Hill Goldsmith
Ph.D., University of Minnesota
Group Coordinator, Social and Affective Sciences Group
Fluno Bascom Professor & Leona Tyler Professor of Psychology

Contact Information:
UW-Madison
328 Psychology Building, W J Brogden
1202 W Johnson St
Madison, WI 53706
(608) 262-9932
(608) 263-4735
E-mail: hhgoldsm@facstaff.wisc.edu
Web: Wisconsin Twin Research

Research Statement

A principal line of current research, in collaboration with Professor Gernsbacher and others, focuses on autism spectrum disorders. One aspect of this research implies that the current results of genetic (i.e., genome screen) and neuroanatomical (i.e., brain imaging) studies have been less definitive than expected because of the heterogeneity among persons with autistic spectrum disorders. Even when diagnosed according to strict and consistent criteria, symptom profiles of persons with autism vary greatly, suggesting variability in etiology. Thus, we propose to identify and validate a putative subtype of autism, which we refer to as "developmental verbal dyspraxia," or DVD. DVD is a motor-speech programming disorder resulting in difficulty coordinating and sequencing the oral-motor movements necessary to produce and combine speech sounds (phonemes) to form syllables, words, phrases, and sentences. We hypothesize that a sizable minority of minimally verbal or nonverbal persons with autism are characterize d by DVD. Support for our hypothesis comes from behavioral, genetic, and neuroanatomical evidence. Our project seeks to identify and validate a DVD subtype of autism by screening all children with autism (under age 16) in a metropolitan area; identifying the members of this group who are also characterized by DVD; selecting an autism control group of children not characterized by DVD and a typically developing control group; collecting extensive behavioral, medical, and developmental histories of all children in these groups. We shall also construct indices of the DVD subtype from diagnostic instruments currently being used in full genome screens (e.g., the ADI-R and A-DOS), with the future aim of pro-viding these indices to the research groups who have conducted the genome screens. This research will lay the foundation for identifying other subtypes of autism spectrum disorder. In related research, we have also begun to identify potential participants for a statewide twin study of autism spectrum disorder. Epidemiological research on autism, in collaboration with other Waisman Center investigators, is also in the planning stage.

A second project, underway for several years, is the fine-grained, longitudinal Genetics of Emotional Ontogeny project. This project includes multimodal, comprehensive assessment of emotion and temperament as well as selective assessment of cognition, motor development, physiology, social interaction, and the home environment from birth t o age 3 years. The final sample size will total about 500 twin pairs. The project incorporates an unusually broad set of methods, including lab-based elicitation of behavior, home observation, testing by examiner, telephone interviews, hospital records, diaries, narrative constructions, language inventories, and parent-child and sibling interaction episodes. The chief issues addressed by this project are the nature, sources, and functional consequences of emotional individuality.

A third project uses the resources of our statewide panel of twins. In collaboration with Professor Lemery, we are engaged in a twin study of young children at risk for (1) internalizing problems such as anxiety, social withdrawal, and depression; (2) externalizing problems, such as motor excess, oppositional and conduct problems, and disinhibition; and (3) attentional problems, particularly ADHD. The nature of the risk is assessed and verified by parental questionnaire, structured interview, observation of children's emotional individuality, observation of interpersonal interactions, and multiple biological measures. These measures are also collected on cotwins and on a control sample. The main goals of the project are to estimate the heritable influence on various forms of childhood psychopathology using both categorical and dimensional approaches, to study the relation of temperamental traits and psychopathology within a behavior-genetic context (including family history information), to consider possible risk-reducing factors related to resiliency and adaptability, such as the capacity to experience and express pleasure, and to collect, extract, and store DNA samples for future analyses once more potential markers of the disorders and more genes involved in relevant neural system. Even more broadly, the project approaches behavioral disorders with the conceptual and empirical tools of developmental psychobiology in addition to the more typical clinical orientation.

A fourth project extends our recently completed behavior-genetic research with infant twins to a new sample of 250 pairs of 6-9 year-old twins, with the inclusion of measures to provide a comprehensive assessment of physiology related to affective reactivity, and particularly to anxiety. Physiological measures are obtained in the laboratory under multiple baseline and emotion-elicitation conditions. These measures include EEG asymmetry, basal and reactive cortisol levels, fear-potentiated startle, and cardiac psychophysiology (including impedance cardiography). The study also employs behavioral measures, assessed in the home, that allow us to assess the latency, duration, and intensity of facial, vocal, and motoric responses to affective stimuli. Other child and family characteristics are assessed by interview and questionnaire, and medical histories are obtained. This project contributes to all four types of evidence needed to complete the logical chain of inference involving genetics, physiology, and behavior in this domain. First, a genetic basis for behavioral individuality must be established. Next, a genetic basis for the biological substrates (e.g., prefrontal EEG asymmetry) needs to be established. Then, we investigate whether there is a common genetic basis for the phenotypically associated behaviors and their biological substrates. Finally, as the field advances, specific molecular genetic markers for relevant behavior and physiology need to be identified.

Representative Publications

Wagner AI, Schmidt NL, Lemery-Chalfant K, Leavitt LA, Goldsmith HH. (2009) The Limited Effects of Obstetrical and Neonatal Complications on Conduct and Attention-Deficit Hyperactivity Disorder Symptoms in Middle Childhood Journal of Developmental & Behavioral Pediatrics. 2009 May 8.

Light SN, Coan JA, Frye C, Goldsmith HH, Davidson RJ.(2009) Dynamic variation in pleasure in children predicts nonlinear change in lateral frontal brain electrical activity. Developmental Psychology. 2009 Mar;45(2):525-33.

Burk LR, Park JH, Armstrong JM, Klein MH, Goldsmith HH, Zahn-Waxler C, Essex MJ. (2007) Identification of early child and family risk factors for aggressive victim status in first grade. Journal of Abnormal Child Psychology. 2008 May;36(4):513-26.

Volbrecht MM, Lemery-Chalfant K, Aksan N, Zahn-Waxler C, Goldsmith HH. (2007) Examining the familial link between positive affect and empathy development in the second year. Journal of Genetic Psychology. 2007 Jun;168(2):105-29.

Van Hulle CA, Lemery-Chalfant K, Goldsmith HH. (2007) Genetic and environmental influences on socio-emotional behavior in toddlers: an initial twin study of the infant-toddler social and emotional assessment. Journal of Child Psychology and Psychiatry. 2007 Oct;48(10):1014-24.

Lemery-Chalfant K, Schreiber JE, Schmidt NL, Van Hulle CA, Essex MJ, Goldsmith HH. (2007) Assessing internalizing, externalizing, and attention problems in young children: validation of the MacArthur HBQ. Journal of the American Academy of Child and Adolescent Psychiatry. 2007 Oct;46(10):1315-23.

Goldsmith HH, Lemery-Chalfant K, Schmidt NL, Arneson CL, Schmidt CK. (2007) Longitudinal analyses of affect, temperament, and childhood psychopathology. Twin Research and Human Genetics. 2007 Feb;10(1):118-26.

Crawford TN, Shaver PR, Goldsmith HH. How affect regulation moderates the association between anxious attachment and neuroticism. Attachment & Human Development. 2007 Jun;9(2):95-109.

Lemery-Chalfant K, Goldsmith HH, Schmidt NL, Arneson CL, Van Hulle CA. (2006) Wisconsin Twin Panel: current directions and findings. Twin Research and Human Genetics. 2006 Dec;9(6):1030-7.

Boyce WT, Essex MJ, Alkon A, Goldsmith HH, Kraemer HC, Kupfer DJ. (2006) Early father involvement moderates biobehavioral susceptibility to mental health problems in middle childhood. Journal of the American Academy of Child and Adolescent Psychiatry. 2006 Dec;45(12):1510-20.

Essex MJ, Kraemer HC, Armstrong JM, Boyce WT, Goldsmith HH, Klein MH, Woodward H, Kupfer DJ. (2006) Exploring risk factors for the emergence of children's mental health problems. Archives of General Psychiatry. 2006 Nov;63(11):1246-56.

Schreiber JE, Shirtcliff E, Van Hulle C, Lemery-Chalfant K, Klein MH, Kalin NH, Essex MJ, Goldsmith HH. (2006) Environmental influences on family similarity in afternoon cortisol levels: twin and parent-offspring designs. Psychoneuroendocrinology. 2006 Oct;31(9):1131-7.

Goldsmith, H. H., Van Hulle, C. A., Arneson, C. L., Schreiber, J. E.. & Gernsbacher, M. A. (2006). A population-based twin study of parentally reported tactile and auditory defensiveness in young children. Journal of Abnormal Child Psychology. Jun;34(3):393-407.

Dalton, K. M., Nacewitz, B. M., Johnstone, T., Schaefer, H. S., Gernsbacher, M.A., Goldsmith, H. H., Alexander, A., & Davidson, R. J. (2005). Gaze-aversion and the neuronal circuitry of face processing in autism. Nature Neuroscience, 8, 519-526.

Gernsbacher, M. A., Dawson, M., & Goldsmith, H. H. (2005). Three reasons not to believe in an autism epidemic. Current Directions in Psychological Science, 14, 55-58.

Gernsbacher, M. A., Dissanayake, C., Goldsmith, H. H., Mundy, P.C., Rogers, S.J., & Sigman, M. (2005). Autism and deficits in attachment behavior. Science, 307, 1201-1203. (comment)

Buss, K. A., Goldsmith, H. H., & Davidson, R. J. (2005). Cardiac reactivity is associated with changes in negative emotion in 24-month-olds. Developmental Psychobiology, 46, 118-132.

Goldsmith, H. H., & Davidso , R. J. (2004). Disambiguating the components of emotion regulation. Child Development, 74, 361-365.

Nigg, J. T., Goldsmith, H. H., & Sachek, J. (2004). Temperament and Attention-Deficit/ yperactivity Disorder: The development of a multiple pathway model. Journal of Clinical Child and Adolescent Psychology, 33, 42-53.

Goldsmith, H. H., Lemery, K. S., & Essex, M. J. (2004). Temperament as a liability factor for childhood behavioral disorders: The concept of liability. In L. . DiLalla (Ed.). Behavior genetics principles: Perspectives in development, personality, and psychopathology. (pp. 19-39). Washington, DC: American Psychological Association.

Buss, K. A., Schumacher, J. R., Dolski, I., Kalin, N. H., Goldsmith, H. H., & Davidson, R. J. (2003). Right frontal brain activity, cortisol, and withdrawal behavior in 6-month-old infants. Behavioral Neurosciene, 117, 11-20.

Costello, E. J., Pine, D. S., Hammen, C. March, J. S., Plotsky, P. M., Weissman, M. M., Biederman, J., Goldsmith, H. H., Kaufman, J., Lewinsohn, P. M., Hellander, M., Hoagwood, K., Koretz, D. S., Nelson, C. A., & Leckman, J. F. (2002). Development and natural history of mood disorders. Biological Psychiatry Sep 15;52(6):529-42.

Goldsmith, H. H., & Lemery, K. S. (2000). Linking temperamental fearfulness and anxiety symptoms: A behavior-genetic perspective. Biological Psychiatry.48, 1199-1209.

Goldsmith, H. H., Lemery, K. S., Buss, K. A., & Campos, J. J. (1999). Genetic analyses of focal aspects of infant temperament. Developmental Psychology, 35, 972-985.