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Clinical Atlas Prestige · Evidence-first

Psych VivasFoundations — psychiatric genetics and epigenetics

Psych Vivas · Foundations — psychiatric genetics and epigenetics

Psychiatric genetics and epigenetics — structured clinical viva

Fellowship viva on heritability, GWAS architecture, CNVs/22q11, PRS limits, epigenetics, and counselling ethics.

clinical
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Target exams

FRANZCPMRCPsychABPNMD-DNB

Target exams

FRANZCPMRCPsychABPNMD-DNB
Prompt
FRANZCP/MRCPsych-style viva. Slide 1: table of approximate twin heritabilities (schizophrenia high ~80%, MDD ~30–40%, bipolar high). Slide 2: schematic Manhattan plot labelled PGC schizophrenia. Slide 3: chromosome 22 with 22q11.2 deletion highlight. Follow-ups cover missing heritability, PRS clinical limits, epigenetics (Meaney/Weaver paradigm), and ethics of commercial genetic testing.

Interpretation

Reveal interpretation

Slide 1 — heritabilities. Schizophrenia shows high twin heritability (~80% classically from meta-analysis); major depression moderate (~37% meta-analytic twin estimate); bipolar high with genetic links to unipolar depression dimensions.[1][2] Immediately state: heritability is population variance partition; incomplete MZ concordance; environment remains causal and interventional.

Slide 2 — Manhattan/GWAS. Points to polygenic common-variant architecture. Name PGC 2014 108 loci and later expanded maps prioritising synaptic biology; depression GWAS similarly polygenic at scale.[3][4][5] Mention cross-disorder pleiotropy as explanation for comorbidity genetics.[10] Missing heritability bridges to rare variants/CNVs and imperfect tagging.

Slide 3 — 22q11. Prototype high-impact CNV with multisystem developmental medicine and elevated psychosis risk; management is multidisciplinary, not genetics-only.[6][7]

Epigenetics follow-up. Meaney/Weaver maternal care → GR promoter methylation paradigm illustrates environmental embedding of gene expression; do not claim a clinical methylation diagnostic for human depression on the ward.[8]

PRS/ethics follow-up. Research tool, limited discrimination, ancestry caveats; non-directive counselling; refuse genetic essentialism.[9]

Key points

Variance ≠ personal risk

h2 ~80% for schizophrenia does not mean an 80% chance for each relative.[1]

Architecture is mixed

Common polygenic + rare CNV/coding hits on one liability continuum.[3][4][6]

Clinic still phenotype-led

Genomics informs counselling and syndromic care; standard psychiatric treatment continues.[7][9]

References

  1. [1]Sullivan PF, Kendler KS, Neale MC Schizophrenia as a complex trait: evidence from a meta-analysis of twin studies Arch Gen Psychiatry, 2003.PMID 14662550
  2. [2]Sullivan PF, Neale MC, Kendler KS Genetic epidemiology of major depression: review and meta-analysis Am J Psychiatry, 2000.PMID 11007705
  3. [3]Schizophrenia Working Group of the Psychiatric Genomics Consortium Biological insights from 108 schizophrenia-associated genetic loci Nature, 2014.PMID 25056061
  4. [4]Trubetskoy V, Pardiñas AF, Qi T, et al. Mapping genomic loci implicates genes and synaptic biology in schizophrenia Nature, 2022.PMID 35396580
  5. [5]Wray NR, Ripke S, Mattheisen M, et al. Genome-wide association analyses identify 44 risk variants and refine the genetic architecture of major depression Nat Genet, 2018.PMID 29700475
  6. [6]Malhotra D, Sebat J CNVs: harbingers of a rare variant revolution in psychiatric genetics Cell, 2012.PMID 22424231
  7. [7]McDonald-McGinn DM, Sullivan KE, Marino B, et al. 22q11.2 deletion syndrome Nat Rev Dis Primers, 2015.PMID 27189754
  8. [8]Weaver ICG, Cervoni N, Champagne FA, et al. Epigenetic programming by maternal behavior Nat Neurosci, 2004.PMID 15220929
  9. [9]Lewis CM, Vassos E Polygenic risk scores: from research tools to clinical instruments Genome Med, 2020.PMID 32423490
  10. [10]Cross-Disorder Group of the Psychiatric Genomics Consortium Genomic Relationships, Novel Loci, and Pleiotropic Mechanisms across Eight Psychiatric Disorders Cell, 2019.PMID 31835028