{
  "slug": "gut-microbiome-systemic-causality",
  "completed": true,
  "provider_mode": "Consensus MCP keyword search and paper-record fetch; independent comparison with primary PubMed records and existing topic inventories",
  "queries": [
    "gut microbiota causal systemic disease human randomized fecal microbiota transplantation autoimmune arthritis type 2 diabetes cardiovascular disease mechanisms primary studies",
    "primary human randomized fecal microbiota transplantation trial Kootte 2017 Vrieze 2012 Yu FMT-TRIM autoimmune arthritis segmented filamentous bacteria Wu 2010"
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      "pmid": "20620945",
      "depth": "PubMed abstract_metadata in baseline inventory",
      "result": "Segmented filamentous bacteria drive Th17-associated autoimmune arthritis in a mouse model; bounded animal causality, not broad human systemic primacy.",
      "loadbearing_claim_ids": [
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    {
      "pmid": "24009397",
      "depth": "PubMed abstract, reopened 2026-10-09",
      "result": "Fecal microbiota from obesity-discordant twins transferred body/fat-mass and metabolic phenotypes to germ-free mice; diet-dependent and animal transfer.",
      "loadbearing_claim_ids": [
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    {
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      "depth": "PubMed abstract_metadata in baseline inventory",
      "result": "FMT-TRIM placebo-controlled pilot in obesity did not improve the primary metabolic endpoint; weighs against assuming human systemic metabolic effects from transfer.",
      "loadbearing_claim_ids": [
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    {
      "pmid": "28978426",
      "depth": "PubMed abstract_metadata in baseline inventory",
      "result": "Lean-donor FMT effect on insulin sensitivity depended on baseline microbiota and was short-term; not disease initiation or general systemic cause.",
      "loadbearing_claim_ids": [
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  "grade_changed": false,
  "conclusion": "No grade change: Γ for microbial composition as a broad primary cause across distant human organ diseases. Historical mention is field-level Delphi consensus, not Consensus service provenance; fresh searches are retrospective only.",
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  "status": "completed_retrospective_original_source_reconciliation",
  "score_before": {
    "hsef_level": "Γ",
    "hsef_descriptor": "Mechanistically plausible, partial system support",
    "confidence": "Moderate",
    "confidence_rationale": "Multiple causal animal lines, strong human CDI trials, and emerging but conflicting human systemic interventions support the narrow mechanisms; broad human primacy is not directly tested.",
    "rests_on_non_peer_reviewed_work": false,
    "rationale": "Gut communities can causally modify selected animal phenotypes and recurrent CDI, with mixed context-specific human metabolic, hepatic, and Parkinson signals. No evidence establishes community composition as a primary cause across human distant-organ disease classes."
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