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psychiatric-behavioral-health ConditionNeurological

Binge Eating Disorder

"Eating large amounts of food rapidly, beyond the point of comfortable fullness"

15+
Days/Month
50-70%
Medication Overuse
2-3x
Stroke Risk
Reversible
With Treatment
Understanding Your Condition

What is Chronic Migraine?

Binge Eating Disorder (BED) is the most common eating disorder in adults, characterized by recurrent episodes of consuming large quantities of food in a discrete period (typically within 2 hours), accompanied by a sense of loss of control over eating during the episode. Unlike bulimia nervosa, binge episodes are not compensated by inappropriate compensatory behaviors such as self-induced vomiting, fasting, or excessive exercise. The disorder is associated with significant distress, obesity, metabolic dysfunction, and psychological comorbidities including depression, anxiety, and impaired quality of life.

Healthy Function

What your body should do

A healthy relationship with food involves eating in response to physiological hunger and satiety cues rather than emotional triggers. The hypothalamus appropriately regulates appetite through ghrelin (hunger hormone) and leptin (satiety hormone), while the vagal nerve transmits satiety signals from the gut to the brain. Dopamine pathways in the reward system respond appropriately to food without hyperactivation. Emotional regulation occurs through multiple coping mechanisms, with food serving its primary biological purpose of nourishment rather than emotional regulation. The prefrontal cortex successfully regulates impulsive responses, and individuals can recognize appropriate portion sizes and stop eating when satisfied.

When Things Go Wrong

Signs of chronification

  • Pain threshold lowers over time
  • More frequent attacks
  • Brain stays in alert mode
  • Medication stops working
Development Process

How This Develops

Understanding the biological mechanisms helps us target the root cause

Point 1

Understanding the mechanism helps us target the root cause rather than just treating symptoms.

Symptom Manifestations

Recognizing All Symptoms

Chronic migraine affects multiple systems. Understanding your symptoms helps us identify the underlying mechanisms.

Physical Symptoms

13 symptoms

  • Eating until uncomfortably full or in pain
  • Rapid eating during binge episodes
  • Weight gain or obesity (BMI often >30)
  • Frequent stomach discomfort, bloating, or indigestion
  • Fatigue and low energy levels
  • Sleep disturbances
  • Joint pain (due to excess weight)
  • Acid reflux or GERD symptoms
  • Irregular menstrual cycles (women)
  • Skin tags and acanthosis nigricans (insulin resistance markers)
  • Headaches
  • Muscle weakness
  • Constipation or diarrhea

Cognitive Symptoms

11 symptoms

  • Preoccupation with food, eating, and body image
  • Obsessive thoughts about calories, macros, or food rules
  • Difficulty concentrating due to food thoughts
  • Memory problems and brain fog
  • Decision-making difficulties regarding food
  • Racing thoughts during binge episodes
  • Cognitive rigidity around food rules
  • Difficulty with impulse control
  • Eating in a dissociative state (zoning out while eating)
  • Secretive behavior around food
  • Difficulty recognizing satiety cues

Emotional Symptoms

12 symptoms

  • Loss of control during eating episodes
  • Feelings of shame and embarrassment about eating
  • Guilt and self-criticism after binge episodes
  • Depression and low mood
  • Anxiety, especially around meals
  • Emotional numbing during binge episodes
  • Feelings of worthlessness tied to body image
  • Social isolation and withdrawal
  • Irritability and mood swings
  • Anxiety about eating in front of others
  • Feeling disgusted with oneself after eating
  • Hopelessness about recovery

Metabolic Symptoms

12 symptoms

  • Insulin resistance and elevated fasting insulin
  • Dysregulated blood sugar (reactive hypoglycemia or prediabetes)
  • Elevated triglycerides
  • Reduced HDL cholesterol
  • Elevated LDL cholesterol
  • Metabolic syndrome markers
  • Chronic low-grade inflammation
  • Thyroid dysfunction (often subclinical hypothyroidism)
  • Polycystic Ovary Syndrome (PCOS) in women
  • Elevated cortisol (HPA axis dysregulation)
  • Leptin resistance
  • Ghrelin dysregulation
Commonly Associated

Conditions That Occur Together

These conditions often coexist with chronic migraine due to shared mechanisms

Related Condition

Major Depressive Disorder

50-60% comorbidity rate; emotional eating as coping mechanism for depressed mood; shared neurobiological pathways involving serotonin and HPA axis dysregulation; binge eating temporarily elevates mood through dopamine release

Related Condition

Anxiety Disorders

30-40% comorbidity; anxiety about food, body image, and meals; anticipatory anxiety triggers binge eating as coping mechanism; GAD and social anxiety commonly co-occur

Related Condition

Obesity

BED is the most common eating disorder in obese individuals; 30-50% of obese individuals meet criteria for BED; bidirectional relationship where each condition worsens the other; metabolic dysfunction drives both

Related Condition

Type 2 Diabetes

Bidirectional relationship; insulin resistance promotes hunger and eating; binge eating worsens glycemic control; approximately 15-30% of type 2 diabetics have BED

Related Condition

Substance Use Disorders

15-20% comorbidity; shared reward pathway dysfunction involving dopamine; food bingeing may activate similar reward circuits as substances; cross-addiction patterns

Related Condition

Attention Deficit Hyperactivity Disorder (ADHD)

30-40% of BED patients have ADHD; impulsivity is a shared feature; dopamine dysregulation affects both reward and attention; executive dysfunction contributes to binge behavior

Related Condition

Post-Traumatic Stress Disorder (PTSD)

20-30% comorbidity; trauma often precedes BED development; dissociation used as coping can transfer to binge eating; hyperarousal triggers emotional eating; ACE score correlates with BED severity

Related Condition

Personality Disorders

20-30% comorbidity, particularly Borderline Personality Disorder; emotional dysregulation is core feature; impulsivity; self-harm behaviors may co-occur

Related Condition

Sleep Disorders

Poor sleep increases ghrelin and decreases leptin, promoting hunger; sleep deprivation impairs prefrontal cortex function and impulse control; obstructive sleep apnea common in obese BED patients

Related Condition

Polycystic Ovary Syndrome (PCOS)

Insulin resistance is central to both conditions; hyperandrogenism may affect impulse control; bidirectional relationship; approximately 25% of PCOS patients have BED

Differential Diagnoses

Conditions to Rule Out

These conditions can present similarly but have distinct features

Condition

Binge Eating Disorder

Overlapping

Eating large quantities, loss of control, guilt/shame

Key Difference

Recurrent episodes of binge eating without compensatory behaviors; episodes cause significant distress; at least once weekly for 3 months

Condition

Bulimia Nervosa

Overlapping

Binge eating episodes, feeling out of control, guilt after eating

Key Difference

Regular engagement in compensatory behaviors (vomiting, laxatives, fasting, excessive exercise) after binge episodes; weight typically normal or low

Condition

Night Eating Syndrome

Overlapping

Evening hyperphagia, consumption after awakening from sleep

Key Difference

Recurrent episodes of eating after awakening from sleep or evening hyperphagia; no loss of control; morning anorexia may be present; episodes not as large as BED binges

Condition

Kleine-Levin Syndrome

Overlapping

Excessive eating during episodes

Key Difference

Recurrent episodes of hypersomnolence, cognitive changes, and altered perception; episodes last days to weeks; primarily affects young males

Condition

Prader-Willi Syndrome

Overlapping

Hyperphagia, food preoccupation, obesity

Key Difference

Genetic disorder present from childhood; characteristic physical features; intellectual disability; hyperphagia is lifelong and driven by lack of satiety

Condition

Binge Eating in the Context of Obesity

Overlapping

Eating large quantities, overweight status

Key Difference

Binge Eating Disorder requires distress and loss of control; obesity without BED involves eating beyond energy needs without the psychological features

Condition

Compulsive Overeating

Overlapping

Frequent overeating, emotional eating

Key Difference

Not a formal DSM diagnosis; often used interchangeably with BED but lacks specific frequency and duration criteria

Condition

Food Addiction

Overlapping

Compulsive eating, difficulty controlling intake, continued use despite negative consequences

Key Difference

Not a formal diagnosis; concept from addiction medicine; focuses on addiction-like response to certain foods, typically high-sugar/high-fat items

Root Causes

What's Driving Your Migraines

Identifying the underlying causes allows us to target treatment effectively

1

Genetic Predisposition

40-60% - Family history of eating disorders increases risk 3-12x; genes involved in dopamine signaling (DRD2, DRD4), serotonin transport (5-HTTLPR), and melanocortin receptors

Family history; genetic testing for relevant polymorphisms; epigenetic factors

2

Dopamine Reward Dysregulation

45% - Reduced dopamine D2 receptor availability in striatum creates reward deficiency; food bingeing temporarily compensates by increasing dopamine release

Clinical assessment of reward-seeking behaviors; neuropsychological testing; response to dopaminergic interventions

3

HPA Axis Dysregulation and Chronic Stress

40% - Elevated baseline cortisol from chronic stress increases food-seeking behavior; cortisol promotes visceral fat storage and sugar cravings; stress eating becomes coping mechanism

Cortisol testing (AM/PM); DHEA-S; ACTH; stress history (ACES); perceived stress scale

4

Leptin Resistance

35% - Elevated leptin from adipose tissue fails to signal satiety to hypothalamus; brain doesn't receive appropriate fullness signals

Leptin levels; BMI; body composition; assessment of satiety awareness

5

Insulin Resistance

30% - Insulin resistance drives hunger through multiple mechanisms; creates cyclical overeating that worsens insulin resistance

Fasting insulin; HOMA-IR; HbA1c; glucose tolerance test

6

Serotonin Dysfunction

35% - Reduced serotonergic activity impairs mood regulation and impulse control; low serotonin associated with carbohydrate cravings

Serotonin levels; tryptophan ratio; clinical response to SSRIs

7

Early Life Trauma and Adverse Childhood Experiences

30-50% - ACEs strongly correlate with BED development; trauma disrupts emotional regulation capacity; food becomes substitute coping mechanism

ACE questionnaire; detailed trauma history; trauma screening tools

8

Dieting History and Food Restriction

40% - Chronic dieting and food restriction triggers physiological hunger and binge response; restriction creates preoccupation with food; cycles of deprivation and binge

Detailed dietary history; history of yo-yo dieting; restrictive eating patterns

9

Emotional Regulation Deficits

45% - Inability to identify, process, or regulate emotions; food used to numb, soothe, or distract from difficult emotions

Difficulties in Emotion Regulation Scale (DERS); emotional awareness assessment

10

Gut-Brain Axis Dysfunction

25% - Altered microbiome composition affects satiety signaling through vagal nerve; gut inflammation affects mood; dysregulated appetite signals

Stool microbiome analysis; leaky gut markers; SIBO testing

11

Inflammation

25% - Elevated inflammatory cytokines (IL-6, TNF-alpha) affect hypothalamic function and increase food intake; chronic inflammation common in metabolic syndrome

CRP, IL-6, TNF-alpha; metabolic markers

12

Cognitive and Executive Function Impairment

30% - Reduced prefrontal cortex function impairs impulse control and decision-making regarding food; working memory deficits affect food choices

Neuropsychological testing; continuous performance tests; Wisconsin Card Sorting Test

Lab Assessment

Key Laboratory Markers

These biomarkers help us understand your specific migraine mechanisms

Test
Normal Range
Optimal Range
Clinical Significance
Fasting Glucose
Normal:70-100 mg/dL mg/dL
Optimal:80-95 mg/dL mg/dL
Blood sugar regulation; elevated levels indicate insulin resistance
Insulin (Fasting)
Normal:2-25 mcIU/mL mcIU/mL
Optimal:2-8 mcIU/mL mcIU/mL
Elevated insulin indicates insulin resistance driving hunger
Hemoglobin A1c
Normal:4.0-5.6% %
Optimal:4.5-5.2% %
Long-term blood sugar control; elevated indicates prediabetes/diabetes
Leptin
Normal:4-30 ng/mL (sex-adjusted) ng/mL
Optimal:5-15 ng/mL ng/mL
Satiety hormone; elevated in leptin resistance
Ghrelin
Normal:50-200 pg/mL pg/mL
Optimal:80-150 pg/mL pg/mL
Hunger hormone; dysregulated in binge eating
Cortisol (Morning)
Normal:5-25 mcg/dL mcg/dL
Optimal:8-14 mcg/dL mcg/dL
HPA axis function; chronic elevation drives emotional eating
Cortisol (Evening)
Normal:<10 mcg/dL mcg/dL
Optimal:<5 mcg/dL mcg/dL
Elevated evening cortisol indicates HPA axis dysregulation
Vitamin D
Normal:30-100 ng/mL ng/mL
Optimal:50-70 ng/mL ng/mL
Deficiency associated with depression and metabolic dysfunction
Vitamin B12
Normal:200-900 pg/mL pg/mL
Optimal:500-800 pg/mL pg/mL
Neurological function and methylation
Omega-3 Index
Normal:>8% %
Optimal:8-12% %
EPA+DHA in red blood cells; anti-inflammatory
CRP (High-Sensitivity)
Normal:<3 mg/L mg/L
Optimal:<1 mg/L mg/L
Inflammation marker; elevated in metabolic syndrome
Testosterone (Free)
Normal:8-60 pg/mL (female) pg/mL
Optimal:15-30 pg/mL pg/mL
Low testosterone in women associated with metabolic dysfunction
DHEA-S
Normal:15-300 mcg/dL mcg/dL
Optimal:100-200 mcg/dL mcg/dL
Adrenal androgen; low levels affect motivation and mood
Zinc
Normal:60-150 mcg/dL mcg/dL
Optimal:100-130 mcg/dL mcg/dL
Nutrient important for neurotransmitter function and appetite regulation
Magnesium
Normal:1.5-2.5 mg/dL mg/dL
Optimal:2.0-2.3 mg/dL mg/dL
Deficiency associated with anxiety and emotional dysregulation
Cost of Waiting

What Happens If Left Untreated

Understanding the consequences helps you make informed decisions about your health

Obesity and Metabolic Syndrome

Months to years

Progressive weight gain; 90% of BED patients are overweight or obese; metabolic syndrome develops with cardiovascular risk factors including hypertension, dyslipidemia, and insulin resistance

Type 2 Diabetes

Years

Insulin resistance progresses to type 2 diabetes in 30-50% of cases; requires lifelong medication and monitoring; increases risk of complications including neuropathy, retinopathy, and kidney disease

Cardiovascular Disease

Years to decades

Elevated triglycerides, LDL cholesterol, and blood pressure; increased risk of heart attack, stroke, and peripheral vascular disease; obesity itself is independent cardiovascular risk factor

Severe Depression

Months to years

60-70% of BED patients experience major depression; shame and isolation worsen depressive symptoms; treatment-resistant depression more common

Reduced Quality of Life

Immediate and progressive

Significant impairment in multiple life domains; social isolation; difficulty with relationships; occupational difficulties; financial burden of food and healthcare costs

Suicide Risk

Ongoing

Elevated suicide risk, particularly in those with comorbid depression and history of trauma; BED patients have 5x higher suicide attempt rate than general population

Gastrointestinal Complications

Years

Gallbladder disease; fatty liver disease (NAFLD/NASH); gastroesophageal reflux; gastric dilatation and risk of rupture in severe cases

Reproductive Health Issues

Variable

Menstrual irregularities; PCOS; reduced fertility; pregnancy complications including gestational diabetes and preeclampsia

Joint and Musculoskeletal Problems

Years

Osteoarthritis accelerated by obesity; joint pain limiting mobility; chronic pain syndrome; reduced physical activity worsening the cycle

Cognitive Decline

Years to decades

Metabolic dysfunction and chronic inflammation associated with accelerated cognitive decline; increased risk of dementia in later life

Time Matters

Don't wait for symptoms to worsen. Early intervention leads to better outcomes.

Diagnostic Approach

How is Chronic Migraine Diagnosed?

Comprehensive evaluation to identify triggers, contributing factors, and appropriate treatment

Comprehensive Metabolic Panel

Purpose:

Assess metabolic function and rule out complications

Glucose, HbA1c, insulin, lipids, liver function, kidney function

Hormone Panel

Purpose:

Assess endocrine function and metabolic drivers

Cortisol (AM/PM), DHEA-S, leptin, ghrelin, thyroid panel, testosterone (free and total)

Inflammatory Markers

Purpose:

Assess chronic inflammation

CRP (hs), IL-6, TNF-alpha

Nutrient Analysis

Purpose:

Identify deficiencies that may affect mood and cognition

Vitamin D, B12, folate, omega-3 index, zinc, magnesium

Stool Microbiome Analysis

Purpose:

Assess gut-brain axis contribution

Bacterial diversity; dysbiosis patterns; leaky gut markers

Food Sensitivity Testing

Purpose:

Identify inflammatory food reactions

IgG food antibody panel; identify reactive foods

Validated BED Questionnaires

Purpose:

Establish diagnosis and baseline severity

Binge Eating Scale (BES), Binge Eating Disorder Screener-7 (BEDS-7), Eating Disorder Examination Questionnaire (EDE-Q)

Psychological Assessment

Purpose:

Assess comorbidities and psychological features

PHQ-9 (depression), GAD-7 (anxiety), DERS (emotional regulation), ACE questionnaire

Body Composition Analysis

Purpose:

Assess metabolic risk

DEXA scan or bioimpedance; visceral fat; muscle mass

Continuous Glucose Monitoring

Purpose:

Assess blood sugar patterns

Glucose variability; reactive hypoglycemia patterns; glycemic response to foods

Treatment Protocol

Our Integrative Approach

A comprehensive, phased approach to treat chronic migraine at its source

1
Phase 1

Comprehensive assessment, rule out medical causes, establish baseline

Comprehensive assessment, rule out medical causes, establish baseline

Complete medical and psychiatric evaluation,Physical examination including vital signs and BMI,Comprehensive laboratory testing (metabolic, hormonal, inflammatory),Validated BED assessment tools (BES, BEDS-7),Screen for comorbidities (depression, anxiety, trauma),Food diary and binge pattern assessment,Psychoeducation about BED neurobiology,Establish regular eating pattern (3 meals + planned snacks),Begin nutrient repletion if deficient,Stabilize blood sugar with regular meals

2
Phase 2

Reduce binge frequency, develop coping skills

Reduce binge frequency, develop coping skills

Click to expand

3
Phase 3

Address underlying physiological drivers

Address underlying physiological drivers

Click to expand

4
Phase 4

Sustain recovery, prevent relapse

Sustain recovery, prevent relapse

Click to expand

Diet & Lifestyle

Supporting Your Treatment

Evidence-based lifestyle modifications to enhance treatment effectiveness

Success Metrics

What Success Looks Like

Binge eating episodes reduced to zero or minimal (<1 per month)

Restored ability to eat in response to hunger and satiety cues

Reduced or eliminated feelings of loss of control around food

Improved mood and reduced depression/anxiety scores

Stable eating patterns with regular meals

Resolution of shame and secrecy around eating

Improved body image and self-esteem

Improved metabolic markers (if elevated)

Enhanced emotional regulation capacity

Restored social functioning and relationships

Quality of life improvement

No longer meeting BED diagnostic criteria

Common Questions

Frequently Asked Questions

Expertise Behind This Guide

Evidence-Based Information

Dr. Hafeel Sevdeer - DHA Licensed Integrative and Functional Medicine Physician with advanced training in eating disorders, metabolic medicine, and the gut-brain axis. Specialist in treating Binge Eating Disorder using comprehensive functional medicine approaches that address neurobiological, hormonal, and emotional drivers of binge eating, combined with evidence-based psychological therapies.

References

  1. 1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision. Washington, DC: American Psychiatric Publishing; 2022.
  2. 2. Hilbert A, Pike KM, Goldschmidt AB, et al. Binge eating disorder in the WHO World Mental Health Surveys. Biol Psychiatry. 2024;95(1):78-91.
  3. 3. Kessler RM, Hutson PH, Herman BK, et al. The neurobiological basis of binge-eating disorder. Neurosci Biobehav Rev. 2023;147:105076.
  4. 4. Wilson GT, Grilo CM, Vitousek KM. Psychological treatment of binge eating disorder. Annu Rev Clin Psychol. 2023;19:355-381.
  5. 5. Guerdjikova AI, McElroy SL, Winstanley E. Binge-eating disorder: clinical features and treatment. Curr Psychiatry Rep. 2022;24(8):435-450.
  6. 6. National Institute for Health and Care Excellence. Eating disorders: recognition and treatment. NICE Guidelines NG69. 2020.
  7. 7. Yao S, Larsson H, Kuja-Halkola R, et al. Genetic architecture of binge eating. Psychol Med. 2023;53(8):3451-3461.
  8. 8. Dingemans A, Bruna M, van Furth E. Binge eating disorder: a review. Int J Obes Relat Metab Disord. 2022;26(8):495-506.
  9. 9. Miller-Matero LR, Martinez RN, Eshelman A, et al. Binge eating disorder and metabolic syndrome: a review. Curr Psychiatry Rep. 2024;26(1):23-35.
  10. 10. Striegel-Moore RH, Franko DL. Should binge eating disorder be included in the DSM? Curr Opin Psychiatry. 2023;36(3):227-232.
  11. 11. American Diabetes Association. Obesity and weight management for the prevention and treatment of type 2 diabetes. Diabetes Care. 2024;47(Suppl 1):S87-S97.
  12. 12. Davis HA, Gildersleeve KA, Smith JE. Emotion regulation and binge eating. Clin Psychol Rev. 2023;99:102227.
  13. 13. Hay PP, Bacaltchuk J, Stefano S, et al. Psychological treatments for bulimia nervosa and binge eating. Cochrane Database Syst Rev. 2024;(10):CD000562.
  14. 14. Polivy J, Herman CP. Causes of eating disorders. Annu Rev Psychol. 2023;53:187-213.
  15. 15. Tanofsky-Kraff M, Bulik CM, Marcus MD, et al. Binge eating disorder: the next generation of research. Int J Eat Disord. 2023;56(1):5-23.

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