Eating Disorders

Populations and Risk Factors

Anorexia nervosa: primarily adolescent and young adult women; onset typically 14–18 years; male cases are underdiagnosed (estimated 10–25% of cases); female-to-male ratio approximately 10:1
Bulimia nervosa: onset typically late adolescence to early 20s; female-to-male ratio approximately 10:1; often normal body weight, making recognition more difficult
Binge eating disorder (BED): most common eating disorder; affects men and women more equally (approximately 3:2 female-to-male); associated with obesity; onset typically in early adulthood
Strong genetic component — first-degree relatives have 7–12 times increased risk for anorexia; twin concordance rates 50–80%
Comorbidities: depression (50–75%), anxiety disorders (25–75%), OCD (particularly in anorexia), substance use disorders (particularly in bulimia), personality disorders, PTSD (particularly in those with abuse history)
Survivors of physical, sexual, or emotional abuse — using body weight/control as a coping mechanism
Cultural pressure regarding body image; athletes in weight-sensitive sports (gymnastics, wrestling, dance, running); modeling and entertainment industries
Female athlete triad: eating disorder + amenorrhea + osteoporosis — a specific high-risk clinical entity

Causes and Pathophysiology

Neurochemical and Psychological Drivers

Serotonin dysregulation: Serotonin modulates satiety, mood, and impulse control. In anorexia, caloric restriction paradoxically reduces the anxiety associated with serotonin excess (restricting food reduces serotonin precursors, providing temporary anxiolytic effect — which reinforces the behavior). In bulimia, binge-purge cycles produce rapid serotonin fluctuations that drive the compulsive cycle.
Dopamine reward pathway: The control over food intake activates the dopamine reward system — the sense of control itself becomes addictive. Starvation-induced endorphin release produces a "high" that reinforces restriction.
HPA axis activation: Chronic caloric restriction is a physiological stressor that activates the HPA axis, producing sustained cortisol elevation. This contributes to osteoporosis, muscle catabolism, immune suppression, and the anxiety/depression comorbidity.

Muscle Wasting and Atrophy — The MSK Core

Protein-energy malnutrition (anorexia): Severe caloric restriction forces the body to catabolize muscle protein for gluconeogenesis. Skeletal muscle mass decreases progressively — limb muscles lose bulk first, trunk muscles follow, and eventually cardiac muscle is affected. The wasting is global but most visible in the proximal limb musculature (deltoids, quadriceps, gluteals) and the trunk (erector spinae, abdominal wall).
Myocardial wasting: The heart is a muscle. Prolonged starvation produces myocardial atrophy, reducing cardiac output, causing bradycardia, and predisposing to fatal arrhythmias. Sudden death in anorexia is typically from cardiac failure.
Why this matters for palpation: The muscles are not just thin — they are structurally compromised. Weakened sarcomeres, reduced glycogen stores, and impaired contractile protein mean that even moderate palpation pressure may cause tissue damage that the patient does not perceive (pain thresholds are often altered). Tissue quality on palpation will feel thin, atrophied, and lacking normal contractile resilience.

Bone Density Loss

Mechanism: Three converging pathways destroy bone in eating disorders:

Estrogen deficiency (amenorrhea): Caloric restriction suppresses the hypothalamic-pituitary-gonadal axis, causing estrogen deficiency. Estrogen normally inhibits osteoclast activity — without it, bone resorption exceeds bone formation. Amenorrhea lasting >6 months produces measurable bone density loss.
Cortisol excess: Chronic HPA axis activation from starvation stress produces cortisol that directly inhibits osteoblast function and stimulates osteoclast activity (similar mechanism to glucocorticoid-induced osteoporosis).
Nutritional deficiency: Inadequate calcium, vitamin D, and protein intake removes the building blocks for bone formation.

Clinical consequences: Eating disorder patients — even young women in their 20s — may have bone density equivalent to postmenopausal women. Stress fractures occur with minimal trauma. Vertebral compression fractures produce height loss and kyphotic deformity. The bone fragility is not visible and may not be suspected in a young patient.
Why this matters for MT: Pressure that is safe for a healthy 20-year-old may fracture a bone in an anorexic 20-year-old. Bone fragility is a critical safety parameter that overrides normal pressure-selection guidelines.

Electrolyte Derangement — The Acute Danger

Purging-related electrolyte loss (bulimia): Recurrent vomiting produces loss of gastric acid (hydrochloric acid), causing metabolic alkalosis and hypokalemia (potassium depletion). Laxative and diuretic abuse compounds potassium loss. Potassium is essential for cardiac conduction and muscle contraction.
Hypokalemia effects on muscle: Potassium depletion causes muscle weakness, cramping, and fatigue. Severe hypokalemia (<3.0 mEq/L) can cause paralysis, rhabdomyolysis, and fatal cardiac arrhythmia (ventricular fibrillation).
Why this matters clinically: A bulimic patient who reports recent purging episodes may have acutely dangerous potassium levels. Cardiac arrhythmia is the primary cause of death in bulimia. Symptoms of severe hypokalemia (extreme weakness, palpitations, muscle cramping, confusion) should prompt immediate medical referral.

Fascial Dehydration and Connective Tissue Changes

Chronic dehydration: Inadequate fluid intake, purging, laxative abuse, and diuretic abuse produce chronic dehydration that affects fascial tissue integrity. Fascia requires adequate hydration to maintain its viscoelastic properties — dehydrated fascia becomes brittle, inelastic, and more susceptible to injury. The ground substance of connective tissue (proteoglycans, glycosaminoglycans) loses its gel-like consistency.
Collagen degradation: Protein malnutrition and cortisol excess impair collagen synthesis. Connective tissue (ligaments, tendons, fascial layers) becomes weaker and less resilient. Wound healing is impaired.

Refeeding Syndrome and Recovery Effects

Refeeding edema: When nutritional rehabilitation begins, insulin release promotes sodium and water retention, producing peripheral edema. Fluid shifts can cause rapid weight gain that is alarming to the patient (5–10 lbs in days, which is water, not fat). The edema is transient but may persist for weeks.
Refeeding cardiac risk: Rapid refeeding can cause fatal electrolyte shifts (hypophosphatemia is the most dangerous) leading to cardiac arrhythmia, respiratory failure, and seizures. Patients in early refeeding may be medically fragile even if they appear to be improving.
Why this matters for MT: Patients in recovery may present with edema, tissue sensitivity changes, emotional lability from nutritional and hormonal fluctuations, and ongoing bone/muscle fragility. Recovery does not immediately restore tissue integrity — bone density takes years to recover (if it ever fully does), and muscle rebuilding requires months of adequate nutrition and progressive exercise.

Signs and Symptoms

Anorexia Nervosa — Physical Findings

Extreme thinness (BMI <17.5); wasted proximal musculature (deltoids, quadriceps, gluteals visible through skin)
Lanugo — fine, downy hair on face, trunk, and extremities (body's attempt to insulate against heat loss)
Dry, flaky skin; brittle nails; hair loss on scalp
Amenorrhea (loss of menses) — indicates estrogen deficiency
Hypothermia — basal metabolic rate is reduced; cold extremities, cold intolerance
Bradycardia (HR <60 bpm) — from myocardial wasting and metabolic conservation
Height loss from vertebral compression fractures; history of stress fractures
Sunken eyes; temporal wasting (temporalis muscle atrophy visible as hollow temples)

Bulimia Nervosa — Physical Findings

Often normal body weight — the disorder may be invisible
Russell's sign — calluses or scarring on the dorsum of the hand (from fingers contacting teeth during induced vomiting)
Parotid gland swelling (bilateral) — "chipmunk cheeks" from repeated vomiting
Dental erosion (lingual surfaces) from gastric acid exposure
Esophageal damage — Barrett's esophagus, Mallory-Weiss tears
Metabolic alkalosis from vomiting; hypokalemia; electrolyte instability

Musculoskeletal Findings Common to Both

Muscle wasting — proximal more than distal; trunk more visible in severe cases
Postural deterioration — increased thoracic kyphosis from vertebral compression fractures and trunk muscle weakness; forward head from cervical extensor weakness
Tissue fragility — bones, muscles, and connective tissue are structurally compromised
Dehydration signs: reduced skin turgor (skin tenting when pinched), dry mucous membranes, sunken eyes
In recovery: peripheral edema from refeeding; tissue sensitivity changes; ongoing fragility despite improved nutrition

Comparison Table

Feature	Anorexia Nervosa	Bulimia Nervosa	Binge Eating Disorder
Body weight	Severely underweight (BMI <17.5)	Often normal	Often overweight/obese
Key physical sign	Lanugo, extreme thinness, amenorrhea	Russell's sign, parotid swelling, dental erosion	No characteristic physical sign
Cardiac risk	Myocardial wasting → bradycardia, arrhythmia	Electrolyte derangement → arrhythmia	Obesity-related cardiovascular disease
Bone risk	Severe — osteoporosis from amenorrhea + cortisol + malnutrition	Moderate — less estrogen disruption but cortisol and nutritional deficiency present	Low — bone density usually preserved
Muscle wasting	Severe — progressive skeletal and cardiac muscle atrophy	Moderate — less caloric restriction but nutrient malabsorption	Minimal — muscle mass usually preserved
MT pressure concern	Critical — bone fracture risk, muscle tissue fragility, dehydration	Moderate — electrolyte effects on muscle function, dehydration	Standard — adjust for obesity-related considerations

Assessment Profile

Subjective Presentation

Chief complaint: May present with musculoskeletal symptoms without disclosing the eating disorder: "My back aches all the time." "I'm always cold and tired." "I keep getting stress fractures." Some patients will disclose: "I'm in recovery from anorexia." Others may present for relaxation without connecting their physical state to the eating disorder.
Pain quality: Diffuse aching from muscle wasting and deconditioning; bone pain from osteoporosis or stress fractures; abdominal cramping (GI dysmotility from malnutrition or electrolyte derangement); jaw pain from purging (TMJ stress from repeated vomiting)
Onset: Physical symptoms develop insidiously over months to years as the nutritional deficit accumulates; bone complications may not become apparent until a fracture occurs; patients in recovery may experience new symptoms as the body refeeds and rehydrates
Aggravating factors: Physical activity (stress fractures, muscle fatigue from wasting), cold environments (hypothermia, poor thermoregulation), prolonged standing (orthostatic intolerance), emotional stress about body/appearance
Easing factors: Warmth (compensates for hypothermia), rest (limited muscle reserve fatigues quickly), gentle touch (provides positive body experience), nutritional improvement (gradual)
Red flags: Irregular heartbeat, palpitations, or chest pain → cardiac arrhythmia from electrolyte derangement; emergency referral; do not treat. Severe dizziness or syncope on standing → orthostatic hypotension (dehydration/cardiac compromise); do not treat until medically cleared. Extreme emaciation with inability to maintain body temperature → medical emergency. Report of recent purging with muscle weakness/cramping → possible acute hypokalemia; defer treatment and refer.

Observation

Local inspection: Anorexia: visible wasting — bony prominences (clavicles, ribs, iliac crests, scapulae) prominently visible; lanugo on face/trunk; dry skin; brittle hair; temporal wasting (hollow temples); edema in recovery. Bulimia: often normal appearance; parotid swelling; Russell's sign on hands; dental erosion if mouth is open. BED: may show obesity-related findings. General: look for dehydration signs, cold/mottled extremities, signs of self-harm (scars, bruising — comorbidity).
Posture: Increased thoracic kyphosis (vertebral compression from osteoporosis and trunk muscle weakness); forward head from cervical extensor weakness; overall postural deterioration proportional to severity and duration; in severe anorexia, the patient may appear frail and unstable
Gait: May show generalized weakness — slow, cautious, wide-based gait from muscle wasting and deconditioning; orthostatic instability (swaying or needing support on standing); no specific antalgic pattern unless a stress fracture is present

Palpation

Tone: Globally hypotonic from muscle wasting — muscles feel thin, atrophied, and lacking normal contractile tone; proximal muscles (deltoids, quadriceps, gluteals) most affected; trunk musculature (erector spinae, abdominal wall) wasted in severe cases; no hypertonicity pattern (the neuromuscular system lacks the protein substrate to maintain tone). In bulimia with less caloric restriction, tone may be closer to normal but with fatigue and cramping from electrolyte effects. In recovery, tone gradually improves with nutritional rehabilitation but lags behind weight restoration.
Tenderness: Bony prominences are tender and poorly padded — direct pressure over clavicles, ribs, iliac crests, spinous processes may be painful even with light contact; muscle tenderness may be present from metabolic waste accumulation in deconditioned tissue; abdominal tenderness from GI dysmotility and organ compression; tenderness threshold may be altered (heightened or blunted depending on pain processing changes from malnutrition).
Temperature: Cool extremities — reduced basal metabolic rate and poor peripheral circulation; may feel cold to touch bilaterally; hypothermia is common in severe anorexia; warmth at bony prominences does not indicate inflammation — it reflects reduced subcutaneous insulation
Tissue quality: Critical finding — tissue fragility. Skin is thin, dry, and fragile (tears easily); subcutaneous tissue is minimal (bony prominences palpable with no cushioning); muscle tissue is atrophied, soft, and lacking normal elastic resilience; fascial tissue is dehydrated and inelastic; connective tissue (ligaments, tendons) is weakened from collagen degradation; edema may be present in recovery (pitting edema in lower extremities from refeeding). Skin turgor test: gently pinch dorsal hand skin — if the skin fold persists >2 seconds, significant dehydration is present.

Motion Assessment

AROM: Reduced range from muscle weakness and deconditioning rather than structural restriction; proximal weakness limits shoulder elevation, hip flexion strength, and trunk rotation; movements are slow and effortful; may show compensatory patterns (using momentum rather than muscle control); thoracic extension limited from kyphotic change (may be structural if vertebral compression fractures are present)
PROM / end-feel: Tissue-stretch end-feel in most directions — no capsular restriction unless comorbid OA from altered joint loading; PROM exceeds AROM significantly (the difference reflects muscle weakness, not guarding); end-feel at bony limits may be reached earlier than expected if vertebral compression or other bony changes are present; use caution with PROM — do not apply force to osteoporotic bones; gentle passive movement only
Resisted testing: Weakness — true strength deficit from muscle atrophy and protein malnutrition; generalized and proximal-dominant (not myotomal); grip strength markedly reduced; fatigability is extreme (strength drops rapidly with repetition); in bulimia, acute hypokalemia may produce sudden weakness or cramping during testing

Special Test Cluster

Eating disorders produce musculoskeletal findings through malnutrition-driven tissue degradation rather than structural injury. The cluster below screens for the severity of systemic compromise, identifies safety parameters for treatment, and rules out conditions that may coexist.

Test	Positive Finding	Purpose
Vital signs (resting HR, BP, orthostatic BP) (CMTO)	Bradycardia <60 bpm (anorexia); orthostatic drop >20 mmHg systolic on standing; irregular pulse	Screen for cardiac compromise and orthostatic instability; irregular pulse → do not treat; refer for ECG
Skin turgor test (CMTO)	Skin fold on dorsal hand persists >2 seconds after release	Quantify dehydration severity; dehydrated tissue is more fragile
Grip strength (dynamometry) (supplementary)	Markedly reduced compared to age/sex norms	Objective marker of muscle wasting severity; trackable outcome
Postural assessment (CMTO)	Increased thoracic kyphosis, forward head; may show height loss from vertebral compression	Document structural changes; kyphosis that does not correct with cueing may indicate vertebral compression fracture
Bone fragility screen (history) (CMTO — red flag)	History of stress fractures, vertebral compression, height loss >2 cm; amenorrhea >6 months	Identifies bone fragility — modify pressure to prevent fracture; refer for DEXA scan if not already done

Critical safety note: If the patient presents with irregular pulse, severe orthostatic hypotension (systolic drop >20 mmHg), recent purging with muscle weakness, or extreme emaciation, defer treatment and refer for medical evaluation. These findings indicate acute systemic compromise that makes massage therapy inappropriate until stabilized.

Differential Assessment

Condition	Key Distinguishing Feature
Cancer cachexia	Progressive wasting with anorexia but without body image distortion or food restriction behavior; unexplained weight loss; may have palpable mass, lymphadenopathy, or abnormal blood work; refer for medical evaluation if wasting without known eating disorder
Hyperthyroidism	Weight loss, tachycardia (opposite of anorexia's bradycardia), tremor, heat intolerance; elevated T3/T4 with suppressed TSH; no body image distortion
Malabsorption syndromes (celiac disease, Crohn's)	Weight loss and nutritional deficiency but with GI symptoms (diarrhea, bloating) and without food restriction behavior; laboratory markers (anti-tTG for celiac, CRP/ESR for Crohn's)
Addison disease	Weight loss, fatigue, hypotension, hyperpigmentation; cortisol deficiency (opposite of the elevated cortisol in eating disorders); electrolyte pattern differs (hyperkalemia vs. hypokalemia)
Depression (with appetite loss)	Weight loss from reduced appetite but without body image distortion, purging behavior, or deliberate restriction; flexion posture from psychomotor retardation rather than structural weakness

CMTO Exam Relevance

Classified as a mental health condition with critical medical/systemic consequences
Key differentiation: Anorexia (extreme thinness, lanugo, amenorrhea, bradycardia) vs. bulimia (normal weight, Russell's sign, parotid swelling, dental erosion, electrolyte derangement) vs. BED (obesity, no purging, no characteristic physical signs)
Cardiac red flags are the priority: Bradycardia <60 bpm, irregular pulse, severe orthostatic hypotension → do not treat; refer
Bone fragility: Amenorrhea >6 months + eating disorder = presume osteoporosis until proven otherwise; modify all pressure parameters
Electrolyte awareness: Hypokalemia from purging causes muscle weakness, cramping, and fatal arrhythmia — understand the mechanism (metabolic alkalosis from HCl loss → renal potassium wasting)
Female athlete triad (eating disorder + amenorrhea + osteoporosis) is a commonly tested concept
Understand refeeding syndrome — rapid nutritional rehabilitation can cause fatal electrolyte shifts (hypophosphatemia)

Massage Therapy Considerations

Primary therapeutic target: Providing a safe, nurturing, positive body experience. For many eating disorder patients, massage therapy may be the only context in which they experience their body in a positive, non-judgmental way. The therapeutic value of appropriate touch for patients with disturbed body image should not be underestimated — but it must be delivered within strict safety parameters dictated by tissue fragility.
Sequencing logic: Safety assessment first (vital signs, orthostatic screen, tissue integrity assessment), then conservative treatment within safety parameters. The MSK benefits of massage (improved circulation, gentle tissue mobilization, parasympathetic activation) are secondary to the psychological benefit and must never compromise safety.
Safety / contraindications:
Bone fragility: Presume osteoporosis in any patient with amenorrhea >6 months and eating disorder history. Use light pressure only — no deep tissue, no sustained compression over bony prominences, no joint mobilization without imaging confirmation of bone integrity.
Cardiac compromise: Bradycardia <60 bpm, irregular pulse, or orthostatic drop >20 mmHg systolic → do not treat; refer. Check vitals before every session in known eating disorder patients.
Electrolyte instability: Recent purging with weakness or cramping → defer and refer. Do not treat until medically stable.
Dehydration: Dehydrated tissue tears easily — reduce pressure, increase lubrication, avoid deep friction techniques.
Refeeding edema: Gentle effleurage is appropriate; do not use aggressive lymphatic drainage on refeeding edema (the edema is physiological, not pathological).
Emotional safety: Body image distortion means the patient may have intense anxiety about being unclothed, touched, or assessed. Offer maximum draping, work through clothing if preferred, start with non-threatening areas (arms, hands, feet, upper back).
Heat/cold guidance: Warmth is essential — eating disorder patients are often hypothermic and cold-intolerant; heated table, warm room, warm blankets, moist heat packs. These patients cannot thermoregulate effectively. Cold is absolutely contraindicated — it compounds hypothermia and increases discomfort.

Treatment Plan Foundation

Clinical Goals

Provide a positive, nurturing body experience that counteracts body image disturbance
Gently improve circulation and tissue quality within the constraints of tissue fragility
Promote parasympathetic activation and reduce anxiety associated with body awareness
Address postural deterioration through gentle positioning and supported movement, not aggressive correction

Position

Patient chooses — offer prone, supine, side-lying; some patients prefer to remain partially clothed or fully draped; respect all preferences without question
Maximum bolstering — bony prominences must be padded; standard table padding may be insufficient for severely emaciated patients — add foam padding, folded towels, or gel pads under bony areas (iliac crests, greater trochanters, clavicles, sacrum, ankles)
Heated table or warm blankets — hypothermia is common; warmth is both therapeutic and necessary for basic comfort
Position changes should be minimized and assisted — orthostatic instability makes transitions risky

Session Sequence

Vital sign check — resting HR, BP, orthostatic BP if any concern; do not proceed if HR <50, irregular pulse, or orthostatic drop >20 mmHg systolic
Warming contact — place hands on upper back with gentle, steady warmth; no pressure; allow the patient to settle; assess skin quality and tissue tolerance through this initial contact
Gentle effleurage to the upper back — light pressure using broad-contact palms; assess tissue resilience — if the skin blanches easily or feels paper-thin, further reduce pressure; use ample lubrication to reduce shear stress on fragile skin
Upper extremity work — arms, forearms, hands; these are non-threatening areas with relatively preserved tissue in most patients; gentle kneading and effleurage; provides positive sensory input without vulnerability concerns
Lower extremity work — gentle effleurage to legs and feet; assess for edema (refeeding) and skin integrity; avoid deep pressure over tibial crest, fibular head, and other poorly padded bony prominences; compression stockings may be in use — work around or over them
Posterior trunk — gentle broad-surface techniques along the erector spinae; avoid direct pressure over spinous processes (vertebral compression fracture risk); assess for kyphotic deformity; do not attempt postural correction through force
Gentle scalp and face massage — [if the patient is receptive] — provides nurturing sensory input; temporal region massage addresses temporal wasting discomfort; jaw work only if bruxism/purging-related TMJ involvement is present
Closing — warm blanket; allow extended rest; assist with sitting up slowly (orthostatic risk); check in: "How does your body feel right now?"

Adjunct Modalities

Hydrotherapy: Warmth is the primary modality — heated table, warm blankets, moist heat packs to shoulders and low back. The hydrotherapy goal is thermoregulation and comfort, not tissue preparation for deep work. Cold is absolutely contraindicated — hypothermia risk.
Remedial exercise (on-table): Extremely gentle active-assisted ROM if the patient is able — shoulder circles, ankle pumps, gentle cervical rotation. Purpose is to maintain joint mobility and provide proprioceptive input, not strengthening (the nutritional substrate for muscle building may not yet be present). Diaphragmatic breathing instruction — gentle, without pressure; do not emphasize abdominal expansion (body awareness of the abdomen can be anxiety-provoking for eating disorder patients).

Exam Station Notes

Demonstrate awareness of tissue fragility — verbalize: "Given the patient's nutritional status, I'm going to use light pressure throughout and avoid direct compression over bony prominences to protect bone integrity"
Perform vital sign screening — the examiner expects to see HR, BP, and orthostatic assessment before treatment; identify and verbalize red flags
Demonstrate sensitivity to body image — offer draping choices, work through clothing if preferred, explain techniques before performing them
Show understanding of cardiac/electrolyte red flags — verbalize criteria for deferring treatment

Verbal Notes

Session framing: "My goal today is to help your body feel comfortable and relaxed. We'll go at whatever pace feels right for you. If any area is sensitive or you'd prefer I skip it, just let me know."
Pressure calibration: "I'm using very light pressure. I want to make sure this feels nurturing rather than uncomfortable. Let me know if you'd like any adjustments."
Body-positive language: Avoid any comments about the patient's body size, shape, weight, or appearance. Do not comment on how thin they are, how much weight they've gained or lost, or any changes in appearance. Focus language on sensation: "How does this feel?" not "Your muscles look/feel [descriptor]."
Post-treatment: "Take your time sitting up — I'll be right here if you feel lightheaded. How do you feel?"

Self-Care

Warm baths or warm showers — thermoregulation support; improves circulation; provides positive body sensation in a private, self-directed context; water temperature should be warm but not hot (reduced thermoregulation means burn risk)
Gentle walking — 10–15 minutes at a comfortable pace if medically cleared; improves circulation, mood, and maintains muscle function; do not recommend vigorous exercise (eating disorder patients may compulsively over-exercise as a compensatory behavior — any exercise recommendation should be coordinated with the patient's treatment team)
Self-massage to hands, feet, and forearms — provides positive body contact in a self-directed context; use moisturizing cream to address skin dryness
Nutritional rehabilitation compliance — this is the foundational self-care; all other interventions are secondary to adequate nutrition; reinforce that the treatment team's nutritional plan is the priority without lecturing or moralizing

Key Takeaways

Eating disorders carry the highest mortality rate of any psychiatric illness — primarily from cardiac arrhythmia (electrolyte derangement in bulimia, myocardial wasting in anorexia) and suicide; cardiac screening before every treatment session is essential
Tissue fragility is the primary safety parameter — bone density loss (presume osteoporosis with amenorrhea >6 months), muscle atrophy, dehydrated fascia, and fragile skin require light pressure throughout; standard deep tissue techniques are contraindicated
The key differentiation is anorexia (extreme thinness, lanugo, amenorrhea, bradycardia) versus bulimia (normal weight, Russell's sign, parotid swelling, dental erosion, hypokalemia) versus BED (obesity, no purging)
Electrolyte derangement from purging (hypokalemia → muscle dysfunction, cardiac arrhythmia; metabolic alkalosis) is the most acute danger — irregular pulse or recent purging with weakness → defer treatment and refer
The primary therapeutic value of massage for eating disorder patients is providing a positive, nurturing body experience in a context where the body has been a source of distress — this psychological benefit is as important as any musculoskeletal effect
Refeeding syndrome can cause fatal electrolyte shifts — patients in early recovery may be medically fragile despite appearing to improve; coordinate care with the treatment team