Diadia Transparency Lab
Transparency Reports
Every health claim an AI makes, decomposed into a mechanism, checked against the evidence, and published with the reasoning fully in the open.
Abstract — Generative models now answer health questions in fluent, confident prose. That fluency hides its own reasoning. And when these models are put to work in clinical settings, fluency is not enough: claims that inform care demand a higher bar of scrutiny — each one verified against the published evidence before it is trusted. This resource publishes the reasoning instead: for each claim we show what was asserted, what the evidence supports, and what the system inferred — as an inspectable mechanism graph rather than a verdict to be taken on trust.
Why this exists
State-of-the-art models still hallucinate — they produce fluent, plausible-sounding health claims that are subtly wrong, unsupported, or invented outright, and present each one with the same confidence. In a clinical context the reader cannot tell a well-evidenced claim from a confident guess — and the cost of being wrong is asymmetric.
This project exists to shed light on that gap. Every claim here is put through Diadia’s proprietary claim-verification process — decomposed into its underlying mechanism, checked against the published evidence link by link, and rolled up into an auditable verdict. The aim is not another opaque answer to trust, but clarity: the reasoning, the evidence, and the uncertainty, all in the open.
A library of decomposed claims
Each report is built around one living figure: an interactive mechanism graph whose nodes are biomedical entities — biomarkers, processes, symptoms, outcomes — and whose edges are causal or evidential links. Links are encoded by evidence state through line weight, dash and glyph, never by colour alone, so every figure reads in greyscale and in print.
The catalogue spans nutrition, sleep, immunity, metabolism and mood. Some claims hold; some break; most land in the honest middle — plausible, not proven.
How every claim is checked
The same four steps run on every claim, so reports stay comparable across the library:
- DecomposeThe claim is broken into mechanism steps and drawn as a neutral hypothesis graph — every link an equal hairline.
- Map evidenceStudies reweigh each link. Some thicken to established, some hold moderately, some break, some are left untested.
- EnrichEvidence may reveal explanatory routes the claim never mentioned, surfaced as parallel paths.
- Roll upSurviving paths combine into a single auditable verdict — traceable back to every edge and source.
An edge weight scales its evidence label by confidence, and a path is only as strong as its weakest edge. The verdict is a deterministic label roll-up over every root-to-leaf path — not a numeric score: weights rank and display the evidence, while labels, confidence and critical-edge priority decide the verdict.
The full methodology — and an evaluation of it across frontier models — is detailed in our paper, Claim-Level Transparency Analysis of LLM-Generated Diagnostic Reports ↗.
Browse all claims
2717 claimsDoes insulin resistance and hyperglycemia lead to low T3 and high reverse T3 through impaired peripheral conversion?
Insulin resistance and elevated blood glucose are associated with reduced peripheral conversion of T4 to active T3 and a shift toward higher reverse T3 levels.
Can low ferritin cause hair loss?
Low ferritin (depleted iron stores) is frequently associated with hair loss in women, particularly telogen effluvium and female pattern hair loss.
Low luteal progesterone increases prostaglandin activity and uterine contractility, causing painful periods.
Low luteal progesterone leads to increased prostaglandin synthesis and uterine hypercontractility, which underlies primary dysmenorrhea.
Do progesterone deficiency and estrogen–progesterone imbalance contribute to dysmenorrhea and menstrual migraine?
Progesterone deficiency and a relative estrogen–progesterone imbalance are linked to dysmenorrhea and hormonally triggered menstrual migraine.
Can reduced thyroid hormone signaling cause low luteal progesterone?
Reduced thyroid hormone signaling disrupts ovulation and corpus luteum function, leading to lower luteal-phase progesterone levels.
Does elevated reverse T3 indicate reduced peripheral thyroid hormone signaling?
Elevated reverse T3 reflects a stress- and illness-related reduction in active T3 signaling in peripheral tissues.