{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,20]],"date-time":"2026-10-20T17:56:25Z","timestamp":1792518985787,"version":"4.5.0"},"reference-count":205,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2016,1,19]],"date-time":"2016-01-19T00:00:00Z","timestamp":1453161600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100000765","name":"University College London","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000765","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Child Psychology Psychiatry"],"published-print":{"date-parts":[[2016,3]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Although autism spectrum condition (\n                      <jats:styled-content style=\"fixed-case\">ASC<\/jats:styled-content>\n                      ) is strongly genetic in origin, accumulating evidence points to the critical roles of various environmental influences on its emergence and subsequent developmental course.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      A developmental psychopathology framework was used to synthesise literature on environmental factors associated with the onset and course of\n                      <jats:styled-content style=\"fixed-case\">ASC<\/jats:styled-content>\n                      (based on a systematic search of the literature using PubMed, PsychInfo and Google Scholar databases). Particular emphasis was placed on gene\u2013environment interplay, including gene\u2013environment interaction (G\u00a0\u00d7\u00a0E) and gene\u2013environment correlation (\n                      <jats:styled-content style=\"fixed-case\">rGE<\/jats:styled-content>\n                      ).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Before conception, advanced paternal and maternal ages may independently enhance offspring risk for\n                      <jats:styled-content style=\"fixed-case\">ASC<\/jats:styled-content>\n                      . Exogenous prenatal risks are evident (e.g. valproate and toxic chemicals) or possible (e.g. selective serotonin reuptake inhibitors), and processes endogenous to the materno\u2010foeto\u2010placental unit (e.g. maternal diabetes, enhanced steroidogenic activities and maternal immune activation) likely heighten offspring vulnerability to\n                      <jats:styled-content style=\"fixed-case\">ASC<\/jats:styled-content>\n                      . Folate intake is a prenatal protective factor, with a particular window of action around 4\u00a0weeks preconception and during the first trimester. These prenatal risks and protective mechanisms appear to involve G\u00a0\u00d7\u00a0E and potentially\n                      <jats:styled-content style=\"fixed-case\">rGE<\/jats:styled-content>\n                      . A variety of perinatal risks are related to offspring\n                      <jats:styled-content style=\"fixed-case\">ASC<\/jats:styled-content>\n                      risk, possibly reflecting\n                      <jats:styled-content style=\"fixed-case\">rGE<\/jats:styled-content>\n                      . Postnatal social factors (e.g. caregiver\u2013infant interaction, severe early deprivation) during the first years of life may operate through\n                      <jats:styled-content style=\"fixed-case\">rGE<\/jats:styled-content>\n                      to influence the likelihood of manifesting a full\n                      <jats:styled-content style=\"fixed-case\">ASC<\/jats:styled-content>\n                      phenotype from a \u2018prodromal\u2019 phase (a proposal distinct to the discredited and harmful \u2018refrigerator mother hypothesis\u2019); and later postnatal risks, after the full manifestation of\n                      <jats:styled-content style=\"fixed-case\">ASC<\/jats:styled-content>\n                      , shape life span development through transactions mediated by\n                      <jats:styled-content style=\"fixed-case\">rGE<\/jats:styled-content>\n                      . There is no evidence that vaccination is a postnatal risk for ASC.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Future investigations should consider the specificity of risks for\n                      <jats:styled-content style=\"fixed-case\">ASC<\/jats:styled-content>\n                      versus other atypical neurodevelopmental trajectories, timing of risk and protective mechanisms, animal model systems to study mechanisms underlying gene\u2013environment interplay, large\u2010sample genome\u2013envirome designs to address G\u00a0\u00d7\u00a0E and longitudinal studies to elucidate how\n                      <jats:styled-content style=\"fixed-case\">rGE<\/jats:styled-content>\n                      plays out over time. Clinical and public health implications are discussed.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/jcpp.12501","type":"journal-article","created":{"date-parts":[[2016,1,19]],"date-time":"2016-01-19T01:48:45Z","timestamp":1453168125000},"page":"271-292","source":"Crossref","is-referenced-by-count":232,"title":["Annual Research Review: The role of the environment in the developmental psychopathology of autism spectrum condition"],"prefix":"10.1111","volume":"57","author":[{"given":"William","family":"Mandy","sequence":"first","affiliation":[{"name":"Research Department of Clinical, Educational and Health Psychology University College London London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Meng\u2010Chuan","family":"Lai","sequence":"additional","affiliation":[{"name":"Child and Youth Mental Health Collaborative at The Centre for Addiction and Mental Health and The Hospital for Sick Children Toronto ON 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