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Anorexia Essay: How to Work with a Scary Topic and Do It Right

Jilian Woods

Table of Contents

When you study at the Nutrition department or prepare to become a medical specialist, you’re sure to get an eating disorder essay assignment one day. This problem has become quite commonplace, with a complex of eating problems awaiting people who are too obsessed with slim body images on social media and want to lose weight at all costs.

Because of the popularity of slim body images and young people’s obsession with the sporty body, the problem of anorexia is getting acuter day by day. So, when you get an anorexia essay assignment, be ready to do some thorough research, develop strong arguments, and compose a paper in line with academic writing rules.

If you’re confused about this task, here are some working tips to get the process going.

What Is Anorexia and How to Talk About It

Problems with eating surface not that quickly. At first, individuals may limit their portion sizes and refuse some products that they believe are dangerous for their weight. Next, they refrain from several meals a day, leaving only 1-2 food intakes to stay slim and not to overeat. As a result of such severe limitations in eating, some people develop anorexia nervosa.

This disease goes far beyond a permanent loss of appetite and manifests itself in various neurological and gastrointestinal problems. Its common symptoms are:

  • Extreme, uncontrollable weight loss
  • Unhealthy thinness
  • Fatigue experienced during a significant part of the day
  • Unexpected attacks of dizziness and frequent fainting
  • Thinning hair and breaking nails
  • Intolerance to cold
  • Hypertension
  • The inability of the gastrointestinal tract to process the consumed food – nausea and vomiting after food intakes

Given such an abundance of symptoms and clinical manifestations of this condition, you can approach the subject from several angles. Some students discuss the psychological causes of the disorder in their anorexia essay papers. Others focus on the biological mechanisms of anorexia development. Another interesting approach is to consider clinical evidence of therapeutic methods to treat anorexic people and help them regain a healthy weight.

How to Write an Eating Disorder Thesis Statement

The first task that you should complete in crafting your anorexia essay is developing a solid, clear thesis statement. It is a crucial element of your assignment that will guide the readers from the introduction to the concluding part, giving them a firm grasp of your logic and argument flow.

Thus, to build a robust and believable thesis, you need to follow these guidelines:

  • Choose a sub-topic within the subject of eating disorders. Formulate for yourself what you think about this topic first.
  • Try to express your central idea in one sentence, showing your primary arguments and focus.
  • Mention the arguments supporting your central claim briefly in this statement, without going into too much detail.
  • Place the thesis statement correctly at the end of your introductory section to ensure that the readers and supervisor will locate it.

Anorexia Essay Outline

Now let’s consider a sample outline for an anorexia essay, which can serve as your guidance in future work on such papers.

INTRODUCTION

Introduce the broad context. Give some stats and facts. Delineate a concrete problem and its significance. Formulate a thesis statement.

Diet – a personal choice or a disorder? Global population (2.9 mln) affected by anorexia. No apparent cause identified yet (genetic, neurological factors). A variety of treatment modalities available today and their varying effectiveness. 

Paragraphs #1-3

Present a topic sentence with one central idea per paragraph. Add some credible evidence from external sources to support the points. Interpret the information you’ve provided.

Paragraph #1 – the process of anorexia development, extreme dieting, forced vomiting after eating to control body weight, obsession with slim body images. The result – clinical anorexia symptoms.

Paragraph #2 – the inability of anorexic individuals to reverse the process (return to healthy eating after achieving the weight loss goal). Clinical complications of anorexia (osteoporosis, infertility, heart damage). Forced feeding of anorexic individuals to prevent terminal organ failure.

Paragraph #3 – Treatment modalities – psychotherapy, healthy weight gain, and addressing the problematic behaviors (forced vomiting, food refusal). Effectiveness of CBT and family therapy. Pharmacological treatments.

Make a summary of what’s been said and reinforce the readers’ impression by referencing the broader context (public health, teen health, the devastating impact of social media, etc.).

Anorexia is not a strict diet. It is a neurological disorder that can cause morbidity and mortality among patients. Because of the absence of a clear understanding of its underlying causes, anorexia needs to be treated on a case-by-case basis by giving each patient an individual treatment plan in line with their health state and anorexia triggers. 

Eating Disorders: Conclusion That’ll Earn You A+ Grade

A conclusion of your anorexia essay should summarize all the evidence you provided in the body of your paper and return to the problem’s significance in the broader context of public health. Depending on your essay’s topic, you can draw some recommendations on helping young people avoid anorexia or some workable methods for managing this condition more efficiently.

Sample Essay on How We Should Treat People with Anorexia

Our writing experts have crafted a short essay sample based on the outline presented in the section above. Use it as a reference when preparing your following paper on this subject.

For many people, choosing what to eat and when to do it is a voluntary act. For those with anorexia nervosa, eating has become an impossible challenge, an act that they cannot commit voluntarily, even for the sake of their survival. At present, over 2.9 million people are affected by anorexia worldwide, suffering extreme weight loss, multiple organ problems, osteoporosis, heart damage, and a complex of other devastating consequences of strict dieting and food refusal. Thus, what starts as a diet for the sake of healthy weight loss and body slimming often ends with a clinical disorder with no cure. Still, the issue is grave for people affected by this condition as they need efficient, professional treatment to start eating normally again and avoid lethal malnourishment. This paper discusses the causes, manifestations, and treatment modalities for anorexia nervosa known today in an effort to find workable solutions for the affected patients.

No single cause of anorexia development has yet been identified, with a mixture of genetic, environmental, and psychological factors coming into play. Jameson (2009) discovered that anorexic patients often view themselves as overweight (even if they are thin) and deny any weight loss or nutrition problems. As a result of the distorted body image and an obsession with slimness, anorexic people force themselves to vomit, refuse many food types, engage in excessive exercise and use laxatives to prevent excessive body fat accumulation (Mary, 2007).

As a result, the process of body weight loss becomes irreversible and cannot be dropped even after the clinical problem is clear. Individuals with anorexia often develop osteoporosis, suffer from irreversible organ failure, and lose fertility (especially females). Anorexic patients refuse therapeutic interventions, vomit secretly, and avoid treatment in all ways. Thus, such severe manifestations of anorexia are commonly treated by forced feeding via nasogastric tubes upon a competent psychiatrist’s diagnosis of the patient’s psychological incompetence.

Other treatment methods include psychotherapy and family therapy to identify the underlying psychological causes for food refusal and change the false perceptions and prejudices of patients. Kale (2020) found CBP to be effective with young female anorexics, with 78% of the surveyed sample reporting significant improvements in body image perceptions and weight regain. Thus, psychotherapeutic methods are popular in anorexia treatment as they allow dealing with underlying psychological problems of patients and correct their beliefs about body image in the long run.

As the provided evidence suggests, anorexia nervosa is a severe clinical problem that millions of patients face worldwide. With no clear causes and specific clinical guidelines for its treatment, anorexia remains a pressing challenge for medical professionals and patients. Case-by-case management of anorexia cases is suggested, while a combination of pharmacological and psychotherapeutic treatments suggests the greatest efficiency thus far.

More Helpful Tips & Tricks

Tasked with an anorexia essay? Here are some valuable tips to follow to get an outstanding grade for this assignment:

  • The underlying causes of this disorder are still unclear. So, you can surprise your tutor by presenting an in-depth analysis of the existing theories about the origin of anorexia.
  • Treatments for anorexia differ, ranging from CBT to pharmacological care. You can compose in-depth research about the clinical evidence of each treatment modality’s effectiveness for various population groups.
  • The psychological component of anorexia is powerful. An excellent paper can result from research on the psychological triggers and accompanying psychological disorders among anorexic individuals.

Here’s How a Professional Writer Can Help You

Still unsure how to compose an anorexia essay that will win you a high grade? Having little time to think over the subject thoroughly and develop workable arguments? Lacking a couple of free hours to attend the library and find the relevant, credible evidence to support your points? No problem, as our experts can do it for you.

Contact us today to get a perfectly written and well-proofread paper about eating disorders. We’ll surely impress your supervisor with original ideas and credible evidence. In this way, you’re sure to save crucial time for other academic priorities and avoid getting an F for a failed deadline.

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112 Anorexia Essay Topic Ideas & Examples

🏆 best anorexia topic ideas & essay examples, 📌 simple & easy anorexia essay titles, 👍 good essay topics on anorexia, ❓ research questions about anorexia nervosa.

  • Anorexia as Eating Disorder However, due to limitation in scope, the rest of the chapter will explore anorexia nervosa by tracing the historical background of the condition, reviewing prevalence of the disorder in terms of gender, culture and geographical […]
  • Anorexiants: Pharmacology and Pharmacological Effects The purpose of this presentation is to examine the pharmacology and pharmacological effects of popular anorexiant substances.
  • Anorexia Nervosa in Psychological Point of View Anorexia nervosa is more common in the industrialized countries, where being thin is considered to be more attractive, and is more frequent in Whites than the nonwhite populations. In the age group of 10-14 years, […]
  • Differential Diagnosis in a Patient: Anorexia Nervosa The first step is to avoid malingering and make sure that a patient is not pretending to be sick. Julia’s and the roommate’s stories are not contradictory; hence, it is safe to say that Julia […]
  • Anorexia as Social and Psychological Disease Many who were used to his weight knew, though Bob is not the most handsome, but a charming person, kind and friendly.
  • Anorexia Nervosa and Its Treatment Anorexia nervosa is a treatable eating disorder when people significantly limit the number of calories and types of foods they eat, which leads to excessive weight loss. The objectives of anorexia treatment include weight recovery, […]
  • Genetic Disorder: “A Genetic Link to Anorexia” The author effectively proves that the development of anorexia nervosa may occur not only due to the exposure to the social pressure of beauty standards, but also the presence of a genetic predisposition.
  • Controlling the Problem and the Treatment Anorexia Nervosa Finally, the paper will be looking at the possible measures of controlling the problem and the treatment of the victims. When female are in their teenage, most of them are affected by the problem of […]
  • Daily Patterns of Anxiety in Anorexia Nervosa The researchers failed to indicate the distinct and important sections such as the study objectives and the significance of the study.
  • Anorexia Nervosa and Life-Sustaining Treatment Therefore, the primary care for patients with anorexia nervosa requires administration of various dietary and mental medical interventions and a clear understanding of different concepts and ethical issues related to the treatment of the disorder.
  • Anorexia Studies. “Thin” Documentary The nutrition of a single person has a strong cultural aspect, being influenced by traditions of a family circle and the whole nation.
  • Eating Disorders: Anorexia and Bulimia Anorexia Nervosa is the disease in which the patient avoids eating because of the fear of getting fat. Bulimia Nervosa refers to the pattern of binge eating.
  • The Anorexia Nervosa as a Mental Illness While tracing the history of the disease, many authors have come to the conclusion that the disease is to some extent due to the living styles that people have adopted over the years and also […]
  • Anorexia Nervosa: Medical Issues In response to this, the writer wishes to state that the purpose of this paper is to present a brief outline of anorexia and its causes to the millions of Americans out there without knowledge […]
  • The Portrayal of Women With Anorexia Body image distortion, wherein the individual has an inaccurate perception of body shape and size is considered to be the cause of the intense fear of gaining weight or becoming fat witnessed in individuals with […]
  • The Role of Family in Developing and Treating Anorexia The rest of the poem confused and inspired me as a reader because Smith, as well as millions of people around the globe, proved the impossibility to have one particular definition of anorexia in modern […]
  • The Problem of Anorexia: “There Was a Girl” by Katy Waldman In her essay, the writer strives to embrace the concept of anorexia and explore the mindset that encourages the development of the specified disorder.
  • “Skinny Boy: A Young Man’s Battle and Triumph Over Anorexia” by Gary A. Grahl Grahl suffered from anorexia in his youth, and the book is a memoir-like account of the event, serving to open the door to the psychology of the disease in the male populace a vulnerable population […]
  • Anorexia Nervosa and Its Perception by Patients In the control group, 80 laymen and women were selected randomly to participate in the study and they completed a modified IPQ-R questionnaire to elicit their perceptions towards AN.
  • Anorexia Nervosa (AN) and LGBTQ Suicide Awareness Concerning the format, the design of the poster is good and the words are readable. The colors and contrasts enhance the readability of the content and stress the key points, such as AN indicators, risk […]
  • Anthropology: Anorexia and Idiopathic Seizures Considering the relation between this disease and cultural issues, it is possible to refer to life of people in society. It is essential to consider anorexia and idiopathic epilepsy from the point of view of […]
  • Anorexia Nervosa: Diagnosis and Treatment in Psychotherapy In the meantime, it is, likewise, vital to determine the cause of the condition’s appearance and point out the necessary alterations.
  • Influence of Media on Anorexia As the children grow, they disregard big-bodied people, and try as much as possible to maintain a slim figure, as they see from the magazines and televisions.
  • Psychological Factors Underlying Anorexia Nervosa The condition also occurs where individuals deny hunger as well as restrict energy and nutrients to levels that are minimal and inadequate to maintain the functioning of the normal body health and mass. In addition, […]
  • The Problem of Anorexia in Modern American Society However, in spite of frightening statistics, nowadays many sufferers have a good chance to recover due to increasing number of programs and campaigns aimed at overcoming this disease. 7% – Hispanic people, and the rest […]
  • The Eating Disorder – Anorexia Nervosa It is noted that majority of the people that suffer from anorexia disorder are those that suffer from low-self esteem. The eating disorder makes bodies of people suffering from Anorexia nervosa struggle to manage insufficient […]
  • Healthy Lifestyles in the Context of Anorexia and Obesity In addition, a thorough evaluation of one’s lifestyle is imperative so as to rectify that which is causing the anorexia. As discussed in this paper, it is clear that physical activity and a healthy balanced […]
  • Anorexia Nervosa: Signs, Effects and Therapies Nurses in the labor and delivery units need to be trained on the proper way of diagnosing and handling anorexia patients to reduce cases of infant mortality. A combination of medical attention and accommodating psychotherapy […]
  • Treatments of Anorexia Nervosa Because the mortality rates and co-morbidity incidence of aneroxia nervosa remains critically high despite the array of various intervention strategies that are currently available to health professionals, it is justifiable to have a reassessment of […]
  • Anorexia in Teens: Media Impact This research focuses on the impact of the media as the ultimate key player for the development of the dangerous disorder among the contemporary young girls in the society.
  • Eating Disorders: Anorexia, Bulimia and Compulsive Overeating Anorexia is a both eating and psychological disorder that is initiated as a person begins to diet in order to lose weight.
  • Psychological Disorders: Bulimia Nervosa vs. Anorexia Nervosa Although people with the condition are able to recover if the disorder is properly managed, Eysenck states that the near starvation state that most anorexics live with during the period of the disorder can be […]
  • Eating Disorders: A Session With Sufferers of Obesity and Anorexia One of the myths that surrounds anorexia is that the only cause of this disorder is the wish to lose weight; some people even refer to the condition as the ‘slimmer’s disease’.
  • The Issue of Anorexia Nervosa Disease: Symptoms, Treatments and Reasons Why It’s Become so Common
  • The Characteristics of People Suffering from Anorexia Nervosa
  • The Morality in Helping Others With the Anorexia Nervosa, a Psychological Disorder
  • Randomized Controlled Trial of a Treatment for Anorexia and Bulimia Nervosa
  • The Characteristics and Symptoms of Anorexia Nervosa, an Eating Disorder
  • The Causes, Symptoms, Effects, and Treatment of Anorexia Nervosa
  • Relationship Between Environmental Factors and Anorexia Nervosa in Adolescent Girls
  • The Mental Problem Connected to the Eating Disorder Anorexia Nervosa
  • The Causes and Treatment of Eating Disorders Bulimia and Anorexia
  • Restrictive Food Intake Disorder And Anorexia Nervosa
  • The Exploration of Anorexia in Regards to Nyasha
  • The Causes, Manifestation and Treatment of Anorexia Nervosa
  • Several Possible Reasons for the Increasing Cases of Anorexia Nervosa
  • Society’s Influence On Teenagers: Anorexia Nervosa And Bulimia Nervosa
  • The Potential Causes and Factors Leading to the Eating Disorder, Anorexia Nervosa
  • The Main Diagnostic Components Of Anorexia Nervosa
  • Symptoms Of Anorexia Nervosa, The Most Visible Eating Disord
  • The Predictors, Prevention And Intervention Of Anorexia
  • The Maudsley Model of Family-Based Treatment for Anorexia Nervosa
  • The Dancing with Anorexia, An Introduction to the Disease by Natalie Moon
  • Signs, Causes, and Treatment of Bulimia and Anorexia Eating Disorders
  • The Pervasiveness Of Eating Disorders Essay – Anorexia therapy, Eating
  • The Description of the Eating Disorder Anorexia Nervosa
  • Taking Control of Eating with Bulemia or Anorexia
  • Symptoms, Causes, And Treatments For Anorexia Nervosa
  • The Hidden Causes and Effects of Anorexia and Bulimia
  • The Effects of Anorexia to Marian in the Edible Woman, a Novel by Margaret Atwood
  • The Effectiveness of Treatment for Anorexia Nervosa and Bulimia
  • The Effects Of Pharmacological Treatment On Anorexia Nervosa
  • The Influence of Perfect Bodies Advertisements Leading to Anorexia among Teenagers
  • The Impact of the Fashion Industry in the Proliferation of Anorexia Nervosa
  • The Importance of Maintaining an Adequate and Nutritional Diet Among Anorexia Nervosa Patients
  • The Unattainable Goals of Anorexia Nervosa: Are you Starving Yourself
  • The Problem of Women in the United States: Anorexia Nervosa and Bulimia Nervosa
  • Understanding the Causes and Treatment of Anorexia Nervosa
  • The Prevention and Treatment of the Mental Illness, Anorexia Nervosa
  • The Question of Craving in the Eating Disorder Anorexia Nervosa
  • The Problem of Anorexia and Bulimia Nevrosa in the United States
  • The Rise in the Number of Girls Suffering from Anorexia
  • The Signs, Symptoms and Treatment for Anorexia Nervosa
  • The Real Skinny on Anorexia A Merciless Battle with the Mirror
  • The Truth about Anorexia a Disease That Strikes Both Men and Women
  • The Unfortunate Mindset Of A Patient With Anorexia
  • What Are The Symptoms Of Anorexia Nervosa
  • To Eat or Not to Eat: a Comparison of Anorexia and Obesity
  • Treatment For Anorexia Nervos A Comparison Of Cognitive
  • How Does American Advertising Cause Anorexia in Women and Female Teenagers?
  • Could Dopamine Agonists Aid in Drug Development for Anorexia Nervosa?
  • How Does Food Taste in Anorexia and Bulimia Nervosa?
  • What Are the Symptoms of Anorexia Nervosa?
  • How Does Anorexia Affect the Human Body and How One Can Recover?
  • What Does Blushing Have to Do With Anorexia?
  • How Does the Media Cause Bulimia and Anorexia?
  • What Are the Differences Between Anorexia Nervosa and Bulimia?
  • How Does Low Self-Esteem Affect Anorexia?
  • Why Is the Diagnosis of Anorexia Significant Amongst Youngsters?
  • How Will Anorexia Nervosa and Bulimia Influence the Emotions and Attitudes of Kids Towards Others?
  • Who Are Susceptible to Anorexia Nervosa and Bulimia?
  • How Will Anorexia and Bulimia Affect the Social Lifestyle of Kids?
  • Would You Say Unhappiness and Physical Shame About the Body Worsens Bulimia and Anorexia?
  • How Do the Symptoms of Anorexia and Bulimia Overlap?
  • Do You Think Diagnosis for Anorexia Are Often Underrated?
  • How Does Subconscious Feature of Bulimia and Anorexia Develop Amongst Girls?
  • Is There Much Evidence for Specific Features of Cognitive Behavioural Therapy Being Effective in the Treatment of Anorexia Nervosa?
  • How Do Anorexia and Bulimia Affect Women’s Libido?
  • What’s the Difference Between Bodily Shame and Body Dissatisfaction? What Role Do These Variables Play in Anorexia Onset?
  • How Do Western Communities React to Anorexia?
  • What Is the Death Rate of Anorexia?
  • Are Certain Personality Traits More Common in Individuals With Anorexia?
  • What Is Age Group Most Likely to Suffer From Anorexia?
  • Is There a Psychological Assessment Recommendation That Measures the Tendency for Anorexia Nervosa?
  • What Is the Risk of Cancer in Anorexia Nervosa?
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State or trait: the neurobiology of anorexia nervosa — contributions of a functional magnetic resonance imaging study

Selma göller.

1 Department of Psychosomatic Medicine and Psychotherapy, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany

Kathrin Nickel

2 Department of Psychiatry and Psychotherapy, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany

Isabelle Horster

Dominique endres, almut zeeck, katharina domschke.

4 Center for Basics in Neuromodulation, Faculty of Medicine, University of Freiburg, Freiburg, Germany

Claas Lahmann

Ludger tebartz van elst, simon maier, andreas a. b. joos.

3 Department of Psychosomatic Medicine and Psychotherapy, Ortenau Klinikum, Lahr, Academic Teaching Hospital of the University of Freiburg, Lahr, Germany

Associated Data

Data are available from the senior authors on reasonable request.

The understanding of the cerebral neurobiology of anorexia nervosa (AN) with respect to state- versus trait-related abnormalities is limited. There is evidence of restitution of structural brain alterations with clinical remission. However, with regard to functional brain abnormalities, this issue has not yet been clarified.

We compared women with AN (n = 31), well-recovered female participants (REC) (n = 18) and non-patients (NP) (n = 27) cross-sectionally. Functional magnetic resonance imaging was performed to compare neural responses to food versus non-food images. Additionally, affective ratings were assessed.

Functional responses and affective ratings did not differ between REC and NP, even when applying lenient thresholds for the comparison of neural responses. Comparing REC and AN, the latter showed lower valence and higher arousal ratings for food stimuli, and neural responses differed with lenient thresholds in an occipital region.

Conclusions

The data are in line with some previous findings and suggest restitution of cerebral function with clinical recovery. Furthermore, affective ratings did not differ from NP. These results need to be verified in intra-individual longitudinal studies.

Supplementary Information

The online version contains supplementary material available at 10.1186/s40337-022-00598-7.

Plain English summary

There is abundant evidence of structural and functional brain alterations during the acute stage of anorexia nervosa (AN), although affected brain areas differ based on various study methodologies. Meanwhile, investigations indicate that brain structure normalizes with weight and clinical restitution. The current cross-sectional investigation examines acutely ill AN patients, healthy controls, i.e. non-patients (NP) and well-recovered individuals (REC), with respect to brain function. Functional cerebral responses of participants exposed to food pictures were investigated. Neither in terms of function nor emotional experience of food stimuli, the REC differed from the NP group. This study points to brain function normalizing with clinical and weight restoration, which should be verified in intra-individual longitudinal studies.

Anorexia nervosa (AN) is an eating disorder largely affecting young women with high morbidity, chronicity and mortality [ 1 ]. Apart from a restriction of energy intake leading to a significant weight loss, an intense fear of gaining weight and body image disturbance are key symptoms. The etiology is not well understood, though genetic disposition is one important factor, accompanied by psychosocial factors [ 2 ]. Maintaining factors include consequences of malnutrition, as well as consequences of isolation and depression [ 3 ]. Brain imaging studies point towards shrinkage of white (WM) and grey matter (GM) and complementary increase of the cerebrospinal spaces [ 4 , 5 ]. Longitudinal investigations show restitution of GM and WM volumetric alterations following long-term weight restoration [ 4 ]. Apart from structural brain alterations, also the function of various domains has been reported to be affected in acute AN [ 6 , 7 ], although the involved brain areas differed [ 8 ]. Due to significant loss of weight, cerebral aberrations might be associated with metabolic changes, i.e. starvation, and it is difficult to disentangle other factors associated with eating disorder psychopathology and/or predisposing factors [ 9 ].

Hence, the question remains which abnormalities are state phenomena, i.e. occur only during the acute phase of the disease, and which are trait-related. Persistent cerebral aberrations could be a predisposing phenomenon and might therefore represent endophenotypes [ 10 ], but they may also represent sequels, i.e. “scars” of the acute disease. As AN is a disorder with low prevalence [ 2 ], it is methodically difficult to study individuals who might develop AN longitudinally in order to shed light on the question of endophenotypic cerebral aberrations. Therefore, a first step to clarify questions about state and trait is to investigate individuals recovered from AN (REC).

With respect to the issue of state-trait in AN, previous studies examined psychological, cognitive and behavioral variables [ 11 , 12 ] as well as metabolic, structural and functional correlates of the brain [ 13 – 15 ]. Overall, research on reversibility of psychological, cognitive and behavioral functioning in REC presents a heterogeneous picture [ 16 – 18 ]. In terms of structural cerebral alterations, neuroimaging studies provide strong evidence of remission with clinical recovery [ 5 , 19 , 20 ]. Findings of functional magnetic resonance imaging (fMRI) studies comparing REC and non-patients (NP) show divergent results. With respect to visual food cues, some authors reported no alteration in brain activation in REC (when compared to NP) [ 21 – 23 ], while Uher et al. [ 24 ] detected increased activation of prefrontal and anterior cingulate cortices (ACC) and a reduction of activity in parietal regions in a small group of REC. Further studies found hypoactivation of the insula [ 25 ] or increased caudate activation [ 26 ] in response to food pictures. With regard to other disorder specific paradigms (e.g. taste, body shape), both increased and decreased functional neural brain responses for REC (compared to NP) were found in various brain regions [ 13 , 27 – 30 ], while two studies detected no altered brain activity in REC [ 31 , 32 ]. However, a majority of fMRI studies using non-disorder specific stimuli (e.g., fear, intimacy, reward) reported no or only minimal functional aberrations in REC [ 33 – 36 ]. Longitudinal fMRI studies with non-disorder specific paradigms yielded conflicting results in delay discounting tasks [ 37 , 38 ], a normalization in a working memory and set-shifting task [ 39 , 40 ], and persisting changes in theory of mind and reward learning paradigms [ 41 , 42 ]. For further details and an overview of previous studies, see Additional file 1 .

This investigation focuses on the question of restitution vs. non-restitution of functional brain abnormalities using a cross-sectional design in order to address the topic state and trait of the neurobiology in AN. In this context, the comparison of NP and REC is of particular interest. It complements previous studies on disease-specific food stimuli in REC [ 21 – 26 ]. The paradigm has already been employed previously in a study of AN with some REC participants [ 24 , 43 ] and a study focusing on NP versus AN [ 44 ]. Data from the current study comparing NP and AN has been reported previously, with a focus on replicability issues [ 45 ]: Group comparisons yielded higher blood oxygenation-level dependent (BOLD) responses of AN compared to NP in midcingulate, pre/postcentral and parietal areas when using a lenient initial threshold, and no significant group differences with a conservative initial threshold.

Based on results of preceding whole-brain analyses [ 23 , 25 ], we expected no differences between REC and NP in neural response to food stimuli or behavioral/experiential response, i.e., affective ratings of stimuli [ 22 , 24 , 46 ]. Additionally, we performed exploratory analyses of affective ratings and insula activation, as earlier studies found a positive correlation between food pleasantness ratings and insula activation in the NP group [ 22 , 25 ], but not in the AN [ 25 ] or REC groups [ 22 ].

Participants

AN and REC participants were recruited via the Department of Psychosomatic Medicine and Psychotherapy of the University Medical Center Freiburg. NP were recruited via local advertisements. The study was performed following written informed consent from the participants. The data was collected between March 2015 and October 2017.

Thirty-one AN, 18 REC and 27 NP were included in the final analysis. AN participants had to fulfill DSM-5 criteria. The following inclusion criteria were defined for the REC group: (1) Absence of eating disorder symptomatology for more than 12 months and an Eating Disorder Examination (EDE) [ 47 ] within one standard deviation of normal; (2) The Body Mass Index (BMI) was aimed at ≥ 20 kg/m 2 , which we achieved for most REC. The BMI of four participants was slightly below 20 kg/m 2 (between 19.3 and 19.7 kg/m 2 ) and of one participant 18.8 kg/m 2 . We decided to include these participants because they were clinically completely recovered and had always had a BMI in this range before the onset of the disease. Three AN patients were of the binge eating/purging type, all other AN and REC were of the restrictive type. Patients with AN were seen in the outpatient clinic for diagnostic reasons while nine were right at the beginning of inpatient treatment. Exclusion criteria had been reported previously [ 45 ].

The participants examined in the current study largely overlap with those of our previous investigations [ 5 , 14 , 19 , 34 , 35 , 45 ].

The study was approved by the local Ethics Committee (EK 520/13). Participants were assessed by means of the SCID interview [ 48 , 49 ], the EDE [ 47 , 50 ] and the following self-report questionnaires: Beck Depression Inventory-II (BDI-II) [ 51 ], Eating Disorder Inventory-2 (EDI-2) [ 52 ], State-Trait Anxiety Inventory (STAI) [ 53 ], and a crystalline intelligence test (MWT-B) [ 54 ]. All participants were studied in the second half of the menstrual cycle or the corresponding phase with estrogen and progesterone when taking oral contraception. In the morning around 8 a.m., participants were provided with a standardized breakfast, the calories consumed were counted, and the feeling of satiety was rated on a Likert-scale from 0 (very hungry) to 9 (very satiated).

Participants viewed via a mirror photographs of food and non-food items of similar structure [ 43 – 45 ] presented on a BOLDScreen monitor at the rear of the scanner bore. In a block design with five blocks per condition of 30 s each, 10 consecutive food or non-food pictures were presented alternately per block.

Participants were asked to look attentively at the pictures. Examples of the picture stimuli are displayed in Fig.  1 .

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Examples of food and non-food stimuli (cf. [ 45 ])

Behavioral data

After scanning, participants rated a selection of images (10 food and 10 non-food images) with respect to three emotion dimensions (valence, arousal and dominance) using “manikin ratings” based on the International Affective Picture System on scales from zero to eight [ 54 ]. The dominance scale assesses how much the viewer feels controlled or in control when watching the images [ 55 ]. Ratings of two AN and two NP could not be included due to incomplete data.

Image acquisition and processing

A T1-weighted Magnetization-prepared rapid gradient echo (MPRAGE) sequence (TR = 2300 ms, TE = 2.98 ms, flip angle = 9°, FOV = 240 * 256 mm 2 , voxel size = 1 × 1 × 1 mm 3 ) was recorded as an anatomical reference. 138 functional echo-planar T2*-weighted (EPI) images (TR = 2500 ms, TE = 30 ms, flip angle = 90°, FOV = 192 * 192 mm 2 , Matrix volume = 64 × 64, 38 slices, voxel size = 3 × 3 × 3 mm 3 ) were recorded with a Siemens 3 T Prisma MAGNETOM (Siemens Medical Systems, Erlangen) using a 20-channel head coil. All EPI images were automatically rigid-body transformed to correct for head motion and a distortion correction algorithm was applied [ 56 ]. Preprocessing and statistical analysis of the functional data was performed with the statistical parametric mapping software SPM12 (Wellcome Trust Centre of Imaging Neuroscience, London; for details, see [ 57 ]). The first two volumes of each run were disregarded and an artifact detection algorithm (ArtRepair toolbox, SPM) was applied to detect head motion and possible spiking artifacts. The functional raw images were realigned to the first volume to generate six head motion parameters (rotation and translation in x, y, z direction), which were used as regressors of no interest in the first-level statistical analysis to correct for influences of head motion. The ‘Artrepair’ tool implemented in SPM12 was used to correct movement artifacts over half a voxel size by interpolating the measurement time points before and after the movement. Participants whose head movements were larger than half a voxel size (corresponding to 1.5 mm for a voxel size of 3 × 3 × 3 mm 3 ) were excluded from the analysis if more than two consecutive measurement time points (= "volumes") were affected or more than two corrections had to be made in the time series. In the case of spiking artifacts again the ‘Artrepair’ toolbox was used to correct single slices by interpolating the slice below and above the affected slice. If several slices of a single volume were affected, we interpolated (correspondingly to motion artifacts) the measurement time points before and after the volume affected by spiking artifacts. If two consecutive volumes or more than two volumes in total were affected by spiking artifacts, the subject was excluded. The motion corrected images were spatially normalized into the MNI (Montreal Neurological Institute) reference system applying the anatomical MPRAGE image. To increase the signal-to-noise ratio and to compensate for inter-individual differences in location of corresponding functional areas, the data was spatially smoothed with a three-dimensional isotropic Gaussian kernel (8 mm FWHM). Low frequency artifacts across the time-series were removed applying a high-pass filter (128 s).

Statistical analysis

Demographic, clinical and behavioral data were assessed by analyses of variance with a level of significance of p  < 0.05 (two-sided).

Food and non-food regressors were convolved with a canonical hemodynamic response function and fitted together with the six regressors for head motion parameters in a linear regression model (general linear model (GLM)) with the functional signal time courses for each voxel and participant.

Within-group activation

In the second-level whole brain analysis, we tested for within-group differences (group activation) by performing a one-sample t -test for the food > non-food contrast of the first-level beta estimates of the food and non-food regressors.

Between-group comparison

For group comparisons, the first-level food > non-food contrast was used to compare AN > REC, REC > AN, NP > REC, and REC > NP in a two-sample t-test.

For both, the within- and between-group analysis: (1) We added age as a covariate. (2) We performed whole brain analyses with a cluster-defining threshold, i.e., initial height threshold, of p uncorr.  < 0.001 and a minimum cluster size of 10 voxels (k ≥ 10) (3) Results were corrected for multiple comparisons on a cluster level applying family-wise error correction with a threshold of p corr.  < 0.05.

For the between-group analysis, we additionally performed analyses with a cluster-defining threshold of p uncorr.  < 0.01 and a minimum cluster size of 10 voxels, as previous studies had used lenient thresholds of p uncorr.  < 0.01 [ 24 , 44 ] or even lower ( p uncorr.  < 0.05) [ 22 , 25 ].

Moreover, we performed ROI-based (region of interest) small volume correction (SVC) for insula and amygdala ROIs according to the AAL3 atlas [ 58 ].

Comparisons of the AN and NP group are not reported as they have already previously been published [ 45 ].

Multiple regression analysis

For all groups and for each group separately, SPM multiple regression analyses were performed to calculate the correlation of the first-level BOLD contrast (food and non-food) with the valence and arousal ratings of the food stimuli. We tested for positive and negative linear effects of stimulus ratings and included the factor group as a regressor of non-interest (to adjust for possible group differences). We set up an interaction model with the factors group and stimulus ratings as regressors of interest and age as regressor of non-interest and compared the regression slopes of AN > NP, AN > REC, and NP > REC and vice versa.

We set-up three separate Analysis of Variance (ANOVA) models for valence/arousal/dominance (dependent variable) with the independent factor group followed by post-hoc Tukey Kramer tests to assess for between-group differences.

One hundred and eight female participants (40 AN, 24 REC, 44 NP) were recruited. Thirty-two data sets had to be discarded due to insufficient data quality, spiking head motion or incomplete data (Fig.  2 ). The food paradigm was performed towards the end of the imaging session (after approximately 35 min). This might have resulted in increased head motion (three subjects) and termination of the session by the participants (five). Spiking artifacts were also more likely to occur at the end of a scanning session, possibly due to the scanner heating up, requiring the exclusion of further 22 participants (Fig.  2 ). Seventy-six functional data sets could finally be analyzed: 31 AN, 18 REC and 27 NP.

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Exclusion flow chart. AN anorexia nervosa, NP  non-patients, REC  recovered AN

Post-hoc power calculation

A post-hoc power calculation for the food > non-food contrast with Random Field Theory control was performed separately for the final AN (power 0.81 with cluster-defining threshold p  < 0.001, power 0.59 with cluster-defining threshold p  < 0.01), REC (power 0.32 with cluster-defining threshold p  < 0.001, power 0.24 with cluster-defining threshold p  < 0.01) and NP (power 0.88 with cluster-defining threshold p  < 0.001, power 0.54 with cluster-defining threshold p  < 0.01) samples applying the “Neuro-Powertool” ( http://neuropowertools.org/ ; retrieval date 05th May, 2022).

Demographic and clinical characteristics

Patients with AN had typical features of psychopathology and a lower BMI compared to the REC and NP group. REC participants showed good restitution of all clinical data (Table ​ (Table1). 1 ). The NP group was matched to the AN group and therefore younger than REC (Table ​ (Table1). 1 ). Lowest BMI and duration of illness did not differ between REC and AN. Patients with AN consumed fewer calories than REC and NP, but did not differ in feeling of satiety.

AN (n = 31)REC (n = 18)NP (n = 27)ANOVAPost hoc test Tukey–Kramer*
MeanSDMeanSDMeanSD
Age (years)24.14.327.47.723.63.0F = 3.7;  < 0.03REC > NP
Current BMI (kg/m )16.31.420.81.222.12.2F = 92.1;  < 0.001NP > REC > AN
Lowest-lifetime BMI (kg/m )14.81.414.42.920.91.8F = 40.85;  < 0.001NP > REC,AN
Duration of illness (in months)69.447.565.062.0F = 0.076;  = 0.784
Duration of recovery (in months)52.777.1
EDE—mean3.31.00.70.40.40.3F = 142.9;  < 0.001AN > REC,NP
EDE—sum score 74.426.415.09.09.97.0F = 111.1;  < 0.001AN > REC,NP
EDI—total score61.99.447.75.244.63.1F = 51.85;  < 0.001AN > REC,NP
EDI-2— (t-values)83.620.048.013.344.66.4F = 58.6;  < 0.001AN > REC,NP
EDI-2— (t-values)61.812.950.39.546.68.0F = 15.8;  < 0.001AN > REC,NP
STAI— 38.86.735.75.332.84.8F = 7.9;  = 0.001AN > NP
STAI— 45.67.731.97.929.36.8F = 38.3;  < .001AN > REC,NP
BDI-II22.410.26.56.22.32.7F = 59.2;  < 0.001AN > REC,NP
MWT-B28.45.429.84.928.04.3F = 0.7;  = 0.477
Calorie intake at breakfast160.1180.7300.6124.9386.385.7F = 19.0;  < 0.001NP, REC > AN
Satiety6.41.86.61.76.71.0F = 0.221;  = 0.802

AN anorexia nervosa, BDI-II Beck Depression Inventory II, BMI body mass index, EDE Eating Disorder Examination, EDI-2 Eating Disorder Inventory-2, NP non-patients, MWT-B multiple-choice vocabulary intelligence test (German: Mehrfachwahl-Wortschatz-Intelligenztest), REC recovered AN, SD standard deviation, STAI State-Trait Anxiety Inventory

* p  < 0.05 (cf [ 45 ])

The contrast food > non-food showed increased BOLD activation of frontoinsular cortices in all three groups (Table ​ (Table2, 2 , Fig.  3 a). Within-group analyses showed no significant results in any of the three groups for the contrast non-food > food.

Within-group differences for the contrast food > non-food (cluster-defining threshold of p uncorr.  < 0.001, k ≥ 10 voxels)

HemisphereVoxels MNIT-score
Middle occipital gyrusL1086 < 0.0010.001− 21− 9787.05
Occipital gyrusR0.01333− 73− 76.06
Lingual gyrusR0.01515− 88− 45.98
R0.02721− 88− 45.73
Inferior occipital gyrusL0.042− 30− 76− 45.53
InsulaR5474 < 0.0010.0040− 31356.63
Inferior occipital gyrusL0.008− 1220656.27
Superior frontal gyrusL0.034− 1850355.56
R0.0291538505.70
R0.030− 914265.68
Posterior medial frontal cortexL0.028− 653385.71
L0.034− 65685.62
R0.044917685.50
Superior frontal gyrus, medial partL0.032059235.65
Middle frontal gyrus, orbital partL0.039− 956− 75.50
Medial cingulate cortexL0.045− 9− 7325.49
PrecuneusL0.046− 6− 52205.44
Supramarginal gyrusR320 < 0.0010.02260− 16295.82
PrecuneusL375 < 0.0010.022− 33− 1145.82
Postcentral gyrusR780.1020.028 − 60− 16265.70
InsulaL1370.0020.001− 36− 4119.92
L0.007− 395− 138.38
R520.0960.016 39− 127.86
Superior orbital gyrusL299 < 0.0010.008− 2135− 138.32
Superior frontal gyrusL1090.0070.326 39− 125.67
Thalamus1040.0080.387 0− 725.52
Calcarine gyrusR1140.0140.00518− 9456.91
Superior frontal gyrusL674 < 0.0010.006− 1547446.84
Superior occipital gyrusL244 < 0.0010.012− 18− 9126.51
Superior parietal lobuleL1960.0010.012− 24− 76476.50
InsulaL1970.0010.013− 36− 7116.47
Supramarginal gyrusR660.0800.016 − 60− 16326.36

FWE-corr. family wise error corrected, MNI standardised brain according to Montreal Neurological Institute

† only significant at a cluster level, FWE-corrected

‡ only significant at a peak/voxel level, FWE-corrected

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A T-maps of within-group differences for the contrast food > non-food for AN, REC and NP, p uncorr.  < 0.001, k ≥ 10 voxels. Color bars represent the t-scores (white/yellow = high, red = low). B Behavioral data. Mean valence (0 = negative to 8 = positive valence), arousal (0 = unaroused to 8 = very aroused) and dominance (0 = not dominant to 8 = very dominant) ratings for the three groups (AN, REC, NP) and the two conditions (food and non-food). * p  < 0.01, ** p  < 0.001. AN anorexia nervosa; NP non-patients, REC  recovered AN (cf. [ 45 ])

Applying the initial threshold of p uncorr.  < 0.001, the two-sample t-test revealed no significant BOLD differences between groups for any of the comparisons (AN > REC, REC > AN, NP > REC, REC > NP).

At a lenient cluster-forming initial threshold of p uncorr.  < 0.01, there were no differences between REC and NP neither. AN showed a higher BOLD response of an occipital area compared to REC (Additional file 2 ). Comparisons of AN and NP have been reported previously [ 45 ], where AN showed higher BOLD responses compared to NP in midcingulate, pre/postcentral and parietal areas when using a lenient initial threshold, and no significant group differences with recommended more stringent initial cluster-forming thresholds [ 45 , 59 ]. Neither the SVC analysis for the insula nor for the amygdala ROIs survived family-wise error correction.

None of the regression models yielded results that exceeded the significance threshold. Additional file 3  depicts the results of the performed multiple regression models for the affective ratings (arousal/valence).

The AN group had lower valence and higher arousal ratings compared to both REC and NP, while REC did not differ from NP (Table ​ (Table3; 3 ; Fig.  3 b). There were no group differences in the ratings of non-food stimuli.

ANRECNPANOVA F(df); ppost-hoc Tukey test *
MeanSDMeanSDMeanSD
Valence3.701.855.201.366.281.4317.98 (2); < 0.001NP,REC > AN
Arousal4.692.162.941.683.191.616.518(2); < 0.01AN > NP,REC
Dominance5.232.165.751.115.285.340.643 (2); 0.529
Valence4.911.595.230.825.041.460.289 (2); 0.75
Arousal3.071.712.241.452.921.501.638 (2); 0.202
Dominance5.701.495.620.735.341.13

0 = negative valence to 8 = positive valence, 0 = unaroused to 8 = very aroused, 0 = not dominant to 8 = very dominant. AN  anorexia nervosa, NP non-patients, REC  recovered AN

* p  < 0.05 (cf. [ 45 ])

This cross-sectional fMRI study on functional neural correlates towards disease-related stimuli (food vs. non-food images) revealed no group differences between REC and NP with neither a conservative initial height threshold [ 45 ] nor a lenient one. REC and NP also showed no difference in affective ratings, i.e. with respect to the subjective experience of the stimuli. Furthermore, there was no significant correlation of the valence and arousal ratings with the BOLD response towards food stimuli in the insular cortex.

The lack of group differences between REC and NP in functional neural correlates to visual food cues is in line with results of previous studies, which also detected no differences between REC and NP [ 21 – 23 ]. However, some studies reported differences between groups [ 24 – 26 ], which was only the case in region-of-interest analyses, but not whole-brain in the Holsen et al. sample [ 25 ]. These inconsistencies are likely due to a variety of reasons, some of which are associated with limited reliability and replicability [ 45 ]. Further, it is likely that studies yielded false-positive results due to small sample sizes as well as different statistical methods (e.g., region of interest vs. whole brain analyses, statistical thresholds, etc.) [ 60 , 61 ]. Comparability of studies is hampered due to heterogeneity across participants (BMI, duration of illness and recovery, etc.), within participants (daytime, hormonal level, etc.), and across study sites (study design, scanner hardware, etc.) [ 45 , 62 ]. This, once again, supports the need of replication studies [ 63 ], especially in the field of fMRI [ 64 , 65 ]. With respect to the early study of Uher et al. [ 24 ], which reported group differences of functional neural correlates and which used visual stimuli similar to ours, these factors likely account for the differing results.

Naturally, recovery criteria are another important topic with respect to state and trait. Recovery in AN in principle requires the absence of eating disorder psychopathology and a minimal BMI for a certain period of time [ 66 – 69 ], although the exact quantitative values vary.

For further detailed discussion of this topic with respect to recovery, remission and relapse see for example Khalsa et al. [ 69 ]. We used conservative measures in the current study, i.e. absence of eating disorder pathology for at least 12 months, an EDE score within one standard deviation of normal. Most REC were in the BMI ≥ 20 kg/m 2 range with a few exceptions. In consequence, our sample of REC represents clinically stable long-term recovered individuals, which seems important in order to avoid cerebral aberrations and dysfunction—which might still be present after short term—due to insufficient clinical recovery.

However, most previous studies used such recovery criteria (see Additional file 1 ), and we could not detect any pattern with respect to the rather divergent study results.

We aimed to put behavioral and cerebral response to visual food cues in the context of state and trait. In contrast to AN, REC participants did not differ psychometrically or in their valence and arousal ratings to food stimuli from NP, indicating unimpaired cognitive and emotional processing of food stimuli. This is accompanied by a cerebral neural activation pattern which is similar to NP, i.e. which is not different between groups, even when applying a very lenient initial height threshold statistically. These data are comparable to two recent studies using a food paradigm [ 21 , 23 ].

In contrast to previous studies [ 22 , 25 ], correlation and interaction analysis showed no significant results. However, although our study has a larger sample size than the previous ones [ 22 , 25 ], it is possible that the effects are still too small to be detected with the group size of this study [ 70 ].

Comparing REC and AN, experiential data differed. The BOLD responses showed no regions of higher activation of REC as suggested by Uher et al. [ 24 ]. Applying a lenient initial height threshold, we however also found increased activation in occipital areas in AN when compared to REC, but this was located on the left side, while in the other study it was right-sided [ 24 ]. With respect to the meaning of possible occipital differences, these do not represent brain areas associated with emotional and motivational processing, but visual processing and might be unspecific [ 43 ]. Finally, we point to a recent report on neurobiological markers of 55 REC, which did not find differences between NP and REC, which can be regarded as a complementary finding to our results [ 71 ].

Not only neuronal and glial damage appear to be state phenomena [ 4 , 71 ] but, according to our results, neural processing and affective rating of food stimuli also seem to be state-related. Certain neuropsychological characteristics seem to persist in some patients with AN after clinical recovery, such as difficulties in set-shifting abilities and weaker central coherence [ 72 ]. Consequently, functional cerebral aberrations are likely no candidates for endophenotypes in AN.

The study has limitations. REC were slightly older than the other groups, which is due to the course of the illness. When including age as a covariate, the results remained significant. Larger cohorts and in particular longitudinal intra-individual designs will complement our knowledge — ideally through repeated measurements. However, AN is a disease with low prevalence and high chronicity, and therefore it is difficult to recruit large enough samples — in particular in single-center studies. A further limitation of the current study represents that AN consumed less calories before the imaging protocol — which, however, is also difficult to compensate/equalize methodically. Due to the differences in calorie intake between AN and REC/NP, food processing might be due to a temporary situation of hunger during measurement and not representing a stable finding in acute AN. Although our findings suggest a restitution of brain function with regard to food stimuli, the paradigm might not be sensitive enough to detect weaker effects. Furthermore, it cannot be ruled out that there may be other areas where abnormalities persist, such as in the perception of one's own body.

In summary, similar to the restitution of structural cerebral abnormalities [ 5 , 20 ] and serum neuronal biomarkers [ 71 ], functional brain aberrations also seem to be a state phenomenon , at least in terms of processing of food stimuli. However, this should be proven experimentally by longitudinal studies in AN and larger cohorts, which is not easily feasible methodically. Replicability is affected by several methodological issues, which we discussed in more detail elsewhere [ 45 ]. From a clinical perspective, the restitution of structural and functional cerebral alterations is an interesting issue concerning the transition of neuroscientific knowledge into clinical practice [ 73 ].

Abbreviations

ANAnorexia nervosa
BDIBeck depression inventory
BOLDBlood oxygenation level dependent
BMIBody mass index
EDEEating disorder examination
EDIEating disorder inventory
fMRIFunctional magnetic resonance imaging
FOVField of view
MPRAGEMagnetization-prepared rapid gradient echo
MNIMontreal Neurological Institute
MWTMultiple choice vocabulary test
NPNon-patients
RECRecovered
SCIDStructured clinical interview for DSM
SPMStatistical parametric mapping
STAIState trait anxiety inventory
TEEcho time
TRRepetition time

Author contributions

All authors contributed to and reviewed the study and manuscript and gave consent to its publication. All authors approved the final manuscript.

Open Access funding enabled and organized by Projekt DEAL. German Research Foundation, JO 744/2-1 (Principal Investigator: A. Joos).

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Anorexia Essay: How to Write a Good Paper on This Critical Issue

Today, the range of topics you can highlight in a written assignment is limitless. The world is fickle, and the number of things you can describe and discuss in your school essay is always growing. Students write about artificial intelligence, the problems of social networks, and video game addiction, issues that are becoming more pressing with each day.

One of the most significant areas students discuss in their papers is health. In our article , we are going to focus on the anorexia essay and study the four approaches you can use for writing. We want to emphasize the importance of discussing and highlighting this issue, which has been slowly and steadily spreading throughout the modern world. Therefore, we hope that our guide to the essay about anorexia will help you cope with this specific paper and make you think about some undereating issues that might not seem like a big deal at first.

Purpose of the Anorexia Nervosa Essay

The first question you are likely to face while preparing a paper on this disputable topic is what to write about in your essay . Every second student has heard of anorexia and knows what it is. However, you are to write a thoughtful essay, not a column in a glossary. That means a mere definition of anorexia is not enough to get a high or any grade.

If you don't know what you should write about in your paper , then the first thing you are to do is define the central purpose of your task. That usually depends on the essay type, the principles of which will determine the way you develop the writing. Based on those, you might have to convince your reader of a standpoint, argue a specific idea about anorexia, explain the consequences of this disorder, or present possible solutions to this issue. Of course, your essay will revolve around the anorexia nervosa, but your objective will vary depending on the angle you choose.

Argumentative Essay on Anorexia

Here, you should decide on your viewpoint and back it by substantial evidence. When speaking about the argumentative essay on anorexia, there are a lot of concepts related to this disorder you could easily use for your writing. For example, you could question the very definition of anorexia. Is it dangerous to weigh less than forty kilograms? Tell why it is essential to pay attention to this issue, agree or express disagreement with some opinions on this matter. Remember that a good argumentative essay on anorexia is impossible without a solid foundation of evidence.

Persuasive Essay on Anorexia

How to persuade the reader if your essay is on anorexia? Think about all the "why" and "how" questions. Formulate your opinion about this problem and think of how to prove the validity of your viewpoints to the audience . What to include in your persuasive essay? Think about the following ideas:

  • Why is anorexia an ideal in the model business?
  • How important is it to control your diet?
  • Anorexia as a dream (or nightmare) of any girl.

Dig deeper, and you will be surprised with how many non-trivial ideas you can find.

Problem-Solution Essay on Anorexia

Anorexia holds many problems behind its name. These may be not just health problems but also bullying, low self-esteem, or mental disorders. Your task while preparing a problem solution essay on anorexia is to choose which of the issues you would like to discuss and to find possible ways to solve it. You can mention the already-known methods (work on mental problems, proper nutrition, visiting the therapist, etc.) and explain your attitude towards them. Besides, you are free to express any non-trivial ideas and assumptions if you can support them with pertinent facts or examples.

Cause and Effect Essay on Anorexia

The health of young people as a new generation is probably the most discussed topic in different areas such as psychology or medicine. Anorexia can be the root of many problems and raise some critical questions:

  • What can difficulties with nutrition entail?
  • What dire consequences await for adolescents who flip through fashion magazines with admiration?
  • What problems hide behind strict diets?

You can answer all those questions in your cause and effect essay about anorexia. Any carelessness or indifference can cause a challenging struggle with this condition.

Your Anorexia Essay Structure

To express ideas or assumptions logically and understandably, you must follow some standard structure rules. All the parts of your writing should be interlinked with each other and keep to one central idea. But, that doesn't mean every sentence of your paper should contain the same information. Therefore, you should be aware of what is appropriate for mentioning in each part of your paper.

Introduction

This part must contain the thesis statement, which you will address throughout the paper. Usually, in an anorexia essay introduction, you raise a particular issue that you want to explore and emphasize or state a specific opinion. Often, a central idea here is placed in one of the last sentences of this part because then goes an essay body, the content of which directly depends on the purpose of your writing. One of the introduction's last sentences may sound like:

  • But what if anorexia isn't as harmful as we think?
  • What can you face if your nutrition continues to be unregular?
  • There is no doubt that TV shows promoting anorexia should be prohibited.

The Body Paragraphs

Let's see what to write in the central part of your paper on anorexia? As we mentioned above, it depends on the purpose of your writing. Nevertheless, your essay should be well-grounded, and all your ideas, as well as statements about anorexia nervosa that you want to argue, should be reasonable and relevant. To find the sources you can research and use in your body paragraphs, you can:

  • Look through the previous successful research on this theme.
  • Explore medicine- or psychology-oriented online sources and libraries.
  • Visit the nearest hospital and try to talk to doctors (if you're brave enough).
  • Check the Internet for some books, tv-shows, or documentaries about this terrible eating disorder.

Ready to make a thought-provoking conclusion? Think about whether there are any open questions or what-ifs left. There is a chance your anorexia essay conclusion will be met with doubts and arguments because this issue is highly debatable - many men, many minds. Your task is to predict such an outcome and make your final part as refined and doubt-proof as possible. Otherwise, don't worry because you have already made your essay so impressive that it will make your readers ponder. But be careful because your conclusion shouldn't anything new (information, ideas, etc.).

Anorexia Essay Topics You Can Use

To focus your attention on the most relevant anorexia-related issues, we want to offer you some ideas to inspire you or give a good foundation for your topic. Here is a list of anorexia essay topics that will grab anyone's attention:

  • High price for low weight: What does the anorexia hold?
  • Glamorous anorexia. Does being a model mean giving up on your health?
  • America's Next Top Anorexic and the popularity of plus-size models.
  • Why "40 kilos" isn't an "anorexia" tag anymore.
  • "I'm not hungry" or why it's essential to spot an eating disorder.
  • Why do teenage girls dream about losing weight?
  • Skinny girls on TV as an unreachable aspiration.
  • Why there's no such thing as "perfect" body.
  • Anorexia as a result of mental health issues.
  • Mockery of anorexic people and its consequences.

Anorexia Essay Outline Example

Here is our outline example with key ideas to develop in each paragraph. Study it and see how to add logic and coherence to your essay .

  • Introduction Anorexia among teenagers is a result of mental illness.
  • Backing evidence 1 Bullying at school makes teenagers think about themselves as not attractive or defective. Such thoughts can lead to mental trauma resulting in the loss of appetite and weight.
  • Backing evidence 2 According to previous psychological and medical studies, the majority of anorexic people seek help from therapists first because they see anorexia as not a physical but mental disorder.
  • Backing evidence 3 Advertising and various TV-shows promote unhealthy skinny bodies as perfection and influence teenagers psychologically, making them change their bodies "for the better."
  • Conclusion To predict and avoid any signs of anorexia, we should pay attention not only to our weight but our mental state as well. Don't let anyone think about your body as "not skinny enough."

We hope this essay outline example will be useful to you. Such an assignment is your chance to show your competence, analytical thinking skills, and extensive background knowledge.

Where to look for inspiration

As a conclusion, we would like to offer you an inspirational tip, especially if you are going to write about anorexia in teenage females.

Nowadays teenagers enjoy watching various TV-series and movies that try bring to light the issue of anorexia nervosa. Look through some of them (or recall if you have watched some) and share your impression with your readers and professors:

  • Red Band Society, 2014 (Emma Chota)
  • Skins, 2007 (Cassie Ainsworth)
  • To the Bone, 2017 (Ellen)
  • Girl, Interrupted, 1999 (Daisy Randone)
  • Binge, 2017 (Nancy)

As you can see, this eating disorder has been a pressing issue for many years. Express your standpoint about the problem and write a perfect essay by using our tips!

Subscribe to get free samples

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Peripheral biomarkers of anorexia nervosa: a meta-analysis.

thesis statement anorexia nervosa

1. Introduction

2. materials and methods, 2.1. study selection and search strategy, 2.2. data extraction, 2.3. quality appraisal, 2.4. calculating effect sizes, 2.5. meta-analysis, 3.1. search outcome, 3.2. characteristics of included studies, 3.3. quality of studies, 3.4. meta-analysis results, 3.5. publication bias, 4. discussion, 4.1. key findings, 4.2. limitations, 5. conclusions, supplementary materials, author contributions, data availability statement, conflicts of interest.

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Click here to enlarge figure

Peripheral Biomarkerskg SE (g )CI LCI UpTau I z (PEESE)z p
(PEESE)
X (TPSM)X  p
(TPSM)
g+ adjp adjCI L adjCI U adj
25-Oh-Vitamin D5−0.360.42−1.180.450.380.7990.89−0.7080.4790.1630.687−0.5130.262−1.4090.384
Acylated Ghrelin60.810.170.481.140000.3980.6910.1350.7130.7350.0060.2121.258
Adiponectin110.290.33−0.360.930.381.0590.2−2.7740.0068.2880.004−0.7700.123−1.7490.209
Adrenocorticotropic Hormone50.460.20.060.860.020.0627.89−0.5980.5500.1840.6680.3850.056−0.0090.779
Albumin 1000.1−0.180.190.98000.4900.6240.5280.467−0.0360.732−0.2450.172
Bone Alkaline Phosphatase30.60.69−0.741.950.381.2891.71.2010.2300.8930.345−0.1130.906−1.9741.749
Brain-Derived Neurotrophic Factor 4−0.220.2−0.610.180.280.0957.55−1.9140.056NANANANANANA
Calcium 5−0.420.44−1.280.440.340.8690.09−4.1580.0005.0450.025−1.0160.082−2.1610.130
Carboxy-Terminal Collagen Crosslinks40.460.170.130.780.010.0329.170.1890.8500.0030.955−0.5860.004−0.990−0.183
CD3 Positive4−0.510.21−0.91−0.10.01000.4560.6490.0210.884−0.5040.016−0.913−0.095
CD4 Cell Counts 4−0.340.22−0.770.080.1200−0.1000.9210.0650.798−0.3330.136−0.7710.105
CD8 Cell Counts 4−0.460.22−0.89−0.030.04000.0130.9890.0320.858−0.4540.041−0.891−0.018
Cholecystokinin30.360.4−0.421.130.370.3166−2.2460.0257.1060.008−0.9830.002−1.620−0.347
Cholesterol100.470.140.20.7400.0842.88−0.3630.716NANANANANANA
Cortisol251.110.190.731.4900.7685.292.3350.0202.8350.092−0.1290.301−0.3720.115
C-Peptide 4−0.210.59−1.370.950.721.2390.633.5240.0000.0000.9830.4530.331−0.4611.367
C-Reactive Protein3−0.590.21−0.99−0.180001.0110.3120.7800.377−0.5860.004−0.990−0.183
Creatinine4−2.280.83−3.9−0.650.012.4591.4−2.6140.0090.1560.693−2.1740.008−3.781−0.566
Des-Acyl Ghrelin41.240.230.781.700.015.28−1.6440.1000.6030.4371.3950.0000.8251.966
Estradiol18−1.350.14−1.62−1.0800.2266.45−3.6560.0000.0130.908−1.3460.000−1.614−1.077
Fatty Acids50.270.46−0.631.180.560.984.270.7240.4690.3410.559−0.0260.964−1.1831.130
Follicle-Stimulating Hormone7−0.620.23−1.08−0.170.010.2875.61−0.7070.4800.4300.512−0.5640.040−1.101−0.027
Free Thyroxine 12−1.210.2−1.6−0.8200.3579.38−3.5740.0000.0920.762−1.1940.000−1.581−0.808
Free Triiodithyronine 13−1.70.37−2.43−0.9701.6494.07−3.2590.0011.3660.242−1.4700.007−2.536−0.405
Ghrelin131.070.230.621.5200.5483.774.9580.0003.2900.0700.5150.312−0.4831.514
Glucose24−1.120.13−1.38−0.8600.2665.22−4.1710.0000.1380.711−1.1120.000−1.379−0.846
Glycerol 50.330.53−0.711.360.541.1182.493.3030.0010.9190.3381.3560.388−1.7214.433
Growth Hormone120.620.160.310.9300.1658.981.0520.2930.6750.4110.4640.056−0.0120.941
Hdl Cholesterol70.560.39−0.221.330.160.9992.69−1.1840.2360.7410.3890.9650.099−0.1822.113
Insulin25−0.760.16−1.08−0.4500.4979.39−3.6030.0000.0020.965−0.7640.000−1.110−0.418
Insulin-Like Growth Factor 122−1.280.19−1.66−0.9100.6685.49−3.1310.0021.4250.233−1.3580.000−1.703−1.014
Insulin-Like Growth Factor-Binding Protein−3 4−0.750.42−1.570.060.070.573.33−2.9590.0030.1960.658−0.6800.099−1.4880.128
Ldl Cholesterol70.370.25−0.120.850.140.3482.47−3.6280.0003.1300.077−1.6700.000−1.906−1.433
Leptin40−1.620.13−1.89−1.3600.5782.01−1.0150.3107.4670.006−1.5040.032−0.129−2.880
Luteinizing Hormone6−1.230.46−2.12−0.330.011.1391.91−2.4540.0140.6850.408−1.0120.139−2.3530.329
Lymphocyte (%)4−0.550.16−0.87−0.23003.23−1.5880.1120.0080.930−0.5470.001−0.863−0.232
Melatonin (N-Acetyl−5 Methoxytryptamine)30.360.62−0.861.570.561.0288.45−4.4090.0000.1450.7030.6300.475−1.0982.359
Na5−0.740.45−1.630.150.10.8383.58−0.3060.7590.9030.342−0.3970.673−2.2421.448
Norepinephrine4−0.10.56−1.210.861.0684.090.6690.5043.6910.0552.1320.468−3.6287.892
Obestatin51.510.330.862.1600.3666.251.6310.103NANANANANANA
Osteocalcin5−0.690.41−1.50.110.090.7591.05−0.4290.6681.4170.234−0.1230.928−2.7752.529
Parathyroid Hormone3−0.230.26−0.750.290.390.1467.12−0.7330.464NANANANANANA
Peptide Tyrosine Tyrosine70.670.58−0.461.80.252.1995.530.0650.9484.6550.0312.2260.0220.3194.132
Potassium 5−0.50.29−1.070.070.080.2867.09−0.0880.9300.3510.554−0.4300.228−1.1300.270
Prolactin10−0.90.3−1.49−0.300.7586.17−0.8150.4151.3670.242−0.6640.201−1.6830.354
Resistin 4−0.20.21−0.610.210.340.0632.722.1860.0290.0920.762−0.2080.431−0.7240.309
Sex Hormone-Binding Globulin30.920.56−0.162.010.10.8188.741.3770.1680.0030.9540.9260.161−0.3682.220
Soluble Leptin Receptor 40.730.170.41.060000.1020.919NANANANANANA
Testosterone80.030.42−0.780.850.941.2593.262.4210.0154.6460.0311.9180.224−1.1715.006
Thyroid-Stimulating Hormone12−0.010.12−0.240.220.920.0744.910.0150.9880.1400.708−0.0350.700−0.2140.144
Total Protein6−0.550.37−1.280.170.140.6782.46−1.3750.1691.4710.225−0.8030.006−1.375−0.231
Triglycerides90.120.29−0.460.690.690.6686.692.1430.0320.1620.687−0.0330.938−0.8630.797
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Wu, Y.-K.; Watson, H.J.; Del Re, A.C.; Finch, J.E.; Hardin, S.L.; Dumain, A.S.; Brownley, K.A.; Baker, J.H. Peripheral Biomarkers of Anorexia Nervosa: A Meta-Analysis. Nutrients 2024 , 16 , 2095. https://doi.org/10.3390/nu16132095

Wu Y-K, Watson HJ, Del Re AC, Finch JE, Hardin SL, Dumain AS, Brownley KA, Baker JH. Peripheral Biomarkers of Anorexia Nervosa: A Meta-Analysis. Nutrients . 2024; 16(13):2095. https://doi.org/10.3390/nu16132095

Wu, Ya-Ke, Hunna J. Watson, Aaron C. Del Re, Jody E. Finch, Sabrina L. Hardin, Alexis S. Dumain, Kimberly A. Brownley, and Jessica H. Baker. 2024. "Peripheral Biomarkers of Anorexia Nervosa: A Meta-Analysis" Nutrients 16, no. 13: 2095. https://doi.org/10.3390/nu16132095

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  • Introduction
  • Conclusions
  • Article Information

Participants diagnosed with binge eating disorder were referred to another study. BMI indicates body mass index (calculated as weight in kilograms divided by height in meters squared); ED, eating disorder.

Data points represent means, including error bars for their SEs. Bulimic episodes were measured over the past 28 days.

Trial Protocol

eFigure 1. Interface and Course of the Web-Based Intervention Selfapy for Bulimia Nervosa

eTable 1. Results for Primary and Secondary Outcomes Applying Last Observation Carried Forward

eTable 2. Baseline Differences in Demographic Characteristics Between Control and Intervention Group

eTable 3. Baseline Differences in Clinical Outcomes Between Control and Intervention Group

eFigure 2. Trajectories of the Number of Binge-eating Episodes During the Study Period

eFigure 3. Trajectories of the Number of Compensatory Behaviors During the Study Period

eFigure 4. Weekly Trajectories in Bulimic Episodes During the Study Period

eTable 4. Changes in Daily Eating Disorder Symptoms from Baseline to Posttreatment

eFigure 5. Trajectories of Daily Eating Disorder Symptoms from Baseline to Posttreatment

eTable 5. Results from Moderator Analyses on the Treatment Effect

eFigure 6. Johnson-Neyman Plot for the Moderator Analysis of Illness Duration

eTable 6. Previous Treatments and Treatment Uptake During the Study Period

eTable 7. Adverse Effects Attributed to the Web-Based Intervention

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Hartmann S , Timm C , Barnow S , Rubel JA , Lalk C , Pruessner L. Web-Based Cognitive Behavioral Treatment for Bulimia Nervosa : A Randomized Clinical Trial . JAMA Netw Open. 2024;7(7):e2419019. doi:10.1001/jamanetworkopen.2024.19019

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Web-Based Cognitive Behavioral Treatment for Bulimia Nervosa : A Randomized Clinical Trial

  • 1 Department of Psychology, Heidelberg University, Germany
  • 2 Department of Psychology, University of Osnabrück, Germany

Question   Can a web-based cognitive behavioral self-help intervention reduce eating disorder symptoms and address disease-related features in bulimia nervosa?

Findings   In this randomized clinical trial of 154 adults with bulimia nervosa, receiving a web-based intervention led to a significantly higher reduction in binge-eating episodes, global eating disorder symptoms, and clinical impairment compared with a waiting-list control group. There were no effects on compensatory behaviors.

Meaning   These findings underscore the effectiveness of web-based cognitive behavioral treatments for bulimia nervosa and suggest that these interventions can complement face-to-face therapies.

Importance   Despite the existence of effective treatments, many individuals with bulimia nervosa (BN) do not receive evidence-based therapies. Integrating digital interventions into routine care might reach more patients and reduce the clinical burden of BN.

Objective   To evaluate the effectiveness of a web-based cognitive behavioral self-help intervention for individuals with BN.

Design, Setting, and Participants   A 2-group randomized clinical trial without follow-up was conducted between February 2, 2021, and July 9, 2022, in Germany. Participants aged between 18 and 65 years who met the diagnostic criteria for BN were enrolled online via self-referral. Data analyses were conducted from October 24, 2022, to December 23, 2023.

Interventions   A web-based cognitive behavioral self-help intervention including 12 weekly modules was compared with a waiting-list control group only having access to routine care.

Main Outcomes and Measures   The primary outcome was the change in the number of bulimic episodes between baseline and posttreatment. Secondary outcomes included changes in global eating disorder symptoms, clinical impairment, well-being, work capacity, comorbid symptoms, self-esteem, and emotion regulation complemented by weekly measures and ecological momentary assessment. Intention-to-treat analyses were performed.

Results   Participants (N = 154; mean [SD] age, 29.6 [8.6] years; 149 [96.8%] female) receiving the web-based intervention demonstrated a significantly greater decrease in bulimic episodes compared with the control group (Cohen d  = −0.48; 95% CI, −0.75 to −0.20; P  < .001), representing a significant change in binge-eating episodes (Cohen d =  −0.61; 95% CI, −0.89 to −0.33; P  < .001), but not in compensatory behaviors (Cohen d  = −0.25; 95% CI, −0.51 to 0.02; P  = .21). The intervention was superior in improving global eating disorder symptoms (Cohen d =  −0.61; 95% CI, −0.89 to −0.32; P  < .001) and clinical impairment (Cohen d =  −0.62; 95% CI, −0.92 to −0.33; P  < .001). No significant effects were found for well-being (Cohen d =  −0.08; 95% CI, −0.37 to 0.22; P  > .99) and work capacity (Cohen d =  −0.01; 95% CI, −0.68 to 0.66; P  = .99). Exploratory analyses indicated significant changes in self-esteem and emotion regulation difficulties, but not in comorbid symptoms.

Conclusions and Relevance   In this randomized clinical trial, a web-based cognitive behavioral self-help intervention effectively decreased eating disorder symptoms and illness-related burden in individuals with BN, underlining the potential of digital interventions to complement established treatments.

Trial Registration   ClinicalTrials.gov Identifier: NCT04876196

Approximately 1% to 2% of the global population is affected by bulimia nervosa (BN) during their lifetime and experiences recurrent binge-eating episodes and inappropriate compensatory behaviors accompanied by an excessive influence of shape or weight on self-evaluations. 1 - 3 These symptoms are associated with functional impairment, reduced well-being, increased mortality, and immense societal costs. 4 - 7 Therefore, developing and implementing effective treatments is essential to reduce the increasing global burden of BN. 5 , 8

Cognitive behavioral therapy (CBT) targets key etiologic factors of BN, such as biased cognitive schemes, limited emotion regulation abilities, low self-esteem, and interpersonal problems, and has been established as an evidence-based treatment. 9 - 11 Notwithstanding, most patients with BN do not receive adequate care. 7 , 8 , 12 A vicious circle of illness-related characteristics and health care–related barriers leads to low treatment rates even compared with other mental disorders. 13 - 15 Consequently, individuals with BN often spend years without receiving evidence-based care, increasing their distress. 12 - 15

Possibly reducing the barriers of face-to-face treatments by being more flexible, accessible, and cost-efficient, web-based interventions have been developed to complement established therapies and are increasingly integrated into routine care settings. 16 - 26 While meta-analyses suggest that web-based interventions may reduce eating disorder symptoms, there is a scarcity of research investigating treatments tailored to BN, and previous studies are often limited regarding their generalizability to clinical practice. 17 - 20 , 24 , 25 , 27 Therefore, more research is needed to evaluate the effectiveness of web-based interventions targeting patients diagnosed with BN, especially when applied in naturalistic settings.

Addressing this research gap, this randomized clinical trial aimed to evaluate the effectiveness of a 12-week, web-based cognitive behavioral self-help intervention for patients with BN in reducing the number of binge-eating episodes and compensatory behaviors. To generalize our results to key eating disorder–related mechanisms and account for the high clinical burden of BN, our secondary aim was to explore changes in global eating disorder symptoms, clinical impairment, well-being, work capacity, comorbidities, emotion regulation, and self-esteem. Moreover, including weekly and everyday measurements may increase the temporal resolution and ecological validity of our results. 28 - 30

This randomized clinical trial comparing a web-based cognitive behavioral self-help intervention and a waiting-list control group received ethical approval by the institutional review board at Heidelberg University. The study design has been published, 31 and the trial protocol is available in Supplement 1 . The study included a baseline (study entrance), a midtreatment (6 weeks after baseline), and a posttreatment (12 weeks after baseline) assessment. No follow-up assessment was conducted. Study data were collected from February 2, 2021, to July 9, 2022. All participants provided written informed consent online and received monetary compensation (10€ [$10.89]) for each assessment. International data privacy regulations and European Union legislation were considered to ensure participant confidentiality and safety. This report followed the Consolidated Standards of Reporting Trials ( CONSORT ) reporting guideline.

The study was coordinated at Heidelberg University, with recruitment, data assessment, and treatment conducted entirely online. German-speaking individuals with eating disorder symptoms were recruited through self-referral by distributing advertisement material online and in inpatient and outpatient treatment centers, resembling enrollment to online therapy in the German health care system. 32 After the initial screening, trained clinical interviewers administered video-based interviews, including the Eating Disorders Examination Interview 33 and the Diagnostic Interview for Psychological Disorders. 34 Each decision on study eligibility was discussed within the research team, supervised by 2 licensed clinical psychologists (C.T. and L.P.). Interrater reliability based on 19 interviews was almost perfect (κ = 0.90). Noneligible individuals were encouraged to seek professional help, and those diagnosed with binge eating disorder were directed to a parallel study. 35

Eligible participants needed to (1) meet the diagnostic criteria for BN according to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition , 1 (2) be aged between 18 and 65 years, (3) have adequate language skills (German C1), and (4) have a smartphone with internet access. Exclusion criteria were (1) a body mass index below 18.5 (calculated as weight in kilograms divided by height in meters squared), (2) current psychotherapy or pharmacotherapy for eating disorders, (3) lifetime bipolar or psychotic disorder, (4) acute substance dependence, (5) current severe depressive episodes, and (6) acute suicidality. Inclusion and exclusion criteria were selected to represent clinical practice while ensuring participants’ safety.

After completing the baseline assessment, participants were randomized to the intervention or control group by an independent and blinded researcher in a 1:1 ratio using a computer-based algorithm. 36 The interviewers were thus blinded to treatment allocation (allocation sequence concealment). 37 Immediately after randomization, participants either received access to the intervention or were informed of the waiting period of 12 weeks via email. All data assessments were initiated automatically to ensure unbiased data collection. 36

Patients in the intervention group received access to a web-based 12-week CBT self-help intervention specialized for treating BN (Selfapy). 38 - 42 The program introduces a diathesis-stress model and then targets key eating disorder mechanisms, allowing participants to work individually on their symptoms. During the treatment, interactive evidence-based CBT techniques complemented by stress management and mindfulness-based exercises are introduced in 6 mandatory and 6 additional weekly modules. After receiving 3 reminders to register for the program, only minimal guidance was provided, including technical support and security monitoring. For a detailed description of the intervention, refer to the trial protocol in Supplement 1 and eFigure 1 in Supplement 2 . Additional treatment uptake during the study period was allowed and assessed mid- and posttreatment.

Participants in the control group did not receive any treatment as part of the study but were allowed to seek professional help, including pharmacologic and psychological therapies. All health care service uptakes were captured at each assessment. After the study period, individuals in the control group received the web-based intervention.

The primary outcome was the change in bulimic episodes during the study period, determined by the total number of binge-eating episodes and compensatory behaviors within the preceding 28 days of each assessment, using the Eating Disorder Examination Questionnaire. 43 Additional symptom measures were global eating disorder symptoms (Eating Disorders Examination Questionnaire) 43 and weekly bulimic episodes (Weekly Binges Questionnaire). 29 Furthermore, eating disorder–related daily difficulties (Clinical Impairment Assessment Questionnaire), 44 well-being (World Health Organization Well-Being Index), 45 and work capacity (iMTA [institute for Medical Technology Assessment] Productivity Cost Questionnaire) 46 were assessed as secondary outcomes.

Possible changes in depressive (Patient Health Questionnaire-9) 47 and anxiety (General Anxiety Disorder Scale-7) symptoms, 48 self-esteem (Rosenberg Self-Esteem Scale), 49 and emotion regulation (Difficulties in Emotion Regulation Scale 50 ; Heidelberg Form for Emotion Regulation Strategies 51 ) were included as exploratory outcomes.

These questionnaires were complemented by a smartphone-based 5-day ecological momentary assessment protocol at baseline and posttreatment. In these recurrent assessments, daily eating disorder symptoms, such as binge-eating tendency, the current urge to compensate, and shape and weight concerns, were assessed on an 11-point Likert scale.

In addition to measures of change, the Attitudes Toward Psychological Online Interventions Scale, 52 the Patient Questionnaire on Therapy Expectation and Evaluation, 53 and the Client Sociodemographic and Service Receipt Inventory–European Version 54 were used. Adverse effects and their impact were quantified using the Negative Effects Questionnaire. 55

An a priori power analysis assuming a medium effect of Cohen d  = 0.50 based on meta-analytic evidence for self-help interventions for eating disorders, 18 , 56 an intraclass correlation of 0.40, a power of 0.80, and an α level of .05 indicated a required sample size of greater than or equal to 152. 57 , 58 Data analyses were conducted from October 24, 2022, to December 23, 2023. Following our analysis plan, linear mixed models with restricted maximum likelihood estimation were run in line with the intention-to-treat principle. A random intercept and fixed effects for time (baseline, midtreatment, posttreatment), treatment (control, intervention), and their interaction were added stepwise to model continuous symptom change while considering the repeated measures design. 59 The treatment effect was derived from the treatment × time interaction and standardized as Cohen d effect size. 60 For the secondary analyses, error rates were adjusted using the unweighted Bonferroni-Holm correction, and for the analysis of the weekly and ecological momentary assessment data, the models were modified to include the higher number of measurements. Complementing these analyses, a minimal clinically important difference (MCID = baseline SD [√(1−r)]) score was calculated to evaluate the clinical significance of within-group changes. 61

Enhancing the robustness of our results, missing values were addressed by conducting a sensitivity analysis using multiple imputations by chained equations. Given its questionable accuracy, the registered last observation carried forward analysis was emphasized less and is only reported in eTable 1 in Supplement 2 . 62 Moderator analyses were run for baseline symptom severity (Eating Disorder Examination global score), illness duration, age, previous treatments, new treatment uptake, patient expectancies, adherence, satisfaction, and attitudes toward online therapy by adding the moderators as a covariate to the mixed models. All statistical tests were conducted using R Statistics (R Foundation for Statistical Computing) 63 and the lme4 package, version 1.1.27.1 (R Project for Statistical Computing). 64 A 2-tailed 5% level of statistical significance was used.

A total of 1757 individuals were screened, of whom 154 were equally randomized (mean [SD] age, 29.6 [8.6] years; 149 [96.8%] female; 3 [2.0%] male; 2 [1.3%] nonbinary) to the 2 study arms. Baseline participant characteristics are reported in Table 1 . Participants in both groups reported similar demographic characteristics and clinical outcomes at baseline, except for the years since illness onset, which were higher in the control group, and global eating disorder symptoms and emotion regulation difficulties, which were slightly higher in the intervention group (eTable 2 and eTable 3 in Supplement 2 ). The CONSORT flow diagram summarizes the study flow ( Figure 1 ). The clinical assessments were completed by 136 participants (88.3%) at midtreatment and 129 (83.8%) at posttreatment.

There was a moderately higher decrease in bulimic episodes in the intervention group compared with the control group (Cohen d  = −0.48; 95% CI, −0.75 to −0.20; P  < .001) ( Table 2 and Figure 2 ). A clinically meaningful decrease in bulimic episodes was found in the intervention group ( b  = −16.27; 95% CI, −19.59 to −12.95; MCID =12.53), but not in the control group ( b  = −4.58; 95% CI, −9.90 to 0.74; MCID =12.53). Separate analyses on binge-eating episodes and compensatory behaviors revealed a moderate effect for binge-eating episodes (Cohen d  = −0.61; 95% CI, −0.89 to −0.33; P  < .001) with a substantial clinical symptom reduction in the intervention group ( b  = −7.45; 95% CI, −9.41 to −5.49; MCID =4.75), but not in the control group ( b  = −0.14; 95% CI, −3.36 to 3.07; MCID =4.75) (eFigure 2 in Supplement 2 ). For compensatory behaviors, there was no significant effect (Cohen d  = −0.25; 95% CI, −0.51 to 0.02; P  = .21) and neither a clinically meaningful change in the intervention group ( b  = −8.82; 95% CI, −11.29 to −6.34; MCID =9.16) nor in the control group ( b  = −4.43; 95% CI, −7.45 to −1.42; MCID =9.16) was found (eFigure 3 in Supplement 2 ). Underlining the robustness of our findings, these results were replicated in our sensitivity analysis ( Table 2 ).

Medium differences in the changes from baseline to posttreatment favoring the intervention group were found for global eating disorder symptoms (Cohen d  = −0.61; 95% CI, −0.89 to −0.32; P  < .001) and clinical impairment (Cohen d  = −0.62; 95% CI, −0.92 to −0.33; P  < .001). In contrast, no meaningful effects were detected for well-being (Cohen d  = −0.08; 95% CI, −0.37 to 0.22; P  > .99) and the restoration of work capacity (Cohen d  = −0.01; 95% CI, −0.68 to 0.66; P  = .99). The same pattern of results occurred in the sensitivity analysis ( Table 2 ). Concerning the weekly symptom measurements, bulimic behaviors decreased more substantially in the intervention group compared with the control group ( b  = −0.15; 95% CI, −0.24 to −0.06; Cohen d  = −0.29; 95% CI, −0.46 to −0.11; P  = .005) (eFigure 4 in Supplement 2 ).

Exploratory analysis indicated a moderately higher increase in self-esteem (Cohen d  = 0.33; 95% CI, 0.11 to 0.56; P  = .003) and a more substantial reduction in emotion regulation difficulties (Cohen d  = −0.61; 95% CI, −0.88 to −0.34; P  < .001) in the intervention group. There were no substantial differences in the pre-post changes for comorbid symptoms (depressive symptoms: Cohen d  = −0.24; 95% CI, −0.56 to 0.07; P  = .13; anxiety symptoms: Cohen d  = −0.09; 95% CI, −0.39 to 0.21; P  = .57) and the repertoire of adaptive emotion regulation strategies (Cohen d  = 0.18; 95% CI, −0.11 to 0.46; P  = .22) ( Table 3 ). Confirming the results from the questionnaires, the ecological momentary assessment analyses demonstrated a notably higher reduction in binge-eating tendency, urges to compensate, and shape and weight concerns in daily life (all β > .18) (eTable 4 and eFigure 5 in Supplement 2 ).

Age, participants’ treatment expectancies, baseline global eating disorder symptoms, and attitudes toward online interventions did not moderate the treatment × time interaction (eTable 5 in Supplement 2 ). However, a more prolonged illness duration was associated with a higher symptom reduction (eTable 5 and eFigure 6 in Supplement 2 ).

Regarding previous treatment experiences, 48 of the 77 participants (62.3%) in the control group and 43 of the 77 participants (55.8%) in the intervention group had received prior psychotherapeutic or pharmacologic treatments. During the study period, 6 participants (8.0%) in the control group and 7 participants (10.6%) in the intervention group sought additional professional help (eTable 6 in Supplement 2 ). Previous treatments or the uptake of a new therapy did not moderate changes in bulimic behaviors (eTable 5 in Supplement 2 ).

Seventy-six of 77 participants (98.7%) allocated to the intervention group started the web-based intervention and finished a mean (SD) of 7.4 (4.1) of 12 modules. Forty-seven participants (61.0%) completed the main course consisting of 6 modules, and 26 participants accessed all offered contents (33.8%). A mean (SD) satisfaction of 60.6 (23.4) was reported on a scale from 0 (no satisfaction) to 100 (complete satisfaction). Adherence based on the number of finished modules and satisfaction did not moderate symptom changes (eTable 5 in Supplement 2 ). Adverse effects caused by the intervention mostly concerned the intervention’s quality and the occurrence of psychological symptoms (eTable 7 in Supplement 2 ).

A maladaptive interplay of dysfunctional self-evaluations, binge-eating episodes, and compensatory behaviors dominates the life of individuals with BN, leading to a high illness-related burden. 1 , 3 - 7 While the effectiveness of face-to-face psychotherapies for BN has been established, web-based treatments have not been investigated to a similar extent. 9 , 11 , 17 - 20 , 23 - 25 Targeting this imbalance in research, the present 2-armed clinical trial indicates that a web-based cognitive behavioral self-help intervention for patients with BN can lead to a substantial reduction in binge-eating episodes, global eating disorder symptoms, and clinical burden. Supporting the validity of these results, changes in symptoms were also observed when examining weekly and momentary real-time assessments.

These findings complement previous results on web-based treatments for eating disorders by obtaining a similar effect in a sample of individuals diagnosed with BN. 17 - 20 , 23 , 24 Apart from changes in eating disorder symptoms, web-based self-help also reduced psychosocial impairments and emotion regulation difficulties, and improved self-esteem. Thus, the present intervention successfully targeted key symptoms and etiologic mechanisms of eating disorders. 10 , 65 , 66 Demonstrating the feasibility of the web-based intervention for BN, the dropout rates and adverse effects mirror those obtained in previous studies. 67 , 68 Regarding the participants’ adherence, the number of completers was similar to previous studies, 17 while the mean number of finished modules was slightly lower, probably due to 6 modules being optional. 24 , 67 Satisfaction ratings, possibly influenced by the substantial proportion of participants reporting prior therapies, were moderate. This fits research on unguided interventions but falls below the satisfaction levels observed in programs with clinical support. 67 , 69

While aligning with previous results on web-based interventions, the effects are smaller than the ones reported in meta-analyses on face-to-face psychotherapies. 9 , 11 , 18 Moreover, in contrast to established therapies, the present intervention did not lead to substantial improvements in compensatory behaviors, comorbid symptoms, and overall well-being. 9 , 11 , 70 Mixed findings for changes in compensatory behaviors have been found for other web-based interventions for BN, indicating that more prolonged and more extensive treatments (eg, with more guidance) might be needed to establish changes in these domains. 9 , 11 , 24 , 27 , 56 Compared with findings on guided web-based interventions, posttreatment symptom levels were still high. 24 , 67 Reasons for this might have been the negative influences of the COVID-19 pandemic during the study period and that the effects of internet-based interventions might need more time to unfold. 27 , 71

The current study has limitations that may affect the interpretation of the results. First, this randomized clinical trial did not include an active control group and patients in the control group were aware that they would receive treatment after the study period, possibly minimizing their intrinsic motivation to address their symptoms independently. Second, participants enrolled in the study via self-referral, raising the possibility that the sample might not represent the overall BN population. Still, similar demographic data and baseline symptom severity were observed in previous studies on BN. 18 , 72 Third, the web-based intervention was designed to address German participants, and the study design was adjusted to the German health care system, possibly limiting its generalizability. Fourth, the present trial did not include follow-up assessments, and the long-term stability of the treatment effects remains unclear.

This randomized clinical trial showed that a web-based CBT self-help intervention can effectively reduce eating disorder symptoms and the burden of BN. Therefore, considering their low threshold, integrating web-based interventions into routine care might increase access to effective treatments for BN. Likewise, the high scalability of these interventions can assist in treating hard-to-reach patient groups with or without a formal diagnosis. 73 Building on these results, future research should test whether more extensive interventions (ie, blended or ecological momentary interventions) can impact compensatory behaviors, comorbid symptoms, and overall well-being more effectively. 74 Overall, web-based self-help can support patients to work on their symptoms autonomously and has the potential to complement established health care structures. 73

Accepted for Publication: April 26, 2024.

Published: July 3, 2024. doi:10.1001/jamanetworkopen.2024.19019

Open Access: This is an open access article distributed under the terms of the CC-BY-NC-ND License . © 2024 Hartmann S et al. JAMA Network Open .

Corresponding Author: Steffen Hartmann, MS, Department of Psychology, Heidelberg University, Hauptstr 47-51, 69117, Heidelberg, Germany ( [email protected] ).

Author Contributions: Mr Hartmann and Ms Pruessner had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.

Concept and design: All authors.

Acquisition, analysis, or interpretation of data: Hartmann, Timm, Pruessner.

Drafting of the manuscript: Hartmann.

Critical review of the manuscript for important intellectual content: Timm, Barnow, Rubel, Lalk, Pruessner.

Statistical analysis: Hartmann, Pruessner.

Obtained funding: Timm, Barnow, Pruessner.

Administrative, technical, or material support: Timm, Barnow, Rubel, Pruessner.

Conflict of Interest Disclosures: No disclosures were reported.

Funding/Support: This study was supported by the European Regional Development Fund awarded to Selfapy GmbH. An independent evaluation of the web-based intervention for bulimia nervosa was commissioned by Selfapy GmbH to the Department of Psychology at Heidelberg University to ensure adherence to the highest scientific standards. The publication costs were partially funded by the German Research Foundation (Deutsche Forschungsgemeinschaft) and Heidelberg University.

Role of the Funder/Sponsor: Selfapy GmbH had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication.

Data Sharing Statement: See Supplement 3 .

Additional Contributions: We thank Maria Brinkhof, BS, Katrin Fischer, MS, Leonie Hans, BS, Tanja Hauser, MS, Nina Helwig, MS, Luisa Jung, BS, Theresa Kloss, BS, Lena Komorowski, MS, Laura Kristalis, MS, Jana Reich, BS, Elena Rettweiler, BS, Marlene Sayer, MS, and Leoni Weintz, MS, for their assistance with recruitment and data collection during their thesis work (all Department of Psychology, Heidelberg University, Germany, at the time of the study). No financial compensation was received.

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  1. (PDF) Anorexia nervosa: A literature review

    Anorexia nervosa is a food intake disorder. characterized by a cute weight loss that it could cause. severe psychosomatic problems [1]. Diagnostic criteria for Anorexia nervosa. include an intense ...

  2. Conceptualization of anorexia nervosa : a theoretical synthesis of self

    Psychiatric Association, 2013) defines anorexia nervosa as "persistent energy intake restriction; intense fear of gaining weight or of becoming fat; and a disturbance in self-perceived weight or shape" (APA, 2013). The main diagnostic criterion for anorexia nervosa is a body weight below the expected age, sex, and height of the patient (APA, 2013).

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    Anorexia nervosa is a complex psychiatric illness associated with food restriction and high mortality. Recent brain research in adolescents and adults with anorexia nervosa has used larger sample sizes compared with earlier studies and tasks that test specific brain circuits. ... Funding Statement. This work was supported by National Institute ...

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    It includes anorexia nervosa (AN), bulimia nervosa (BN), binge eating disorder (BED), ARFID, rumination disorder, pica, other specified feeding or eating disorder, and unspecified feeding or eating disorder. 1 The modifications of the diagnostic criteria appearing in the DSM-5 are relatively few, although significant, and involve clarifications ...

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    1. Introduction. Anorexia nervosa (AN) is a complex psychiatric disorder with a high rate of mortality and a relatively low rate of remission [].Using DSM-V criteria, the lifetime prevalence of AN in females is estimated to be as high as 4% [].The lifetime prevalence in males has been estimated to be between 0.1% and 0.3%, although this is likely an underestimate [].

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  13. Peripheral Biomarkers of Anorexia Nervosa: A Meta-Analysis

    The pathogenesis of anorexia nervosa (AN) has been hypothesized to involve several biological systems. However, reliable biomarkers for AN have yet to be established. This study was aimed to identify statistically significant and clinically meaningful peripheral biomarkers associated with AN.

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    The weight of an anorexia nervosa patient is at least 15% less than the average weight according to the height. Also, the BMI (body mass index) is under 16. For women with anorexia nervosa missing your period or not having your period at all is also a strong physical sign. Skin can be very dry and covered with thin, light hairs called lanugos.

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    Anorexia Nervosa and Its Treatment. Anorexia nervosa is a treatable eating disorder when people significantly limit the number of calories and types of foods they eat, which leads to excessive weight loss. The objectives of anorexia treatment include weight recovery, […] Genetic Disorder: "A Genetic Link to Anorexia".

  19. The role of the reward system in Anorexia Nervosa

    Anorexia Nervosa (AN) is a complex mental disorder characterized by a significant reduction in food intake, leading to severe weight loss and emaciation. Despite its prevalence, especially among young adolescents, the exact causes of this multifactorial disease remain unknown, posing challenges for effective treatment. Patients with AN exhibit various neurobiological alterations, though it is ...

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    Anorexia nervosa (AN) is an eating disorder largely affecting young women with high morbidity, chronicity and mortality . Apart from a restriction of energy intake leading to a significant weight loss, an intense fear of gaining weight and body image disturbance are key symptoms.

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    The pathogenesis of anorexia nervosa (AN) has been hypothesized to involve several biological systems. However, reliable biomarkers for AN have yet to be established. This study was aimed to identify statistically significant and clinically meaningful peripheral biomarkers associated with AN. A systematic literature search was conducted to identify studies published in English from inception ...

  23. Web-Based Cognitive Behavioral Treatment for Bulimia Nervosa

    Key Points. Question Can a web-based cognitive behavioral self-help intervention reduce eating disorder symptoms and address disease-related features in bulimia nervosa?. Findings In this randomized clinical trial of 154 adults with bulimia nervosa, receiving a web-based intervention led to a significantly higher reduction in binge-eating episodes, global eating disorder symptoms, and clinical ...

  24. Anorexia Nervosa.pdf

    Thesis Statement: Anorexia Nervosa effects a person both physically and mentally. Anorexia represents one percent of most prevalent eating disorder diseases. The word anorexia itself means, " lack of appetite". Anorexia is an all-encompassing pursuit of thinness. The person effected by Anorexia has an absolute fear of becoming obese (Matthew 4). ). Approximately one percent of adolescent ...

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  26. Enriching a randomized controlled treatment trial for anorexia nervosa

    Materials & Methods: The manuscript is a participatory publication co‐written by individuals with lived experience with anorexia nervosa and eating disorder researchers. Results: We report on motivations for this approach, our collaboration principles, structures and shared experience of working together in the trial, the potential burdens ...

  27. arXiv:2406.15470v1 [cs.CL] 15 Jun 2024

    Ethics Statement When conducting an analysis of social media con-tent pertaining to mental disorders, it is essential to ... Ph.D. thesis, Université ... Anorexia nervosa: A serious eating disorder characterized by extreme self-starvation and weight loss, leading to a low body weight. ...