literature review on stress disorder

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Peer-reviewed

Research Article

Post-traumatic stress disorder and associated factors among internally displaced persons in Africa: A systematic review and meta-analysis

Roles Conceptualization, Data curation, Formal analysis, Investigation, Methodology, Software, Validation, Visualization, Writing – original draft, Writing – review & editing

* E-mail: [email protected]

Affiliation Department of Environmental and Occupational Health and Safety, Institute of Public Health, College of Medicine and Health Sciences, University of Gondar, Gondar, Ethiopia

Roles Formal analysis, Investigation, Methodology, Validation, Visualization, Writing – original draft

Affiliation Department of Clinical Pharmacy, School of Pharmacy, College of Medicine and Health Sciences, University of Gondar, Gondar, Ethiopia

Roles Methodology, Visualization, Writing – review & editing

Roles Methodology, Supervision, Visualization, Writing – review & editing

Roles Data curation, Investigation, Visualization, Writing – review & editing

Affiliation Department of Nursing, College of Medicine and Health Sciences, Jigjiga University, Jigjiga, Ethiopia

Roles Data curation, Methodology, Supervision, Visualization, Writing – review & editing

Affiliation Department of Environmental Health, College of Medicine and Health Sciences, Wollo University, Dessie, Ethiopia

Roles Data curation, Methodology, Validation, Visualization, Writing – review & editing

Affiliation Department of Immunology and Molecular Biology, School of Biomedical and Laboratory Sciences, College of Medicine and Health Science, University of Gondar, Gondar, Ethiopia

Roles Data curation, Formal analysis, Investigation, Methodology, Writing – review & editing

Affiliation Department of Epidemiology and Biostatistics, Institute of Public Health, College of Medicine and Health Sciences, University of Gondar, Gondar, Ethiopia

Roles Data curation, Investigation, Methodology, Supervision, Validation, Visualization, Writing – review & editing

• Amensisa Hailu Tesfaye, 
• Ashenafi Kibret Sendekie, 
• Gebisa Guyasa Kabito, 
• Garedew Tadege Engdaw, 
• Girum Shibeshi Argaw, 
• Belay Desye, 
• Abiy Ayele Angelo, 
• Fantu Mamo Aragaw, 
• Giziew Abere

• Published: April 1, 2024
• https://doi.org/10.1371/journal.pone.0300894
• Peer Review
• Reader Comments

Internally displaced people (IDPs), uprooted by conflict, violence, or disaster, struggle with the trauma of violence, loss, and displacement, making them significantly more vulnerable to post-traumatic stress disorder (PTSD). Therefore, we conducted a systematic review and meta-analysis to assess the prevalence and associated factors of PTSD among IDPs in Africa.

A comprehensive search of electronic databases was conducted to identify relevant studies published between 2008 and 2023. The search included electronic databases such as PubMed, CABI, EMBASE, SCOPUS, CINHAL, and AJOL, as well as other search sources. The Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines were followed. Data were extracted using Microsoft Excel, and analysis was performed using STATA 17 software. The quality of the included studies was assessed using the JBI quality appraisal tool. A random-effects model was used to estimate the pooled prevalence of PTSD and its associated factors. The funnel plot and Egger’s regression test were used to assess publication bias, and I 2 test statistics was used to assess heterogeneity. The protocol for this review has been registered with PROSPERO (ID: CRD42023428027).

A total of 14 studies with a total of 7,590 participants met the inclusion criteria. The pooled prevalence of PTSD among IDPs in Africa was 51% (95% CI: 38.-64). Female gender (OR = 1.99, 95% CI: 1.65–2.32), no longer married (OR = 1.93, 95% CI: 1.43–2.43), unemployment (OR = 1.92, 95% CI: 1.17–2.67), being injured (OR = 1.94, 95% CI: 1.50–1.50), number of traumatic events experienced [4-7(OR = 2.09, 95% CI: 1.16–3.01), 8–11 (OR = 2.09, 95% CI: 2.18–4.12), 12–16 (OR = 5.37, 95% CI: 2.61–8.12)], illness without medical care (OR = 1.92, 95% CI: 1.41–2.29), being depressed (OR = 2.97, 95% CI: 2.07–3.86), and frequency of displacement more than once (OR = 2.13, 95% CI: 1.41–2.85) were significantly associated with an increased risk of PTSD.

Conclusions

The findings of this systematic review and meta-analysis highlight the alarming prevalence of PTSD among IDPs in Africa. Female gender, marital status, number of traumatic events, ill health without medical care, depression, and frequency of displacement were identified as significant risk factors for PTSD. Effective interventions and the development of tailored mental health programs are needed to prevent PTSD among IDPs, focusing on the identified risk factors.

Citation: Tesfaye AH, Sendekie AK, Kabito GG, Engdaw GT, Argaw GS, Desye B, et al. (2024) Post-traumatic stress disorder and associated factors among internally displaced persons in Africa: A systematic review and meta-analysis. PLoS ONE 19(4): e0300894. https://doi.org/10.1371/journal.pone.0300894

Editor: Roberto Ariel Abeldaño Zuñiga, University of Helsinki, FINLAND

Received: December 6, 2023; Accepted: March 5, 2024; Published: April 1, 2024

Copyright: © 2024 Tesfaye et al. This is an open access article distributed under the terms of the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Data Availability: All relevant data are within the manuscript and its Supporting information files ( S3 File ).

Funding: The author(s) received no specific funding for this work.

Competing interests: The authors have declared that no competing interests exist.

Introduction

Internally displaced persons (IDPs) are individuals forced to flee their homes due to conflict, natural disasters, or other man-made or natural events [ 1 ]. These individuals face numerous challenges, including physical and psychological trauma, witnessing violence, loss of livelihoods, and separation from family and friends [ 2 , 3 ]. These challenges can contribute to the development of post-traumatic stress disorder (PTSD), a common mental health condition characterized by flashbacks, nightmares, hypervigilance, avoidance, and emotional numbness [ 4 – 6 ].

PTSD can have a profound and debilitating impact on the lives of IDPs, posing significant challenges to their recovery and reintegration into society [ 3 ]. The impact of PTSD on IDPs extends beyond the individual, affecting their families and communities as well. The emotional turmoil and behavioral changes associated with PTSD can strain relationships within families, leading to conflict, neglect, and further emotional distress [ 1 , 7 ]. PTSD can also lead to secondary problems such as substance abuse, self-harm, and suicide [ 8 , 9 ]. Moreover, the inability of IDPs with PTSD to contribute fully to their communities can hinder collective recovery efforts and exacerbate existing social and economic vulnerabilities [ 1 , 7 , 10 ]. The impact could have been highly significant in Africa because of several factors, including insufficient mental health services, the stigma associated with mental health problems, and the logistical challenges of providing mental health services to IDPs who are often living in remote areas [ 11 – 13 ].

Globally, more than 71 million people are internally displaced as of the end of 2022 across 120 countries because of conflict, violence, and disasters. This number shows an increase of 20% from the previous year [ 14 ]. Human and natural disasters that could potentially cause IDPs have been prominently reported in sub-Saharan Africa [ 15 ]. In 2020, Africa accounted for almost 40% of all new internal displacements globally, with natural disasters being the primary cause of displacement in 32 out of 54 African countries [ 16 ]. According to the United Nations Human Rights Commission (UNHCR), 42% of all IDP people globally have lived in Africa [ 17 ].

The prevalence of PTSD among IDPs varies widely, ranging from 3% to 88% depending on the specific country and population studied [ 18 , 19 ]. The prevalence of PTSD in East Africa ranges from 11% to 80.2% [ 20 – 22 ]. Similarly, a meta-analysis study conducted in sub-Saharan African countries reveals that the magnitude of PTSD ranges from 12.3% in Central Sudan to 85.5% in Nigeria, and the majority of them reported to have more than 50% of the magnitude of PTSD [ 23 ]. This suggests that PTSD is a significant public health problem among IDPs in Africa.

Several factors have been identified as being associated with an increased risk of PTSD among IDPs. These factors include: female gender, young age, trauma, experiencing or witnessing violence, depression, anxiety, stress, low level of educational status, lack of social support, and economic hardship [ 20 , 23 , 24 ]. Beyond the previously mentioned factors, a number of other factors may also increase the likelihood of PTSD in IDPs in Africa. These factors include political instability and ongoing conflict, which can prolong the trauma and displacement cycle and make it more challenging for IDPs to find stability and security. This ongoing exposure to stress and uncertainty can exacerbate PTSD symptoms and hinder recovery efforts. Poverty and food insecurity are also common among IDPs in Africa, creating additional stressors and challenges. These socio-economic factors can contribute to feelings of hopelessness, despair, and a sense of being trapped in a difficult situation, further exacerbating PTSD among these vulnerable groups [ 25 – 28 ].

Despite the high prevalence of PTSD among IDPs in different African countries, there is a lack of comprehensive studies that show the pooled impact of PTSD and the nature of risk factors. Thus, a comprehensive study that can address the overall public health impact of internal displacement in terms of causing PTSD could be important to provide mental health services for IDPs. Therefore, the purpose of this systematic review and meta-analysis is to synthesize existing evidence on the prevalence of PTSD and its associated factors among IDPs in Africa. This information will be used to inform the development of interventions to prevent and treat PTSD among IDPs in Africa.

Methods and materials

Study setting.

The study provides a comprehensive synthesis of existing research on PTSD prevalence rates and examines risk factors contributing to the development of PTSD among IDPs in African countries. According to the African Development Bank, there are 54 countries in Africa today [ 29 ].

Protocol and registration

The protocol for this review was registered in the International Prospective Register of Systematic Reviews (PROSPERO), the University of York Centre for Reviews and Dissemination (Record ID: CRD42023428027, May 31 st , 2023).

Data sources and search strategy

This review and meta-analysis were conducted according to the guidelines of Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). The three phases drawn from the PRISMA flowchart were documented in the results to show the study selection process from identification to the included studies [ 30 ]. The PRISMA checklist was also used in the reporting of the systematic review and meta-analysis ( S1 File ).

We extensively searched articles on PubMed/MEDLINE, CABI, EMBASE, SCOPUS, CINHAL, and African Journal Online (AJOL) up to June 11, 2023. According to the African Development Bank, there are 54 countries in Africa [ 29 ]. The search terms were selected to capture relevant articles on PTSD and IDPs in African countries. The search was conducted using a combination of keywords and controlled vocabulary (MeSH terms). The search strategy was adapted for each database as per their specific syntax and indexing terms. For the PubMed search, the following key terms were used in combination with the Boolean operators "AND" and "OR". ("Post-traumatic stress disorder" [All Fields] OR "Posttraumatic stress disorder" [All Fields] OR "PTSD" [All Fields]) AND ("Internally displaced persons" [All Fields] OR "Internally displaced people"[All Fields] OR "Internally displaced individuals" [All Fields] OR "IDP" [All Fields]) AND ("Associated factors" [All Fields] OR "Determinant factors" [All Fields] OR "Risk factors" [All Fields]) AND "Africa" [All Fields].

In addition to these electronic database searches, we searched the grey literature using website searches such as BioMed Central and National Institute of Mental Health, Behavioral and Brain Sciences—Cambridge University Press, etc., Google Search, and Google Scholar. We also searched the reference lists (bibliographies) of the included studies for additional relevant studies.

Eligibility criteria

Inclusion criteria..

Articles that met the following criteria were considered for inclusion in this systematic review and meta-analysis.

• Population: internally displaced persons (IDPs).
• Outcomes: articles reported the quantitative outcome of the prevalence of PTSD and associated factors among IDPs in Africa.
• Study design: a cross-sectional study.
• Study setting: studies conducted in African countries.
• Publication issue: peer-reviewed journal articles published before 11 June 2023.

Exclusion criteria.

Systematic reviews, qualitative studies, letters to editors, short communications, and commentaries were excluded. In addition, articles that were not fully accessible after three personal email contacts with the corresponding author and articles that did not indicate the outcome interest of this study were all excluded.

Study selection process

The Endnote X9.2 (Thomson Reuters, Philadelphia, PA, USA) software reference manager was used to collect and organize search results and to remove duplicate articles. Three investigators (AHT, FMA, and GA) independently screened articles by their title, abstract, and full text to identify eligible articles using predetermined inclusion and exclusion criteria. The screened articles were then compiled together by three investigators (AHT, GSA, and AKS), and the disagreement between authors that arises during data abstraction and selection is solved based on evidence-based discussion and the involvement of other investigators (AKS, GTE, and AAA).

Data extraction and management

Data were extracted using the Joanna Briggs Institute (JBI) data extraction checklist. Four review authors (AHT, FMA, GGK, and BD) extracted the data independently using a Microsoft Excel spreadsheet. The data extraction format included (name of first author, publication year, study country, study design, sample size, response rate, prevalence of PTSD, total number of participants, factors associated with PTSD with their respective OR with 95% CI, and risk of bias). Disagreements between the review authors were resolved by a review by the other review authors based on an evidence-based discussion.

Quality assessment of the studies

The quality of the included articles was assessed using the Joanna Briggs Institute (JBI) quality appraisal tools for analytical cross-sectional studies [ 31 ]. Three investigators (AHT, AKS, and GA) independently assessed the quality of the included articles. The assessment tool contains eight criteria: (1) clear inclusion and exclusion criteria; (2) description of the study subject and study setting; (3) use of a valid and reliable method to measure the exposure; (4) standard criteria used for measurement of the condition; (5) identification of confounding factors; (6) development of strategies to deal with confounding factors; (7) use of a valid and reliable method to measure the outcomes; and (8) use of appropriate statistical analysis. The risks for biases were classified as low (total score, 6 to 8), moderate (total score, 3 or 5), or high (total score, 0 to 2) ( S2 File ). Finally, articles with low and moderate biases were considered in this review. Disagreements that arose during the full-text quality assessment were resolved through evidence-based discussion with the involvement of other review authors (GGK, GA, and BD).

Outcome of interest

The primary outcome of this review was the pooled prevalence of post-traumatic stress disorder (PTSD). It was reported as a percentage (%). The second outcome of this review was the pooled measure of the association between PTSD and associated factors among IDPs in Africa. It was determined using the pooled odds ratio (OR) with a 95% confidence interval.

Statistical methods and data analysis

The extracted data were exported from a Microsoft Excel spreadsheet to STATA version 17 for further analysis. Heterogeneity among the included studies was quantitatively measured by the index of heterogeneity (I 2 statistics), in which 25%-51%, 50%-75%, and>75% represented low, moderate, and high heterogeneity, respectively [ 32 ]. The overall pooled estimate of PTSD among IDPs in Africa was computed using the metaprop STATA command. A subgroup analysis was conducted by a study country to see the difference in the pooled prevalence of PTSD between countries. The influence of a single study on the overall pooled estimate was assessed using a sensitivity analysis. Furthermore, the small-study effect was evaluated using the funnel plot test and Egger’s regression test, with a p-value <0.05 as a cutoff point to declare the presence of publication bias. A p-value <0.05 was used to declare factors associated with PTSD to be statistically significant with a pooled odds ratio (OR) at the 95% confidence level. The results were presented using graphs, tables, text, and a forest plot.

Searching process

A total of 4622 articles were identified using electronic databases and manual searching. After removing duplicate records, 3427 records were screened for this review. Based on their titles and abstracts, 3351 articles were excluded. In addition, 62 articles were excluded based on the exclusion criteria. Finally, a total of 14 articles were included in this review. The PRISMA flow diagram was used to summarize the selection process ( Fig 1 ).

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https://doi.org/10.1371/journal.pone.0300894.g001

Characteristics of the included studies

In this review, the publication year, country of study, study design, sample size, and prevalence of PTSD are summarized in Table 1 . By design, all included studies were cross-sectional. This study included a total of 7,590 participants [ 2 , 10 , 20 , 21 , 24 , 26 , 33 – 40 ]. The included articles were published between 2008–2023. The included study sample sizes ranged from 93 to 1291. In this review, a study conducted in Sudan, South Darfur, at the Darfur Campaign study site, showed the lowest prevalence of PTSD (14.9%) [ 35 ], while a study conducted in IDP camps in Yobe State in northeastern Nigeria showed the highest prevalence of PTSD (94.2%) [ 2 ]. Three studies were from Ethiopia [ 20 , 26 , 33 ]; five studies were from Nigeria [ 2 , 24 , 38 – 40 ] and the remaining studies were from Kenya [ 34 ], Somalia [ 10 ], Sudan [ 35 ], South Sudan [ 36 ], Uganda [ 21 ] and the Democratic Republic of Congo (DRC) [ 37 ]. The included studies were categorized as having a low risk of bias (quality score 6 to 8). The description of the included studies is presented in Table 1 .

https://doi.org/10.1371/journal.pone.0300894.t001

Assessment methods of PTSD.

This research review included studies with varying screening methods for PTSD. While standardized questionnaires were common, most lacked clinical confirmation, raising potential concerns about the accuracy of PTSD diagnoses. However, some studies employed both questionnaires and clinical confirmation, offering a more robust approach to assessing PTSD. Details of these assessment methods used in the original studies are summarized in Table 2 .

https://doi.org/10.1371/journal.pone.0300894.t002

Meta-analysis

Pooled prevalence of ptsd among idps in africa.

The pooled prevalence estimate of PTSD was found to be 51% (95% CI: 38–64; I 2 = 99.38%). In this analysis, the lowest prevalence of PTSD was found in Sudan at 15% (95% CI: 9–25) [ 35 ] and the highest prevalence of PTSD was found in Nigeria at 94% (95% CI: 92–96) [ 2 ]. A forest plot shows the prevalence estimates of PTSD among IDPs in Africa ( Fig 2 ).

https://doi.org/10.1371/journal.pone.0300894.g002

Subgroup analysis

Subgroup analysis was done to see the pooled prevalence of PTSD by country. According to the result, of in-country subgroup analysis, the pooled prevalence of PTSD was 62% (95% CI: 41–82) in Nigeria and 54% (95% CI: 36–72) in Ethiopia. Subgroup analysis of the study showed that the highest and lowest prevalence of PTSD was in Nigeria, 62% (95% CI: 41–82), and Sudan, 15% (95% CI: 9–25), respectively ( Fig 3 ). A subgroup analysis was also performed with clinically confirmed cases of PTSD and positive screening cases of PTSD as different subgroups. Accordingly, the pooled prevalence of clinically confirmed cases of PTSD was 31% (95% CI: 15–46) and positive screening cases of PTSD was 55% (95% CI: 44–65) (Figs 4 & 5 ).

https://doi.org/10.1371/journal.pone.0300894.g003

https://doi.org/10.1371/journal.pone.0300894.g004

https://doi.org/10.1371/journal.pone.0300894.g005

Heterogeneity and publication bias

The presence of heterogeneity and publication bias (small study effect) was assessed within the included studies. The included studies had a high degree of heterogeneity (I 2 = 99.38%, p = 0.00). Publication bias was assessed using a funnel plot and Egger’s regression test at a p-value <0.05. The funnel plot showed that the distribution of studies was asymmetrical, whereas Egger’s test was found to be not statistically significant for the estimated prevalence of PTSD (p = 0.063), meaning that there was no evidence of publication bias ( Fig 6 ).

https://doi.org/10.1371/journal.pone.0300894.g006

Sensitivity analysis test

A sensitivity analysis was performed to assess the effect of each study on the pooled estimate of PTSD. However, the results of the sensitivity analysis showed that there was no single study effect on the pooled prevalence of PTSD in the fitted meta-analytic model, as shown in Fig 7 .

https://doi.org/10.1371/journal.pone.0300894.g007

Factors associated with PTSD among IDPs in Africa.

Factors associated with PTSD were identified based on the pooled effect of two or more studies. In this meta-analysis, factors associated with PTSD were assessed using 14 studies [ 2 , 10 , 20 , 21 , 24 , 26 , 33 – 40 ]. The analysis showed that in 4 of these studies [ 20 , 21 , 33 , 36 ], female IDPs were found to have a twofold higher risk of developing PTSD compared to male IDPs (OR = 1.99, 95% CI: 1.65–2.32). The pooled results of three studies [ 21 , 33 , 36 ] revealed that individuals who were no longer married (divorced, separated, widowed, or forcefully separated) had 1.93 times higher likelihood of PTSD compared to those who were married or single (OR = 1.93, 95% CI: 1.43–2.43). Similarly, the pooled findings of two studies [ 10 , 26 ] showed that the likelihood of PTSD was 1.92 times higher for unemployed IDPs compared to employed IDPs (OR = 1.92, 95% CI: 1.17–2.67). Furthermore, two studies’ combined results [ 33 , 36 ] revealed that the likelihood of PTSD was 1.94 times higher for injured IDPs than for uninjured ones (OR = 1.94, 95% CI: 1.50–2.37).

Moreover, the pooled results of two studies [ 20 , 21 ] of this meta-analysis revealed a positive correlation between the likelihood of developing PTSD and the commutative number of traumatic incidents encountered. The odds of PTSD were higher in IDPs who had experienced four or more of the sixteen traumatic events (OR = 2.09, 95% CI: 1.16–3.01), 3.15 times higher in those who had experienced eight to eleven traumatic events (OR = 2.09, 95% CI: 2.18–4.12), and 5.37 times higher in those who had experienced twelve or more traumatic events (OR = 5.37, 95% CI: 2.61–8.12) compared to those who had experienced zero to three traumatic events. The combined findings of two studies [ 21 , 36 ] revealed that the odds of having PTSD were 1.92 times higher for IDPs with poor health who did not receive medical care than for those who did receive medical care (OR = 1.92, 95% CI: 1.41–2.29). Furthermore, the pooled result from four studies [ 2 , 20 , 24 , 26 ] revealed that people with depression had a 2.97-fold increased risk of developing PTSD compared to people without depression (OR = 2.97, 95% CI: 2.07–3.86). Additionally, the current analysis discovered a substantial correlation between PTSD and a higher frequency of displacement. The meta-analysis’s combined findings showed that those who were internally relocated more than once had a 2.13-fold increased risk of developing PTSD ( Table 3 ).

https://doi.org/10.1371/journal.pone.0300894.t003

Internally displaced persons (IDPs) are particularly vulnerable to PTSD because they have often experienced traumatic events such as violence, loss of loved ones, and destruction of their homes [ 41 , 42 ]. They may also have difficulty accessing mental health care, which can make it harder to recover from PTSD. Investigating the overall impact and risk factors might be important to the development of interventions to prevent and treat PTSD among IDPs in Africa. The current review presents comprehensive findings on the pooled magnitude of PTSD and its associated factors among IDPs in Africa.

This systematic review and meta-analysis found that the pooled prevalence of PTSD among IDPs in Africa was 51% (95% CI: 38–64%). The prevalence of PTSD in this review was aligned with the studies carried out in the Kurdistan region of Iraq (60%) [ 43 ], and Sri Lanka (56%) [ 44 ]. Moreover, this finding is in concordance with a systematic review and meta-analysis study in Syria which reported a pooled estimate of 36% PTSD [ 45 ]. On the other hand, the prevalence of PTSD in this review was lower than that of the study done in Medellin, Colombia (88%) [ 46 ]. There are several possible explanations for these disparities. One possibility could be a difference in methodological approaches. Another possibility is that the studies were conducted with different populations in different cultural and social contexts to manage problems related to displacements [ 47 ]. Antithetically, the estimated prevalence of PTSD in the current review was higher than the studies carried out in another study in Sri Lanka (2.3%) [ 48 ], Georgia (23.3%) [ 49 ], Iraq (20.8%) [ 50 ], and India (9%) [ 51 ]. Furthermore, the prevalence of PTSD in the current study is higher than in a systematic review and meta-analysis of an epidemiological study done by Nexhmedin M. et al which reported a 26% pooled prevalence of PTSD among survivors living in war-afflicted regions [ 52 ].

The subgroup meta-analysis of this review showed that the pooled prevalence of clinically confirmed cases of PTSD was 31% (95% CI: 15–46) and positive screening cases of PTSD was 55% (95% CI: 44–65). One possible explanation for the higher prevalence rate among positive screening cases (55%) compared to clinically confirmed cases (31%) could be related to the sensitivity of the screening tool used. Screening tools are designed to identify individuals who may be at risk or likely to have the condition, but they may also capture individuals with false positives those who screen positive but may not meet the diagnostic criteria upon further clinical assessment. These false positives could inflate the prevalence rate among positive screening cases. On the other hand, clinically confirmed cases undergo a more comprehensive diagnostic evaluation, which includes clinical interviews, symptom assessment, and adherence to specific diagnostic criteria. This process is typically conducted by trained professionals such as qualified mental health professional and aims to ensure a more accurate diagnosis of PTSD. By applying stricter criteria, the diagnostic process may exclude individuals who had initially screened positive but do not meet the clinical diagnostic threshold. Consequently, the prevalence rate among clinically confirmed cases may be lower compared to positive screening cases [ 53 – 55 ].

Several factors may also contribute to the differences. The first possible reason could be due to the impact of conflict, mass displacement, and the level of property destruction repeatedly encountered in the African region where this review was conducted. This may include a combination of war and political and ethnic conflict [ 22 ]. In addition, this difference may be related to the differences in the accessibility and affordability of mental health care services in those different settings [ 23 ]. Furthermore, it is also possible that the studies were conducted at different times, and that the prevalence of PTSD has changed over time.

A meta-analysis of this review found that females were at higher risk of PTSD than men. Several factors could contribute to the higher prevalence of PTSD among females compared to males. Numerous studies across different countries have documented the higher prevalence of PTSD among females compared to males [ 13 , 23 , 56 – 60 ]. These factors can broadly be related to biological, psychological, and social factors. Hormonal differences between females and males that estrogen may enhance emotional reactivity and memory consolidation, potentially increasing the risk of PTSD [ 61 ]. Social factors could also contribute to increased PTSD in females because females are more likely to experience interpersonal trauma, such as sexual assault or domestic violence compared with males [ 23 , 62 , 63 ], which are associated with a higher risk of PTSD compared to other types of traumas. Gender roles and expectations of females may also emphasize emotional expressiveness and vulnerability, which could make them more susceptible to developing PTSD symptoms. Furthermore, psychological factors like coping strategies and social support might be among the factors contributing to the occurrence of PTSD among female IDPs. Females may be more likely to use emotion-focused coping strategies, such as rumination and suppression, which may exacerbate PTSD symptoms. Males, on the other hand, may favor problem-focused coping, which may be more effective at managing stress. In addition, females often have stronger social networks, which can provide emotional support and buffer against stress. However, these networks may also expose females to more trauma-related discussions, potentially increasing the risk of PTSD. Therefore, understanding these factors is crucial for developing effective prevention and treatment strategies for PTSD in this population. This finding may also suggest that it could be important to give more attention to females to provide psychological and general support to minimize the impact on their daily lives.

In this review, being divorced, separated, and widowed was found to be more associated with PTSD compared with being married and/or single. The finding is also consistent with previous studies [ 23 , 64 ]. Marital status can influence an individual’s vulnerability to PTSD in several ways: social support and emotional buffer, joint problem-solving and resource sharing, and sociocultural factors that marriage can provide a strong source of social support and emotional buffering, which can help individuals cope with stress and trauma. These findings suggest that marital status can play a significant role in influencing the risk of PTSD among IDPs. The supportive and protective aspects of marriage can help individuals cope with the challenges of displacement and trauma, reducing their vulnerability to PTSD. However, it is important to note that the relationship between marital status and PTSD may not always be straightforward. In some cases, some studies showed that marital strain or conflict can increase the risk of PTSD among married individuals [ 65 , 66 ]. Therefore, the impact of marital status on PTSD may vary depending on individual circumstances, cultural factors, and the specific nature of the traumatic event.

Consistent with earlier findings [ 10 ], employment status was also found to have a significant association with PTSD among IDPs. Several factors contribute to this association: loss of routine and structure that unemployment disrupts an individual’s daily routine and structure, which can be particularly destabilizing for IDPs who have already experienced the upheaval of displacement; financial strain, and economic hardship, adding to the stress and anxiety of displacement; limited access to mental health care that can hinder an individual’s ability to access mental health care, either due to financial constraints or the lack of employer-sponsored health insurance. These findings underscore the importance of employment in promoting mental health and well-being among IDPs. Supporting employment opportunities and providing vocational training can help IDPs regain a sense of normalcy, purpose, and control, reducing their risk of developing PTSD and improving their overall quality of life.

This review revealed that being injured is significantly associated with the existence of PTSD among IDPs, which is in line with other studies [ 23 , 42 , 67 ]. Experiencing physical injury during displacement can significantly increase an individual’s risk of developing PTSD because of direct trauma and physical pain, psychological impact of injury, impact on daily living and functioning, limited access to healthcare and support, trauma reactivation, and reminders of injury. These findings highlight the importance of addressing physical injuries and providing comprehensive support services for IDPs to mitigate the risk of developing PTSD. Timely and effective medical care, rehabilitation services, and psychological support can significantly improve the physical and mental health outcomes of IDPs who have experienced injuries.

The current finding has shown, consistent with earlier evidence [ 23 , 45 , 68 , 69 ], that the number of trauma events experienced was positively associated with the risk of PTSD. There is a well-established relationship between the number of trauma events experienced and the risk of PTSD among IDPs. Research suggests that each additional trauma event increases the likelihood of developing PTSD. This association can be attributed to several factors, such as accumulation of stress and emotional overload. Each trauma event exposes an individual to significant stress and emotional overload, taxing their coping mechanisms and increasing their vulnerability to developing PTSD. The cumulative effect of multiple trauma events can overwhelm an individual’s ability to process and integrate these experiences, leading to the development of PTSD symptoms. In addition, repeated exposure to traumatic events can heighten an individual’s sensitivity to trauma cues, making them more likely to experience flashbacks, nightmares, and intrusive thoughts related to the traumatic experiences. This sensitization can maintain the state of hypervigilance and emotional arousal characteristic of PTSD. These findings may underscore the importance of preventing and addressing trauma exposure among IDPs to reduce the risk of developing PTSD. Providing early intervention and mental health support services can help IDPs cope with the effects of trauma and prevent the development of PTSD.

Illness in the absence of medical care was found to be significantly associated with the presence of PTSD among IDPs and this is in line with other findings [ 21 ]. The absence of medical care significantly elevates the risk of developing PTSD among IDPs. This association stems from several interconnected factors including unmet physical and psychological needs. Lack of access to medical care can lead to the neglect of both physical and psychological needs following a traumatic event. These findings highlight the importance of providing comprehensive healthcare services to IDPs, including both physical and mental healthcare. Addressing their medical needs can significantly reduce the risk of developing PTSD and promote their overall well-being.

In the current review, the presence of depression is found to have a significant association with PTSD among IDPs, which is in line with earlier studies [ 10 , 21 , 23 ]. The co-occurrence of depression and post-traumatic stress disorder (PTSD) is prevalent among internally displaced persons (IDPs). This could be because of shared etiological factors that both depression and PTSD share common risk factors, such as exposure to trauma, genetic predisposition, and neurobiological alterations. Both depression and PTSD involve dysregulation of stress hormones, such as cortisol and norepinephrine. These hormonal imbalances can contribute to the development and maintenance of both conditions. In addition, IDPs face a range of social and environmental stressors, such as displacement, loss of social support, and economic hardship. These stressors can contribute to both depression and PTSD by exacerbating emotional distress and reducing resilience. These findings implicate the importance of addressing both depression and PTSD simultaneously in IDPs. Integrated treatment approaches that target both conditions can significantly improve the mental health outcomes of IDPs.

The current review also revealed that an increased frequency of displacement was also found to be significantly associated with PTSD. The finding is consistent with previous studies [ 21 , 23 , 42 , 67 , 68 ]. The number of times an individual had been displaced was positively associated with the risk of PTSD. Multiple factors contribute to the increased risk of PTSD among IDPs who experience repeated displacements. This could be because each displacement experience exposes an individual to significant stress and emotional overload, taxing their coping mechanisms and increasing their vulnerability to developing PTSD. Repeated displacements lead to an accumulation of traumatic experiences, making it increasingly difficult to process and integrate these experiences, ultimately increasing the risk of PTSD. Frequent displacements can heighten an individual’s sensitivity to trauma cues, making them more likely to experience flashbacks, nightmares, and intrusive thoughts related to the traumatic experiences. This sensitization perpetuates the state of hypervigilance and emotional arousal characteristic of PTSD. These findings suggest the importance of preventing and addressing repeated displacements to reduce the risk of PTSD among IDPs. Providing stable housing, livelihood support, and mental health services can help IDPs cope with the effects of displacement and prevent the development of PTSD.

Strengths and limitations of the study

This study was a first-of-its-kind systematic review and meta-analysis that estimated the pooled prevalence and associated risk factors of PTSD among IDPs in Africa. The study identified several significant risk factors for PTSD among IDPs. This information can be used to develop targeted interventions to prevent PTSD. This study has its limitations. Firstly, it was a cross-sectional study, so it could not establish cause-effect relationships. In addition, the lack of studies from countries other than those included may limit the continental representativeness of the study. Overall, the study is a valuable contribution to our understanding of PTSD among IDPs in Africa. The findings can be used to inform the development of targeted interventions to prevent PTSD among this vulnerable population.

The findings of this systematic review and meta-analysis highlight the alarming prevalence of PTSD among IDPs in Africa. The estimated pooled prevalence of 51% is significantly higher than the general population prevalence of PTSD, demonstrating the unique challenges faced by IDPs in coping with trauma and displacement. The study’s identification of significant risk factors, including female gender, marital status, traumatic events, ill health without medical care, depression, and frequency of displacement, provides valuable insights for targeted interventions. Effective interventions and the development of tailored mental health programs are needed to prevent and treat PTSD among IDPs, with focusing on the identified risk factors. Future studies focusing on the determinant factors of PTSD and their impacts on IDPs need to be welcomed.

Supporting information

S1 file. prisma checklist used in the reports of systematic review and meta-analysis..

https://doi.org/10.1371/journal.pone.0300894.s001

S2 File. JBI quality appraisal/result of the quality assessment of the studies.

https://doi.org/10.1371/journal.pone.0300894.s002

S3 File. Data set used in generating and analyzing of systematic review and meta-analysis.

https://doi.org/10.1371/journal.pone.0300894.s003

Acknowledgments

The authors would like to thank the University of Gondar, Ethiopia, for providing an office and free internet service. Moreover, the authors thanked and recognized the articles included in this study and used them as a basis for this systematic review and meta-analysis.

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Traumatic Stress and Homelessness: A Review of the Literature for Practitioners

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• Published: 22 November 2021
• Volume 50 , pages 218–230, ( 2022 )

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• Brenda Wiewel   ORCID: orcid.org/0000-0003-4640-9920 1 &
• Laura Hernandez   ORCID: orcid.org/0000-0002-9115-7593 2  

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A growing body of evidence connects traumatic stress and homelessness, which illustrates the importance of trauma and-resiliency-informed care (TIC) to appropriately serve persons experiencing homelessness (PEH). This paper reviews the literature on traumatic stress, including the biology of trauma as well as psychosocial, environmental, and systemic factors. These areas of knowledge constitute necessary elements when designing systems of care for PEH in order to provide effective services, avoid re-traumatization, and create healing environments to foster resilience. The authors identify trauma-specific evidence-based therapies, and comprehensive programmatic approaches that stem from established trauma-informed core values. Practical applications of the reviewed literature are utilized to demonstrate how organizations can adopt a trauma and resiliency-informed approach, based on both the reviewed literature as well as the authors’ collective clinical experience. A key takeaway is an emerging consensus that service providers must consider trauma when designing and offering services to persons with a history of homelessness. The authors offer recommendations for future pathways to create outcome measurement tools for social service providers based on the theory of self-efficacy and using concrete, quantifiable variables.

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Acknowledgements

We thank Dr. Gary Painter and the staff of the Homeless Research Policy Institute at the Sol Price School of Public Policy, University of Southern California for useful feedback on an early version of this paper. We also acknowledge a manuscript review provided by Melissa Singh, EdD, LCSW, Clinical Associate Professor of Social Work at the USC Suzanne Dworak-Peck School of Social Work.

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Substance Use Disorders in Patients With Posttraumatic Stress Disorder: A Review of the Literature

• Leslie K. Jacobsen , M.D. ,
• Steven M. Southwick , M.D. , and
• Thomas R. Kosten , M.D.

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OBJECTIVE: Alcohol use disorders and other substance use disorders are extremely common among patients with posttraumatic stress disorder (PTSD). This article reviews studies pertaining to the epidemiology, clinical phenomenology, and pathophysiology of comorbid PTSD and substance use disorders. METHOD: Studies were identified by means of computerized and manual searches. The review of research on the pathophysiology of PTSD and substance use disorders was focused on studies of the hypothalamic-pituitary-adrenal axis and the noradrenergic system. RESULTS: High rates of comorbidity suggest that PTSD and substance use disorders are functionally related to one another. Most published data support a pathway whereby PTSD precedes substance abuse or dependence. Substances are initially used to modify PTSD symptoms. With the development of dependence, physiologic arousal resulting from substance withdrawal may exacerbate PTSD symptoms, thereby contributing to a relapse of substance use. Preclinical work has led to the proposal that in PTSD, corticotropin-releasing hormone and noradrenergic systems may interact such that the stress response is progressively augmented. Patients may use sedatives, hypnotics, or alcohol in an effort to interrupt this progressive augmentation. CONCLUSIONS: Vigorous control of withdrawal and PTSD-related arousal symptoms should be sought during detoxification of patients with comorbid PTSD and substance use disorders. Inclusion of patients with comorbid PTSD and substance use disorders in neurobiologic research and in clinical trials will be critical for development of effective treatments for this severely symptomatic patient population.

Substance use disorders, particularly abuse of and dependence on central nervous system (CNS) depressants, are common in patients with posttraumatic stress disorder (PTSD). This article reviews clinical, epidemiologic, and neurobiologic studies relevant to the problem of comorbid PTSD and substance use disorders and discusses the clinical implications of these findings.

Clinical Phenomenology and Epidemiology

PTSD develops in some people after exposure to a severe traumatic event. The DSM-IV diagnosis of PTSD consists of symptoms in three clusters: 1) reexperiencing symptoms, including intrusive recollections of the trauma that are triggered by exposure to cues symbolizing the trauma; 2) avoidance symptoms, which involve diminished participation in activities and avoidance of thoughts, people, places, and memories associated with the trauma; and 3) arousal symptoms, which include difficulty sleeping, irritability, difficulty concentrating, hypervigilance, and exaggerated startle response.

Although intoxication and withdrawal symptoms vary across abused substances, all substance use disorders share key features. They include a maladaptive pattern of substance use leading to failure to fulfill work, school, or home obligations; legal problems; and substance-related interpersonal problems. Substance dependence further includes tolerance, withdrawal symptoms upon cessation of use, unsuccessful efforts to control use, and continued use despite persistent substance-related physical or psychological problems.

Persons with PTSD have elevated rates of comorbid psychiatric disorders. Studies of both combat veterans and civilians with PTSD have demonstrated that, among men with PTSD, alcohol abuse or dependence is the most common co-occurring disorder, followed by depression, other anxiety disorders, conduct disorder, and nonalcohol substance abuse or dependence (1 , 2) . Among women with PTSD, rates of comorbid depression and other anxiety disorders are highest, followed by alcohol abuse and dependence (1 , 2) . High rates of comorbidity of PTSD and substance use disorders were first reported in war-related studies, in which as many as 75% of combat veterans with lifetime PTSD also met criteria for alcohol abuse or dependence (2) . Among civilian populations, estimates of the prevalence of lifetime substance use disorders have ranged from 21.6% to 43.0% in persons with PTSD, compared with 8.1% to 24.7% in persons without PTSD (1 , 3 , 4) . Similarly, among substance abusers in the general population, the reported rate of PTSD is 8.3% (5) . Rates of PTSD appear to be higher among patients in inpatient substance abuse treatment (up to 42.5%) (6) and among pregnant women in residential treatment for substance abuse (62%) (7) . Surveys of substance-dependent adolescents have also found rates of PTSD ranging up to 19.2% (8) .

Patients with both PTSD and a substance use disorder have significantly higher rates of comorbid axis I and II disorders, psychosocial and medical problems, substance- or alcohol-related inpatient admissions, and relapse to substance use, compared with patients whose substance use is not complicated by PTSD (4 , 9) . Furthermore, patients with PTSD and substance use disorders tend to suffer from more severe PTSD symptoms, particularly those in the avoidance and arousal symptom clusters, than do patients with PTSD alone (10) . Conversely, one longitudinal study of patients with PTSD and a comorbid substance use disorder found at 6-month posttreatment follow-up that patients whose PTSD symptoms had remitted reported significantly less substance use than did patients with unremitted PTSD (11) .

Relationship of Substance Use to PTSD Symptoms

Elevated rates of comorbid depressive and anxiety disorders in patients with PTSD greatly complicate any effort to develop a model of the relationship between PTSD and substance use. High rates of comorbidity suggest that PTSD and substance use disorders are functionally related to one another. Two primary pathways have been described to explain these high rates of comorbidity. In the first, substance abuse precedes PTSD. To sustain their habit, some substance abusers repetitively place themselves in dangerous situations and, as a result, experience high levels of physical and psychological trauma (5) . For example, in a study of patients with PTSD and comorbid cocaine abuse, patients whose cocaine abuse developed first later developed PTSD as a result of trauma sustained in the context of procurement and use of cocaine (12) . Given that chronic substance use can lead to higher levels of arousal and anxiety as well as to sensitization of neurobiologic stress systems (13) , substance abuse may result in a higher level of vulnerability to development of PTSD after exposure to trauma.

In the second pathway, PTSD precedes development of substance use disorders. In this model, the use of substances is a form of self-medication. Patients report that CNS depressants, such as alcohol, cannabis, opioids, and benzodiazepines acutely improve PTSD symptoms (14) . Consistent with this, patients with PTSD report that onset and severity of substance abuse parallel the onset and escalation of PTSD symptoms (14) . In addition, clinical evidence suggests that the choice of substances of abuse (CNS depressants versus CNS stimulants) may stem from the particular constellation of PTSD symptoms that patients experience. For example, PTSD patients with alcohol dependence exhibit significantly more arousal symptoms that do PTSD patients with cocaine dependence (10) .

In the second model, withdrawal from substances, particularly CNS depressants, may initiate a cycle that perpetuates relapse and continued substance use. The withdrawal syndromes associated with many CNS depressants overlap extensively with the arousal symptoms of PTSD (15) ( Figure 1 ). Substances may be taken initially to ameliorate PTSD symptoms. As noted earlier, patients with PTSD have reported that CNS depressants acutely provide symptom relief (14) . Furthermore, objectively measured startle responses are reduced by alcohol (16) . However, the physiologic arousal resulting from substance withdrawal may have an additive effect with arousal symptoms stemming from PTSD. The resulting hyperaroused state may serve as a conditioned reminder of traumatic events and thus precipitate an increase in reexperiencing symptoms. Exacerbation of PTSD symptoms may then prompt relapse to substance use in an attempt to self-medicate. Thus, for the PTSD patient who already has symptoms of arousal, the additional arousal that accompanies withdrawal from substances may be intolerable. Alternatively, substances may be used to cope with the traumatic event itself (17) . This pattern may particularly apply when trauma that leads to PTSD occurs during adulthood. The initial calming effects from substance use may cue patients to resume substance use when PTSD symptoms reemerge.

Most published data support the second model, in which substance use follows or parallels traumatic exposure and the development of PTSD (18) . In a longitudinal study conducted by Chilcoat and Breslau (19) , 1,007 adults were reevaluated 3 and 5 years after an initial assessment. The researchers found that preexisting substance abuse did not increase subjects’ risk of subsequent exposure to trauma or their risk of developing PTSD after exposure to trauma. The relationship between exposure to trauma and increased risk for development of a substance use disorder was found to be specific to PTSD, as exposure to trauma without subsequent development of PTSD did not increase risk for development of a substance use disorder (19) . Of note, one study of patients with cocaine dependence and PTSD found that patients in whom PTSD preceded the onset of cocaine use were significantly more likely to suffer from comorbid major depression and to use benzodiazepines and opiates than were patients in whom PTSD developed after the onset of cocaine use (12) .

Pathophysiology

Our review of the literature on the pathophysiologic basis of comorbid PTSD and addiction selectively focuses on studies of the hypothalamic-pituitary-adrenal (HPA) axis and the noradrenergic system, as these have been most extensively studied in PTSD. It must be emphasized that many other neurobiological systems are involved in both the acute and chronic adaptation to stress and to substance use. These systems include the dopaminergic, γ-aminobutyric acid, benzodiazepine, and serotonergic systems, as well as the thyroid axis. Interactions among these systems in patients with comorbid PTSD and substance dependence are enormously complex. Thus, the potential relationships we discuss between the HPA axis, the noradrenergic system, and symptoms in patients with comorbid PTSD and substance use disorders should be viewed as one part of a far more complex whole.

HPA Axis in PTSD and Addiction

In humans and animals, acute stress elicits a cascade of neurohormonal events, including increased turnover of norepinephrine in terminal projection regions of the locus ceruleus and liberation of hypothalamic corticotropin-releasing hormone (CRH) into the pituitary portal system, which stimulates release of ACTH from the pituitary, which in turn triggers release of cortisol (human) or corticosterone (rat) from the adrenals (20) . Animal and human research has implicated this cascade in the pathophysiology of both substance use disorders and PTSD.

Humans with substance dependence most frequently identify stress and negative mood states as reasons for relapse and ongoing substance abuse (21) . Recently, a personalized stress imagery task was shown to reliably increase cocaine craving and salivary cortisol in cocaine-dependent patients (22) . Animal studies have shown that stress induces relapse to heroin and to cocaine self-administration in rats trained to self-administer these substances and then subjected to a prolonged drug-free period (23 , 24) . Similarly, in animals naive to illicit substances, a large range of stressors increases the proclivity toward drug self-administration (25) . Initial work on the pathophysiology of this phenomenon indicated that stress-induced or stress-enhanced drug self-administration is mediated by corticosterone (26) .

Evidence has accumulated to support a role for CRH in mediating the effects of stress on drug self-administration. Central, but not peripheral, administration of CRH has been shown to induce a long-lasting enhancement (sensitization) of the locomotor response to d-amphetamine (27) , and pretreatment with a CRH antagonist has been shown to block the development of stress-induced sensitization to d-amphetamine (28) . Indeed, central administration of anti-CRH antibody or the CRH receptor antagonist α-helical CRH has been found to block the locomotor hyperactivity induced by cocaine (29) .

Withdrawal from chronic cocaine or alcohol administration in rats produces anxiety-like behavior and decreased exploration that is associated with selective increases in CRH in the hypothalamus, amygdala, and basal forebrain (30 , 31) . Pretreatment with anti-CRH immunoserum or α-helical CRH, blocking the effects of CRH, completely prevents the development of these withdrawal-associated behaviors (30) . Consistent with these observations, CSF CRH is elevated in humans in acute alcohol withdrawal and then normalizes or decreases below normal levels with extended abstinence and resolution of withdrawal symptoms (32) . Shaham and colleagues (33) found that intracerebroventricular injection of CRH reinstated heroin seeking after extinction in rats trained to self-administer the drug. In addition, α-helical CRH attenuated the reinstatement effect of footshock stress (33) . Neither adrenalectomy nor chronic or acute exposure to the corticosterone synthesis inhibitor metyrapone interfered with the reinstatement effects of priming injections of heroin or of footshock stress. A potent, selective CRF1 receptor antagonist, CP-154,526, has been found to attenuate reinstatement of drug seeking induced by footshock stress after up to 14 days of extinction in rats trained to self-administer heroin or cocaine (34) .

Findings from both animal and human studies of the effects of chronic stress or of PTSD on HPA axis function vary depending on the experimental paradigm used or the population studied. In patients with PTSD, elevated (35) , reduced (36) , and normal (37) levels of cortisol secretion have been reported. A series of studies performed by Yehuda and colleagues demonstrated that patients with PTSD have an elevated number of lymphocyte glucocorticoid receptors (38) , enhanced suppression of cortisol after administration of dexamethasone (39) , a greater than normal decrease in the number of lymphocyte glucocorticoid receptors after administration of dexamethasone (39) , and higher than normal increases in ACTH after metyrapone blockade of cortisol synthesis (40) . All of these findings suggest that glucocorticoid negative feedback is enhanced in PTSD.

Animal studies examining the effects of uncontrollable stress on HPA axis function have reported initial increases of corticosterone secretion, followed by normalization of corticosterone secretion with ongoing chronic stress (41) . However, some investigators have failed to demonstrate normalization of corticosterone secretion with chronic uncontrollable stress (42) , particularly in animals that have been reared under stressful conditions (43) or when levels of chronic stress are high (44) . In a pattern similar to that found in humans with PTSD, animals subjected to a single episode of prolonged stress and then briefly restressed after a stress-free period showed enhancement of glucocorticoid negative feedback (45) .

Although both animal and human studies have suggested that glucocorticoid negative feedback may be enhanced in PTSD, the implications of these observations for CRH secretion in this disorder are unclear. As noted earlier, CRH-producing cells and CRH receptors exist both in the hypothalamus and in extrahypothalamic sites. Findings from some studies have suggested that hypothalamic and extrahypothalamic CRH-producing cells may respond differently to corticosterone. Specifically, corticosterone appears to restrain hypothalamic CRH-producing cells while stimulating extrahypothalamic CRH-producing cells, particularly those in the amygdala (46) . Replacement of corticosterone in adrenalectomized rats decreases CRH production in the parvocellular nucleus of the hypothalamus while increasing CRH production in the central nucleus of the amygdala (47) . This region-specific pattern of regulation is also seen in adrenally intact rats treated with high-stress levels of corticosterone for extended periods of time (48) . Thus, while glucocorticoid feedback may decrease CRH production and release in the hypothalamus, it may stimulate CRH production and release in other brain regions, including the amygdala. This possibility has been addressed in two studies of patients with PTSD, one that examined CSF concentrations of CRH at a single time point (49) and one that examined CSF concentrations of CRH at serial time points over a 6-hour period (37) . Both found significantly higher levels of CSF CRH in patients with PTSD than in normal comparison subjects. However, although elevated CSF CRH suggests that brain CRH may be elevated, the specific brain tissues producing CRH elevations cannot be determined from CSF data alone.

The possibility that brain CRH levels are elevated in PTSD is of great interest because of a rich preclinical literature indicating that elevated levels of CRH in the brain, particularly in the amygdala, potentiate fear-related behavioral responses, including the startle response (50) . These anxiogenic effects of CRH are reversed by administration of CRH antagonists (50) . As noted earlier, findings from animal and human studies have supported a role for CRH in mediating some effects of drugs of abuse, including stress- or priming-induced relapse to drug self-administration and symptoms of withdrawal (27 , 28 , 32 – 34) . Thus, elevated levels of CRH in the brain in PTSD may mediate both the symptoms of hyperarousal as well as the increased risk for substance abuse and dependence seen in this disorder. More specifically, elevated levels of CRH in the brain in PTSD may enhance the euphorigenic properties of certain drugs, such as stimulants, and may worsen the severity of withdrawal symptoms, thereby prompting patients to relapse to drug use. Conversely, brain CRH elevations induced by withdrawal from substance use may exacerbate symptoms of hyperarousal, which could trigger other symptoms of PTSD, prompting relapse to substance use.

Noradrenergic System in PTSD and Addiction

During chronic uncontrollable stress, norepinephrine turnover increases in specific brain regions, including the locus ceruleus, hypothalamus, hippocampus, amygdala, and cerebral cortex (51) . Evidence for noradrenergic dysregulation in patients with PTSD has included elevated 24-hour urinary epinephrine and norepinephrine excretion, a lower than normal number of platelet α 2 -adrenergic receptors, elevated 24-hour plasma norepinephrine, and exaggerated cardiovascular and 3-methoxy-4-hydroxyphenylglycol (MHPG) (a norepinephrine metabolite) responses to intravenous yohimbine (52) . Noradrenergic dysregulation has also been reported during states of withdrawal from chronic self-administration of alcohol and other abused substances. The levels of noradrenaline, norepinephrine, and MHPG in both plasma and CSF have been found to be increased and the number of platelet α 2 -adrenergic receptors decreased in alcoholics during acute withdrawal (53 , 54) . The severity of alcoholic withdrawal symptoms has been positively correlated with the concentration of MHPG in CSF (54) . Evidence for noradrenergic dysregulation in opiate withdrawal has included findings of elevated plasma MHPG in humans and elevated plasma and brain MHPG in animals (55 , 56) . In animals, the level of noradrenergic activity was significantly correlated with the severity of withdrawal symptoms (56) . These findings have prompted the use of the α 2 -adrenergic receptor agonist clonidine in the treatment of both opiate withdrawal symptoms and PTSD (57 , 58) .

Noradrenergic System/HPA Axis Interactions

Evidence that brain CRH and noradrenergic systems modulate each other has been reported. Stress has been shown to increase CRH levels in the locus ceruleus (59) , a primary source of noradrenergic projections to all cortices as well as to the thalamus and hypothalamus, while intraventricular administration of CRH has been found to increase the discharge rates of locus ceruleus neurons and to increase norepinephrine turnover in hippocampus, hypothalamus, and prefrontal cortex (60 – 62) . Conversely, stress-induced activation of the locus ceruleus has been blocked by administration of CRH antagonists (63) . Similar evidence exists for the interaction of the CRH and noradrenergic systems in the hypothalamus (64) and the amygdala, where stress induces increases in both CRH and norepinephrine (65) . Furthermore, norepinephrine in the amygdala appears to stimulate release of CRH (66) .

These observations have prompted the proposal by Koob (20) that interactions of the CRH and noradrenergic systems in the brain may, under some conditions, function as a feed-forward system, leading to the progressive augmentation of the stress response with repeated stress exposure that is characteristic of PTSD. This progressive augmentation of response with repeated stress has previously been conceptualized as kindling (67) . A feed-forward interaction between the CRH and noradrenergic systems may represent one neurobiologic underpinning of both PTSD and substance use disorders. More specifically, stress, including stress related to self-administration of or withdrawal from substances, may stimulate CRH release in the locus ceruleus, leading to activation of the locus ceruleus and release of norepinephrine in the cortex, which in turn may stimulate the release of CRH in the hypothalamus and amygdala (20) . Such an interaction between the brain noradrenergic and CRH systems may mediate the symptoms of hyperarousal seen in PTSD, including exaggerated startle response. The proclivity toward misuse of CNS depressants by patients with PTSD may reflect an attempt to interrupt this feed-forward interaction by suppressing activity of the locus ceruleus with these agents (68) .

Conclusions

Clinical and epidemiologic studies confirm that comorbidity of PTSD with substance use disorders is common and that the symptoms of patients with this comorbidity tend to be more severe and more refractory to treatment than those of patients suffering from either disorder alone. Despite the frequency with which patients with both diagnoses present for treatment, no systematic treatment approach of proven efficacy has been developed for this population. Furthermore, little is known about the impact on substance use disorder outcomes of the medications and psychosocial interventions commonly used to treat PTSD, or vice versa.

These limitations notwithstanding, the research conducted to date can inform both clinical practice and future clinical and preclinical research. For example, clinical research suggests that PTSD patients with substance dependence, particularly those who are addicted to CNS depressants, may find the physiologic arousal resulting from substance withdrawal intolerable due to additive effects with preexisting arousal symptoms related to PTSD. Successful detoxification of these patients may thus require inpatient admission to permit vigorous control of withdrawal and PTSD-related arousal symptoms.

Neurobiologic research indicates that high levels of CRH in the brain, particularly in the amygdala, may be common to both PTSD and to substance withdrawal states. Further, CRH antagonists reduce both the anxiety and the enhanced response to illicit substances (sensitization) that are induced by higher levels of brain CRH. These observations suggest that CRH antagonists could potentially have a role in the treatment of patients with PTSD and comorbid substance dependence. Although at present no CRH antagonist has been approved for human use, a series of CRH antagonists that can be administered peripherally have been developed and have been shown to cross the blood brain barrier (34 , 69) . These agents will be important tools for further defining the potential role of CRH antagonism in the treatment of patients with PTSD and substance dependence and will hopefully lead to development of orally active preparations.

Evidence of noradrenergic dysregulation in both PTSD and in withdrawal from CNS depressants has prompted the use of the α 2 -adrenoceptor agonist clonidine in both disorders (57 , 58) . Data from both preclinical and clinical research suggest that this agent, as well as the selective α 2 -adrenoceptor agonist guanfacine, would be effective in reducing noradrenergic hyperactivity in patients with PTSD and comorbid substance dependence. Guanfacine, given its greater selectivity, may offer a more favorable side effect profile. Given the dearth of established treatments for this patient population, controlled clinical trials to establish the efficacy of these agents are clearly indicated.

Finally, although preclinical work has resulted in considerable progress toward delineating the contributions of the HPA axis and noradrenergic systems to the pathophysiologic underpinnings of PTSD with comorbid substance dependence, few neurobiologic studies have been conducted in this patient population. The inclusion of subjects with this comorbidity may render such studies more complicated, but the data emerging from this work would better inform the clinical management of the difficult-to-treat symptoms of these frequently encountered patients. At the minimum, patients who participate in studies of PTSD or of substance dependence must be thoroughly evaluated for the presence of this comorbidity to permit adequate control of the effects of the comorbid condition on the neurobiologic processes under study.

Received May 11, 2000; revision received Aug. 22, 2000; accepted Nov. 17, 2000. From the Department of Psychiatry, Yale University School of Medicine, New Haven, Conn., and the VA Connecticut Healthcare System. Address correspondence to Dr. Jacobsen, Department of Psychiatry (116A), VA Connecticut Healthcare System, Yale University–West Haven Campus, 950 Campbell Ave., West Haven, CT 06516; [email protected] (e-mail). Supported in part by grants DA-00167, DA-04060, and DA-09250 from the National Institute on Drug Abuse.

Figure 1. Symptoms of Increased Arousal in PTSD and Symptoms Associated With Withdrawal From CNS Depressants a

a From the DSM-IV criteria for PTSD, alcohol withdrawal, and sedative, hypnotic, or anxiolytic withdrawal.

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Prevalence and associated factors of post-traumatic stress disorder in Lebanon: A literature review

Affiliation.

• 1 Partner 4 Health, Oslo, Norway. Electronic address: [email protected].
• PMID: 34340165
• DOI: 10.1016/j.ajp.2021.102800

Lebanon has been under continuous conflict for more than four decades, putting millions of Lebanese at a high risk for post-traumatic stress disorder (PTSD) and creating a complex collective trauma. This paper aimed to review all studies from Lebanon reporting on PTSD in order to describe the prevalence of PTSD and its associated risk factors among Lebanese adults. A search of the MEDLINE/PubMed database was conducted in February/March 2021 to identify research articles on PTSD in Lebanese adults. A total of 1064 articles were identified, out of which 11 articles (5875 participants) published between 2003 and 2020 were included. PTSD prevalence estimates were highly variable across the individual studies, ranging from 2 % to 98 %. Female sex, economic hardship, lower educational level, being unemployed, number of witnessed/experienced traumatic events, and presence of comorbid psychological disorders were associated with higher PTSD rates. In light of the increasing PTSD risk in the Lebanese population as a result of the recent Beirut blast and ongoing social and economic crises, further culturally competent research is needed to provide rigorous evidence on the prevalence, course, and severity of PTSD in Lebanon.

Keywords: Lebanon; Post-traumatic stress disorder; Prevalence; Risk factors; Trauma.

Copyright © 2021 Elsevier B.V. All rights reserved.

Publication types

• Lebanon / epidemiology
• Risk Factors
• Stress Disorders, Post-Traumatic* / epidemiology

First Responders and PTSD: A Literature Review

The time has come to put the mental health needs of our first responders before their call of duty, writes Ashley Fitzpatrick.

The mental health of first responders is often overlooked. Increases in mental health issues, post-traumatic stress disorder (PTSD) and rates of suicide have prompted research into what first responders need in order to stay emotionally healthy. The time has come to put the mental health needs of our first responders before their call of duty. Exposure to traumatic events has been linked to psychological distress and many frontline workers experience these traumas on a daily basis. Literature suggests that the increased incidences of psychological distress requires extensive scientific inquiry into the mental health of first responders worldwide.

• Ohio Moves Forward with PTSD Bill for First Responders
• Toward a Better Understanding of Post-Traumatic Stress Disorder (PTSD)
• Psychological Trauma: The Silent Stalker

First Responders Suffering

There is a silent crisis happening worldwide. First responders are quietly suffering because of the stigma surrounding the utilization of mental health services. First responders are more likely to suffer from psychological distress due to job stress, repeated exposure to trauma, lack of sleep, the physical demands of the job, lack of resources and working long hours or multiple jobs.

The community of first responders have been neglected and now they are beginning to show the consequences of such neglect. The immediacy of care is of the utmost importance for all individuals suffering with a mental illness or condition.

The community of first responders must begin accepting mental illness as they would any other physiological condition. 1 The first responder community must end the stigmatization of mental health and bring awareness, as well as normalcy, to end this silent killer. The trauma that first responders experience throughout their careers are not normal instances however seeking help is what should be considered normal. 

A review of existing literature published within the last 10 years was completed utilizing the electronic databases PubMed and Google Scholar. Forty-eight articles were further evaluated for this literature review, 15 were utilized. Articles were chosen based on the following inclusion criteria: (1) the article examines one or more first responder occupations defined as police officers, firefighters, emergency medical services, emergency medical technicians, paramedics and/or dispatchers; (2) presents data on one or more of the following topics: post traumatic stress disorder (PTSD), suicide, substance abuse, dual diagnosis, depression and/or anxiety, non pharmacological interventions, pharmacological interventions, therapy; (3) published in English.

Articles were excluded if they contained the following: (1) large scale incident studies; (2) military-specific articles; (3) first responders responding to mental health crisis patients.

The three themes signify how the data from the articles was separated. Theme one reports findings in relation to police, fire, and EMS. Theme two discusses PTSD and suicide. Lastly, theme three examines different treatment modalities and their outcomes.

Emergency Medical Services, Fire and Police

All literature points to the same conclusions. The data suggests that first responders are at an increased risk of PTSD and issues with mental health however rigourous studies need to be conducted in order to be able to generalize the data and apply it to all first responders. In a survey study completed in Canada, researchers found that out of 5,813 participants (32.5% women) were grouped into six categories (i.e., call center operators/dispatchers, correctional workers, firefighters, municipal/provincial police, paramedics, Royal Canadian Mounted Police). Substantial proportions of participants reported current symptoms consistent with one (i.e., 15.1%) or more (i.e., 26.7%) mental disorders based on the screening measures. 2

The researchers reported that the participants’ symptom clusters were consistent with one or more mental disorders, concluding that the incidences of mental illness were higher than previously published estimates compared to the general population.

Harvey et. al examined the impact of repeated trauma exposure in firefighters from Australia. A cross-sectional survey was completed by current (n=488) and retired (n=265) firefighters from Fire and Rescue New South Wales, Australia.

Among current fire-fighters, rates of post-traumatic stress disorder and depression were 8% and 5%, respectively; while 4% reported consumption of more than 42 alcoholic drinks per week. Retired firefighters reported significantly greater levels of symptomatology, with the prevalence estimates of post-traumatic stress disorder at 18% (p = 0.001), depression at 18% (p < 0.001) and heavy drinking at 7%. There was a significant positive linear relationship between the number of fatal incidents attended and rates of post-traumatic stress disorder, depression and heavy drinking. 3

Conclusions can be drawn from this study that there is a link between trauma exposure, PTSD, depression and substance abuse. Not only do the studies find a correlation between trauma exposure and psychological distress in paid firefighters, it has also been observed in volunteer fire services. Milligan-Saville et al. notes that volunteer fire services in Western countries (Australia) have a significant lack of access to support services for mental health issues.

In a cross-sectional survey of an Australian volunteer fire service (n=459), it was found that: The risk of probable PTSD was significantly higher for those with the most frequent involvement with distressing incidents and the highest levels of cumulative trauma exposure. Being trapped in a dangerous situation or being assaulted by other people, resulted in the greatest odds of developing a mental disorder. Volunteer fire service members with the highest levels of trauma exposure and involvement with particular types of critical incidents are at elevated risk of mental health problems. 4

Results yielded that the “estimated prevalence of probable PTSD and psychological distress in the sample were 5.4% and 9.8% respectively, with 11.8% suffering from probable mental disorder.” There is a correlation in their study between the number of traumatic events and greater odds of PTSD (p=0.01), psychological distress (p=0.02), and probable mental disorder (p=0.01). The more traumatic events a firefighter responded to, the higher incidence of PTSD, psychological distress, or probable mental disorder.

Lee et al. evaluated police officers in South Korea utilizing a cross-sectional study. 5 Their goal was to evaluate police officers job characteristics and their risk for PTSD. Using the Impact of Event Scale (revised Korean version) they defined police officers to be high risk with a score of greater than or equal to 26. Police officers (n=3187) that had experienced a traumatic event within a one year period were included in the study. Results showed that “41.11% were classified as having a high risk of PTSD.”

Comparatively, Nelson and Smith studied police officers (n=134) and their mental health in Jamaica. The study aimed to examine the relationship between work and mental health. The goal was to assess if there was a correlation between work (job satisfaction and job stress) and mental health outcomes using a cross-sectional survey design. Results reported that: negative work characteristics, lower levels of positive work factors and work support and emotion-focused coping styles were associated with increased levels of depression (F(8, 125) = 7.465, P < 0.001). Subjective feelings of anxiety were positively associated with negative work characteristics and emotion-focused coping (F(8, 125) = 7.586, P < 0.001). The relationship between work characteristics and mental health outcomes was mediated by perceived stress. 6 Nelson and Smith recommended that intervention programs should address working conditions and should monitor stress levels.

There is a noteworthy relationship between emergency medical services, firefighters and police officers when comparing all of the articles. Studies show that first responders are at an increased risk of post-traumatic stress disorder and additional mental health issues including substance abuse. The data does not conflict between articles. Concluding statements for most of the articles note that there is a lack of large, national or international studies to verify results between these groups. Though the compilation of data is compelling, the need for additional research is imperative. 2,3,5,6

Post-traumatic Stress Disorder and Suicide

PTSD is immensely underreported as utilizing mental health services is seen as weakness in the prehospital and first responder communities. A study conducted using in-hospital and prehospital providers found that “prehospital providers were significantly more likely to screen positive for PTSD compared to the in-hospital providers (42% vs. 21%, P<0.001).” 7

Interestingly, this survey found that only 55% of respondents had ever received any information or education about PTSD, and only 13% of respondents sought treatment for their symptoms. Astoundingly, though emergency service personnel experience prominently higher rates of post traumatic stress, there are no rigorously conducted trials for PTSD in this population. 8

According to the National Fallen Firefighters Foundation, firefighters are three times more likely to die by suicide than a line of duty death. “In 2016,  The Badge of Life, a police suicide prevention program, revealed that nearly 108 law enforcement officers took their own lives. According to the Firefighter Behavioral Health Alliance, an estimated 113 firefighters and paramedics took their own lives in 2015.” 1

From a study published in the Journal of Emergency Medical Services researchers found that first responders (EMS) in the United States were approximately 10 times more likely to have suicidal ideations and/or attempt suicide compared to the CDC national average. “The results showed that 3,447 (86%) of the 4,022 respondents experienced CS, but the shocking discovery was that 1,383 (37%) of the respondents had contemplated suicide and 225 (6.6%) had actually tried to take their own life.” (Barber et al., 2015). In the survey, CS (critical stress) was defined as “the stress we undergo either as a result of a single critical incident that had a significant impact upon you, or the accumulation of stress over a period of time. This stress has a strong emotional impact on providers, regardless of their years of service.” 9

In some states, emergency medical services (EMS) are not considered an essential service. In these places, EMS does not receive taxpayer money for their services, thus their access to resources and funding is significantly lower than their emergency counterparts. This issue leads to increased stress in the workplace, in addition to “their experiences of life-threatening situations and acute stress” which could further lead to the development of posttraumatic stress disorder (PTSD) or posttraumatic stress symptoms. 10

Firefighters were also found to have an increased risk of suicidal thoughts and behaviors. In a study conducted by Stanley et al. (2015), data was obtained via online cross-sectional survey that was distributed nationwide (n=1027) to both active and retired firefighters. Suicidal ideations and behaviors were assessed using a modified version of the Self-Injurious Thoughts and Behaviors Interview-Short Form (SITBI- SF). This study reports the career prevalence estimates of 46.8% (suicidal ideations), 19.2% (has a suicidal plan), 15.5% (suicidal attempts), and 16.4% (non-suicidal self-injury).

The researchers noted that the “key factors associated with increased risk for reporting suicidal thoughts and behaviors included lower firefighter rank, fewer years of firefighter service, membership in an all-volunteer department, a history of professionally responding to a suicide attempt or death, and active duty military status.” 11 These numbers are frighteningly high and require immediate intervention in the prevention and treatment of firefighter suicidality.

Treatment Modalities

In the world of behavioral health, there are a variety of treatment modalities utilized for different diagnoses. Cognitive behavioral therapy (CBT) has presented positive outcomes in treating first responders with PTSD. CBT sets a goal-oriented, teleological, problem-focused, well-structured–in the here and now–approach, which also focuses on therapeutic alliance and rapport between the CBT therapist and the client. 12,10

A study completed by Bryant et al. (2017) examined the efficacy of exposure based cognitive behavior therapy for PTSD in emergency service personnel in a randomized clinical trial. The trial examined the efficacy of brief exposure to traumatic memories (CBT-B) versus prolonged exposure to traumatic memories (CBT-L). Participants were randomized into three groups: CBT-B, CBT-L, and WL (waitlist). The cognitive behavioral therapy groups included 12 weeks of individualized therapy and education, CBT skills building, imaginal exposure (40 minutes for CBT-L, 10 minutes for CBT-B), in vivo exposure, and cognitive restructuring and relapse prevention.

Participants were assessed at their baseline, post-treatment, and had a six-month follow up. Results showed that participants in the CBT groups had greater reductions in PTSD severity (Clinician Administered PTSD Scale), depression, maladaptive appraisals about oneself and the world, and had increased improvements on psychological and social quality of life than the waitlist group whom did not receive any interventions. Researchers did not find a difference in outcomes between the CBT-B and CBT-L groups, and note “that CBT, which can include either long or brief imaginal exposure, is efficacious in reducing PTSD in emergency service personnel.” 8

In contrast to cognitive behavioral therapy, Sessa (2017) reports that resistance to treatment for PTSD is high and has found that trauma-focused psychotherapy can be difficult for those who have issues with recalling traumatic memories. Sessa (2017) suggests that using MDMA in conjunction with psychotherapy “appears to facilitate recall of traumatic memories without the user feeling overwhelmed by the negative affect that usually accompanies such memories.” 13 Another study completed in 2018 by Mithoefer et al. examined 3,4-methylenedioxymethamphetamine (MDMA)-assisted psychotherapy for post- traumatic stress disorder in military veterans, firefighters, and police officers. The study aimed to examine the efficacy and safety of 3,4-methylenedioxymethamphetamine (MDMA)-assisted psychotherapy for treating chronic PTSD in first responders.

This study was a randomized, double-blind, dose-response, phase two clinical trial that was completed in an outpatient clinic in the United States. Criteria included service personnel ages 18 years or older, with chronic PTSD (duration of at least six months) and had a Clinician-Administered PTSD Scale (CAPS-IV) total score of 50 or greater. Participants were administered MDMA (either 30mg, 75mg, or 125mg) orally in two 8-h sessions with concomitant psychotherapy. “Participants in the 30 mg and 75 mg groups subsequently underwent three 100-125 mg MDMA-assisted psychotherapy sessions in an open-label crossover, and all participants were assessed 12 months after the last MDMA session. Safety was monitored through adverse events, spontaneously reported expected reactions, vital signs, and suicidal ideation and behavior. This study is registered with ClinicalTrials.gov, number NCT01211405.” 14

The study concluded that those whom had received the full dose of MDMA (75mg and 125mg) had a significant decrease in PTSD symptoms compared to the 30mg group. Symptom severity was decreased in the 30mg group after receiving the additional three psychotherapy sessions with the full dose of MDMA (100-125mg). “PTSD symptoms were significantly reduced at the 12-month follow-up compared with baseline after all groups had full-dose MDMA (mean CAPS-IV total score of 38.8 [SD 28.1] vs 87.1 [16.1]; p<0.0001).” 14 Trials and studies do show positive outcomes when therapy is involved however for those who have chronic PTSD, have suppressed traumatic memories, or have issues recalling traumatic incidences, the use of MDMA is showing to have encouraging outcomes in clinical trials. 

Additional non-pharmacological interventions recommended to treat post-traumatic stress disorder are recreational therapy, animal-assisted therapy, yoga, and acupuncture as well as alternative delivery methods for psychotherapy. 15 However, these complementary alternative methods are dependent upon patient preferences and therapy availability. Additional research is also required to examine the efficacy of complementary practices and PTSD. 

In a literature review by Lewis-Schroeder et al. (2018), as previously discussed, evidence indicates that the prevalence of posttraumatic stress disorder (PTSD) is higher among first responders than the general population. However, they present an interesting topic that requires additional research when discussing the treatment of women and PTSD. There are “notable gaps in the literature including the need to investigate why and how women present with different PTSD symptoms than men, and how these differences need to be taken into account in determining appropriate treatment for women.” 16

Treatment can begin through identification of a mental health issue by a primary care provider. Robertson (2019) identified that first responders during their annual fitness for duty exams were screened for physical fitness, not emotional wellness for their occupation. 17 Utilizing the PTSD Checklist for the Diagnostic and Statistical Manual of Mental Disorders, 5 th Edition (PCL-5) screening tool, first responders (n=152 post intervention) were screened during their primary care visit. Out of the seven responders that screened positive, five (71%) responders received a referral for mental health services. Early identification of psychological distress and PTSD symptoms with education and referral is beneficial to the mental health of first responders.

The author’s primary intention of this literature review is to clearly identify and bluntly express that an issue exists within the world of emergency services and it is not being adequately addressed. Early identification, intervention, and referrals to mental health providers may be a key in helping to treat PTSD and decrease the incidence of suicide in first responders. The author’s secondary intention of this literature review was to study the efficacy of mental health services in first responders with PTSD, in comparison with those whom do not utilize mental health support services.

The literature reports positive outcomes with both cognitive behavioral therapy and medication supported psychotherapy, dependent upon the severity and chronicity of PTSD symptoms. Utilizing healthy coping mechanisms and exploring the use of complementary and alternative medicinal practices such as meditation or yoga, can have a positive impact on mental wellbeing. First responders must acknowledge that this is a life-threatening issue and it is one that requires immediate intervention.

The problem is extensive as it involves emergency medical services, firefighters, and police officers globally. “As we begin treating mental illness as a normal condition and mental healthcare as a normal avenue for treatment; we will begin the process of promoting a healthier life among those that serve as first responders.” 1 Do not think for a moment that a problem does not exist simply because it cannot be outwardly visualized.

1. Brown, A. D. (2017). First responders and mental health.  Psychology Today,  Retrieved from  https://www.psychologytoday.com/us/blog/towards-recovery/201705/first-responders-and-mental-health .

2. Carleton, R. N., Afifi, T. O., Turner, S., Taillieu, T., Duranceau, S., LeBouthillier, D. M., . . . Asmundson, G. J. G. (2018). Mental disorder symptoms among public safety personnel in canada. Canadian Journal of Psychiatry.Revue Canadienne De Psychiatrie, 63 (1), 54-64. doi:10.1177/0706743717723825 [doi].

3. Harvey, S. B., Milligan-Saville, J. S., Paterson, H. M., Harkness, E. L., Marsh, A. M., Dobson, M., . . . Bryant, R. A. (2016). The mental health of fire-fighters: An examination of the impact of repeated trauma exposure. The Australian and New Zealand Journal of Psychiatry, 50 (7), 649-658. doi:10.1177/0004867415615217 [doi].

4. Milligan-Saville, J., Choi, I., Deady, M., Scott, P., Tan, L., Calvo, R. A., . . . Harvey, S. B. (2018). The impact of trauma exposure on the development of PTSD and psychological distress in a volunteer fire service. Psychiatry Research, 270 , 1110-1115. doi:S0165-1781(17)32292-8 [pii].

5. Lee, J. H., Kim, I., Won, J. U., & Roh, J. (2016). Post-traumatic stress disorder and occupational characteristics of police officers in republic of korea: A cross-sectional study. BMJ Open, 6 (3), e009937-009937. doi:10.1136/bmjopen-2015-009937 [doi].

6. Nelson, K. V., & Smith, A. P. (2016). Occupational stress, coping and mental health in jamaican police officers. Occupational Medicine (Oxford, England), 66 (6), 488-491. doi:10.1093/occmed/kqw055 [doi].

7. Luftman, K., Aydelotte, J., Rix, K., Ali, S., Houck, K., Coopwood, T. B., . . . Davis, M. (2017). PTSD in those who care for the injured. Injury, 48 (2), 293-296. doi:S0020-1383(16)30722-7 [pii].

8. Bryant, R. A., Kenny, L., Rawson, N., Cahill, C., Joscelyne, A., Garber, B., . . . Nickerson, A. (2019). Efficacy of exposure-based cognitive behaviour therapy for post-traumatic stress disorder in emergency service personnel: A randomised clinical trial. Psychological Medicine, 49 (9), 1565-1573. doi:10.1017/S0033291718002234 [doi].

9. Barber, E., Newland, C., Young, A., & Rose, M. (2015). Survey reveals alarming rates of EMS provider stress and thoughts of suicide. 40 (10) Retrieved from  https://www.jems.com/2015/09/28/survey-reveals-alarming-rates-of-ems-provider-stress-and-thoughts-of-suicide/ .

10. Papazoglou, K. (2017). Examining the psychophysiological efficacy of CBT treatment for first responders diagnosed with PTSD: An understudied topic. Sage Open, 7 (3), 2158244017729407. 

11. Stanley, I. H., Hom, M. A., Hagan, C. R., & Joiner, T. E. (2015). Career prevalence and correlates of suicidal thoughts and behaviors among firefighters. Journal of Affective Disorders, 187 , 163-171. doi:10.1016/j.jad.2015.08.007 [doi].

12. Rector, N. A. (2010). Cognitive-behavioural therapy: An information guide. Toronto, Ontario, Canada: Centre for Addiction and Mental Health. 

13. Sessa, B. (2017). MDMA and PTSD treatment: “PTSD: From novel pathophysiology to innovative therapeutics”. Neuroscience Letters, 649 , 176-180. doi:S0304-3940(16)30490-6 [pii].

14. Mithoefer, M. C., Mithoefer, A. T., Feduccia, A. A., Jerome, L., Wagner, M., Wymer, J., . . . Doblin, R. (2018). 3,4-methylenedioxymethamphetamine (MDMA)-assisted psychotherapy for post- traumatic stress disorder in military veterans, firefighters, and police officers: A randomised, double-blind, dose-response, phase 2 clinical trial. The Lancet.Psychiatry, 5 (6), 486-497. doi:S2215-0366(18)30135-4 [pii].

15. Wynn, G. H. (2015). Complementary and alternative medicine approaches in the treatment of PTSD. Current Psychiatry Reports, 17 (8), 600-2. doi:10.1007/s11920-015-0600-2 [doi].

16. Lewis-Schroeder, N. F., Kieran, K., Murphy, B. L., Wolff, J. D., Robinson, M. A., & Kaufman, M. L. (2018). Conceptualization, assessment, and treatment of traumatic stress in first responders: A review of critical issues. Harvard Review of Psychiatry, 26 (4), 216-227. doi:10.1097/HRP.0000000000000176 [doi].

17. Robertson, E. W. (2019). Implementation of a standardized screening protocol to improve post- traumatic stress disorder surveillance in first responders. Journal of Occupational and Environmental Medicine, 61 (12), 1041-1044. doi:10.1097/JOM.0000000000001732 [doi].

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• Open access
• Published: 05 September 2022

Psychiatric and medical comorbidities of eating disorders: findings from a rapid review of the literature

• Ashlea Hambleton 1 ,
• Genevieve Pepin 2 ,
• Anvi Le 3 ,
• Danielle Maloney 1 , 4 ,
• National Eating Disorder Research Consortium ,
• Stephen Touyz 1 , 4 &
• Sarah Maguire 1 , 4  

Journal of Eating Disorders volume  10 , Article number:  132 ( 2022 ) Cite this article

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Eating disorders (EDs) are potentially severe, complex, and life-threatening illnesses. The mortality rate of EDs is significantly elevated compared to other psychiatric conditions, primarily due to medical complications and suicide. The current rapid review aimed to summarise the literature and identify gaps in knowledge relating to any psychiatric and medical comorbidities of eating disorders.

This paper forms part of a rapid review) series scoping the evidence base for the field of EDs, conducted to inform the Australian National Eating Disorders Research and Translation Strategy 2021–2031, funded and released by the Australian Government. ScienceDirect, PubMed and Ovid/Medline were searched for English-language studies focused on the psychiatric and medical comorbidities of EDs, published between 2009 and 2021. High-level evidence such as meta-analyses, large population studies and Randomised Control Trials were prioritised.

A total of 202 studies were included in this review, with 58% pertaining to psychiatric comorbidities and 42% to medical comorbidities. For EDs in general, the most prevalent psychiatric comorbidities were anxiety (up to 62%), mood (up to 54%) and substance use and post-traumatic stress disorders (similar comorbidity rates up to 27%). The review also noted associations between specific EDs and non-suicidal self-injury, personality disorders, and neurodevelopmental disorders. EDs were complicated by medical comorbidities across the neuroendocrine, skeletal, nutritional, gastrointestinal, dental, and reproductive systems. Medical comorbidities can precede, occur alongside or emerge as a complication of the ED.

Conclusions

This review provides a thorough overview of the comorbid psychiatric and medical conditions co-occurring with EDs. High psychiatric and medical comorbidity rates were observed in people with EDs, with comorbidities contributing to increased ED symptom severity, maintenance of some ED behaviours, and poorer functioning as well as treatment outcomes. Early identification and management of psychiatric and medical comorbidities in people with an ED may improve response to treatment and overall outcomes.

Plain English Summary

The mortality rate of eating disorders is significantly elevated compared to other psychiatric conditions, primarily due to medical complications and suicide. Further, individuals with eating disorders often meet the diagnostic criteria of at least one comorbid psychiatric or medical disorder, that is, the individual simultaneously experiences both an ED and at least one other condition. This has significant consequences for researchers and health care providers – medical and psychiatric comorbidities impact ED symptoms and treatment effectiveness. The current review is part of a larger Rapid Review series conducted to inform the development of Australia’s National Eating Disorders Research and Translation Strategy 2021–2031. A Rapid Review is designed to comprehensively summarise a body of literature in a short timeframe, often to guide policymaking and address urgent health concerns. The Rapid Review synthesises the current evidence base and identifies gaps in eating disorder research and care. This paper gives a critical overview of the scientific literature relating to the psychiatric and medical comorbidities of eating disorders. It covers recent literature regarding psychiatric comorbidities including anxiety disorders, mood disorders, substance use disorders, trauma and personality disorders and neurodevelopmental disorders. Further, the review discusses the impact and associations between EDs and medical comorbidities, some of which precede the eating disorder, occur alongside, or as a consequence of the eating disorder.

Introduction

Eating Disorders (EDs) are often severe, complex, life-threatening illnesses with significant physiological and psychiatric impacts. EDs impact individuals across the entire lifespan, affecting all age groups (although most often they emerge in childhood and adolescence), genders, socioeconomic groups and cultures [ 1 ]. EDs have some of the highest mortality rates of all psychiatric illnesses and carry a significant personal, interpersonal, social and economic burdens [ 2 , 3 ].

Adding to the innate complexity of EDs, it is not uncommon for people living with an ED to experience associated problems such as psychological, social, and functional limitations [ 2 ] in addition to psychiatric and medical comorbidities [ 4 , 5 , 6 ]. Comorbidity is defined as conditions or illnesses that occur concurrently to the ED. Evidence suggests that between 55 and 95% of people diagnosed with an ED will also experience a comorbid psychiatric disorder in their lifetime [ 4 , 6 ]. Identifying psychiatric comorbidities is essential because of their potential impact on the severity of ED symptomatology, the individual’s distress and treatment effectiveness [ 7 , 8 ].

The mortality rate of EDs is significantly higher than the general population, with the highest occurring in Anorexia Nervosa (AN) due to impacts on the cardiovascular system [ 9 ] and suicide. [ 10 ] Mortality rates are also heightened in Bulimia Nervosa (BN) and Other Specified Feeding and Eating Disorder (OSFED) [ 11 ]. Suicide rates are elevated across the ED spectrum, and higher rates are observed in patients with a comorbid psychiatric disorder [ 10 , 12 ]. Of concern, the proportion of people with an ED not accessing treatment is estimated to be as high as 75% [ 13 ], potentially a consequence of comorbidities which impact on motivation, the ability to schedule appointments or require clinical prioritisation (i.e., self-harm or suicidal behaviours) [ 14 ]. Further, for many of those diagnosed with an ED who access treatment, recovery is a lengthy process. A longitudinal study found approximately two-thirds of participants with AN or BN had recovered by 22 years follow-up [ 15 ]. Although recovery occurred earlier for those with BN, illness duration was lengthy for both groups with quality of life and physical health impacts [ 15 ]. Further, less is known regarding the illness trajectory for those who do not receive treatment.

Medical comorbidities associated with EDs can range from mild to severe and life-threatening, with complications observed across all body systems, including the cardiac, metabolic and gastrointestinal, and reproductive systems [ 5 ]. These comorbidities and complications can place people at increased risk of medical instability and death [ 5 ]. Therefore, understanding how co-occurring medical comorbidities and complications impact EDs is critical to treatment and recovery.

In addition to ED-associated medical comorbidities, EDs often present alongside other psychiatric conditions. Psychiatric comorbidities in people with EDs are associated with higher health system costs, emergency department presentations and admissions [ 16 ]. Comorbidities may precede the onset of the ED, be co-occurring, or result from symptoms and behaviours associated with the ED [ 17 , 18 ]. Individuals with an ED, their carers and care providers often face a complex and important dilemma; the individual with an ED requires treatment for their ED but also for their psychiatric comorbidities, and it can be difficult for treatment providers to determine which is the clinical priority [ 19 ]. This is further complicated by the fact that EDs and comorbidities may have a reciprocal relationship, whereby the presence of one impact the pathology, treatment and outcomes of the other.

The current Rapid Review (RR) forms part of a series of reviews commissioned by the Australian Federal Government to inform the Australian National Eating Disorders Research and Translation Strategy 2021–2031 [ 20 ]. In response to the impact of psychiatric and medical comorbidities on outcomes, this rapid review summarises the recent literature on the nature and implications of psychiatric and medical comorbidities associated with EDs.

The Australian Government Commonwealth Department of Health funded the InsideOut Institute for Eating Disorders (IOI) to develop the Australian Eating Disorders Research and Translation Strategy 2021–2031 [ 20 ] under the Psych Services for Hard to Reach Groups initiative (ID 4-8MSSLE). The strategy was developed in partnership with state and national stakeholders including clinicians, service providers, researchers, and experts by lived experience (both consumers and families/carers). Developed through a two-year national consultation and collaboration process, the strategy provides the roadmap to establishing EDs as a national research priority and is the first disorder-specific strategy to be developed in consultation with the National Mental Health Commission. To inform the strategy, IOI commissioned Healthcare Management Advisors (HMA) to conduct a series of RRs to assess all available peer-reviewed literature on all DSM-5 listed EDs.

A RR Protocol [ 21 ] was utilised to allow swift synthesis of the evidence in order to guide public policy and decision-making [ 22 ]. This approach has been adopted by several leading health organisations including the World Health Organisation [ 17 ] and the Canadian Agency for Drugs and Technologies in Health Rapid Response Service [ 18 ], to build a strong evidence base in a timely and accelerated manner, without compromising quality. A RR is not designed to be as comprehensive as a systematic review—it is purposive rather than exhaustive and provides actionable evidence to guide health policy [ 23 ].

The RR is a narrative synthesis adhering to the PRISMA guidelines [ 24 ]. It is divided by topic area and presented as a series of papers. Three research databases were searched: ScienceDirect, PubMed and Ovid/Medline. To establish a broad understanding of the progress made in the field of EDs, and to capture the largest evidence base from the past 12 years (originally 2009–2019, but expanded to include the preceding two years), the eligibility criteria for included studies were kept broad. Therefore, included studies were published between 2009 and 2021, written in English, and conducted within Western healthcare systems or health systems comparable to Australia in terms of structure and resourcing. The initial search and review process was conducted by three reviewers between 5 December 2019 and 16 January 2020. The re-run for the years 2020–2021 was conducted by two reviewers at the end of May 2021.

The RR had a translational research focus with the objective of identifying evidence relevant to developing optimal care pathways. Searches therefore used a Population, Intervention, Comparison, Outcome (PICO) approach to identify literature relating to population impact, prevention and early intervention, treatment, and long-term outcomes. Purposive sampling focused on high-level evidence studies encompassing meta-analyses; systematic reviews; moderately sized randomised controlled studies (RCTs) (n > 50); moderately sized controlled-cohort studies (n > 50); and population studies (n > 500). However, the diagnoses ARFID and UFED necessitated less stringent eligibility criteria due to a paucity of published articles. As these diagnoses are newly captured in the DSM-5 (released in 2013, within the allocated search timeframe), the evidence base is still emerging, and few studies have been conducted. Thus, smaller studies (n =  ≤ 20) and narrative reviews were also considered and included. Grey literature, such as clinical or practice guidelines, protocol papers (without results) and Masters’ theses or dissertations, were excluded. Other sources (which may not be replicable when applying the current methodology) included the personal libraries of authors, yielding two additional studies (see Additional file 1 ). This extra step was conducted in line with the PRISMA-S: an extension to the PRISMA Statement for Reporting Literature Searches in Systematic Reviews [ 25 ].

Full methodological details including eligibility criteria, search strategy and terms and data analysis are published in a separate protocol paper, which included a total of 1320 studies [ 26 ] (see Additional file 1 : Fig. S1 for PRISMA flow diagram). Data from included studies relating to psychiatric and medical comorbidities of EDs were synthesised and are presented in the current review. No further analyses were conducted.

The search included articles published in the period January 2009 to May 2021. The RR identified 202 studies for inclusion. Of these, 58% related to psychiatric comorbidities (n = 117) and 42% to medical comorbidities (n = 85). A full list of the studies included in this review and information about population, aims and results can be found in Additional file 2 : Tables S3, S4. Results are subdivided into two categories: (1) psychiatric comorbidities and (2) medical complications. Tables 1 and 2 provide high-level summaries of the results.

Psychiatric comorbidities

The study of psychiatric comorbidities can assist with developing models of ED aetiology, conceptualising psychopathology and has relevance for treatment development and outcomes. Given that common psychological factors are observed across psychiatric disorders [ 87 ], it is not surprising that there are high prevalence rates of co-occurring psychiatric conditions with EDs. Comorbidity rates of EDs and other psychiatric conditions are elevated further in ethnic/racial minority groups [ 88 ]. When looking at the evidence from studies conducted with children and young people, one study of children with ARFID found that 53% of the population had a lifetime comorbid psychiatric disorder [ 89 ]. It emerged from the RR that research regarding psychiatric comorbidities generally focussed on the prevalence rates of comorbidities among certain ED subgroups, with some also exploring implications for treatment and ED psychopathology.

Anxiety disorders

Research indicates that EDs and anxiety disorders frequently co-occur [ 8 , 27 ]. The high prevalence rates of anxiety disorders in the general population are also observed in people with EDs; with a large population study finding anxiety disorders were the most frequently comorbid conditions reported [ 8 ]. In a study of women presenting for ED treatment, 65% also met the criteria for at least one comorbid anxiety disorder [ 28 ]. Of note, 69% of those endorsing the comorbidity also reported that the anxiety disorder preceded the onset of the ED [ 28 ]. Another study explored anxiety across individuals with an ED categorised by three weight ranges (individuals whose weight is in the ‘healthy weight’ range, individuals in the ‘overweight’ range and individuals in the ‘obese’ range). While anxiety was elevated across all groups, the authors did note that individuals in the overweight group reported significantly higher rates of anxiety than individuals within the healthy weight group [ 90 ]. One study that explored temperamental factors provided some insight into factors that may mediate this association; anxiety sensitivity (a predictor of anxiety disorders) was associated with greater ED severity among individuals in a residential ED treatment facility [ 29 ]. Further, this association was mediated by a tendency to engage in experiential avoidance—the authors noting that individuals with greater ED symptoms were more likely to avoid distressing experiences [ 29 ].

Generalised anxiety disorder (GAD)

Studies have noted the potential genetic links between EDs and GAD, noting that the presence of one significantly increases the likelihood of the other [ 8 , 30 ]. Further, there appears to be a relationship between the severity of ED behaviours and the co-occurrence of GAD, with comorbidity more likely when fasting and excessive exercise are present, as well as a lower BMI [ 30 ]. The authors noted the particularly pernicious comorbidity of EDs (specifically AN) and GAD may be amplified by the jointly anxiolytic and weight loss effects of food restriction and excessive exercise [ 30 ].

Social anxiety

A meta-analysis of 12 studies found higher rates of social anxiety across all ED diagnoses, with patients with BN demonstrating the highest rate of comorbidity at 84.5%, followed by both BED and AN-BP both at 75% [ 31 ]. High levels of social anxiety were also associated with more severe ED psychopathology [ 31 ] and higher body weight [ 91 ]. This particular comorbidity may also impact on access to treatment for the ED; a large follow-up study of adolescents found that self-reported social phobia predicted not seeking treatment for BN symptoms [ 32 ]. Interestingly, two studies noted that anxiety symptoms improved following psychological treatments that targeted ED symptoms, possibly due to a shared symptom profile [ 29 , 31 ].

Obsessive–compulsive disorder

Similarities between the symptoms of Obsessive–Compulsive Disorder (OCD) and EDs, such as cognitive rigidity, obsessiveness, detail focus, perfectionism and compulsive routines have long been reported in the literature [ 34 ]. Given the symptom overlap, a meta-analysis sought to clarify the lifetime and current (that is, a current diagnosis at the time of data collection) comorbidity rates of OCD and EDs, noting the lifetime comorbidity rate was 18% and current comorbidity rate was 15% [ 33 ]. However, the authors noted that this prevalence may double over longer periods of observation, with some follow-up data demonstrating comorbidity rates of 33% [ 33 ]. Prevalence rates of OCD seemed to be highest among people with AN (lifetime = 19% and current = 14%) compared to other ED subtypes. In addition to the symptom crossover, this RR found evidence of a complex relationship between OCD and EDs, including a potential association between OCD and greater ED severity [ 34 ].

Network analysis found that doubts about simple everyday things and repeating things over and over bridged between ED and OCD symptoms. Further, a pathway was observed between restricting and checking compulsions and food rigidity as well as binge eating and hoarding. However, as the data was cross-sectional, directional inferences could not be made [ 36 ]. An earlier study explored how changes in OCD symptoms impact ED symptoms among an inpatient sample [ 35 ]. As was hypothesised, decreases in OCD symptoms accounted for significant variance in decreases in ED symptoms, and this effect was strongest among ED patients with comorbid OCD. The study also found that irrespective of whether patients had comorbid OCD or not, when ED symptoms improved, so did symptoms of OCD [ 35 ]. The authors concluded that perhaps there is a reciprocal relationship between OCD and ED symptoms, whereby symptoms of both conditions interact in a synergistic, bidirectional manner, meaning that improvement in one domain can lead to improvement in another [ 35 ]. These findings were somewhat supported in a study by Simpson and colleagues (2013), which found exposure and response prevention (a specialised OCD treatment) resulted in a significant reduction in OCD severity, as was expected, and an improvement in ED symptoms. In their study, individuals with BN showed more improvement than those with AN–nevertheless, BMI still increased among those underweight [ 92 ].

Mood disorders

Depression and major depressive disorder (mdd).

This RR also found high levels of comorbidity between major depression and EDs. A longitudinal study of disordered eating behaviours among adolescents found that disordered eating behaviours and depressive symptoms developed concurrently [ 37 ]. Among the sample, over half the adolescent sample had a depressive disorder. Prevalence rates were similar for AN (51.5%) and BN (54%) [ 37 ]. The study also explored the neurological predictors of comorbid depression in individuals with EDs, noting that lower grey matter volumes in the medial orbitofrontal, dorsomedial, and dorsolateral prefrontal cortices predicted the concurrent development of purging and depressive symptoms [ 37 ]. The results suggested that alterations in frontal brain circuits were part of a neural aetiology common to EDs and depression [ 37 ].

This RR found much support for a strong relationship between depression and ED symptomatology. In a study of patients with AN, comorbid MDD was associated with a greater AN symptom severity [ 93 ], and this relationship between the symptoms of MDD and AN was bidirectional in a study of adolescents undergoing treatment for AN, whereby dietary restraint predicted increased guilt and hostility (symptoms of low mood) and fear predicted further food restriction [ 94 ]. Further studies noted the association between BN, BED and NES, with a higher prevalence of depression and more significant depression symptoms [ 95 , 96 , 97 ]. However, other studies have failed to find support for this association–for example, a Swedish twin study found no association between NES and other mental health disorders [ 98 ].

The impact of the relationship between depression and EDs on treatment outcomes was variable across the studies identified by the RR. One study noted the impact of depression on attrition; patients with BN and comorbid depression attending a university clinic had the highest rates of treatment drop-out [ 99 ]. However, in a sample of patients with AN, the comorbidity of depression (or lack of) did not impact treatment outcome and the severity of depression was not associated with changes in ED symptoms [ 100 ]. This finding was supported in another study of inpatients with AN; pre-treatment depression level did not predict treatment outcome or BMI [ 101 ].

Bipolar disorders

Notable comorbidity rates between bipolar disorders (BD) and EDs were reported in the literature reviewed, however evidence about the frequency of this association was mixed. Studies noted comorbidity rates of BD and EDs ranging between 1.9% to as high as 35.8% [ 38 , 39 , 40 ]. In order to better understand the nature of comorbidity, a recent systematic review and meta-analysis found BD (including bipolar 1 disorder and bipolar 2 disorder) and ED comorbidity varied across different ED diagnostic groups (BED—12.5%, BN—7.4%, AN—3.8%) [ 102 ]. However, the authors noted the scant longitudinal studies available, particularly in paediatric samples. An analysis of comorbidity within a sample of patients with BD identified that 27% of participants also met criteria for an ED; 15% had BN, 12% had BED, and 0.2% had AN [ 103 ]. Two other studies noted considerable comorbidity rates of BD; 18.6% for binge eating [ 104 ] and 8.8% for NES [ 105 ]. Some studies suggested the co-occurrence of BD and EDs were seen most in people with AN-BP, BN and BED—all of which share a binge and/or purge symptom profile [ 38 , 106 ]. Specifically, BED and BN were the most common co-occurring EDs with BD [ 40 ], however, these EDs are also the most prevalent in the population. Therefore, it is unclear if this finding is reflective of the increased prevalence of BN and BED, or if it reflects a shared underlying psychopathology between BD and these EDs [ 40 ].

Comorbid ED-BD patients appear to experience increased ED symptom severity, poorer daily and neuropsychological functioning than patients with only a ED or BD diagnosis [ 107 ]. In an effort to understand which shared features in ED-BD relate to quality of life, one study assessed an adult sample with BD [ 108 ]. Binge eating, restriction, overevaluation of weight and shape, purging and driven exercise were associated with poorer clinical outcomes, quality of life and mood regulation [ 108 ]. Additionally, a study of patients undergoing treatment for BD noted patients with a comorbid ED had significantly poorer clinical outcomes and higher scores of depression [ 109 ]. Further, quality of life was significantly lower among patients with comorbid ED-BD [ 109 ]. The comorbidity of ED and BD has implications for intervention and clinical management, as at least one study observed higher rates of alcohol abuse and suicidality among patients with comorbid ED and BD compared to those with BD only [ 40 ].

Personality disorders

This RR identified limited research regarding the comorbidity between personality disorders (PD) and EDs. A meta-analysis sought to summarise the proportion of comorbid PDs among patients with AN and BN [ 41 ]. There was a heightened association between any type of ED and PDs, and this was significantly different to the general population. For specific PDs, the proportions of paranoid, borderline, avoidant, dependant and obsessive–compulsive PD were significantly higher in EDs than in the general population. For both AN and BN, Cluster C PDs (avoidant, dependant and obsessive–compulsive) were most frequent. The authors noted that the specific comorbidity between specific EDs and PDs appears to be associated with common traits—constriction/perfectionism and rigidity is present in both AN and obsessive–compulsive PD (which had a heightened association), as was the case with impulsivity, a characteristic of both BN and borderline PD [ 41 ]. This symptom association was also observed in a study of adolescents admitted to an ED inpatient unit whereby a significant interaction between binge-purge EDs (AN-BP and BN), childhood emotional abuse (a risk factor for PD) and borderline personality style was found [ 110 ].

This comorbidity may be associated with greater patient distress and have implications for patient outcomes [ 41 , 42 ]. Data from a nine-year observational study of individuals with BN reported that comorbidity with a PD was strongly associated with elevated mortality risk [ 111 ]. In terms of treatment outcomes, an RCT compared the one- and three-year treatment outcomes of four subgroups of women with BN, defined by PD complexity; no comorbid PD (health control), personality difficulties, simple PD and complex PD [ 112 ]. At pre-treatment, the complex PD group had greater ED psychopathology than the other three groups. Despite this initial difference, there were no differences in outcomes between groups at one-year and three-year follow up [ 112 ]. The authors suggested this result could be due to the targeting of the shared symptoms of BN and PD by the intervention delivered in this study, and that as ED symptoms improve, so do PD symptoms [ 112 ]. Suggesting that beyond symptom overlap, perhaps some symptoms attributed to the PD are better explained by the ED. This was consistent with Brietzke and colleagues’ (2011) recommendation that for individuals with ED and a comorbid PD, treatment approaches should target both conditions where possible [ 113 ].

Substance use disorders

Comorbid substance use disorders (SUDs) are also often noted in the literature as an issue that complicates treatment and outcomes of EDs [ 114 ]. A meta-analysis reported the lifetime prevalence of EDs and comorbid SUD was 27.9%, [ 43 ] with a lifetime prevalence of comorbid illicit drug use of 17.2% for AN and 18.6% for BN [ 115 ]. Alcohol, caffeine and tobacco were the most frequently reported comorbidities [ 43 ]. Further analysis of SUDs by substance type in a population-based twin sample indicated that the lifetime prevalence of an alcohol use disorder among individuals with AN was 22.4% [ 115 ]. For BN, the prevalence rate was slightly higher at 24.0% [ 115 ].

The comorbidity of SUD is considered far more common among individuals with binge/purge type EDs, evidenced by a meta-analysis finding higher rates of comorbid SUD among patients with AN-BP and BN than AN-R [ 44 ]. This trend was also observed in population data [ 116 ]. Further, a multi-site study found that patients with BN had higher rates of comorbid SUD than patients with AN, BED and Eating Disorder Not Otherwise Specific (EDNOS) (utilised DSM-IV criteria) [ 117 ]. Behaviourally, there was an association between higher frequencies of binge/purge behaviours with high rates of substance use [ 117 ]. The higher risk of substance abuse among patients with binge/purge symptomology was also associated with younger age of binge eating onset [ 118 ]. A study explored whether BN and ED subtypes with binge/purge symptoms predicted adverse outcomes and found that adolescent girls with purging disorder were significantly more likely to use drugs or frequently binge drink [ 119 ]. This association was again observed in a network analysis of college students, whereby there was an association between binge drinking and increased ED cognitions [ 120 ].

Psychosis and schizophrenia

The RR identified a small body of literature with mixed results regarding the comorbidity of ED and psychosis-spectrum symptoms. A study of patients with schizophrenia found that 12% of participants met full diagnostic criteria for NES, with a further 10% meeting partial criteria [ 45 ]. Miotto and colleagues’ (2010) study noted higher rates of paranoid ideation and psychotic symptoms in ED patients than those observed in healthy controls [ 121 ]. However, the authors concluded that these symptoms were better explained by the participant's ED diagnosis than a psychotic disorder [ 121 ]. At a large population level, an English national survey noted associations between psychotic-like experiences and uncontrolled eating, food dominance and potential EDs [ 122 ]. In particular, these associations were stronger in males [ 122 ]. However, the true comorbidity between psychotic disorders and ED remains unclear and further research is needed.

Body dysmorphic disorder

While body image disturbances common to AN, BN and BED are primarily related to weight and shape concerns, individuals with body dysmorphic disorder (BDD) have additional concerns regarding other aspects of their appearance, such as facial features and skin blemishes [ 46 , 123 ]. AN and BDD share similar psychopathology and both have a peak onset period in adolescence, although BDD development typically precedes AN [ 46 ]. The prevalence rates of BDD among individuals with AN are variable. In one clinical sample of female AN patients, 26% met BDD diagnostic criteria [ 124 ]. However, much higher rates were observed in another clinical sample of adults with AN, where 62% of patients reported clinically significant 'dysmorphic concern' [ 125 ].

As the RR has found with other mental health comorbidities, BDD contributes to greater symptom severity in individuals with AN, making the disorder more difficult to treat. However, some research suggested that improved long-term outcomes from treatments for AN are associated with the integration of strategies that address dysmorphic concerns [ 124 , 126 ]. However, there remains little research on the similarities, differences and co-occurrence of BDD and AN, and with even less research on the cooccurrence of BDD and other EDs.

Neurodevelopmental disorders

Attention deficit hyperactivity disorder

Several studies noted the comorbidity between Attention Deficit Hyperactivity Disorder (ADHD) and EDs. A systematic review found moderate evidence for a positive association between ADHD and disordered eating, particularly between overeating and ADHD [ 47 ]. The impulsivity symptoms of ADHD were particularly associated with BN for all genders, and weaker evidence was found for the association between hyperactivity and restrictive EDs (AN and ARFID) for males, but not females [ 47 ]. Another meta-analysis reported a two-fold increased risk of ADHD in individuals with an ED [ 48 ] and studies have noted particularly strong associations between ADHD and BN [ 49 , 50 ]. In a cohort of adults with a diagnosis of an ED, 31.3% had a 'possible' ADHD [ 127 ]. Another study considered sex differences; women with ADHD had a significantly higher lifetime prevalence of both AN and BN than women without ADHD [ 128 ]. Further, the comorbidity rates for BED were considerably higher among individuals with ADHD for both genders [ 128 ].

Further evidence for a significant association between ADHD and EDs was reported in a population study of children [ 51 ]. Results revealed that children with ADHD were more like to experience an ED or binge, purge, or restrictive behaviours above clinical threshold [ 51 ]. Another study of children with ADHD considered gender differences; boys with ADHD had a greater risk of binge eating than girls [ 129 ]. However, the study found no significant difference in AN's prevalence between ADHD and non-ADHD groups. Further, among patients attending an ED specialist clinic, those with comorbid ADHD symptoms had poorer outcomes at one-year follow-up [ 130 ].

Autism spectrum disorder

There is evidence of heightened prevalence rates of autism spectrum disorder (ASD) among individuals with EDs. A systematic review found an average prevalence of ASD with EDs of 22.9% compared with 2% observed in the general population [ 52 ]. With regards to AN, several studies have found symptoms of ASD to be frequently exhibited by patients with AN [ 53 , 54 ]. An assessment of common phenomena between ARFID and ASD in children found a shared symptom profile of eating difficulties, behavioural problems and sensory hypersensitivity beyond what is observed in typically developing children (the control group) [ 55 ]. While research in this area is developing, the findings indicated these comorbidities would likely have implications for the treatment and management of both conditions [ 55 ].

Post traumatic stress disorder

Many individuals with EDs report historical traumatic experiences, and for a proportion of the population, symptoms of post traumatic stress disorder (PTSD). A broad range of prevalence rates between PTSD and EDs have been reported; between 16.1–22.7% for AN, 32.4–66.2% for BN and 24.02–31.6% for BED [ 56 ]. A review noted self-criticism, low self-worth, guilt, shame, depression, anxiety, emotion dysregulation, anger and impulsivity were linked to the association between EDs and trauma [ 57 ]. It was suggested that for individuals with trauma/PTSD, EDs might have a functional role to manage PTSD symptoms and reduce negative affect [ 57 ]. Further, some ED behaviours such as restriction, binge eating, and purging may be used to avoid hyperarousal, in turn maintaining the association between EDs and PTSD [ 57 ].

Few studies have explored the impact of comorbid PTSD on ED treatment outcomes. A study of inpatients admitted to a residential ED treatment service investigated whether PTSD diagnosis at admission was associated with symptom changes [ 56 ]. Cognitive and behavioural symptoms related to the ED had decreased at discharge, however, they increased again at six-month follow up. In contrast, while PTSD diagnosis was associated with higher baseline ED symptoms, it was not related to symptom change throughout treatment or treatment dropout [ 56 ]. Given previous research identified that PTSD and EDs tend to relate to more complex courses of illness, greater rates of drop out and poorer outcomes, a study by Brewerton and colleagues [ 131 ], explored the presence of EDs in patients with PTSD admitted to a residential setting. Results showed that patients with PTSD had significantly higher scores of ED psychopathology, as well as depression, anxiety and quality of life. [ 131 ]. Further, those with PTSD had a greater tendency for binge-type EDs.

Suicidality

Suicide is one of the leading causes of death for individuals with EDs [ 58 ]. In a longitudinal study of adolescents, almost one quarter had attempted suicide, and 65% reported suicidal ideation within the past 6 months [ 37 ]. EDs are a significant risk factor for suicide, with some evidence suggesting a genetic association between suicide risk and EDs [ 59 , 60 ]. This association was supported in the analysis of Swedish population registry data, which found that individuals with a sibling with an ED had an increased risk of suicide attempts with an odds ratio of 1.4 (relative cohort n  = 1,680,658) [ 61 ]. For suicide attempts, this study found an even higher odds ratio of 5.28 (relative cohort n  = 2,268,786) for individuals with an ED and 5.39 (relative cohort n  = 1,919,114) for death by suicide [ 61 ]. A comparison of individuals with AN and BN indicated that risk for suicide attempts was higher for those with BN compared to AN [ 61 ]. However, the opposite was true for death by suicide; which was higher in AN compared to BN [ 61 ]. This result is consistent with the findings of a meta-analysis—the incidence of suicide was higher among patients with AN compared to those with BN or BED [ 62 ].

The higher incidence of suicide in adults with AN [ 132 ] is potentially explained by the findings from Guillaume and colleagues (2011), which suggested that comparative to BN, AN patients are more likely to have more serious suicide attempts resulting in a higher risk of death [ 133 ]. However, death by suicide remains a significant risk for both diagnoses. As an example, Udo and colleagues (2019) study reported that suicide attempts were more common in those with an AN-BP subtype (44.1%) than AN-R (15.7%), or BN (31.4%) [ 134 ]. Further, in a large cohort of transgender college students with EDs, rates of past-year suicidal ideation (a significant risk factor for suicide attempts) was 75.2%, and suicide attempts were 74.8%, significantly higher than cisgender students with EDs and transgender students without EDs [ 135 ]. The RR found that the risk of suicidal ideation and behaviour was associated with ED diagnosis and the presence of other comorbidities. Among a community-based sample of female college students diagnosed with an ED, 25.6% reported suicidal ideation, and this was positively correlated with depression, anxiety and purging [ 136 ]. In support of this evidence, Sagiv and Gvion (2020) proposed a dual pathway model of risk of suicide attempt in individuals with ED, which implicates trait impulsivity and comorbid depression [ 137 ]. In two large transdiagnostic ED patient samples, suicidal ideation was associated with different aspects of self-image between ED diagnoses. For example, suicidal ideation was associated with higher levels of self-blame among individuals with BED, while among patients with AN and OSFED, increased suicidal ideation was associated with a lack of self-love [ 138 , 139 ].

Anorexia nervosa

Amongst adults with AN, higher rates of suicide have been reported amongst those with a binge-purge subtype (25%) than restrictive subtype (8.65%) [ 58 , 140 ]. Further, comorbid depression and prolonged starvation were strongly associated with elevated suicide attempts for both subtypes [ 58 , 140 ]. In another study, the risk of attempted suicide was associated with depression, but it was moderated by hospital treatment [ 93 ]. Further, suicidal ideation was related to depression. A significant 'acquired' suicide risk in individuals with AN has been identified by Selby et al. (2010) through an increased tolerance for pain and discomfort resultant from repeated exposure to painful restricting and purging behaviours [ 141 ].

Bulimia nervosa

Further research among individuals diagnosed with BN found an increased level of suicide risk [ 142 ]. Results from an extensive study of women with BN indicated that the lifetime prevalence of suicide attempts in this cohort was 26.9% [ 143 ]. In one study of individuals diagnosed with severe BN, 60% of deaths were attributed to suicide [ 144 ]. The mean age at the time of death was 29.6 years, and predictive factors included previous suicide attempts and low BMI. Further, in a sample of children and adolescents aged 7 to 18 years, higher rates of suicidal ideation were associated with BN, self-induced vomiting and a history of trauma [ 12 ].

A large population-based study of adolescents and adults explored the frequency and correlates of suicidal ideation and attempts in those who met the criteria for BN [ 145 ]. Suicidal ideation was highest in adolescents with BN (53%), followed by BED (34.4%), other non-ED psychopathology (21.3%) or no psychopathology (3.8%). A similar trend was observed for suicide plans and attempts [ 145 ]. However, for adults, suicidality was more prevalent in the BN group compared to no psychopathology, but not statistically different to the AN, BED or other psychopathology groups [ 145 ].

Consistent with Crow and colleagues’ (2014) results, in a sample of women with BN, depression had the strongest association with lifetime suicide attempts [ 146 ]. There were also associations between identity problems, cognitive dysregulation, anxiousness, insecure attachment and lifetime suicide attempts among the sample. Depression was the most pertinent association, suggesting that potential comorbid depression should be a focus of assessment and treatment among individuals with BN due to the elevated suicide risk for this group [ 146 ]. Insecure attachment is associated with childhood trauma, and a systematic review found that suicide attempts in women with BN were significantly associated with childhood abuse and familial history of EDs [ 58 ].

Binge eating disorder

The RR found mixed evidence for the association between suicidal behaviour and BED. A meta-analysis found no suicides for patients with BED [ 62 ]. However, evidence from two separate large national surveys found that a significant proportion of individuals who had a suicide attempt also had a diagnosis of BED [ 134 , 147 ].

Non-suicidal self injury

Non-suicidal self-injury (NSSI), broadly defined, is the intentional harm inflicted to one’s body without intent to die [ 148 ]. Recognising NSSI is often a precursor for suicidal ideation and behaviour [ 149 ], together with the already heightened mortality rate for EDs, several studies have examined the association between EDs and NSSI. Up to one-third of patients with EDs report NSSI at some stage in their lifetime, with over one quarter having engaged in NSSI within the previous year [ 63 ]. Similarly, a cohort study [ 148 ] found elevated rates of historical NSSI amongst patients with DSM-IV EDs; specifically EDNOS (49%), BN (41%) and AN (26%). In a Spanish sample of ED patients, the most prevalent form of NSSI was banging (64.6%) and cutting (56.9%) [ 63 ].

Further research has explored the individual factors associated with heightened rates of NSSI. Higher levels of impulsivity among patients with EDs have been associated with concomitant NSSI [ 64 ]. This was demonstrated in a longitudinal study of female students, whereby NSSI preceded purging, marking it a potential risk factor for ED onset [ 65 ]. In a study of a large clinical sample of patients with EDs and co-occurring NSSI, significantly higher levels of emotional reactivity were observed [ 150 ]. The highest levels of emotional reactivity were reported by individuals with a diagnosis of BN, who were also more likely to engage in NSSI than those with AN [ 150 ]. In Olatunji and colleagues’ (2015) cohort study, NSSI was used to regulate difficult emotions, much like other ED behaviours. NSSI functioning as a means to manage negative affect associated with EDs was further supported by Muehlenkamp and colleagues’ [ 66 ] study exploring the risk factors in inpatients admitted for an ED. The authors found significant differences in the prevalence of NSSI across ED diagnoses, although patients with binge/purge subtype EDs were more likely to engage in poly-NSSI (multiple types of NSSI). Consistent with these findings, a study of patients admitted to an ED inpatient unit found that 45% of patients displayed at least one type of NSSI [ 151 ]. The function of NSSI among ED patients was explored in two studies, one noting that avoiding or suppressing negative feelings was the most frequently reported reason for NSSI [ 151 ]. The other analysed a series of interviews and self-report questionnaires and found patients with ED and comorbid Borderline Personality Disorder (BPD) engaged in NSSI as a means of emotion regulation [ 152 ].

Medical comorbidities

The impact of EDs on physical health and the consequential medical comorbidities has been a focus of research. Many studies reported medical comorbidities resulting from prolonged malnutrition, as well as excessive exercise, binging and purging behaviours.

Cardiovascular complications

As discussed above, although suicide is a significant contributor to the mortality rate of EDs, physical and medical complications remain the primary cause of death, particularly in AN, with a high proportion of deaths thought to result from cardiovascular complications [ 153 ]. AN has attracted the most research focus given its increased risk of cardiac failure due to severe malnutrition, dehydration and electrolyte imbalances [ 67 ].

Cardiovascular complications in AN can be divided by conduction, structural and ischemic diseases. A review found that up to 87% of patients experience cardiovascular compromise shortly following onset of AN [ 153 ]. Within conduction disease, bradycardia and QT prolongation occur at a high frequency, largely due to low body weight and resultant decreased venous return to the heart. Whereas, atrioventricular block and ventricular arrhythmia are more rare [ 153 ]. Various structural cardiomyopathies are observed in AN, such as low left ventricular mass index (occurs frequently), mitral prolapse and percardial effusion (occurs moderately). Ischemic diseases such as dyslipidemia or acute myocardial infarction are more rare.

Another review identified cardiopulmonary abnormalities that are frequently observed in AN; mitral valve prolapse occurred in 25% of patients, sinus bradycardia was the most common arrhythmia, and pericardial effusion prevalence rates ranged from 15 to 30%. [ 68 ] Sudden cardiac death is thought to occur due to increased QT interval dispersion and heart rate variability. [ 68 ] A review of an inpatient database in a large retrospective cohort study found that coronary artery disease (CAD) was lower in AN patients than the general population (4.4% and 18.4%, respectively). Consistent with trends in the general population, the risk of cardiac arrest, arrhythmias and heart failure was higher in males with AN than females with AN [ 69 ].

Given that individuals with AN have compromised biology, may avoid medical care, and have higher rates of substance use, research has examined cancer incidence and prognosis among individuals with AN. A retrospective study noted higher mortality from melanoma, cancers of genital organs and cancers of unspecified sites among individuals with AN, however, there was no statistically significant difference compared to the general population [ 70 ]. No further studies of cancer in EDs were identified.

Gastrointestinal disorders

The gastrointestinal (GI) system plays a pivotal role in the development, maintenance, and treatment outcomes for EDs, with changes and implications present throughout the GI tract. More than 90% of AN patients report fullness, early satiety, abdominal distention, pain and nausea [ 68 ]. Although it is well understood that GI system complaints are complicated and exacerbated by malnutrition, purging and binge eating [ 154 , 155 ], the actual cause of the increased prevalence of GI disorders and their contribution to ED maintenance remain poorly understood.

To this end, a review aimed to determine the GI symptoms reported in two restrictive disorders (AN and ARFID), as well as the physiologic changes as a result of malnutrition and function of low body weight and the contribution of GI diseases to the disordered eating observed in AN and ARFID [ 156 ]. The review found mixed evidence regarding whether GI issues were increased in patients with AN and ARFID. This was partly due to the relatively limited amount of research in this area and mixed results across the literature. The review noted that patients with AN and ARFID reported a higher frequency of symptoms of gastroparesis. Further, there was evidence for a bidirectional relationship between AN and functional gastrointestinal disorders (FGIDs) contributing to ongoing disordered eating. The review found that GI symptoms observed in EDs develop due to (1) poorly treated medical conditions with GI-predominant symptoms, (2) the physiological and anatomical changes that develop due to malnutrition or (3) FGIDs.

There was a high rate of comorbidity (93%) between ED and FGIDs, including oesophageal, bowel and anorectal disorders, in a patient sample with AN, BN and EDNOS [ 157 ]. A retrospective study investigating increased rates of oesophageal cancer in individuals with a history of EDs could not conclude that risk was associated with purging over other confounding factors such as alcohol abuse and smoking [ 158 ].

Given that gut peptides like ghrelin, cholecystokinin (CCK), peptide tyrosine (PYY) and glucagon-like peptide 1 (GLP-1) are known to influence food intake, attention has focussed on the dysregulation of gut peptide signalling in EDs [ 159 ]. A review aimed to discuss how these peptides or the signals triggered by their release are dysregulated in EDs and whether they are normalised following weight restoration or weight loss (in the case of people with higher body weight) [ 159 ]. The results were inconsistent, with significant variability in peptide dysregulation observed across EDs [ 159 ]. A systematic review and meta-analysis explored whether ghrelin is increased in restrictive AN. The review found that all forms of ghrelin were raised in AN’s acute state during fasting [ 160 ]. In addition, the data did not support differences in ghrelin levels between AN subtypes [ 160 ]. Another study examined levels of orexigenic ghrelin and anorexigenic peptide YY (PYY) in young females with ARFID, AN and healthy controls (HC) [ 161 ]. Results demonstrated that fasting and postprandial ghrelin were lower in ARFID than AN, but there was no difference between ARFID and AN for fasting and postprandial PYY [ 161 ].

Oesophageal and gastrointestinal dysfunction have been observed in patients with AN and complicate nutritional and refeeding interventions [ 155 ]. Findings from a systematic review indicated that structural changes that occurred in the GI tract of patients with AN impacted their ability to swallow and absorb nutrients [ 162 ]. Interestingly, no differences in the severity of gastrointestinal symptoms were observed between AN-R and AN-BP subtypes [ 155 ].

A systematic review of thirteen studies aimed to identify the most effective treatment approaches for GI disorders and AN [ 163 ]. An improvement in at least one or more GI symptoms was reported in 11 of the 13 studies, with all studies including nutritional rehabilitation, and half also included concurrent psychological treatment [ 163 ]. Emerging evidence on ED comorbidity with chronic GI disorders suggested that EDs are often misdiagnosed in children and adolescents due to the crossover of symptoms. Therefore, clinicians treating children and adolescents for GI dysfunction should be aware of potential EDs and conduct appropriate screening [ 164 ]. There has been an emerging focus on the role of the gut microbiome in the regulation of core ED symptoms and psychophysiology. Increased attention is being paid to how the macronutrient composition of nutritional rehabilitation should be considered to maximise treatment outcomes. A review found that high fibre consumption in addition to prebiotic and probiotic supplementation helped balance the gut microbiome and maintained the results of refeeding [ 165 ].

Bone health

The RR found evidence for bone loss/poor bone mineral density (BMD) and EDs, particularly in AN. The high rates of bone resorption observed in patients with AN is a consequence of chronic malnutrition leading to osteoporosis (weak and brittle bones), increased fracture risk and scoliosis [ 166 ]. The negative impacts of bone loss are more pronounced in individuals with early-onset AN when the skeleton is still developing [ 67 ] and among those who have very low BMI [ 71 ], with comorbidity rates as high as 46.9% [ 71 ]. However, lowered BMD was also observed among patients with BN [ 72 ].

A review [ 167 ] explored the prevalence and differences in pathophysiology of osteoporosis and fractures in patients with AN-R and AN-BP. AN-R patients had a higher prevalence of osteoporosis, and AN-BP patients had a higher prevalence of osteopenia (loss of BMD) [ 167 ]. Further, the authors noted the significant increase in fracture risk that starts at disease onset and lasts throughout AN, with some evidence that risk remains increased beyond remission and recovery [ 167 ]. Findings from a longitudinal study of female patients with a history of adolescent AN found long-term bone thinning at five and ten-year follow-up despite these patients achieving weight restoration [ 168 ].

Given this, treatment to increase BMD in individuals with AN has been the objective of many pharmacotherapy trials, mainly investigating the efficacy of hormone replacement [ 169 , 170 ]. Treatments include oestrogen and oral contraceptives [ 169 , 170 , 171 , 172 ]; bisphosphonates [ 169 , 173 ]; other hormonal treatment [ 174 , 175 , 176 , 177 ] and vitamin D [ 178 ]. However, the outcomes of these studies were mixed.

Refeeding syndrome

Nutritional rehabilitation of severely malnourished individuals is central to routine care and medical stabilisation of patients with EDs [ 179 ]. Within inpatient treatment settings, reversing severe malnutrition is achieved using oral, or nasogastric tube feeding. However, following a period of starvation, initiating/commencing feeding has been associated with ‘refeeding syndrome’ (RFS), a potentially fatal electrolyte imbalance caused by the body's response to introducing nutritional restoration [ 180 , 181 ]. The studies identified in the RR focused predominantly on restrictive EDs/on this population group—results regarding RFS risk were mixed [ 73 ].

A retrospective cohort study of inpatients diagnosed with AN with a very low BMI implemented a nasogastric feeding routine with vitamin, potassium and phosphate supplementation [ 182 ]. All patients achieved a significant increase in body weight. None developed RFS [ 182 ], suggesting that even with extreme undernutrition, cautious feeding within a specialised unit can be done safely without RFS. For adults with AN, aminotransferases are often high upon admission, however are normalised following four weeks of enteral feeding [ 183 , 184 ]. Further, the RR identified several studies demonstrating the provision of a higher caloric diet at intake to adolescents with AN led to faster recoveries and fewer days in the hospital with no observed increased risk for RFS [ 75 , 76 , 77 ]. These findings were also noted in a study of adults with AN [ 179 ].

However, the prevalence of RFS among inpatients is highly variable, with one systematic review noting rates ranging from 0 to 62% [ 74 ]. This variability was largely a reflection of the different definitions of RFS used across the literature [ 74 ]. A retrospective review of medical records of patients with AN admitted to Intensive Care Units (ICUs) aimed to evaluate complications, particularly RFS, that occurred during the ICU stay and the impact of these complications on treatment outcomes [ 185 ]. Of the 68 patients (62 female), seven developed RFS (10.3%) [ 185 ].

Although easily detectable and treatable, hypophosphatemia (a low serum phosphate concentration) may lead to RFS which is the term used to describe severe fluid and electrolyte shifts that can occur when nutrition support is introduced after a period of starvation. Untreated hypophosphatemia may lead to characteristic signs of the RFS such as respiratory failure, heart failure, and seizures [ 76 , 179 , 186 , 187 , 188 ]. A retrospective case–control study of inpatients with severe AN identified [ 189 ]. A retrospective study of AN and atypical AN patients undergoing refeeding found that the risk of hypophosphatemia was associated with a higher level of total weight loss and recent weight loss rather than the patient’s weight at admission [ 190 ]. The safe and effective use of prophylactic phosphate supplementation during refeeding was supported by the results from Agostino and colleagues’ chart review study [ 191 ], where 90% of inpatients received supplementation during admission.

Higher calorie refeeding approaches are considered safe in most cases, however the steps necessitated to monitor health status are costly to health services [ 192 ]. The most cost-effective approach would likely involve prophylactic electrolyte supplementation in addition to high calorie refeeding, which would decrease the need for daily laboratory monitoring as well as shortening hospital stays [ 75 , 191 , 192 ]. A systematic review noted that much of the research regarding refeeding, particularly in children and young people, has been limited by small sample sizes, single-site studies and heterogeneous designs [ 181 ]. Further, the differing definitions of RFS, recovery, remission and outcomes leading to variable results. While RFS appears safe for many people requiring feeding, the risk and benefits of it are unclear [ 193 ] due to the limited research on this topic. Following current clinical practice guidelines on the safe introduction of nutrition is recommended.

Metabolic syndrome

Metabolic syndrome refers to a group of factors that increase risks for heart disease, diabetes, stroke and other related conditions [ 194 ]. Metabolic syndrome is conceptualised as five key criteria; (1) elevated waist circumference, (2) elevated triglyceride levels, (3) reduced HDL-C, (4) elevated blood pressure and (5) elevated fasting glucose. The binge eating behaviours exhibited in BN, BED and NES have been linked to the higher rates of metabolic syndrome observed in these ED patients [ 78 , 195 ].

An analysis of population data of medical comorbidities with BED noted the strongest associations were with diabetes and circulatory systems, likely indexing components of metabolic syndrome [ 196 ]. While type 1 diabetes is considered a risk factor for ED development, both BN and BED have increased risk for type 2 diabetes [ 78 ]. A 16-year observation study found that the risk of type 2 diabetes was significantly increased in male patients with BED compared to the community controls [ 78 ]. By the end of the observation period, 33% of patients with BED had developed type 2 diabetes compared to 1.7% of the control group. The prevalence of type 2 diabetes among patients with BN was also slightly elevated at 4.4% [ 78 ]. Importantly, the authors were not able to control for BMI in this study. In another study, BED was the most prevalent ED in a cohort of type 2 diabetes patients [ 197 ]. Conversely, the prevalence of AN among patients with type 2 diabetes is significantly lower, with a review of national data reporting comorbidity rates to be 0.06% [ 198 ].

Metabolic dysfunction was observed in a relatively large sample of individuals with NES, including metabolic syndrome and type 2 diabetes, with women reporting slightly higher rates (13%) than men (11%) [ 199 ]. In another group of adults with type 2 diabetes, 7% met the diagnostic criteria for NES [ 200 ]. These findings suggested a need for increased monitoring and treatment of type 2 diabetes in individuals with EDs, particularly BED and NES. Another study found BED had a significant impact on metabolic abnormalities, including elevated cholesterol and poor glycaemic control [ 201 ].

The RR identified one intervention study, which examined an intervention to address medical comorbidities associated with BN and BED [ 195 ]. The study compared cognitive behaviour therapy (CBT) to an exercise and nutrition intervention to increase physical fitness, decrease body fat percentage and reduce the risk for metabolic syndrome. While the exercise intervention improved participants' physical fitness and body composition, neither group reduced cardiovascular risk at one-year follow-up [ 195 ].

Oral health

Purging behaviour, particularly self-induced vomiting, has been associated with several oral health and gastrointestinal dysfunctions in patients with EDs. A case–control study of ED patients with binge/purge symptomology found that despite ED patients reporting an increased concern for dental issues and engaging in more frequent brushing, their oral health was poorer than controls. [ 79 ] Further, a systematic review and meta-analysis aimed to explore whether EDs increase the risk of tooth erosion [ 80 ]. The analysis found that patients with EDs had more risk of dental erosion, especially among those who self-induced vomiting [ 80 ]. These findings were also found in a large cohort study, where the increased risk for BN was associated with higher rates of dental erosion but not dental cavities [ 81 ].

However, a systematic review of 10 studies suggested that poor oral health may be common among ED patients irrespective of whether self-induced vomiting forms part of their psychopathology [ 202 ]. One study reported that AN-R patients had poorer oral health outcomes and tooth decay than BN patients [ 203 ]. Two studies identified associations between NES and poor oral health, including higher rates of missing teeth, periodontal disease [ 204 , 205 ]. Another study of a group of patients with AN, BN and EDNOS, demonstrated the impact of ED behaviours on dental soft tissue, whereby 94% of patients had oral mucosal lesions, and 3% were found to have dental erosion [ 206 ].

Vitamin deficiencies

The prolonged periods of starvation, food restriction (of caloric intake and/or food groups), purging and excessive exercise observed across the ED spectrum have detrimental impacts on micronutrient balances [ 207 ]. The impact of prolonged vitamin deficiencies in early-onset EDs can also impair brain development, substantially reducing neurocognitive function in some younger patients even after weight restoration [ 82 ]. Common micronutrient deficiencies include calcium, fat soluble vitamins, essential fatty acids selenium, zinc and B vitamins [ 183 ]. One included study looked at prevalence rates of cerebral atrophy and neurological conditions, specifically Wernicke's encephalopathy in EDs and found that these neurological conditions were very rare in people with EDs [ 208 ].

Cognitive functioning

The literature included in RR regarding the cognitive changes in ED patients with AN following weight gain was sparse. It appears that some cognitive functions affected by EDs recover following nutritional restoration, whereas others persist. Cognitive functions, such as flexibility, central coherence, decision making, attention, processing speed and memory, are hypothesised to be impacted by, and influence the maintenance of EDs. A systematic review explored whether cognitive functions improved in AN following weight gain [ 83 ]. Weight gain appeared to be associated with improved processing speed in children and adolescents. However, no improvement was observed in cognitive flexibility following weight gain. Further, the results for adults were inconclusive [ 83 ].

Reproductive health

Infertility and higher rates of poor reproductive health are strongly associated with EDs, including miscarriages, induced abortions, obstetric complications, and poorer birth outcomes [ 84 , 85 ]. Although amenorrhea is a known consequence of AN, oligomenorrhea (irregular periods) was common among individuals with BN and BED [ 86 ]. A twin study found women diagnosed with BN and BED were also more likely to have poly cystic ovarian syndrome (PCOS), leading to menstrual irregularities [ 209 ]. The prevalence of lifetime amenorrhea in this sample was 10.4%, and lifetime oligomenorrhea was 33.7%. An epidemiological study explored the association of premenstrual syndrome (PMS) and premenstrual dysphoric disorder (PMDD) in women with BN and BED and found prevalence rates as high as 42.4% for PMS and 4.2% for PMDD [ 210 ].

Given the increased rates of menstrual irregularities and issues, questions have been raised regarding whether this complication is reversed or improves with recovery. A review of five studies monitoring reproductive functions during recovery over a 6- to 18-year follow up period [ 211 ] noted no significant difference between the pooled odds of childbirth rates between the AN and general population—demonstrating that if patients undergo treatment for AN, achieve weight restoration, and continue to maintain wellness, reproductive functions can renormalise [ 211 ].

An observational study of women with AN, BN or EDNOS found higher rates of low birth rate, pre-term deliveries, caesarean deliveries, and intrauterine growth restrictions [ 84 ]. Increased caesarean delivery was also observed in a large cohort of women diagnosed with BED [ 212 ]. However, these women had higher birth weight babies [ 212 ]. Further, women with comorbid ED and epilepsy were found to have an increased risk of pregnancy-related comorbidities, including preeclampsia (gestational hypertension and signs of damage to the liver and kidneys ) , gestational diabetes and perinatal depression [ 213 ].

The results from this review identified that the symptomology and outcomes of EDs are impacted by both psychiatric and medical factors. Further, EDs have a mortality rate substantially higher than the general population, with a significant proportion of those who die from an ED dying by suicide or as a result of severe medical complications.

This RR noted high rates of psychiatric and medical comorbidities in people with EDs, with comorbidities contributing to increased ED symptom severity, maintenance of some ED behaviours, compromised functioning, and adverse treatment outcomes. Evidence suggested that early identification and management of psychiatric and medical comorbidities in people with an ED may improve response to treatment and outcomes [ 29 , 35 , 83 ].

EDs and other psychiatric conditions often shared symptoms and high levels of psychopathology crossover were noted. The most prevalent psychiatric comorbidities were anxiety disorders, mood disorders and substance use disorders [ 8 , 100 , 119 ]. perhaps unsurprising given the prevalence of these illnesses in the general population. Of concern is the elevated suicide rate noted across the ED spectrum, the highest observed in AN [ 58 , 140 , 149 ]. For people with AN, suicide attempts were mostly associated with comorbid mood and anxiety disorders [ 136 ]. The review noted elevated rates of NSSI were particularly associated with binge/purge subtype EDs [ 150 ], impulsivity and emotional dysregulation (again, an example of psychopathological overlap).

With regards to PDs, studies were limited to EDs with binge-purge symptomology. Of those included, the presence of a comorbid personality disorder and ED was associated with childhood trauma [ 110 ] and elevated mortality risk [ 111 ]. There appeared to be a link between the clinical characteristics of the ED (e.g., impulsivity, rigidity) and the comorbid PD (cluster B PDs were more associated with BN/BED and cluster C PDs were more associated with AN). There was mixed (albeit limited) evidence regarding the comorbidity between EDs and psychosis and schizophrenia, with some studies noting an association between EDs and psychotic experiences [ 45 ]. Specifically, there was an association between psychotic experiences and uncontrolled eating and food dominance, which were stronger in males [ 122 ]. In addition, the review noted the association between EDs and neurodevelopmental disorders-specifically ADHD—was associated with features of BN and ASD was more prevalent among individuals with AN [ 53 , 54 ] and ARFID [ 55 ].

EDs are complicated by medical comorbidities across the neuroendocrine, skeletal, nutritional, gastrointestinal, dental, and reproductive systems that can occur alongside, or result from the ED. The RR noted mixed evidence regarding the effectiveness and safety of enteral feeding [ 180 , 181 ], with some studies noting that RFS could be safely managed with supplementation [ 191 ]. Research also described the impacts of restrictive EDs on BMD and binge eating behaviour on metabolic disorders [ 78 , 195 ]. Purging behaviours, particularly self-induced vomiting [ 79 ], were found to increase the risk of tooth erosion [ 81 ] and damage to soft tissue within the gastrointestinal tract [ 206 ]. Further, EDs were associated with a range of reproductive health issues in women, including infertility and birth complications [ 84 ].

Whilst the RR achieved its aim of synthesising a broad scope of literature, the absence of particular ED diagnoses and other key research gaps are worth noting. A large portion of the studies identified focused on AN, for both psychiatric and medical comorbidities. This reflects the stark lack of research exploring the comorbidities for ARFID, NES, and OSFED compared to that seen with AN, BN and BED. There were no studies identified exploring the psychiatric and medical comorbidities of Pica. These gaps could in part be due to the timeline utilised in the RR search strategy, which included the transition from DSM-IV to DSM-5. The update in the DSM had significant implications for psychiatric diagnosis, with the addition of new disorders (such as Autism Spectrum Disorder and various Depressive Disorders), reorganisation (for example, moving OCD and PTSD out of anxiety disorders and into newly defined chapters) and changes in diagnostic criteria (including for AN and BN, and establishing BED as a discrete disorder). Although current understanding suggests EDs are more prevalent in females, research is increasingly demonstrating that males are not immune to ED symptoms, and the RR highlighted the disproportionate lack of male subjects included in recent ED research, particularly in the domain of psychiatric and medical comorbidities.

As the RR was broad in scope and policy-driven in intent, limitations as a result of this methodology ought to be considered. The RR only considered ‘Western’ studies, leading to the potential of important pieces of work not being included in the synthesis. In the interest of achieving a rapid synthesis, grey literature, qualitative and theoretical works, case studies or implementation research were not included, risking a loss of nuance in developing fields, such as the association and prevalence of complex/developmental trauma with EDs (most research on this comorbidity focuses on PTSD, not complex or developmental trauma) or body image dissatisfaction among different gender groups. No studies regarding the association between dissociative disorders and EDs were included in the review. However, dissociation can co-occur with EDs, particularly AN-BP and among those with a trauma history [ 214 ]. Future studies would benefit from exploring this association further, particularly as trauma becomes more recognised as a risk factor for ED development.

The review was not designed to be an exhaustive summary of all medical comorbidities. Thus, some areas of medical comorbidity may not be included, or there may be variability in the level of detail included (such as, limited studies regarding the association between cancer and EDs). Studies that explored the association between other autoimmune disorders (such as Type 1 Diabetes, Crohn’s disease, Addison’s disease, ulcerative colitis, and coeliac disease) and EDs [ 215 , 216 ] were not included. Future reviews and research should examine the associations between autoimmune disorders and the subsequent increased risk of EDs, and likewise, the association between EDs and the subsequent risk of autoimmune disorders.

An important challenge for future research is to explore the impact of comorbidity on ED identification, development and treatment processes and outcomes. Insights could be gained from exploring shared psychiatric symptomology (i.e., ARFID and ASD, BN/BED and personality disorders, and food addiction). Particularly in disorders where the psychiatric comorbidity appears to precede the ED diagnosis (as may be the case in anxiety disorders [ 28 ]) and the unique physiological complications of these EDs (e.g., the impact of ARFID on childhood development and growth). Further, treatment outcomes would benefit from future research exploring the nature of the proposed reciprocal nature between EDs and comorbidities, particularly in those instances where there is significant shared psychopathology, or the presence of ED symptoms appears to exacerbate the symptoms of the other condition—and vice versa.

The majority of research regarding the newly introduced EDs has focused on understanding their aetiology, psychopathology, and what treatments demonstrate efficacy. Further, some areas included in the review had limited included studies, for example cancer and EDs. Thus, in addition to the already discussed need for further review regarding the association between EDs and autoimmune disorders, future research should explore the nature and prevalence of comorbidity between cancers and EDs. There was variability regarding the balance of child/adolescent and adult studies across the various comorbidities. Some comorbidities are heavily researched in child and adolescent populations (such as refeeding syndrome) and others there is stark child and adolescent inclusion, with included studies only looking at adult samples. Future studies should also address specific comorbidities as they apply to groups underrepresented in current research. This includes but is not limited to gender, sexual and racial minorities, whereby prevalence rates of psychiatric comorbidities are elevated. [ 88 ] In addition, future research would benefit from considering the nature of psychiatric and medical comorbidity for subthreshold and subclinical EDs, particularly as it pertains to an opportunity to identify EDs early within certain comorbidities where ED risk is heightened.

This review has identified the psychiatric and medical comorbidities of EDs, for which there is a substantial level of literature, as well as other areas requiring further investigation. EDs are associated with a myriad of psychiatric and medical comorbidities which have significant impacts on the symptomology and outcomes of an already difficult to treat, and burdensome illness.

Availability of data and materials

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Abbreviations

Anorexia nervosa—restricting type

Anorexia nervosa—binge-purge type

Avoidant restrictive food intake disorder

Body mass index

Borderline personality disorder

Diagnostic and statistical manual of mental disorders, 5th edition

Eating disorder

Generalised anxiety disorder

International classification of diseases, 11th edition

Major depressive disorder

Night eating syndrome

Other specified feeding or eating disorder

Post-traumatic stress disorder

Rapid review

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Acknowledgements

The authors would like to thank and acknowledge the hard work of Healthcare Management Advisors (HMA) who were commissioned to undertake the Rapid Review. Additionally, the authors would like to thank all members of the consortium and consultation committees for their advice, input, and considerations during the development process. Further, a special thank you to the carers, consumers and lived experience consultants that provided input to the development of the Rapid Review and wider national Eating Disorders Research & Translation Strategy. Finally, thank you to the Australian Government—Department of Health for their support of the current project.

National Eating Disorder Research Consortium: Phillip Aouad, Sarah Barakat, Robert Boakes, Leah Brennan, Emma Bryant, Susan Byrne, Belinda Caldwell, Shannon Calvert, Bronny Carroll, David Castle, Ian Caterson, Belinda Chelius, Lyn Chiem, Simon Clarke, Janet Conti, Lexi Crouch, Genevieve Dammery, Natasha Dzajkovski, Jasmine Fardouly, Carmen Felicia, John Feneley, Amber-Marie Firriolo, Nasim Foroughi, Mathew Fuller-Tyszkiewicz, Anthea Fursland, Veronica Gonzalez-Arce, Bethanie Gouldthorp, Kelly Griffin, Scott Griffiths, Ashlea Hambleton, Amy Hannigan, Mel Hart, Susan Hart, Phillipa Hay, Ian Hickie, Francis Kay-Lambkin, Ross King, Michael Kohn, Eyza Koreshe, Isabel Krug, Anvi Le, Jake Linardon, Randall Long, Amanda Long, Sloane Madden, Sarah Maguire, Danielle Maloney, Peta Marks, Sian McLean, Thy Meddick, Jane Miskovic-Wheatley, Deborah Mitchison, Richard O’Kearney, Shu Hwa Ong, Roger Paterson, Susan Paxton, Melissa Pehlivan, Genevieve Pepin, Andrea Phillipou, Judith Piccone, Rebecca Pinkus, Bronwyn Raykos, Paul Rhodes, Elizabeth Rieger, Sarah Rodan, Karen Rockett, Janice Russell, Haley Russell, Fiona Salter, Susan Sawyer, Beth Shelton, Urvashnee Singh, Sophie Smith, Evelyn Smith, Karen Spielman, Sarah Squire, Juliette Thomson, Marika Tiggemann, Stephen Touyz, Ranjani Utpala, Lenny Vartanian, Andrew Wallis, Warren Ward, Sarah Wells, Eleanor Wertheim, Simon Wilksch & Michelle Williams

The RR was in-part funded by the Australian Government Department of Health in partnership with other national and jurisdictional stakeholders. As the organisation responsible for overseeing the National Eating Disorder Research & Translation Strategy, InsideOut Institute commissioned Healthcare Management Advisors to undertake the RR as part of a larger, ongoing, project. Role of Funder: The funder was not directly involved in informing the development of the current review.

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Authors and affiliations.

InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, Charles Perkins Centre (D17), University of Sydney, Camperdown, NSW, 2006, Australia

Ashlea Hambleton, Danielle Maloney, Stephen Touyz & Sarah Maguire

School of Health and Social Development, Faculty of Health, Deakin University, Geelong, VIC, 3220, Australia

Genevieve Pepin

Healthcare Management Advisors, Melbourne, VIC, Australia

Sydney Local Health District, Camperdown, NSW, Australia

Danielle Maloney, Stephen Touyz & Sarah Maguire

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National Eating Disorder Research Consortium

• Phillip Aouad
• , Sarah Barakat
• , Robert Boakes
• , Leah Brennan
• , Emma Bryant
• , Susan Byrne
• , Belinda Caldwell
• , Shannon Calvert
• , Bronny Carroll
• , David Castle
• , Ian Caterson
• , Belinda Chelius
• , Lyn Chiem
• , Simon Clarke
• , Janet Conti
• , Lexi Crouch
• , Genevieve Dammery
• , Natasha Dzajkovski
• , Jasmine Fardouly
• , Carmen Felicia
• , John Feneley
• , Amber-Marie Firriolo
• , Nasim Foroughi
• , Mathew Fuller-Tyszkiewicz
• , Anthea Fursland
• , Veronica Gonzalez-Arce
• , Bethanie Gouldthorp
• , Kelly Griffin
• , Scott Griffiths
• , Ashlea Hambleton
• , Amy Hannigan
• , Susan Hart
• , Phillipa Hay
• , Ian Hickie
• , Francis Kay-Lambkin
• , Ross King
• , Michael Kohn
• , Eyza Koreshe
• , Isabel Krug
• , Jake Linardon
• , Randall Long
• , Amanda Long
• , Sloane Madden
• , Sarah Maguire
• , Danielle Maloney
• , Peta Marks
• , Sian McLean
• , Thy Meddick
• , Jane Miskovic-Wheatley
• , Deborah Mitchison
• , Richard O’Kearney
• , Shu Hwa Ong
• , Roger Paterson
• , Susan Paxton
• , Melissa Pehlivan
• , Genevieve Pepin
• , Andrea Phillipou
• , Judith Piccone
• , Rebecca Pinkus
• , Bronwyn Raykos
• , Paul Rhodes
• , Elizabeth Rieger
• , Sarah Rodan
• , Karen Rockett
• , Janice Russell
• , Haley Russell
• , Fiona Salter
• , Susan Sawyer
• , Beth Shelton
• , Urvashnee Singh
• , Sophie Smith
• , Evelyn Smith
• , Karen Spielman
• , Sarah Squire
• , Juliette Thomson
• , Marika Tiggemann
• , Stephen Touyz
• , Ranjani Utpala
• , Lenny Vartanian
• , Andrew Wallis
• , Warren Ward
• , Sarah Wells
• , Eleanor Wertheim
• , Simon Wilksch
•  & Michelle Williams

Contributions

DM, PM, ST and SM oversaw the Rapid Review process; AL carried out and wrote the initial review; AH and GP wrote the first manuscript; all authors edited and approved the final manuscript.

Corresponding author

Correspondence to Ashlea Hambleton .

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Not applicable.

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Competing interests.

ST receives royalties from Hogrefe and Huber, McGraw Hill and Taylor and Francis for published books/book chapters. He has received honoraria from the Takeda Group of Companies for consultative work, public speaking engagements and commissioned reports. He has chaired their Clinical Advisory Committee for Binge Eating Disorder. He is the Editor in Chief of the Journal of Eating Disorders. ST is a committee member of the National Eating Disorders Collaboration as well as the Technical Advisory Group for Eating Disorders. AL undertook work on this RR while employed by HMA. A/Prof Sarah Maguire is a guest editor of the special issue “Improving the future by understanding the present: evidence reviews for the field of eating disorders.”

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Supplementary Information

Additional file 1..

PRISMA diagram.

Additional file 2.

Studies included in the Rapid Review.

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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 10 , 132 (2022). https://doi.org/10.1186/s40337-022-00654-2

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Received : 08 July 2022

Accepted : 15 August 2022

Published : 05 September 2022

DOI : https://doi.org/10.1186/s40337-022-00654-2

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