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Dive into the research topics where Renate Houts is active.

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Featured researches published by Renate Houts.


Proceedings of the National Academy of Sciences of the United States of America | 2011

A gradient of childhood self-control predicts health, wealth, and public safety

Terrie E. Moffitt; Louise Arseneault; Daniel W. Belsky; Nigel Dickson; Robert J. Hancox; HonaLee Harrington; Renate Houts; Richie Poulton; Brent W. Roberts; Stephen A. Ross; Malcolm R. Sears; W. Murray Thomson; Avshalom Caspi

Policy-makers are considering large-scale programs aimed at self-control to improve citizens’ health and wealth and reduce crime. Experimental and economic studies suggest such programs could reap benefits. Yet, is self-control important for the health, wealth, and public safety of the population? Following a cohort of 1,000 children from birth to the age of 32 y, we show that childhood self-control predicts physical health, substance dependence, personal finances, and criminal offending outcomes, following a gradient of self-control. Effects of childrens self-control could be disentangled from their intelligence and social class as well as from mistakes they made as adolescents. In another cohort of 500 sibling-pairs, the sibling with lower self-control had poorer outcomes, despite shared family background. Interventions addressing self-control might reduce a panoply of societal costs, save taxpayers money, and promote prosperity.


JAMA | 2008

Moderate-to-vigorous physical activity from ages 9 to 15 years.

Philip R. Nader; Robert H. Bradley; Renate Houts; Susan L. Mcritchie; Marion O'Brien

CONTEXT Decreased physical activity plays a critical role in the increase in childhood obesity. Although at least 60 minutes per day of moderate-to-vigorous physical activity (MVPA) is recommended, few longitudinal studies have determined the recent patterns of physical activity of youth. OBJECTIVE To determine the patterns and determinants of MVPA of youth followed from ages 9 to 15 years. DESIGN, SETTING, AND PARTICIPANTS Longitudinal descriptive analyses of the 1032 participants in the 1991-2007 National Institute of Child Health and Human Development Study of Early Child Care and Youth Development birth cohort from 10 study sites who had accelerometer-determined minutes of MVPA at ages 9 (year 2000), 11 (2002), 12 (2003), and 15 (2006) years. Participants included boys (517 [50.1%]) and girls (515 [49.9%]); 76.6% white (n = 791); and 24.5% (n = 231) lived in low-income families. MAIN OUTCOME MEASURE Mean MVPA minutes per day, determined by 4 to 7 days of monitored activity. RESULTS At age 9 years, children engaged in MVPA approximately 3 hours per day on both weekends and weekdays. Weekday MVPA decreased by 37 minutes per year [corrected], while weekend MVPA decreased by 39 minutes per year [corrected]. By age 15 years, adolescents were only engaging in MVPA for 50 minutes per weekday [corrected] and 36 minutes per weekend day [corrected]. Boys were more active than girls, spending 18 and 14 more minutes per day [corrected] in MVPA on the weekdays and weekends, respectively. The rate of decrease in MVPA was the same for boys and girls. The estimated age at which girls crossed below the recommended 60 minutes of MVPA per day was approximately 13.2 years for weekday [corrected] activity compared with boys at 14.9 years [corrected], and for weekend activity, girls crossed below the recommended 60 minutes of MVPA at 12.7 years [corrected] compared with boys at 13.6 years [corrected]. CONCLUSION In this study cohort, measured physical activity decreased significantly between ages 9 and 15 years.


Proceedings of the National Academy of Sciences of the United States of America | 2012

Persistent cannabis users show neuropsychological decline from childhood to midlife

Madeline H. Meier; Avshalom Caspi; Antony Ambler; HonaLee Harrington; Renate Houts; Richard S.E. Keefe; Kay McDonald; Aimee L. Ward; Richie Poulton; Terrie E. Moffitt

Recent reports show that fewer adolescents believe that regular cannabis use is harmful to health. Concomitantly, adolescents are initiating cannabis use at younger ages, and more adolescents are using cannabis on a daily basis. The purpose of the present study was to test the association between persistent cannabis use and neuropsychological decline and determine whether decline is concentrated among adolescent-onset cannabis users. Participants were members of the Dunedin Study, a prospective study of a birth cohort of 1,037 individuals followed from birth (1972/1973) to age 38 y. Cannabis use was ascertained in interviews at ages 18, 21, 26, 32, and 38 y. Neuropsychological testing was conducted at age 13 y, before initiation of cannabis use, and again at age 38 y, after a pattern of persistent cannabis use had developed. Persistent cannabis use was associated with neuropsychological decline broadly across domains of functioning, even after controlling for years of education. Informants also reported noticing more cognitive problems for persistent cannabis users. Impairment was concentrated among adolescent-onset cannabis users, with more persistent use associated with greater decline. Further, cessation of cannabis use did not fully restore neuropsychological functioning among adolescent-onset cannabis users. Findings are suggestive of a neurotoxic effect of cannabis on the adolescent brain and highlight the importance of prevention and policy efforts targeting adolescents.


Pediatrics | 2006

Identifying Risk for Obesity in Early Childhood

Philip R. Nader; Marion O'Brien; Renate Houts; Robert H. Bradley; Jay Belsky; Robert Crosnoe; Sarah L. Friedman; Zuguo Mei; Elizabeth J. Susman

OBJECTIVES. Our aim with this study was to assist clinicians by estimating the predictive value of earlier levels of BMI status on later risk of overweight and obesity during the middle childhood and early adolescent years. METHODS. We present growth data from the National Institute of Child Health and Human Development Study of Early Child Care and Youth Development, a longitudinal sample of 1042 healthy US children in 10 locations. Born in 1991, their growth reflects the secular trend of increasing overweight/obesity in the population. Height and weight of participating children in the study were measured at 7 time points. We examined odds ratios for overweight and obesity at age 12 years comparing the frequency with which children did versus did not reach specific BMI percentiles in the preschool- and elementary-age periods. To explore the question of whether and when earlier BMI was predictive of weight status at age 12 years, we used logistic regression to obtain the predicted probabilities of being overweight or obese (BMI ≥85%) at 12 years old on the basis of earlier BMI. RESULTS. Persistence of obesity is apparent for both the preschool and elementary school period. Children who were ever overweight (>85th percentile), that is, ≥1 time at ages 24, 36, or 54 months during the preschool period were >5 times as likely to be overweight at age 12 years than those who were below the 85th percentile for BMI at all 3 of the preschool ages. During the elementary school period, ages 7, 9, and 11 years, the more times a child was overweight, the greater the odds of being overweight at age 12 years relative to a child who was never overweight. Sixty percent of children who were overweight at any time during the preschool period and 80% of children who were overweight at any time during the elementary period were overweight at age 12 years. Follow-up calculations showed that 2 in 5 children whose BMIs were ≥50th percentile by age 3 years were overweight at age 12 years. No children who were <50th percentile for BMI at all points during elementary school were overweight at age 12 years. Children who have higher range BMIs earlier, but not at the 85th percentile, are also more likely to be overweight at age 12 years. Even at time points before and including age 9 years, children whose BMIs are between the 75th and 85th percentile have an ∼40% to 50% chance of being overweight at age 12 years. Children at 54 months old whose BMIs are between the 50th and 75th percentile are 4 times more likely to be overweight at age 12 years than their contemporaries who are <50th percentile, and those whose BMIs are between the 75th and 85th percentile are >6 times more likely to be overweight at age 12 years than those <50th percentile. CONCLUSIONS. The data from this study indicate that children with BMIs >85th percentile, as well as with BMIs in the high reference range are more likely than children whose BMI is <50th percentile to continue to gain weight and reach overweight status by adolescence. Pediatricians can be confident in counseling parents to begin to address the at-risk childs eating and activity patterns rather than delaying in hopes that overweight and the patterns that support it will resolve themselves in due course. Identifying children at risk for adolescent obesity provides physicians with an opportunity for earlier intervention with the goal of limiting the progression of abnormal weight gain that results in the development of obesity-related morbidity.


Clinical psychological science | 2014

The p Factor: One General Psychopathology Factor in the Structure of Psychiatric Disorders?

Avshalom Caspi; Renate Houts; Daniel W. Belsky; Sidra Goldman-Mellor; HonaLee Harrington; Salomon Israel; Madeline H. Meier; Sandhya Ramrakha; Idan Shalev; Richie Poulton; Terrie E. Moffitt

Mental disorders traditionally have been viewed as distinct, episodic, and categorical conditions. This view has been challenged by evidence that many disorders are sequentially comorbid, recurrent/chronic, and exist on a continuum. Using the Dunedin Multidisciplinary Health and Development Study, we examined the structure of psychopathology, taking into account dimensionality, persistence, co-occurrence, and sequential comorbidity of mental disorders across 20 years, from adolescence to midlife. Psychiatric disorders were initially explained by three higher-order factors (Internalizing, Externalizing, and Thought Disorder) but explained even better with one General Psychopathology dimension. We have called this dimension the p factor because it conceptually parallels a familiar dimension in psychological science: the g factor of general intelligence. Higher p scores are associated with more life impairment, greater familiality, worse developmental histories, and more compromised early-life brain function. The p factor explains why it is challenging to find causes, consequences, biomarkers, and treatments with specificity to individual mental disorders. Transdiagnostic approaches may improve research.


American Educational Research Journal | 2008

Classroom Effects on Children’s Achievement Trajectories in Elementary School

Robert C. Pianta; Jay Belsky; Nathan Vandergrift; Renate Houts; Frederick J. Morrison

This nonexperimental, longitudinal field study examines the extent to which variation in observed classroom supports (quality of emotional and instructional interactions and amount of exposure to literacy and math activities) predicts trajectories of achievement in reading and math from 54 months to fifth grade. Growth mixture modeling detected two latent classes of readers: fast readers whose skills developed rapidly and leveled off, and a typical group for which reading growth was somewhat less rapid. Only one latent class was identified for math achievement. For reading, there were small positive associations between observed emotional quality of teacher-child interactions and growth. Growth in math achievement showed small positive relations with observed emotional interactions and exposure to math activities. There was a significant interaction between quality and quantity of instruction for reading such that at higher levels of emotional quality there was less of a negative association between amount of literacy exposure and reading growth.


American Journal of Psychiatry | 2010

Static and Dynamic Cognitive Deficits in Childhood Preceding Adult Schizophrenia: A 30-Year Study

Abraham Reichenberg; Avshalom Caspi; HonaLee Harrington; Renate Houts; Richard S.E. Keefe; Robin M. Murray; Richie Poulton; Terrie E. Moffitt

OBJECTIVE Premorbid cognitive deficits in schizophrenia are well documented and have been interpreted as supporting a neurodevelopmental etiological model. The authors investigated the following three unresolved questions about premorbid cognitive deficits: What is their developmental course? Do all premorbid cognitive deficits follow the same course? Are premorbid cognitive deficits specific to schizophrenia or shared by other psychiatric disorders? METHOD Participants were members of a representative cohort of 1,037 males and females born between 1972 and 1973 in Dunedin, New Zealand. Cohort members underwent follow-up evaluations at specific intervals from age 3 to 32 years, with a 96% retention rate. Cognitive development was analyzed and compared in children who later developed schizophrenia or recurrent depression as well as in healthy comparison subjects. RESULTS Children who developed adult schizophrenia exhibited developmental deficits (i.e., static cognitive impairments that emerge early and remain stable) on tests indexing verbal and visual knowledge acquisition, reasoning, and conceptualization. In addition, these children exhibited developmental lags (i.e., growth that is slower relative to healthy comparison subjects) on tests indexing processing speed, attention, visual-spatial problem solving ability, and working memory. These two premorbid cognitive patterns were not observed in children who later developed recurrent depression. CONCLUSIONS These findings suggest that the origins of schizophrenia include two interrelated developmental processes evident from childhood to early adolescence (ages 7-13 years). Children who will grow up to develop adult schizophrenia enter primary school struggling with verbal reasoning and lag further behind their peers in working memory, attention, and processing speed as they get older.


Molecular Psychiatry | 2013

Exposure to violence during childhood is associated with telomere erosion from 5 to 10 years of age: a longitudinal study

Idan Shalev; Terrie E. Moffitt; Karen Sugden; Benjamin Williams; Renate Houts; Andrea Danese; Jonathan Mill; Louise Arseneault; Avshalom Caspi

There is increasing interest in discovering mechanisms that mediate the effects of childhood stress on late-life disease morbidity and mortality. Previous studies have suggested one potential mechanism linking stress to cellular aging, disease and mortality in humans: telomere erosion. We examined telomere erosion in relation to childrens exposure to violence, a salient early-life stressor, which has known long-term consequences for well-being and is a major public-health and social-welfare problem. In the first prospective-longitudinal study with repeated telomere measurements in children while they experienced stress, we tested the hypothesis that childhood violence exposure would accelerate telomere erosion from age 5 to age 10 years. Violence was assessed as exposure to maternal domestic violence, frequent bullying victimization and physical maltreatment by an adult. Participants were 236 children (49% females; 42% with one or more violence exposures) recruited from the Environmental-Risk Longitudinal Twin Study, a nationally representative 1994–1995 birth cohort. Each childs mean relative telomere length was measured simultaneously in baseline and follow-up DNA samples, using the quantitative PCR method for T/S ratio (the ratio of telomere repeat copy numbers to single-copy gene numbers). Compared with their counterparts, the children who experienced two or more kinds of violence exposure showed significantly more telomere erosion between age-5 baseline and age-10 follow-up measurements, even after adjusting for sex, socioeconomic status and body mass index (B=−0.052, s.e.=0.021, P=0.015). This finding provides support for a mechanism linking cumulative childhood stress to telomere maintenance, observed already at a young age, with potential impact for life-long health.


Epigenetics | 2010

A longitudinal study of epigenetic variation in twins.

Chloe Wong; Avshalom Caspi; Benjamin Williams; Ian Craig; Renate Houts; Antony Ambler; Terrie E. Moffitt; Jonathan Mill

DNA methylation is a key epigenetic mechanism involved in the developmental regulation of gene expression. Alterations in DNA methylation are established contributors to inter-individual phenotypic variation and have been associated with disease susceptibility. The degree to which changes in loci-specific DNA methylation are under the influence of heritable and environmental factors is largely unknown. In this study, we quantitatively measured DNA methylation across the promoter regions of the dopamine receptor 4 gene (DRD4), the serotonin transporter gene (SLC6A4/SERT) and the X-linked monoamine oxidase A gene (MAOA) using DNA sampled at both ages 5 and 10 years in 46 MZ twin-pairs and 45 DZ twin-pairs (total n=182). Our data suggest that DNA methylation differences are apparent already in early childhood, even between genetically identical individuals, and that individual differences in methylation are not stable over time. Our longitudinal-developmental study suggests that environmental influences are important factors accounting for interindividual DNA methylation differences, and that these influences differ across the genome. The observation of dynamic changes in DNA methylation over time highlights the importance of longitudinal research designs for epigenetic research.


American Journal of Psychiatry | 2015

Is Adult ADHD a Childhood-Onset Neurodevelopmental Disorder? Evidence From a Four-Decade Longitudinal Cohort Study

Terrie E. Moffitt; Renate Houts; Philip Asherson; Daniel W. Belsky; David L. Corcoran; Maggie Hammerle; HonaLee Harrington; Sean Hogan; Madeline H. Meier; Guilherme V. Polanczyk; Richie Poulton; Sandhya Ramrakha; Karen Sugden; Benjamin Williams; Luis Augusto Rohde; Avshalom Caspi

OBJECTIVE Despite a prevailing assumption that adult ADHD is a childhood-onset neurodevelopmental disorder, no prospective longitudinal study has described the childhoods of the adult ADHD population. The authors report follow-back analyses of ADHD cases diagnosed in adulthood, alongside follow-forward analyses of ADHD cases diagnosed in childhood, in one cohort. METHOD Participants belonged to a representative birth cohort of 1,037 individuals born in Dunedin, New Zealand, in 1972 and 1973 and followed to age 38, with 95% retention. Symptoms of ADHD, associated clinical features, comorbid disorders, neuropsychological deficits, genome-wide association study-derived polygenic risk, and life impairment indicators were assessed. Data sources were participants, parents, teachers, informants, neuropsychological test results, and administrative records. Adult ADHD diagnoses used DSM-5 criteria, apart from onset age and cross-setting corroboration, which were study outcome measures. RESULTS As expected, childhood ADHD had a prevalence of 6% (predominantly male) and was associated with childhood comorbid disorders, neurocognitive deficits, polygenic risk, and residual adult life impairment. Also as expected, adult ADHD had a prevalence of 3% (gender balanced) and was associated with adult substance dependence, adult life impairment, and treatment contact. Unexpectedly, the childhood ADHD and adult ADHD groups comprised virtually nonoverlapping sets; 90% of adult ADHD cases lacked a history of childhood ADHD. Also unexpectedly, the adult ADHD group did not show tested neuropsychological deficits in childhood or adulthood, nor did they show polygenic risk for childhood ADHD. CONCLUSIONS The findings raise the possibility that adults presenting with the ADHD symptom picture may not have a childhood-onset neurodevelopmental disorder. If this finding is replicated, then the disorders place in the classification system must be reconsidered, and research must investigate the etiology of adult ADHD.

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Jay Belsky

University of California

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