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Psychiatric Times

Vol 40, Issue 4
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Co-occurring Substance Use and Eating Disorders

What does existing research say about the connection between substance use disorders and eating disorders?

PORNCHAI SODA_AdobeStock

PORNCHAI SODA_AdobeStock

There have been many studies analyzing co-occurrences between substance use disorders (SUDs) and eating disorders (EDs). The DSM-5 describes different EDs, including anorexia nervosa (AN), bulimia nervosa (BN), and binge-eating disorder (BED).

AN is mainly characterized by a low body weight due to a persistent restriction of food intake, a fear of gaining weight, and a body image distortion.

Two AN subtypes have been proposed: AN-restrictive (AN-R) and AN-binge/purge (AN-BP). BN is characterized by recurrent episodes of binge eating (the consumption, in a discrete period of time, of an objectively large amount food with a sense of loss of control during the episode). The episodes are accompanied by extreme, inappropriate weight-control behaviors such as self-induced vomiting, excessive exercise, misuse of laxatives or diuretics, or extreme dietary restriction.

BED is the most prevalent ED and is characterized by binges (compulsive episodes of excessive consumption of highly palatable foods) and an intense sense of loss of control, without a compensatory purging behavior.1 Binge-eating episodes are usually followed by anxiety, shame, and guilt.1

Co-occurrence

Prevalence estimates of co-occurrences between EDs and SUDs differ across studies.2 Most research has focused on the frequency of SUDs in individuals with EDs.3 For example, in a study with a large clinical sample of patients with EDs (N = 11,588), 10.1% were identified as also having SUDs.4

Some authors have suggested that substance use and SUDs are not limited to a specific ED,2 and that individuals with EDs show higher rates of SUDs than seen in the general population. However, data suggest that SUDs may be particularly common in individuals with binge/purge subtypes of EDs. Moreover, among individuals with EDs, those with co-occurring SUDs have higher mortality.5

Alcohol, tobacco, and caffeine appear to be the most commonly used substances in individuals with EDs.6 However, when exploring SUDs with illicit drugs in individuals with EDs, there are differences in drug preferences among individuals with different EDs. For example, individuals with AN or unspecified ED often show a greater preference for sedatives/hypnotics, whereas individuals with BN often prefer specific illicit substances such as hallucinogens or ecstasy.7

AN and SUDs

Figure. Results From a Recent Systematic Review and Meta-Analysis Examining the Prevalence of Substance Use and SUDs in AN

Figure. Results From a Recent Systematic Review and Meta-Analysis Examining the Prevalence of Substance Use and SUDs in AN

A recent systematic review and meta-analysis examined the prevalence of substance use and SUDs in AN.8 After analyzing 52 studies, a 16% prevalence rate of SUDs in AN was detected, and prevalence was higher in the case of AN-BP as compared with AN-R types. The co-occurring SUDs included alcohol use disorder (AUD; 10%), cannabis use disorder (6%), amphetamine use disorder (5%), cocaine and polysubstance use disorder (3%), narcotic and sedative/hypnotic use disorder (1%), and other substances (4%).

Different explanations for the overlap between AN and SUDs have been proposed. On one hand, it has been postulated that AN behaviors of restriction, binge and purge, and substance use are maladaptive coping mechanism for distress and chaotic inner experiences. Both substance use and AN-related eating behaviors may generate temporary feelings of well-being. On the other hand, it has been suggested that both disorders share risk factors such as high perfectionism, rigidity, and, in the case of AN-BP, high impulsivity.8

BN and SUDs

Co-occurrences between BN and SUDs have been less explored. In one study, 30.1% of women who were in treatment for AUD were diagnosed with an ED. Alcohol may be used by individuals with BN to suppress appetite and, consequently, to maladaptively cope with eating problems. However, efforts to stop using alcohol by individuals with BN (mainly because of calories in alcoholic beverages) may subsequently lead to binge drinking.9

BED and SUDs

Some studies have reported frequent co-occurrences between SUDs and BED.10,11 More specifically, it has been suggested that 23% to 68% of individuals with BED may report SUDs.11-15

A recent systematic review and meta-analysis explored the lifetime prevalence of AUD in individuals with BED.16 Of 18 studies included, the pooled lifetime prevalence was found to be 19.9%. When comparing individuals with BED with those without, the former had a 1.5-fold higher likelihood of having a lifetime AUD. The prevalence of AUD was higher in community samples compared with clinical samples and in those studies in which the proportion of women was lower.

A possible explanation for the co-occurrence between BED and AUD is that both substances (alcohol and food) may activate the reward system, so both disorders may show common neurobiological mechanisms.16 Likewise, both substances may be used as maladaptive coping strategies in response to negative emotional states.16

Some studies have explored co-occurrences between BED and SUDs and familial transmissions. For example, it has been suggested that female relatives of individuals with BED are more likely to report SUDs, regardless of co-occurring disorder in the relatives.17 However, more empirical evidence is required to reach solid conclusions.

Recently, several studies have highlighted overlaps between both disorders. For example, it has been suggested that alterations that individuals with BED show in reward-related responses and brain activation patterns have similarities with those shown by individuals with SUDs.18 Likewise, it has been proposed that craving, high impulsivity, and emotional dysregulation may present in both BEDs and SUDs.19

At a diagnostic level, an overlap between the 2 disorders has also been proposed, taking into account the use of food or substances (eg, bingeing) in greater quantities than intended, use of food/substances despite negative consequences, and the reduction of other pleasurable activities while using substances/bingeing.20

Case Example: Co-occurring AUD and BED

“Mr Rhodes” is a 23-year-old single man with secondary education working as an administrative assistant in a logistics company. Mr Rhodes consulted an addiction care unit because of harmful alcohol consumption that had developed over the course of years. He began using alcohol around the age of 15 years, and this became problematic when he was 19.

A desire to enjoy nights out and to escape from reality were triggers for drinking. Mr Rhodes turned to alcohol not only to connect better with others, become less inhibited, and fit in with others, but also to get away from worries and frustration.

Things were seemingly going well for him, and this was corroborated by both family members and friends. However, Mr Rhodes felt empty and without purpose. In addition, he felt uncomfortable with his body image and was ashamed of his weight and physical shape.

Mr Rhodes reported having started drinking socially and with the intention of having fun. At first, he would have a few drinks until he felt in a better mood, more relaxed, and open to having fun, and he said that he was able to stop drinking after he had had a few drinks. Gradually, however, there was an increase in the frequency of nights out, the amount of alcohol he drank, and the occasions when he woke up in the morning without remembering details of what had happened the night before. However, he was reluctant to admit that he had lost control over his drinking to his family and friends.

Mr Rhodes also reported problems with eating behaviors that started when he was 17 years old, compatible with a diagnosis of BED, for which he was referred to a specialized eating disorders unit for evaluation. He reported regular episodes of overeating (2 to 3 binges per week), without subsequent compensatory behavior and with a feeling of significant loss of control.

The food ingested during binge episodes included predominantly carbohydrates (2000 to 2500 kcal). These episodes were triggered by both internal factors (negative moods) and external factors (environmental situations that acted as triggers for this abnormal eating behavior and, subsequently, difficulties following more healthy diets). Mr Rhodes was obese upon initial presentation (weight, 98 kg; body mass index [BMI], 32.7).

Regarding other conditions, Mr Rhodes had been diagnosed previously with depressive and anxiety disorders and was treated with paroxetine (20 mg/day), alprazolam (0.25 mg/day), and propranolol (20 mg/day). He also met criteria for a tobacco use disorder, smoking 20 to 30 cigarettes each day. He had no other addictive disorders (either substance or behavioral). Per family history, he had a second-degree relative with a gambling disorder and a first-degree relative with an anxiety disorder.

On clinical examination, Mr Rhodes described affective symptoms in part related to his personal situation. He met criteria for an AUD and BED, with the consequences of both disorders being severe and impacting individual, financial, family, and work domains. For the BED, he participated in a group psychological treatment program, with a cognitive-behavioral orientation, of 4 months of weekly outpatient sessions and a follow-up of up to 2 years.

It was also recommended that he continue treatment for his AUD in parallel. The treatment followed included nalmefene 18 mg/day as needed, to be used if he perceived risk of alcohol use, in addition to 12 face-to-face weekly sessions of cognitive-behavioral outpatient therapy.

At discharge, Mr Rhodes was abstinent, with no desire or thoughts of consuming alcohol. He was able to identify risk situations and had alternative strategies to avoid relapse. With regard to his eating behavior, he had significantly reduced the number of binges, normalized his food intake and eating behaviors, and reduced his weight to 88 kg (BMI 29.3). However, he dropped out of treatment after the 6-month follow-up session, and the subsequent evolution of his case is unknown.

Discussion of the Case

SUDs and EDs share multiple clinical and behavioral characteristics and neurobiological correlates.21,22 As described previously, there is strong evidence of co-occurrence among them, especially in patients with bingeing behaviors, with co-occurrence ranging from 40% to 50% and often involving alcohol and cannabis.23,24

Patients with co-occurring disorders typically present with greater clinical severity, more symptomatology, greater general psychopathology, more dysfunctional personality-related features (eg, impulsivity), worse cognitive functioning, and poorer prognosis.23,25,26

The present case is one example of what is described in the current literature, in which an ED involving bingeing co-occurs with an AUD. The fact that this case involves a man is relatively unusual for BED, given that this condition in men is usually less common (9% of individuals with EDs seeking treatment at our program in Spain are men).

As described, dual pathology is usually associated with worse prognosis and more frequent dropping out, and therefore a concurrent multidisciplinary approach is important.

Limitations of the Existing Literature

The main limitation of studies exploring co-occurring SUDs and EDs, as discussed previously,27 is that many groups with different SUDs or EDs are combined in single heterogeneous categories, perhaps erroneously assuming that individuals with different disorders (eg, alcohol vs other substances) constitute a homogeneous clinical population.

Likewise, most studies have focused on populations with EDs, and few have explored the presence of EDs in individuals with SUDs.3 In this regard, most populations studied are predominantly female, so there is a relative lack of studies examining these relationships in men.

Clinical Implications and Future Research

The study of co-occurring EDs and SUDs has suggested that the restrictive behaviors of AN-R and BN-R may be less associated with SUDs.9 Bingeing and purging behaviors of AN-BP, BN-BP, and BED more frequently co-occur with SUDs.9

At a clinical level it is important to evaluate the presence of SUDs, exploring each of the substances independently in every subtype of EDs. Moreover, in line with other authors,3 it is essential to examine the presence of active or remitted EDs in individuals with SUDs, and not only in those who are underweight or overweight.

At a research level, future studies could explore these co-occurrences in larger gender-balanced clinical samples. Future studies could focus specifically on each of the 10 substances proposed by the DSM-5, as well as on individual EDs and their subtypes.

Dr Mestre-Bach is a postdoctoral researcher at Universidad Internacional de La Rioja in Spain. Dr Fernández-Aranda is a full professor at the University of Barcelona in Spain; director of the Eating Disorders Unit at the Bellvitge University Hospital in L’Hospitalet de Llobregat and scientific director of the Biomedical Research Institute of Bellvitge. Dr Jiménez-Murcia is a professor at the University of Barcelona, director of the Behavioral Addictions Unit at the Bellvitge University Hospital, and director of the Psychological Services of the University of Barcelona.

Dr Potenza is a professor of psychiatry in the Child Study Center and of neuroscience, director of the Division of Addictions Research, director of the Center of Excellence in Gambling Research, and director of the Yale Program for Research on Impulsivity and Impulse Control Disorders at Yale School of Medicine in New Haven, Connecticut.

References

1. Hutson PH, Balodis IM, Potenza MN. Binge-eating disorder: clinical and therapeutic advances. Pharmacol Ther. 2018;182:15-27.

2. Root TL, Pisetsky EM, Thornton L, et al. Patterns of co-morbidity of eating disorders and substance use in Swedish females. Psychol Med. 2010;40(1):105-115.

3. Courbasson CMA, Smith PD, Cleland PA. Substance use disorders, anorexia, bulimia, and concurrent disorders. Can J Public Heal. 2005;96(2).

4. Ulfvebrand S, Birgegård A, Norring C, et al. Psychiatric comorbidity in women and men with eating disorders results from a large clinical database. Psychiatry Res. 2015;230(2):294-299.

5. Mellentin AI, Mejldal A, Guala MM, et al. The impact of alcohol and other substance use disorders on mortality in patients with eating disorders: a nationwide register-based retrospective cohort study. Am J Psychiatry. 2022;179(1):46-57.

6. Hambleton A, Pepin G, Le A, et al. Psychiatric and medical comorbidities of eating disorders: findings from a rapid review of the literature. J Eat Disord. 2022;10(1):132.

7. Skøt L, Mejldal A, Guala MM, et al. Eating disorders and subsequent risk of substance use disorders involving illicit drugs: a Danish nationwide register-based cohort study. Soc Psychiatry Psychiatr Epidemiol. 2022;57(4):695-708.

8. Devoe DJ, Dimitropoulos G, Anderson A, et al. The prevalence of substance use disorders and substance use in anorexia nervosa: a systematic review and meta-analysis. J Eat Disord. 2021;9(1):161.

9. Eskander N, Chakrapani S, Ghani MR. The risk of substance use among adolescents and adults with eating disorders. Cureus. 2020;12(9):e10309.

10. Munn-Chernoff MA, Baker JH. A primer on the genetics of comorbid eating disorders and substance use disorders. Eur Eat Disord Rev. 2016;24(2):91-100.

11. Hudson JI, Hiripi E, Pope HG Jr, Kessler RC. The prevalence and correlates of eating disorders in the National Comorbidity Survey replication. Biol Psychiatry. 2007;61(3):348-358.

12. Citrome L. Binge-eating disorder and comorbid conditions: differential diagnosis and implications for treatment. J Clin Psychiatry. 2017;78(suppl 1):9-13.

13. Udo T, Grilo CM. Prevalence and correlates of DSM-5–defined eating disorders in a nationally representative sample of U.S. adults. Biol Psychiatry. 2018;84(5):345-354.

14. Keski-Rahkonen A. Epidemiology of binge eating disorder: prevalence, course, comorbidity, and risk factors. Curr Opin Psychiatry. 2021;34(6):525-531.

15. Grilo CM, White MA, Masheb RM. DSM-IV psychiatric disorder comorbidity and its correlates in binge eating disorder. Int J Eat Disord. 2009;42(3):228-234.

16. Bogusz K, Kopera M, Jakubczyk A, et al. Prevalence of alcohol use disorder among individuals who binge eat: a systematic review and meta-analysis. Addiction. 2021;116(1):18-31.

17. Lilenfeld LRR, Ringham R, Kalarchian MA, Marcus MD. A family history study of binge-eating disorder. Compr Psychiatry. 2008;49(3):247-254.

18. Kessler RM, Hutson PH, Herman BK, Potenza MN. The neurobiological basis of binge-eating disorder. Neurosci Biobehav Rev. 2016;63:223-238.

19. Schulte EM, Grilo CM, Gearhardt AN. Shared and unique mechanisms underlying binge eating disorder and addictive disorders. Clin Psychol Rev. 2016;44:125-139.

20. Schreiber LRN, Odlaug BL, Grant JE. The overlap between binge eating disorder and substance use disorders: diagnosis and neurobiology. J Behav Addict. 2013;2(4):191-198.

21. Munn‐Chernoff MA, Johnson EC, Chou YL, et al. Shared genetic risk between eating disorder‐ and substance‐use‐related phenotypes: evidence from genome‐wide association studies. Addict Biol. 2021;26(1):e12880.

22. Mallorquí-Bagué N, Fagundo AB, Jimenez-Murcia S, et al. Decision making impairment: a shared vulnerability in obesity, gambling disorder and substance use disorders? PLoS One. 2016;11(9):e0163901.

23. Krug I, Treasure J, Anderluh M, et al. Present and lifetime comorbidity of tobacco, alcohol and drug use in eating disorders: a European multicenter study. Drug Alcohol Depend. 2008;97(1-2):169-179.

24. Miranda-Olivos R, Agüera Z, Granero R, et al. Food addiction and lifetime alcohol and illicit drugs use in specific eating disorders. J Behav Addict. 2022;11(1):102-115.

25. Lozano-Madrid M, Clark Bryan D, Granero R, et al. Impulsivity, emotional dysregulation and executive function deficits could be associated with alcohol and drug abuse in eating disorders. J Clin Med. 2020;9(6):1936.

26. Del Pino-Gutiérrez A, Jiménez-Murcia S, Fernández-Aranda F, et al. The relevance of personality traits in impulsivity-related disorders: from substance use disorders and gambling disorder to bulimia nervosa. J Behav Addict. 2017;6(3):396-405.

27. Dunn EC, Neighbors C, Fossos N, Larimer ME. A cross-lagged evaluation of eating disorder symptomatology and substance-use problems. J Stud Alcohol Drugs. 2009;70(1):106-116.

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