Eating Disorders: The Functional Medicine Perspective

When the War with Food Is a War with the Body

Eating disorders are the deadliest psychiatric conditions. Anorexia nervosa carries a mortality rate of 5-10% — higher than depression, bipolar disorder, or schizophrenia. Yet they are routinely trivialized as vanity problems or phases. Behind the diagnostic labels lives a tangle of neurobiology, trauma, perfectionism, gut dysfunction, and nutrient depletion so intertwined that pulling on any single thread moves all the others.

Functional medicine does not treat eating disorders alone. This must be stated clearly and repeatedly: eating disorders require a multidisciplinary team — psychiatrist, therapist, dietitian, and medical monitor at minimum. What functional medicine offers is the biological layer that traditional treatment often overlooks: the zinc deficiency driving the loss of appetite, the gut devastation perpetuating the symptoms, the hormonal collapse that will not reverse without targeted support.

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The Spectrum

Eating disorders are not monolithic:

• Anorexia nervosa (AN): restriction, fear of weight gain, distorted body image. Restrictive subtype and binge-purge subtype.
• Bulimia nervosa (BN): binge episodes followed by compensatory behaviors — purging, laxatives, excessive exercise, fasting.
• Binge eating disorder (BED): recurrent binge episodes without compensatory behaviors. The most common eating disorder, often invisible.
• ARFID (Avoidant/Restrictive Food Intake Disorder): severe food avoidance based on sensory characteristics, fear of choking/vomiting, or lack of interest. Not driven by body image concerns. Common in autism spectrum and anxiety disorders.
• Orthorexia: obsessive pursuit of “healthy” or “clean” eating that becomes pathologically restrictive. Not yet in the DSM but clinically recognized.

Each requires different nutritional strategies, but all share common biological disruptions.

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The Medical Emergency: Refeeding Syndrome

When a starved body suddenly receives calories, the metabolic shift from catabolic to anabolic state can kill. Insulin surges. Electrolytes — particularly phosphorus, potassium, and magnesium — rush intracellularly. Serum levels plummet. Cardiac arrhythmias follow.

Refeeding syndrome prevention is the first priority in severe malnutrition:

• Start low, go slow: begin at 1000-1200 kcal/day (or even lower in extreme cases), increase by 200-300 kcal every 2-3 days
• Monitor: phosphorus, potassium, magnesium, glucose, and cardiac telemetry for the first 7-14 days
• Supplement prophylactically: phosphorus (if levels <3.0 mg/dL, supplement before refeeding), potassium, magnesium, thiamine (200-300mg IV or oral — before any carbohydrate loading)
• Cardiac monitoring: bradycardia is common in starvation; QTc prolongation can occur during refeeding

This is inpatient medicine. No functional medicine practitioner should manage severe refeeding outside a medical setting.

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Nutritional Deficiencies by Disorder Type

Anorexia Nervosa

The deficiency list reads like a review of the periodic table:

• Zinc: Birmingham et al. (1994) demonstrated that 14mg of supplemental zinc doubled the rate of weight gain in anorexic patients compared to placebo. This single study should have changed treatment protocols worldwide. Zinc deficiency causes loss of taste and smell (anosmia/ageusia), which perpetuates appetite loss. A zinc-deficient person literally cannot taste food properly, reinforcing avoidance.
• Iron and B12: depleted through inadequate intake, often masked by hemoconcentration (dehydration makes blood values appear normal)
• Folate: critical for methylation, mood, and DNA repair
• Calcium and vitamin D: chronic depletion drives the osteoporosis that makes anorexia lethal long after weight restoration — vertebral compression fractures in 30-year-olds
• Essential fatty acids: cell membrane integrity collapses; dry skin, brittle hair, cognitive impairment
• Protein malnutrition: hypoalbuminemia, edema, muscle wasting, impaired wound healing

Bulimia Nervosa

Purging creates specific deficiency patterns:

• Potassium: the most dangerous purging-related deficiency. Hypokalemia causes cardiac arrhythmias. Every bulimic patient needs regular potassium monitoring.
• Sodium and chloride: lost in vomitus
• Magnesium: depleted through vomiting and laxative abuse
• Dental enamel erosion: from gastric acid exposure. Irreversible.
• Esophageal damage: Mallory-Weiss tears, Barrett’s esophagus with chronic exposure

Binge Eating Disorder

Paradoxically, BED patients are often malnourished despite excess calories:

• Magnesium, zinc, chromium: depleted by high-sugar, high-processed-food intake
• Omega-3 to omega-6 ratio: severely skewed toward pro-inflammatory omega-6
• Vitamin D: often low, especially in individuals with higher body fat (vitamin D is fat-soluble, sequestered in adipose)

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The Zinc-Taste Test

The zinc tally test is a simple clinical tool: the patient holds 10mL of aqueous zinc sulfate solution in their mouth. Four possible responses:

1. No taste at all: severe zinc deficiency
2. Delayed mineral/furry taste (after 10+ seconds): moderate deficiency
3. Immediate slight taste: mild deficiency
4. Immediate strong, unpleasant metallic taste: adequate zinc

In anorexia, the cycle is vicious: restriction depletes zinc, zinc depletion kills appetite and taste, impaired taste reinforces restriction. Breaking this cycle with zinc supplementation (15-30mg elemental zinc as zinc picolinate or zinc carnosine, taken away from meals) is one of the highest-yield interventions in ED treatment.

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Gut Complications: The Devastation Below

Starvation, bingeing, and purging each wreak distinct havoc on the GI tract:

Gastroparesis: the stomach loses motility during starvation. Refeeding causes bloating, nausea, and early satiety that patients interpret as confirmation that they “shouldn’t eat.” This is not psychological resistance — it is a paralyzed stomach. Management: small, frequent meals; prokinetics (ginger, motility agents); time and patience.

SIBO (Small Intestinal Bacterial Overgrowth): starvation-induced hypomotility allows bacteria to colonize the small intestine. Bloating, gas, and pain worsen eating aversion. Testing via lactulose breath test; treatment with antimicrobials (rifaximin, herbal protocols).

Constipation: universal in restriction. Laxative abuse creates a dependent, atonic colon. Recovery of bowel function may take months. Magnesium citrate (400-800mg), vitamin C to bowel tolerance, fiber (introduced slowly), adequate hydration, and movement.

Microbiome devastation: starvation produces a distinctive microbiome profile — reduced diversity, increased Methanobrevibacter (methane-producing archaea), decreased Roseburia and Faecalibacterium (butyrate producers). This altered microbiome may independently drive anxiety and food avoidance through the gut-brain axis.

IBS-type symptoms: many eating disorder patients meet criteria for IBS. The question is which came first — sometimes the GI dysfunction preceded and contributed to disordered eating patterns.

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The Gut-Brain Axis in Eating Disorders

Appetite regulation is a hormonal symphony that eating disorders disrupt at every level:

• Ghrelin (the hunger hormone): paradoxically elevated in anorexia — the body screams for food, but the signal is overridden. Chronically elevated ghrelin may contribute to the anxiety and hyperactivity seen in AN.
• Leptin (the satiety hormone): plummets in starvation, contributing to amenorrhea, bone loss, and metabolic slowdown. Does not normalize immediately with weight restoration.
• Peptide YY (PYY): elevated in anorexia, contributing to early satiety and slowed gastric emptying.
• Microbiome composition shifts: certain bacteria produce caseinolytic protease B (ClpB), a protein that mimics alpha-melanocyte-stimulating hormone (a satiety signal). Altered microbiome composition may directly modulate appetite signaling.

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HPA Axis and Hormonal Collapse

Cortisol: chronically elevated in starvation — the body’s stress response to energy deprivation. Elevated cortisol drives bone loss, muscle catabolism, immune suppression, and insomnia.

Amenorrhea: hypothalamic amenorrhea occurs when the brain shuts down the reproductive axis (GnRH suppression) to conserve energy. Not a minor inconvenience — it signals estrogen deficiency, which accelerates bone loss. Return of menses is a key recovery marker but may lag behind weight restoration by months.

Thyroid: the body downregulates T3 (the active thyroid hormone) to slow metabolism during starvation. Low T3 syndrome (euthyroid sick syndrome). Do not treat with thyroid medication — it will increase metabolic demand in a body that cannot afford it. Nutrition restores thyroid function.

Bone loss: the combination of estrogen deficiency, cortisol elevation, calcium/vitamin D depletion, and low body weight produces osteoporosis of a severity normally seen in postmenopausal women — in teenagers and young adults. DEXA scanning is essential. Weight restoration is the only intervention proven to reverse bone loss in anorexia.

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The Serotonin Paradox

Here is a biological twist that helps explain the addictive quality of restriction: caloric restriction temporarily increases the ratio of tryptophan available for brain serotonin synthesis (by reducing competition with other large neutral amino acids for blood-brain barrier transport). In a person with constitutionally low serotonin — which may predispose to anxiety, perfectionism, and obsessive traits — restriction can feel calming.

Conversely, carbohydrate bingeing triggers insulin release, which clears competing amino acids from the blood, increasing tryptophan transport to the brain and boosting serotonin. The binge is serotonin self-medication.

Understanding this removes moral judgment and replaces it with biochemistry: the patient is not weak. They are medicating a neurotransmitter imbalance through the only means their body has found.

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The Functional Medicine Treatment Sequence

Order matters. You cannot do psychological work on a brain that lacks the nutrients to think clearly.

1. Medical stabilization: correct electrolyte abnormalities, prevent refeeding syndrome, cardiac monitoring if indicated
2. Nutritional rehabilitation: gradual caloric increase, protein adequacy (1.2-1.5g/kg goal), balanced macronutrients
3. Gut repair: address gastroparesis, SIBO, constipation, microbiome restoration. Small frequent meals. Prokinetics. Probiotics introduced gradually.
4. Nutrient repletion: zinc (15-30mg elemental), omega-3 (2-4g EPA/DHA), vitamin D (5000 IU, titrate to 50-70 ng/mL), magnesium glycinate (400mg), B-complex (activated forms — methylfolate, methylcobalamin, P5P), iron if deficient
5. Hormonal recovery: monitored through lab work — cortisol normalization, return of menses, thyroid recovery. Most hormonal disruption resolves with adequate nutrition and weight restoration.
6. Psychological work: now the brain has the resources to engage. DBT, family-based treatment, body-based therapies, trauma processing.

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Body Image, Inflammation, and Interoception

Eating disorders distort interoception — the ability to accurately sense and interpret internal body signals. Hunger cues are misread or ignored. Fullness is catastrophized. Emotional states are confused with physical ones.

The polyvagal framework (Porges) applies here: many ED patients live in a dorsal vagal state (freeze/shutdown) or a sympathetic state (anxiety/hypervigilance) with respect to their bodies. The body is not a home — it is a threat. Body-based therapies aim to rebuild ventral vagal safety in relationship to one’s own physical self.

Inflammation may contribute to distorted body perception. Elevated cytokines alter interoceptive processing. The leaky gut that accompanies eating disorders drives systemic inflammation, which drives neuroinflammation, which distorts the very brain circuits responsible for body awareness. Healing the gut may improve body image — not through cognition, but through biology.

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Integrative Therapies

• DBT (Dialectical Behavior Therapy): the gold standard for bulimia and BED. Teaches distress tolerance, emotional regulation, mindfulness, and interpersonal effectiveness.
• Family-Based Treatment (FBT/Maudsley method): the strongest evidence base for adolescent anorexia. Parents take temporary charge of feeding. Removes the burden of food decisions from the patient.
• Body-based therapies: somatic experiencing, sensorimotor psychotherapy, dance/movement therapy. Essential for reconnecting with the body.
• Yoga: Carei et al. (2010) demonstrated that yoga reduced eating disorder symptoms in adolescents. Must be taught with sensitivity — no mirrors, no competitive language, no focus on physical appearance.

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The Practitioner’s Role: Adjunctive, Never Solo

A functional medicine practitioner managing an eating disorder without a full treatment team is practicing outside scope. The severity of medical risk, the complexity of psychological dynamics, and the lethality of these conditions demand collaboration. The functional medicine role is to:

• Identify and correct nutrient deficiencies that perpetuate the disorder
• Repair gut damage that impairs recovery
• Monitor and support hormonal recovery
• Provide the biological foundation for psychological treatment to work
• Communicate regularly with the treatment team

This is not solo medicine. It is ensemble medicine, and the patient’s life may depend on every player knowing their part.

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What if the body you have been fighting is not your enemy, but a messenger — starving not for control, but for the very nutrients that would restore your ability to hear its voice?