Psychoneuroendocrinology and psychoimmunology — MEQ

(i) Definitions and HPA. Psychoneuroendocrinology: bidirectional CNS–pituitary–peripheral endocrine regulation of behaviour and psychopharmacology. Psychoimmunology: bidirectional neural–immune signalling. HPA: limbic/hypothalamic CRH → pituitary ACTH → adrenal cortisol; GR/MR negative feedback; allostatic load = cumulative cost of chronic adaptation. [1][2]

(ii) Depression models. Holsboer: impaired GR signalling drives HPA dysregulation. Gold–Chrousos: melancholic features as relatively high CRH/NE organisation versus atypical features as relatively low CRH/NE organisation — conceptual, not a lab test. [3][5]

(iii) Immune models. Sickness behaviour: fatigue, anhedonia, social withdrawal, anorexia, sleep change, slowing. Routes: neural (vagus), humoral (circumventricular/transport), cellular. Human model: IFN-alpha–associated depression-like syndrome; inflammation relevant in a subset. [4][8]

(iv) Tests and prolactin. DST historically studied for melancholia but not a routine modern diagnostic for MDD. CRP/IL-6 are not DSM/ICD diagnostic tests. Hyperprolactinaemia: D2 blockade removes tuberoinfundibular inhibition; assess symptoms, pregnancy where relevant, consider dose reduction/switch (e.g. aripiprazole/quetiapine) and endocrine referral if needed. [7][2][6]

(v) Application. Diagnose depression clinically; treat medical inflammation and depression in parallel; use biomarkers for physical health and formulation, never as sole diagnosis or suicide risk tools; evidence-based psych treatments remain core. [8][2]