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. Author manuscript; available in PMC: 2015 Dec 1.
Published in final edited form as: Int J Eat Disord. 2014 Jan 15;47(8):874–877. doi: 10.1002/eat.22247

Do Emotional Eating Urges Regulate Affect? Concurrent and Prospective Associations and Implications for Risk Models of Binge Eating

Alissa A Haedt-Matt 1, Pamela K Keel 2,*, Sarah E Racine 3, S Alexandra Burt 4, Jean Yueqin Hu 5, Steven Boker 6, Michael Neale 7, Kelly L Klump 4
PMCID: PMC4099307  NIHMSID: NIHMS553201  PMID: 24431328

Abstract

Objective

Emotional eating (EE) reflects an urge to eat in response to emotional rather than physical cues and is a risk factor for the development of binge eating. EE has been conceptualized as an attempt to regulate negative affect (NA), a posited maintenance factor for binge eating. However, no study has examined whether EE urges regulate affect. Further, no studies have examined longitudinal associations between EE urges and positive affect (PA).

Method

We examined within-subject longitudinal associations between affect and EE urges in a community-based sample of female twins (mean age=17.8 years). Participants (N=239) completed ratings of affect and EE urges for 45 consecutive days.

Results

Greater NA was concurrently associated with greater EE urges. Additionally, greater EE urges predicted worse NA for both concurrent and prospective (next-day) analyses. Finally, lower PA was associated with greater EE urges in concurrent analyses, but there were no prospective associations between changes in PA and EE urges.

Discussion

EE urges do not appear to effectively regulate affect. EE urges in a community-based sample appears to have the same functional relationship with affect as binge eating in clinical samples, further supporting EE as a useful dimensional construct for examining processes related to binge eating.


The affect regulation model for binge eating posits that changes in affective states trigger and maintain binge episodes (1). According to this model, individuals experience a desire or urge to eat in response to increased negative emotions, referred to as emotional eating (EE)(2,3). Theoretically, EE promotes the consumption of excessive quantities of food and development of binge eating because eating is reinforced by a reduction in negative affect (NA) instead of being regulated by physiological cues of hunger and satiation. Supporting this model, several studies have found significant associations between EE and binge eating in clinical (4,5) and non-clinical samples (68), and EE was a prospective predictor of binge-eating onset among adolescent girls (6). However, no studies have established whether EE is maintained by reductions in NA. Thus, a key assumption regarding how EE contributes to the development of binge eating remains untested.

Longitudinal data are needed to determine the emotional precipitants and consequences of EE. In addition, although affect regulation models typically propose that maladaptive behaviors function to decrease NA, regulation may include increases in positive affect (PA)(9) as dopamine release following food consumption has been associated with subjective pleasure (10). Thus, EE may regulate affect through increases in PA. The current study examined concurrent and prospective associations between affect (positive and negative) and EE urges using a longitudinal, within-subjects design in a large, community-based sample. Such samples are ideal for informing risk models as they can examine longitudinal associations before clinical problems become established and thus can disambiguate consequences of clinical problems from their possible antecedents. Given meta-analytic findings for binge eating (11) as well as theoretical models regarding the role of NA in precipitating EE, we hypothesized that greater NA would predict increases in EE urges. A key question of this study, however, is whether EE urges will successfully regulate affect or whether EE urges would be followed by further deterioration of mood. If EE urges are associated with subsequent increases in NA, this would further challenge affect regulation models for dysregulated eating.

METHODS

Participants

Participants were 239 female twins, ages 16–25 years, (M(SD)=17.79(1.65)), drawn from the Twin Study of Hormones and Behavior across the Menstrual Cycle (12) within the Michigan State University Twin Registry (MSUTR (13,14)). Participant-reported ethnicity was 83.2% Caucasian, non-Hispanic; 12.6% African American; and 4.2% Hispanic. Participants had a mean (SD) body mass index of 23.98(5.66) kg/m2.

Procedure and measures

Participants completed daily self-report measures after 5:00p.m. for 45 consecutive days using either a secure on-line system or pre-printed scantrons; 91% of eligible participants completed the study. This research study was reviewed and approved by an institutional review board; all participants completed informed consent prior to participation.

Emotional eating urges

The Dutch Eating Behavior Questionnaire-Emotional Eating subscale (DEBQ-EE (2)) measures desire to eat in response to affective cues (e.g., sadness, anger). The instructions were modified with permission to ask participants how well each item was “true in relation to you TODAY” to capture EE urges at the daily level. Internal consistencies using the unmodified and modified instructions are excellent (α=.93 and α=.98, respectively (15)). This scale has demonstrated discriminant (16) and criterion validity (17), and has demonstrated significant associations with continuous measures of binge eating (15), supporting the relevance of the DEBQ-EE for assessing and understanding pathological eating behaviors. The DEBQ-EE has demonstrated unique associations with ovarian hormones that were not mediated by NA (15), supporting that the DEBQ-EE is not simply an alternative measure of NA. Internal consistency in the current study was α=.90.

Positive and negative affect

The Positive and Negative Affect Schedule (PANAS (18)) assesses 10 positive (e.g., excited) and 10 negative (e.g., sadness) emotions at the daily level. Good internal consistency, convergent validity, and discriminant validity have been demonstrated for the PANAS (18). In the current study, average internal consistency was α=.85 (NA) and α=.88 (PA).

Statistical analyses

Raw scores for EE urges, NA, and PA were log-transformed to correct for positive skew and multiplied by 10 to prevent boundary constraints. Predictor variables were person-centered on mean values. Multilevel models (MLM) with full maximum-likelihood estimation were used to examine how within-person changes in EE urges were associated with within-person changes in affect. MLM permitted inclusion of participants with missing data (6.82% of observations). A three-level model with random intercepts and slopes was used to control for the non-independence of repeated measures (level 1) within individuals (level 2) and the non-independence of individuals within families (level 3). Separate models were fit to examine the main effects of affect on EE urges and EE urges on affect. Concurrent (same-day) analyses examined associations between affect and EE urges, but are subject to bidirectional interpretations. Thus, time-lagged analyses also examined prospective associations between affect and next-day EE urges and between EE urges and next-day affect. To account for within-variable stability over time in longitudinal data, each dependent variable was entered as a covariate in prospective analyses (e.g., EE urges was entered as a covariate in analyses of affect and next-day EE urges to control for associations due to stability of EE urges across days).

RESULTS

Descriptive statistics were: mean (SD) EE urges=0.35(0.50), range=0–3.69; mean (SD) NA=15.11(5.50), range=10–47; mean (SD) PA=23.62(7.94), range=10–50. Results from concurrent models predicting EE urges and affect measured on the same day are presented in Table 1. Greater NA was concurrently associated with greater EE urges, and lower PA was concurrently associated with greater EE urges. Additionally, greater EE urges were a significant predictor of greater same-day NA and lower same-day PA. Results from prospective models predicting EE urges while controlling for within-variable stability of EE urges indicated that neither NA nor PA significantly predicted next-day EE urges (Table 2). However, greater EE urges were associated with greater next-day NA while controlling for within-variable stability of NA. EE urges did not predict PA on the following day.

Table 1.

Concurrent Models

Fixed Effects Emotional Eating Urges
Estimate (SE) t (df) p
 Intercept 1.07 (.07) 14.94 (238.00) <.001
 Negative Affect .17 (.01) 22.68 (9828.04) <.001
 Positive Affect −.03 (.01) −4.82 (9828.03) <.001
Fixed Effects Negative Affect
Estimate (SE) t (df) p
 Intercept 11.57 (.07) 176.89 (237.96) <.001
 Emotional Eating Urges .30 (.01) 23.01 (9841.04) <.001
Fixed Effects Positive Affect
Estimate (SE) t (df) p
 Intercept 13.46 (.08) 173.10 (237.87) <.001
 Emotional Eating Urges −.09 (.01) −6.08 (9840.97) <.001

Table 2.

Prospective Models

Fixed Effects Next-Day Emotional Eating Urges
Estimate (SE) t (df) p
 Intercept 1.09 (.07) 15.46 (238.00) <.001
 Emotional Eating Urges −.15 (.01) −14.90 (8029.44) <.001
 Negative Affect <.01 (.01) .60 (6991.69) .55
 Positive Affect .01 (.01) 1.52 (7509.58) .13
Fixed Effects Next-Day Negative Affect
Estimate (SE) t (df) p
 Intercept 11.57 (.07) 176.68 (237.75) <.001
 Negative Affect −.22 (.01) −21.38 (7644.96) <.001
 Emotional Eating Urges .04 (.01) 2.47 (8803.91) .005
Fixed Effects Next-Day Positive Affect
Estimate (SE) t (df) p
 Intercept 13.45 (.08) 171.39 (237.78) <.001
 Positive Affect .36 (.01) 36.74 (3918.82) <.001
 Emotional Eating Urges .02 (.01) 1.14 (3419.05) .25

DISCUSSION

NA was positively associated with EE urges, and greater EE urges predicted worse NA in both concurrent and prospective analyses. However, greater NA did not predict changes in next-day EE urges. Thus, NA may serve as a proximal trigger for EE urges (reflected in concurrent analyses) rather than a distal trigger (reflected in prospective analyses). The desire to eat in response to NA appears to maintain or increase NA over time, consistent with a meta-analysis of longitudinal studies demonstrating that NA is an immediate trigger of binge eating and that NA increases further following binge eating (11).

Theoretically, EE represents an attempt to regulate NA; however, current results suggest that this does not work. Instead, there appear to be reciprocal relations in which EE urges contribute to worsening affect, which then contributes to EE urges, resulting in a downward spiral that potentially explains prospective associations between EE and development of binge-eating episodes (6). Our results do not support that EE urges regulate affect through increasing positive feelings (10) because lower PA was concurrently associated with greater EE urges, and there were no significant prospective associations between PA and EE urges.

Taken together, EE urges in a community-based sample may have the same functional relationship with affect as binge eating in clinical samples (11). This is consistent with research demonstrating that EE urges in non-clinical samples has the same functional relationship with ovarian hormones across the menstrual cycle (12,15) as binge eating in clinical samples (19). Current findings and studies of dysregulated eating in children (20) suggest that EE urges may be useful in identifying early disordered eating patterns and etiological processes of binge eating. Research on EE may inform our understanding of the development and course of binge eating, consistent with the Research Domain Criteria initiative (21,22).

Strengths of this study included use of a longitudinal, within-subject design in a large community-based sample with a high retention rate. Study measures demonstrated strong psychometric properties, and study duration minimized concerns regarding the impact of reactivity on daily assessments and random error. This study filled a critical gap in the existing literature by examining both NA and PA, and by investigating both the influence of affect on EE urges and the influence of EE urges on affect. Finally, participants completed ratings in their own homes, which increases ecological validity (23).

The present study was limited by the use of once daily assessments of EE urges and affect. Patients often describe significant day-to-day fluctuations in binge eating (19), suggesting that “day” is a clinically meaningful unit of analysis. Nonetheless, it is possible that EE urges may improve affect during or immediately after eating, which would not be captured in the current study. Future research incorporating ecological momentary assessment is needed to examine immediate, momentary relations between affect and EE. A second limitation includes our assessment of the desire or urge to eat in response to negative emotions rather than actual eating behavior. However, previous research supports the reliability and validity of our measure of EE urges as tapping behavioral changes that have been directly linked to food intake in both human and animal studies (15), and another study supports the criterion validity of EE urges for assessing dysregulated eating in this sample (17). Finally, longitudinal studies cannot permit causal interpretations. Experimental designs are needed to determine whether food intake triggered by experimental manipulations in affect causes improvement or deterioration in mood.

In summary, EE urges appear to lead to worsening affect on subsequent days. These predictable increases in NA following EE urges may be incorporated into psycho-educational components of treatment to counter patients’ belief that eating relieves negative emotions (1,24). Treatments that emphasize exposure to and tolerance of NA, such as exposure plus response prevention (25) or Dialectical Behavior Therapy (26), may help break the link between NA and eating. These approaches also may be integrated into prevention programs to reduce EE given that EE has been demonstrated to be a risk factor for binge eating (6).

Acknowledgments

This research was supported by grants from the National Institute of Mental Health (R01 MH082054 awarded to Drs. Klump, Boker, Burt, Keel, Neale, Sisk; F31 MH085456 awarded to Dr. Haedt-Matt) and from the Canadian Institutes of Health Research (MDR-96630 awarded to Dr. Racine). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institute of Mental Health or the Canadian Institutes of Health Research. We also wish to acknowledge the scientific contributions of Dr. Cheryl Sisk to this study.

Footnotes

Disclosure of Conflicts

None.

References

  • 1.Hawkins RC, Clement PF. Binge eating: Measurement problems and a conceptual model. In: Hawkins RC, Fremouw WJ, Clement PF, editors. The Binge Purge Syndrome: Diagnosis, Treatment, and Research. New York, NY: Springer; 1984. [Google Scholar]
  • 2.Van Strien T, Frijters JE, Bergers GP, Defares PB. The Dutch Eating Behavior Questionnaire (DEBQ) for assessment of restrained, emotional, and external eating behavior. International Journal of Eating Disorders. 1986;5(2):295–315. [Google Scholar]
  • 3.Arnow B, Kenardy J, Agras WS. The Emotional Eating Scale: the development of a measure to assess coping with negative affect by eating. Int J Eat Disord. 1995;18(1):79–90. doi: 10.1002/1098-108x(199507)18:1<79::aid-eat2260180109>3.0.co;2-v. [DOI] [PubMed] [Google Scholar]
  • 4.Masheb RM, Grilo CM. Emotional overeating and its associations with eating disorder psychopathology among overweight patients with binge eating disorder. Int J Eat Disord. 2006;39(2):141–6. doi: 10.1002/eat.20221. [DOI] [PubMed] [Google Scholar]
  • 5.Ricca V, Castellini G, Lo Sauro C, Ravaldi C, Lapi F, Mannucci E, et al. Correlations between binge eating and emotional eating in a sample of overweight subjects. Appetite. 2009;53(3):418–21. doi: 10.1016/j.appet.2009.07.008. [DOI] [PubMed] [Google Scholar]
  • 6.Stice E, Presnell K, Spangler D. Risk factors for binge eating onset in adolescent girls: a 2-year prospective investigation. Health Psychol. 2002;21(2):131–8. [PubMed] [Google Scholar]
  • 7.Tanofsky-Kraff M, Theim KR, Yanovski SZ, Bassett AM, Burns NP, Ranzenhofer LM, et al. Validation of the emotional eating scale adapted for use in children and adolescents (EES-C) Int J Eat Disord. 2007;40(3):232–40. doi: 10.1002/eat.20362. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 8.Van Strien T, Engels RC, Van Leeuwe J, Snoek HM. The Stice model of overeating: tests in clinical and non-clinical samples. Appetite. 2005;45(3):205–13. doi: 10.1016/j.appet.2005.08.004. [DOI] [PubMed] [Google Scholar]
  • 9.Gross JJ. Handbook of emotion regulation. New York, NY US: Guilford Press; 2007. [Google Scholar]
  • 10.Small DM, Jones-Gotman M, Dagher A. Feeding-induced dopamine release in dorsal striatum correlates with meal pleasantness ratings in healthy human volunteers. Neuroimage. 2003;19(4):1709–15. doi: 10.1016/s1053-8119(03)00253-2. [DOI] [PubMed] [Google Scholar]
  • 11.Haedt-Matt AA, Keel PK. Revisiting the affect regulation model of binge eating: a meta-analysis of studies using ecological momentary assessment. Psychol Bull. 2011;137(4):660–81. doi: 10.1037/a0023660. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 12.Klump KL, Keel PK, Racine SE, Burt SA, Burt AS, Neale M, et al. The interactive effects of estrogen and progesterone on changes in emotional eating across the menstrual cycle. J Abnorm Psychol. 2013;122(1):131–7. doi: 10.1037/a0029524. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 13.Burt SA, Klump KL. The Michigan State University Twin Registry (MSUTR): an update. Twin Res Hum Genet. 2013;16(1):344–50. doi: 10.1017/thg.2012.87. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 14.Klump KL, Burt SA. The Michigan State University Twin Registry (MSUTR): genetic, environmental and neurobiological influences on behavior across development. Twin Res Hum Genet. 2006;9(6):971–7. doi: 10.1375/183242706779462868. [DOI] [PubMed] [Google Scholar]
  • 15.Klump KL, Keel PK, Culbert KM, Edler C. Ovarian hormones and binge eating: exploring associations in community samples. Psychol Med. 2008;38(12):1749–57. doi: 10.1017/S0033291708002997. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 16.Wardle J. Eating style: a validation study of the Dutch Eating Behaviour Questionnaire in normal subjects and women with eating disorders. J Psychosom Res. 1987;31(2):161–9. doi: 10.1016/0022-3999(87)90072-9. [DOI] [PubMed] [Google Scholar]
  • 17.Racine SE, Keel PK, Burt SA, Sisk CL, Neale M, Boker S, Klump KL. Exploring the relationship between negative urgency and dysregulated eating: etiologic associations and the role of negative affect. J Abnorm Psychol. 2013;122(2):433–44. doi: 10.1037/a0031250. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 18.Watson D, Clark LA, Tellegen A. Development and validation of brief measures of positive and negative affect: the PANAS scales. J Pers Soc Psychol. 1988;54(6):1063–70. doi: 10.1037//0022-3514.54.6.1063. [DOI] [PubMed] [Google Scholar]
  • 19.Edler C, Lipson SF, Keel PK. Ovarian hormones and binge eating in bulimia nervosa. Psychol Med. 2007;37(1):131–41. doi: 10.1017/S0033291706008956. [DOI] [PubMed] [Google Scholar]
  • 20.Tanofsky-Kraff M, Shomaker LB, Olsen C, Roza CA, Wolkoff LE, Columbo KM, et al. A prospective study of pediatric loss of control eating and psychological outcomes. J Abnorm Psychol. 2011;120(1):108–18. doi: 10.1037/a0021406. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 21.Insel T, Cuthbert B, Garvey M, Heinssen R, Pine DS, Quinn K, et al. Research domain criteria (RDoC): toward a new classification framework for research on mental disorders. Am J Psychiatry. 2010;167(7):748–51. doi: 10.1176/appi.ajp.2010.09091379. [DOI] [PubMed] [Google Scholar]
  • 22.Sanislow CA, Pine DS, Quinn KJ, Kozak MJ, Garvey MA, Heinssen RK, et al. Developing constructs for psychopathology research: research domain criteria. J Abnorm Psychol. 2010;119(4):631–9. doi: 10.1037/a0020909. [DOI] [PubMed] [Google Scholar]
  • 23.Shiffman S, Stone AA, Hufford MR. Ecological momentary assessment. Annu Rev Clin Psychol. 2008;4:1–32. doi: 10.1146/annurev.clinpsy.3.022806.091415. [DOI] [PubMed] [Google Scholar]
  • 24.Stickney MI, Miltenberger RG, Wolff G. A descriptive analysis of factors contributing to binge eating. J Behav Ther Exp Psychiatry. 1999;30(3):177–89. doi: 10.1016/s0005-7916(99)00019-1. [DOI] [PubMed] [Google Scholar]
  • 25.Jansen A, Broekmate J, Heymans M. Cue-exposure vs self-control in the treatment of binge eating: a pilot study. Behav Res Ther. 1992;30(3):235–41. doi: 10.1016/0005-7967(92)90069-s. [DOI] [PubMed] [Google Scholar]
  • 26.Linehan MM, Cochran BN, Kehrer CA. Dialectical behavior therapy for borderline personality disorder. In: Barlow DH, editor. Clinical handbook of psychological disorders: A step-by-step treatment manual. 3. New York, NY US: Guilford Press; 2001. pp. 470–522. [Google Scholar]

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