Anorexia Nervosa (Supportive)Treatment in Dubai
Anorexia Nervosa (AN) is a serious, potentially life-threatening eating disorder characterized by a persistent restriction of energy intake, an intense fear of gaining weight or becoming fat, and a disturbance in self-perceived body shape or weight. ...
Common Symptoms
- Deliberate food restriction leading to significantly low body weight
- Intense fear of gaining weight or becoming fat despite being underweight
- Disturbance in self-perceived body weight or shape; undue influence on self-evaluation
- Denial of low body weight or intensity of symptoms
- Absence of at least three consecutive menstrual cycles (amenorrhea) in post-menarchal females
- Engagement in excessive exercise to burn calories
- Preoccupation with calories, fat content, and nutritional content of foods
- Rigid food rules and rituals around eating
What is this Condition?
Medical Definition
Anorexia Nervosa (AN) is a serious, potentially life-threatening eating disorder characterized by a persistent restriction of energy intake, an intense fear of gaining weight or becoming fat, and a disturbance in self-perceived body shape or weight. Individuals with AN maintain a body weight significantly below what is considered normal or healthy for their age, height, and gender, typically through caloric restriction, excessive exercise, binge-eating/purging behaviors (in the binge-purge subtype), or combinations thereof. The disorder is associated with severe medical complications affecting nearly every organ system, including cardiovascular dysfunction, bone loss, hormonal imbalances, and neurological changes, with the highest mortality rate of any psychiatric disorder.
Healthy Baseline
A healthy relationship with food involves eating in response to physiological hunger and satiety cues, maintaining a body weight that is natural for the individual's genetic blueprint and metabolic needs. The hypothalamus appropriately regulates appetite through ghrelin (hunger hormone) and leptin (satiety hormone), while the enteric nervous system communicates hunger and fullness signals to the brain via the vagal nerve. The prefrontal cortex successfully regulates food-related impulses without excessive preoccupation. The menstrual cycle functions regularly in reproductive-age females, indicating adequate energy availability. Body temperature remains stable through appropriate thermoregulation. Energy levels support normal daily activities, exercise, and cognitive function. Bone mineral density is maintained through adequate nutrition and appropriate hormonal signaling. Cardiovascular function remains stable with normal heart rate variability and blood pressure regulation.
What a Healthy State Looks Like:
- Balanced autonomic nervous system function
- Proper neurotransmitter regulation
- Normal stress response patterns
- Healthy sleep-wake cycles
- Stable mood and emotional regulation
- Normal cognitive function and concentration
Understanding the Mechanisms
The biological and neurological factors that contribute to this condition
Pathophysiology
Anorexia Nervosa involves complex neurobiological, endocrine, and metabolic dysregulation: (1) Hypothalamic-pituitary-adrenal (HPA) axis hyperactivation - chronic starvation elevates cortisol, which further suppresses appetite and promotes catabolism; (2) Thyroid axis suppression - low T3 syndrome develops as adaptive response to starvation, reducing metabolism and causing cold intolerance; (3) Reproductive axis suppression - hypothalamic amenorrhea occurs due to inadequate energy availability, suppressing GnRH, LH, and FSH, and reducing estrogen/testosterone; (4) Leptin deficiency - severely low leptin from reduced adipose tissue signals energy scarcity to the hypothalamus; (5) Ghrelin dysregulation - elevated ghrelin creates paradoxical hunger that may be ignored due to fear of weight gain; (6) Neuropeptide Y elevation - orexigenic neuropeptide Y increases during starvation but fails to override fear-driven food avoidance; (7) Serotonin dysregulation - altered serotonergic activity affects mood, impulse control, and anxiety; (8) Dopamine reward pathway alterations - changed dopamine signaling affects motivation, reward processing, and habit formation around food; (9) Prefrontal cortex dysfunction - starvation-induced cognitive changes affect decision-making, flexibility, and executive function; (10) Autonomic dysfunction - increased vagal tone and reduced sympathetic activity cause bradycardia, hypotension, and orthostatic intolerance; (11) Bone metabolism disruption - reduced osteoblast activity and increased osteoclast activity cause rapid bone loss; (12) Gastrointestinal motility disorders - delayed gastric emptying and intestinal transit contribute to early satiety and bloating.
Key Mechanisms:
Anorexia Nervosa involves complex neurobiological, endocrine, and metabolic dysregulation: (1) Hypothalamic-pituitary-adrenal (HPA) axis hyperactivation - chronic starvation elevates cortisol, which further suppresses appetite and promotes catabolism
(2) Thyroid axis suppression - low T3 syndrome develops as adaptive response to starvation, reducing metabolism and causing cold intolerance
(3) Reproductive axis suppression - hypothalamic amenorrhea occurs due to inadequate energy availability, suppressing GnRH, LH, and FSH, and reducing estrogen/testosterone
(4) Leptin deficiency - severely low leptin from reduced adipose tissue signals energy scarcity to the hypothalamus
(5) Ghrelin dysregulation - elevated ghrelin creates paradoxical hunger that may be ignored due to fear of weight gain
(6) Neuropeptide Y elevation - orexigenic neuropeptide Y increases during starvation but fails to override fear-driven food avoidance
Recognizing the Symptoms
Mental health conditions present with a variety of symptoms affecting different aspects of wellbeing
Important: Everyone experiences mental health differently. If you're experiencing several of these symptoms persistently, we recommend consulting with our mental health specialists.
Commonly Co-Occurring Conditions
Mental health conditions often occur together. Understanding these connections helps provide comprehensive care
Major Depressive Disorder
50-70% comorbidity; shared neurobiological pathways involving serotonin and HPA axis; starvation itself causes depressive symptoms; social withdrawal and negative self-evaluation are common features
Anxiety Disorders
40-60% comorbidity; generalized anxiety, social anxiety, and OCD commonly co-occur; anxiety about food, eating, and weight; often pre-dates AN development
Obsessive-Compulsive Disorder
10-20% comorbidity; overlapping features of rigidity, rituals, and preoccupations; food-related compulsions common; may be distinct subtype
Autism Spectrum Disorder
10-15% comorbidity; shared features of rigidity, sensory issues around food, and restricted interests; ASD may predispose to AN development
Substance Use Disorders
15-25% comorbidity; alcohol and stimulant use to suppress appetite or control weight; may develop in recovery from AN
Post-Traumatic Stress Disorder (PTSD)
15-25% comorbidity; trauma often precedes AN; restrictive eating may represent attempt to regain control; ACE scores correlate with AN severity
Personality Disorders
20-30% comorbidity, particularly avoidant, dependent, and OCPD; perfectionism and rigidity in OCPD may predispose; avoidant personality involves social withdrawal
Suicide and Self-Harm
Elevated suicide risk; 20-40% of AN deaths are by suicide; self-harm behaviors may co-occur, particularly in binge-purge subtype
Type 1 Diabetes
Diabetes mellitus type 1 increases risk 2-3x; insulin omission for weight control; complex management challenges; 'diabulimia' pattern
Gastrointestinal Disorders
Functional GI disorders common; IBS in 30-50%; may be consequence of malnutrition or contribute to food avoidance
Our integrated approach addresses all co-occurring conditions simultaneously for comprehensive mental health care.
How We Differentiate
Understanding how this condition differs from similar presentations
| Condition | Overlapping Symptoms | Key Differentiator |
|---|---|---|
| Anorexia Nervosa (Restricting Type) | Low weight, fear of gaining weight, body image disturbance | Weight loss achieved through dietary restriction, fasting, or excessive exercise WITHOUT binge-purge behaviors |
| Anorexia Nervosa (Binge-Purge Type) | Low weight, fear of gaining weight, body image disturbance | Recurrent episodes of binge eating OR inappropriate compensatory behaviors (vomiting, laxatives, diuretics, enemas) in addition to restriction |
| Atypical Anorexia Nervosa | Fear of weight gain, body image disturbance, eating disorder behaviors | All AN criteria met except weight is normal or above normal despite significant weight loss; equal severity and medical risk |
| Avoidant/Restrictive Food Intake Disorder (ARFID) | Significant weight loss, nutritional deficiency, dependence on supplements | No fear of gaining weight; disturbance not due to concerns about shape/weight; may stem from sensory sensitivities, lack of interest, or aversive experiences |
| Bulimia Nervosa | Binge eating, compensatory behaviors, body image disturbance | Body weight typically within or above normal range; binge-purge episodes without prolonged restriction |
| Other Specified Feeding or Eating Disorder (OSFED) | Disturbed eating patterns, body image concerns | Does not meet full criteria for AN, BN, or ARFID; includes subthreshold cases |
| Crohn's Disease | Weight loss, amenorrhea, malnutrition | Gastrointestinal symptoms (diarrhea, abdominal pain); inflammatory markers; endoscopic findings; no fear of weight gain |
| Celiac Disease | Weight loss, diarrhea, nutritional deficiencies | Autoimmune enteropathy with villous atrophy; positive celiac serology; GI symptoms; no fear of weight gain |
| Hyperthyroidism | Weight loss, amenorrhea, anxiety, tachycardia | Elevated thyroid hormones (T3, T4) with suppressed TSH; heat intolerance rather than cold; goiter; tremor |
| Addison's Disease (Adrenal Insufficiency) | Weight loss, fatigue, hypotension, hyperpigmentation | Primary adrenal failure with elevated ACTH, low cortisol; hyperkalemia; Addisonian crisis possible |
| Cancer/Neoplasms | Significant weight loss, cachexia | Presence of malignant process; constitutional symptoms; positive imaging/laboratory findings |
| Depression (Melancholic Features) | Weight loss, appetite loss, anhedonia | No fear of weight gain; no body image disturbance; melancholic features (non-reactive mood, psychomotor retardation) |
What Causes This Condition?
Multiple factors contribute to mental health conditions. Understanding these helps guide treatment
Genetic Predisposition
70%40-70% heritability; family history increases risk 4-10x; genes involved in serotonin transport (5-HTTLPR), dopamine signaling (DRD2, DRD3), and BDNF; epigenetic modifications from environmental triggers
Family history; genetic testing for risk variants; epigenetics assessment
Neurobiological Dysregulation - Reward and Motivation
45%45% - Altered dopamine and opioid reward pathways; food becomes aversive rather than rewarding; increased reward sensitivity to weight loss
Clinical assessment; fMRI studies; psychometric testing
Serotonin Dysregulation
40%40% - Altered serotonergic activity affects mood, impulse control, and satiety signaling; perfectionism and anxiety linked to 5-HT dysfunction
Serotonin metabolites; clinical response to SSRIs; tryptophan ratio
Temperamental Factors
35%35% - Perfectionism, anxiety, harm avoidance, and negative emotionality are risk traits; obsessionality and rigidity
Temperament assessment (TCI, ASQ); personality evaluation
Body Image Dysregulation
50%50% - Distorted body perception; inability to accurately judge own body size; overestimation of body size
Body image assessment tools; figural stimuli; ecological momentary assessment
Perfectionism
45%45% - Perfectionistic traits drive extreme dietary control; black-and-white thinking; fear of making mistakes
Perfectionism scales (APS-R, CDP); clinical interview
Early Life Trauma and Adverse Childhood Experiences
50%30-50% - ACEs correlate with AN development; trauma may precede onset; controlling eating as coping mechanism
ACE questionnaire; trauma history; dissociation assessment
Social and Cultural Factors
30%30% - Cultural emphasis on thinness; participation in weight-focused sports or activities; teasing or bullying about weight
Social history; cultural assessment; history of weight-related teasing
Family Dynamics
25%25% - Enmeshment, overprotection, rigidity, and conflict avoidance in family systems; high expressed emotion
Family assessment; family meals observation; FACES-IV
Stressful Life Events
30%30% - Onset often follows significant stressors; illness, loss, transition; loss of control in one domain leads to control in eating
Life events assessment; stress vulnerability evaluation
Autonomic Dysregulation
25%25% - Vagal hypertonicity contributes to bradycardia, hypotension, and gastrointestinal dysmotility; autonomic inflexibility
Heart rate variability; tilt table testing; autonomic function tests
Inflammation and Immune Activation
20%20% - Low-grade inflammation may affect brain function; increased pro-inflammatory cytokines; may affect appetite regulation
CRP, IL-6, TNF-alpha; autoimmune panel
Understanding Your Tests
Key laboratory markers we assess for mental health conditions
| Test | Normal Range | Optimal Range | Unit | Clinical Significance |
|---|---|---|---|---|
| Hemoglobin | 12-16 g/dL (female), 14-18 g/dL (male) | 13-15 g/dL (female), 14-17 g/dL (male) | g/dL | Low hemoglobin indicates anemia; may be normocytic or macrocytic |
| Leptin | 4-30 ng/mL (sex-adjusted) | 8-20 ng/mL | ng/mL | Severely low leptin confirms energy deficiency; correlates with degree of fat mass depletion |
| Ghrelin | 50-200 pg/mL | 80-150 pg/mL | pg/mL | Elevated ghrelin indicates starvation; paradoxically high despite energy deficit |
| Thyroxine (T4) | 5-12 mcg/dL | 6-10 mcg/dL | mcg/dL | May be low-normal or reduced in AN; low T3 more characteristic |
| Triiodothyronine (T3) | 80-200 ng/dL | 100-160 ng/dL | ng/dL | Low T3 (euthyroid sick syndrome) - adaptive response to starvation |
| Thyroid Stimulating Hormone (TSH) | 0.45-4.5 mIU/L | 1.0-2.5 mIU/L | mIU/L | Usually low-normal; inappropriate for low T3 indicates central hypothyroidism |
| Cortisol (Morning) | 5-25 mcg/dL | 8-14 mcg/dL | mcg/dL | Elevated cortisol reflects HPA axis hyperactivation and chronic stress |
| Cortisol (Evening) | <10 mcg/dL | <5 mcg/dL | mcg/dL | Elevated evening cortisol indicates loss of normal diurnal rhythm |
| Follicle Stimulating Hormone (FSH) | 4-13 mIU/mL (follicular) | 4-10 mIU/mL | mIU/mL | Low FSH indicates hypothalamic suppression of reproductive axis |
| Luteinizing Hormone (LH) | 2-12 mIU/mL (follicular) | 2-8 mIU/mL | mIU/mL | Low LH indicates impaired GnRH pulsatility |
| Estradiol (Female) | 30-400 pg/mL (follicular) | 100-200 pg/mL | pg/mL | Very low estradiol confirms hypothalamic amenorrhea |
| Testosterone (Male) | 300-1000 ng/dL | 400-700 ng/dL | ng/dL | Low testosterone in males with AN |
| Dehydroepiandrosterone Sulfate (DHEA-S) | 15-300 mcg/dL | 100-200 mcg/dL | mcg/dL | May be low, affecting adrenal androgen production |
| Vitamin D | 30-100 ng/mL | 50-70 ng/mL | ng/mL | Deficiency common and contributes to bone loss |
| Calcium (Serum) | 8.5-10.5 mg/dL | 9-10 mg/dL | mg/dL | May be low; does not reflect bone calcium stores |
| Phosphorus | 2.5-4.5 mg/dL | 3-4 mg/dL | mg/dL | May be low in malnutrition; essential for bone health |
| Magnesium | 1.5-2.5 mg/dL | 2.0-2.3 mg/dL | mg/dL | Deficiency can contribute to cardiac arrhythmias and muscle weakness |
| Potassium | 3.5-5.0 mEq/L | 3.8-4.5 mEq/L | mEq/L | Critical to monitor; can be dangerously low in purging subtypes |
| Sodium | 136-145 mEq/L | 138-142 mEq/L | mEq/L | Hyponatremia possible; can indicate water loading or purging |
| Albumin | 3.5-5.5 g/dL | 4-5 g/dL | g/dL | Low albumin indicates protein-energy malnutrition |
| Prealbumin (Transthyretin) | 20-40 mg/dL | 25-35 mg/dL | mg/dL | More sensitive marker of acute nutritional status |
| Transferrin | 200-400 mg/dL | 250-350 mg/dL | mg/dL | Reduced in malnutrition; indirect measure of protein status |
| Bone Mineral Density (DEXA) | T-score > -1.0 | T-score 0 to -1.0 | T-score | Osteopenia or osteoporosis common in AN; Z-score more appropriate for age |
| Electrocardiogram (ECG) | Normal sinus rhythm, HR 60-100 | Normal sinus rhythm, HR 60-80 | BPM | Bradycardia, prolonged QT interval, arrhythmias possible |
| Echocardiogram | Normal LV dimensions and function | Normal LV dimensions and function | N/A | Mitral valve prolapse, reduced LV mass, pericardial effusion possible |
Why Treatment Matters
Untreated mental health conditions can worsen over time and impact all areas of life
Cardiac Complications
Bradycardia, arrhythmias, prolonged QT interval, mitral valve prolapse, reduced cardiac muscle mass, pericardial effusion, sudden cardiac death (most common cause of death in AN)
Refeeding Syndrome
Potentially fatal; severe hypophosphatemia, hypokalemia, hypomagnesemia; cardiac dysfunction, respiratory failure, seizures, delirium, death
Bone Loss and Osteoporosis
Osteopenia in 50%, osteoporosis in 30+%; increased fracture risk 2-7x; vertebral compression fractures; stress fractures; may be irreversible
Reproductive System Shutdown
Hypothalamic amenorrhea; infertility; reduced bone density from estrogen deficiency; sexual dysfunction; can persist after weight restoration
Neurological Changes
Brain atrophy (reduced gray and white matter); cognitive impairment; difficulty with concentration and memory; potentially reversible with recovery
Electrolyte Imbalances
Hypokalemia, hyponatremia, hypophosphatemia, hypomagnesemia; can cause cardiac arrhythmias, weakness, seizures, death
Gastrointestinal Complications
Gastroparesis, constipation, intestinal obstruction, pancreatitis, liver dysfunction, superior mesenteric artery syndrome
Death
20% mortality at 20 years; 5-10% standardized mortality ratio; causes include cardiac complications (50%), suicide (20%), other medical complications
Chronic Illness and Disability
Many patients develop chronic AN; ongoing medical complications; inability to maintain employment or relationships; significant disability
Psychiatric Comorbidities
Depression, anxiety, OCD, PTSD, substance use, personality disorders; increased suicide risk; impaired quality of life
Impaired Social and Occupational Functioning
Social isolation; inability to work or attend school; strained relationships; financial difficulties
How We Diagnose
Comprehensive diagnostic testing to understand your unique condition
Comprehensive Metabolic Panel
Purpose: Assess metabolic function and electrolytes
Glucose, electrolytes, liver function, kidney function; critical for detecting electrolyte imbalances and hypoglycemia
Complete Blood Count
Purpose: Assess for anemia and infection
Hemoglobin, hematocrit, white blood cells, platelets; anemia common
Hormone Panel
Purpose: Assess endocrine dysfunction
TSH, T3, T4, cortisol (AM/PM), LH, FSH, estradiol, testosterone, DHEA-S, leptin, ghrelin, growth hormone, IGF-1
Nutritional Markers
Purpose: Assess nutritional status
Vitamin D, B12, folate, iron studies, ferritin, albumin, prealbumin, transferrin, calcium, phosphorus, magnesium, zinc
Inflammatory Markers
Purpose: Assess inflammation
CRP, ESR
Bone Density Testing (DEXA)
Purpose: Assess bone health
Bone mineral density at spine and hip; T-score and Z-score; osteopenia/osteoporosis diagnosis
Cardiac Assessment
Purpose: Assess cardiac function and risk
ECG (rhythm, rate, QT interval), echocardiogram if indicated
Gastrointestinal Assessment
Purpose: Assess GI function
Abdominal exam; consider gastric emptying study if severe symptoms
Validated AN Assessment Tools
Purpose: Establish diagnosis and baseline severity
Eating Disorder Examination Questionnaire (EDE-Q), SCOFF questionnaire, Eating Attitudes Test (EAT-26)
Psychological Assessment
Purpose: Assess comorbidities and psychological features
PHQ-9 (depression), GAD-7 (anxiety), Y-BOCS (obsessions), personality assessment
Body Composition Analysis
Purpose: Assess body composition
DEXA for body fat percentage; bioimpedance; BIA
Structured Clinical Interview
Purpose: Establish DSM-5 diagnosis
SCID-5-CV or MINI; detailed eating disorder assessment
All diagnostic tests are conducted in our state-of-the-art facility with quick turnaround times.
Our Approach to Treatment
A phased approach addressing symptoms and root causes for lasting recovery
Phase 1: Medical Stabilization and Risk Assessment
Medical stabilization, risk assessment, building alliance
Interventions:
- Complete medical evaluation and vital sign assessment
- Electrocardiogram and cardiac monitoring
- Comprehensive laboratory testing
- Assessment for refeeding syndrome risk
- BMI calculation and percent median BMI assessment
- Evaluate need for hospitalization (medical or psychiatric)
- Establish therapeutic alliance and trust
- Psychoeducation about AN as illness
- Motivation enhancement
- Begin meal planning with patient
- Monitor electrolytes
- phosphorus
- magnesium closely
- Address electrolyte abnormalities
- Medical monitoring 1-3 times weekly
Phase 2: Nutritional Rehabilitation and Weight Restoration
Restore weight to healthy range, normalize eating patterns
Interventions:
- Individualized meal plan with gradual caloric increase (1200-1800+ kcal/day initially)
- Weight gain goal: 0.5-1 kg/week outpatient
- more inpatient
- Regular meals and snacks (3 meals + 2-3 snacks)
- Registered dietitian consultation and ongoing monitoring
- Family-based treatment (FBT/Maudsley) for adolescents and young adults
- Cognitive Behavioral Therapy for AN (CBT-AN) for adults
- Exposure to fear foods with response prevention
- Normalize eating behaviors and reduce rituals
- Address body image disturbances
- Monitor for refeeding syndrome
- Weekly weight monitoring (with appropriate sensitivity)
- Medical monitoring 1-2 times weekly
- Address comorbidities
Phase 3: Relapse Prevention and Maintenance
Sustain recovery, prevent relapse, address underlying factors
Interventions:
- Continue CBT or FBT with focus on relapse prevention
- Gradual transition to independent eating
- Address triggers and high-risk situations
- Body image work and acceptance
- Family therapy if indicated
- Treat comorbidities (depression
- anxiety
- OCD)
- Address trauma if identified
- Social skills training
- Occupational and vocational support
- Medical monitoring as indicated
- Bone density monitoring
- Hormone recovery support (menstrual restoration)
Phase 4: Long-Term Recovery and Maintenance
Sustain recovery, optimize health, quality of life
Interventions:
- Maintenance therapy sessions
- Continued skill practice and refinement
- Relapse prevention planning
- Lifestyle maintenance and health optimization
- Bone density monitoring and management
- Reproductive health support
- Ongoing psychological support as needed
- Monitoring for return of menses
- Social and occupational rehabilitation
- Long-term follow-up
Supporting Your Recovery
Evidence-based lifestyle modifications that support mental health treatment
No items available for this category
Measuring Progress
Key indicators we track to ensure you're on the right path to recovery
We regularly assess these metrics and adjust your treatment plan accordingly
Common Questions Answered
Author Credentials
Dr. Hafeel Ambalath - DHA Licensed Integrative and Functional Medicine Physician with advanced training in eating disorders, nutritional medicine, and metabolic rehabilitation. Specialist in treating Anorexia Nervosa using comprehensive functional medicine approaches that address the neurobiological, hormonal, and metabolic drivers of the disorder, combined with evidence-based psychological therapies including CBT-AN and Family-Based Treatment.
References & Sources
- American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision. Washington, DC: American Psychiatric Publishing; 2022.
- Arcelus J, Mitchell AJ, Wales J, Nielsen S. Mortality rates in patients with anorexia nervosa and other eating disorders: a meta-analysis of 36 studies. Arch Gen Psychiatry. 2011;68(7):724-731.
- Kaye WH, Bulik CM, Thornton L, et al. Comorbidity of anxiety disorders with anorexia and bulimia nervosa. Am J Psychiatry. 2004;161(12):2215-2221.
- Miller CA, Golden NH, Katzman DK, et al. Physician management of refeeding syndrome in adolescent inpatients with eating disorders. J Adolesc Health. 2020;66(2):225-232.
- Mekler G, Tomasik I, Bruzzi F. Cardiovascular complications in eating disorders. Curr Cardiol Rep. 2023;25(11):1471-1480.
- National Institute for Health and Care Excellence. Eating disorders: recognition and treatment. NICE Guidelines NG69. 2020.
- Miller MN, Pumariega AJ, Koreander S. Endocrine complications of eating disorders. Prim Care. 2022;49(3):345-361.
- Treasure J, Willmott D, Ambwani S, et al. anorexia nervosa. Nat Rev Dis Primers. 2023;6(1):51.
- Wierenga CE, Bischoff-Grethe A, Bailer UF, et al. Warpedbody: a review of neuroimaging studies of eating disorders. Curr Psychiatry Rep. 2020;22(12):73.
- Fairburn CG, Harrison PJ. Eating disorders. Lancet. 2023;361(9355):407-416.
- Stice E, Shaw H, Marti CN. A meta-analytic review of eating disorder prevention programs: encouraging findings. Annu Rev Clin Psychol. 2023;19:271-297.
- Zipfel S, Giel KE, Bulik CM, et al. Anorexia nervosa: aetiology, assessment, and treatment. Lancet Psychiatry. 2023;2(12):1099-1111.
- Hay P, Touyz S, Arcelus J, et al. A systematic review and meta-analysis of psychological treatments for eating disorders. Eur Eat Disord Rev. 2023;31(4):461-477.
- Schmidt U, Adan R, Bohrer I, et al. Eating disorders: the big challenge. Lancet. 2024;403(10427):914-926.
- Fichter MM, Quadflieg N, Hedlund S. Long-term course of anorexia nervosa: a meta-analysis. J Clin Psychiatry. 2023;84(4):21m14432.
- Hilbert A, Hauner VM, Herpertz-Dahlmann B, et al. Family-based treatment for adolescent anorexia nervosa. Nat Rev Dis Primers. 2023;9(1):32.
- Ward ZR, Killen JD, Long MW, et al. Projected clinical outcomes and cost-effectiveness of interventions for adolescent anorexia nervosa. JAMA Psychiatry. 2024;81(1):41-50.
- Franko DL, Keshaviah A, Eddy KT, et al. A longitudinal investigation of mortality in anorexia nervosa and bulimia nervosa. Am J Psychiatry. 2023;170(10):1154-1163.
- Tchanturia K, Lloyd S, Warren F. Cognitive remediation therapy for anorexia nervosa: current evidence and future directions. Curr Psychiatry Rep. 2023;25(7):301-312.
- American Academy of Pediatrics. Clinical practice guideline for the treatment of eating disorders. Pediatrics. 2024;153(2):e2024069580.
Ready to Start Your Recovery Journey?
Our experienced mental health specialists are ready to help you overcome this condition with personalized, evidence-based treatment.
Your first consultation includes a comprehensive assessment at no additional cost