vida: extract claims from 2026-05-05-pmc12835689-semaglutide-atypical-anorexia-adolescent-case

- Source: inbox/queue/2026-05-05-pmc12835689-semaglutide-atypical-anorexia-adolescent-case.md
- Domain: health
- Claims: 1, Entities: 0
- Enrichments: 4
- Extracted by: pipeline ingest (OpenRouter anthropic/claude-sonnet-4.5)

Pentagon-Agent: Vida <PIPELINE>

domains/health/glp1-adolescent-eating-disorder-risk-amplified-by-developmental-timing.md

@@ -10,9 +10,16 @@ agent: vida
 sourced_from: health/2025-xx-pmc-glp1-eating-disorders-double-edged-sword.md
 scope: causal
 sourcer: PMC / Journal of Clinical Medicine
-related: ["glp1-eating-disorder-risk-subtype-specific-protective-bed-harmful-restrictive", "glp1-social-media-cosmetic-misuse-creates-eating-disorder-pathway"]
+related: ["glp1-eating-disorder-risk-subtype-specific-protective-bed-harmful-restrictive", "glp1-social-media-cosmetic-misuse-creates-eating-disorder-pathway", "glp1-adolescent-eating-disorder-risk-amplified-by-developmental-timing"]
 ---
 
 # Adolescents face compounded GLP-1 eating disorder risk because ED prevalence peaks during adolescence while social media exposure is highest
 
 The review identifies adolescents as the highest-risk population for GLP-1-induced eating disorder harm through a developmental timing mechanism. Two factors converge: (1) eating disorder prevalence peaks during adolescence, creating a large vulnerable population, and (2) adolescent social media use is highest, maximizing exposure to cosmetic GLP-1 promotion. This creates a compounding risk structure where the population most vulnerable to eating disorder onset is also most exposed to the cultural messaging that drives cosmetic GLP-1 misuse. The review explicitly names adolescents as an at-risk population requiring special consideration, alongside patients obtaining GLP-1s for cosmetic purposes without medical supervision and individuals with prior ED history. This is distinct from general GLP-1 eating disorder risk because it identifies a specific demographic where two independent risk factors (developmental vulnerability + cultural exposure) multiply rather than add.
+
+
+## Supporting Evidence
+
+**Source:** PMC12835689, January 2026
+
+Adolescent case progressed from prescription to life-threatening cardiac complications (bradycardia 38 bpm, pericardial effusion) within 6 months, demonstrating rapid escalation in developmentally vulnerable population. Patient experienced panic attack upon gaining 1 kg followed by suicidal ideation requiring psychiatric hospitalization.

domains/health/glp1-adolescent-prescribing-requires-eating-disorder-screening-because-subclinical-restriction-invisible-without-assessment.md

@@ -0,0 +1,19 @@
+---
+type: claim
+domain: health
+description: Case evidence shows 18-month pre-prescription restrictive substrate went undetected, leading to severe atypical anorexia with cardiac complications within 6 months of semaglutide initiation
+confidence: experimental
+source: PMC12835689 case report, published January 2026
+created: 2026-05-05
+title: GLP-1 adolescent prescribing requires eating disorder screening because subclinical restrictive behaviors are clinically invisible without structured assessment
+agent: vida
+sourced_from: health/2026-05-05-pmc12835689-semaglutide-atypical-anorexia-adolescent-case.md
+scope: structural
+sourcer: PMC12835689
+supports: ["glp1-atypical-anorexia-screening-gap-creates-invisible-high-risk-population", "glp1-eating-disorder-screening-gap-structural-capacity-not-clinical-knowledge"]
+related: ["medical-care-explains-only-10-20-percent-of-health-outcomes-because-behavioral-social-and-genetic-factors-dominate", "glp1-atypical-anorexia-screening-gap-creates-invisible-high-risk-population", "glp1-eating-disorder-screening-gap-structural-capacity-not-clinical-knowledge", "glp1-eating-disorder-screening-protocol-scoff-plus-history-plus-behavioral-assessment-recommended-for-pre-treatment-risk-stratification", "glp1-eating-disorder-pharmacovigilance-signal-class-effect-obesity-population-specific", "glp1-pre-treatment-eating-disorder-screening-recommended-not-required"]
+---
+
+# GLP-1 adolescent prescribing requires eating disorder screening because subclinical restrictive behaviors are clinically invisible without structured assessment
+
+This case report documents an adolescent prescribed semaglutide who developed severe atypical anorexia nervosa with life-threatening cardiac complications (bradycardia 38 bpm, pericardial effusion) within 6 months. The critical finding is that 18 months of pre-prescription restrictive behaviors—increasing exercise, decreasing food intake, distorted body image—were present but undetected by the prescribing general practitioner who conducted no psychological screening. The patient was prescribed semaglutide because she was 'previously on the verge of being overweight with weight-related dysphoria'—language that itself suggests unrecognized eating disorder psychopathology. The proposed mechanism is that semaglutide's appetite suppression combined with underlying eating disorder substrate created compounding restriction effects. This is not evidence of de novo eating disorder induction, but rather a screening failure: the behavioral substrate existed but was invisible to an unscreened prescriber. The severity of the outcome (near-fatal cardiac complications within 6 months) demonstrates that subclinical restrictive patterns, when combined with pharmacological appetite suppression in adolescents, can rapidly progress to medical crisis. The case authors explicitly recommend eating disorder screening before GLP-1 prescription, particularly for distorted body image and restrictive patterns, regardless of BMI.

domains/health/glp1-eating-disorder-screening-protocol-scoff-plus-history-plus-behavioral-assessment-recommended-for-pre-treatment-risk-stratification.md

@@ -11,9 +11,16 @@ sourced_from: health/2026-05-05-pmc12694361-glp1-appetite-eating-disorders-syste
 scope: functional
 sourcer: PMC12694361
 supports: ["glp1-managed-access-operating-systems-require-multi-layer-infrastructure-beyond-formulary"]
-related: ["glp1-eating-disorder-screening-gap-structural-capacity-not-clinical-knowledge", "glp1-pre-treatment-eating-disorder-screening-recommended-not-required", "glp-1-therapy-requires-nutritional-monitoring-infrastructure-but-92-percent-receive-no-dietitian-support", "glp1-social-media-cosmetic-misuse-creates-eating-disorder-pathway", "who-glp1-guideline-omits-eating-disorder-screening-despite-pharmacovigilance-signal", "glp1-eating-disorder-risk-subtype-specific-protective-bed-harmful-restrictive"]
+related: ["glp1-eating-disorder-screening-gap-structural-capacity-not-clinical-knowledge", "glp1-pre-treatment-eating-disorder-screening-recommended-not-required", "glp-1-therapy-requires-nutritional-monitoring-infrastructure-but-92-percent-receive-no-dietitian-support", "glp1-social-media-cosmetic-misuse-creates-eating-disorder-pathway", "who-glp1-guideline-omits-eating-disorder-screening-despite-pharmacovigilance-signal", "glp1-eating-disorder-risk-subtype-specific-protective-bed-harmful-restrictive", "glp1-eating-disorder-screening-lacks-reimbursement-infrastructure-despite-identified-risk-population"]
 ---
 
 # GLP-1 eating disorder screening protocol combining SCOFF questionnaire, recent ED history review, and compensatory behavior assessment is recommended for pre-treatment risk stratification
 
 The systematic review identifies a specific pre-treatment screening protocol for GLP-1 receptor agonist prescribing: (1) SCOFF questionnaire administration, (2) recent ED history review, (3) assessment for compensatory behaviors, and (4) weight-suppression history evaluation. This represents a clinical governance recommendation addressing the 92 percent dietitian support gap documented in existing claims. The review also establishes red flags during treatment: rapid weight loss, dizziness/syncope, escalating restriction, and purging or laxative use. This screening infrastructure addresses the structural capacity gap identified in glp1-eating-disorder-screening-gap-structural-capacity-not-clinical-knowledge. The protocol is positioned as 'recommended' not 'required,' reflecting the absence of regulatory mandate despite clinical consensus. This creates a parallel to the ambient-ai-scribes-create-three-party-liability-exposure-outside-fda-oversight pattern where clinical best practice outpaces regulatory infrastructure.
+
+
+## Extending Evidence
+
+**Source:** PMC12835689, January 2026
+
+Case authors explicitly recommend screening for eating disorder vulnerability—particularly distorted body image and restrictive patterns—before prescribing GLP-1 agonists to adolescents, regardless of BMI. The case demonstrates that 'weight-related dysphoria' language itself may signal unrecognized eating disorder psychopathology requiring assessment.

domains/health/glp1-induced-gi-side-effects-reinforce-existing-purging-cycles-but-no-clinical-evidence-supports-de-novo-eating-disorder-induction.md

@@ -18,3 +18,10 @@ related: ["glp1-gi-side-effects-trigger-purging-behaviors-pharmacological-harm-p
 # GLP-1-induced GI side effects may reinforce pre-existing purging cycles but no clinical evidence supports de novo eating disorder induction in patients without behavioral vulnerability
 
 This systematic review provides the strongest current evidence synthesis on GLP-1 receptor agonists and eating disorder risk. The review explicitly states: 'To date, no clinical evidence links GLP-1RA use to the onset or worsening of AN.' This is a definitive closure of the de novo causation hypothesis for anorexia nervosa. The review identifies that 'gastrointestinal symptoms such as nausea and vomiting may complicate treatment, particularly in patients with purging behaviours, where these side effects could inadvertently reinforce or exacerbate existing cycles' — critically, the qualifier is 'existing cycles,' not new onset. The mechanism requires pre-existing behavioral vulnerability: vulnerability markers include high perfectionism, obsessive-compulsive traits, elevated baseline emotional eating, mixed binge-purge patterns, and weight suppression history. The review characterizes evidence quality as 'low-to-moderate confidence throughout' with BED/BN findings 'preliminary' and restrictive ED evidence 'scarce and inconclusive.' This closes the GI-mediated purging disconfirmation hypothesis from session 36 — the pharmacological pathway requires behavioral substrate.
+
+
+## Supporting Evidence
+
+**Source:** PMC12835689, January 2026
+
+Case report shows 18-month pre-prescription history of restrictive behaviors (increasing exercise, decreasing food intake, distorted body image) that went undetected. Semaglutide worsened existing subclinical restriction rather than creating de novo eating disorder. Patient developed severe atypical AN with cardiac complications (bradycardia 38 bpm, pericardial effusion) within 6 months, but behavioral substrate clearly preceded medication.

domains/health/glp1-starvation-spiral-hypothesis-caloric-deficit-triggers-obsessive-restriction.md

@@ -17,3 +17,10 @@ related: ["glp1-eating-disorder-pharmacovigilance-signal-class-effect-obesity-po
 # GLP-1-mediated caloric deficit may trigger starvation-response restriction through neurobiological misinterpretation of pharmacological appetite suppression as famine
 
 Multiple clinicians quoted in NBC News describe a progression pattern: beneficial appetite suppression → pathological restriction → 'atypical anorexia nervosa' presentation. The proposed mechanism is that the brain 'may interpret dramatic sudden weight loss as starvation, triggering obsessive food thoughts' — a neurobiological feedback loop where pharmacological caloric reduction activates evolutionary starvation-response circuits that then reinforce restriction behavior. The Cynthia Landrau case exemplifies this: 28-year-old consuming 'only about one-third of calories recommended for a woman her age' with 'no mentioned prior ED history' (though absence of evidence is not evidence of absence). This differs from the population-selection hypothesis (GLP-1s prescribed to people with subclinical ED risk) by proposing a direct pharmacological → neurological → behavioral pathway. Critical limitation: 'no mentioned prior history' ≠ 'confirmed no prior history' — the NBC reporter did not probe for subclinical body image concerns or dietary restriction patterns. All evidence is case-report level with no systematic data on incidence rates or risk factors.
+
+
+## Supporting Evidence
+
+**Source:** PMC12835689, January 2026
+
+Patient continued weight loss through restriction for months after discontinuing semaglutide at month 6, losing 20 kg total. Medication discontinuation did not halt restrictive spiral, suggesting pharmacological appetite suppression triggered self-sustaining behavioral restriction pattern.

inbox/archive/health/2026-05-05-pmc12835689-semaglutide-atypical-anorexia-adolescent-case.md

@@ -7,10 +7,13 @@ date: 2026-01-01
 domain: health
 secondary_domains: []
 format: article
-status: unprocessed
+status: processed
+processed_by: vida
+processed_date: 2026-05-05
 priority: high
 tags: [glp-1, semaglutide, eating-disorders, anorexia, atypical-anorexia, case-report, adolescent, screening-failure]
 intake_tier: research-task
+extraction_model: "anthropic/claude-sonnet-4.5"
 ---
 
 ## Content