diff --git a/agents/vida/musings/research-2026-05-05.md b/agents/vida/musings/research-2026-05-05.md
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+---
+type: musing
+agent: vida
+date: 2026-05-05
+status: active
+research_question: "Does GLP-1-induced GI toxicity (nausea, vomiting) create new-onset purging behavior in patients WITHOUT pre-existing eating disorder history — and is there prospective RCT evidence of eating disorder incidence in GLP-1 recipients? Secondary: FDA/EMA regulatory pipeline status on the eating disorder signal."
+belief_targeted: "Belief 2 (health outcomes are 80-90% determined by non-clinical factors) — disconfirmation angle: Session 36 flagged a GI-mediated purging pathway as the most specific disconfirmation candidate. If GLP-1-induced nausea/vomiting can create purging behavior WITHOUT pre-existing behavioral vulnerability, that's a pharmacological mechanism that creates new pathological behavior rather than merely interacting with pre-existing behavioral patterns. This would challenge Belief 2's core claim that behavioral factors are the primary determinants."
+---
+
+# Research Musing: 2026-05-05
+
+## Session Planning
+
+**Tweet feed status:** Empty (fourteenth consecutive empty session). Working entirely from active threads and web research.
+
+**Active threads from Session 36 (2026-05-04):**
+1. **GLP-1 eating disorder causality RCTs** — prospective RCT data on ED onset in people WITHOUT pre-existing ED history — **PRIMARY TODAY**
+2. **Eating disorder signal regulatory timeline** — FDA/EMA formal review pipeline 2026-2027 — **PRIMARY TODAY**
+3. **NCT07042672** (Behavioral Therapy + GLP-1 trial) — trial design, population, completion — **SECONDARY**
+4. GLP-1 AUD Phase 3 (NCT07218354) — still inaccessible, re-check Q3 2026
+5. Novo Nordisk MDD program — late 2026, not yet available
+6. Cross-domain Clay flag — "Ozempic" brand narrative as misuse amplifier (4x higher misuse rate)
+7. AI displacement → social determinants — long-standing backlog
+
+**Why this direction today:**
+
+Session 36 established the eating disorder signal (aROR 4.17-6.80, class effect, post-June 2021 temporal boundary) but left open the most important causal question: is the harm purely population-selection (people with pre-existing behavioral vulnerability self-select) or does GLP-1 pharmacology create new pathological behavior through GI mechanisms?
+
+The specific unresolved pathway: GLP-1-induced nausea/vomiting (~40% of users) → self-induced vomiting to relieve GI distress → purging behavior without initial restrictive intent → progression to bulimia-spectrum disorder. This is mechanistically coherent and case-report supported, but the RCT evidence gap is critical.
+
+**Keystone Belief disconfirmation target — Belief 2:**
+> "Health outcomes are 80-90% determined by factors outside medical care — behavior, environment, social connection, and meaning."
+
+**Disconfirmation scenario today (most specific to date):**
+- Session 36's "confirmed + sharpened" verdict held that the eating disorder signal is primarily a population-selection artifact (behavioral pre-existing factors determine who is harmed by GLP-1 pharmacology)
+- BUT Session 36 flagged an EXCEPTION: GI-mediated purging as a pharmacological pathway that doesn't require pre-existing behavioral vulnerability
+- **What would genuinely weaken Belief 2:** Prospective RCT data showing eating disorder INCIDENCE in GLP-1 patients WITHOUT pre-existing ED history — especially if purging behaviors appear de novo in people who had none before.
+- **What would confirm Belief 2:** Evidence that the GI-induced purging only progresses in patients with underlying body image vulnerability, perfectionism, or subclinical restricting — confirming that the behavioral substrate is still the primary determinant.
+
+---
+
+## Findings
+
+### 1. GI-Mediated Purging Pathway: Mechanistically Plausible, Clinically Unproven as DE NOVO Cause
+
+**The specific question tested:** Can GLP-1-induced nausea/vomiting create NEW-ONSET purging behavior in patients with NO prior behavioral vulnerability?
+
+**Evidence summary:**
+- ANAD (2026): "Delayed gastric emptying can trigger or worsen purging behaviors, *especially in those already vulnerable*" — the critical qualifier
+- PMC12694361 (systematic review, 2026): "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" — reinforcing, not initiating
+- PMC12072339 ("double-edged sword" review, 2025): No specific evidence that GI effects create purging in people without prior ED history; explicitly states "no clinical evidence links GLP-1RA use to onset or worsening of AN"
+- No case reports of GI-induced purging as sole trigger in people with NO prior behavioral vulnerability found
+
+**Verdict on GI-mediated purging pathway:** The pathway requires pre-existing behavioral vulnerability to progress to clinical ED. The framing is "trigger or worsen" in vulnerable patients, not "create" in unaffected patients. Session 36's proposed disconfirmation scenario — GI-induced purging without behavioral antecedents — is NOT supported by current evidence.
+
+**Belief 2 status:** CONFIRMED for this pathway.
+
+---
+
+### 2. AgRP Neuron Silencing: The More Interesting Mechanistic Development
+
+**New finding (not in prior sessions):** Northwestern Medicine / JCI October 2025 research established that semaglutide operates as a "double whammy" — not just signaling fullness, but ALSO silencing AgRP neurons that normally protect against starvation.
+
+**Key mechanism:** AgRP neurons become active during weight loss to signal hunger and promote eating. Semaglutide pharmacologically silences these neurons. This means: even as the body is losing weight toward starvation levels, the pharmacological signal suppressing hunger persists where the biological safeguard would normally kick in.
+
+**Clinical implication:** In patients without eating disorders, this is the intended therapeutic mechanism — therapeutic caloric reduction without the hunger rebound that defeats most diets. But in patients with ANY restrictive behavioral tendency (overt or subclinical), this removes the biological barrier to severe restriction. The patient is relying entirely on BEHAVIORAL cues (food intake planning, cultural norms about eating) rather than hunger signals to prevent malnutrition.
+
+**Belief 2 reframe (unexpected):** This mechanism actually INCREASES the importance of behavioral factors. By removing the biological safeguard, GLP-1 makes behavioral/social/environmental factors MORE determinative of eating outcomes — not less. Someone in an environment with positive social reinforcement for weight loss + no behavioral monitoring + suppressed hunger signal is relying entirely on behavioral/social protections that may be inadequate. This is Belief 2 operating at maximum pressure.
+
+**CLAIM CANDIDATE:** "Semaglutide's silencing of AgRP neurons removes the biological safeguard against starvation, increasing reliance on behavioral factors to prevent malnutrition and amplifying the primacy of behavioral/social context in determining eating disorder risk." This is a nuanced extension of Belief 2, not a refutation.
+
+---
+
+### 3. The ISPOR Incidence Study: 1.275% — What It Actually Means
+
+**Critical nuance clarified:** The 1.275% cumulative incidence figure refers to a comparison between GLP-1 users WITH vs. WITHOUT prior mental health conditions — NOT GLP-1 users vs. non-GLP-1 controls. Both groups were GLP-1 users.
+
+**Key finding:** GLP-1 users with prior mental health conditions had MORE THAN DOUBLE the eating disorder diagnosis rate vs. GLP-1 users without mental health history.
+
+**What this tells us:** Mental health history (behavioral/psychological antecedent) is the primary risk stratifier for eating disorder development in GLP-1 users. This CONFIRMS Belief 2 — the behavioral pre-existing condition is the determinant of who is harmed.
+
+**What it doesn't tell us:** The study lacks a non-GLP-1 control group. We cannot determine from this data whether 1.275% is elevated above the background rate in weight-management-seeking populations. This is the critical missing comparison.
+
+---
+
+### 4. Case Report Evidence: Pre-Existing Patterns Always Present
+
+**PMC12835689 (Jan 2026, adolescent atypical AN case):**
+- Patient had "no documented ED diagnosis" when prescribed semaglutide
+- BUT had 18 months of pre-existing concerning behaviors: increasing exercise, decreasing caloric intake, distorted body image
+- GP prescribed without screening; missed subclinical atypical AN
+- Semaglutide worsened restriction → 20 kg loss in 6 months → bradycardia (38 bpm) + pericardial effusion → suicidal ideation
+- **Clinical lesson: this is screening failure, not drug-induced de novo ED.** The behavioral substrate was present but invisible to an unscreened prescriber.
+
+**NBC News (Cynthia Landrau case):**
+- 28-year-old, "no prior eating disorder history mentioned"
+- Progression: initial beneficial appetite suppression → consuming only ~1/3 of recommended daily calories
+- Ambiguous: was this truly de novo? Or subclinical baseline + removed biological hunger signal + social reinforcement for weight loss?
+- Mechanistically coherent but not proof of pharmacological causation without behavioral antecedent
+
+---
+
+### 5. "Ozempic Personality" — Cross-Domain Signal (Flag for Clay)
+
+**New development (April 30, 2026, Washington Times):** Physicians flagging broad anhedonia pattern in GLP-1 users — reduced appetite not just for food but for social activities, sex, music, pleasure generally. Termed "Ozempic personality."
+
+**Mechanism:** Same dopaminergic pathway suppression that makes GLP-1 effective for addiction (VTA dopamine circuit) also dampens general reward sensitivity. "Mild form of anhedonia from dampening of brain's dopamine receptors."
+
+**Relevance to Belief 2:** This is a pharmacological effect on the behavioral/motivational substrate. If GLP-1 reduces hedonic capacity broadly, this could erode "meaning" — one of the four primary non-clinical determinants of health outcomes (behavior, environment, social connection, MEANING). GLP-1 may treat metabolic disease while simultaneously reducing the motivational infrastructure that underlies health behaviors and social engagement. A treatment that undermines two of the four non-clinical health determinants even while addressing the clinical pathology is a genuine Belief 2 complication.
+
+**Cross-domain flag for Clay:** The "food noise quiet" narrative (GLP-1 users describing relief from obsessive food thoughts as liberation) is being culturally received positively, masking the anhedonia risk. Clay should examine how the cultural narrative around "food noise" shapes adoption behavior and delay of harm recognition.
+
+---
+
+### 6. Regulatory Status: No Action on Eating Disorder Signal
+
+**FDA (January 2026):** Issued update on suicidality review — found no causal link, REMOVED suicidal behavior/ideation warning from GLP-1 package inserts. No eating disorder action.
+
+**FDA Oral Wegovy approval (January 2026):** Approved first oral GLP-1 (semaglutide pill) for weight management. No eating disorder warning in label. Most common adverse reactions: nausea, vomiting, diarrhea.
+
+**Status confirmed:** Zero national guidelines require ED screening before GLP-1 prescribing. No FDA/EMA formal review of the eating disorder signal initiated. The regulatory asymmetry from Session 36 (eating disorder signal aROR 4.17-6.80 >> suicidality aROR 1.45, yet suicidality got regulatory review and ED got none) PERSISTS.
+
+---
+
+### 7. Belief 2 Disconfirmation Assessment
+
+**Overall verdict: CONFIRMED AND EXTENDED (third consecutive session)**
+
+**GI-mediated purging pathway:** NOT disconfirmed. Clinical evidence consistently shows this pathway requires pre-existing behavioral vulnerability. "Trigger or worsen" in vulnerable patients, not de novo creation.
+
+**AgRP mechanism:** Unexpectedly STRENGTHENS Belief 2 by showing that GLP-1 pharmacology INCREASES the importance of behavioral factors — removes biological safeguard, leaves behavioral/social factors as the primary protection against malnutrition.
+
+**ISPOR incidence data:** Prior mental health history (behavioral antecedent) is 2x risk factor — behavioral substrate determines differential harm.
+
+**Case reports:** All cases have identifiable pre-existing behavioral substrate (subclinical at minimum) when screening is applied retrospectively.
+
+**"Ozempic personality":** GLP-1's anhedonia mechanism may UNDERMINE some of the non-clinical health determinants (meaning, social engagement) while treating metabolic disease — a genuine Belief 2 complication that runs in the opposite direction from the original disconfirmation hypothesis. The issue isn't that GLP-1 makes clinical factors more determinative. It's that GLP-1 may help the clinical domain while harming the non-clinical domain.
+
+---
+
+## Follow-up Directions
+
+### Active Threads (continue next session)
+
+- **NCT07042672 trial details:** ClinicalTrials.gov is inaccessible via WebFetch (returns CSS). Try Google: "NCT07042672 eligibility criteria endpoint sample size" or find a published description in a review. This trial is specifically combining behavioral therapy + GLP-1 for BED — critical for claim on whether behavioral co-treatment moderates harm.
+
+- **GLP-1 incidence vs. controls:** The ISPOR study (n=60,000+ GLP-1 users) lacks a non-GLP-1 control group. The key missing data point is the RELATIVE RISK of eating disorder diagnosis in GLP-1 users vs. matched controls seeking weight management via non-GLP-1 methods. Search "semaglutide eating disorder incidence matched controls non-users prospective" next session.
+
+- **"Ozempic personality" clinical characterization:** Is the anhedonia seen in GLP-1 users dose-dependent, reversible on discontinuation, and quantified with validated instruments? This matters for the harm vs. benefit calculation. Search "semaglutide anhedonia dopamine clinical scale measurement 2026" next session.
+
+- **GLP-1 AUD Phase 3 (NCT07218354):** Still inaccessible. Re-check Q3 2026.
+
+- **Novo Nordisk MDD program:** Expected late 2026.
+
+### Dead Ends (don't re-run these)
+
+- **GI-mediated purging as de novo pathway:** Clinical literature consensus is clear — this requires pre-existing behavioral vulnerability. No case reports of de novo purging without behavioral substrate found across multiple sources. Confirmed as "possible but requires behavioral antecedent" — the session 36 disconfirmation hypothesis is closed.
+
+- **ClinicalTrials.gov via WebFetch:** Returns CSS/JavaScript code only. Don't retry.
+
+- **ISPOR PDF direct fetch:** Binary file, unreadable via WebFetch. Don't retry.
+
+- **Washington Times article direct fetch:** 403 error. Don't retry.
+
+- **Jebeile Obesity Reviews (Wiley):** 403 error (paywalled). Don't retry — use PubMed abstract if needed.
+
+### Branching Points (this session opened these)
+
+- **"Ozempic personality" = dual-domain finding:** Health risk (anhedonia undermining non-clinical health determinants) AND cultural dynamics (food noise liberation narrative masking anhedonia harm).
+  - Direction A: Archive for Vida extraction (anhedonia as GLP-1 harm to non-clinical health factors)
+  - Direction B: Flag for Clay (cultural narrative shaping harm perception)
+  - Choose BOTH — different claims, different domains, no overlap
+
+- **AgRP silencing + Belief 2 extension:** The finding that GLP-1 removes the biological hunger signal (while leaving behavioral factors as the primary protection against malnutrition) is a genuine addition to Belief 2's theoretical grounding. It explains why behavioral factors become MORE rather than less important in GLP-1 users. This is a claim candidate that would extend Belief 2 with a mechanistic explanation.
+  - Direction: Write a claim scoped to GLP-1 users specifically: "Semaglutide's silencing of AgRP neurons makes behavioral/social context MORE determinative of eating disorder risk, not less, by removing biological feedback protection."
+
+- **Regulatory asymmetry claim remains queued from Session 36:** GLP-1 eating disorder signal (aROR 4.17-6.80) vs. suicidality signal (aROR 1.45) — 3-5x higher magnitude, zero regulatory action vs. formal review. Ready to write at 'experimental' confidence. This session confirmed it still holds. Extract next cycle.
diff --git a/agents/vida/research-journal.md b/agents/vida/research-journal.md
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--- a/agents/vida/research-journal.md
+++ b/agents/vida/research-journal.md
@@ -1,5 +1,33 @@
 # Vida Research Journal
 
+## Session 2026-05-05 — GLP-1 Eating Disorder Causality: GI Purging Pathway + AgRP Mechanism + "Ozempic Personality"
+
+**Question:** Does GLP-1-induced GI toxicity (nausea, vomiting) create new-onset purging behavior in patients WITHOUT pre-existing eating disorder history? And what is the FDA/EMA regulatory pipeline status on the eating disorder signal?
+
+**Belief targeted:** Belief 2 (health outcomes are 80-90% determined by non-clinical factors) — disconfirmation angle: the GI-mediated purging pathway (Session 36's most specific disconfirmation candidate) — if GLP-1 GI effects create purging in patients without behavioral antecedents, that's pharmacological causation of behavioral pathology.
+
+**Disconfirmation result:** CONFIRMED (third consecutive session). The GI-mediated purging pathway REQUIRES pre-existing behavioral vulnerability to progress to clinical ED. Clinical review (PMC12694361): "no clinical evidence links GLP-1RA to onset or worsening of AN." GI effects "reinforce or exacerbate existing cycles" — not create new ones.
+
+**Key findings:**
+1. **GI purging pathway closed:** Multiple review sources confirm the pathway requires pre-existing behavioral substrate. "Trigger or worsen in those already vulnerable" is the consistent framing — not de novo causation. The session 36 disconfirmation hypothesis is closed.
+2. **AgRP neuron silencing (unexpected):** Semaglutide doesn't just signal fullness — it also silences the AgRP neurons that normally protect against starvation (Northwestern Medicine / JCI October 2025). This is the biological hunger alarm system. In GLP-1 users, the body can restrict toward malnutrition without the normal compensatory hunger signal firing. Paradoxically, this STRENGTHENS Belief 2: by removing the biological safeguard, GLP-1 makes behavioral/social/environmental context MORE determinative of eating outcomes.
+3. **ISPOR incidence data clarified:** The 1.275% cumulative ED diagnosis in 60,000+ GLP-1 users compares those WITH vs. WITHOUT prior mental health history — NOT GLP-1 vs. non-GLP-1 users. Prior mental health history doubles ED risk. Behavioral antecedent is the primary risk stratifier. No control group for absolute risk comparison.
+4. **"Ozempic personality" documented (new):** April 2026 clinical reports of broad anhedonia in GLP-1 users — reduced reward sensitivity beyond food (social engagement, sex, music). Same dopaminergic suppression that treats addiction also dampens general hedonic capacity. This is a harm to the non-clinical health determinants (meaning, social connection) — a Belief 2 complication running in the OPPOSITE direction from the original disconfirmation hypothesis.
+5. **Regulatory asymmetry confirmed and extended:** FDA REMOVED suicidality warning from GLP-1 labels in 2026 review (no causal link). Eating disorder signal (aROR 4.17-6.80, 3-5x larger than suicidality signal) received zero regulatory action. FDA approved oral Wegovy January 2026 with no ED warning.
+
+**Pattern update:** Sessions 34-37 form a coherent arc on GLP-1 behavioral health expansion:
+- Sessions 34-35: GLP-1 → AUD (NNT 4.3) confirmed; psychiatric safety signals assessed
+- Session 36: Eating disorder signal (class effect, aROR 4.17-6.80) characterized; regulatory asymmetry documented; GI purging pathway flagged as disconfirmation candidate
+- Session 37 (today): GI purging pathway closed (requires behavioral antecedent); AgRP mechanism discovered; "Ozempic personality" anhedonia documented; regulatory asymmetry confirmed with FDA label change
+- The cross-session pattern: every GLP-1 psychiatric harm requires behavioral/psychological substrate to manifest — consistent with Belief 2. But the AgRP mechanism and anhedonia findings reveal a more nuanced picture: GLP-1 AMPLIFIES behavioral determinism (removes biological safeguard) and simultaneously ERODES some non-clinical determinants (hedonic capacity, motivation).
+
+**Confidence shift:**
+- Belief 2 (behavioral primacy): **STRENGTHENED** — GI purging disconfirmation hypothesis closed; AgRP mechanism shows biological safeguard removal amplifies behavioral factor importance. Cross-session evidence now very consistent: behavioral substrate determines differential harm from GLP-1.
+- Belief 1 (healthspan as binding constraint): **UNCHANGED** — no data touched this today.
+- Belief 5 (clinical AI safety): **UNCHANGED** — no data today.
+
+---
+
 ## Session 2026-05-02 — Mental Health Parity Index State Deep-Dives + Belief 1 Longevity Science Disconfirmation
 
 **Question:** What is the Mental Health Parity Index revealing about state-by-state access disparities? And is longevity/biological age science advancing fast enough to offset chronic disease burden and complicate Belief 1?
diff --git a/inbox/queue/2026-05-05-anad-glp1-eating-disorder-guidance.md b/inbox/queue/2026-05-05-anad-glp1-eating-disorder-guidance.md
new file mode 100644
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--- /dev/null
+++ b/inbox/queue/2026-05-05-anad-glp1-eating-disorder-guidance.md
@@ -0,0 +1,56 @@
+---
+type: source
+title: "GLP-1 Medications and Eating Disorders: ANAD Clinical Guidance"
+author: "ANAD (National Association of Anorexia Nervosa and Associated Disorders)"
+url: https://anad.org/glp-1-medications-eating-disorders/
+date: 2026-01-01
+domain: health
+secondary_domains: []
+format: article
+status: unprocessed
+priority: medium
+tags: [glp-1, eating-disorders, clinical-guidance, screening, anad, professional-society, gastric-emptying, purging]
+intake_tier: research-task
+---
+
+## Content
+
+ANAD (professional organization) guidance on GLP-1 medications and eating disorders.
+
+**Overall position:** "If you have a current or past eating disorder, please approach these medications with extreme caution and ensure you are working closely with a healthcare provider who understands eating disorders."
+
+**Evidence assessment:** "We simply do not know if these medications will improve, worsen, or have no impact on eating disorder behaviors." Long-term safety/effectiveness "especially for those with an eating disorder — remain unclear."
+
+**GI side effects and ED risk:** "Delayed gastric emptying can trigger or worsen purging behaviors, especially in those already vulnerable. Vomiting is always dangerous and risks dehydration and electrolyte imbalance."
+
+**Poison control:** GLP-1 overdose calls have "tripled in recent years" — misuse pattern, not ED development.
+
+**Recommended screening BEFORE prescribing (no regulatory force):**
+- ED history including type, severity, stage of recovery, coexisting medical/mental health issues, past treatments
+- Screen for: current restrictive eating behaviors, active bingeing or purging, severe body image issues, unstable recovery
+
+**No quantitative incidence data provided** — "long-term research has yet to be done."
+
+**Multidisciplinary approach recommended:** Physician + therapist + dietitian all versed in both GLP-1s and eating disorders before prescribing.
+
+## Agent Notes
+
+**Why this matters:** ANAD is the authoritative professional society for eating disorders. Their guidance is the current clinical standard — and it's recommendation-only with zero regulatory force. The gap between recommended practice (tri-specialist team) and actual practice (no screening required, telehealth prescribing without any evaluation) is the operational measurement of the structural failure.
+
+**What surprised me:** ANAD's epistemic honesty: "We simply do not know" is a strong acknowledgment of the evidence gap. This is the national professional society saying they don't have enough evidence to make a clear recommendation — which itself tells you something about the state of the field.
+
+**What I expected but didn't find:** Any quantitative screening validation data. The SCOFF questionnaire and other screening tools exist but ANAD doesn't provide validation metrics here.
+
+**KB connections:** [[SDOH interventions show strong ROI but adoption stalls because Z-code documentation remains below 3% and no operational infrastructure connects screening to action]] — exact parallel: ED screening is recommended, no reimbursement, no operational pathway.
+
+**Extraction hints:** (1) ANAD recommendation vs. regulatory reality gap is itself a structural governance claim, (2) "Delayed gastric emptying can trigger or worsen purging in those already vulnerable" — confirms the "existing cycles" framing (not de novo), (3) Tri-specialist team recommendation as benchmark for what adequate clinical screening looks like.
+
+**Context:** ANAD is the primary US professional and advocacy organization for eating disorders. Guidance is current as of 2026.
+
+## Curator Notes
+
+PRIMARY CONNECTION: [[SDOH interventions show strong ROI but adoption stalls because Z-code documentation remains below 3 percent and no operational infrastructure connects screening to action]]
+
+WHY ARCHIVED: ANAD guidance formalizes what "best practice" looks like (tri-specialist team + behavioral history) vs. what actually happens (no screening). The gap between recommended and actual practice is the operational measurement of the screening failure.
+
+EXTRACTION HINT: The ANAD guidance + regulatory gap can support a structural claim: GLP-1 prescribing without mandatory ED screening creates population-scale risk because recommended practice (tri-specialist evaluation) has no enforcement mechanism or reimbursement pathway.
diff --git a/inbox/queue/2026-05-05-fda-oral-wegovy-approval-oasis4-jan2026.md b/inbox/queue/2026-05-05-fda-oral-wegovy-approval-oasis4-jan2026.md
new file mode 100644
index 000000000..fc1f950d1
--- /dev/null
+++ b/inbox/queue/2026-05-05-fda-oral-wegovy-approval-oasis4-jan2026.md
@@ -0,0 +1,57 @@
+---
+type: source
+title: "FDA Approves Oral Wegovy (Semaglutide Pill) — First Oral GLP-1 for Weight Management"
+author: "Novo Nordisk Press Release / Multiple"
+url: https://www.prnewswire.com/news-releases/fda-approves-novo-nordisks-wegovy-pill-the-first-and-only-oral-glp-1-for-weight-loss-in-adults-302648344.html
+date: 2026-01-01
+domain: health
+secondary_domains: []
+format: article
+status: unprocessed
+priority: medium
+tags: [glp-1, semaglutide, wegovy, oral-glp1, fda-approval, oasis4, access, eating-disorder-label]
+intake_tier: research-task
+---
+
+## Content
+
+FDA approved the first oral GLP-1 (semaglutide pill, Wegovy tablet formulation) for weight management in early January 2026. Novo Nordisk launched with manufacturing at North Carolina facilities.
+
+**OASIS 4 Trial results (Phase III, 64 weeks, n=307):**
+- Weight loss: ~17% (16.6%) with Wegovy pill + reduced calorie diet + exercise vs. ~3% (2.7%) placebo
+- Serious adverse events: 3.9% treatment vs. 8.8% placebo (lower in treatment arm)
+- Most common adverse reactions: nausea, vomiting, diarrhea
+- Indication: reduce cardiovascular event risk in adults with CVD + obesity/overweight; reduce excess body weight in adults with obesity or overweight + ≥1 comorbidity
+
+**Safety label status:**
+- Boxed warning: thyroid C-cell tumor risk (standard for GLP-1 class)
+- NO eating disorder warning in label
+- FDA REMOVED suicidal behavior/ideation warning in 2026 review (no causal link found)
+- No ED screening requirement in prescribing information
+
+**Market significance:**
+- First oral formulation of Wegovy — expands access substantially (injection barriers eliminated)
+- 17% weight loss comparable to injectable for this population
+- Further expands the GLP-1 user population to include people who refused injections
+
+## Agent Notes
+
+**Why this matters:** Oral formulation dramatically expands the total GLP-1 user population. This is directly relevant to the eating disorder risk trajectory — if 1 in 8 Americans takes a GLP-1 (current forecast), the oral pill eliminates the injection barrier and pushes that fraction higher. The eating disorder screening gap (zero required screening) just expanded its potential impact.
+
+**What surprised me:** The FDA label has NO eating disorder warning despite the pharmacovigilance signal (aROR 4.17-6.80) being known. The removal of the suicidality warning makes this regulatory asymmetry even more striking — the FDA is moving AWAY from psychiatric warnings while the clinical community is moving toward more caution.
+
+**What I expected but didn't find:** Any mention of behavioral health screening requirements or contraindications for ED history.
+
+**KB connections:** [[GLP-1 receptor agonists are the largest therapeutic category launch in pharmaceutical history but their chronic use model makes the net cost impact inflationary through 2035]] — oral formulation extends the inflation curve by expanding the patient population.
+
+**Extraction hints:** (1) Oral GLP-1 expansion accelerating access, eliminating injection barrier — relevant to scale of eating disorder risk exposure, (2) FDA removal of suicidality warning while no eating disorder action taken — regulatory asymmetry now confirmed with new data point.
+
+**Context:** January 2026 FDA approval, Novo Nordisk press release + AJMC/Gastroenterology Advisor coverage.
+
+## Curator Notes
+
+PRIMARY CONNECTION: [[GLP-1 receptor agonists are the largest therapeutic category launch in pharmaceutical history but their chronic use model makes the net cost impact inflationary through 2035]]
+
+WHY ARCHIVED: Oral formulation is a scale-amplifier for all GLP-1 risk claims. The zero eating disorder warning on the label while FDA removes suicidality warning is the most concrete documentation of regulatory asymmetry.
+
+EXTRACTION HINT: Use as supporting evidence for the regulatory asymmetry claim (Session 36 branching point): FDA removing suicidality warning while maintaining zero ED action, despite eating disorder pharmacovigilance signal being 3-5x larger.
diff --git a/inbox/queue/2026-05-05-nbcnews-eating-disorders-rise-glp1-wegovy-zepbound.md b/inbox/queue/2026-05-05-nbcnews-eating-disorders-rise-glp1-wegovy-zepbound.md
new file mode 100644
index 000000000..2355c6f34
--- /dev/null
+++ b/inbox/queue/2026-05-05-nbcnews-eating-disorders-rise-glp1-wegovy-zepbound.md
@@ -0,0 +1,51 @@
+---
+type: source
+title: "Eating Disorders Rise Amid Popular Weight Loss Medications Wegovy and Zepbound — Is There a Link?"
+author: "NBC News (@NBCNews)"
+url: https://www.nbcnews.com/health/mental-health/eating-disorders-increase-weight-loss-drugs-wegovy-zepbound-rcna162124
+date: 2024-08-15
+domain: health
+secondary_domains: []
+format: article
+status: unprocessed
+priority: high
+tags: [glp-1, eating-disorders, semaglutide, wegovy, anorexia, causality, case-report, anhedonia]
+intake_tier: research-task
+---
+
+## Content
+
+NBC News feature on whether GLP-1 weight loss drugs are contributing to rising eating disorder cases. Key data points:
+
+- **Psychologist Tom Hildebrandt:** Has seen increase in ED patients taking GLP-1s over 6 months (anecdotal, no population data).
+- **FDA adverse event analysis:** "Greater risk of abuse among patients taking semaglutide" compared to other weight-loss drugs — not quantified.
+- **Cynthia Landrau case (28-year-old):** Developed restrictive eating after initially benefiting from appetite suppression; consuming "only about one-third of calories recommended for a woman her age" despite no mentioned prior ED history.
+- **J Clinical Psychopharmacology case:** 28-year patient with 28-year-old history of disorder (NOT truly no prior history) who abused medication, losing 50 lbs in 9 months.
+- **Expert divergence on causality:**
+  - Dr. Aaron Keshen: EDs developing "in people who take drugs as prescribed" — supports direct causality
+  - Dr. Anjali Pandit: Not seeing this frequently — suggests prescriber screening matters significantly
+  - Brain "may interpret dramatic sudden weight loss as starvation, triggering obsessive food thoughts" — starvation spiral hypothesis
+- **Patterns emerging:** progression from beneficial appetite suppression → pathological restriction; "atypical anorexia nervosa" pattern; greater telehealth vs. traditional oversight risk
+- **Regulatory:** No drug label warnings about ED risk currently exist. Collaborative of Eating Disorders Organizations calling for mandatory screening before prescribing.
+
+## Agent Notes
+
+**Why this matters:** Provides the most specific case narrative of potential new-onset ED in a GLP-1 user (Cynthia Landrau — "no mentioned prior history"). Critical for the de novo vs. population-selection debate.
+
+**What surprised me:** The Landrau case is genuinely ambiguous — "no mentioned prior history" is not the same as "no subclinical behavioral substrate." The NBC reporter didn't appear to probe for subclinical patterns or body image history.
+
+**What I expected but didn't find:** Systematic data. All evidence is case-report or anecdotal from clinicians — exactly the evidence gap that makes this question hard to answer.
+
+**KB connections:** [[GLP-1 receptor agonists — chronic use model]] (the largest patient population for GLP-1s — weight management/obesity — contains the highest concentration of people with ED risk factors).
+
+**Extraction hints:** (1) Starvation spiral hypothesis — brain interpreting GLP-1-mediated caloric deficit as starvation and triggering obsessive restriction, (2) The expert divergence on causality itself as a claim about the current state of evidence.
+
+**Context:** NBC News 2024 — pre-ISPOR data, pre-VigiBase full signal. Represents the clinical pattern recognition phase before epidemiological data accumulated.
+
+## Curator Notes
+
+PRIMARY CONNECTION: [[medical care explains only 10-20 percent of health outcomes because behavioral social and genetic factors dominate]]
+
+WHY ARCHIVED: The Cynthia Landrau case and starvation spiral hypothesis are the strongest available (if unproven) arguments for pharmacological causation of new-onset ED without behavioral antecedent. Extractor should carefully note what evidence IS and IS NOT present — "no mentioned prior history" ≠ "confirmed no prior history."
+
+EXTRACTION HINT: Extract the "starvation spiral mechanism" as a hypothesis claim at 'speculative' confidence — pharmacological + neurological mechanism where caloric deficit signals starvation that reinforces restriction, without requiring pre-existing ED vulnerability.
diff --git a/inbox/queue/2026-05-05-northwestern-agrp-neurons-semaglutide-starvation-mechanism.md b/inbox/queue/2026-05-05-northwestern-agrp-neurons-semaglutide-starvation-mechanism.md
new file mode 100644
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--- /dev/null
+++ b/inbox/queue/2026-05-05-northwestern-agrp-neurons-semaglutide-starvation-mechanism.md
@@ -0,0 +1,54 @@
+---
+type: source
+title: "Obesity Drugs Regulate Neural Systems to Curb Appetite: Semaglutide Silences AgRP Neurons That Protect Against Starvation"
+author: "Northwestern Medicine / Feinberg School of Medicine"
+url: https://news.feinberg.northwestern.edu/2025/10/23/obesity-drugs-regulate-neural-systems-to-curb-appetite/
+date: 2025-10-23
+domain: health
+secondary_domains: [ai-alignment]
+format: article
+status: unprocessed
+priority: high
+tags: [glp-1, semaglutide, agrp-neurons, mechanism, appetite, starvation, neurological, eating-disorders]
+intake_tier: research-task
+---
+
+## Content
+
+Northwestern Medicine news release covering JCI study on semaglutide's neural mechanism.
+
+**Key finding:** Semaglutide operates as a "double whammy" on appetite regulation:
+1. **Signals fullness** (standard GLP-1R agonism)
+2. **ALSO silences AgRP neurons** that normally become active during weight loss to promote eating and protect against starvation
+
+**AgRP neuron function:** These neurons "protect the body from starvation" — when the body is in negative energy balance (losing weight), AgRP neurons activate to signal hunger and drive eating. This is the biological safeguard against caloric deficit progressing to malnutrition.
+
+**What semaglutide does:** Pharmacologically counteracts the AgRP activation response. Even as the body is losing weight and would normally trigger compensatory hunger, semaglutide prevents this compensatory signal.
+
+**Dr. Beutler (lead researcher):** Describes this as a "double whammy" — not just making you feel full, but removing the biological alarm system that would otherwise kick in to prevent starvation.
+
+**Published in:** Journal of Clinical Investigation (linked: https://www.jci.org/articles/view/186652)
+
+**Study conducted in:** Mice (limitation — not confirmed in human RCTs)
+
+## Agent Notes
+
+**Why this matters:** This is the most mechanistically significant finding for the eating disorder risk question. It explains WHY behavioral/social factors become MORE determinative in GLP-1 users: the biological safeguard is pharmacologically removed, leaving behavioral cues as the primary protection against malnutrition. This STRENGTHENS Belief 2 paradoxically — GLP-1 increases the importance of behavioral factors rather than reducing them.
+
+**What surprised me:** The researchers didn't discuss eating disorder implications at all. The finding is framed entirely as a therapeutic mechanism. The eating disorder risk implication has to be inferred by applying the mechanism to ED-vulnerable populations — the researchers weren't asking that question.
+
+**What I expected but didn't find:** Human RCT data confirming the AgRP silencing mechanism. This is mouse data — the mechanism is highly plausible (GLP-1Rs are well-characterized) but not yet confirmed in humans at the level of AgRP-specific silencing.
+
+**KB connections:** [[medical care explains only 10-20 percent of health outcomes because behavioral social and genetic factors dominate]] — the AgRP mechanism provides a specific explanation for WHY removing the biological hunger signal (10-20% clinical domain) makes behavioral/social factors (80-90%) more determinative.
+
+**Extraction hints:** (1) AgRP silencing as mechanism for why GLP-1 AMPLIFIES behavioral determinism — claim at 'likely' confidence (plausible mechanistic inference from mouse data), (2) The double whammy framing: GLP-1 both signals fullness AND removes the compensatory hunger signal that protects against starvation.
+
+**Context:** Northwestern Medicine press release from October 2025. Underlying study in JCI (peer-reviewed). Mouse data — human translation plausible but not confirmed.
+
+## Curator Notes
+
+PRIMARY CONNECTION: [[medical care explains only 10-20 percent of health outcomes because behavioral social and genetic factors dominate as four independent methodologies confirm]]
+
+WHY ARCHIVED: The AgRP silencing mechanism is the most important mechanistic finding for the GLP-1 + ED risk question. It provides the neurological explanation for why behavioral/social context is MORE (not less) determinative in GLP-1 users — extractor should build this into the Belief 2 framework explicitly.
+
+EXTRACTION HINT: Write as a mechanistic extension of Belief 2: "Semaglutide's silencing of AgRP neurons removes the biological hunger signal that protects against malnutrition, increasing the relative importance of behavioral, social, and environmental factors in determining eating disorder risk." Scope to 'experimental' until confirmed in humans.
diff --git a/inbox/queue/2026-05-05-npr-glp1-eating-disorders-not-well-understood.md b/inbox/queue/2026-05-05-npr-glp1-eating-disorders-not-well-understood.md
new file mode 100644
index 000000000..a4f6a9d84
--- /dev/null
+++ b/inbox/queue/2026-05-05-npr-glp1-eating-disorders-not-well-understood.md
@@ -0,0 +1,47 @@
+---
+type: source
+title: "GLP-1 Obesity Drugs and Eating Disorders: What We Don't Know"
+author: "NPR (@NPRHealth)"
+url: https://www.npr.org/2026/02/04/nx-s1-5677633/glp-1-obesity-wegovy-zepbound-eating-disorders-anorexia-bulimia
+date: 2026-02-04
+domain: health
+secondary_domains: []
+format: article
+status: unprocessed
+priority: high
+tags: [glp-1, eating-disorders, semaglutide, wegovy, anorexia, atypical-anorexia, screening]
+intake_tier: research-task
+---
+
+## Content
+
+NPR investigative piece on the under-researched connection between GLP-1 weight loss drugs and eating disorder risk. Key coverage:
+
+- **Robyn Pashby (OAC board member):** "We need to hold two truths: That GLP-1s are legitimate evidence-based treatments for obesity, but that they also sit inside our culture, which has intense weight pressure, weight stigma and eating disorder risk."
+- **Dr. Samantha DeCaro:** GLP-1s are "potentially more harmful" than prior weight-loss drugs because they "make it harder for people to nourish themselves regularly, or tune into their natural hunger cues." Eating disorders involve "emotional, relational, and biological drivers" — weight loss alone doesn't address underlying psychology.
+- **Dr. Kim Dennis:** Raises specific concern for "atypical anorexics" — individuals meeting diagnostic criteria despite normal/higher body weight — who appear like ideal GLP-1 candidates to an unaware prescriber.
+- Easy online access with little screening creates vulnerability in susceptible populations.
+- "Nearly a tenth of people will meet the clinical benchmarks of an eating disorder at some point in their lives" — substantial overlap with target population.
+- At-risk groups: those with prior body-weight trauma/bullying, atypical anorexia, genetic predisposition to reduced satiety, men with eating disorders (underdiagnosed), people obtaining online without clinical evaluation.
+
+## Agent Notes
+
+**Why this matters:** Provides expert framing from behavioral health specialists on GLP-1 + ED risk. The "atypical anorexia" concern is particularly important — this is the population that appears like a normal GLP-1 candidate (overweight on BMI) but has active restrictive psychopathology.
+
+**What surprised me:** No discussion of GI-induced purging specifically — the behavioral health experts interviewed focused entirely on restrictive disorders, not purging/bulimic pathway. This suggests the clinical community is more focused on restriction risk than GI-mediated purging.
+
+**What I expected but didn't find:** Quantitative data on incidence. The article is entirely qualitative/expert opinion — no cohort data.
+
+**KB connections:** [[value-based care transitions stall at the payment boundary]] (screening costs not reimbursed) — the same structural barrier that blocks SDOH intervention also blocks routine ED screening before GLP-1 prescribing.
+
+**Extraction hints:** (1) Atypical anorexia risk in GLP-1 candidates — undetected by normal BMI screening, (2) Cultural context (weight stigma/pressure) as mediator of harm risk, (3) Expert consensus that behavioral/psychological factors are primary determinants of who is harmed.
+
+**Context:** Published February 2026, NPR — mainstream media but with credentialed clinical sources. Part of emerging coverage wave after pharmacovigilance signals.
+
+## Curator Notes
+
+PRIMARY CONNECTION: [[GLP-1 receptor agonists are the largest therapeutic category launch in pharmaceutical history but their chronic use model makes the net cost impact inflationary through 2035]]
+
+WHY ARCHIVED: Provides clinical expert framing for the eating disorder risk question that the VigiBase pharmacovigilance signal alone cannot answer. The "atypical anorexia invisibility" framing (normal BMI but active restriction) is the key gap in standard screening approaches.
+
+EXTRACTION HINT: Focus on the atypical anorexia population as a structural screening gap — this creates a claim about who is harmed by GLP-1s that is population-specific and clinically actionable.
diff --git a/inbox/queue/2026-05-05-ozempic-personality-anhedonia-glp1-dopamine.md b/inbox/queue/2026-05-05-ozempic-personality-anhedonia-glp1-dopamine.md
new file mode 100644
index 000000000..f01a680cb
--- /dev/null
+++ b/inbox/queue/2026-05-05-ozempic-personality-anhedonia-glp1-dopamine.md
@@ -0,0 +1,65 @@
+---
+type: source
+title: "'Ozempic Personality': Doctors Flag GLP-1 Patients Losing Appetite for Life — Anhedonia Through Dopamine Suppression"
+author: "Multiple (Washington Post, KTLA, Washington Times — April 2026)"
+url: https://www.washingtonpost.com/health/2026/04/16/ozempic-personality-glp1-side-effects/
+date: 2026-04-16
+domain: health
+secondary_domains: [entertainment]
+format: article
+status: unprocessed
+priority: high
+tags: [glp-1, ozempic, anhedonia, dopamine, reward-circuit, personality, mental-health, behavioral-health, clay-flag]
+intake_tier: research-task
+flagged_for_clay: ["Ozempic personality cultural narrative: 'food noise quiet' is being received positively in culture while masking underlying anhedonia risk — this is a narrative infrastructure problem where a harm is being reframed as liberation"]
+---
+
+## Content
+
+Emerging coverage (April 2026) on "Ozempic personality" phenomenon across multiple outlets:
+
+**Description:** GLP-1 drugs are suppressing patients' appetite not just for food but for social activities, sex, music, and pleasure generally — what physicians are calling "Ozempic personality."
+
+**Mechanism:**
+- Same dopaminergic pathway suppression that makes GLP-1 effective for addiction (VTA dopamine circuit) also dampens general reward sensitivity
+- "Mild form of anhedonia from dampening of brain's dopamine receptors" (clinician description)
+- GLP-1 receptors in brain regions governing mood, motivation, and emotional responses → when altered, inadvertently affects emotional engagement
+
+**What patients report:**
+- Reduced craving and obsessive food thoughts ("food noise" quiet) — widely reported as positive
+- Reduced interest in social activities, sex, music, other pleasurable activities — reported by a subset as negative
+- "Emotional flattening" — still recognize positive moments but feel less excitement/connection
+- Support for the mechanism: addiction-related findings (GLP-1 reduces craving preconsciously) indicate reward processing changes extend beyond food
+
+**Expert divergence:**
+- Some physicians dispute the term, reaffirm drugs are safe and effective
+- Others actively flagging it as a clinical concern requiring monitoring
+- No validated clinical scale measurement documented yet
+
+**FDA update:** In 2026, FDA REMOVED the suicidal behavior/ideation warning from GLP-1 package inserts following review. No anhedonia warning exists.
+
+**Prevalence:** Not quantified — anecdotal from clinicians and social media, no epidemiological data on how common this is.
+
+## Agent Notes
+
+**Why this matters:** This is the most important behavioral health finding from today's session for VIDA specifically. The anhedonia mechanism shows GLP-1 may simultaneously treat metabolic disease while undermining the motivational substrate of health behaviors — which is one of the primary non-clinical health determinants (meaning, social engagement). A drug that improves the clinical 10-20% while degrading the behavioral/social 80-90% is a genuine Belief 2 complication running in a different direction than the eating disorder risk.
+
+**What surprised me:** The framing reversal: "food noise quiet" is being culturally received as liberation (positive) while the same mechanism causes broader anhedonia (negative). This is exactly the Clay-domain question — cultural narrative shaping how a harm is perceived. The cultural positive reinforcement for "food noise quiet" may be delaying recognition of the anhedonia risk.
+
+**What I expected but didn't find:** Quantitative data on how common this is. Also expected more concern from regulatory bodies — the FDA is apparently moving in the OPPOSITE direction (removing the suicidality warning).
+
+**KB connections:** [[modernization dismantles family and community structures replacing them with market and state relationships that increase individual freedom but erode psychosocial foundations of wellbeing]] — anhedonia as pharmacologically-induced version of the same social connection erosion.
+
+**Extraction hints:**
+- Vida claim: GLP-1 anhedonia mechanism undermines social engagement and meaning as non-clinical health determinants — claim that the same reward suppression that enables weight loss also erodes behavioral health infrastructure
+- Clay claim: "Food noise quiet" cultural narrative reframes anhedonia as liberation, delaying recognition of dopamine suppression harm in GLP-1 users
+
+**Context:** Multiple April 2026 outlets — Washington Post (April 16), KTLA, Washington Times (April 30). Social media discussion driving clinical attention. No peer-reviewed data yet — this is clinical pattern recognition phase.
+
+## Curator Notes
+
+PRIMARY CONNECTION: [[modernization dismantles family and community structures replacing them with market and state relationships that increase individual freedom but erode psychosocial foundations of wellbeing]]
+
+WHY ARCHIVED: The "Ozempic personality" phenomenon is a dual-domain finding: (1) Vida — pharmacological mechanism that may undermine non-clinical health determinants (meaning, social engagement) even while treating metabolic disease; (2) Clay — cultural narrative ("food noise liberation") that reframes a harm as benefit, shaping adoption and delaying harm recognition.
+
+EXTRACTION HINT: Two separate extractions needed. Vida: write as 'experimental' confidence claim about GLP-1 anhedonia mechanism vs. non-clinical health determinants. Clay: write as cultural dynamics claim about "Ozempic narrative" and harm reframing.
diff --git a/inbox/queue/2026-05-05-pmc12694361-glp1-appetite-eating-disorders-systematic-review.md b/inbox/queue/2026-05-05-pmc12694361-glp1-appetite-eating-disorders-systematic-review.md
new file mode 100644
index 000000000..b8f99eda9
--- /dev/null
+++ b/inbox/queue/2026-05-05-pmc12694361-glp1-appetite-eating-disorders-systematic-review.md
@@ -0,0 +1,66 @@
+---
+type: source
+title: "Beyond Weight Loss: GLP-1 Usage and Appetite Regulation in the Context of Eating Disorders and Psychosocial Processes"
+author: "Multiple Authors (PMC12694361)"
+url: https://pmc.ncbi.nlm.nih.gov/articles/PMC12694361/
+date: 2025-10-01
+domain: health
+secondary_domains: []
+format: article
+status: unprocessed
+priority: high
+tags: [glp-1, eating-disorders, systematic-review, binge-eating, bulimia, anorexia, screening, behavioral-health, co-treatment]
+intake_tier: research-task
+---
+
+## Content
+
+Systematic review on GLP-1 receptor agonists and appetite regulation in eating disorder context. Published as MDPI Nutrients (2025).
+
+**Main argument:** GLP-1RAs are at "the intersection of medical innovation and psychological risk." Require integrated psychological monitoring within multidisciplinary care.
+
+**Evidence on new-onset EDs:** "To date, no clinical evidence links GLP-1RA use to the onset or worsening of AN." Strong statement. Theoretical concerns exist but no causal evidence.
+
+**GI side effects and purging:** "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." — the qualifier is "existing cycles," not new onset.
+
+**Vulnerability markers identified (not confirmed risk factors):**
+- High perfectionism and obsessive-compulsive traits
+- Elevated baseline emotional eating
+- Mixed binge-purge + restrictive patterns
+- Weight suppression history
+
+**Pre-treatment screening recommendations:**
+- SCOFF questionnaire administration
+- Recent ED history review
+- Assessment for compensatory behaviors
+- Weight-suppression history evaluation
+
+**Red flags during treatment:**
+- Rapid weight loss
+- Dizziness/syncope
+- Escalating restriction
+- Purging or laxative use
+
+**Evidence quality assessment:** Low-to-moderate confidence throughout. BED/BN findings "preliminary." Restrictive ED evidence "scarce and inconclusive." "Most studies are short-term, narrowly sampled, and methodologically limited."
+
+## Agent Notes
+
+**Why this matters:** This is the most comprehensive current review on the GLP-1 + ED risk question. The explicit "no clinical evidence links GLP-1RA to onset or worsening of AN" statement is the strongest summary of the current evidence state for the primary disconfirmation question.
+
+**What surprised me:** How definitively the review frames the absence of evidence for de novo AN. This is not "evidence of absence" framing — this is "the mechanism requires pre-existing vulnerability, and we have no evidence of pharmacological causation."
+
+**What I expected but didn't find:** Long-term follow-up data (>1 year). The review explicitly identifies this as missing: "most studies are short-term."
+
+**KB connections:** [[human-in-the-loop clinical AI degrades to worse-than-AI-alone]] — parallel structural point about how well-intentioned interventions can harm vulnerable populations when proper screening/safeguards aren't in place.
+
+**Extraction hints:** (1) "No clinical evidence links GLP-1RA use to onset or worsening of AN" — this is the strongest current statement closing the de novo causation question, (2) Screening protocol (SCOFF + history + behavioral assessment) as a clinical governance recommendation, (3) GI effects reinforce EXISTING purging cycles, not create new ones.
+
+**Context:** October 2025 systematic review, MDPI Nutrients (peer-reviewed).
+
+## Curator Notes
+
+PRIMARY CONNECTION: [[medical care explains only 10-20 percent of health outcomes because behavioral social and genetic factors dominate as four independent methodologies confirm]]
+
+WHY ARCHIVED: This review provides the most authoritative current evidence synthesis for the GLP-1 de novo ED question. The "no clinical evidence for onset" statement + "GI effects exacerbate existing cycles" together close the session 36 disconfirmation hypothesis — behavioral substrate is necessary.
+
+EXTRACTION HINT: This source closes the GI-mediated purging disconfirmation hypothesis definitively enough to write a claim: "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." Scope carefully — 'experimental' confidence given limited RCT evidence.
diff --git a/inbox/queue/2026-05-05-pmc12835689-semaglutide-atypical-anorexia-adolescent-case.md b/inbox/queue/2026-05-05-pmc12835689-semaglutide-atypical-anorexia-adolescent-case.md
new file mode 100644
index 000000000..c404b280c
--- /dev/null
+++ b/inbox/queue/2026-05-05-pmc12835689-semaglutide-atypical-anorexia-adolescent-case.md
@@ -0,0 +1,57 @@
+---
+type: source
+title: "Semaglutide-Associated Worsening of Atypical Anorexia Nervosa in an Adolescent Girl: Case Report"
+author: "Case Report Authors (PMC12835689)"
+url: https://pmc.ncbi.nlm.nih.gov/articles/PMC12835689/
+date: 2026-01-01
+domain: health
+secondary_domains: []
+format: article
+status: unprocessed
+priority: high
+tags: [glp-1, semaglutide, eating-disorders, anorexia, atypical-anorexia, case-report, adolescent, screening-failure]
+intake_tier: research-task
+---
+
+## Content
+
+Case report (received March 2025, accepted October 2025, published January 2026) of adolescent girl developing severe atypical anorexia nervosa during semaglutide treatment.
+
+**Patient background:**
+- Prescribed semaglutide because "previously on the verge of being overweight with weight-related dysphoria"
+- AT TIME OF PRESCRIPTION: No documented ED diagnosis
+- BUT: Had 18 months of pre-prescription concerning behaviors — increasing exercise, decreasing food intake, distorted body image
+- General practitioner prescribed without psychological screening
+
+**Clinical course:**
+- Months 1-3: Semaglutide 0.25mg injection
+- Months 1-6: 20 kg total weight loss
+- Month 6: Discontinued medication but continued weight loss through restriction
+- Later: Panic attack upon gaining 1 kg → suicidal ideation → psychiatric hospitalization
+- Cardiac: Bradycardia 38 bpm + pericardial effusion
+
+**Proposed mechanism:** "Semaglutide can affect mental health in patients who are prone to mental disorders." The medication's appetite suppression combined with underlying eating disorder psychopathology created compounding restriction effects.
+
+**Clinical lesson:** Prescribers must screen for eating disorder vulnerability — particularly distorted body image and restrictive patterns — before prescribing GLP-1 agonists to adolescents, regardless of BMI.
+
+## Agent Notes
+
+**Why this matters:** The highest-quality single-case evidence of GLP-1-associated ED worsening. More importantly, this case exemplifies the atypical AN invisibility problem: the behavioral substrate (18 months of restricting + distorted body image) was present but undetected by an unscreened prescriber.
+
+**What surprised me:** The severity of the cardiac outcome (bradycardia at 38 bpm + pericardial effusion) — this is near-fatal restriction, not just mild disordered eating. The time course was rapid (6 months from prescription to cardiac complications).
+
+**What I expected but didn't find:** Evidence that this was truly de novo ED. On review, the 18-month pre-prescription history of restricting behavior is a clear behavioral antecedent. This is a screening failure, not a case of GLP-1 creating ED without prior behavioral substrate.
+
+**KB connections:** [[social isolation costs Medicare 7 billion annually]] — parallel structural point: clinically significant conditions (loneliness, subclinical ED) are present but undetected because screening infrastructure doesn't exist.
+
+**Extraction hints:** (1) Atypical AN risk in adolescent GLP-1 users: behavioral substrate present but invisible without screening → claim on screening requirement, (2) Case evidence that GLP-1 worsens pre-existing (subclinical) ED rather than causing de novo ED.
+
+**Context:** This is the strongest individual case in the literature. Published January 2026, peer-reviewed.
+
+## Curator Notes
+
+PRIMARY CONNECTION: [[medical care explains only 10-20 percent of health outcomes because behavioral social and genetic factors dominate]]
+
+WHY ARCHIVED: Definitively documents the atypical AN screening failure pattern: behavioral substrate present but undetected → catastrophic outcome. Extractor should scope this as evidence for "GLP-1 worsens subclinical/undetected restrictive ED" not "GLP-1 causes de novo ED."
+
+EXTRACTION HINT: This case is the clearest evidence for a mandatory ED screening requirement before GLP-1 prescribing. Write as a clinical governance claim: behavioral assessment before GLP-1 prescription prevents catastrophic outcomes in patients with undiagnosed subclinical restriction.
diff --git a/inbox/queue/2026-05-05-statnews-true-risk-eating-disorders-glp1-april2026.md b/inbox/queue/2026-05-05-statnews-true-risk-eating-disorders-glp1-april2026.md
new file mode 100644
index 000000000..69c0e656e
--- /dev/null
+++ b/inbox/queue/2026-05-05-statnews-true-risk-eating-disorders-glp1-april2026.md
@@ -0,0 +1,53 @@
+---
+type: source
+title: "What's the True Risk for Eating Disorders With GLP-1s?"
+author: "STAT News"
+url: https://www.statnews.com/2026/04/27/health-news-true-risk-of-eating-disorders-and-wegovy-ozempic/
+date: 2026-04-27
+domain: health
+secondary_domains: []
+format: article
+status: unprocessed
+priority: high
+tags: [glp-1, eating-disorders, semaglutide, incidence, regulatory-gap, screening, evidence-gap, pharmacovigilance]
+intake_tier: research-task
+---
+
+## Content
+
+STAT News investigative feature (April 27, 2026) on the evidence base for eating disorder risk with GLP-1 medications.
+
+**Key finding — ISPOR real-world analysis:**
+- More than 60,000 people taking GLP-1s analyzed via medical records
+- 1.28% diagnosed with eating disorder within two years
+- Note: This is total incidence in GLP-1 users — no control group for comparison (limitation)
+
+**Scale calculation:** If ~1 in 8 Americans takes a GLP-1, more than 420,000 people could develop an eating disorder based on this rate.
+
+**Expert assessment:** "Physicians, trialists, regulators, policymakers, and drug developers are unprepared for this coming wave" — attributed to "Banks" (identity unclear in search results).
+
+**Research gap acknowledged:** "Actual research on this topic is scant" — the article explicitly characterizes the evidence base as insufficient.
+
+**Full article content inaccessible** (subscription/paywall — STAT News). Full summary above derived from search result excerpts and corroborating sources.
+
+## Agent Notes
+
+**Why this matters:** STAT News has the most credibility among health science journalists for quantitative accuracy. The April 27, 2026 date (one week ago) makes this the most current synthesis available. The 1.28% figure is the best available real-world incidence estimate, even without controls.
+
+**What surprised me:** The STAT News framing "true risk" in the headline suggests the article is specifically addressing the causality vs. population-selection debate — this is exactly the question from this session. Unfortunately the full article is paywalled.
+
+**What I expected but didn't find:** Full article content — it's behind the STAT News paywall. The extract doesn't give the full causality assessment.
+
+**KB connections:** [[healthcare AI creates a Jevons paradox because adding capacity to sick care induces more demand for sick care]] — analogous structure: increasing GLP-1 access induces more eating disorder exposure.
+
+**Extraction hints:** The 1.28% incidence figure needs careful scoping: this is total incidence in GLP-1 users, not GLP-1 vs. matched controls. The 420,000 person projection is a useful frame for the scale of risk even if the causal fraction is uncertain.
+
+**Context:** STAT News — most credible independent health science journalism publication in the US. This is the article that will likely drive regulatory and clinical attention to the eating disorder signal.
+
+## Curator Notes
+
+PRIMARY CONNECTION: [[GLP-1 receptor agonists are the largest therapeutic category launch in pharmaceutical history but their chronic use model makes the net cost impact inflationary through 2035]]
+
+WHY ARCHIVED: This is the most current synthesis of the eating disorder risk question from the most credible health journalism source. The 1.28% figure and the "420,000 people" projection give the extractor a population-scale frame for the claim.
+
+EXTRACTION HINT: Use the 1.28% figure CAREFULLY — scope to "incidence in GLP-1 user population without controlled comparison" rather than "GLP-1 causes 1.28% ED rate." The missing control group is the critical methodological gap.
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+---
+type: source
+title: "The Dark Side of the GLP-1 Weight Loss Drugs: Eating Disorders"
+author: "Luke Timmerman (Timmerman Report)"
+url: https://timmermanreport.com/2025/11/the-dark-side-of-the-glp-1-weight-loss-drugs-eating-disorders/
+date: 2025-11-01
+domain: health
+secondary_domains: []
+format: article
+status: unprocessed
+priority: medium
+tags: [glp-1, eating-disorders, ispor, pharmacovigilance, regulatory-gap, screening, anorexia]
+intake_tier: research-task
+---
+
+## Content
+
+Timmerman Report investigative piece on GLP-1 and eating disorders. Key data and arguments:
+
+**ISPOR Study (n=60,000+ GLP-1 users):**
+- Cumulative incidence of new eating disorder diagnosis (mainly anorexia nervosa): 1.275% across all GLP-1 users
+- GLP-1 users with PRIOR MENTAL HEALTH CONDITIONS had MORE THAN DOUBLE the ED risk vs. those without mental health history
+- NOTE: Both groups were GLP-1 users — no non-GLP-1 control group for comparison
+- "35% of new eating disorder diagnoses" estimate from people on GLP-1 agonists — uncited, presented without source attribution
+
+**Regulatory gap described:**
+- No standard protocol for ED screening before prescribing
+- No safety database for monitoring GLP-1-induced ED
+- No required clinical follow-up structure
+- Semaglutide labels do not include a warning for restrictive ED risk
+
+**Key argument:** "Physicians, trialists, regulators, policymakers, and drug developers are unprepared for this coming wave" (attributed to an unspecified author "Banks")
+
+**Access gap:** "Rigorous studies about the incidence of eating disorders in people taking GLP-1 agonists are lacking" — author acknowledges the evidence base is thin
+
+## Agent Notes
+
+**Why this matters:** Contains the ISPOR study summary with the critical clarification that "both groups" = GLP-1 users WITH vs. WITHOUT prior mental health conditions (not GLP-1 vs. non-GLP-1). This resolves ambiguity about what the 1.275% figure means.
+
+**What surprised me:** The "35% of new ED diagnoses" statistic has NO cited source in the article — it's presented as an estimate but appears to be either uncited or from an undocumented calculation. Should NOT be used as data.
+
+**What I expected but didn't find:** The non-GLP-1 control comparison that would tell us whether GLP-1 elevates ED risk above background in weight-management-seeking populations.
+
+**KB connections:** [[SDOH interventions show strong ROI but adoption stalls because Z-code documentation remains below 3%]] — parallel structural barrier: screening would catch ED risk but there's no reimbursement or requirement to do it.
+
+**Extraction hints:** (1) ISPOR finding: prior mental health history 2x risk in GLP-1 users — this confirms behavioral antecedent as primary risk stratifier, (2) Regulatory gap claim: no screening requirement despite known risk population.
+
+**Context:** Timmerman Report — biotech industry newsletter with analytical credibility. November 2025 publication.
+
+## Curator Notes
+
+PRIMARY CONNECTION: [[value-based care transitions stall at the payment boundary because 60 percent of payments touch value metrics but only 14 percent bear full risk]]
+
+WHY ARCHIVED: The ISPOR data clarification (it's a within-GLP-1-users comparison, not GLP-1 vs. controls) is critical for correct interpretation of the 1.275% figure. Prior mental health history doubling risk confirms behavioral substrate primacy.
+
+EXTRACTION HINT: The behavioral mental health history as primary risk stratifier in GLP-1 ED incidence (ISPOR: 2x risk) is the extractable finding — scope to 'experimental' confidence since no control group for absolute incidence comparison.