My research is focused on the exploration of the distribution of childhood onset neuropsychiatric disorders and disruptive behavioral problems including autism and bullying, and on the understanding of the causes of these conditions, including genetics and environmental risk factors as well as their interactions.
To achieve these goals in my research, a large number of children and their families are recruited from the community, survey and biological sample collections are carried out, and laboratory analyses are followed.
My research on autism has taken place in Korean children, extensively, while my research on bullying has been conducted in both Korean and American children.
Extensive Research Description
Dr. Kim’s major research efforts involve three areas: 1) The social and psychopathological consequences of school bullying; 2) Epidemiology of childhood onset neuropsychiatric disorders; and, 3) The genetics and genetic epidemiology of childhood onset neuropsychiatric disorders.
Dr. Kim developed an interdisciplinary research team and completed a series of bullying studies in Korean elementary and middle schools. The purpose of these studies are to examine: (a) the time trend change of prevalence of bullying (either victim, perpetrator or victim-perpetrator); (b) trajectories of bullying behaviors; (c) risk factors that predict bullying behavior; and, (d) bullying as a risk factor in the development of psychopathology and suicidal ideations/behaviors. Parallel studies and anti-bullying intervention studies in US children and adolescents are under preparation.
Currently, Dr. Kim is conducting epidemiological studies, genetic studies, Gene-Environmental Interaction Studies and Neuroimaging Studies of Autistic Spectrum Disorder (ASD) in South Korea.
1) The international research team screen and assess all school-aged children (N=45,000) from Ilsan (population 513,024). Cases are identified through the disability registry, school surveys and records and self-referrals, and subsequent diagnosis are made by employing a variety of standardized instruments: Korean versions of the Autism Spectrum Screening Questionnaire (ASSQ), the Autism Behavior Checklist (ABC), Autism Diagnostic Observation Schedule (ADOS) and the Autism Diagnosis Interview-Revised (ADI-R) and the Korean Wechsler Scale.
2) Leveraging already established infrastructure and research design in the community, our team continue to examine 6-year cumulative incidence of ASD in a prospective design for 2000 and 2001 birth cohorts. This study will provide first accurate incidence rate that was prospectively examined in a total population.
3) Third area of research is to examine the roles of genes, environment and gene-environment interactions in the etiology of childhood onset neuropsychiatric disorders. Dr. Kim completed a family-based association study to examine dopaminergic and serotonergic system genetic markers in Korean children with ADHD. Currently, a genetic epidemiological study of ASD is underway with epidemiologically-ascertained Korean ASD cohort in which the phenotype is carefully determined using state-of-the-art, standardized assessment methods and to generate hypotheses about genotypes, environments and GE interactions.
4) Another large cohorts of children (N=10,000) have been recruited for genetics and GE interactions studies in CheonAn area. Social reciprocity of these children were measured by ASSQ, Social Responsiveness Scale (SRS) and Behavioral Assessment Scale for Children-II (BASC-II) by their parents, their blood or saliva samples have been collected for the genetic analyses, and environmental exposures are measured biologically and with questionnaires.
5) Children with ASD identified from ongoing prevalence and incidence studies and their sex, age and IQ matched control groups have been recruited for sMRI, fMRI and DTI studies to examine brain structure and function. Additionally, these data will serve for neuroigmaing-genetics study for ASD.
- Prevalence study of ASD in Korean school-aged children;
- Prospective examination of 6-year cumulative incidence of ASD in Korean children;
- Genetic Epidemiology of ASD in Korean children;
- Genetics and GE interactions of social reciprocity in Korean epidemiological sample;
- Neuroimaging study of Korean children with ASD;
- Causes and consequences of bullying in adolescents; and
- Effectiveness of anti-bullying intervention in American children
- A Gene Environment Interaction in the Etiology of Autism Spectrum Disorder
- Kim YS, Leventhal B, Koh YJ, Fombonne E, Laska E, Lim EC, Cheon KA, Kim SJ, Kim YK, Lee HK, Song DH, Grinker RR. (2011). Prevalence of autism spectrum disorders in a total population sample. Am J Psychiatry, 2011 0: appi.ajp.2011.10101532. PMID: 21558103
- Kim YS+, Boyce WT, Koh YJ, Leventhal BL. (2009). Time trends, trajectories and demographic predictors of bullying: a prospective study in Korean adolescents. J Adolesc Health,Vol. 45, No. 4, pp360-7.
- Kim YS, Leventhal BL, Koh YJ, Boyce WT. (2009). Bullying increased suicide risk: Prospective study of Korean adolescents. Arch Suicide Res, Vol. 13, No. 1, pp15-30.
- Kim YS, Leventhal BL, Koh YJ, Hubbard A, Boyce WT. (2006). School bullying and youth violence: causes or consequences of psychopathology? Arch Gen Psychiatry Vol. 63, No. 9, pp1035-41.
- Kim SJ, Kim YS, Lee HS, Kim SY, Kim CH. (2006). An interaction between the serotonin transporter promoter region and dopamine transporter polymorphisms contributes to harm avoidance and reward dependence traits in normal healthy subjects. J Neural Transm,
- Kim SJ, Kim YS, Kim SY, Lee HS, Kim CH. j(2006). An association study of catechol-O-methyltransferase and monoamine oxidase A polymorphisms and personality traits in Korean. Neurosci Lett Vol. 401, No. 1, pp154-8.
- Leckman J, Kim YS (2006). A “primary” candidate gene for OCD? Arch Gen Psychiatry Vol. 63, No. 7, pp717-20.
- Kim SJ, Badner J, Cheon KA, Kim BN, Yoo HJ, Kim SJ, Cook EH Jr., Leventhal BL, Kim YS. (2005). Family-based association study of the serotonin transporter gene polymorphisms in Korean ADHD trios. Am J Med Genet B Neuropsychiatr Genet, 39(1), 14-18. PMID: