Evidence, and replication thereof, that molecular-genetic and environmental risks for psychosis impact through an affective pathway


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Van Os J., Pries L., Ten Have M., De Graaf R., Van Dorsselaer S., Delespaul P., ...Daha Fazla

Psychological Medicine, cilt.52, sa.10, ss.1910-1922, 2022 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 52 Sayı: 10
  • Basım Tarihi: 2022
  • Doi Numarası: 10.1017/s0033291720003748
  • Dergi Adı: Psychological Medicine
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Social Sciences Citation Index (SSCI), Scopus, Academic Search Premier, ASSIA, IBZ Online, PASCAL, Abstracts in Social Gerontology, AgeLine, CAB Abstracts, CINAHL, EMBASE, MEDLINE, Psycinfo, Public Affairs Index, Veterinary Science Database
  • Sayfa Sayıları: ss.1910-1922
  • Anahtar Kelimeler: Affective pathway, childhood adversity, environment, genetics, psychosis, MENTAL-HEALTH SURVEY, SCHIZOPHRENIA SPECTRUM DISORDERS, 1ST EPISODE PSYCHOSIS, CHILDHOOD TRAUMA, PSYCHIATRIC-DISORDERS, CLINICAL PSYCHOSIS, GENERAL-POPULATION, NEGATIVE SYMPTOMS, NETWORK APPROACH, SHORT-FORM
  • Orta Doğu Teknik Üniversitesi Adresli: Hayır

Özet

Copyright © The Author(s) 2020. Published by Cambridge University Press.Background There is evidence that environmental and genetic risk factors for schizophrenia spectrum disorders are transdiagnostic and mediated in part through a generic pathway of affective dysregulation. Methods We analysed to what degree the impact of schizophrenia polygenic risk (PRS-SZ) and childhood adversity (CA) on psychosis outcomes was contingent on co-presence of affective dysregulation, defined as significant depressive symptoms, in (i) NEMESIS-2 (n = 6646), a representative general population sample, interviewed four times over nine years and (ii) EUGEI (n = 4068) a sample of patients with schizophrenia spectrum disorder, the siblings of these patients and controls. Results The impact of PRS-SZ on psychosis showed significant dependence on co-presence of affective dysregulation in NEMESIS-2 [relative excess risk due to interaction (RERI): 1.01, p = 0.037] and in EUGEI (RERI = 3.39, p = 0.048). This was particularly evident for delusional ideation (NEMESIS-2: RERI = 1.74, p = 0.003; EUGEI: RERI = 4.16, p = 0.019) and not for hallucinatory experiences (NEMESIS-2: RERI = 0.65, p = 0.284; EUGEI: -0.37, p = 0.547). A similar and stronger pattern of results was evident for CA (RERI delusions and hallucinations: NEMESIS-2: 3.02, p < 0.001; EUGEI: 6.44, p < 0.001; RERI delusional ideation: NEMESIS-2: 3.79, p < 0.001; EUGEI: 5.43, p = 0.001; RERI hallucinatory experiences: NEMESIS-2: 2.46, p < 0.001; EUGEI: 0.54, p = 0.465). Conclusions The results, and internal replication, suggest that the effects of known genetic and non-genetic risk factors for psychosis are mediated in part through an affective pathway, from which early states of delusional meaning may arise.