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Bio basis for illness: Schizophrenia, Biological basis, OUTLINE, Diathesis…

- - - - baseline HPA activity elevated in SZD and other psychoses
      - antipsychotic meds typically reduce cortisol
      - prescription and rec drugs that exacerbate psychotic symptoms also increase HPA activity
      - illness ass. with increased cortisol (eg Cushing's syndrome) linked to heightened psych risk
      - gluc.cort. receptors in SZD seem downregulated (reduced neg feedback)
      - reduced hippocampal volume (correlate of hypercortisoleme) among most reported brain abnorm in psychotic patients
      - normative increase in HPA reactivity in adolescence (onset time)
      - increase in cortisol secretion appears to precede and predict onset of psychosis in at risk ppl
- - - - risk of SZD -> low SES
  - - - Brookwell, Bentall and Varese (2013)
        
        auditory hallucinations due to misattribution of internally generated content
    - - Janssen et al (2003)
        
        paranoid beliefs linked to chronic victimisation and powerlessness
    - - Bentall and Kaney (1996)
        
        externalising attributions to protect self esteem
        
        Bucket et al (2023)
        
        SZD -> hostile attribution bias
    - - over-reliance on antipsychotics
      - Moritz et al (2018)
        
        MCT+ effective
  - - - ELS, urban, birth comp, social isolation
- - - - reduced GMV and WMV + increased ventricular
    - - recuced hippocampal vol. most replicated finding
    - - Fusar-Poli (2013)
        
        meta-anal of longitudinal studies using MRI scans. GMV decreases associated with cumulative exposure to antipsychotics
  - - - DISC1 gene known as risk factor for SZD, associated with dopamine impairments
      - DA hypothesis based on finding that affinity of antipsychotic meds for dopamine receptors is closely related to clinical potency
  - - - Moritz et al (2018)
        
        awareness of prognosis for SZD increases suicide risk
    - - Linkage approaches fail to identify responsible genes. Still thinks twin studies etc point to the 1 gene
    - - Exploring SCZ one gene at a time difficult and expensive. Early studies underpowered with low rates of replication
      - review of epigenetic mech. Clinical heterogeneity and relatiionship with epigenetic expression remains poorly evidenced