Environment, Developmental Origins, and Attention-Deficit/Hyperactivity Disorder

Nigg, Joel T.

doi:10.1001/archpediatrics.2011.905

Cited by 8 publications

(7 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our findings highlight the importance of preventing children from developing mental health difficulties following early diagnosis of ADHD and DBDs. Even among disorders of neurodevelopmental nature and presumed heritable predisposition, environmental adaptations and social experience are expected to have significant impact on outcomes [57]. For instance, parent training interventions focusing on addressing early DBDs have proven to be effective in improving adverse and antisocial outcomes [58].…”

Section: Discussionmentioning

confidence: 99%

Onset and Severity of Early Disruptive Behavioral Disorders in Treatment-Seeking Substance Use Disorder Patients with and without Attention-Deficit/Hyperactivity Disorder

et al. 2020

View full text Add to dashboard Cite

This study addressed the age of onset of conduct disorder (CD) and oppositional defiant disorder (ODD) in treatment-seeking substance use disorder (SUD) patients with and without adult attention-deficit/hyperactivity disorder (ADHD) and its association with early onset of SUD. Methods: We examined data from the 2nd International ADHD in Substance Use Disorders Prevalence Study, including 400 adults in SUD treatment from Puerto Rico, Hungary, and Australia. ADHD, SUD, and CD/ODD were assessed with the Conners Adult ADHD Diagnostic Interview for DSM-IV, the MINI International Neuropsychiatric Interview, and the K-SADS, respectively. Cox regression analyses modeled time to emergence of CD/ODD separately for SUD patients with and without adult ADHD. Linear regression models examined associations between age of onset of SUD and presence of ADHD and adjusted for sex, age, and country. To assess the mediating role of CD/ODD on the association of ADHD with onset of SUD, adjusted regression models were estimated. Results: Treatment-seeking SUD patients with ADHD presented an earlier onset of CD/ODD compared with those without ADHD. CD/ODD symptom loads were higher among González et al.

show abstract

Section: Discussionmentioning

confidence: 99%

Onset and Severity of Early Disruptive Behavioral Disorders in Treatment-Seeking Substance Use Disorder Patients with and without Attention-Deficit/Hyperactivity Disorder

et al. 2020

View full text Add to dashboard Cite

show abstract

“…The Developmental Origins of Health and Disease hypothesis (DOHaD; Gluckman and Hanson 2004;Mill and Petronis 2008;Nigg 2012;Swanson and Wadhwa 2008) builds on the theory of ''fetal programming'' (Barker 2007) and provides an integrative framework to conceptualize the interplay between environmental, genetic and epigenetic factors in determining birth and health outcomes. Briefly, DOHaD posits that the prenatal environmental influences are associated with birth outcomes.…”

Section: Developmental Origins Of Adhd: Epigenetic Programming and Nementioning

confidence: 99%

“…Multiple genetic and prenatal environmental risk factors for ADHD have been identified; however, it is unclear how genetic and environmental risk factors coalesce to alter ADHD risk. Researchers have begun to examine how genetic pathways may impact molecular and cellular processes and ADHD risk (Poelmans et al 2011;Yang et al 2013); however, there remains a significant need to understand the role of prenatal environmental risk factors in the etiology of ADHD (Nigg 2012).…”

Section: Introductionmentioning

confidence: 99%

Pre- and Perinatal Ischemia-Hypoxia, the Ischemia-Hypoxia Response Pathway, and ADHD Risk

et al. 2016

View full text Add to dashboard Cite

This review focuses on how measured pre- and perinatal environmental and (epi)genetic risk factors are interrelated and potentially influence one, of many, common developmental pathway towards ADHD. Consistent with the Developmental Origins of Health and Disease hypothesis, lower birth weight is associated with increased ADHD risk. Prenatal ischemia-hypoxia (insufficient blood and oxygen supply in utero) is a primary pathway to lower birth weight and produces neurodevelopmental risk for ADHD. To promote tissue survival in the context of ischemia-hypoxia, ischemia-hypoxia response (IHR) pathway gene expression is altered in the developing brain and peripheral tissues. Although altered IHR gene expression is adaptive in the context of ischemia-hypoxia, lasting IHR epigenetic modifications may lead to increased ADHD risk. Taken together, IHR genetic vulnerability to ischemia-hypoxia and IHR epigenetic alterations following prenatal ischemia-hypoxia may result in neurodevelopmental vulnerability for ADHD. Limitations of the extant literature and future directions for genetically-informed research are discussed.

show abstract

“…Early life risk factors for ADHD span the prenatal period (e.g., pregnancy complications), the perinatal period (e.g., low birth weight, delivery complications), and the early postnatal period (e.g., household poverty, psychosocial adversity) (Das Banerjee, Middleton, & Faraone, 2007;Froehlich et al, 2011;Russell, Ford, Rosenberg, & Kelly, 2014;Sciberras, Mulraney, Silva, & Coghill, 2017;Thapar, Cooper, Jefferies, & Stergiakouli, 2012). These risk factors are assumed to interact with genetic susceptibility and/or to initiate epigenetic processes that lead to disruptions to neural and cognitive development that underlie ADHD (Nigg, 2012a(Nigg, , 2012bThapar, Cooper, Eyre, & Langley, 2013). Virtually all studies that have investigated early life risk factors for ADHD have ignored variations in the age of ADHD symptom onset.…”

mentioning

confidence: 99%

Early life predictors of attention deficit/hyperactivity disorder symptomatology profiles from early through middle childhood

et al. 2019

View full text Add to dashboard Cite

This study used repeated measures data to identify developmental profiles of elevated risk for ADHD (i.e., six or more inattentive and/or hyperactive-impulsive symptoms), with an interest in the age at which ADHD risk first emerged. Risk factors that were measured across the first 3 years of life were used to predict profile membership. Participants included 1,173 children who were drawn from the Family Life Project, an ongoing longitudinal study of children's development in low-income, nonmetropolitan communities. Four heuristic profiles of ADHD risk were identified. Approximately two thirds of children never exhibited elevated risk for ADHD. The remaining children were characterized by early childhood onset and persistent risk (5%), early childhood limited risk (10%), and middle childhood onset risk (19%). Pregnancy and delivery complications and harsh-intrusive caregiving behaviors operated as general risk for all ADHD profiles. Parental history of ADHD was uniquely predictive of early onset and persistent ADHD risk, and low primary caregiver education was uniquely predictive of early childhood limited ADHD risk. Results are discussed with respect to how changes to the age of onset criterion for ADHD in DSM5 may affect etiological research and the need for developmental models of ADHD that inform ADHD symptom persistence and desistance.

show abstract

Environment, Developmental Origins, and Attention-Deficit/Hyperactivity Disorder

Cited by 8 publications

References 22 publications

Onset and Severity of Early Disruptive Behavioral Disorders in Treatment-Seeking Substance Use Disorder Patients with and without Attention-Deficit/Hyperactivity Disorder

Onset and Severity of Early Disruptive Behavioral Disorders in Treatment-Seeking Substance Use Disorder Patients with and without Attention-Deficit/Hyperactivity Disorder

Pre- and Perinatal Ischemia-Hypoxia, the Ischemia-Hypoxia Response Pathway, and ADHD Risk

Early life predictors of attention deficit/hyperactivity disorder symptomatology profiles from early through middle childhood

Contact Info

Product

Resources

About