This paper reviews several converging lines of research that suggest that prenatal exposure to environmental stress may increase risk for Autistic Disorder (AD). We first discuss studies finding that prenatal exposure to stressful life events is associated with significantly increased risk of AD, as well as other disorders, such as schizophrenia and depression. We then review evidence from animal and human studies that prenatal stress can produce both (a) abnormal postnatal behaviors that resemble the defining symptoms of AD, and (b) other abnormalities that have elevated rates in AD, such as learning deficits, seizure disorders, perinatal complications, immunologic and neuroinflammatory anomalies, and low postnatal tolerance for stress. We explain why an etiologic role for prenatal stress is compatible with genetic factors in AD, and describe how stress can disrupt fetal brain development. Finally, we discuss implications for understanding underlying processes in AD, including potential gene-environment interactions, and developing new therapies and early prevention programs.

Studies of creativity and affective illness typically focus on eminent individuals in specific fields. This is the first study to select subjects solely by diagnosis, and then evaluate their overall creative accomplishments. Seventeen manic-depressives, 16 cyclothymes, and 11 normal first-degree relatives we compared with 33 controls with no personal or family history of major affective disorder, cyclothymia, or schizophrenia; 15 controls were normal and 18 carried another diagnosis. Peak creativity was assessed by raters blind to subjects' diagnosis with the use of the Lifetime Creativity Scales. Orthogonal contrasts showed (a) creativity to be significantly higher among the combined index subjects (manic-depressive, cyclothymes, and normal relatives) than among controls (/>< .05), (b) no significant difference between normal and ill controls, and (c) suggestively higher creativity among normal index relatives than among manic-depressives (p < . 10). (Cyclothymes fell close to normal relatives.) Liability for manic-depressive illness may carry advantages for creativity, perhaps particularly among those individuals who are relatively better functioning.Bipolar manic-depressive illness (MDI) tends to run in families. Adoption and twin studies support a marked genetic conion to this familial pattern (e.g., Bertelsen, 1979;Mendlewicz & Ranier, 1977;Wender et al., 1986). In this study we investigated whether manic-depressive pathology might be associated with positive behavioral characteristics that run in the same families. Such a compensatory advantage to genes that increase vulnerability to illness has been proposed for behavioral disorders such as schizophrenia (e.g., Kinney & Matthysse, 1978). A rough analogy may be drawn to sickle cell anemia, although the genetics of affective disorder are likely more complex. In the sickle-cell case, individuals homozygous for the mutant gene typically have severe anemia with clinical complications and often suffer an early death. In contrast, the much larger number of heterozygous carriers of the gene are frequently asymptomatic and have the advantage of increased resistance to malaria.A version of this article was presented at the 93rd annual meeting of the American Psychological Association, Los Angeles, August 1985.We are grateful to Paul Wendei; Seymour Kety, Fini Schulsinger, and David Rosen thai for permission to use the present sample and interview data base for this study of creativity, and to the Spencer Foundation for its support of the further development and refinement of the Lifetime Creativity Scales. We wish to thank Seymour Kety, Steven Matthysse, Sandow Ruby, and Christine Waternaux for their helpful suggestions. Sincere thanks are also extended to Beth Gerstels and Carol Paik for their assistance in making creativity assessments, and to Heidi Daniels and Karen Linkins for work on data analysis and preparation of tables.

Hurricanes and tropical storms served as natural experiments for investigating whether autism is associated with exposure to stressful events during sensitive periods of gestation. Weather service data identified severe storms in Louisiana from 1980 to 1995 and parishes hit by storm centers during this period. Autism prevalences in different cohorts were calculated using anonymous data on birth dates and parishes of children diagnosed with autism in the state mental health system, together with corresponding census data on all live births in Louisiana. Prevalence increased in dose-response fashion with severity of prenatal storm exposure, especially for cohorts exposed near the middle or end of gestation (p < 0.001). Results complement other evidence that factors disrupting development during sensitive gestational periods may contribute to autism.