# Inflammatory Depression Hypothesis

Inflammation can alter mood and contribute to defined depressive syndromes; a causal high-inflammation MDD subtype still needs prospective confirmation.

Overall Γ follows registered SC3. Baseline prediction is Β, and sustained immune-treatment-related syndromes earn a restricted Ε at SC2. Neither narrow immune exposure nor exploratory high-CRP response establishes prospectively identifiable inflammatory MDD causation. Genuine positive clinical pilot findings are retained alongside larger or prospectively stratified nulls. The next clinical subtype boundary remains open rather than being declared refuted.

Age, sex, insomnia, physical illness, cytokine exposure, symptom domain and baseline assay/threshold were retained. They map context-specific immune effects but do not permit responder-based eligibility or automatic acute-to-sustained transfer.