hypothesis on eating disorders

Eating Disorders

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Anorexia nervosa ; Binge eating disorder ; Bulimia nervosa ; EDs ; Fear of weight gain ; Food restriction

Eating disorders are a category of psychological disorders characterized by abnormal eating and related thoughts and emotions. People with eating disorders often have a preoccupation with food and their body image.

Introduction

Eating disorders (EDs) are a category of psychological disorders. The three main classifications in the category of feeding and eating disorders are anorexia nervosa (AN), bulimia nervosa (BN), and binge eating disorder (BED). A fourth category is “eating disorders not otherwise specified,” in which individuals have eating-related problems but do not meet the diagnostic criteria for anorexia, bulimia, or binge eating. Eating disorders are characterized by abnormal eating behaviors and related thoughts and emotions (Parekh 2017 ). People who suffer from eating disorders are often preoccupied with food and their body image or weight and tend to...

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Locke, A., Arnocky, S. (2020). Eating Disorders. In: Shackelford, T., Weekes-Shackelford, V. (eds) Encyclopedia of Evolutionary Psychological Science. Springer, Cham. https://doi.org/10.1007/978-3-319-16999-6_696-1

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Eating disorder outcomes: findings from a rapid review of over a decade of research

• Jane Miskovic-Wheatley 1 , 2 ,
• Emma Bryant 1 , 2 ,
• Shu Hwa Ong 1 , 2 ,
• Sabina Vatter 1 , 2 ,
• Anvi Le 3 ,
• National Eating Disorder Research Consortium ,
• Stephen Touyz 1 , 2 &
• Sarah Maguire 1 , 2  

Journal of Eating Disorders volume  11 , Article number:  85 ( 2023 ) Cite this article

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Eating disorders (ED), especially Anorexia Nervosa (AN), are internationally reported to have amongst the highest mortality and suicide rates in mental health. With limited evidence for current pharmacological and/or psychological treatments, there is a grave responsibility within health research to better understand outcomes for people with a lived experience of ED, factors and interventions that may reduce the detrimental impact of illness and to optimise recovery. This paper aims to synthesise the literature on outcomes for people with ED, including rates of remission, recovery and relapse, diagnostic crossover, and mortality.

This paper forms part of a Rapid Review series scoping the evidence for the field of ED, 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 studies published between 2009 and 2022 in English. High-level evidence such as meta-analyses, large population studies and Randomised Controlled Trials were prioritised through purposive sampling. Data from selected studies relating to outcomes for people with ED were synthesised and are disseminated in the current review.

Of the over 1320 studies included in the Rapid Review, the proportion of articles focused on outcomes in ED was relatively small, under 9%. Most evidence was focused on the diagnostic categories of AN, Bulimia Nervosa and Binge Eating Disorder, with limited outcome studies in other ED diagnostic groups. Factors such as age at presentation, gender, quality of life, the presence of co-occurring psychiatric and/or medical conditions, engagement in treatment and access to relapse prevention programs were associated with outcomes across diagnoses, including mortality rates.

Results are difficult to interpret due to inconsistent study definitions of remission, recovery and relapse, lack of longer-term follow-up and the potential for diagnostic crossover. Overall, there is evidence of low rates of remission and high risk of mortality, despite evidence-based treatments, especially for AN. It is strongly recommended that research in long-term outcomes, and the factors that influence better outcomes, using more consistent variables and methodologies, is prioritised for people with ED.

Plain English summary

Eating disorders are complex psychiatric conditions that can seriously impact a person’s physical health. Whilst they are consistently associated with high mortality rates and significant psychosocial difficulties, lack of agreement on definitions of recovery, remission and relapse, as well as variations in methodology used to assess for standardised mortality and disability burden, means clear outcomes can be difficult to report. 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 to guide policymaking and address urgent health concerns. This Rapid Review synthesises the current evidence-base for outcomes for people with eating disorders and identifies gaps in research and treatment to guide decision making and future clinical research. A critical overview of the scientific literature relating to outcomes in Western healthcare systems that may inform health policy and research in an Australian context is provided in this paper. This includes remission, recovery and relapse rates, diagnostic cross-over, the impact of relapse prevention programs, factors associated with outcomes, and findings related to mortality.

Introduction

Eating disorders (ED), especially Anorexia Nervosa (AN), have amongst the highest mortality and suicide rates in mental health. While there has been significant research into causal and maintaining factors, early identification efforts and evidence-based treatment approaches, global incidence rates have increased from 3.4% calculated between 2000 and 2006 to 7.8% between 2013 and 2018 [ 1 ]. While historically seen as a female illness, poorer outcomes are increasingly seen in other genders, including males [ 2 ].

Over 3.3 million healthy life years are lost worldwide due to ED each year, and many more lost to disability due to medical and psychiatric complications [ 3 ]. Suicide accounts for approximately 20% of non-natural deaths among people with ED [ 4 ]. As this loss of healthy life is preventable, there is a grave responsibility to better understand outcomes for people with ED, including factors which may minimise the detrimental impact they have on individuals, carers, and communities, as well as to optimise recovery.

There has been considerable debate within the clinical, scientific and lived experience (i.e., patient, consumer, carer) communities about the definition and measurement of key outcomes in ED, including ‘remission’ from illness (a period of relief from symptoms), ‘relapse’ (a resumption of symptoms) and ‘recovery’ (cessation of illness) [ 5 , 6 ], which can compromise outcome comparisons. Disparities include outcome variables relating to eating behaviours as well as medical, psychological, social and quality of life factors. There is increasing awareness in the literature of the elevated likelihood of diagnostic crossover [ 7 ]; research examining specific diagnostic profiles potentially misses outcomes where symptom experience transforms rather than alleviates. Methodological approaches in outcomes research are varied, the most significant being length of time to follow up, compromising direct study comparisons.

The aim of this Rapid Review (RR) is to synthesise the literature on outcomes for people with ED, including rates of remission, recovery and relapse, diagnostic crossover, and mortality. Factors influencing outcomes were summarised including demographic, illness, treatment, co-morbidities, co-occurring health conditions, societal factors, and impact of relapse prevention programs. This RR forms one of a series of reviews scoping the field of ED commissioned to inform the Australian National Eating Disorders Research and Translation Strategy 2021–2031 [ 8 ]. The objective is to evaluate the current literature in ED outcomes to identify areas of consensus, knowledge gaps and suggestions for future research.

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 [ 8 ] 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 (including consumers and families/carers). Developed through a 2 year national consultation and collaboration process, the strategy provides the roadmap to establishing ED 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 broadly assess all available peer-reviewed literature on the six DSM-V [ 9 ] listed ED. RR’s were conducted in the following domains: (1) population, prevalence, disease burden, Quality of Life in Western developed countries; (2) risk factors; (3) co-occurring conditions and medical complications; (4) screening and diagnosis; (5) prevention and early intervention; (6) psychotherapies and relapse prevention; (7) models of care; (8) pharmacotherapies, alternative and adjunctive therapies; and (9) outcomes (including mortality) (current RR), with every identified paper allocated to only one of the above domains from abstract analysis by two investigators. Each RR was submitted for independent peer review to the Journal of Eating Disorders special edition, “Improving the future by understanding the present: evidence reviews for the field of eating disorders”.

A RR Protocol [ 10 ] was utilised to swiftly synthesise evidence to guide public policy and decision-making [ 11 ]. This approach has been adopted by several leading health organisations, including the World Health Organization [ 12 ] and the Canadian Agency for Drugs and Technologies in Health Rapid Response Service [ 13 ], to build a strong evidence base in a timely and accelerated manner, without compromising quality. RR was chosen as the most suitable design as it is conducted with broader search terms and inclusion criteria allowing to gain a better understanding of a specific field, returning a larger number of search results and providing a snapshot of key findings detailing the current state of a field at study [ 10 ]. 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 [ 14 ].

The RR is a narrative synthesis adhering to the PRISMA guidelines [ 15 ]. 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 eating disorders, and to capture the largest evidence base on the past 13 years (originally 2009–2019, but expanded to include the preceding two years), the eligibility criteria for included studies into the RR were kept broad. Therefore, included studies were published between 2009 and 2022, 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 and a final run for 2022 conducted in January 2023 to ensure the most up to date publications were included prior to publication.

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 such as: meta-analyses; systematic reviews; moderately sized randomised controlled trials (RCTs) ( n  > 50); moderately sized controlled-cohort studies ( n  > 50), or population studies ( n  > 500). However, the diagnoses Avoidant Restrictive Food Intake Disorder (ARFID), Eating Disorder Not Otherwise Specified (EDNOS), Other Specified Feeding or Eating Disorder (OSFED) and Unspecified Feeding or Eating Disorder (UFED) necessitated a less stringent eligibility criterion due to a paucity of published articles. As these diagnoses are newly captured in the DSM-V [ 9 ] (released in 2013, within the allocated search timeframe), the evidence base is emerging, and fewer 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, was excluded.

Full methodological details including eligibility criteria, search strategy and terms and data analysis are published in a separate protocol paper [ 10 ]. The full RR included a total of over 1320 studies (see Additional file 1 : Fig. S1). Data from included studies relating to outcomes for eating disorders were synthesised and are presented in the current review.

Of the 1320 articles included in the RR, the proportion of articles focused on outcomes in ED was relatively small, just less than 9% ( n  = 116) (see Additional file 2 : Table S1). Studies typically examined outcomes in AN, Bulimia Nervosa (BN) and Binge Eating Disorder (BED), with limited research in other diagnostic groups. Whereas most outcome studies reported recovery, remission and relapse rates, others explored factors impacting outcomes, such as quality of life, co-occurring conditions, and outcomes from relapse prevention programs.

ED, particularly AN, have long been associated with an increased risk of mortality. The current review summarises best available evidence exploring this association. Several factors complicate these findings including a lack of consensus on definitions of remission, recovery and relapse, widely varying treatment protocols and research methodologies, and limited transdiagnostic outcome studies or syntheses such as meta-analyses. Table 1 provides a summary of outcomes reported by studies identified in this review. There is considerable heterogeneity in the reported measures.

Overall outcomes

A good outcome for a person experiencing ED symptomatology is commonly defined as either remission or no longer meeting diagnostic criteria, as well as improved levels of psychosocial functioning and quality of life [ 28 , 29 ]. However, such a comprehensive approach is rarely considered, and there is no consensus on a definition for recovery, remission, or relapse for any of the ED diagnoses [ 30 , 31 ]. To contextualise this variation, definitions and determinants for these terms are presented in Table 2 .

The terms ‘remission’ and ‘recovery’ appear to be used interchangeably in the literature. Whilst ‘remission’ is usually defined by an absence of diagnostic symptomatology, and ‘recovery’ an improvement in overall functioning, the period in which an individual must be symptom-free to be considered ‘remitted’ or ‘recovered’ varies greatly between studies, follow-up (FU) time periods are inconsistent, and very few studies examine return to psychosocial function and quality of life (QoL) after alleviation of symptoms. The current review uses the terms adopted by the original studies. ‘Relapse’ is typically defined by a return of symptoms after a period of symptom relief. The reviewed studies report a variety of symptom determinants including scores on standardised psychological and behavioural interviews or questionnaires, weight criteria [including Body Mass Index (BMI) or %Expected Body Weight (%EBW)], clinical assessment by a multidisciplinary team, self-reported ED behaviours, meeting diagnostic criteria, or a combination of the above.

Remission, recovery, and relapse

In a global overview of all studies reviewed, remission or recovery rates were reported for around half of the cohort, regardless of diagnostic group. For example, a 30 month FU study of a transdiagnostic cohort of patients found 42% obtained full and 72% partial remission, with no difference between diagnostic groups for younger people; however, bulimic symptoms emerged frequently during FU, regardless of initial diagnosis [ 44 ]. A 6 year study following the course of a large clinical sample ( n  = 793) reported overall recovery rates of 52% for AN, 50–52% for BN, 57% for EDNOS-Anorectic type (EDNOS-A), 60–64% for BED and 64–80% for EDNOS-Bulimic type (EDNOS-B) [ 7 ]. Of those who recorded full remission at end of treatment (EOT), relapse was highest for AN (26%), followed by BN (18%), and EDNOS-B (16%). Relapse was less common for individuals with BED (11–12%), and EDNOS-A (4%). Change in diagnosis (e.g., from AN to BN) was also seen within the relapse group [ 7 ].

Longer-term FU studies may more accurately reflect the high rates of relapse and diagnostic crossover associated with ED. A 17 year outcome study of ED in adult patients found only 29% remained fully recovered, with 21% partially recovered and half (50%) remaining ill [ 52 ], noting the protracted nature of illness for adults with longstanding ED. Relapse is observed at high rates (over 30%) among people with AN and BN at 22 year FU [ 61 ]. In a large clinical study using predictive statistical modelling, full remission was more likely for people with BED (47.4%) and AN (43.9%) compared to BN (25.2%) and OSFED (23.2%) [ 41 ]. This result is distinct from other studies citing AN to have the worst clinical outcomes within the diagnostic profiles [ 52 ]. The cut‐off points for the duration of illness associated with decreased likelihood of remission were 6–8 years for OSFED, 12–14 years for AN/BN and 20–21 years for BED [ 41 ]. As with recovery rates, reported rates of relapse are highly variable due to differing definitions and study methodologies used by researchers in FU studies [ 35 , 61 ].

Evidence from a meta-analysis of 16 studies found four factor clusters that significantly contributed to relapse; however, also noted a substantial variability in procedures and measures compromising study comparison [ 62 ]. Factors contributing to heightened risk of relapse included severity of ED symptoms at pre- and post-treatment, presence and persistence of co-occurring conditions, higher age at onset and presentation to assessment, and longer duration of illness. Process treatment variables contributing to higher risk included longer duration of treatment, previous engagement in psychiatric and medical treatment (including specialist ED treatment) and having received inpatient treatment. These variables may indicate more significant illness factors necessitating a higher intensity of treatment.

Importantly, full recovery is possible, with research showing fully recovered people may be indistinguishable from healthy controls (HCs) on all physical, behavioural, and psychological domains (as evaluated by a battery of standardised assessment measures), except for anxiety (those who have fully recovered may have higher general anxiety levels than HCs) [ 29 ].

Diagnostic crossover

Most studies reported outcomes associated with specific ED diagnoses; however, given a significant proportion of individuals will move between ED diagnoses over time, it can be challenging to determine diagnosis-specific outcomes. Results from a 6 year FU study indicated that overall individuals with ED crossed over to other ED diagnoses during the FU observational period, most commonly AN to BN (23–27%), then BN to BED (8–11%), BN to AN (8–9%) and BED to BN (7–8%) [ 7 ]. Even higher crossover trends were observed in the subgroup reporting relapse during the FU period, with 61.5% of individuals originally diagnosed with AN developing BN, 27.2% and 18.1% of individuals originally diagnosed with BN developing AN and BED respectively, and 18.7% of people with a previous diagnosis of BED developing BN [ 7 ].

A review of 79 studies also showed a significant number of individuals with BN (22.5%) crossed over to other diagnostic groups (mostly OSFED) at FU [ 63 ]. A large prospective study of female adolescents and young adults in the United States ( n  = 9031) indicated that 12.9% of patients with BN later developed purging disorder and between 20 and 40% of individuals with subthreshold disorders progressed to full threshold disorders [ 64 ]. Progression from subthreshold to threshold eating disorders was higher for BN and BED (32% and 28%) than for AN (0%), with researchers suggesting higher risk for binge eating [ 66 ]. Progression from subthreshold to full threshold BN and BED was also common in adolescent females over the course of an 8 year observational study [ 33 ]. Some researchers contend that such diagnostic ‘instability’ demonstrates a need for ‘dimensional’ approaches to research and treatment which have greater focus on the severity rather than type of symptoms [ 7 ]. Diagnostic crossover is common and should be considered in the long-term management and monitoring of people with an ED.

Anorexia nervosa (AN)

People with restrictive-type ED have the poorest prognosis compared to the other diagnostic groups, particularly individuals displaying severe AN symptomatology (including lower weights and higher body image concerns) [ 44 ]. There is a paucity of effective pharmacological and/or psychological treatments for AN [ 65 ]. Reported rates of recovery vary and include 18% [ 56 ] to 52% at 6 year FU [ 7 ] to 60.3% at 13 year FU [ 20 ] and 62.8% at 22 year-FU [ 61 ]. Reported relapse rates in AN also vary, for example, 41.0% at 1 year post inpatient/day program treatment [ 35 ] to 30% at 22 year FU [ 61 ]. Average length of illness across the reviewed studies also varies from 6.5 years [ 56 ] to 14 years [ 41 ].

A variety of reported outcomes from treatment studies is likely due to the breadth of treatments under investigation, diverse study protocols and cohorts. For example, in a mixed cohort of female adult patients with AN and Atypical AN (A-AN), 33% were found to have made a full recovery at 3 year FU after treatment with cognitive behavioural therapy (CBT) [ 57 ], while 6.4% had a bad outcome and 6.4% a severe outcome. However, in a 5–10 year FU study of paediatric inpatients (mean age 12.5 years) approximately 41% had a good outcome, while 35% had intermediate and 24% poor outcome [ 66 ]. Multimodal treatment approaches including psychiatric, nutritional, and psychological rehabilitation have been found to be most efficacious for moderate to severe and enduring AN but noting a discrete rate of improvement [ 67 ].

Very few factors were able to predict outcomes in AN. Higher baseline BMI was consistently found to be the strongest predictor of recovery, and better outcomes were associated with shorter duration of illness [ 7 , 55 , 61 , 66 ]. Earlier age of illness onset [ 59 , 68 , 69 ] and older age at presentation to treatment [ 30 ] were related to chronicity of illness and associated with poorer outcome.

There was a consensus across a variety of studies that engagement in binge/purge behaviours (Anorexia Nervosa Binge/Purge subtype; AN-BP) was associated with a poorer prognosis [ 20 , 56 , 70 ]. Similarly, individuals with severe and enduring AN restrictive sub-type (AN-R) are likely to have a better outcome than individuals with AN-BP. AN-BP was associated with a two-fold greater risk of relapse compared to AN-R [ 30 , 35 ]. Some studies, however, were unable to find an association between AN subtype and outcome [ 55 ]. Other factors leading to poorer outcome and higher probability of relapse were combined ED presentations, such as combined AN/BN [ 35 ], higher shape concern [ 57 ], lower desired weight/BMI [ 44 ], more ED psychopathology at EOT, low or decreasing motivation to recover, and comorbid depression [ 35 , 61 ].

Preliminary genetic work has found associations between a single nucleotide polymorphism (SNP) in a ghrelin production gene (TT genotype at 3056 T-C) and recovery from AN-R [ 71 ], and the S-allele of the 5-HTTLPR genotype increasing the risk susceptibility for both depressive comorbidity and diagnostic crossover at FU of AN patients [ 72 ]. These studies, however, need to be interpreted with caution as they were conducted over a decade ago and have not since been replicated. Research in eating disorder genetics is a rapidly emerging area with potential clinical implications for assessment and treatment.

Bulimia nervosa (BN)

Overall, studies pertaining to a diagnostic profile of BN report remission recovery rates of around 40–60%, depending on criteria and FU period, as detailed below. Less than 40% of people achieved full symptom abstinence [ 73 ] and relapse occurred in around 30% of individuals [ 61 ]. A meta-analysis of 79 case series studies reported rates of recovery for BN at 45.0% for full recovery and 27.0% for partial remission, with 23.0% experiencing a chronic course and high rates of treatment dropout [ 63 ]. At 11 year FU, 38.0% reported remission in BN patients, increasing to 42.0% at 21 year [ 45 ]. At 22 year FU, 68.2% with BN were reported to have recovered [ 41 ]. Higher frequency of both objective binge episodes and self-induced vomiting factors influencing poorer outcomes [ 44 ].

Considering impact of treatment, analysis of engagement in self-induced vomiting as a predictor for outcome indicated there were no differences between groups in treatment dropout or response to CBT among a sample of 152 patients with various types of EDs (AN-BP, BN, EDNOS) at EOT [ 74 ]. Meta-analysis of results from 45 RCTs on psychotherapies for BN found 35.4% of treatment completers achieved symptom abstinence [ 73 ] with other studies indicating similar rates of recovery (around 52–59% depending on DSM criteria) [ 7 ].

Studies delivering CBT or other behavioural therapies reported the best outcomes for BN [ 73 ]. Specifically, early treatment progression, elimination of dietary restraint and normalisation of eating behaviour resulted in more positive outcomes [ 22 ]. These findings are supported by results from a study comparing outcomes of CBT and integrative cognitive-affective therapy (ICAT) [ 75 ]. Additional moderating effects were shown at FU (but not EOT), with greater improvements for those with less baseline depression, higher stimulus seeking (the need for excitement and stimulation) and affective lability (the experience of overly intense and unstable emotions) in the ICAT-BN group and lower stimulus seeking in the Enhanced Cognitive Behavioural Therapy (CBT-E) group. Lower affective lability showed improvements in both treatment groups [ 75 ]. Such findings indicate personality factors may deem one treatment approach more suitable to an individual than another.

A review of 4 RCTs of psychotherapy treatments for BN in adolescents (including FBT and CBT) reported overall psychological symptom improvement by EOT predicting better outcomes at 12 months, which underscored the need for not only behavioural but psychological improvement during 6 month treatment [ 31 ]. Other factors leading to poorer outcomes included less engagement in treatment, higher drive for thinness, less global functioning, and older age at presentation [ 45 ]. More research is needed into consistent predictors, mediators and moderators focused on treatment engagement and outcomes [ 22 ].

While many studies combine findings for BN and BED, one study specifically considered different emotions associated with binge eating within the two diagnostic profiles [ 60 ]. At baseline, binge eating was associated with anger/frustration for BN and depression for BED. At FU, objective binge eating (OBE) reduction in frequency (a measure of recovery) was associated with lower impulsivity and shape concern for BN but lower emotional eating and depressive symptoms for BED. These differences may provide approaches for effective intervention targets for differing presentations; however, how these may play out within a transdiagnostic approach requires further enquiry.

Binge eating disorder (BED)

BED is estimated to affect 1.5% of women and 0.3% of men worldwide, with higher prevalence (but more transient) in adolescents. Most adults report longstanding symptoms, 94% lifetime mental health conditions and 23% had attempted suicide, yet only half were in recognised healthcare or treatment [ 76 ].

Compared with AN and BN, long-term outcomes, and treatment success for individuals with BED were more favourable. Meta-analysis of BED abstinence rates suggests available psychotherapy and behavioural interventions are more effective for this population [ 77 ]. Additionally, stimulant medication (i.e., Vyvanse) has been found to be particularly effective to reduce binge eating [see [ 78 ] for full review]. Results from a study of people who received 12 months of CBT for BED indicated high rates of treatment response and favourable outcomes, maintained to 4 year FU. Significant improvements were observed with binge abstinence increasing from 30.0% at post-treatment to 67.0% at FU [ 79 ]. A meta-analysis reviewing psychological or behavioural treatments found Interpersonal Therapy (IPT) to be the treatment producing the greatest abstinence rates [ 73 ]. In a comparative study of IPT and CBT, people receiving CBT experienced increased ED symptoms between treatment and 4 year FU, while those who received IPT improved during the same period. Rates of remission at 4 year FU were also higher for IPT (76.7%) versus CBT (52.0%) [ 80 ].

One study specifically explored clinical differences between ED subtypes with and without lifetime obesity over 10 years. Prevalence of lifetime obesity in ED was 28.8% (ranging from 5% in AN to 87% in BED), with a threefold increase in lifetime obesity observed over the previous decade. Observed with temporal changes, people with ED and obesity had higher levels of childhood and family obesity, older-age onset, longer ED duration, higher levels of ED (particularly BED and BN) and poorer general psychopathology than those who were not in the obese weight range [ 81 ], suggesting greater clinical severity and poorer outcomes for people of higher weight.

Comparison of 6 year treatment outcomes between CBT and Behavioural Weight Loss Treatment (BWLT) found CBT more effective at post-treatment but fading effectiveness over time, with remission rates for both interventions lower than other reported studies (37%) [ 82 ]. A meta-analytic evaluation of 114 published and unpublished psychological and medical treatments found psychological treatments, structured self-help, and a combination of the two were all effective at EOT and 12 month FU but noted a wide variation in study design and quality, and the need for longer term FU. Efficacy and FU data for pharmacological and surgical weight loss treatments were lacking [ 77 ].

Whilst high weight and associated interventions (such as bariatric surgery) can be associated with any ED, they are frequently studied in relation to BED. A significant proportion of individuals seeking bariatric surgery (up to 42%) displayed binge eating symptomatology [ 83 ], yet little is known about the effect of these interventions on ED psychopathology and whether this differs by type of intervention. A systematic review of 23 studies of changes in ED behaviour following three different bariatric procedures found no specific procedure led to long term changes in ED profiles or behaviours [ 84 ]; however, another study investigating the placement of an intragastric balloon in obese patients found post-surgical reductions in grazing behaviours, emotional eating and EDNOS scores [ 85 ]. Bariatric surgery in general is associated with a reduction in ED, binge eating and depressive symptoms [ 86 ].

Outcomes among patients receiving bariatric surgery with and without BED were assessed where weight loss was comparable between the groups at 1 year FU. However, compared with participants receiving a BWLT-based lifestyle modification intervention instead of surgery, bariatric surgery patients lost significantly less weight at a 10.3% difference between groups. There was no significant difference between lifestyle modification and surgery groups in BED remission rates [ 87 ]. These results indicate that BLWT-type interventions are more effective than surgery at promoting weight loss in individuals with BED over a 1 year FU period, and people with BED and higher BMI were able to maintain weight loss in response to psychotherapy (CBT) at up to 5 year FU [ 88 ]. In analysis of health-related quality of life (HRQoL) in people with BED who received various levels of CBT (therapist-led, therapist-assisted and self-help), evaluation indicated that all modalities resulted in improvements to HRQoL. Poorer outcomes were associated with obesity and ED symptom severity at presentation, stressing the importance of early detection and intervention measures [ 89 ]. Research into the role of CBT in strengthening the effect of bariatric surgery for obesity is ongoing but promising [ 90 ].

EDNOS, OSFED and UFED

Similarly to BED, a diagnosis of DSM-IV EDNOS (now OSFED) was associated with a more favourable outcome than AN or BN, including shorter time to remission. One study reported remission rates for both EDNOS and BED at 4 year FU of approximately 80% [ 21 ]. The researchers suggested that an ‘otherwise specified’ diagnostic group might be comprised of individuals transitioning into or out of an ED rather than between diagnostic categories; however, more work is needed in this area to fully understand this diagnostic profile. The reported recovery rate from EDNOS-A has been found to be much lower at 57% than for EDNOS-B at 80% (DSM-V). One factor suggested leading to poorer outcomes for EDNOS-A was a higher association with a co-occurring condition of major depression and/or dysthymia not found in other EDNOS subtypes [ 7 ]. Another study found purging occurred in 6.7% from total (cross-diagnostic) ED referrals, but this subtype did not have different post-treatment remission rates or completion rates compared to non-purging profiles [ 91 ], so results are mixed.

Acknowledging the scarcity of research within these diagnostic groups, remission rates for adolescents including those with a diagnosis of Other Specified Feeding or Eating Disorder (OSFED) and Unspecified Feeding or Eating Disorder (UFED) was reported to be 23% at 12 month FU in the one study reviewed, but no detail was provided on recovery rates by diagnosis [ 26 ]. No available evidence was identified specifically for the DSM-V disorders OSFED or UFED for adults.

Avoidant/Restrictive Food Intake Disorder (ARFID)

Research into outcomes for people with ARFID is lacking, with only three studies meeting criteria for the review [ 23 , 24 , 25 ]. While, like AN, recovery for people with ARFID is usually measured by weight gain targets, one of the three studies [ 63 ] identified by this review instead reported on outcomes in terms of meeting a psychiatric diagnosis, making comparison between the studies difficult.

In a cross-diagnostic inpatient study, individuals presenting with ARFID were younger, had fewer reported ED behaviours and co-occurring conditions, less weight loss and were less likely to be bradycardic than individuals presenting with AN [ 25 ]. Although both groups received similar caloric intakes, ARFID patients relied on more enteral nutrition and required longer hospitalisations but had higher rates of remission and fewer readmissions than AN patients at 12 months. This study highlights the need for further investigation into inpatient treatment optimisation for different diagnostic profiles.

People with ARFID who had achieved remission post-treatment were able to maintain remission until 2.5 year FU, with most continuing to use outpatient treatment services [ 23 ]. In a 1 year FU study assessing ARFID, 62.0% of patients had achieved remission as defined by weight recovery and no longer meeting DSM-V criteria [ 25 ]. In a study following children treated for ARFID to a mean FU of 16 years post-treatment (age at FU 16.5–29.9 years), 26.3% continued to meet diagnostic criteria for ARFID with no diagnostic crossover, suggesting symptom stability [ 24 ]. Rates of recovery for ARFID patients in this study were not significantly different to the comparison group who had childhood onset AN, indicating similar prognoses for these disorders. No predictors of outcome for patients with ARFID were identified by the articles reviewed [ 63 ].

Community outcomes

While most outcome studies derive from health care settings, two studies were identified exploring outcomes of ED within the community. The first reported the 8 year prevalence, incidence, impairment, duration, and trajectory of ED via annual diagnostic interview of 496 adolescent females. Controlling for age, lifetime prevalence was 7.0% for BN/subthreshold BN, 6.6% for BED/subthreshold BED, 3.4% for purging disorder, 3.6% for AN/atypical AN, and 11.5% for feeding and eating disorders not otherwise classified. Peak onset age across the ED diagnostic profiles was 16–20 years with an average episode duration ranging from 3 months for BN to a year for AN; researchers noted that these episodes were shorter than the average duration estimates reported in similar research and may be representative of the transient nature of illness rather than longer term prognosis. ED were associated with greater functional impairment, distress, suicidality, and increased use of mental health treatment [ 27 ].

A second study followed 70 young people (mean age of 14 years at study commencement) meeting DSM-IV criteria for a binge eating or purging ED and found 44% no longer met criteria at ages 17 or 20, while 25% still met criteria at age 20 (the latter individuals were more likely to have externalising behaviour problems and purging behaviour at age 17). Those who experienced a persistent ED were less likely to complete secondary education and report higher depressive and anxiety symptoms at age 20, indicating the ongoing impacts of ED on education and quality of life [ 92 ]. These studies provide information about the course and outcome of early onset ED at the population level with indicators of predictive and maintaining factors.

Factors relating to outcomes

Several factors relating to outcomes have been studied across ED presentations and in specific diagnostic profiles. These include predictors of outcome, moderators or mediators of outcome, and illness reinforcers, considering age of presentation and duration of illness, ED symptomatology, presence of co-occurring medical and psychiatric conditions, and treatment characteristics.

Age of presentation

Age of presentation to treatment has been shown to have a significant impact on outcome in all diagnoses. One study considering ED in general (including AN, BN and EDNOS) showed presentation at mid-life drastically decreased chances of achieving a good outcome in response to treatment (“good” outcome defined as BMI ≥ 18.5, 3 month remission of symptoms and Eating Disorder Examination Questionnaire (EDE-Q) scores within or better than normal range). Six percent of mid-life (≥ 40 years) presentations achieved a good outcome post-treatment compared to 14% of young adults (18–39 years) and 28% of younger people (< 18 years) [ 28 ]. This finding has also been seen in research comparing 22 year outcomes of AN and BN [ 61 ].

People presenting in mid-life often have more complex medical and psychiatric profiles as well as life circumstances. They are also far more likely to have a sustained length of illness by the time of initial presentation: 27.8 years compared with 1.2 years for youths [ 28 ]. Longer duration of illness is associated with greater increase in self-reported clinical impairment [ 93 ]; however, illness duration does not necessarily influence treatment outcome, though wide variation in study protocol and quality limit the interpretability of these findings [ 37 , 94 ]. The disparity in rates of favourable outcome between age groups highlights the importance of prevention, screening, awareness of ED in primary care settings and early intervention programs, as well as targeted programs for those presenting with more complex psychosocial and life challenges.

Clinical features and co-occurring conditions

A systematic review assessed the average duration of untreated illness duration in help-seeking populations at first contact to treatment services at 29.9 months for AN, 53.0 months for BN and 67.4 months for BED [ 69 ]. ED clinical factors significantly influence outcomes, with poorer prognosis in those with time of untreated illness, primary diagnosis of AN [ 95 ], lower BMI at presentation [ 93 ], and presence of binge/purge symptomatology [ 20 , 56 ]. Certain ED behaviours and cognitions at intake predict better outcome such as lower rates of purging behaviour, higher rates of body image flexibility [ 96 ], and lower EDE-Q scores at baseline [ 97 ].

There is strong evidence for the presence of co-occurring medical and psychiatric conditions as a predictor of outcome in ED. At 22 year FU, the presence of co-occurring psychiatric conditions including Major Depressive Disorder (MDD) and Substance Use Disorder (SUD) were negatively correlated with recovery, with those who had recovered from an ED being 2.17 times less likely to have MDD and 5.33 times less likely to have SUD [ 98 ]. Co-occurring mood disorders consistently lead to poorer outcomes [ 47 , 51 , 55 , 99 ] and greater chance of moving between ED diagnoses [ 7 ]. In one study, presence of a mood disorder was the strongest predictor of classification of AN-R (but not AN-BP) [ 61 ]. Comorbid personality disorder was found in several studies to be the most common predictor of poorer outcome in ED [ 20 , 41 , 44 , 67 ].

In an adolescent sample, 39% of individuals with AN met criteria for at least one other psychiatric disorder and poorer prognosis was associated with co-occurring diagnoses of Obsessive Compulsive Disorder (OCD) and autistic traits [ 59 ]. In a large community childhood health longitudinal study, presence of any ED profile was predictive of later anxiety and mood disorders. AN was prospectively associated with long term low weight, while BN and BED with obesity, drug use and deliberate self-harm compared to age-matched children who did not have an ED profile [ 100 ].

Personality traits have also been found to be associated with poorer outcomes such as low persistence and harm avoidance in AN, lower self-directedness (BN) and reward dependence (BED) [ 41 ]. Higher perfectionism at intake predicted a lower likelihood of remission at 12 months in an adolescent sample [ 26 ], a finding consistent with previous research in adult cohorts [ 41 ].

Medical comorbidities such as malnutrition [ 72 ], concurrent type 1 diabetes [ 39 , 42 ], bodily pain [ 55 ] and viral infections [ 72 ] have been identified as risk factors for poorer outcomes and increased rates of relapse. Other co-occurring factors associated with poorer outcomes for people with ED include anxiety [ 47 , 56 , 93 ], dissociative experiences [ 101 ], impulsivity [ 56 ], adjustment disorder [ 95 ], use of psychotropic medications [ 30 ], and autistic traits have been associated with greater use of ED treatment [ 102 ].

Psychosocial, environmental and health factors

A large United States community study found positive correlation between higher rates of smoking behaviour and ED in women [ 99 ]. The same study also reported birth-related outcomes in women with ED including having a later first birth, pregnancy health concerns, experience of miscarriage or abortion [ 99 ], and women with ED may have increased experience of adverse pregnancy and neonatal outcomes, and lower numbers of children [ 3 ]. For women with a history of ED, ED symptoms tend to alleviate during pregnancy; however, they commonly resurface during the postnatal period, and up to a third of women with ED report postnatal depression [ 103 , 104 ].

Demographic factors leading to poorer prognosis include being male [ 72 ], of the LGBTQIA + community [ 105 ], being from a non-white ethnic background, low family education levels [ 99 ], lower socioeconomic status, living in a remote or rural area [ 72 ], poor employment and social adjustment [ 30 ], functional impairment [ 47 ], and having a family member with an ED [ 99 ]. Complicating prognosis are additional factors such as financial stress (individuals with ED face yearly health care costs 48% higher than the general population, while the presence of co-occurring psychiatric conditions is associated with 48% lower yearly earnings [ 3 ]. These financial challenges limit ability to access evidence-based treatments (especially in countries lacking in publicly funded health care) which may prolong illness.

There is strong evidence to suggest QoL is reduced in people with an ED [ 3 , 106 ]. It is important to consider associations between QoL, ED symptomatology and treatment outcome. Evidence-based treatments have demonstrated positive effects on QoL in addition to reduction in ED symptomatology, for example, improvements in QoL and psychological functioning and well-being were seen in response to CBT in a cross-diagnostic sample [ 43 ]. However, a meta-analysis of ED outcome studies found that the QoL of recovered ED patients remained lower than in healthy populations, highlighting the importance of prevention efforts [ 107 ] and restoration of QoL in relapse prevention. These studies highlight the high public health and clinical burden of eating disorders and the need to consider co-occurring medical and psychiatric conditions during comprehensive assessment history-taking, treatment planning and provision.

Treatment factors

Early progression in treatment can provide indication of treatment outcomes. In an RCT comparing Family Based Treatment (FBT) and Adolescent Focused Therapy (AFT) for adolescents with AN, most people who achieved remission at 1 year FU maintained recovery to 4 years FU regardless of treatment arm with remission rates tended to remain stable after 1 year [ 108 ]. The First Episode Rapid Early Intervention for Eating Disorders (FREED) service model for young adults with AN reported significant and rapid clinical improvements in over 53.2% of people compared to 17.9% TAU and also reported more cost-effective treatment [ 109 ]. In a transdiagnostic study comparing inpatient vs outpatient settings, rapid response to treatment (defined here as a clinically meaningful reduction in disorder-specific symptoms within the first ten sessions) was the only outcome predictor accounting for 45.6% of variance in ED symptoms, suggesting future work should evaluate mediators and moderators of rapid response [ 37 ]. A systematic review of outcome predictors and mediators in response to CBT indicated that early behavioural and cognitive change was associated with positive outcomes across ED diagnoses [ 22 ]. Similarly, a recent systematic review and meta-analysis of 20 years of accumulated evidence concluded early response to treatment the most robust predictor of better treatment outcomes, however, only half of people investigated across numerous studies showed early change, and more research was needed to determine outcome predictors [ 110 ]. Ongoing assessment to identify individuals who do not show early response to treatment (defined by healthy weight and absence of ED behaviours at 12 month FU), as well as provision of targeted engagement approaches, may improve outcomes [ 47 ].

Due to the frequent need for medical stabilisation in the early and acute stages of AN, the role of hospitalisation needs to be considered in the evaluation of treatment outcomes. In a large patient cohort study ( n  = 7505) with 5 year FU, a clear trend was observed with the per-patient 5 year cumulated number of inpatient days decreasing by 6% per annum after adjustment for age at diagnosis, parental mental health, and household income. The number of hospital admissions decreased by 2% per year, although there was no change in outpatient visits [ 111 ]. Factors contributing to better outcomes were not identified in this study, but in other research, early change in %EBW and ED psychopathology in adolescent inpatients predicted later change in the same ED variables [ 18 ]. Another study showed longer first admission predicted increased use of the health system in young adults [ 112 ].

In a multicentre RCT there was no difference between higher or lower calorie refeeding on clinical remission or medical hospitalisation to 12 month FU [ 113 ]. A systematic scoping review of 49 studies found adolescent day programs (intensive treatment programmes that do not involve an overnight stay at the treatment facility) can be an effective alternative to inpatient hospitalisation or step up/down in treatment intensity and are generally associated with weight gain and improvements in ED and comorbid psychopathology [ 114 ]. Outcomes in the review were sustained from 3 months to 2 years from EOT; however, due to large variability in the content, structure and theoretical underpinnings of reviewed programs, findings should be interpreted with caution.

Difficulties with emotion regulation are also associated with poor outcome across diagnostic profiles. There is evidence to suggest emotion-focused treatment is beneficial both to emotional functioning and mood as well as ED severity for people with elevated emotion regulation issues at baseline with positive effects lasting up to 5 years FU [ 115 ].

Self-esteem, self-compassion, and motivation

There is little conclusive evidence regarding predictors of poor response to evidence-based treatments [ 22 , 58 ]; however, low self-esteem has been implicated across all ED diagnoses [ 98 , 101 ], particularly AN [ 55 ]. A meta-analysis exploring the role of self-esteem on treatment outcomes indicated that while self-esteem did not predict remission or long-term weight related outcomes, it did mediate progression during inpatient treatment (greater increase in self-esteem during inpatient treatment was associated with higher remission and lower relapse rates at FU) [ 116 ]. Relatedly, high fear of self-compassion was associated with greater severity of ED symptoms in individuals with an active ED, suggesting that a fearful unwillingness to become more self-compassionate, rather than the absence of self-compassion, may lead to more detrimental outcomes [ 117 ].

Greater pre-treatment motivation has also been associated with ED symptom improvement and management of co-occurring anxiety and depression, in a systematic review and meta-analysis of 42 longitudinal studies [ 118 ]. Therapeutic interventions that include enhancement of motivation, self-esteem and self-compassion have been shown across studies to improve treatment outcomes across diagnostic profiles [ 117 ].

Relapse prevention programs

Whilst the role of treatment is crucial in the alleviation of symptoms and restoration of wellbeing, active provision of evidence-based post-treatment recovery care may be an important determining factor in relapse prevention. Research suggests the period in which individuals are at greatest risk of relapse is between four and nine-months following discharge [ 35 ], with between 31 and 41% relapsing at one to two years post-discharge [ 62 ].

To reduce readmission among a group of females receiving inpatient treatment for AN at an Australian specialist child and adolescent ED service, a 10 week transition ‘day’ program was developed and evaluated. The delivered program allowed for a ‘step down’ option and was found to have significant benefit for participants, who achieved an average weight gain of over 1 BMI point and decreased ED symptomatology at six-month FU [ 65 ]. Promising findings were also seen in a 6-session post-(inpatient and/or outpatient) treatment relapse prevention program designed by clinicians, parents, and patients in the Netherlands, which included a take-home workbook and appointments up to 18 months (frequency dependent on patient progress). Evaluated with young people with AN-R and AN-BP, 70% maintained post-discharge recovery to the end of the study period [ 36 ]. Such programs were evaluated in the context of a comprehensive specialist service with no control group comparison to measure the impact of the specific intervention, and there was no FU assessment following conclusion of the intervention to assess maintenance. Although more work is needed, these studies indicate the value of targeted relapse prevention programs.

Online relapse prevention programs

There is emerging evidence to support the safety and efficacy of internet-based relapse prevention programs aimed at preventing readmission to intensive ED treatment following discharge. These programs have the potential to be widely disseminated to individuals who may otherwise disengage from ongoing support due to access issues (e.g., living in an underserviced area, financial burden) or personal reasons such as stigma or shame [ 119 , 120 ].

A 9-session (1/month) CBT-based online relapse prevention program for women with AN discharged from inpatient treatment (baseline BMI x̄  = 17.7) found participants who completed the program had significant gains in BMI at end of program ( x̄  = 19.1) while the treatment as usual (TAU) control group did not ( x̄  = 17.7). Of note, participants who were 1–2 sessions short of completing the program maintained a higher BMI ( x̄  = 18.0) than the TAU group, whereas participants with less than 50% completion had a significantly lower BMI than any group including TAU ( x̄  = 17.0) [ 121 ]. A similar CBT-based online program targeted toward women discharged from inpatient treatment for BN found that the intervention group reported 46.0% fewer vomiting episodes compared to TAU, with some improvement in symptom abstinence (intervention group: 21.4%, TAU control = 18.9%), although this finding was not statistically significant [ 122 ].

In Hungary, an internet-based aftercare support program for individuals who had received inpatient or outpatient treatment for BN or related EDNOS in the 12 months prior to the study included information and support offered via 30 min chat sessions with peers and clinicians. Results showed 40.6% of the intervention group reported improvement compared to TAU waitlist controls (24.4%), although this difference was not statistically significant. The study noted that, although on the waitlist for the internet-based aftercare support program, the TAU group could still access additional treatment if so required. Evaluation findings report the program was feasible and well accepted [ 123 ].

Text messaging-based interventions have also been trialled to maintain engagement post-treatment, whereby participants send regular symptom reports to the clinical team with feedback provided. A 12 week ‘mobile therapy’ study with a group of women exiting CBT treatment for BN resulted in significant improvement in binge/purge frequency, ED and depressive symptoms from baseline to FU, with high rates of protocol adherence (87.0%), although there was no control group comparison [ 124 ]. Further evidence was provided in a 16 week weekly symptom report study of women with BN following inpatient discharge, with a significantly larger proportion of the intervention group achieving remission (51%) compared with TAU (36%) at 8 months FU. There was no significant difference between groups in terms of outpatient service use [ 125 ]. Results from these studies conflict with evidence from a systematic review of 15 studies, which was unable to support the effectiveness of text messaging-based programs for people with ED as either a sole or adjunctive component of the intervention [ 126 ]; however, this review noted the lack of a common evaluation framework making comparison difficult.

Despite advances in awareness and treatment, ED, particularly AN, continue to be associated with increased risk of mortality [ 4 ]. Studies identified that focus on the assessment of ED mortality, as well as data from the Global Burden of Disease Study 2016 are discussed in this section. Importantly, there are several different metrics used to report mortality. These include the Standardised Mortality Ratio (SMR), or the number of observed deaths in a cohort versus the number of expected deaths in a reference population (where a rate greater than one is interpreted as excess mortality); Weighted Mortality Ratio (WMR), or the weighted average of age-specific mortality rates per 100,000 persons; Crude Mortality Rate (CMR) , or the number of deaths in a given period divided by the population exposed to risk of death in that period; and Years of Life Lost (YLL), a summary measure of premature mortality calculated by subtracting the age at death from the standard life expectancy in a reference population.

Standardised, weighted, and crude mortality

AN is consistently described as having the highest mortality rate of the ED, but actual rate difference varies between studies. A summary of Standardised Mortality Ratios across studies is presented in Table 3 . SMRs from a meta-analysis suggest that measured mortality of AN is approximately three times as high as for other ED diagnoses, and in a UK study of ED patients ( n  = 1892) accessing services between 1992 and 2004, the SMR for AN was almost five times higher than other ED [ 127 ]. This is consistent with other research (a meta-analysis summarising 41 studies) reporting people with AN were 5.2 [3.7–7.5] times more likely to die prematurely from any cause [ 128 ]. A longitudinal study ( n  = 246) found SMR of AN to be only twice as high compared to BN, but still 6.5 times the rate expected in the general population [ 49 ].

Some studies did not report higher SMR for AN compared to other ED, however, methodological differences need to be considered. For example, some studies reported comparable SMR for AN to other ED, but subthreshold AN cases were included (previously catagorised as EDNOS) which may have reduced the calculated AN SMR [ 104 , 108 ]. In a British study using English National Hospital Episodes Statistics (2001–2009) comparing AN and BN, little difference in SMRs was reported [ 132 ]. The diagnosis of BN was less likely than other diagnosis to be recorded as the primary diagnosis and may not have been representative.

In a 22 year trial FU of a large sample of inpatients treated for BN, 2.4% had died [ 45 ]; the CMR for BN was 0.32% [ 63 ] and in severely malnourished patients, the crude mortality rate rose to 11.5% with SMR 15.9 [CI 95% (11.6–21.4)], just over 5 years post-treatment [ 137 ]. WMR has been found to be 5.1 for AN, 1.7 for BN, and 3.3 for EDNOS. SMRs were 5.86 for AN, 1.93 for BN, 1.92 for EDNOS [ 4 ] and 1.5–1.8 for BED [ 76 ].

Mortality rates in AN were highest during the first year after admission to treatment, while in BN it is in the first two years [ 134 ], with a higher risk in adolescence [ 140 ]. In AN, peak age of risk of death has been reported to be 15 years of age, BN 22 years and EDNOS 18–22 years [ 141 ]. Substance use disorders (including alcohol and/or cannabis) increased mortality in people with eating disorders across the diagnostic profiles [ 142 ].

In ED, peak age of risk for males may be earlier than females [ 141 ]. SMRs are higher for males (SMR = 7.24; 95% CI 6.58–7.96) relative to females (SMR = 4.59; 95% CI 4.34–4.85) overall, and in all age groups [ 131 ]. This may be due to the lower likelihood of males to self-identify or be identified with ED resulting in treatment delays and higher severity of illness when finally seeking help [ 131 ]. In mortality research conducted with a male-only sample, similarly high SMRs for males with BN and particularly AN as in majority female samples [ 2 ] were reported; however, mortality rates of EDNOS in males were considerably higher than those reported in female-dominant or female-only samples. Moreover, a case-controlled study found there was a sex difference across all diagnostic categories in CMR, with male to female being 15–5% in AN, 8–3% in BN, and 4–3% in EDNOS, but there were no significant sex differences in SMR for any diagnostic group, with males showing a shorter survival time after onset [ 2 ]. Researchers have suggested that increased mortality in males could be due to several factors, including reluctance to seek treatment and current treatment approaches being less effective in males [ 138 ]. Further research in males with ED is required to better understand the impact and response in male patients. Regardless of the mortality metric used, these studies indicate the vital importance of considering elevated mortality risk across the range of ED diagnoses.

Years of life lost/years lived with disability

The Global Burden of Disease Study 2016 reported that YLL due to premature death attributable to AN was 0.4 per 100,000. No YLL were attributed to BN; however, cause-specific mortality (CSM)—where each death is attributed to a single underlying cause—was, per thousand, 0.5 for AN (with a 2.9% increase from 1980 to 2016) and 0.1 for BN (21.8% increase from 1980 to 2016) [ 143 ]. The 2019 extension advocated for the inclusion of BED and OSFED in the Global Burden of Disease Study, previously excluded, as both diagnostic groups accounted for the majority of global ED cases and accounted for an unrepresented 41.9 million people living with ED [ 144 ].

Estimates are that over 3.3 million healthy life years are lost per year worldwide due to eating disorders. Years lived with a disability (YLDs) have increased from 2007 to 2017 for both AN (6.2% increase) and BN (10.3%), a higher rate than other mental disorders (− 0.1%). ED outcomes include reduced self-reported quality of life and estimated health care costs at 48% higher than for the general population [ 3 ].

Risk factors

Little is known about specific risk factors for mortality, although some variables have been reported in the literature. People who receive inpatient treatment for AN have more than five to seven times mortality risk when matched to age and gender and compared to other ED diagnoses [ 3 , 131 , 133 ]. For individuals receiving AN or BN treatment in outpatient settings, the risk is still twice that of controls [ 3 ]. Older age of presentation is a significant risk; adult presentations are associated with much higher mortality rates than adolescent presentations likely due to longer duration of illness at presentation, higher rates of medical and psychiatric complications and less engagement in treatment [ 4 , 28 , 68 , 137 , 139 ]. Higher mortality rates (especially in AN) are associated with lower BMI, longer duration of illness at service presentation [ 4 , 49 , 68 , 137 , 139 ], diuretic use [ 68 ], and occurrence of an in-hospital suicide attempt [ 68 , 137 ]. Certain treatment factors may be associated with higher risk of mortality, including transfer to medical intensive care unit, discharge against medical advice, and shorter hospital stays [ 137 ]. Other factors associated with increased risk of mortality include poor psychosocial functioning, substance use [ 28 , 49 ] and absence of family ED history [ 28 ].

Cause of death

Results from a large prospective 20 year (1985–2005) longitudinal study of individuals admitted to inpatient services in Germany ( n  = 5839) showed people with AN were likely to die from health issues caused by their disorder, most commonly circulatory failure, cachexia, and multiple organ failure [ 133 ]. Other studies have identified somatic risk factors including anaemia, dysnatremia, infection, cardiac complications and haematological comorbidities [ 137 ]. A 2021 study reported rates of medical complications for severe AN, which included anaemia (79%), neutropenia (53.9%), hypertransaminasemia (53.7%), osteoporosis (46.3%), hypokalemia (39.5%), hypophosphatemia (26%), hypoglycaemia (13.8%), infectious complications (24.3%), cardiac dysfunction (7.1%), and proven gelatinous bone marrow transformation (6.5%). Five (1.4%) of the patients in this study died of the following causes: septic shock of pulmonary origin ( n  = 1), septic shock of urinary origin ( n  = 1) and suicide ( n  = 3) [ 145 ].

Suicide is the most common non-natural cause of death in people with AN, BN, BED and EDNOS [ 133 ]. High rates of suicidality were reported in a meta-analysis of 36 studies published between 1966 and 2010 with data showing one in five individuals who died from an ED did so by suicide [ 4 ]. Risk of suicide may be particularly elevated in AN [Hazard Ratio (HR) 5.07; 95% CI 1.37–18.84] and BN (HR 6.07; 95% CI 2.47–14.89) even when specialised treatments are available [ 134 ]: people with AN are 18.1 [11.5–28.7] times more likely to die by suicide than 15–34 year old females in the general population [ 128 ]. This is supported by results from a meta-review exploring risk of all-cause and suicide across major mental disorders. 1.7 million patients and over a quarter of a million deaths were examined, finding all mental health disorders had an increased mortality rate to the general population; however, substance use and AN were the highest, translating into 10–20 year reductions in life expectancy, with borderline personality disorder, AN, depression and bipolar disorder having the highest suicide risk [ 146 ].

This rapid review, which synthesised the available literature on ED remission, relapse and recovery rates including associated moderating and mediating variables such as psychosocial and treatment characteristics, highlighted significant challenges of synthesising outcome literature. This includes a wide variety of ways in which key outcomes ‘remission’, ‘relapse’ and ‘recovery’ are not only defined but also how they are measured and analysed. There is no consensus among clinical or research communities on these definitions for any of the ED diagnoses [ 30 , 31 , 94 ]; thus, comparison between studies is challenging.

As EDs have amongst the highest rates of mortality of the mental health disorders, including one in five deaths caused by suicide, research into preventable causes of death, mitigatable risk, prevention and treatment efficacy is of paramount importance. It is noteworthy that current reported YLL and YLD for ED are likely an underestimate due to lack of robust epidemiological data, methodological limitations of burden of disease studies, absence of the illness group from national surveys and underreporting of mortality [ 147 ].

‘Relapse’ is typically defined by a return of symptoms after a period of reduced symptomatology; however, reviewed studies report a variety of methods to measure this, including multidisciplinary healthcare team assessment, scores on standardised psychological and behavioural interviews or questionnaires, weight criteria (including BMI or %EBW), reported eating disorder behaviours, meeting DSM (IV or V) diagnostic criteria, or a combination of the above. More difficult is determining if there is a difference between ‘remission’ and ‘recovery’, with remission usually determined by an absence of diagnostic symptomatology (again, characterised by a variety of methods), and recovery an improvement in overall functioning. Many studies report remission and recovery interchangeably, and very few incorporate returns to psychosocial functioning and QoL post alleviation of symptoms [ 29 ]. More standardised definitions may progress research [ 148 ] by allowing direct comparison between outcome studies, improving the ability of future investigations to predict and report relapse versus recovery rates and to comprehensively evaluate intervention and relapse prevention approaches.

An additional challenge across studies is a highly variable period between initial assessment or baseline and the time at which ‘outcome’ is assessed—ranging from as little as one week up to 25 years. As rates of relapse increase with illness progression, relatively short FU periods may compromise the understanding of true long-term outcomes. Longer-term FU studies are crucial to understand optimised models of care for sustained recovery and wellbeing.

Along with illness progression over time in individuals, the shift of diagnostic profiles among the individual may differ the definition of relapse or remission and thus impacts on outcome measures. Most research protocols adopt a firm inclusion/exclusion criterion, focusing on specific diagnostic profiles; however, findings from this review suggest considering a transdiagnostic approach in outcomes research which may better reflect the potentially transient nature of ED symptomatology [ 44 ]. This may have implications for diagnoses such as OSFED, potentially a transient category [ 21 ], rather than categorisation in or out of full ED diagnostic syndromes. Identification and consideration of transdiagnostic profiles, combined ED presentations and co-occurring mental health conditions should be considered in the long-term management and monitoring of individuals.

Studies within this review reported on cohorts of individuals with a formal diagnosis and research conducted within treatment settings. However, previous research has suggested that incidence rates within the community are considerable, and yet help-seeking of any type for a problem related to ED symptoms is uncommon, ranging between 22 and 40% [ 106 ] and there can be a significant time delay from first symptom experience [ 69 ]. A recent large community survey of the impact of COVID-19 on people with ED reported up to 70% of people who experienced ED symptoms were not in treatment [ 149 ] suggesting a significant proportion of people with an ED are not captured within this outcome review. Outcomes for this population are largely unknown [ 150 ] but preliminary research suggests they may be less favourable [ 151 , 152 ].

Improved QoL has been shown to be a significant predictor of positive outcome and is an opportunity for broader scope interventions for people with ED [ 107 ], and yet consistent and more wholistic markers of life quality are rarely integrated into research or clinical decision making [ 153 , 154 ]. It is also noted that outcome determinants in the reviewed studies are predominantly biometric (e.g., weight) and ED symptom related, whereas qualitative lived experience evidence suggests a broader range of person-centred metrics should be used to measure outcome. These include supportive relationships (e.g., receiving support, advice and encouragement from others, including family, friends, and/or professional carers), sense of hope, identity, meaning and purpose, feelings of empowerment and self-compassion [ 155 ]. Involvement of those to whom the work pertains (i.e., individuals with lived experience) is essential in future outcomes research to add richness and utility to theoretical frameworks, methodological approaches and conclusions [ 156 ].

Key findings

ED frequently take a chronic course, with less than half of individuals achieving recovery at long-term FU [ 41 , 44 , 52 ]. Between 30 and 41% of people will relapse within two years of receiving treatment [ 35 , 61 ], and between 20 and 61% will experience more than one type of eating disorder [ 7 , 63 , 64 ]. As with much of the extant ED literature, most outcome research has been conducted in AN. Restrictive ED are consistently associated with the poorest prognosis. This review identified recovery rates in the range of 18–60% for AN and an average length of illness of between 6.5 and 14 years [ 41 , 56 ]. Binge/purge symptomatology within AN is associated with worse outcome [ 20 , 56 ]. Recovery rates for BN are slightly more optimistic at 35–59% [ 7 , 45 , 63 , 157 ], and similarly for BED at 37–77% [ 79 , 80 , 82 ]. There is limited data available on outcomes in ARFID, OSFED, and UFED.

Factors associated with a more positive long-term outcome include lower age of presentation [ 28 , 61 ], shorter duration of illness at first presentation [ 69 , 93 , 94 ], higher pre-treatment motivation to recover [ 116 ], and demonstrated early response to treatment [ 18 , 75 , 110 , 112 ]. Factors associated with poorer outcome are lower BMI at presentation [ 93 ], presence of binge/purge symptomatology [ 20 , 30 , 44 , 56 ], and presence of comorbid psychiatric condition/s such as depression, anxiety, or personality disorder [ 44 , 47 , 51 , 55 , 67 , 98 , 99 ]. Males, LGBTQIA + community [ 104 , 105 ], neurodiversity [ 102 ], individuals from non-white/ethnic backgrounds, and those from lower socioeconomic brackets or rural/remote communities are also more likely to experience a poor outcome [ 18 , 72 , 76 , 77 ].

Relapse following ED treatment is common [ 11 , 35 , 36 , 62 , 148 ] and is most likely to occur 4–9 months post discharge [ 35 ]. Up to 41% of individuals will relapse by the second-year post-discharge [ 62 ]. Aftercare relapse prevention programs, including online and face-to-face initiatives such as text-message based interventions, daily feedback to clinicians and intensive day programs have been shown to increase chance of maintaining recovery [ 121 , 123 – 125 ]. The implementation of such programs may be key to improving long-term recovery rates particularly for those individuals who may otherwise disengage from treatment for access reasons (such as living in an underserviced area) or because of the stigma of engaging with mental health care [ 119 , 120 ]. There is emerging evidence in the effectiveness of online intervention for preventing relapse and promoting treatment gains when individuals are motivated to change; however, evidence is not conclusive potentially due to the high variability of the interventions and evaluations of such programs.

ED are associated with unacceptably high mortality rates, and particularly high risk of suicide [ 128 , 133 ]. Of the ED, AN carries the highest mortality risk [ 49 , 127 , 128 ]. Standardised mortality ratios (SMRs) identified by this review ranged between 1.2 and 15.9 for AN; 1.4 and 4.8 for BN; 1.01 and 3.3 for BED; and 1.3 to 4.7 for EDNOS/OSFED [ 2 , 4 , 20 , 121 , 127 , 128 , 132 , 134 , 135 , 137 , 139 ]. Factors associated with increased risk of mortality include having received inpatient treatment [ 3 , 131 , 133 ], longer duration of untreated illness [ 4 , 28 , 68 , 68 , 137 , 139 ] and lower BMI at presentation [ 4 , 49 , 68 , 137 , 139 ]. Males are at higher risk of death than females [ 2 ].

Strengths and limitations

This rapid review has several strengths inherent to the methodological approach of the series, conducted to inform the Australian Eating Disorders Research and Translation Strategy 2021–2031 [ 1 ]. The RR process broadly assessed all available high-level evidence peer-reviewed literature swiftly [ 24 ], included all diagnostic categories covering transdiagnostic continuums, considered the full demographic range available and reported a variety of methodological designs including clinical trials (across a variety of settings), systematic reviews, meta-analyses, and population-level research. It aimed to provide the most comprehensive and current review possible with coordination of complex findings into a more cohesive structure. It was noted where applicable the limitations of conclusions drawn from this review, such as the widely disparate definitions and measurements for key outcome data (i.e., remission, relapse, and recovery rates), crossover from DSM-IV to DSM-V criteria (due to timeframe of search), vastly different periods of follow up impacting findings, and conflicting evidence. As with the series of rapid reviews, the inclusion criteria of evidence may have potentially excluded relevant evidence, and it is noted that evidence is always emerging.

This RR of outcomes in ED identified several gaps in current knowledge and provides direction for future strategic research directives, specifically, defining the key outcomes of remission, recovery, and relapse, with consensus of determinants and inclusion of broader QoL measures and lived experience. Identifying and refining risk factors, mediating and moderating factors that may influence outcomes is ongoing, with longer-term FU research needed to track remission versus relapse, diagnostic crossover and optimisation of treatment engagement and recovery. Regarding mortality literature, this review noted considerable gaps [ 146 ], with variety reporting methods, a paucity of research between population level reporting and small hospital outcome studies, and minimal investigation into life circumstances relating to death, especially as many of these deaths may be preventable. With low rates of remission despite evidence-based care and high risk of mortality, especially for AN, it is strongly recommended that focused, long-term follow-up research is prioritised for people with ED.

Availability of data and materials

Not applicable—all citations provided.

Abbreviations

Atypical anorexia nervosa

Adolescent focused therapy

• Anorexia nervosa

Anorexia nervosa binge/purge subtype

Anorexia nervosa restricting subtype

Avoidant restrictive food intake disorder

• Binge eating disorder

Body mass index

• Bulimia nervosa

Behavioural weight loss therapy

Cognitive behaviour therapy

Enhanced cognitive behavioural therapy

Crude mortality rate

Diagnostic and statistical manual of mental disorders

Expected body weight

• Eating disorders

Eating disorder examination questionnaire

Eating disorder not otherwise specified

Eating disorder not otherwise specified-anorectic type

Eating disorder not otherwise specified-bulimic type

End of treatment

Family-based therapy

Healthcare management advisors

Health related quality of life

Integrative cognitive-affective therapy

InsideOut Institute

Interpersonal therapy

Major depressive disorder

Objective binge eating

Obsessive compulsive disorder

Other specified feeding or eating disorder

Quality of life

Randomised controlled trial

National eating disorder research & translation strategy rapid review

Standardised mortality ratio

Substance use disorder

Treatment as usual

Unspecified feeding or eating disorder

Weighted mortality ratio

Years of life lost

Years lived with a disability

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Acknowledgements

The InsideOut Institute is a collaboration between the University of Sydney and Sydney Local Health District. We thank all the staff from the Institution for their support of this significant project. 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 Members (alphabetical order of surname): *indicates named authors. Phillip Aouad InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Sarah Barakat InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Robert Boakes School of Psychology, Faculty of Science, University of Sydney, NSW Australia. Leah Brennan School of Psychology and Public Health, La Trobe University, Victoria, Australia. Emma Bryant* InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Susan Byrne School of Psychology, Western Australia, Perth, Australia. Belinda Caldwell Eating Disorders Victoria, Victoria, Australia. Shannon Calvert Perth, Western Australia, Australia. Bronny Carroll InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. David Castle Medicine, Dentistry and Health Sciences, University of Melbourne, Victoria, Australia. Ian Caterson School of Life and Environmental Sciences, University of Sydney, Sydney, New South Wales, Australia. Belinda Chelius Eating Disorders Queensland, Brisbane, Queensland, Australia. Lyn Chiem Sydney Local Health District, New South Wales Health, Sydney, Australia. Simon Clarke Westmead Hospital, Sydney, New South Wales, Australia. Janet Conti Translational Health Research Institute, Western Sydney University, Sydney NSW Australia. Lexi Crouch Brisbane, Queensland, Australia. Genevieve Dammery InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Natasha Dzajkovski InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Jasmine Fardouly School of Psychology, University of New South Wales, Sydney, New South Wales, Australia. John Feneley New South Wales Health, New South Wales, Australia. Amber-Marie Firriolo University of Sydney, NSW Australia. Nasim Foroughi Translational Health Research Institute, Western Sydney University, Sydney NSW Australia. Mathew Fuller-Tyszkiewicz School of Psychology, Faculty of Health, Deakin University, Victoria, Australia. Anthea Fursland School of Population Health, Faculty of Health Sciences, Curtain University, Perth, Australia. Veronica Gonzalez-Arce InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Bethanie Gouldthorp Hollywood Clinic, Ramsay Health Care, Perth, Australia. Kelly Griffin InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Scott Griffiths Melbourne School of Psychological Sciences, University of Melbourne, Victoria, Australia. Ashlea Hambleton InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Amy Hannigan Queensland Eating Disorder Service, Brisbane, Queensland, Australia. Mel Hart Hunter New England Local Health District, New South Wales, Australia. Susan Hart St Vincent’s Hospital Network Local Health District, Sydney, New South Wales, Australia. Phillipa Hay Translational Health Research Institute, Western Sydney University, Sydney NSW Australia. Ian Hickie Brain and Mind Centre, University of Sydney, Sydney, Australia. Francis Kay-Lambkin School of Medicine and Public Health, University of Newcastle, New South Wales, Australia. Ross King School of Psychology, Faculty of Health, Deakin University, Victoria, Australia. Michael Kohn Paediatrics & Child Health, Children's Hospital, Westmead, Sydney, Australia. Eyza Koreshe InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Isabel Krug Melbourne School of Psychological Sciences, University of Melbourne, Victoria, Australia. Jake Linardon School of Psychology, Faculty of Health, Deakin University, Victoria, Australia. Randall Long College of Medicine and Public Health, Flinders University, South Australia, Australia. Amanda Long Exchange Consultancy, Redlynch, New South Wales, Australia. Sloane Madden Eating Disorders Service, Children’s Hospital at Westmead, Sydney, New South Wales, Australia. Sarah Maguire* InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Danielle Maloney InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Peta Marks InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Sian McLean The Bouverie Centre, School of Psychology and Public Health, La Trobe University, Victoria, Australia. Thy Meddick Clinical Excellence Queensland, Mental Health Alcohol and Other Drugs Branch, Brisbane, Queensland, Australia. Jane Miskovic-Wheatley* InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Deborah Mitchison Translational Health Research Institute, Western Sydney University, Sydney NSW Australia. Richard O’Kearney College of Health & Medicine, Australian National University, Australian Capital Territory, Australia. Shu Hwa Ong* InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Roger Paterson ADHD and BED Integrated Clinic, Melbourne, Victoria, Australia. Susan Paxton La Trobe University, Department of Psychology and Counselling, Victoria, Australia. Melissa Pehlivan InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Genevieve Pepin School of Health & Social Development, Faculty of Health, Deakin University, Geelong, Victoria, Australia. Andrea Phillipou Swinburne Anorexia Nervosa (SWAN) Research Group, Centre for Mental Health, School of Health Sciences, Swinburne University, Victoria, Australia. Judith Piccone Children's Health Queensland Hospital and Health Service, Brisbane, Queensland, Australia. Rebecca Pinkus School of Psychology, Faculty of Science, University of Sydney, NSW Australia. Bronwyn Raykos Centre for Clinical Interventions, Western Australia Health, Perth, Western Australia, Australia. Paul Rhodes School of Psychology, Faculty of Science, University of Sydney, NSW Australia. Elizabeth Rieger College of Health & Medicine, Australian National University, Australian Capital Territory, Australia. Karen Rockett New South Wales Health, New South Wales, Australia. Sarah-Catherine Rodan InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Janice Russell Central Clinical School Brain & Mind Research Institute, University of Sydney, New South Wales, Sydney. Haley Russell InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Fiona Salter Ramsay Health Care, Perth, Australia. Susan Sawyer Department of Paediatrics, The University of Melbourne, Australia. Beth Shelton National Eating Disorders Collaboration, Victoria, Australia. Urvashnee Singh The Hollywood Clinic Hollywood Private Hospital, Ramsey Health, Perth, Australia. Sophie Smith Sydney, New South Wales, Australia. Evelyn Smith Translational Health Research Institute, Western Sydney University, Sydney NSW Australia. Karen Spielman InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Sarah Squire The Butterfly Foundation, Sydney, Australia. Juliette Thomson The Butterfly Foundation, Sydney, Australia. Stephen Touyz* InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Ranjani Utpala The Butterfly Foundation, Sydney, Australia. Lenny Vartanian School of Psychology, University of New South Wales, Sydney, New South Wales, Australia. Sabina Vatter* InsideOut Institute, Central Clinical School, Faculty of Medicine and Health, University of Sydney, NSW Australia. Andrew Wallis Eating Disorder Service, The Sydney Children’s Hospital Network, Westmead Campus, Sydney, Australia. Warren Ward Department of Psychiatry, University of Queensland, Brisbane, Australia. Sarah Wells University of Tasmania, Tasmania, Australia. Eleanor Wertheim School of Psychology and Public Health, La Trobe University, Victoria, Australia. Simon Wilksch College of Education, Psychology and Social Work, Flinders University, South Australia, Australia. Michelle Williams Royal Hobart, Tasmanian Health Service, Tasmania, Australia.

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.

Faculty of Medicine and Health, InsideOut Institute for Eating Disorders, University of Sydney, Level 2, Charles Perkins Centre (D17), Sydney, NSW, 2006, Australia

Jane Miskovic-Wheatley, Emma Bryant, Shu Hwa Ong, Sabina Vatter, Phillip Aouad, Sarah Barakat, Emma Bryant, Bronny Carroll, Genevieve Dammery, Natasha Dzajkovski, Veronica Gonzalez-Arce, Kelly Griffin, Ashlea Hambleton, Eyza Koreshe, Sarah Maguire, Danielle Maloney, Peta Marks, Jane Miskovic-Wheatley, Shu Hwa Ong, Melissa Pehlivan, Sarah-Catherine Rodan, Haley Russell, Karen Spielman, Stephen Touyz, Sabina Vatter, Stephen Touyz & Sarah Maguire

Sydney Local Health District, Sydney, Australia

Healthcare Management Advisors, Melbourne, Australia

School of Psychology, Faculty of Science, University of Sydney, Sydney, NSW, Australia

Robert Boakes, Rebecca Pinkus & Paul Rhodes

School of Psychology and Public Health, La Trobe University, Victoria, Australia

Leah Brennan & Eleanor Wertheim

School of Psychology, Perth, Western Australia, Australia

Susan Byrne

Eating Disorders Victoria, Victoria, Australia

Belinda Caldwell

Perth, Australia

Shannon Calvert

Medicine, Dentistry and Health Sciences, University of Melbourne, Victoria, Australia

David Castle

School of Life and Environmental Sciences, University of Sydney, Sydney, NSW, Australia

Ian Caterson

Eating Disorders Queensland, Brisbane, QLD, Australia

Belinda Chelius

Sydney Local Health District, New South Wales Health, Sydney, Australia

Westmead Hospital, Sydney, NSW, Australia

Simon Clarke

Translational Health Research Institute, Western Sydney University, Sydney, NSW, Australia

Janet Conti, Nasim Foroughi, Phillipa Hay, Deborah Mitchison & Evelyn Smith

Brisbane, Australia

Lexi Crouch

School of Psychology, University of New South Wales, Sydney, NSW, Australia

Jasmine Fardouly & Lenny Vartanian

University of Sydney, Sydney, NSW, Australia

Carmen Felicia & Amber-Marie Firriolo

New South Wales Health, Sydney, NSW, Australia

John Feneley & Karen Rockett

School of Psychology, Faculty of Health, Deakin University, Victoria, Australia

Mathew Fuller-Tyszkiewicz & Ross King

School of Population Health, Faculty of Health Sciences, Curtain University, Perth, Australia

Anthea Fursland

Hollywood Clinic, Ramsay Health Care, Perth, Australia

Bethanie Gouldthorp & Jake Linardon

Melbourne School of Psychological Sciences, University of Melbourne, Victoria, Australia

Scott Griffiths & Isabel Krug

Queensland Eating Disorder Service, Brisbane, QLD, Australia

Amy Hannigan

Hunter New England Local Health District, New Lambton, NSW, Australia

St Vincent’s Hospital Network Local Health District, Sydney, NSW, Australia

Brain and Mind Centre, University of Sydney, Sydney, Australia

School of Medicine and Public Health, University of Newcastle, Newcastle, NSW, Australia

Francis Kay-Lambkin

Westmead Hospital, Sydney, Australia

Michael Kohn

College of Medicine and Public Health, Flinders University, Adelaide, SA, Australia

Randall Long

Exchange Consultancy, Redlynch, NSW, Australia

Amanda Long

Eating Disorders Service, Children’s Hospital at Westmead, Sydney, NSW, Australia

Sloane Madden

The Bouverie Centre, School of Psychology and Public Health, La Trobe University, Victoria, Australia

Sian McLean

Clinical Excellence Queensland, Mental Health Alcohol and Other Drugs Branch, Brisbane, QLD, Australia

Thy Meddick

College of Health and Medicine, Australian National University, Canberra, ACT, Australia

Richard O’Kearney & Elizabeth Rieger

ADHD and BED Integrated Clinic, Melbourne, VIC, Australia

Roger Paterson

Department of Psychology and Counselling, La Trobe University, Victoria, Australia

Susan Paxton

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

Genevieve Pepin

Swinburne Anorexia Nervosa (SWAN) Research Group, Centre for Mental Health, School of Health Sciences, Swinburne University, Victoria, Australia

Andrea Phillipou

Children’s Health Queensland Hospital and Health Service, Brisbane, QLD, Australia

Judith Piccone

Centre for Clinical Interventions, Western Australia Health, Perth, WA, Australia

Bronwyn Raykos

Central Clinical School Brain & Mind Research Institute, University of Sydney, Sydney, NSW, Australia

Janice Russell

Ramsay Health Care, Perth, Australia

Fiona Salter

Department of Paediatrics, The University of Melbourne, Parkville, Australia

Susan Sawyer

National Eating Disorders Collaboration, Victoria, Australia

Beth Shelton

The Hollywood Clinic Hollywood Private Hospital, Ramsey Health, Perth, Australia

Urvashnee Singh

Sydney, Australia

Sophie Smith

The Butterfly Foundation, Sydney, Australia

Sarah Squire, Juliette Thomson & Ranjani Utpala

Eating Disorder Service, The Sydney Children’s Hospital Network, Westmead Campus, Sydney, Australia

Andrew Wallis

Department of Psychiatry, University of Queensland, Brisbane, Australia

Warren Ward

University of Tasmania, Hobart, TAS, Australia

Sarah Wells

College of Education, Psychology and Social Work, Flinders University, Adelaide, SA, Australia

Simon Wilksch

Royal Hobart, Tasmanian Health Service, Hobart, TAS, Australia

Michelle Williams

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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
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Contributions

AL carried out and wrote the initial review from the first search; JMW conducted subsequent reviews, analysed results, wrote the first manuscript and the final edit; EB, SHO and SV contributed to specific sections, detailed tables and figures, responded to review comments and contributed to ongoing drafts to manuscript completion; the National Eating Disorder Research Consortium reviewed and provided expert feedback; ST and SM provided project direction, methodological design, comprehensively reviewed the manuscript and provided overall supervision and leadership. All authors read and approved the final manuscript.

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Correspondence to Jane Miskovic-Wheatley .

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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. He 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. JMW and SM are guest editors of the special issue “Improving the future by understanding the present: evidence reviews for the field of eating disorders.”

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Studies included in the Rapid Review.

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Miskovic-Wheatley, J., Bryant, E., Ong, S.H. et al. Eating disorder outcomes: findings from a rapid review of over a decade of research. J Eat Disord 11 , 85 (2023). https://doi.org/10.1186/s40337-023-00801-3

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Eating Disorder Behaviors Alter Reward Response in the Brain

NIH-funded study finds changes can affect food intake control circuitry and cause disorders to progress

June 30, 2021 • Press Release

Researchers have found that eating disorder behaviors, such as binge-eating, alter the brain’s reward response process and food intake control circuitry, which can reinforce these behaviors. Understanding how eating disorder behaviors and neurobiology interact can shed light on why these disorders often become chronic and could aid in the future development of treatments. The study, published in  JAMA Psychiatry , was supported by the National Institutes of Health.

“This work is significant because it links biological and behavioral factors that interact to adversely impact eating behaviors,” said Janani Prabhakar, Ph.D., of the  Division of Translational Research  at the National Institute of Mental Health, part of NIH. “It deepens our knowledge about the underlying biological causes of behavioral symptom presentation related to eating disorders and will give researchers and clinicians better information about how, when, and with whom to intervene.”

Eating disorders  are serious mental illnesses that can lead to severe complications, including death. Common eating disorders include anorexia nervosa, bulimia nervosa, and binge-eating disorder. Behaviors associated with eating disorders can vary in type and severity and include actions such as binge-eating, purging, and restricting food intake.

In this study,  Guido Frank, M.D.   , at the University of California San Diego, and colleagues wanted to see how behaviors across the eating disorder spectrum affect reward response in the brain, how changes in reward response alter food intake control circuitry, and if these changes reinforce eating disorder behaviors. The study enrolled 197 women with different eating disorders (including anorexia nervosa, bulimia nervosa, binge-eating disorder, and other specified feeding and eating disorders) and different body mass indexes (BMIs) associated with eating disorder behaviors, as well as 120 women without eating disorders.

The researchers used cross-sectional functional brain imaging to study brain responses during a taste reward task. During this task, participants received or were denied an unexpected, salient sweet stimulus (a taste of a sugar solution). The researchers analyzed a brain reward response known as “prediction error,” a dopamine-related signaling process that measures the degree of deviation from the expectation, or how surprised a person was receiving the unexpected stimulus. A higher prediction error indicates that the person was more surprised, while a lower prediction error indicates they were less surprised. They also investigated whether this brain response was associated with ventral-striatal-hypothalamic circuitry, a neural system associated with food intake control.

The researchers found that there was no significant correlation between BMI, eating disorder behavior, and brain reward response in the group of women without eating disorders. In the group of women with eating disorders, higher BMI and binge-eating behaviors were associated with lower prediction error response. Further, for the women with eating disorders, the direction of ventral striatal-hypothalamic connectivity was the reverse of those without eating disorders, with connectivity directed from the ventral striatum to the hypothalamus. This connectivity was positively related to the prediction error response and negatively related to feeling out of control after eating.

These results suggest that for the women with eating disorders, eating disorder behaviors and excessive weight loss or weight gain modulated the brain’s dopamine-related reward circuit response, altering brain circuitry associated with food intake control, and potentially reinforcing eating disorder behaviors. For example, women with anorexia nervosa, restrictive food intake, and low BMIs had a high prediction error response. This response may strengthen their food intake-control circuitry, leading these women to be able to override hunger cues. In contrast, the opposite seems to be the case for women with binge-eating episodes and higher BMIs.

“The study provides a model for how behavioral traits promote eating problems and changes in BMI, and how eating disorder behaviors, anxiety, mood, and brain neurobiology interact to reinforce the vicious cycle of eating disorders, making recovery very difficult,” said Dr. Frank.

Overall, this study suggests that behavioral traits, including food intake behavior, contribute to eating disorder maintenance and progression by modulating one’s internal reward response and altering food intake control circuitry. However, further research is needed to investigate treatments that could target and change behaviors for individuals with eating disorders to achieve lasting recovery.

Frank, G. K. W., Shott, M. E., Stoddard, J., Swindle, S., & Pryor, T. (2021) Reward processing across the eating disorders spectrum implicates body mass index and ventral striatal-hypothalamic circuitry.  JAMA Psychiatry.  doi:10.1001/jamapsychiatry.2021.1580

MH096777  ,  MH103436 

About the National Institute of Mental Health (NIMH): The mission of the NIMH  is to transform the understanding and treatment of mental illnesses through basic and clinical research, paving the way for prevention, recovery and cure. For more information, visit the NIMH website .

About the National Institutes of Health (NIH) : NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH  and its programs, visit the NIH website  .

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The sexual competition hypothesis for eating disorders

Affiliation.

• 1 Department of Psychiatry, Rotherham District General Hospital, UK.
• PMID: 9875960
• DOI: 10.1111/j.2044-8341.1998.tb01007.x

A hypothesis is presented for eating disorders, based on Darwinian theory, that contends that these syndromes together with the phenomenon of the pursuit of thinness are manifestations of female intra-sexual competition. It is suggested that eating disorders originate in the human female's psychological adaptation of concern about physical attractiveness which is an important component of female 'mate attraction' and 'mate retention' strategies. It is argued that present-day environment of Western countries presents a range of conditions which have led to the overactivation or the disruption of the archaic female sexual strategy of maximizing 'mate value'. The present hypothesis deals with the ultimate level of causation and is therefore compatible with a range of theories of proximate causation. Although the present hypothesis is not directly testable, it makes predictions that are testable and refutable. Finally it is suggested that the sexual competition hypothesis has more explanatory power than existing evolutionary theories of eating disorders.

• Biological Evolution*
• Feeding and Eating Disorders / genetics
• Feeding and Eating Disorders / psychology*
• Reproduction
• Selection, Genetic*
• Sexual Behavior*

• Eating Disorders

Ethical Considerations for Patients With Eating Disorders

What are the benefits and drawbacks of in-person or virtual relationships.

Posted May 31, 2024 | Reviewed by Tyler Woods

• What Are Eating Disorders?
• Find counselling to heal from an eating disorder

From the mid-1990s until 2014, I founded and was the Executive Director of Cedar Associates, an outpatient treatment center for eating disorders with two locations in Westchester County, New York. We were a group of qualified eating disorder specialists joined together for a common cause—to provide coordinated and expert care to our patients.

One ethical issue we pondered was whether or not we had created a cottage industry for those most vulnerable. We wondered if we were somehow taking advantage of those in need as we were part of the new 'niche' industry created by the rapid increase in the prevalence of eating disorders. There was now a steady influx of patients in desperate need of help. Having an eating disorder is terrifying, debilitating, and costly for patients and their families. Eating disorders remain the leading cause of death among all mental health conditions.

Our dilemma was about money. We simultaneously believed that we were entitled to a solid living wage and that patients were entitled to solid and expert care; both could be true and acceptable. Most healthcare practitioners struggle with healthcare services' delivery, costs, and payment. These ethical issues remain unresolved due to the politicization of healthcare, the complexity of insurance, and other factors. However, clinicians have always been able to assert their training, competency, and expertise in providing treatment unequivocally; these bona files remain ethically foundational.

We now have a choice of mental health care delivery, which has created new ethical considerations. COVID-19 set precedence for conducting sensitive meetings virtually, especially in health care. Whether to see a patient in-person or virtually is now part of the clinical decision-making mix. Deciding whether or when to treat in person versus virtually takes a mindful and clinically astute clinician.

Some factors to consider when deciding between in-person and virtual meetings:

Establishing a prudent care plan involves routinely choosing the type of treatment based on the patient's clinical needs. Eating disorders, like others with complex symptoms, occur among the most psychologically vulnerable people. Assessing the level of severity can be very difficult. Keep in mind all the factors that help in assessment: type, frequency, and use of the symptom are all important, as well as assessing the level of depression , how isolated the person is, the family dynamics, and the level of support the person has in the recovery process.

Since eating disorders manifest in many and with various constellations of symptoms, it isn't always easy to tell by looking at someone what state they are in. Patients can conceal their bodies through layered clothing and hide the truth about their behavior due to shame , anger , and fear .

• Eating disorders are also disorders of relationships—the ones we have with our self-concept and our relationships with others. (Zerbe, 2008, Scheel, 2011). Is the clinician confident that a relationship that fosters support, safety, and appropriate boundaries is possible virtually? Is the clinician comfortable not experiencing the most nuanced communication during online sessions? Since eating disorders are the vehicle for communication about relationships, internal conflicts, and lability in mood, does seeing a person virtually contribute to further relational disconnect? Is a real relationship possible virtually?
• Eating disorder clinicians often must face working with families in despair, who would never have consented to the treatment had it not been for their child, adolescent, or adult child in physical distress. The family member with the eating disorder is often the family symptom-bearer. Family members can blame and attack those who are most trying to help; they can sometimes bully school officials and therapists and can resist recommendations or, worse, manipulate or lie about therapeutic interventions to save their reputations. Is the clinician prepared to coordinate care among various professionals while being able to reduce or eliminate divisiveness among family members and other involved professionals? It can be enormously complex for family members to accept the psychological underpinnings of the eating disorder and the metaphoric use of the symptom to talk about family dynamics and issues. Will virtual sessions impede this process of discovery?

In the past, clinicians relied solely on their transparency to patients about their training in treating eating disorders. Although this remains true today, there is a certification process and credentials for clinicians to treat eating disorders, further qualifying competency and commitment to ethical treatment standards (IAEDP). Certified eating disorder specialists (CEDSs) now provide the care, and most clinicians incur additional costs in ongoing training, supervision, and personal therapy.

We need competent and expert therapists. More therapists are receiving advanced training; however, training in evidence-based treatment alone cannot allow someone to understand the complexities of a severe condition. Trauma , major depression, debilitating anxiety , borderline personality disorder, and a high degree of family dysfunction surround and underlie the development of an eating disorder. Do virtual appointments add another layer to an oversimplification of the needs of this population?

Skills in here-and-now approaches like cognitive behavioral therapy, acceptance and commitment therapy, short-term interpersonal therapies, mindfulness , and motivational approaches are insufficient in treating eating disorders. Therapists require additional training in understanding human motivation , even the use of the eating disorder as a symbol and metaphor. Are virtual appointments ethically consistent with providing a holistic treatment protocol for a patient with an eating disorder? (Freeman, 2007)

Telehealth contributions and considerations:

Telehealth has allowed vast populations to have access to mental health treatment, sometimes for the first time. Medically and psychologically home-bound people, rural communities with difficult access to larger towns, adult family members who cannot easily drive their child to treatment, and many others praise telehealth's ability to service specific populations and meet the demands of more and more people considering psychotherapy for the very first time.

• Is some form of therapy, like telehealth, better than no therapy? Absolutely, but with the caveat that these treatments are best suited for those who are not suffering from major depressive conditions, significant anxiety, personality disorders masquerading as 'merely' relationship issues, or those with severe symptoms like an eating disorder. Often, patients with minor anxiety do very well in teletherapy because of the protective veil of physical distance and how the camera orients eye contact.
• Mental health issues confront one in every five Americans (CDC). Adding a layer of disconnect via telehealth requires prudent decision-making to proceed, especially when the therapist is new to the field of eating disorders, or new to the field of treating mental health conditions.
• Serious assessment and consideration are required to determine which patients may be most suited to benefit from telehealth and those for whom it poses risks.

We are in an age of disconnect from human contact, with artificial intelligence , virtual meetings, and connections based and maintained on social media . If only we could extract our humanity from being human, we might be in better mental health living in a virtual world.

CDC.gov. Center for Disease Control: mental health statistics (2024).

Freeman, C. & Power, M. Handbook of Evidence-Based Psychotherapies: A guide for research and practice. 1st edition. Wiley. (2007).

Greenson, R. The technique and practice of psychoanalysis: Volume 1. England: Routledge Press. (1967).

iaedp.com. International association of eating disorders. certified eating disorder specialist overview. (2024)

Scheel, J. When Food is Family: A loving approach to heal eating disorders. Washington: Idyll Arbor Inc. (2011).

Zerbe, K. Integrated Treatment of Eating Disorders: Beyond the Body Betrayed. New York: W.W. Norton & Co. (2008)

Judy Scheel, Ph.D., L.C.S.W. , is the author of When Food Is Family , and is the founder and Executive Director of the Cedar Associates Foundation.

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Research offers hope and reassurance for adults with eating disorders

by Curtin University

New Curtin University research has found an inpatient treatment approach can help adults with eating disorders improve not only their physical health, but also their psychological health. The research is published in the Journal of Eating Disorders .

"High-energy refeeding" is frequently used to treat malnourished adolescents with anorexia nervosa and involves patients consuming a progressively higher energy intake over a short period of time, to quickly restore their nutritional health.

It's been thought this approach could prove problematic when treating adults with the same condition. However, this may not be the case.

Researchers from Curtin's School of Population Health investigated 97 voluntary hospital inpatients (55 adults and 42 adolescents) with eating disorders, the majority anorexia nervosa, who were treated using a high-energy refeeding protocol.

The team found both age groups responded well to high-energy refeeding, reporting very similar positive weight change and improvements in measurements of their psychological health .

Masters student and study lead Fiona Salter said there had been previous concerns that adult patients undergoing high-energy refeeding could be at increased risk of developing refeeding syndrome, a potentially fatal condition which can occur when a severely malnourished person starts eating again and causes a sudden shift in fluid and electrolytes.

"In addition, more frequent mental health issues in adult patients could complicate their medical care ," Ms. Salter said. "However, only one adult participant in our study did not tolerate the high-energy protocol due to oedema, which is an excess of fluid accumulating in body tissues."

Study co-author Dr. Emily Jeffery said the findings indicate high-energy refeeding in adults who are mildly and moderately malnourished can be administered safely and has both nutritional and psychological benefits.

"However, clinicians need to be aware [that] severely malnourished adults may require adjustments to prevent complications," Dr. Jeffery said.

Ms. Salter said the improvements in adult patients ' psychological well-being were critically important in using high-energy refeeding in the future.

"There was some concern feeding too quickly could put them under too much distress, which is why we wanted to measure these psychological scores," Ms. Salter said.

"We found psychosocial questionnaire scores improved significantly over the hospital admission, but psychological recovery from an eating disorder takes months and years, so while it's great we can physically restore someone's nutritional health quite quickly, the important thing is to keep that going. It needs to be maintained after they leave hospital for their longer-term psychological recovery."

With this in mind, Ms. Salter said the next step was to see how patients with a similar severity of illness respond to high-energy refeeding in a less structured environment, such as an intensive treatment day program.

"We'll be investigating whether a similar high energy refeeding protocol to that used in the hospital study has the same outcomes when patient meals are only partially supervised," she said.

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Eating Disorders and Eating Disorder Awareness

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The present Research Topic wishes to focus on the four recognized eating disorders by the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-V): Anorexia Nervosa, Bulimia Nervosa, Binge Eating Disorder (BED), and Avoidant/Restrictive Food Intake Disorder (ARPID). Given the rising incidence of cases of people affected by eating disorders and some studies even suggesting an “epidemic” of eating disorders, we would like to analyze via an interdisciplinary approach the current situation and disseminate the latest findings. Knowledge in this field is constantly expanding, especially in the last 10 years, with authors providing new and fascinating results. However, there are several areas where research is still lacking. We would like to encourage you to share the latest findings in the field. We welcome the submission of manuscripts (original research, brief research report, focused review, hypothesis and theory, perspective, data report, case report, community case study) related, but not limited to: • Causes and risk factors. • Socio-cultural factors. • Psychological factors. • Family factors through enmeshment and criticism. • Peer influence • The impact of the media, by spreading the ideal of thinness. • Negative affect, low self-esteem, and body dissatisfaction. • Biological and genetic bases. • Brain functioning in eating disorders. • Epidemiology, statistics, and mortality. • Diagnostics. • Physiological consequences of eating disorders. • Psycho-therapeutic intervention. • Progresses and challenges related to eating disorders. • Prevention. • Evolution. • Adverse effects. • Eating disorders as coping mechanisms.

Keywords : Eating Disorders, Anorexia Nervosa, Bulimia Nervosa, Binge Eating Disorder, Avoidant/Restrictive Food Intake Disorder (ARPID), Causes, Media, Psychology, Diagnostics, Prevention, Psycho-therapeutic Intervention

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Lack of Sleep Could be Causing an Increase in Mental Health Disorders

Without the proper amount of sleep, your brain can’t function properly, which could lead to an increased risk of mental health disorders..

Three o’clock in the morning — for some people, it’s the most anxiety-producing time. It’s when they wake up after just a few hours of shut-eye and then fail to fall back asleep.

For other people, it’s the dreaded hour when they realize they have yet to fall asleep. The clock is ticking toward their wake-up time, and they haven’t even hit a dream cycle.

Missing sleep can lead to more than just a sluggish day. Sleep medicine scientists have established that poor sleep is related to poor health. And in more recent years, sleep medicine researchers have also gained a greater understanding of how a lack of sleep can jeopardize mental health.

Scientists and advocates are calling for more research and attention into what they warn is a growing public health concern.   

Why We Need Sleep

The body needs sleep, but not everyone is able to sleep well. Sleep medicine researchers say this is akin to not having clean air, nutritious food, or fresh water.

“Sleep is not just something we do because we like it or because it’s good for you. Sleep is a biological requirement for human life. It’s non-negotiable,” says Michael A. Grandner, an associate professor of psychiatry and the director of the Sleep & Health Research Program and the Behavioral Sleep Medicine Clinic at the University of Arizona College of Medicine.

After the Industrial Revolution, Grandner says disorders like insomnia became romanticized and seen as part of a work culture in which people who slept less were admired for being strong, devoted, and capable of working more. He says that standards are changing, and people are beginning to recognize that a lack of sleep impacts a person’s physical and mental health.

“We are in this period of change in how our society looks at sleep health in general,” he says.

Read More: The Importance of Sleep for Your Body

How Sleep Affects Mental Health

Part of the change in how people view their own sleep health is due to a growing understanding of the relationship between sleep and psychiatric disorders. Sleep disorders like insomnia are a risk factor for mental health issues such as anxiety or depression.

Researchers are still learning about the relationship, but they are increasingly seeing how sleep disorders can predict the development of a psychiatric disorder.  

Sleep and Memory

Although scientists are still examining the relationship between sleep and psychiatric disorders, Grandner says there are several theories, and one involves memory. When a person sleeps, their brain processes and stores memories . Sleep disorders like insomnia disturb this process, and the person may miss out on memory consolidation.

Thus, these memories may be missing when a person needs to interpret social situations. Grandner gives the example of a person seeing someone frown in their direction. Past memories could help the person see the scowl as a part of the other person’s bad day, which could spark empathy. But without those memories, the frown could seem personal. This could cause the person to feel anxious or threatened.

“Memory and emotion are at the core of a lot of common mental health issues,” Grandner says. 

Sleep and Suicide Risk

Another theory considers how the brain functions in the middle of the night when the body is meant to be asleep. The Mind After Midnight hypothesis holds that in the overnight hours, a tired brain that is unable to sleep is not functioning optimally — a risk factor for more extreme behavior.  

The brain should be asleep and performing maintenance tasks like memory processing and storage or emotional regulation. Instead, it’s being forced into action mode when “cognitive capacity and mood regulation are diminished.”

During the overnight hours, self-harm, thoughts of suicide, and violent crime spike. Unhealthy behaviors like substance abuse or poor food choices are also likely. The hypothesis holds that it’s during these sleep-deprived times that a stage is set for future psychiatric disorders.

“When your body wants to be asleep, you don’t make good choices,” Grandner says. 

Read More: This Is Your Brain Without Sleep

The 5 Sleep Disorders

The International Classification of Sleep Disorders (ICSD) is a diagnostic manual that puts sleep disorders into seven main groups.

There are insomnia disorders, which relate to the inability to fall asleep or stay asleep. Sleep-breathing disorders involve conditions like sleep apnea, in which a person stops breathing. The third group, central disorders of hypersomnolence, include narcolepsy and other forms of excessive sleepiness. Circadian rhythm sleep-wake disorders consist of disorders in which a person’s sleep-wake cycle is out of sync.

The fifth group, parasomnia, entails abnormal movements such as walking, talking, or eating. This group also includes nightmares, night terrors, and sleep paralysis . Parasomnia is distinct from the sixth group, sleep-related movement disorders, which are characterized by movements that disturb sleep, like restless leg syndrome. Lastly, the ICSD has an “other” category for disorders that do not fit into the other groups.

Read More: What Really Happens During Sleep Paralysis and How to Stop It

Which Sleep Disorder Is Most Common?

Insomnia is likely the most common sleep disorder. But scientists can’t say with certainty how many people suffer from it.

“We actually don’t know the prevalence in the population of most sleep disorders,” Grandner says.

Part of the problem is that sleep studies are needed to diagnose disorders like sleep apnea, Grandner says. For some people, this can mean an overnight stay in a sleep clinic or wearing diagnostic equipment at home. These barriers keep people from seeking out a diagnosis and prevent scientists from fully knowing the epidemiology. 

Read More: Irregular Sleep Schedules Can Lead to Health Risks

Studying Sleep Disorders

Scientists who study sleep medicine say that more research is needed. In the spring of 2024, almost three dozen members of Congress signed a letter supporting funding for sleep health research, which would possibly allow agencies like the Centers for Disease Control and Prevention to study sleep disorders in the American population and get a better sense of the epidemiology. 

“It’s something that’s getting voted on that those of us in the community are advocating for — we’re saying, ‘Please, we need this information,’” Grandner says.

Read More: Can Animals Have Sleep Disorders?

Article Sources

Our writers at Discovermagazine.com use peer-reviewed studies and high-quality sources for our articles, and our editors review for scientific accuracy and editorial standards. Review the sources used below for this article:

Neurologic clinics. Psychiatric disorders and sleep

Frontiers in Network Physiology . The Mind After Midnight: Nocturnal Wakefulness, Behavioral Dysregulation, and Psychopathology

American Academy of Sleep Medicine. The AASM International Classification of Sleep Disorders – Third Edition, Text Revision (ICSD-3-TR)

American family physician . Common Sleep Disorders in Adults: Diagnosis and Management

Sleep Review. Congress Members Rally Behind Sleep Health Funding and Awareness

Emilie Lucchesi has written for some of the country's largest newspapers, including The New York Times, Chicago Tribune and Los Angeles Times. She holds a bachelor's degree in journalism from the University of Missouri and an MA from DePaul University. She also holds a Ph.D. in communication from the University of Illinois-Chicago with an emphasis on media framing, message construction and stigma communication. Emilie has authored three nonfiction books. Her third, "A Light in the Dark: Surviving More Than Ted Bundy," releases October 3, 2023 from Chicago Review Press and is co-authored with survivor Kathy Kleiner Rubin.

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• Open access
• Published: 30 May 2024

Treating depression in patients with borderline personality disorder: clinical clues on the use of antidepressants

• Carmine Tomasetti 1 ,
• G. Autullo 2 ,
• A. Ballerini 3 ,
• A. de Bartolomeis 4 ,
• B. Dell’Osso 5 ,
• A. Fiorentini 6 ,
• F. Tonioni 7 ,
• V. Villari 2 &
• D. De Berardis 8  

Annals of General Psychiatry volume  23 , Article number:  21 ( 2024 ) Cite this article

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Metrics details

Personality disorders (PD) are described as enduring patterns of markedly deviant and pervasive inner experiences and behaviors, with onset in adolescence, which lead to severe distress or impairment. Patients suffering from major depressive disorder (MDD) display higher rates of comorbidity with personality disorders, often complicating the treatment, and worsening the outcomes. Borderline personality disorder (BPD) is the most common of PD and is frequently associated with MDD, with which shares several features. The most part of research agrees on the fact that comorbid BPD in MDD patients quite doubles the poor response to treatments. Moreover, no treatment strategy stands out currently to emerge as more effective in these cases, thus urging the call for the need of new approaches. Herein, we revise the current literature on BPD, its neurobiology and comorbidity with MDD, as well as the more recent treatment strategies used. Then, based on its pharmacology, we propose a possible role of trazodone as a valuable tool to approach comorbid BPD-MDD.

Introduction

Major Depressive Disorder (MDD) is a leading contributor to global burden of disease, being considered as a major cause of disability worldwide, with approximately 3.8% of population affected and over 700.000 people dying of suicide every year [ 1 ]. Despite multiple treatment strategies have been developed, MDD remains a serious challenge for psychiatrists, since approximate 30% of patients do not adequately respond to therapies. The largest MDD trial, the so-called STAR*D (Sequenced Treatment Alternatives to Relieve Depression), demonstrated that, even after 4 consequential steps of treatment, the cumulative remission rate reached 67% after 14 months [ 2 ].

Since MDD is a heterogeneous disorder, multiple reasons have been put forward to support these high rates of treatment resistance: misdiagnosis (e.g., bipolar depression, or mixed states); comorbid substance use; untreated medical conditions (e.g., dysthyroidism); undiagnosed underlying traumata (i.e., post-traumatic stress disorder); cognitive impairment (i.e., neurocognitive disorders) [ 3 ].

In addition to the above-mentioned contributors, a large body of evidence points out the essential role of underpinning and/or understated personality disorders (PD) in the scarce responsivity of MDD to treatments. PDs comorbidity has been recognized in almost half of MDD patients in different meta-analyses [ 4 , 5 ]. Indeed, the pervasive symptoms of PDs, such as low self-esteem, self-criticism, mood instability, feeling of emptiness or hopelessness, suicidal thoughts or behaviors, may all represent substantial contributors to worsen or complicate depression, or even to make depressive symptoms persistent and resistant [ 6 ]. Several studies have examined the relationships amongst personality disorders traits and the quality, the severity, and the outcomes of MDD [ 7 , 8 ]. Personality disorders have been correlated to earlier onset of MDD, to specific subtypes of depression (melancholic vs. non melancholic depression) [ 5 ], as well as to severer symptoms (i.e., suicidal behaviors, self-harming, impaired cognition), and poorer outcomes (e.g., greater resistance to pharmacological and non-pharmacological treatments) [ 9 ]. Thus, the frequent association between PDs and MDD poses the classical question whether came first the chicken or the egg, since from a psychological point of view some predisposing risk factors may be associated to both the conditions [ 10 ]. Moreover, given this entangled relationship, a diagnostic issue should be considered, when assessing a patient with MDD; but, more important, a complete revision of therapeutic approaches to the treatment of depression should be contemplated, based on the possible influence of underlying preponderant personality traits in depressed patients.

In the next sections, we will consider the impact of the most devastating PD, the Borderline Personality Disorder, on MDD, and we will discuss the possible revision of classical antidepressant treatments in the light of an integrated neurobiological-psychological approach to MDD therapy.

The influence of comorbid Borderline Personality Disorder on Major Depressive Disorder

Borderline Personality Disorder (BPD) is described in the Diagnostic and Statistical Manual of Mental Disorders, fifth edition, text revision 2022, (DSM-5-TR) [ 11 ] as a “pervasive pattern of instability of interpersonal relationships, self-image, and affects, and marked impulsivity, beginning by early adulthood and present in a variety of contexts”. Sensation of abandonment, unstable relationships, identity disturbances, impulsivity, recurrent suicidal behaviors, affective instability, feelings of emptiness, anger and, occasionally, transient dissociative or psychotic symptoms during periods of distress may be all features of BPD. All these features can be grouped in three main categories (“factors”, according to DSM-5-TR): disturbed relatedness, behavioral dysregulation, and affective dysregulation; all of these being strongly correlated with each others, thus representing a unique construct, although with broad and pleiotropic manifestations [ 12 ]. BPD is the most common PD, with a reported prevalence of 10% in all psychiatric outpatients [ 13 ], and 5.9% in non-clinical population [ 14 ]. Moreover, the most part of BPD patients seem not to access psychiatric care, but they represent a significant part of primary care patients, since BPD has been described as four-times more prevalent amongst general practitioners’ costumers as compared to general population [ 15 ].

Several studies have reported a high frequency of co-occurrence between BPD and MDD, since 83–85% of BPD patients have been described to suffer from MDD episodes, with high recurrences [ 16 , 17 , 18 ]. Moreover, amongst PDs, BPD seems to have the highest correlation with both genetic and environmental risk factors of MDD [ 19 ].

Manifold studies have tried to dig up the intrinsic connections between BPD and MDD, and just as many theories and models have been developed, with the precise aim to improve diagnosis and therapy of these disorders, above all when comorbid. Personality has been characteristically described as a dynamic construct of two main components: temperament, the biologically-based structure of emotion regulation, and character, which instead is modulated by social relations [ 20 ]. According to the Five Factors Model (FFM), personality traits may be taxonomically subdivided in five principal characteristics, the so-called Big Fives: neuroticism, extraversion, conscientiousness, agreeableness, and openness to experience. Given the hierarchical relationships amongst these factors, they may be further grouped in two big clusters: positive emotionality and negative emotionality [ 21 ]. There is increasing evidence that, although personality traits have solid genetical and biological bases, they are not rigid constructs, but may be dynamically modulated by development and life experiences [ 22 ]. Psychologically, MDD is characterized by a substantial deficiency in positive emotionality, with a prevalence of negative emotions, such as sadness, guilt, shame, anhedonia, depressed mood, and numbness (i.e., the inability of feeling feelings) [ 23 ]. However, it is not rare that MDD patients may manifest irritability, anger, hostility, which are all factors often correlated to self-harming or suicide [ 24 , 25 ]. By contrast, the whole symptomatologic cortege of BPD is mainly hinged on impulsivity traits, with emotional dysregulation, anger, dyscontrol, dysphoria, self-harming, and hostility [ 26 ]. Nevertheless, some typical features of BPD may resemble those seen in MDD patients, such as the feeling of emptiness, sadness, loneliness of hopelessness [ 27 ].

Therefore, BPD may add an “impulsivity color” to MDD symptoms framework, when the two disturbs manifest comorbidly. Different studies, indeed, reported that BPD patients experiencing MDD show increased levels of anger, fear, and hostility [ 28 ], as well as they manifest considerably higher impulsivity than MDD-only patients [ 29 ]. Moreover, BPD patients diagnosed with MDD tend to describe their depressive symptoms as more serious as compared to MDD-only patients, even severer than those objectively assessed by physicians [ 30 , 31 ].

Notably, BPD has been demonstrated to show significant comorbidity also with Bipolar Disorder (BD). Indeed, by analyzing data from the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC), McDermid et al. found that the lifetime prevalence of BPD was about 29% in BD type I and 24% in BD type II, and that comorbid BPD-BD had severer presentation as compared to BD alone [ 32 ]. Successive studies confirmed that BPD may represent a risk factor for BD, and remarked the negative impact of BPD in BD, such as the higher prevalence of suicidality and the treatment-resistance [ 33 ]. Moreover, about 40% of MDD-diagnosed patients have been reported to have a history of subthreshold hypomania symptoms, this subgroup showing earlier onset and more episodes of depression, as well as more comorbidities as compared to non-hypomanic patients [ 34 ]. Last, MDD episodes where psychomotor agitation and racing thoughts are found (the so-called “agitated depression”) have been robustly associated to mixed states, unfavorably predicting the emergence of suicidal ideation and contraindicating antidepressant therapy [ 35 ]. This tight intermingling between hypomanic symptoms, MDD, and BPD may challenge the dichotomic vision of unipolar-bipolar depression, suggesting a more comprehensive “mood spectrum” diagnostic approach [ 36 ].

Thus, it is possible that the inherent “bipolarity” of BPD may colorize MDD with unstable emotional traits, lending this disorder an increased resistance to treatments, as compared to MDD alone. The Collaborative Longitudinal Personality Disorders Study (CLPS) analyzed the longitudinal course of BPD patients, as compared to other PDs and MDD-only patients [ 37 ]. Amongst the other interesting results, CLPS reported that 80% of BPD patients assessed had MDD, and that MDD-only patients showed a remission rate dramatically faster (80% by 1 year) as compared to BPD patients (30% by one year), thus indicating how much BPD comorbidity may influence MDD outcome. These results have been confirmed by the National Epidemiological Study of Alcoholism and Related Disorders, which reported that BPD was the major predictor of persistent MDD [ 38 ]. The McLean Study of Adult Development (MSAD) further demonstrated that, when BPD and MDD coexist, the remission of MDD strictly depends upon the remission of BPD symptoms [ 39 ], thus confirming a previous landmark study, in which an improvement in MDD symptoms was found when treating BPD symptoms, but not vice versa [ 40 ]. However, the mainstay treatment for MDD, antidepressant drugs, have been demonstrated to promote only partial responses in MDD-BPD patients [ 39 ]. Thus, there is a peculiar tendence to poly-treat BPD patients, which have been described to averagely take three-to-five medications, an over-prescription that could be only reduced by a BPD-specific psychotherapy regimens [ 41 ]. Also, non-pharmacological treatments, such as electroconvulsive therapy (ECT) and transcranial magnetic stimulation (TMS) have demonstrated partial efficacy in treating comorbid MDD and BPD [ 42 , 43 ]. Therefore, it appears rather obvious that the treatment of MDD in course of BPD relies on an efficacious BPD treatment. Hence, some specific psychotherapy regimens, such as Dialectical behavioral therapy (DBT) have demonstrated a good efficacy in improve MDD symptoms by improving BPD [ 44 ].

So, is there a biological basis on which the BPD-induced MDD treatment-resistance relies? And, in the light of this possible underlying basis, should it be possible to reconsider a targeted pharmacological approach to help reducing the impact of BPD on MDD?

Digging in the deep: the neurobiological bases of BPD and the underpinnings of comorbid MDD

Although BPD has been classically envisioned as a complex multifactorial disorder, in which environmental risk factors (e.g., traumata, abuses, neglect) seems to be preponderantly responsible for its development [ 45 ], increasing evidence has been pointing out the essential role of the genetic factors underlying the specific personality traits at the basis of the disorder. Indeed, twin studies have demonstrated that BPD has a heritability ranging from 46 to 69% [ 46 , 47 ]. Recently, different genome-wide association studies (GWAS) have been performed, in order to study genetic association of the “Big Five” factors of FFM with PDs in general population. BPD was found closely associated with personality traits of neuroticism and openness [ 48 ], and, more interestingly, it was reported to share positive genetic correlations with MDD, Bipolar Disorder and Schizophrenia [ 49 ]. As above-mentioned, BPD represents a unique construct intermingling specific personality traits, such as disturbed relatedness, behavioral and emotional dysregulation. However, despite the manifold researches stating the large heritability of BPD, only a few genetic studies exist, which tried to correlate these personality traits to specific gene dysfunctions. As previously mentioned, Witt and collaborators found a significant overlap of BPD-associated genes with those associated to MDD, Bipolar Disorder and Schizophrenia [ 49 ]. Two genes reached genome-wide significance: dihydropyrimidine dehydrogenase (DPYD) and Plakophilin-4 (PKP4). DPYD is implicated in pyrimidine metabolism and contains a binding site for the micro-RNA miR-137, which has been found associated to Schizophrenia [ 50 ]. PKP4 is involved in the regulation of cell adhesion and cytoskeletal modifications, which have been substantially implicated in cell junction deficits associated to MDD [ 51 ]. Previously, Lubke et al. have described a specifical association of BPD with the serine incorporator 5 gene (SERINC5), which seems to have a peculiar role in myelination, and has been involved in the development of psychiatric disorders characterized by lack of social interactions [ 52 , 53 ]. Finally, a genome-wide linkage study found a significant association of BPD features with chromosome 9 loci, which have been significantly associated also to Bipolar Disorder and Schizophrenia [ 54 ].

Given the essential role of environment in BPD development, it is not surprising that a large number of studies have reported abnormalities in BPD in epigenetic modifications, which are considered the “portal” through which environment may impact gene expression changes, via DNA methylation, histone deacetylation and non-coding RNA silencing [ 55 ]. Altered methylation of specific genes, such as dopamine D2 receptors, serotonin 3A receptors, glucocorticoid receptors and brain-derived neurotrophic factor (BDNF) receptors have been all associated to BPD [ 56 , 57 , 58 , 59 ]. It is interesting to note that these alterations may be directly correlated to the severity of childhood abuse in BPD patients [ 60 ], as well as to the intensity of depressive symptoms, and may be reinstated by specific psychotherapy regimens [ 61 ].

As already discussed, the core symptoms of BPD rely on a substantial emotional dysregulation. Different studies reported altered emotional interoception in BPD patients, the so-called alexithymia (i.e., “no words for emotions”): while their amygdaloid system highly responds to negative emotions, they have a blunted self-report of the experienced emotions [ 62 ]. This may be due to an altered regulatory control of amygdala-based emotion system: indeed, BPD patients have been described to have altered connections between prefrontal cortex and amygdala, thus probably having an impaired top-down emotional modulation [ 63 ]. Moreover, both substance use, and dissociative episodes have been reported to dampen the hyperactive emotional responses in BPD patients, thereby explaining the frequent comorbidity of BPD with substance use disorder (SUD), as well as the higher frequency of dissociative experiences in BPD patients [ 64 , 65 ]. Interestingly, altered amygdaloid responses and neuroplasticity have been demonstrated in MDD patients [ 66 ]. Moreover, a particular kind of treatment-resistant depression, called “dissociative depression”, has been characterized as frequent in younger patients with childhood traumata, and is defined by the higher frequency in dissociative episodes, as well as by its chronicity, mood instability, and often by comorbid BPD [ 67 ]. Finally, SUD is frequently diagnosed also in MDD patients, and some etiopathogenetic models propose that substances may help depressed patients to cope with their altered affective states [ 68 ].

Besides emotional dysregulation, as previously mentioned, BPD patients experience an essential disrupted relatedness, with interpersonal sensitivity leading to social difficulties.

Several studies have associated BPD social dysfunctionality to altered opioidergic and neuropeptidergic neurotransmission. Primarily, opioidergic neurotransmission is correlated in humans with pain responses. Increasing evidence suggests that µ-opioid receptors may mediate both sensory and affective dimension of pain, in different cerebral regions [ 69 ]; moreover, pain may be literally perceived in social exclusion and rejection by means of µ-opioid mediation in brain [ 70 , 71 ]. BPD patients have been demonstrated to possess a lower sensitivity to acute pain, but a heightened sensitivity to chronic pain [ 72 , 73 ]. This altered sensitivity to pain may be essentially due to an abnormal µ-opioid transmission: indeed, BPD patients have been demonstrated to possess a greater number of cortical µ-opioid receptors, probably due to a scarce baseline opioidergic transmission, with altered and enhanced compensatory opioid responses to acute stimuli [ 74 ]. Besides its primary role in pain responses modulation, µ-opioid neurotransmission has been associated to the right development of attachment behaviors in mammals [ 75 , 76 ]. Interestingly, altered µ-opioid gene expression has been found in adolescents prone to develop MDD reactions to social rejection life events [ 77 ].

Oxytocinergic neurotransmission has been also found abnormal in BPD patients, which were reported to have lower levels of oxytocin as compared to healthy individuals, these levels being correlated with childhood traumata and disrupted attachment [ 78 , 79 ]. Moreover, while in healthy subjects oxytocin administration usually enhances social behaviors, in BPD patients it may provoke counterintuitive aversive behaviors, especially correlated to history of childhood traumata [ 80 ]. Last, genetic alterations in oxytocin receptors have been directly correlated to the development of BPD in abused children [ 81 , 82 ]. The increasing evidence of a substantial role of oxytocin in the etiopathogenesis of MDD, as well as in its possible treatments, represents a further bridge between BPD and MDD [ 83 , 84 ].

Monoaminergic neurotransmission has been implicated in personality since long ago. Particularly, personality dimensions as described by Cloninger, and later by the FFM, may be directly linked to dopaminergic, serotonergic, and noradrenergic neurotransmissions [ 85 , 86 , 87 ].

Dopamine dysfunctions, for example, have been associated to three specific dimensions of BPD: impulsivity, emotional dysregulation, and cognitive impairment [ 88 ]. Specific genetic polymorphisms of the dopamine transporter gene (DAT1) have been peculiarly associated with increased risk of BPD in MDD patients [ 89 ]. Moreover, the same polymorphism has been associated to angry-impulsive traits in comorbid BPD-MDD patients [ 90 ]. On the other hand, both serotonin transporter (5HTT) and serotonin A1 receptor (5HT1A) genes have been associated with BPD [ 91 , 92 ]. Specifically, 5HT1A gene alterations have ben correlated to abnormal amygdala structure and emotional responses in BPD-MDD comorbid patients [ 91 ]. Serotonin alterations seem to be tightly correlated to the “impulsivity color” of MDD, when comorbid with BPD, as well as with an increased risk of suicide [ 93 , 94 ]. Recent studies demonstrated that serotonin and dopamine neurotransmissions closely interact in defining the personality traits underlying BPD, and the simultaneous presence of both dysfunctions may interplay in favoring the risk of BPD development [ 95 ]. Norepinephrine, along with cortisol, has been associated to dissociative responses in BPD [ 96 ].

Targeting depression in BPD: clinical clues on the use of antidepressants. Focus on trazodone

BPD patients, with their pleiotropic symptomatologic manifestations, represent a huge burden for health systems. In fact, as above mentioned, BPD is frequently associated to coexisting psychiatric disorders, above all MDD, anxiety, substance use, and it is as much as frequently misdiagnosed [ 97 ]. Due to their comorbidities, as well as to their over-endorsement of symptoms, BPD patients often tend to self-medicate (even with substances) or to access primary cares, where they are not often understood and well-treated [ 98 ]. Although BPD patients have been described to have good chances to remit over the long period [ 99 ], during the trajectory of the disorder, they have frequent relapses and serious outbursts, which lead to multiple accesses to mental health services for specialized cares or hospitalizations [ 100 ].

All the most recent guidelines for the treatment of BPD seems to agree on the fact that a specific regimen of psychotherapy should be the first line treatment, whereas medications should be used with caution for intense and disruptive symptoms during decompensation acuity, and only for the shortest possible time [ 101 , 102 , 103 , 104 ]. However, while European guidelines—which include NICE (National Institute for Health Care and Excellence) ones—suggest to pharmacologically treat only comorbid disorders in BPD [ 103 , 104 ], APA (American Psychiatric Association) and WFSBP (World Federation of Societies of Biological Psychiatry) suggest using specific classes of medications to treat specific symptom domains [ 101 , 102 ]: thus, antidepressants should be be used to treat emotional dysregulation and impulsivity, similarly to mood stabilizers, while antipsychotics should be used for dissociative and cognitive-perceptual symptoms.

Although scarce evidence exists on the efficacy of antidepressant treatments in BPD, SSRIs (Selective Serotonin Reuptake Inhibitors) are currently the most prescribed medications [ 105 ]. The most part of RCTs examining the efficacy of antidepressants in BPD are outdated, and they have not been replicated since 2010. The main antidepressants for which data are available in the treatment of BPD are: fluoxetine, fluvoxamine, sertraline, amitriptyline, phenelzine, venlafaxine, mianserin. A Cochrane review [ 106 ] reported that antidepressants had no significant effects on the overall BPD severity; no beneficial effects were noticed on impulsivity, as well as on suicidal behaviors, whereas a worsening of suicidal ideation was noticed with fluoxetine; affective instability was slightly ameliorated by fluvoxamine, while no significant effects were noticed for self-harming, feeling of emptiness, anger; the only significant effects on depression were found with amitriptyline.

Similar results were obtained in a comparative meta-analysis by Vita et al. [ 107 ], with a documented, although slight, effect of antidepressants only on affective dysregulation.

Significant results have been achieved on MDD comorbid to BPD when antidepressants were combined to mentalizing psychotherapies (DBT, IPT [Interpersonal Psychotherapy]) [ 108 , 109 ].

It is worth noting that all the antidepressant drugs chosen to be tested in BPD patients, as above described, were selected based on their well-documented efficacy on MDD, which is primarily due to serotonergic effects (i.e., serotonin re-uptake inhibition), with generally scarce impact on other neurotransmitters, such as dopamine or norepinephrine [ 110 ]. On the other hand, the most significant effects in reported RCTs were obtained by means of antidepressant drugs that involved more than the sole serotonin neurotransmission, such as phenelzine, amitriptyline and fluoxetine, or even by combined treatments (e.g. fluoxetine plus olanzapine), which were able to control—although slightly—the core affective/emotional instability, which is the typical signature of BPD [ 106 ].

As above described, BPD core depressive symptoms have been hypothesized to involve multiple neurobiological substrates, such as opioidergic and oxytocinergic neurotransmission, and specific monoamine receptors, such as dopamine D2 and serotonin 2A receptors, which interplay with each others to generate the symptoms of comorbid MDD-BPD. Thus, a more targeted pharmacological approach might help to relieve, if only partially, depressive symptoms in BPD.

In this light, a revision of “old” antidepressant treatments, relying on the enhancement of their possible efficacy, based on their peculiar pharmacodynamic properties, might represent a valuable approach. According to this view, trazodone may be a useful tool to address the unmet needs of MDD in BPD.

The history itself of trazodone appears intriguing, if envisioned in the light of the abovementioned neurobiological underpinnings of BPD. Indeed, it is a triazolopyridine derivative, which was developed in 1960s in Italy based on the “mental pain” hypothesis of MDD, correlating depressive states to altered pain interoception [ 111 ]. Along with nefazodone, trazodone represents the prototype of the so-called serotonin antagonist/reuptake inhibitor antidepressants (SARIs). It is a powerful antagonist at 5HT2A serotonin receptors, which are bound already at low doses, together with alpha1- and alpha2- adrenergic receptors and H1 histamine receptors, thus exerting potent anxiolytic and sedative/hypnotic effects at these doses [ 112 ]. Trazodone also weakly binds the serotonin transporter (SERT), 5HT2B and 5HT2C serotonin receptors, even if it is not clear if it acts as a full agonist, a partial agonist or an antagonist at these last receptors [ 112 ]. Another peculiar characteristic is the strong binding to 5HT1A serotonin receptors, where it acts as a partial agonist with high intrinsic activity [ 113 ]. Moreover, trazodone has an active metabolite, the meta-chlorophenylpiperazine (mCPP), which is known to exert pro-serotonergic psychoactive functions similar to fenfluramine and MDMA (“ecstasy”), in addition to being a well-recognized agonist to multiple serotonin receptors (e.g., 5HT1A, 5HT1B, 5HT1D, 5HT2A, 5HT2B, 5HT2C, 5HT3, and 5HT7 receptors) [ 114 , 115 ]. Thus, trazodone shapes up to be a peculiar multimodal antidepressant, which may exert differential functions at different doses. In fact, the progressive recruitment of serotonin receptors—in particular 5HT2A and 5HT1A—at incremental dosages has been described to exert incremental antidepressant effects by means of multiple—and not completely understood-- mechanisms: (1) 5HT1A receptors activation may mediate some neurotrophic factors’ genes expression, which has been associated to antidepressant actions; (2) 5HT1A receptors may progressively inhibit glutamate release from cortical pyramidal neurons, whose hyperactivity has been implicated in cognitive symptoms of MDD; (3) 5HT2A and 5HT2C serotonin receptors blockade has been associated to the increase in dopamine and noradrenaline cortical release, which are complementary to serotonin in relieving depressive symptoms [ 112 ].

Currently, trazodone is marketed in three different formulations: immediate release (IR), prolonged release (PR), and once-a-day extended release (OAD). Trazodone IR has a rapid plasma peak (1 h) and a short half-life (6.6 h); trazodone PR has a slower plasma peak (4 h) and a longer half-life (12 h), and trazodone OAD shows a plateau plasma level for the entire day, with longer antidepressant concentration as compared to the other formulations [ 113 ]. A large amount of data supports the fact that trazodone has similar efficacy to all the other antidepressants when compared to placebo [ 116 ]. Moreover, the OAD formulation has been described to grant a higher antidepressant efficacy than a placebo with a once-a-day administration, with side effects comparable to other antidepressants [ 117 ]. Finally, trazodone displays high tolerability, even when administered in patients with comorbid clinical conditions, thus granting a safety profile in poly-pharmaco-treated patients [ 118 ].

Several characteristics of trazodone may let lean forward its valuable use in comorbid BPD-MDD patients.

As previously described, the concurrent blockade of 5HT2A/2C receptors and of SERT, the partial agonist activity at 5HT1A receptors, and the antagonism at 5HT7 receptors may boost the antidepressant action of trazodone by increasing serotonin postsynaptic action and the subsequent disinhibition of dopamine and noradrenaline cortical release, together with glutamate-modulated neurotrophic factors’ gene expression [ 112 , 119 ]. Indeed, some studies have described the rapid onset of trazodone antidepressant effects. Sheehan et al. [ 117 ] demonstrated that trazodone OAD (150-225 mg/day) may induce a substantial reduction in depressive symptoms within a week of treatment, and that these effects may persist until 56 weeks. Fagiolini et al. [ 120 ] reported a faster antidepressant response (within 7 days) in patients treated with trazodone OAD (150 mg/die) as compared to venlafaxine XR (75 mg/die). This faster antidepressant effects of trazodone were not only exerted, as mainly expected, on the sleep component of depressive symptoms, but also on the cognitive aspects of depression [ 121 ].

The rapid antidepressant action of trazodone could be really useful during the fast emotional outbursts of BPD patients, which often lead to hospitalization. Peculiarly, this fast action seems not to be accompanied by a heightened risk of suicidal behaviors, even in high-risk patients treated with trazodone [ 122 ].

Trazodone has been demonstrated to exert antinociceptive effects even at low dosages, possibility via a µ-opioid receptors-mediated mechanism [ 123 , 124 ]. These properties may be helpful in manage the altered pain interoception of BPD patients—their “mental pain”—, as well as in treating their susceptibility to auto-medication with analgesics or substances. Indeed, diverse studies provided evidence of a good efficacy of trazodone in the treatment of alcohol, benzodiazepines, and opioid abuse [ 125 , 126 ].

The off-label clinical use of trazodone as hypnotic is well-established [ 126 ]. Some BPD patients have been described to have particularly disrupted sleep, with frequent nightmares, which in turn have been correlated to an increased risk of dissociative experiences and suicidal behaviors [ 127 ], above all if related to childhood traumatic events [ 128 ]. Trazodone has been demonstrated to be particularly effective in improving the quality of sleeping and reducing nightmares in post-traumatic stress disorders-affected war veterans [ 129 ].

Conclusions

BPD is a devastating personality disorder, with multiple symptomatologic presentations, and often comorbid with mood disorders, particularly with MDD, thereby making it substantially treatment resistant. SSRIs have been demonstrated to be scarcely efficacious on BPD-MDD patients. However, the neurobiological underpinnings of BPD may suggest that a more targeted antidepressant approach may helpful in relieving BPD-MDD coexisting symptoms. Since its multimodal action on serotonin, dopamine, noradrenalin, opioid and glutamate neurotransmissions, as well as its incremental effectiveness, trazodone seems to embody all the characteristics which may make it a clinical valuable tool to be used in BPD-MDD patients. More specifically designed studies are warranted to corroborate these clinical clues.

Data availability

No datasets were generated or analysed during the current study.

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Tomasetti, C., Autullo, G., Ballerini, A. et al. Treating depression in patients with borderline personality disorder: clinical clues on the use of antidepressants. Ann Gen Psychiatry 23 , 21 (2024). https://doi.org/10.1186/s12991-024-00507-z

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Social Media, Thin-Ideal, Body Dissatisfaction and Disordered Eating Attitudes: An Exploratory Analysis

Pilar aparicio-martinez.

1 Departamento de Enfermería, Universidad de Córdoba, Campus de Menéndez Pidal, 1470 Córdoba, Spain

2 Usher Institute of Population Health Sciences and Informatics, University of Edinburgh, Edinburgh EH8 9YL, UK

3 Grupo Investigación epidemiológica en Atención primaria (GC-12) del Instituto Maimónides de Investigación Biomédica de Córdoba (IMIBIC), Hospital Universitario Reina Sofía, 14071 Córdoba, Spain; se.ocu@oreuqavm

Alberto-Jesus Perea-Moreno

4 Departamento de Física Aplicada, Universidad de Córdoba, ceiA3, Campus de Rabanales, 14071 Córdoba, Spain; se.ocu@aerepa (A.-J.P.-M.); se.ocu@pijam1af (M.P.M.-J.)

María Pilar Martinez-Jimenez

María dolores redel-macías.

5 Departamento Ingeniería Rural, Ed Leonardo da Vinci, Campus de Rabanales, Universidad de Córdoba, Campus de Excelencia Internacional Agroalimentario, ceiA3, 1470 Cordoba, Spain; se.ocu@lederdm

Claudia Pagliari

6 eHealth Research Group, Usher Institute of Population Health Sciences and Informatics, University of Edinburgh, Edinburgh EH8 9YL, UK; [email protected]

Manuel Vaquero-Abellan

Disordered eating attitudes are rapidly increasing, especially among young women in their twenties. These disordered behaviours result from the interaction of several factors, including beauty ideals. A significant factor is social media, by which the unrealistic beauty ideals are popularized and may lead to these behaviours. The objectives of this study were, first, to determine the relationship between disordered eating behaviours among female university students and sociocultural factors, such as the use of social network sites, beauty ideals, body satisfaction, body image and the body image desired to achieve and, second, to determine whether there is a sensitive relationship between disordered eating attitudes, addiction to social networks, and testosterone levels as a biological factor. The data ( N = 168) was obtained using validated surveys (EAT-26, BSQ, CIPE-a, SNSA) and indirect measures of prenatal testosterone. The data was analysed using chi-square, Student’s t-test, correlation tests and logistic regression tests. The results showed that disordered eating attitudes were linked to self-esteem ( p < 0.001), body image ( p < 0.001), body desired to achieve ( p < 0.001), the use of social media ( p < 0.001) and prenatal testosterone ( p < 0.01). The findings presented in this study suggest a relationship between body image, body concerns, body dissatisfaction, and disordered eating attitudes among college women.

1. Introduction

Mental health problems have increased, especially among young people, over the last decade [ 1 ]. The most common mental problems are behavioural, emotional, and hyperkinetic disorders. Among these illnesses, disordered eating behaviours are rapidly increasing in a short time, especially among young women [ 2 , 3 ]. These disordered attitudes are defined as afflictions in which people suffer severe disruption in their eating behaviours, thoughts and emotions. The people who suffer from these complaints are usually preoccupied with food and weight. In this sense, disordered eating is used to describe a range of irregular eating behaviours that may or may not warrant a diagnosis of a specific disordered eating attitude [ 4 ].

These disorders usually occur in women in their twenties or during adolescence [ 3 ]. People who suffer these disorders usually present altered attitudes, behaviours, weight perception and physical appearance [ 5 ]. Moreover, disordered eating behaviours or attitudes are defined as unhealthy or maladaptive eating behaviours, such as restricting or binging and/or purging [ 6 ]. These behaviours are not categorized as an eating disorder, though they are considered a phase of diagnosed eating disorders [ 7 ].

The concern from health care systems is based on the fact that these severe mental disorders usually puts in danger the well-being and health of the people who suffer them [ 5 ]. One-third of the women in the world have suffered from these mental problems at some point in their life [ 6 ]. If they are inadequately treated, they may develop severe clinical disorders [ 8 ]. Moreover, around 1% of the people with these disordered eating attitudes struggle with unhealthy and emotional problems through all their lives [ 6 ].

Out of the population with disordered eating attitudes, 16% of them present overeating, 20% purged by vomiting, and 61% food restraining [ 9 ]. These frequencies changed as people aged, with food restriction being more common in older women and vomiting during adolescence [ 10 ]. Moreover, recent data have discussed the increase of how the minimum age of the people with disorders is around 12 years of age and decreasing. Meanwhile, the prevalence of disordered eating attitudes appears to increase as young adults or adolescents grow older [ 10 ].

Although these diseases have a crucial psychobiological component, social and cultural factors have a significant influence. Among these factors, advertising has been described as an internalizing or normalizing means to spread unrealistic beauty ideals. Therefore, a higher incidence of these diseases is presented in advanced and modern societies and people with the best living conditions, mostly caused by the popularization of thin and muscular ideals [ 11 , 12 , 13 ].

Several biological factors have been linked to disordered eating attitudes, with up to 50% of disordered eating being described as familiarly transmitted [ 5 , 14 ]. Researchers have also suggested that neurotransmitters in the brain are involved in disordered eating attitudes and, therefore, eating disorders [ 15 , 16 ]. Additionally, the hormones have been linked as factors to puberty, body perception and body concerns [ 17 , 18 ]. Testosterone is included among those hormones highly studied, with blood samples providing a more precise method of examination. Nevertheless, different researchers pointed out the possibility of using indirect markers to avoid taking biological samples and creating risks for the participants. In this sense, most studies have linked testosterone and estrogenic levels via the 2D:4D digital ratio as an indirect indicator [ 19 ], which heavily dictates attractiveness [ 17 ]. This ratio, which is based on the difference in length of the phalanges of the hands (2D:4D ratio) having a lower ratio as an indicator of the existence of a higher level of testosterone, is used for the determination of intrauterine testosterone levels during gestation [ 20 ]. This ratio has reflected the relationship with self-perception, body image, body dissatisfaction, and disordered eating behaviours [ 20 , 21 ]. Based on these studies, the hormone levels, and the indirect marker, might appear to have essential roles in disordered eating attitudes [ 22 ]. Nevertheless, other authors have described how biological or genetic factors are essential, but may not determine, these disordered eating attitudes [ 23 ].

Other factors, such as ethical or familiar factors, contribute to the development of this disordered eating behaviours [ 24 ]. In this sense, previous studies have established that the probability of developing a disordered eating attitude or a diagnosis of eating disorders is higher if the mother had a disordered eating or self-esteem problems [ 25 , 26 ]. Moreover, ethnicity has been linked to the perception of beauty ideals, self-esteem and body perception [ 27 , 28 ].

Another critical factor is the media by which beauty ideals have been promoted. The media plays a vital role in formulating what is attractive in society, increasing the thin beauty ideal among females being unattainable [ 29 , 30 ]. These ideals confirmed the way young people perceived themselves and, therefore, how they value themselves [ 10 , 31 ]. This contradiction between what society portrays as a role model and the real body that many young women have has resulted in body concerns. Body concerns usually maintain over time and increase body dissatisfaction. This body dissatisfaction emerges because of the distortion on the body image, its perception and, therefore, body concern [ 32 , 33 ]. This dissatisfaction also plays an essential role in disordered eating attitudes since it provokes emotional and psychological distress [ 34 ].

In this sense, the theory of social comparison and numerous studies have studied the relationship between body dissatisfaction and disordered eating attitudes to better understand the causes of these illnesses. These previous works showed that real comparisons with other people leads to a distortion of body image and may favour disorderly feeding [ 11 , 29 , 35 ]. Additionally, Fredrickson and Roberts (1997) suggested that sexualization and self-objectification promoted via media should be considered as a risk factor for disordered eating attitudes [ 36 , 37 , 38 ]. Based on previous and recent studies it seems that the role of the media in disordered eating attitudes is noteworthy [ 1 , 11 , 39 ].

This paper presents a research study in which these objectives have been pursued: first, to determine the relationship between disordered eating attitudes in female university students and sociocultural factors, such as the use of social network sites, beauty ideals, body satisfaction, the body image and the body image desired to achieve. Second, to determine whether there is a sensitive relationship between disordered eating attitudes, addiction to social networks, and other biological factors, such as testosterone levels.

2. Background

College-aged women may be at particular risk for body dissatisfaction and disordered eating practices due to the unhealthy weight gain that often occurs during this life stage [ 3 , 31 ]. The promotion of beauty ideals in the media disseminates disordered eating [ 40 , 41 ], drive for thinness and body dissatisfaction among female college students [ 42 ]. Furthermore, the growth of social networking sites (SNS), such as Facebook or Instagram, has also increased the exposure to thin and fit ideals [ 2 , 43 , 44 ]. The social media are more used than any other media as a mean of communication. These internet-based sites pulled the users to create personal profiles and share, view, comment and ‘like’ peer-generated content [ 20 ].

Importantly, young people, almost 90% of them (ages 18–29), reported being active users and being continuously exposed to different content and images in this medium [ 14 , 45 ]. Among the most active users of these media stands out the influencers. These new media role models have a significant impact in the last tendencies, the news and the trends that young people are following [ 46 ]. In this sense, researchers have also pointed out how social media and influencers may have the key to decrease body dissatisfaction and body concerns. Nevertheless, substantial studies have shown that economic interests are linked with the promotion of dieting in social media, or even surgery [ 47 ].

The last publications concluded that the most dangerous social media was Instagram, followed by Facebook and Twitter. These conclusions were based on the instant satisfaction of reviewing and having peer views in the images posted by the users [ 48 ]. Especially on Instagram, the message is accommodated according to the image uploaded [ 47 ].

These studies concluded that the influence of the advertising and the promotion of the thin and muscular ideals might more be connected with the perception that young people has regarding body, dieting and social media [ 49 ]. Additionally, the objectification suggests that the media’s sexual objectification of women modifies their body appearance. Due to this, it could be concluded that self-perception slowly shapes attractiveness resulting in a modification in the body-image, body dissatisfaction and disordered eating attitude. That being said, the proposed hypotheses are as follows:

Among young women, self-image will be linked to body dissatisfaction, the thin-ideal and the desire to change one’s body shape.

The level of body dissatisfaction among female college students will be high and be linked to self-esteem.

The young women’s eating behaviours will be linked to the degree of body dissatisfaction and the frequency of using social media.

The young women’s body image and body description will be slightly connected to prenatal testosterone levels.

3. Methodology

3.1. design and sample.

In the first phase, a cross-sectional study was carried out focused on female college students, aged from 18 to 25 years. The sample was recruited to participate in an in-person survey from April to May 2018 from the University of Cordoba. The selection of the sample was based on non-probability convenience sampling. This method of sampling was selected based on the accessibility of the students and previous scheduling with the professors.

The final sample was constituted by 168 subjects, from biological, education, informatics and nursing degrees who agreed to participate in the study voluntarily. The initial sample was 224, though the final sample was 168 after applying the exclusion terms. The mean age of the sample was 20 ± 0.76.

3.2. Measures

All the surveys used in the study are validated in different languages, including Spanish. Moreover, these surveys are used globally among health professionals and researchers in the health field [ 50 ].

The demographic and anthropometric data were not included in this study since the objective focused on the socio-cultural and individual factors. In this sense, the perception of young people was focused on social media, self-appearance, specific social network sites and distorted eating behaviours.

The EAT-26 with the reduced version of 26 items, was used to assess the frequency of disordered eating attitudes [ 51 , 52 ]. This test measures the low, medium and high risk of having a disordered eating attitude. Moreover, three different disordered eating behaviours can be reflected depending on the answers to each item. In this sense, these three subscales are dieting (focused on questions 1, 6, 7, 10, 11, 12, 14, 16, 17, 22, 23, 24, 26), bulimia and food preoccupation (focused on questions 3, 4, 9, 18, 21, 25) and food oral control (2, 5, 8, 13, 15, 8, 20). Total scores were calculated by taking the sum of the 26 items, based on the value from 0 to 3, where higher scores, over 20 points, indicated higher levels of disordered eating behaviours. This validated survey based on screening disorder eating attitudes when the score is over 20 points [ 52 ]. Nevertheless, this survey does not provide a definite diagnosis of eating disorders; therefore, a clinical evaluation is needed. This evaluation can be carried out via individual interviews.

The body satisfaction questionnaire (BSQ) [ 53 ], whose Spanish adaptation was completed by Raich [ 54 ], was used. The stereotypes perception survey from the University of Granada was also used [ 55 ].

The questions referring to body image included illustrations of women’s bodies. These illustrations comprise seven body images that vary from underweight to obese, numbered from 1 to 7. Additionally, a specific section focused on body satisfaction, examining their satisfaction on a scale from 1 to 7, with lower scores relating to higher levels of body dissatisfaction. In this section, one of the questions examined the steps each young person would take to attain a body type that corresponded to the ideal.

The body image concerns were observed by using the BSQ, a self-report instrument evaluating weight and shape preoccupations [ 54 ]. Sample items include: “Have you been so worried about your shape that you have felt you ought to diet?”; “Have you noticed the shape of others and felt that your shape compared unfavourably?” The questions were answered on a six-point Likert scale (1 = never, five = always).

The Appearance Evaluation (AE) subscale of the Multidimensional Body-Self Relations Questionnaire-Appearance Scales (MBSRQ) was used to measure self-perception and stereotypes [ 56 ]. Participants rate the extent to which they agree with seven statements (e.g., “Most people would consider me good-looking”) on a five-point scale (1 = disagree, 5 = agree) with lower scores indicating lower self-perception and stereotypes.

Finally, self-esteem was evaluated by the Rosenberg survey (CIPE-a) composed of ten questions, which provided us with high, medium or low levels of self-esteem. The questions were given a scale on a four-point scale (1 = disagree, 4 = agree), with lower scores indicating lower self-esteem [ 57 ].

On the other hand, the survey that focused on social networks had preliminary yes/no items about having social network accounts on Twitter, Facebook, Instagram, YouTube or Snapchat. Participants indicated how often they access/check their respective accounts daily on a five-point scale: hardly ever, sometimes, usually, all most all the time and always. Additionally, the participants’ daily use (hours per day in social networks and highly visual social media, i.e., Instagram, Snapchat), number of accounts and importance given to these was rated on a 1 (strongly disagree) to 5 (strongly agree) scale.

Meanwhile, addiction to social networks was evaluated by a validated survey called the Social Networks Addiction Questionnaire (SNSA) [ 50 ]. The survey is based on the DSM-IV-TR [ 27 ], a diagnostic instrument that does not recognize psychological addictions as disorders but as a prior stage that can lead to addiction. The survey is formed by 24 items applying a five-point rating system (from 0 to 4), taking into account the frequency from “never” to “always” [ 56 ].

The study has focused on the indirect determination of intrauterine testosterone levels during the gestation, determined experimentally from the difference in length of the phalanges of the hands (2D:4D ratio). This measure was selected to determine the possible relation with sociocultural factors indirectly. The selection of this method was based on reducing the risks, vulnerability and protecting biological or genetic material from the participants. When the ratio is higher, i.e., the difference between the second and fourth finger, lower levels of testosterone are implied [ 21 ]. 2D:4D is an indicator of testosterone and oestrogen levels [ 58 ], which heavily dictate attractiveness [ 17 ]. Therefore, this digit ratio may be related to self-perception, body image, body dissatisfaction and disordered eating attitudes.

3.3. Instruments

The instruments used to obtain the image of the hands were a Canon Camera EOS700D (produced by Canon Inc., which is a Japanese company founded in Ota, Tokyo) and a Manfrotto Compact Advance tripod (produced by Manfrotto, which is an Italian company founded in, produced and distributed form the USA). Additionally, free access software GeoGebra ( https://www.geogebra.org ), which is a free access software founded in Austria and later updated and mass produced in USA, was used to analyse the indirect marker of testosterone levels (2D:4D ratio).

3.4. Procedure

Participants approved a participant information statement, consent form and questionnaires, followed by the approval of the Research Ethics Committee of Public Health System in Cordoba (Ethical Approval number 273, reference 3773).

The participants were undergraduate students with health, education, life and engineering studies. The recruitment took place in different classrooms of the University, the objective of the study, ethical indications, risks for the participants and voluntary participation in the study being previously explained. During the recruitment a teacher and a researcher were present in the classroom the entire time.

The inclusion of the participants was based on an initial survey, which was provided previously in the same classroom. In this survey, the students were asked about the previous diagnosis of conduct or emotional disorders, addiction to technologies, abuse of substances and having a social network account. Those students that had a previous diagnosis of conduct, emotional disorders, or addiction were eliminated from the sample and were not given the survey of the study. Those students that did not have an account on any social network were also excluded from the study ( Figure 1 ).

Flow chart of the recruitment and selection of the sample.

3.5. Statistical Analysis

Mean and standard deviation (SD) were calculated for the quantitative variables and frequencies in the case of qualitative variables. Firstly, we studied the normalization of the data using the Kolmogorov-Smirnov test ( p < 0.05). Moreover, Cronbach’s alpha test was used for determining the consistency among the scales and subscales and, especially, the SNS test showed acceptable value (0.77) and the EAT-26 (0.83) was excellent. In order to assess the first objective, the χ 2 test was used for the qualitative variables, such as gender and body image, and the Student’s t -test was applied to compare quantitative variables, such as the EAT-26 score and age. Additionally, correlational analyses were used to examine relations between all variables.

Moreover, the second set of analyses examined the impact of the relationship between disordered eating attitudes and the rest the factors measured. For this purpose, the crude and adjusted odds ratio (OR) values were calculated for the logistic regression. In the end, the ROC (receiver operating characteristic) curves and the validity indices were used for the diagnostic accuracy of disordered eating attitudes having body dissatisfaction and social networks addiction.

First Phase

The initial analysis of the data showed that women ( N = 168) had a range of age between 21 and 22, 96.7% of them being Caucasian ethnicity. Moreover, the body image that they had was in range between 3 and 4, which may imply a normal weight. The perception that they had of themselves was fatter (3.56 ± 1.2) when compared to the desired body image (2.99 ± 0.83) ( Table 1 ). Additionally, the most common description of body satisfaction showed low and medium-high levels of body satisfaction (48.7%). In this sense, the difference among the group with lower and higher levels of body satisfaction was related to the body image given by the women (χ 2 = 113.64, p < 0.001).

Mean, standard deviation and confidence intervals.

Moreover, the results from the data showed that almost 93% of the women desired to change at least three zones of their body using at least two different methods (1.98 ± 0.82). The methods most used were physical activity (92%), diet (48%), surgery (24%) and beauty or alimentary products (23%). Among the zones to be modified by a surgical procedure 68% of the women indicated breast implants.

The analysis of the results from the EAT-26 test showed that most of the women had a medium probability of having disordered eating attitudes (18.34 ± 10.7). Figure 2 reflects the frequency of the scores from the EAT-26 related to body satisfaction.

Results from the EAT-26 related to body satisfaction.

The figure displays a higher frequency of scores over 20 points in disordered eating behaviours in the lower points of the body satisfaction scale. This figure implies that there were more values over 20 points when women suffered higher levels of body dissatisfaction. Additionally, the analysis between the score in the disordered eating behaviour test and level of body satisfaction showed significant differences among individuals with low and high levels of body satisfaction and scores over 20 points in the EAT-26 (χ 2 = 375.34, p < 0.001). Moreover, a more in-depth analysis of the data, based on women with more than 20 points in the EAT-26, 48 out of 168 women showed that 40.81% had food oral control, 38.77% presented bulimia and food preoccupation and 20.5% dieting.

Further study of the data was carried out in order to address the possible correlations between the body image that women perceived of themselves and the other variables analysed. In Table 2 , the correlations between the body image and the different variables have shown significant value with numerous factors, including disordered eating attitudes, self-esteem, desired body image or number of methods. These correlations were positive for a fatter body image in higher scores in the EAT-26 and more methods used to modify the body image and the current body image. Moreover, negative correlations were found for a curvier description that the women gave about their body and higher desires for a thinner body image, higher body dissatisfaction and lower levels of self-esteem.

Correlations with body image that women perceived of themselves.

Another variable that determines a “fatter” body image is the level of prenatal testosterone, measured by the 2D:4D ratio. This result displayed a positive relationship implying that a higher 2D:4D ratio, lower levels of intrauterine testosterone, may lead to a fatter body image.

On the other hand, Table 3 exposed the analysis of correlations between the score obtained in EAT-26 for disordered eating attitudes and the other factors analysed. This test displayed a negative correlation between having a higher score in the test and having lower levels of body satisfaction, self-esteem, the desired of having a thinner body image and worse perception of their own body.

Correlations with having higher scores in the disordered eating attitudes test.

Moreover, the positive correlations were obtained for numerous factors studied. The most highlighting positive correlations were reflected for a higher score in the SNS addiction test, a fatter body image and a higher difference in the 2D:4D ratio. These results implied that a higher 2D:4D ratio or fatter body image may lead to a higher score in the EAT-26.

The logistic regression model was used to define a disordered eating behaviour related to having lower levels of body satisfaction, the desired to achieve a thinner body image, lower levels of self-esteem, higher score in the SNS addiction test, higher duration of connection to this media and higher difference between the second and fourth finger ( Table 4 ).

Logistic regression for disordered eating attitudes.

From the analysis based on levels of self-esteem and social networks, the results showed that most women have high levels of self-esteem (31.1 ± 4.7) and low levels of addictive behaviour to social network sites (14.69 ± 10.37). Furthermore, the results of the social network sites presented a high dispersion of the results. In this sense, the confidence intervals (95%) were focused on medium levels regarding addictive behaviour to SNS (13.11–16.26).

Based on this, the correlations for the score in the SNS addition test were studied. The results indicated positive significance for the number of methods used to change their body image (<0.001), higher desired of a thinner body ( p < 0.001), lower levels of self-esteem ( p < 0.001), greater number of social media accounts ( p < 0.001), longer duration of the connections ( p < 0.001) and the importance given to the social networks ( p < 0.001). Nevertheless, the difference between the second and fourth phalange (2D:4D ratio) showed no significance with scores in the social network addiction test.

Finally, based on the results from the logistic regression, a probabilistic model was obtained. This model could diagnose 42.9% of the population with disordered eating attitudes (R 2 Cox and Snell 0.429) by knowing if the person had scored high in the SNS addiction test, body image, body dissatisfaction and high desire of having a thinner body. The specificity (90.3), sensibility (68.9) and valid index (84.6) results were optimal. Finally, the curve of the model was analysed ( Figure 3 ) obtaining an acceptable probabilistic high risk of a disordered eating attitudes (area = 0.94, p < 0.001, CI 0.88–0.97).

ROC curve from the logistic model for disordered eating.

5. Discussion

This study has reflected how different factors, such as the level of self-esteem ( Table 1 ), might play a significant role in disordered eating behaviours. Among these factors the body image that women perceived over themselves stood out as a significant element. In this sense, according to previous researchers, body image is multidimensional, being made of perceptual, behavioural and cognitive-affective domains created by the individual [ 46 ]. This perception is dependent on a variety of elements, including social media and beauty ideals. In the case of social media, the results from this study showed a relationship between the body image, body ideals and the use of social media ( Table 2 and Table 3 ). Furthermore, previous publications explained that the desire to achieve the beauty ideal emerges as the internalization of the portrayed image exposed by the media [ 59 , 60 ]. Homan (2010) discussed how, among female college students, two principal beauty ideals coexist: the athletic-ideal and thin-ideal [ 61 ]. The internalization of the athletic-ideal predicts compulsive exercise [ 61 , 62 , 63 ]. Meanwhile, the thin-ideal internalization predicts food restriction and body dissatisfaction, both leading to disordered eating attitudes and possible origins for eating disorders [ 64 , 65 , 66 ]. These results confirm the association obtained between the desire of having a thinner body image and the use of the media since this media is the primary source to promote such ideals ( Table 3 ).

The issue resides on the fact that the thin-ideal produces a worse body image with a tendency toward frustration based on a fatter body image than desired. This concern among young women results in making different choices to obtain the desired image, such as surgery [ 67 , 68 ]. In this sense, the results from this paper also showed a high frequency of women determined to undergo plastic surgery to improve their image, being focused on breast surgery.

Notwithstanding, internalization of the fit-ideal has been studied as a predictor of the use of social media content related to health and fitness [ 69 , 70 ]. In this case, the fit ideal or athletic ideal may become a replacement for the other ideals, leading to healthier behaviour [ 71 ].

The results ( Table 2 ) have established that body dissatisfaction might be a potential agent in body image and desire to change this body image. These publications also accord with our earlier observations, which showed that levels of body dissatisfaction were associated with the desire of changing the body image in order to achieve a thinner body, especially using dieting [ 72 ]. Based on this, the results appear to match with previous works about how body dissatisfaction and body concerns in young women and teenagers may be related to disordered eating attitudes [ 27 , 73 ].

Another significant outcome was the link between body concerns, body dissatisfaction and levels of self-esteem ( Table 2 ). These data are in accord with recent investigations which connected body dissatisfaction and self-esteem to mental illness and the role of emotional distress in behavioural disorders [ 48 ].

Another study found that body dissatisfaction and disordered eating attitudes could be related to a high level of intrauterine testosterone, measured by the 2D:4D ratio. The prenatal masculinization has been established as a potential intermediate phenotype for the development of these disorders in their offspring [ 74 ]. Following these studies, the results obtained in this paper seem to initially match such conclusions ( Table 3 ) [ 75 ]. These results are partially consistent with the existing literature relating to dieting, alimentary products, such as supplements, negative affect, body dissatisfaction and the tendency to thinness [ 71 ]. Nevertheless, the results obtained regarding the hormonal levels may be related to the environmental conditions during the pregnancy more than the individual level of hormones [ 76 ].

The results of the study ( Table 4 ) have shown how social network sites might play an important role in disordered eating attitudes. In the study carried out by Cohen et al. (2018), the influence of the social networks was determined by the content and the selfies that the users upload to them more than by the assiduity of the connections [ 20 ]. This is partially contradictory to the present results in which the addiction to SNS and the duration of the connections were linked to weight loss and unhealthy dieting. These results match with previous studies in the sociocultural factors, not included among biological measures [ 77 , 78 ]. Withstanding, it is important to note that the regression model obtained in this study have shown the probable role of factors, such as the degree of body satisfaction, self-esteem, use of SNS and other measures, such as the 2D:4D ratio, related to disordered eating behaviours.

Additionally, SNS addiction, which has been related to other mental disorders [ 79 ], has shown correlation with stereotypes, self-esteem, method of change, thinner body image and the desired part of the body to change. In this sense, prior investigations proved the addiction to social media as cause–effect of disordered behaviours [ 80 , 81 ].

The present study raises the possibility that disordered eating attitudes in women might be conditioned by the influence of the ideals of beauty imposed by the social environment and to a lesser extent by the exposure to intrauterine levels of testosterone extracted from the 2D:4D ratio of the phalanges. It is possible, therefore, that disordered eating attitudes are multidimensional disorders produced by the media, hormones, and factors related to body concerns. Although this study has focused on Spanish college students, the results ( Table 2 and Figure 2 ) seem to match with previous works conducted in Caucasian women [ 82 , 83 ]. These studies seem to distant themselves from publications focused on Latina or African American young women or adolescents [ 84 , 85 ]. Nevertheless, it is possible, therefore, that because the study was carried out in Spanish college students, the results might not match university women from other countries.

Nevertheless, as with all research, the current findings need to be considered in light of possible limitations of the study. Therefore, biases and possibly incorrect data may have been included, and causal inferences cannot be drawn. Additionally, as with the majority of the body image literature, the current participants were university students, based on the sample and size of the sample caution is recommended in not generalizing these results to other samples or different samples. Nevertheless, these results seem to provide essential data regarding social media, disordered eating and the perception of the young people about themselves. Another limitation present in this study is the lack of inclusion of further cultural factors, such as the mother–child relationship, and anthropometric data, such as BMI.

All being said, the results from this manuscript and the comparison with previous works suggest how the initial hypothesis has been entirely or partially confirmed, showing how disordered eating behaviours are complex eating attitudes.

6. Conclusions

This paper has argued the relationship between body image, body concerns, body dissatisfaction, and disordered eating behaviours present in college women from the south of Spain. This study has identified that women reported moderate levels of body dissatisfaction and body concerns, which were consistently and strongly associated with disordered eating attitudes. In this sense, this work has established high levels of body dissatisfaction, and the link with the desire to achieve a thinner body image. Additionally, the study has shown how body dissatisfaction and desire to achieve the thin-ideal appear to be universal among college women.

Additionally, one of the more significant findings to emerge from this study was that the thin-ideal seems to be widespread in social media. This ideal can promote unhealthy measures, such as dieting, increase body dissatisfaction and disordered eating attitudes. In this sense, the desire to change the body image and taking unhealthy measures was common, given the proliferation of the use of the social network sites where images and content encourage women to aspire to unrealistic and unattainable body ideals. In this sense, the study associated body dissatisfaction, body concerns, and general mental well-being, demonstrating that interventions to improve body perception and satisfaction are essential. Additionally, this research found that higher levels of prenatal testosterone might decrease the probability of having a disordered eating attitude among women. That said, the current study suggests a connection between disordered eating attitudes, negative impacts of exposure to thin-ideal content, addiction to social media and intrauterine testosterone levels.

Concerning practical implications, researchers have asserted that increasing body appreciation may be easier than attempting to decrease body dissatisfaction and for those disordered eating attitudes. Furthermore, the findings regarding the negative impact of exposure to social media related to women’s body satisfaction and body appreciation are notable. Despite the limitations present in this manuscript, the findings may help us to understand body concerns focused on the impact of exposure to social media.

In the end, future investigations should continue exploring differences in the levels of body dissatisfaction and disordered eating, including the differences between various ethnic groups. Given the findings regarding differences between those with higher and lower score in EAT-26, the role of social media may be essential in levels of body dissatisfaction and disordered eating attitudes within specific gender/age groups. Longitudinal research is needed to determine the direction of the association between the frequency of connections to social media and body dissatisfaction/disordered eating behaviours. Researchers may also consider culturally-relevant factors that may differentially influence such behaviours.

Acknowledgments

We would also like to thank of UCO Social Innova Project Galileo IV from the institution of OTRI of the University of Cordoba, Spain and the funding provided from “IDEP/Escuela de Doctorado” of the University of Cordoba to one of the authors. The content is the responsibility of the authors and does not necessarily represent the official views of the OTRI.

Author Contributions

Conceptualization: P.A.-M. and M.V.A.; methodology: P.A.-M. and M.P.M.-J.; validation: A.-J.P.-M.; formal analysis: P.A.-M. and A.-J.P.-M.; investigation: P.A.-M. and A.-J.P.-M.; resources: M.P.M.-J. and A.-J.P.-M.; data curation: M.D.R.-M.; writing—original draft preparation: P.A.-M., M.P.M.-J. and A.-J.P.-M.; writing—review and editing: M.V.A. and C.P.; visualization: C.P.; supervision: M.D.R.-M., C.P. and M.V.A.; project administration: M.V.A. and M.P.M.-J.; funding acquisition: M.V.A.

UCO Social Innova Project Galileo IV from the institution of OTRI of the University of Cordoba, Spain and the funding provided from “IDEP/Escuela de Doctorado” of the University of Cordoba.

Conflicts of Interest

The authors declare no conflict of interest.