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Dive into the research topics where Kimberly J. Saudino is active.

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Featured researches published by Kimberly J. Saudino.


Journal of Abnormal Child Psychology | 2010

Exploring the Relationship between Autistic-Like Traits and ADHD Behaviors in Early Childhood: Findings from a Community Twin Study of 2-Year-Olds.

Angelica Ronald; Lisa R. Edelson; Philip Asherson; Kimberly J. Saudino

Behaviors characteristic of autism and ADHD emerge in early childhood, yet research investigating their comorbidity has focused on older children. This study aimed to explore the nature of the relationship between autistic-like traits and ADHD behaviors in a community sample of 2-year-olds. Twins from the Boston University Twin Project (Nu2009=u2009312 pairs) were assessed by their parents on autistic-like traits and ADHD behaviors using the Childhood Behavior Checklist. Phenotypic analyses showed that after controlling for general cognitive ability and socioeconomic status, autistic-like traits (total scale as well as social and nonsocial subscales) correlated positively with ADHD behaviors (ru2009=u20090.23–0.26). Structural equation model-fitting analyses revealed that there were modest shared genetic influences between ADHD- and autistic traits (genetic correlation = 0.27) as well as some common environmental influences explaining their covariation. Implications for identifying shared biological pathways underlying autistic-like traits and ADHD behaviors are discussed.


Behavior Genetics | 2010

Wait For It! A Twin Study of Inhibitory Control in Early Childhood

Jeffrey R. Gagne; Kimberly J. Saudino

Inhibitory control (IC) is a dimension of child temperament that emerges in toddlerhood and involves the ability to regulate behavior in response to instructions or expectations. In general, children with low levels of IC have more cognitive and social difficulties, and higher levels of problem behaviors. Unfortunately, there is a paucity of research on the heritability of this important behavioral dimension. The present study used a twin design to examine the extent to which genetic and environmental factors contribute to individual differences in IC. Laboratory and parent assessments of IC were conducted on 294 same-sex twin pairs (133 MZ, 161 DZ) at 24xa0months of age. Model-fitting analyses showed that genetic factors accounted for 38 and 58% of the variance in laboratory- and parent-rated IC, respectively. Multivariate genetic analyses also revealed that the covariance between observed and parent-assessed IC could be predominantly explained by common genetic influences.


Journal of Child Psychology and Psychiatry | 2011

The genetic etiology of inhibitory control and behavior problems at 24 months of age.

Jeffrey R. Gagne; Kimberly J. Saudino; Philip Asherson

BACKGROUNDnTo investigate links between inhibitory control (IC) and behavior problems in early childhood, as well as genetic and environmental covariances between these two constructs.nnnMETHODSnParent and laboratory ratings of IC and parent ratings of externalizing and attention deficit hyperactivity disorder behaviors were administered at 24 months of age on a sample of 291 same-sex twin pairs (131 monozygotic, 160 dizygotic).nnnRESULTSnThere were significant phenotypic associations between both IC assessments and the two areas of behavioral maladjustment (correlations ranged from -.13 to -.57). Multivariate analyses revealed that phenotypic covariance between IC and behavior problems could be substantially explained by common genetic influences (genetic correlations ranged from -.30 to -.74). Parent ratings of IC showed higher phenotypic and genetic correlations with behavior problems than lab ratings of IC.nnnCONCLUSIONSnThis study is the first to examine the etiology of the covariance between IC and related behavioral difficulties in toddlerhood. Findings suggest that low levels of IC can be considered a genetic risk factor for the development of early emerging behavior problems.


Child Development | 2008

Genetic Influences on Activity Level in Early Childhood: Do Situations Matter?

Kimberly J. Saudino; Jeffrey A. Zapfe

Although genetic influences on individual differences in activity level (AL) are well documented, few studies have considered the etiology of AL from a contextual perspective. In the present study, cross-situational and context-specific genetic effects on individual differences in AL at age 2 were examined. The AL of 312 twin pairs (144 monozygotic and 168 dzygotic) was mechanically assessed with actigraphs in the home and in laboratory test and play situations. AL displayed significant genetic variance in all 3 situations. Moreover, actigraph scores significantly correlated across situations. Multivariate genetic model-fitting analyses found that the observed cross-situational continuity in AL was due entirely to genetic factors. Situational differences in AL arise from genetic, shared environmental, and nonshared environmental influences.


Child Development | 2012

Sources of Continuity and Change in Activity Level in Early Childhood

Kimberly J. Saudino

Actigraphs and parent and observer ratings were used to explore genetic influences on continuity and change in activity level (AL) in early childhood. Over 300 pairs of twins wore actigraphs for a 48-hr period in the home and laboratory at ages 2 and 3. AL was genetically influenced at both ages with little evidence of differential heritability across age. For all measures, genetic influences contributed to phenotypic continuity. With the exception of the actigraph measure of AL in the home, new genetic effects emerged at age 3 indicating that genetic factors influence both continuity and change in AL in early childhood. Nonshared environmental influences were also a source of change in AL across the transition from infancy to early childhood.


Genes, Brain and Behavior | 2010

A genetic study of ADHD and activity level in infancy

Nicholas E. Ilott; Kimberly J. Saudino; Alexis C. Wood; Philip Asherson

It is well known that there are strong genetic influences on attention‐deficit hyperactivity disorder (ADHD), with genetic association studies providing good evidence for the involvement of the dopamine neurotransmitter system in its aetiology. Developmental origins of ADHD represent an interesting area of research to understand the genetics that underlie early appearing individual differences. However, understanding the molecular basis of ADHD requires accurate, unbiased, heritable measures that can be used for molecular genetic association analyses. We take two approaches to examine the genetics of ADHD behaviours in infancy. Using quantitative genetic techniques, we explore the relationship between objective measures of activity level (AL) in both home and laboratory environments as well as with parent ratings of ADHD symptoms in a population sample of 2‐year‐old twins. Molecular association analyses of these measures examine candidate genes previously associated with ADHD. We find that ADHD symptoms, AL in the home and AL in the lab represent heritable phenotypes in 2‐year‐old infants. AL measured in the home has a strong genetic correlation with symptoms of ADHD, whereas AL in the lab correlates only modestly with the same ADHD measure. Genetic correlations suggest that AL in the home is more comparable than AL in the lab to ADHD behaviour and support the separation of all three for molecular analyses. There was modest evidence for association between DAT1, NET1 and ADHD symptom scores, as well as between DAT1 and AL in the lab.


Developmental Science | 2009

Do different measures tap the same genetic influences? A multi-method study of activity level in young twins

Kimberly J. Saudino

Activity level (AL) is a highly salient feature of child behaviour that has been linked to developmental outcome. Twin studies of parent-rated, observer-rated and mechanically assessed AL in childhood find that AL is genetically influenced. Few studies, however, consider whether different methods of assessing AL have a shared genetic etiology. Those that do, confound methods and situations. The present study examined whether actigraph and rater-based (parent, observer) measures of AL tap the same genetic influences in a sample of 312 2-year-old twin pairs. Methods were studied within the same situation, thereby controlling for situational influences on AL. The genetic correlation between actigraph and parent-rated AL in the home was .38, indicating modest genetic overlap between the two methods. In contrast, the correlation of genetic effects on actigraph and observer-rated AL in the laboratory was .95, indicating that both laboratory-based measures of AL are influenced by the same genetic effects.


BMC Psychiatry | 2010

Genetic influences on attention deficit hyperactivity disorder symptoms from age 2 to 3: A quantitative and molecular genetic investigation

Nicholas E. Ilott; Kimberly J. Saudino; Philip Asherson

BackgroundA twin study design was used to assess the degree to which additive genetic variance influences ADHD symptom scores across two ages during infancy. A further objective in the study was to observe whether genetic association with a number of candidate markers reflects results from the quantitative genetic analysis.MethodWe have studied 312 twin pairs at two time-points, age 2 and age 3. A composite measure of ADHD symptoms from two parent-rating scales: The Child Behavior Checklist/1.5 - 5 years (CBCL) hyperactivity scale and the Revised Rutter Parent Scale for Preschool Children (RRPSPC) was used for both quantitative and molecular genetic analyses.ResultsAt ages 2 and 3 ADHD symptoms are highly heritable (h2= 0.79 and 0.78, respectively) with a high level of genetic stability across these ages. However, we also observe a significant level of genetic change from age 2 to age 3. There are modest influences of non-shared environment at each age independently (e2= 0.22 and 0.21, respectively), with these influences being largely age-specific. In addition, we find modest association signals in DAT1 and NET1 at both ages, along with suggestive specific effects of 5-HTT and DRD4 at age 3.ConclusionsADHD symptoms are heritable at ages 2 and 3. Additive genetic variance is largely shared across these ages, although there are significant new effects emerging at age 3. Results from our genetic association analysis reflect these levels of stability and change and, more generally, suggest a requirement for consideration of age-specific genotypic effects in future molecular studies.


Behavior Genetics | 2009

Genetic and Environmental Influences on Autistic-Like Behaviors in 2-Year-Old Twins

Lisa R. Edelson; Kimberly J. Saudino

This study aims to explore the genetic and environmental contributions to autistic-like behaviors in a general population sample of toddlers. In a classic twin study of 313 same-sex, 2-year-old twin pairs, autistic-like behaviors were assessed via parent ratings on the pervasive developmental problems subscale of the Child Behavior Checklist and observationally using tester ratings on the orientation/engagement subscale of the Behavior Rating Scale. Analyses show moderate, significant heritabilities for both measures of autistic-like behaviors, as well as modest, but significant shared environmental effects. These genetic and environmental influences overlap greatly between the two measures. Autistic-like behaviors in 2-year-old twins are largely genetic in etiology, but are also influenced by a shared environmental component at this age. This is the first study to examine the etiology of such behaviors in a sample of toddlers, thus providing novel information which could guide future research on genetic and environmental factors that affect these behaviors.


Emotion | 2013

Genetic and environmental influences on individual differences in emotion regulation and its relation to working memory in toddlerhood.

Manjie Wang; Kimberly J. Saudino

This is the first study to explore genetic and environmental contributions to individual differences in emotion regulation in toddlers, and the first to examine the genetic and environmental etiology underlying the association between emotion regulation and working memory. In a sample of 304 same-sex twin pairs (140 MZ, 164 DZ) at age 3, emotion regulation was assessed using the Behavior Rating Scale of the Bayley Scales of Infant Development (BRS; Bayley, 1993), and working memory was measured by the visually cued recall (VCR) task (Zelazo, Jacques, Burack, & Frye, 2002) and several memory tasks from the Mental Scale of the BSID. Based on model-fitting analyses, both emotion regulation and working memory were significantly influenced by genetic and nonshared environmental factors. Shared environmental effects were significant for working memory, but not for emotion regulation. Only genetic factors significantly contributed to the covariation between emotion regulation and working memory.

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Jeffrey R. Gagne

University of Texas at Arlington

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