Solis et al., 2019). Yet, research has primarily focused on high-risk eating during pregnancy (Linna et al., 2014; Sen et al., 2012) and gestational weight gain (Goldstein et al., 2017), with less attention given to postpartum high-risk eating behaviors. The postpartum period is a critical time to identify risk for women’s high-risk eating given potential intergenerational implications: during this time, women spend a lot of time with infants and are actively engaged in feeding and responding to their food cues, all which can shape infant eating behaviors. In fact, empirical evidence shows that how mothers eat during the postpartum period is associated with child eating behaviors and weight outcomes in children ages 2–12 years old (Birch & Fisher, 2000; Burrows et al., 2017; Rodgers et al., 2013). Furthermore, early life eating behaviors endure over time (Fletcher et al., 2017; Rose et al., 2017). Neuroplasticity and adaptation to environmental factors are highest during early development (Gluckman & Hanson, 2008), suggesting that how mothers eat might be most impactful to infants during the early postpartum period and matters for children’s long-term eating trajectories. Research is needed to better understand maternal high-risk eating phenotypes and their psychosocial risk factors during the postpartum period to interrupt the intergenerational transmission of eating-related concerns from mothers to infants.

Food addiction and dietary restraint are high-risk eating phenotypes as they are associated with significant, long-term, negative health outcomes in women like elevated BMI, eating disorders, lower quality of life, more severe psychopathology, and higher likelihood of diet-related disease (Burrows et al., 2018; de Sousa Fern et al., 2020; Gearhardt et al., 2014; Gearhardt & Schulte, 2021; Minhas et al., 2021; van Strien et al., 2014). Food addiction is characterized by “excessive overeating of high-calorie food accompanied by loss of control and intense food cravings” (Gearhardt, Corbin, & Brownell, 2009a, 2009b; Maxwell et al., 2020). In contrast, dietary restraint is the restriction of food intake to lose or maintain weight as self-imposed by an individual (Herman & Polivy, 1975) and includes cognitive efforts to avoid specific foods and reduce overall intake regardless of success (Lowe et al., 2006; Polivy et al., 2020).

There is currently a debate in the field about the utility of food addiction as a construct and how distinct it is from dietary restraint (Wiss & Brewerton, 2020), and thus we chose to focus on these eating phenotypes to address this debate. Eating disorder models have linked food addiction and dietary restraint with some work suggesting that dietary restraint is a necessary antecedent to loss of control eating such as food addiction (Fairburn et al., 2003; Kirkley et al., 1988; Meule, 2019), whereas others show that restraint may be a consequence of loss of control eating like those seen in food addiction to manage weight and shape concerns (Lowe, 2015; Reas & Grilo, 2007). However, dietary restraint is not characteristic of addiction processes, whereas food addiction is characterized by attributes unique to addiction including the importance of the particular substance (in this case, food), withdrawal, and tolerance (Gearhardt et al., 2009a, 2009b; Avena et al., 2012; Schulte et al., 2016). Despite these theoretical arguments there is very little empirical data on how much these constructs overlap or are distinct (Wiss & Brewerton, 2020).

Of the limited research examining associations between food addiction and dietary restraint, findings have been mixed (Gearhardt et al., 2016; Schiestl & Gearhardt, 2018). Significant positive associations have been found between the two phenotypes in non-postpartum adolescents and young adults (Alim et al., 2021; Borisenkov et al., 2020; Schiestl & Gearhardt, 2018), however no significant associations have been identified in non-postpartum adults (Carter et al., 2019; Gearhardt et al., 2012, 2013, 2016; Imperatori et al., 2019; Legendre & Bégin, 2021; Schulte et al., 2018). In postpartum women, dietary restraint and food addiction have only been studied separately (Cahill et al., 2012; Nansel, Lipsky, Burger, et al., 2020; Nansel, Lipsky, & Faith, 2020; Rallis et al., 2007; Stein & Fairburn, 1996). No work has considered these behaviors together or their psychosocial risk factors during the postpartum period. Thus, questions remain about whether these are distinct constructs with specific etiologies during the early postpartum period. The present study is the first of its kind to examine both food addiction and dietary restraint in early postpartum women.

One way to better understand the nature of the association between food addiction and dietary restraint in postpartum women is to examine whether they have common psychosocial risk factors. Yet, no work has examined whether the psychosocial predictors of food addiction and dietary restraint are shared in postpartum women. The postpartum period is a high-stress time where mental health changes can occur, including the activation of women’s childhood trauma in the form of increased emotional dysregulation, fear, and grief about early-life events experienced (Amos et al., 2011; Brand et al., 2010; Fraiberg et al., 1975; Mikoteit et al., 2022) and postpartum depression (Liu et al., 2022; O’Hara, 2009), two potentially important risk factors for these high-risk eating behaviors. If food addiction and dietary restraint have distinct psychosocial risk factors, it could suggest that they have different etiological pathways. Therefore, examining how candidate the psychosocial risk factors of women’s childhood trauma and postpartum depression relate to both food addiction and dietary restraint in postpartum women in the same study could yield new information and identify intervention targets for this population.

1. Childhood trauma exposure and postpartum depression as predictors of food addiction

Childhood trauma exposure is a known risk factor for eating disorders, including food addiction, in adulthood (Guillaume et al., 2016; Imperatori et al., 2016; Mason et al., 2013; Nunes-Neto et al., 2018), and is hypothesized to operate through stress-related disruptions of reward pathways (Wei et al., 2019). For example, childhood trauma exposure and duration was associated with greater risk for food addiction in 57, 321 female nurses (Mason et al., 2013). Likewise, depression symptoms have also been positively associated with food addiction symptoms in adulthood (Borisenkov et al., 2018; Burrows et al., 2018; Racine et al., 2019; Zhao et al., 2018; Şanlier et al., 2016). Across 51 studies, meta-analytic findings showed a significant and strong positive correlation between depression and food addiction (Burrows et al., 2018). Thus, although both childhood trauma and depression have been hypothesized to be predictors of food addiction, and have each been positively associated with adult food addiction in multiple studies, no work has examined this association in postpartum women.

2. Childhood trauma exposure and postpartum depression as predictors of dietary restraint

Childhood trauma is also a hypothesized predictor of dietary restraint in adulthood (Grilo & Masheb, 2001; Guillaume et al., 2016; Rodgers et al., 2019; Strodl & Wylie, 2020). In non-postpartum adults, childhood trauma has been consistently positively associated with dietary restraint (Vartanian et al., 2018; Villarroel et al., 2012). However, the relationship between dietary restraint and depression is less clear. Among non-postpartum samples, some studies found a significant positive association (Spoor et al., 2006; van Strien et al., 2016) while others did not (Goossens et al., 2010; Konttinen et al., 2010; Wardle et al., 2001). Despite the postpartum period being a vulnerable time for the activation of women’s childhood trauma (Fraiberg et al., 1975) and the development of depression (O’hara & McCabe, 2013), to-date no studies have examined the associations of childhood trauma and depression symptoms with dietary restraint in women during this time. Doing so could yield new information about risk for dietary restraint in this population.

3. Etiological pathways of food addiction and dietary restraint in postpartum women

Given the associations of both childhood trauma and adult depression symptoms with food addiction and dietary restraint, it may be that childhood trauma is contributing to food addiction and dietary restraint through depression symptoms in adulthood. Depression is a well-established sequelae of childhood trauma (Anda et al., 2006; Felitti et al., 1998b; Gallo et al., 2018), which has also been specifically linked to postpartum depression (Mahenge et al., 2018; Seng et al., 2013). Therefore, the impact of childhood trauma and depression on food addiction and/or dietary restraint may function via a spillover effect, with childhood trauma leading to postpartum depression, which then leads to one or both high-risk eating phenotypes. Examining this process in postpartum women may provide novel mechanistic information regarding the etiological pathways of food addiction and dietary restraint.

4. Present study

The aim of the present study is to characterize the nature of food addiction and dietary restraint in a community sample of postpartum women by examining the association between these high-risk eating phenotypes, testing psychosocial risk factors that may differentially predict them, and exploring the process by which risk factors may lead to these eating phenotypes. We examined the following research questions among postpartum women: 1) Is food addiction positively associated with dietary restraint? 2) Is women’s childhood trauma exposure positively associated with food addiction and dietary restraint? 3) Are postpartum depression symptoms positively associated with food addiction and dietary restraint? 4) Finally, do postpartum depression symptoms mediate any associations between childhood trauma exposure and food addiction and/or dietary restraint? In other words, is more childhood trauma associated with higher postpartum depression severity and, in turn, more food addiction and/or dietary restraint?

5. Methods

5.1. Participants

Participants were drawn from a broader longitudinal study examining the development of eating behavior in infancy through school age (NICHD R01HD084163). To maximize recruitment, starting in 2016, mother-infant dyads could enroll in the study when infants were 2 weeks, 2 months, or 4 months of age; this resulted in baseline data collected from anywhere from infant age 2 weeks to 4 months. The present study only uses data from these first three study timepoints (when the infants were 2 weeks, 2 months, and 4 months old). 284 participants enrolled in the study by infant age 4 months: 167 of whom entered when their infants were 2 weeks old, 98 when their infants were 2 months old, and 19 when their infants were 4 months old. The present study used a subsample of women (N = 277), which excludes seven women who did not provide any data for the measures of interest in the current study. Table 1 presents the descriptive statistics of the analytic sample.

Table 1.

Descriptive statistics and bivariate correlations for study measures (N = 277).

M (SD)/ % Possible Range 1 2 3 4
1. Childhood trauma exposure 2.06 (2.41) 0.00–10.00 1
2. Postpartum depressive symptoms 3.68 (3.11) 0.00–24.00 .26*** 1
3. Food addiction 1.68 (1.29) 0.00–7.00 .24*** .28*** 1
4. Restraint eating 2.28 (0.73) 1.00–5.00 − .04 0.03 0.06 1
5. Pre-pregnancy BMI 27.79 (7.19) – .23*** 0.14 .26*** .21**
Mother’s age 31.20 (5.02) –
Gestational age 39.49 (1.08) –
Married/in committed relationship 87% –
More than high school degree 90% –
Person of Color 31% –
Income to needs ratio 3.48 (2.23) –
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Note:

**

p < .01,

***

p < .001; Income to needs ratio (ITNR) was calculated by dividing income by the poverty income threshold for a household of that size in the given year; an ITNR of 1.0 indicates that a household is living at the poverty level, with higher values indicating greater income-to-needs (i.e., lower poverty) (Dearing et al., 2001).

5.2. Procedure

Mother-infant dyads were recruited from the community, including prenatal and pediatric clinics in the Midwest United States. The study was described to participants as seeking to “learn more about infant eating behavior and interactions between mothers and babies the first year after your baby’s birth”. Inclusion criteria included: (1) Infant was born at 37.0–42.0 weeks gestation with weight appropriate for gestational age, and (2) no significant perinatal or neonatal complications. Participants were ineligible to participate if: (1) mother was not fluent in English; (2) mother was not a biological parent; (3) mother <18 years of age; (4) infant had medical problems or diagnosis which can affect eating, growth, or development; (5) child protective services involvement in the neonatal period; (6) infant did not consume ≥2 ounces in one feeding from a bottle at least once per week. After participants enrolled, research assistants visited participants’ homes to have mothers complete a set of questionnaires at multiple timepoints (see below). The study was approved by the University of Michigan’s Medicine Institutional Review Board. Mothers provided written informed consent for themselves and their infant.

5.3. Measures

5.3.1. Food addiction

Mothers reported on their own food addiction by completing the Yale Food Addiction Scale (YFAS; Gearhardt et al., 2009a, 2009b) at study enrollment (at either infant age 2 weeks, 2 months, or 4 months). The YFAS is a 25-item questionnaire that measures addictive-like eating behaviors with high fat/sugar foods over the past 12 months based on the seven criteria DSM-IV-TR criteria for substance dependence: 1) Substance taken in larger amount and for longer period than intended; 2) Persistent desire or repeated unsuccessful attempt to quit; 3) Much time/activity to obtain, use, recover; 4) Important social, occupational, or recreational activities given up or reduced; 5) Use continues despite knowledge of adverse consequences; 6) Tolerance (marked increase in amount; marked decrease in effect); 7) Characteristic withdrawal symptoms; substance taken to relieve withdrawal. The 25 items use a combination of Likert and dichotomous scales, which are used to create a total symptom count score (the number of dependence symptoms experienced). The food addiction symptom count score is an index that ranges from 0 to 7 based on the number of DSM-IV substance dependence diagnostic criteria endorsed by participants in the 25 items (α = .67). See Supplementary Table 1 for sample summary statistics of YFAS symptoms and clinical impairment.

5.3.2. Dietary restraint

Mothers reported on their dietary restraint at the 2-month timepoint by completing the 33-item Dutch Eating Behavior Questionnaire (DEBQ; van Strien et al., 1986). The dietary restraint subscale included 10 items asking about eating less to lose or maintain body weight. The questionnaire asked mothers to report their eating behaviors on a 5-point Likert-type scale ranging from never (1) to very often (5). Negatively worded items were reverse scored. The dietary restraint score was calculated as the mean of the 10 restraint items (α = .88). Higher scores indicated greater endorsement of dietary restraint behaviors.

5.3.3. Childhood trauma exposure

Upon study enrollment, mothers completed the Adverse Childhood Experiences Questionnaire (ACE-Q; Felitti et al., 1998a) to assess their own childhood trauma exposure. The 10-item questionnaire asked mothers to report any exposure to trauma (e.g., psychological, physical, and sexual) and household dysfunction (e.g., domestic violence, substance use, and incarceration) during their first 18 years of life (e.g., “Did a household member go to prison?“). Mothers responded no (0) or yes (1) to each item. An ACE total score was calculated by summing the responses (α = .82). Higher scores indicated more childhood trauma exposure.

5.3.4. Depression symptoms

Mothers completed the 8-item Patient Health Questionnaire (PHQ-8; Kroenke et al., 2001) at the 2-month timepoint to assess maternal depression symptoms. Mothers reported how often they were bothered by problems over the last 2 weeks (e.g., “Little interest or pleasure in doing things”) on a scale ranging from not at all (0) to nearly every day (3). A depression severity score was calculated by summing the responses (α = .71). Higher scores indicated more severe depression symptoms.

5.3.5. BMI covariate

Pre-pregnancy BMI was included as a covariate, as BMI has been consistently associated with both food addiction and dietary restraint (Gearhardt et al., 2014; Snoek et al., 2008) and pre-pregnancy BMI, specifically, has been associated with postpartum eating-related outcomes (Ketterl et al., 2018). During the baseline study visit, research staff certified in anthropometry used a Seca 217 portable stadiometer to measure mothers’ height. Mothers also self-reported their weight before becoming pregnant with the index child. Mothers’ pre-pregnancy body mass index (BMI) was then calculated as pre-pregnancy weight in kilograms divided by height in meters squared.

5.3.6. Data analytic strategy

For research question one, we used a bivariate correlation to test the association between food addiction and dietary restraint in postpartum women. To test research questions two through four we used path analysis in Mplus (Mplus version 8; (Muthén & Muthén, 2017), which uses full information maximum likelihood estimation, a robust approach to account for missing data. First, we fit a multivariate model to test the associations of maternal childhood trauma exposure with food addiction and dietary restraint controlling for pre-pregnancy BMI (research question two). We then fit a second multivariate model to test the association of depression symptoms with the two eating phenotypes controlling for pre-pregnancy BMI (research question three). Unstandardized parameter estimates are reported in text. Finally, we fit a sequential mediation model to test the indirect effects of women’s childhood trauma exposure on the two eating phenotypes through postpartum depression symptoms controlling for pre-pregnancy BMI (research question four). To test the sequential mediation model, we employed a bootstrap resample approach (Shrout & Bolger, 2002) with 1,000 resamples in accordance with Hayes and Scharkow (2013). The bootstrap resample approach allowed us to construct bias-corrected bootstrap 95% confidence intervals around the product coefficient for inferring the indirect effects of mother’s childhood trauma exposure via the hypothesized mediational pathway of postpartum depression symptoms on each eating phenotype. All path models were saturated.

Women’s food addiction data were collected at the dyad’s enrollment in the study, at either infant age 2 weeks, 2 months, or 4 months, whereas depression symptoms were only assessed at infant age 2 months. To test research questions one and two that do not include depression symptoms, we used food addiction scores collected at infant age 2 weeks, 2 months, or 4 months in order to use all available data. To test research questions three and four that include depression symptoms, we only used food addiction data collected at 2 months or 4 months to preserve the temporal order of our research questions. In instances when participants enrolled at 2 weeks and reported on food addiction at that time, we treated their food addiction data as missing and estimated their values using full information maximum likelihood estimation (FIML) in Mplus. Because recruitment into the study is random, our missing data technique of FIML addresses this random process to minimize bias in parameter estimates due to missing data (Enders, 2010).

6. Results

Descriptive statistics and correlations for variables in all models are presented in Table 1. Food addiction and restraint were not significantly correlated (p = .571; research question one). Controlling for pre-pregnancy BMI, women’s childhood trauma exposure was significantly associated with food addiction (В = 0.19, se = 0.06, p = .001) but not dietary restraint (В = − 0.10, se = 0.07, p = .138; See Fig. 1; research question two). Controlling for pre-pregnancy BMI, depression symptoms were significantly associated with food addiction (В = 0.27, se = 0.10, p = .005) but not dietary restraint (В = 0.004, se = 0.07, p = .958; See Fig. 2; research question three).

Fig. 1.

Fig. 1.

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Standardized parameter estimates for the associations of childhood trauma exposure with the two high-risk eating phenotypes controlling for pre-pregnancy BMI.

Fig. 2.

Fig. 2.

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Standardized parameter estimates for the associations of postpartum depression symptoms with the two high-risk eating phenotypes controlling for pre-pregnancy BMI.

In the mediation model (research question four; See Fig. 3), women’s childhood trauma exposure was associated with postpartum depression symptoms (В = 0.26, se = 0.07, p < .001), which was, in turn, associated with postpartum food addiction (В = 0.23, se = 0.11, p = .031). The path between childhood trauma exposure and food addiction was not significant (В = 0.16, se = 0.11, p = .140), accounting for postpartum depression. The path between postpartum depression symptoms and dietary restraint was also not significant (В = 0.03, se = 0.07, p = .720), nor was the path between childhood trauma exposure and dietary restraint (b = − 0.11, se = 0.07, p = .147).

Fig. 3.

Fig. 3.

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Mediation model testing the effect of childhood trauma exposure on high-risk eating phenotypes through postpartum depression symptoms with standardized parameter estimates.

There was a significant indirect effect of maternal childhood trauma exposure on food addiction during the postpartum period via postpartum depression symptoms (95% CI [0.003, 0.087]). The direct effect of childhood trauma exposure on food addiction was non-significant (95% CI [−0.091, 0.358]). There was not a significant indirect effect of childhood trauma exposure on dietary restraint via postpartum depression symptoms (95% CI [−0.010 and 0.015]). The direct effect of childhood trauma exposure on dietary restraint was non-significant (95% CI [−0.241, 0.034]). Therefore, controlling for pre-pregnancy BMI, there was a significant indirect effect of maternal childhood trauma exposure on food addiction but not dietary restraint through postpartum depression symptoms.

7. Discussion

The present study sought to characterize the association between food addiction and dietary restraint in a community sample of postpartum women by examining the association between these high-risk eating phenotypes, testing psychosocial risk factors of childhood trauma exposure and depression that may predict them, and exploring the process by which these risk factors may lead to these eating phenotypes. First, we found that food addiction and dietary restraint were not significantly associated in postpartum women. Second, women’s childhood trauma exposure was positively associated with food addiction but not with dietary restraint, such that more childhood trauma exposure was associated with more food addiction. Third, women’s postpartum depression symptoms were positively associated with food addiction but not with dietary restraint, such that higher postpartum depression severity was associated with a higher number of food addiction symptoms. Fourth, postpartum depression symptoms mediated the positive association between women’s childhood trauma exposure and food addiction such that women with more childhood trauma had higher postpartum depression severity and, and, in turn, a higher number of food addiction symptoms. This relationship was not found for dietary restraint.

In the eating disorder literature, questions remain about whether these two high-risk eating phenotypes are distinct constructs with specific etiologies (Wiss & Brewerton, 2020). Findings from the present study align with some prior empirical work showing no correlation between food addiction and dietary restraint among adults (Carter et al., 2019; Gearhardt et al., 2012, 2013, 2016), although other research has found support for their association (Borisenkov et al., 2020) especially during adolescence (Alim et al., 2021; Schiestl & Gearhardt, 2018). Schiestl and Gearhardt (2018) hypothesized that the lack of association in adults may be due to restraint fatigue resulting from high levels of weight cycling common in food addiction (Gearhardt et al., 2014, 2016) and numerous prior dietary restriction attempts that have failed to result in sustained behavior change and/or weight loss. They suggest restraint fatigue in adults may contrast with adolescents who may still use restraint eating to manage weight concerns, as they are under unique shape and weight pressures and likely to have had less experience with failed restriction attempts. Postpartum women with histories of weight cycling may already experience restraint fatigue, consistent with other non-postpartum women, which may be true in our sample. However, we did not assess mother’s prior dieting so are unable to make conclusions regarding if the non-significant correlation between food addiction and dietary restraint is due to restraint fatigue. Furthermore, these women are under unique pressure and stress stemming from the demands of childbirth recovery, sleep deprivation, caring for infants, feeding, and postpartum body changes (Brown, 2014; Cho et al., 2011; Fahey & Shenassa, 2013; Sultan & Carvalho, 2021), which may take precedence over shape and weight concerns. In addition, the all-consuming nature of the demands of the early postpartum period may leave little capacity for efforts to restrain eating (i.e., contributing to further restraint fatigue), consistent with the limited capacity hypothesis that suggests disinhibited eating in restraint eaters results from limitations in cognitive capacity (Boon et al., 2002). Thus, even postpartum women with high levels of food addiction may be so physically and emotionally taxed during this time that the effort needed to engage in dietary restriction may not be available. Of note, levels of food addiction and dietary restraint in the current postpartum sample are equivalent to averages found in the general adult population (Borisenkov et al., 2020; Pursey et al., 2014; Spoor et al., 2006; van Strien et al., 2016). It may also be that these eating behaviors are simply not associated in adulthood, consistent with prior findings that do not demonstrate strong correlations in adult populations (Gearhardt et al., 2012, 2013, 2016).

Our finding that women’s childhood trauma was associated with food addiction in postpartum women (research question two) also supports prior empirical work. Early life stress such as childhood trauma has been robustly linked to addictive processes as a function of permanent neurohormonal and hypothalamic-pituitary-adrenal axis changes, structural brain changes including in the self-regulation areas of the prefrontal cortex, and gene expression changes in the mesolimbic dopamine reward pathway that result from such exposure at developmentally sensitive periods of time (Enoch, 2011; Maté, 2012). Specifically, past research has shown a positive association between childhood trauma and food addiction in adults, though, until now, this relationship has not been examined in women during the postpartum period (Guillaume et al., 2016; Imperatori et al., 2016; Mason et al., 2013; Nunes--Neto et al., 2018). Our finding extends the current state of the literature to suggest that the negative effects of childhood trauma on food addiction risk in adulthood generalize to women in the early postpartum period. This makes sense as although this is a sensitive period for reward-related eating behavior (Betts et al., 2021), there is no evidence to date that early-life sensitization of reward pathways is altered during pregnancy and the postpartum period. However, another explanation for this finding may be that the stress of the early postpartum period may replicate feelings of helplessness and overwhelm experienced during childhood traumatic exposures and thus further compromise access to the self-regulation areas of the prefrontal cortex needed to curb food-related wanting (Nelson et al., 2019). Future research should examine the strength of the positive association between childhood trauma and food addiction in postpartum versus non-postpartum women to further understand the mechanisms by which this early stress may create risk for this high-risk eating phenotype during this sensitive period.

We also found that dietary restraint was not associated with childhood trauma exposure in postpartum women (research question two). In contrast to food addiction, dietary restraint has not been conceptualized as a key mechanistic factor in the development of addictive disorders ( Gearhardt et al., 2009a, 2009b; Avena et al., 2012; Schulte et al., 2016) and thus may not be as affected by early life stress. However, Many previous studies have found a correlation between childhood trauma exposure and dietary restraint (Grilo & Masheb, 2001; Guillaume et al., 2016; Rodgers et al., 2019; Strodl & Wylie, 2020). Of note, these studies used a measure that operationalizes dietary restraint more broadly as disinhibited, emotional, or externally driven eating and also captures diet/overeating cycling (Polivy et al., 2020) which may mimic behaviors common in food addiction. Dietary restraint has recently been better understood to be both behavioral and cognitive efforts to avoid specific foods and reduce overall intake regardless of success (Lowe et al., 2006; Polivy et al., 2020), with empirical evidence showing that restrained eaters do not necessarily decrease caloric intake (Stice et al., 2004). The present study is the first to examine the relationship between childhood trauma and dietary restraint using a measure of dietary restraint that captures both behaviors and attempts to restrain intake while excluding external and emotional disinhibited eating factors (Polivy et al., 2020). It may be that women with histories of childhood trauma are highly sensitized to emotional or environmental cues due to unsafe early environments (Perry et al., 1995). Such sensitivity may be more strongly related to disinhibited or externally-driven eating, common in food addiction, than to internally-driven efforts to control/inhibit intake. Thus, prior studies that have found a positive association between childhood trauma exposure and dietary restraint may have captured restraint related to environmental sensitivity to external factors rather than cognitive or behavioral efforts to restrain eating. Given that the postpartum period is a time of many physical, emotional, and cognitive changes that result in new and intense internal and external/environmental cues, continued research that disentangles restraint related to external versus internal cues during this time can help to better understand this high-risk eating phenotype.

We also found that depression symptoms were associated with food addiction in our sample of postpartum women (research question three). Depression and addiction are robustly associated (Bakken et al., 2007): estimates suggest that almost a third of people who meet criteria for substance use disorder in the United States have a major depressive disorder (Carey, 2019). Prior research suggests that this comorbidity may be in part due to similar brain regions and processes implicated in both depression and addiction (Lalanne et al., 2014; Xu et al., 2020). Our finding aligns with past research that has shown a positive association between depression and food addiction (Burrows et al., 2018) and suggests that postpartum depression symptoms, in particular, are a risk factor for food addiction in postpartum women.

In contrast to food addiction, we did not find that depression was associated with dietary restraint (research question three). Prior research has yielded mixed evidence, with some studies showing a significant positive association between depression and dietary restraint (Spoor et al., 2006; van Strien et al., 2016) and others not (Goossens et al., 2010; Konttinen et al., 2010; Wardle et al., 2001). There are several explanations for our finding. First, anhedonia and significant weight loss/appetite changes can be features of depression (American Psychiatric Association, 2013). Decreased appetite may lead to reduced perceived need to exert effort to restrain intake. Second, depression also includes fatigue and psychomotor retardation, which may leave little energy for significant cognitive efforts like restraining eating, especially during a physically and cognitively demanding time like the postpartum period. Although our findings suggest that postpartum depression symptoms are not a salient psychosocial risk factor for dietary restraint in postpartum women, continued research is needed to discern if this is because of appetite changes, reduced cognitive capacity, or other unknown factors.

Finally, we found that postpartum depression symptoms are a key pathway linking women’s childhood trauma exposure and food addiction during the early postpartum period (research question four). Depression in adulthood (Anda et al., 2006; Felitti et al., 1998b; Gallo et al., 2018) and the postpartum period (Mahenge et al., 2018; Seng et al., 2013) are well established sequelae of childhood trauma. This may be due to the sensitization of the corticotropin-releasing factor (CRF) neuronal systems and the hypothalamic-pituitary-adrenal (HPA) axis, which are centrally implicated in stress response in humans (Nemeroff, 2004). Early trauma exposure may sensitize the system to later stress, which then may manifest as psychopathology, including depression. Our findings extend this current knowledge to suggest that the development of postpartum depression symptoms secondary to childhood trauma exposure is a mechanism by which early life stress may lead to food addiction in postpartum women. The same pathway of risk was not found for dietary restraint, lending further evidence to suggest that food addiction and dietary restraint are distinct constructs with different etiological pathways.

7.1. Strengths and limitations

Despite the fact that the postpartum period is a sensitive time for maternal eating (Brown & Toma, 1986; Faas et al., 2010; Kazma et al., 2020; Orloff & Hormes, 2014) and the intergenerational transmission of eating phenotypes from mothers to children (Birch & Fisher, 2000; Burrows et al., 2017; Rodgers et al., 2013), limited attention has been given to women’s eating in the period right after birth. The current study is the first of its kind to concurrently examine two high-risk eating phenotypes - food addiction and restraint eating - in women during the early postpartum period. This research contributes to the literature by showing that food addiction and dietary restraint are not significantly associated in postpartum women and that the two phenotypes do not share candidate psychosocial risk factors (childhood trauma exposure and postpartum depression symptoms). Finally, we identified mechanistic pathways between these risk factors and two eating phenotypes, finding that the impact of childhood trauma exposure on food addiction during the early postpartum period operated via a spillover effect where more childhood trauma led to more postpartum depression symptoms which then led to more food addiction. This was not the case for dietary restraint. It will be important for future research to identify the unique psychosocial risk factors and etiological pathways to dietary restraint to inform novel intervention targets to interrupt the intergenerational transmission of this eating phenotype. Finally, pre-pregnancy BMI significantly related to both eating phenotypes. As the pre-pregnancy weight status of the sample was in the overweight range, it may be important to consider how findings may replicate in samples with pre-pregnancy obesity.

Despite the aforementioned strengths, there were several study limitations. First, this study did not use a high-risk sample (the cohort had a relatively high mean socio-economic and education level) and therefore findings may not generalize to postpartum women of lower socioeconomic status and less education, or those with more significant childhood trauma, postpartum depression symptoms, or those who have more clinical-level symptoms of food addiction and dietary restraint. Second, the Yale Food Addiction Scale (YFAS; Gearhardt et al., 2009a, 2009b) was used to assess for food addiction in postpartum women, but the measure asks about symptoms over the past twelve months. Although there may be recency bias in reporting symptoms (Davelaar et al., 2005), future research would do well to more precisely specify the postpartum period as the time of interest when assessing for food addiction. Third, our study did not assess emotion dysregulation or distress tolerance in mothers during the postpartum period and therefore we were unable to consider the potentially mechanistic roles of these processes in linking maternal ACEs to postpartum eating. Future work should consider the role of such additional theoretically important constructs as potential mediators. Finally, study findings regarding the etiological pathways of food addiction and dietary restraint relied on sequential mediation which is limited as it does not provide information on the direction and magnitude of bias in the model and thus no way to correct for said bias (Mitchell & Maxwell, 2013). In addition, the effects were small. Future work should assess these constructs over time and use longitudinal mediation to better characterize pathways between childhood trauma exposure, postpartum depression symptoms, and the two high-risk eating phenotypes in postpartum women.

8. Conclusion

The aim of this study was to characterize the association between two high-risk eating phenotypes in women during the early postpartum period, a sensitive time for maternal eating and intergenerational transmission of eating-related concerns. We examined the nature of the association between food addiction to dietary restraint, tested psychosocial risk factors of childhood trauma exposure and postpartum depression symptoms that may predict them, and identified mechanisms by which these risk factors may lead to these eating phenotypes. Findings highlighted that food addiction and dietary restraint have distinct psychosocial predictors and etiological pathways, which suggests important construct validity differences between these two high-risk eating phenotypes. Childhood trauma exposure and postpartum depression symptoms were identified as key psychosocial risk factors for food addiction, in that childhood trauma exposure creates risk for postpartum depression symptoms, which then creates risk for food addiction in the early postpartum period. Interventions seeking to address food addiction in postpartum women and mitigate the impact of this high-risk eating phenotype on the next generation should focus on treating postpartum depression symptoms, especially in women with histories of childhood trauma exposure.

Supplementary Material

Supplementary Table 1. Summary statistics of YFAS symptoms and clinical impairment.

Acknowledgements

We would like to acknowledge the participating families and the research assistants who collected the data.

Funding source

This work was supported by the National Institute of Child Health and Human Development R01HD084163 and the American Heart Association Postdoctoral Fellowship 825916. Funding agencies had no role in study design, collection, analysis and interpretation of data, writing of the report, and the decision to submit the article for publication.

Footnotes

Ethics statement

The study was approved by the University of Michigan Medicine Institutional Review Board (IRB MED; HUM00103575). Written informed consent to participate in this study was provided by participants.

Declaration of competing interest

The authors have no potential conflicts of interest.

Appendix A. Supplementary data

Supplementary data to this article can be found online at https://doi.org/10.1016/j.appet.2023.106589.

Data availability

Data will be made available on request.

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Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Supplementary Materials

Supplementary Table 1. Summary statistics of YFAS symptoms and clinical impairment.
NIHMS1932987-supplement-Supplementary_Table_1___Summary_statistics_of_YFAS_symptoms_and_clinical_impairment_.docx (13.8KB, docx)

Data Availability Statement

Data will be made available on request.

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