Eating Disorder Symptoms,Affect-Regulation Drinking Motives and Drinking-Related Outcomes

Abstract

The present study examined the mediating and moderating effects of affect-regulation (i.e., coping and enhancement) drinking motives in the relationship between eating disorder (ED) pathology and drinking outcomes. The sample included 419 undergraduate college students (52.0% female) who completed self-report questionnaire measures of ED pathology, drinking motives, drinking level, and drinking-related problems. ED pathology was positively associated with both coping and enhancement motivation and drinking-related problems. Results from mediation analyses indicated a positive indirect effect for ED pathology on drinking level through enhancement motivation and positive indirect effects for ED pathology on drinking-related problems (a) through coping motivation and (b) through enhancement motivation and number of heavy drinking days. Little evidence was found for the predicted moderating effects of drinking motives, and few gender differences were observed in the effects of interest. Findings support the notion that distinct motivational pathways underlie the association between ED pathology and alcohol-related outcomes.

Keywords

alcohol use/abuse drinking motives eating behavior/disorders coping drinking motives enhancement drinking motives

Eating disorders (EDs) and alcohol use disorders (AUD) co-occur at remarkably high rates (Bahji et al., 2019; Gadalla & Piran, 2007; Mustelin et al., 2016). An estimated 20.6% of individuals with EDs will be affected by AUD (Bahji et al., 2019) and experience greater psychopathology, increased mortality, and poorer treatment outcomes than those with EDs only (Bulik et al., 1997; Button et al., 2010; Fichter & Quadflieg, 2004). Whereas AUD may be more likely to occur among individuals with binge-purge ED presentations, higher rates of risky drinking and drinking-related harms have been found across the ED diagnostic spectrum (Mustelin et al., 2016). The relationship between problematic eating and drinking behaviors further extends to community samples, in which ED symptom severity is positively correlated with alcohol consumption and alcohol-related problems (Anderson et al., 2006; Arias et al., 2009; Luce et al., 2007; Rolland et al., 2017). Moreover, this association is particularly relevant for college students, a group at high risk for both AUD (Knight et al., 2002; National Institute on Alcohol Abuse and Alcoholism, Task Force on Alcohol Abuse and Alcoholism, 2002) and ED pathology (Harrer et al., 2020). As many as 44% of college students engage in excessive alcohol use (White & Hingson, 2013), while up to 24% have a probable ED diagnosis (Romano et al., 2022). College students with disordered eating behaviors are more likely to engage in problematic drinking; however, the specific mechanisms that underly this relationship remain poorly understood (Cusack et al., 2021; Rush et al., 2016).

Although some frameworks (e.g., Fischer et al., 2004; 2012) posit that EDs and AUD might both arise from a common cause, such as a tendency to act rashly in response to negative affect (i.e., negative urgency), other models propose more direct relationships. For example, tension-reduction models of alcohol use (M. L. Cooper et al., 2016; Greeley & Oei, 1999) maintain that individuals drink, in part, to cope with negative affect and distress arising from life stress. Therefore, to the extent that EDs and subsyndromal ED pathology cause distress and impairment across a variety of domains (Ágh et al., 2016; Patton et al., 2008; Stice et al., 2013; Vannucci et al., 2012), it is appropriate to view ED symptoms as possible antecedents to problematic drinking.

Within the context of incentive motivational models of alcohol use (M. L. Cooper et al., 2016; Cox & Klinger, 1988), the role of EDs as a source of stress can be conceptualized in two ways. First, distress caused by EDs might increase motivation to regulate affective states via alcohol use; i.e., EDs might increase motivation to drink to cope with negative emotions or to drink to enhance positive emotions. Among college students (as in other adolescent and adult samples), these two forms of motivation figure prominently as risk factors for drinking-related problems and heavy drinking, respectively (Cook et al., 2020; M. L. Cooper et al., 2016). Alternatively, affect-regulation drinking motives, especially drinking to cope motivation, might serve as individual difference vulnerability factors that moderate the effects of ED symptoms on drinking-related outcomes. More specifically, individuals who more strongly endorse using alcohol to regulate affective states, compared to those who less strongly endorse such motives, might show a stronger positive association between ED symptoms and alcohol use and related problems.

Relatively few studies have examined EDs in the context of incentive motivational models of drinking, and those that have often focus on specific aspects of EDs or use brief measures designed for ED screening processes. For example, several studies have examined the relationship between drinking motives and binge eating specifically (e.g., Fazzino et al., 2018; Pompili & Laghi, 2019; Stewart et al., 2006; Trojanowski et al., 2019) and found that individuals who binge eat are more likely to drink to cope with negative emotions. Horváth and colleagues’ (2020) study of adolescents examined how ED risk was related to affect-regulation drinking motives and alcohol use. Results indicated that internal drinking motives (i.e., a composite including both coping and enhancement motives) mediated the association between ED risk and alcohol use for women, but not men. However, the authors were unable to distinguish between different types of internal drinking motives – possibly due to their use of brief measures of the constructs – that may differentially influence the relationship between EDs and alcohol use. Additionally, ED risk was assessed with a brief screening questionnaire that is not currently used to generate ED diagnoses and lacks specificity when administered to community samples (Kutz et al., 2020; Parker et al., 2005).

In related work, Luce and colleagues (2008) considered the role of drinking motives across a broader spectrum of ED pathology among college students. They used the Eating Disorder Examination Questionnaire (EDE-Q; Fairburn & Beglin, 1994, 2008) to classify female undergraduates into probable ED diagnostic categories and found that those with bulimia nervosa (BN) and binge eating disorder (BED) were more likely to endorse coping as a drinking motive than those with eating disorder not otherwise specified (EDNOS) or no ED. However, current literature and evidence-based treatments for EDs support a transdiagnostic model of EDs, whereby the same core psychopathology (i.e., overvaluation of eating, shape, weight and their control) maintains EDs and ED symptoms, regardless of the specific ED diagnosis (Fairburn et al., 2003; Giorgio et al., 2011; Jones et al., 2020). The EDE-Q is primarily designed to assess this continuum of ED pathology, as opposed to ED diagnostic criteria (Z. Cooper et al., 1989), and is routinely used to examine associations between transdiagnostic ED pathology and other symptoms and personality traits in both clinical and community samples (Gee & Troop, 2003; Killeen et al., 2015; Marzola et al., 2020).

In the present study, we advanced this area of research in multiple ways. First, we tested the unique mediating effects of negative and positive reinforcement affect-regulation drinking motives (i.e., drinking to cope and drinking to enhance) in the relationship between the core ED pathology identified in the transdiagnostic ED model and drinking outcomes. We explored the pertinence of this model within a sample of college students, for whom the relationship between ED pathology and drinking outcomes is particularly salient (Cusack et al., 2021; Rush et al., 2016). Second, we assessed ED pathology using the questionnaire version of the Eating Disorder Examination interview (EDE; Fairburn & Cooper, 1993), which is considered to be the ‘gold standard’ assessment of ED pathology (Berg et al., 2012). Consistent with the original purpose of the measure, we treated ED pathology as a quantitative predictor by using the EDE-Q global score. Third, we examined separate indicators of drinking level and drinking-related problems. It is commonly found that after controlling for other drinking motives, drinking to cope motivation is a more robust predictor of drinking-related problems compared to drinking level (M. L. Cooper et al., 2016).

We also examined a previously untested moderation model, whereby the association between ED pathology and alcohol outcomes may be stronger for those individuals who are more likely to drink to cope with negative emotions or drink to enhance positive emotions. Although distress associated with ED pathology might contribute to high levels of affect-regulation drinking motives – as purported in the mediation framework – evidence indicates that drinking motives have a considerable trait-like component (O’Hara et al., 2015) and are likely a result of a variety of early life, contextual, and personality factors (M. L. Cooper et al., 2016; Kuntsche et al., 2006). Therefore, drinking motives – and drinking to cope motivation specifically – can be considered a vulnerability factor, such that concerns surrounding eating, shape, and weight might be more likely to be related to alcohol use for those individuals who commonly use alcohol as a means of regulating affective states (especially, negative affect). We examined these associations after controlling for potential confounders related to our variables of interest, including body mass index (BMI) and depressive symptoms (Gage & Patalay, 2021; Lowe et al., 2019) as well as gender (Lewinsohn et al., 2002). Finally, we examined whether these effects were similar for men and women given consistent evidence for gender differences in ED prevalence (Udo & Grilo, 2018) and the mediating role of affect-regulation drinking motives in the ED-alcohol association (Horváth et al., 2020).

Methods

Participants and Procedure

Participants were recruited from an undergraduate psychology department research pool and through campus-wide email advertisements to participate in a larger study on college student daily experience, well-being, and substance use. To be considered for the study, students were required to be at least 18 years old and report drinking alcohol at least twice in the past month. Students were excluded from the study if they had treatment for alcohol abuse. Students who met the eligibility criteria reviewed and signed informed consent and then completed a web-based survey that included a demographic questionnaire (including height and weight) and assessments of ED pathology, drinking motives, drinking level, and drinking-related problems. All participants were paid for their participation and given credit toward their psychology class’s research participation requirement.

Of the 423 participants, four were excluded due to missing questionnaire data. The resulting final sample consisted of 419 participants (52.0% female) with a mean age of 19.28 years (SD = 1.40). Most participants were White (79.2%) and freshmen or sophomores (73.1%). Participants’ BMI ([weight in pounds/height in inches]² x 703) was calculated based on self-reported height and weight. The sample’s BMI ranged from 16.76 to 45.76 (M = 23.54; SD = 3.94).

Measures

Eating Disorder Pathology

We used the 28-item self-report Eating Disorder Examination Questionnaire (EDE-Q; Fairburn & Beglin, 1994; 2008) to measure overvaluation of eating, shape, and weight and their control. Participants rated the severity of ED symptoms, behaviors, and beliefs over the past 28 days (e.g., “Over the past 28 days has your weight influenced how you think about [judge] yourself as a person?”) using a 7-point scale (0 = “Not at all;” 6 = “Markedly”). Frequency of key ED behaviors over the past 28 days were reported as the number of days on which they occurred (e.g., “On how many of the past 28 days you been deliberately trying to limit the amount of food you eat to influence your shape and weight?”). We recoded these values into the 7-point scale of the EDE-Q (0 = “No days;” 6 = “Every day”). Specific items were averaged together to create four subscales (Restraint, Eating Concern, Shape Concern, and Weight Concern), which were then averaged together to calculate an overall global score. Across numerous studies, the EDE-Q has demonstrated high reliability and correlated with measures of similar constructs and related behaviors (Aardoom et al., 2012; Berg et al., 2012). Cronbach’s alpha for our global score was .95.

Depressive Symptoms

Depressive symptoms were measured using the 13 non-somatic items of the Beck Depression Inventory (BDI; Beck et al., 1961). Participants rated the severity of affective and cognitive symptoms of depression using a 4-point Likert-type scale (ranging from 0 to 3). Items were summed to calculate a total score, with higher scores indicating greater depression severity. Cronbach’s alpha was .89.

Drinking Level

We assessed drinking level with two questions. Participants reported the number of days they drank alcohol and the number of days during which they engaged in heavy drinking in the past 30 days. Heavy drinking was defined as four or more drinks for women and five or more drinks for men.

Drinking Motives

We used a slightly modified version of M. L. Cooper’s (1994) drinking motives scale. Specifically, for an unrelated project, the five-item coping motivation subscale was expanded to seven items by splitting the original items concerning “depressed/nervous” and “self-confidence/to be sure of yourself” into two items each, respectively (e.g., “because it helps you when you feel depressed,” “because it helps when you feel nervous” and “to feel more self-confident,” “to feel more sure of self”). All other items were the same. Participants were asked “thinking of all the times you drink, how often would you say that you drink for each of the following reasons?” Responses were made on a 5-point scale (1 = “never/almost never;” 5 = “almost always/always”). Composite scores for the coping subscale and enhancement subscale (e.g., “because it’s fun”) were created by averaging together the corresponding items. Cronbach’s alpha was .90 for the coping subscale and .90 for the enhancement subscale.

Drinking-Related Problems

We assessed drinking-related problems using the Brief Young Adult Alcohol Consequences Questionnaire (BYAACQ; Kahler et al., 2005). Participants indicated how often they experienced each of 24 consequences over the past year on a 4-point scale (0 = “Never;” 4 = “More than 5 times”). Responses were averaged across all items to create a composite alcohol problems score. Cronbach’s alpha was .95.

Results

Descriptive statistics and correlations are shown in Table 1. Using <18.5 kg/m² as a low weight threshold for BMI (Brown et al., 2014), 2.6% of participants were low weight. On the EDE-Q, 7.9% of women scored in the clinically significant range (≥4; Mond et al., 2006) on the Restraint subscale, 2.8% on the Eating Concern subscale, 26.6% on the Shape Concern subscale, 20.2% on the Weight Concern subscale, and 7.3% on the Global Score. For men, 3.1% scored in the clinically significant range for Restraint, 0.5% for Eating Concern, 10.4% for Shape Concern, 5.5% for Weight Concern, and 1.5% on the Global Score. Thus, the rates of ED pathology found in the present sample were comparable to those found in normative samples of college students (Lavender et al., 2010; Luce et al., 2008; Quick & Byrd-Bredbenner, 2013). ED pathology was positively associated with both coping and enhancement motivation and drinking-related problems. Both motivations were positively associated with one another and with all three drinking variables. Women, compared to men, showed higher levels of depressive symptoms and ED pathology but lower levels of BMI, drinking days, and heavy drinking days.

Table 1.

Means, Standard Deviations, and Correlations.

Measure	M (SD)	Range	1	2	3	4	5	6	7	8	9
1. Gender			–
2. BMI	23.54 (3.94)	16.76–45.76	−.10^*	–
3. Depressive symptoms	4.03 (4.92)	0.00–36.00	.17^**	.18^**	–
4. ED pathology	1.50 (1.29)	0.00–5.13	.29^**	.31^**	.48^**	–
5. Coping motivation	1.81 (0.81)	1.00–4.29	−.03	.07	.29^**	.30^**	–
6. Enhancement motivation	2.79 (1.10)	1.00–5.00	.01	.08	.08	.17^**	.54^**	–
7. Drinking days	6.10 (4.46)	0.00–27.00	−.13^**	−.01	−.06	.02	.25^**	.45^**	–
8. Heavy drinking days	3.77 (3.93)	0.00–27.00	−.17^**	.02	−.07	.00	.24^**	.47^**	.81^**	–
9. Drinking-related problems	1.63 (0.56)	1.00–3.92	−.09	.03	.14^**	.19^**	.42^**	.48^**	.57^**	.62^**	–

Note. ED = eating disorder. Gender was coded 0 = male, 1 = female; thus, positive correlations denote higher values for women relative to men.

^*p < .05; ^**p < .01

Mediation Analyses

We conducted mediation analyses using PROCESS model 4 (Hayes, 2022) with core ED pathology as the independent variable and both drinking to cope and drinking to enhance as mediators. Separate analyses were conducted with number of drinking days and number of heavy drinking days as the outcome variable. We also included gender (0 = male, 1 = female), BMI, and depressive symptoms as covariates. Because our outcome variables are not normally distributed, we used the HC3 heteroscedasticity-consistent inference standard error estimator (A. F. Hayes, personal communication, September 13, 2016).

Results for the models are shown in Table 2. Analyses revealed a significant positive association between ED pathology and both coping and enhancement drinking motives. Although there was no direct association between ED pathology and number of drinking days, the total effect was significant due to a significant positive indirect effect of ED pathology on drinking days via enhancement motivation, as indicated by its 95% confidence not including zero. Despite this same indirect effect on number of heavy drinking days, neither the direct nor the total associations were significant in analyses of number of heavy drinking days.

Table 2.

Mediation Analysis Results for Number of Drinking Days and Number of Heavy Drinking Days.

	R ²	b	se	95% CI	β	t	p
DV: Coping motivation	.14
ED pathology		0.16	0.04	0.09, 0.24	0.26	4.11	<.001
DV: Enhancement motivation	.03
ED pathology		0.15	0.05	0.05, 0.24	0.17	2.96	.003
Analyses of drinking days
DV: Number of drinking days	.23
ED pathology		0.11	0.18	−0.25, 0.47	0.03	0.60	.55
Coping motivation		0.12	0.30	−0.46, 0.70	0.02	0.41	.68
Enhancement motivation		1.82	0.23	1.36, 2.27	0.45	7.84	<.001
Total effect model	.03
Total effect of ED pathology		0.40	0.20	0.00, 0.79	0.11	1.98	.05
Direct effect of ED pathology		0.11	0.18	−0.25, 0.47	0.03	0.60	.55
Indirect effects of ED pathology
Via coping motivation		0.02	0.05	−0.08, 0.11	0.01
Via enhancement motivation		0.27	0.10	0.08, 0.47	0.08
Total		0.29	0.10	0.09, 0.49	0.08
Analyses of heavy drinking days
DV: Number of heavy drinking days	.26
ED pathology		0.03	0.16	−0.28, 0.34	0.01	0.19	.85
Coping motivation		0.01	0.29	−0.55, 0.57	0.002	0.03	.98
Enhancement motivation		1.72	0.22	1.29, 2.16	0.48	7.82	<.001
Total effect model	.04
Total effect of ED pathology		0.28	0.18	−0.07, 0.64	0.09	1.56	.12
Direct effect of ED pathology		0.03	0.16	−0.28, 0.34	0.01	0.19	.85
Indirect effects of ED pathology
Via coping motivation		0.001	0.05	−0.10, 0.09	0.001
Via enhancement motivation		0.25	0.09	0.08, 0.45	0.08
Total		0.25	0.09	0.08, 0.44	0.08

Note. DV = dependent variable; b = unstandardized partial slope; se = standard error; β = standardized partial regression slope;

CI = confidence interval.

We next conducted sequential mediation analyses using PROCESS model 80 (Hayes, 2022) with ED pathology as the independent variable and drinking-related problems as the outcome variable. In this model, the mediation pathway goes through drinking to cope and drinking to enhance and then through number of heavy drinking days. We focused on heavy drinking days given its theoretical link with drinking-related problems. We also included gender (0 = male, 1 = female), BMI, and depressive symptoms as covariates and again used the HC3 heteroscedasticity-consistent inference standard error estimator.

Results for this model are shown in Table 3 and Figure 1. Both the total and direct associations between ED pathology and drinking-related problems were significant and positive. In addition, there were significant indirect effects of ED pathology on drinking-related problems via coping motivation and via enhancement motivation and the number of heavy drinking days.

Table 3.

Sequential Mediation Analysis Results for Drinking-Related Problems.

	R ²	b	se	95% CI	β	t	p
DV: Drinking-related problems	.49
ED pathology		0.05	0.02	−0.00, 0.09	0.11	2.19	.03
Coping motivation		0.13	0.04	0.05, 0.20	0.18	3.23	.001
Enhancement motivation		0.06	0.03	0.01, 0.11	0.12	2.37	.02
Number of heavy drinking days		0.07	0.01	0.06, 0.09	0.52	10.44	<.001
Total effect model	.06
Total effect of ED pathology		0.10	0.03	0.04, 0.15	0.23	3.48	<.001
Direct effect of ED pathology		0.05	0.02	0.00, 0.09	0.11	2.19	.03
Indirect effects of ED pathology
Via coping motivation		0.02	0.01	0.01, 0.04	0.05
Via enhancement motivation		0.01	0.00	0.00, 0.02	0.02
Via heavy drinking days		0.00	0.01	−0.02, 0.03	0.01
Via coping and heavy drinking days		0.00	0.00	−0.01, 0.01	0.00
Via enhancement and heavy drinking days		0.02	0.01	0.01, 0.03	0.04
Total		0.05	0.02	0.01, 0.09	0.12

Note. DV = dependent variable; b = unstandardized partial slope; se = standard error; β = standardized partial regression slope;

CI = confidence interval.

Figure 1.

Standardized Associations of Sequential Mediation Analysis in Predicting Drinking-Related Problems. Note: Dotted lines indicate nonsignificant associations. ^*p < .05; ^**p < .01.

Moderation Analyses

Finally, we conducted moderation analyses using PROCESS model 2 (Hayes, 2022) with ED pathology as the independent variable and both drinking to cope and drinking to enhance as moderators. Separate analyses were conducted with number of drinking days, number of heavy drinking days, and drinking-related problems as the dependent variable. We included gender, BMI, and depressive symptoms as covariates in all models and number of heavy drinking days as a covariate in the model predicting drinking-related problems. We again used the HC3 heteroscedasticity-consistent inference standard error estimator. Continuous variables were centered for the construction of product terms.

Results for the models are shown in Table 4. Neither coping nor enhancement motivation moderated associations between ED pathology and number of drinking days or number of heavy drinking days. In analyses predicting drinking-related problems, there was a significant interaction between ED pathology and enhancement motivation. The form of this interaction indicated a positive association between ED pathology and drinking-related problems among individuals with high levels (b = 0.10, p = .002) and average levels (b = 0.05, p = 0.02), of drinking to enhance motivation, but not among individuals with low levels (b = 0.01, p = .81). However, a supplemental analysis showed this effect was no longer significant when the interaction between ED pathology and number of heavy drinking days was included in the model.

Table 4.

Moderating Effects of Drinking Motives.

	R ²	b	se	95% CI	t	p
DV: Drinking days	.23
ED pathology		0.15	0.19	−0.23, 0.52	0.78	.43
Coping motivation		0.29	0.30	−0.39, 0.80	0.66	.51
ED pathology × coping motivation		−0.22	0.25	−0.71, 0.27	−0.89	.37
Enhancement motivation		1.80	0.24	1.34, 2.27	7.61	<.001
ED pathology × enhancement motivation		−0.01	0.22	−0.43, 0.42	−0.03	.98
DV: Heavy drinking days	.26
ED pathology		0.07	0.17	−0.26, 0.39	0.40	.69
Coping motivation		0.07	0.30	−0.51, 0.66	0.25	.81
ED pathology × coping motivation		−0.21	0.25	−0.70, 0.28	−0.84	.40
Enhancement motivation		1.72	0.23	1.27, 2.17	7.49	<.001
ED pathology × enhancement motivation		0.03	0.22	−0.41, 0.46	0.12	.91
DV: Drinking-related problems	.50
Number of heavy drinking days		0.07	0.01	0.06, 0.09	10.49	<.001
ED pathology		0.05	0.02	0.01, 0.10	2.39	.02
Coping motivation		0.13	0.04	0.05, 0.21	3.11	.002
ED pathology × coping motivation		−0.04	0.03	−0.10, 0.02	−1.17	.24
Enhancement motivation		0.06	0.03	0.01, 0.11	2.50	.01
ED pathology × enhancement motivation		0.04	0.02	0.00, 0.08	2.09	.04

Note. b = unstandardized partial slope; se = standard error; CI = confidence interval.

Gender Differences

We examined gender as a moderator of the indirect effects through drinking motives and the direct effect of ED pathology on drinking-related outcomes using PROCESS model 59. We estimated separate models for number of drinking days, number of heavy drinking days, and drinking-related problems (15 total interactions, five for each model; we also controlled for number of heavy drinking days in analyses of drinking-related problems). None of the moderating effects were significant. Finally, we examined gender as an additional moderating variable in our moderation analyses using PROCESS model 3 (18 total interactions, 2 two-way interactions and a three-way interaction each in separate analyses for drinking to cope and drinking to enhance for each of the three outcome variables). Across all analyses, only two moderating effects were significant at the .05 alpha level. Men had a stronger association between enhancement motivation and number of heavy drinking days (b = −0.96, p = .02) and a stronger association between enhancement motivation and drinking-related problems (b = −0.13, p = .01).¹

Discussion

The present study added to the limited body of literature on the relationships among EDs, drinking motives, and alcohol use and related problems among college students. We found some evidence for the mediating role of coping and enhancement drinking motivation in the association between the core ED psychopathology (i.e., overvaluation of eating, shape, and weight and their control) and various alcohol outcomes. Specifically, we found a significant positive indirect effect for ED pathology on drinking level through enhancement but not coping motivation. In contrast, both coping and enhancement motivation played a mediating role in the relationship between ED pathology and drinking-related problems. We found less support for the posited moderating role of affect-regulation motives, with only enhancement motives moderating the association between ED pathology and drinking-related problems.

Our mediation findings clarify and extend those of Horváth and colleagues (2020), who found that a global affect-regulation drinking motivation variable (i.e., a combination of coping and enhancement motivation) mediated the effect of ED risk on an alcohol use composite that mainly reflected use levels. Our findings point to the possibility that two distinct mechanisms might link ED pathology to alcohol-related outcomes: a positive reinforcement pathway wherein alcohol is used to enhance positive emotions and a negative-reinforcement pathway wherein alcohol is used to reduce distress. Moreover, these pathways are linked to distinct outcomes, with the former related to higher levels of use and the latter directly related to greater problems related to drinking. These patterns are generally consistent with the broader literature examining drinking motives’ unique effects on drinking level and drinking-related problems (M. L. Cooper et al., 2016).

We should note that conclusions from our mediation findings are limited given the cross-sectional nature of our data. However, consistent with Hayes’s (2018) and Winer and colleagues’ (2016) perspectives, we believe that results from our atemporal mediation analyses provide insight into plausible theoretical processes of interest. Based on our patterns of associations, we can posit that in certain situations, ED pathology might manifest in a more approach-oriented (i.e., enhancement) motivational style toward drinking and possibly other behavior such as binge eating. For example, when certain individuals with high levels of ED pathology are at parties and other convivial settings, this motivational inclination might result in both increased alcohol use and eating to augment their positive emotions, particularly following a period of dietary restraint (Farmer et al., 2001). In addition, ED pathology might increase the risk of engaging in more avoidance-oriented drinking behavior. For example, drinking in response to the feelings of guilt and depressive symptoms associated with a binge eating episode, or more generally, the negative affect and distress associated with chronic eating, shape, and weight concerns (Puccio et al., 2016). Past research suggests that engaging in coping-related drinking in scenarios like this might exacerbate distress (Armeli et al., 2014; Wycoff et al., 2021), possibly through alcohol-myopia related processes (i.e., crying-in-your-beer effect), thus exacerbating problems commonly associated with drinking (e.g., feeling guilty or bad about oneself after drinking). Future studies should examine how the alcohol use motivated by these distinct motives coincides with the initiation and aftermath of disordered eating behaviors.

An improved understanding of these links could help inform prevention and intervention efforts targeting both eating and alcohol use pathology. In alcohol use interventions for college students, increasing students’ use of protective behavioral strategies has been found to reduce not only alcohol use, but also other risky behaviors (Looby et al., 2019; Pearson, 2013). Regarding drinking motives, there is evidence that providing college students with education and personalized feedback on their drinking motives reduces problematic alcohol use (Blevins & Stephens, 2016). While the extent to which these findings might apply to individuals experiencing both ED and alcohol-related pathology remains an area for further study, the current research offers a potential model to help clinicians organize and understand college students’ symptoms and presenting problems, such as in the cognitive behavioral treatment of co-occurring eating and substance use disorders (Hail et al., 2014). This study also provides additional support for the assessment of drinking motives as part of prevention and treatment programs serving college students. Intervention studies focusing on individuals with these co-occurring issues would clarify whether addressing drinking motives as a maintaining mechanism of problematic drinking might also reduce ED pathology.

This study was also the first to test whether individual differences in drinking motivations act as vulnerability factors that exacerbate the effects of ED pathology. Contrary to predictions, we found no support for our main prediction that individuals high in drinking to cope motivation would show stronger relationships between ED pathology and drinking outcomes. Our only significant interactive effect indicated that high enhancement motivation individuals showed a stronger positive association between ED pathology and drinking-related problems. Given the number of interactions tested and the possibility that this might simply represent a spurious effect, and the fact that this moderating effect was confounded with heavy drinking level, we hesitate to offer an interpretation until replicated. In addition, future studies might also examine whether state-like aspects of affect-regulation drinking motives (i.e., drinking episode-specific levels), rather than the trait-like components that we examined, might moderate the effects of proximal levels of ED symptom severity on drinking-related outcomes.

Finally, we did not replicate Horváth and colleagues’ (2020) gender moderating effects. This might be a result of the relatively lower power of our study to detect small effects. Horváth and colleagues’ (2020) study had over 5000 participants and detected only a small difference in the effects of ED symptoms on internal drinking motives. Other factors such as differences in the developmental period of participants (college students in our study compared to high school students) and the measures used make it difficult to contrast our results. Additional research on gender differences in these processes is needed to better understand these discrepant findings.

One limitation to community samples is the relatively low levels of eating and drinking pathology observed. However, the rates of ED pathology reported by our sample were similar to what has been found in other community samples of college students. We also note that our sample included observations in the clinically relevant range, although they represented a relatively small proportion of the cases. This somewhat restricted level of variability might have attenuated our observed associations. This might be especially relevant for detecting interaction effects which are sensitive to the joint distributions of the variables involved. Future studies that oversample individuals in the clinically significant range are needed to further evaluate the interaction effects of interest.

Several other limitations of the present study merit mention. Our sample was primarily White, college-aged, and from one university, warranting additional research with more diverse ages and sociocultural backgrounds. In addition, our cross-sectional design not only precluded causal inferences about mediation processes, but also limited our interpretation of all the associations. For example, not only might stress elicit ED pathology as specified in our framework, but ED pathology might also generate life stress. Future studies using both intensive and long-term longitudinal designs are needed to better evaluate the temporal unfolding of these processes. Finally, while the measures used in this study improved upon previous methodologies, their reliance on self-report and recall data may have led to inaccuracies and biases in participant reporting. In the case of ED pathology, clinical interviews are preferable to self-report questionnaires; however, there is some evidence that individuals may be more willing to disclose disordered eating behavior when responding in a questionnaire format (Decaluwé & Braet, 2004; Fairburn & Beglin, 1994). These limitations notwithstanding, the present study advances our understanding of the association between ED pathology and problematic drinking by highlighting the possibility of distinct motivational pathways through which these pathologies might be related. Such knowledge could help inform prevention and intervention efforts by tailoring such efforts to these distinct pathways.

Footnotes

Declaration of conflicting interests

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: Funding for this study was provided by NIAAA Grant 5P50-AA027055.

ORCID iDs

Stephen Armeli

Hannah R. Hamilton

Note

Author Biographies

Catherine R. Drury is a PhD Candidate in Clinical Psychology at Fairleigh Dickinson University. Her research interests center around improving eating disorder assessment and treatment for at-risk and underserved populations.

Dr. Stephen Armeli is a Professor in the Department of Psychology at Fairleigh Dickinson University in Teaneck, New Jersey. His research program examines young adult alcohol use and reasons for drinking across the transition from college to post-college years.

Dr. Hannah R. Hamilton is an Assistant Instructional Professor in the Master of Arts Program in the Social Sciences at the University of Chicago whose research explores relations among the need to belong, interpersonal interactions, and health behaviors such as college students' alcohol consumption.

Dr. Katharine L. Loeb is Director of Research and Training at the Chicago Center for Evidence Based Treatment. She has devoted the majority of her career in academia to conducting research on eating and weight disorders in children and adolescents. Dr. Loeb has been inducted as a Fellow in the Academy for Eating Disorders and in the Association for Psychological Science.

Dr. Howard Tennen is a University of Connecticut Board of Trustees Distinguished Professor. His research examines stress, coping and adjustment to threatening encounters, the daily dynamics of chronic pain, stress and alcohol use, and the application of intensive longitudinal methods in clinical trials.

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