Mobiele menu

Emotion regulation in parent-toddler interactions: potential mechanism to prevent the development of ADHD

Projectomschrijving

ADHD kan een grote impact hebben op het leven van een kind en het gezin. Huidige behandelingen kunnen de symptomen van ADHD verminderen, maar niet genezen of het langetermijnbeloop beïnvloeden. Het is daarom cruciaal na te gaan hoe ADHD ontstaat en of preventie mogelijk is. Opvallend genoeg is de preventie van ADHD een nauwelijks verkend onderzoeksterrein.

Doel

Ditonderzoek volgt 700 kinderen met een leeftijd vanaf 3 maanden tot 6 jaar. Dit is de periode vóór het ontstaan van ADHD. In deze leeftijdsgroep zullen we de vroege bio-psychosociale processen die gezamenlijk leiden tot ADHD bepalen. Op basis van deze informatie ontwikkelt dit project een screeningstool waarmee kinderen die een hoog risico lopen op het ontwikkelen van ADHD kunnen worden geïdentificeerd.

De verwachting is dat een substantieel deel van de kinderen die als peuter forse problemen hebben met emotiebeheersing later ADHD ontwikkelt. In dit onderzoek wordt ook onderzocht of het ontstaan van ADHD op latere leeftijd kan worden voorkomen door ouders te trainen het kind emotiebeheersingsvaardigheden te leren.

Verslagen


Samenvatting van de aanvraag

Background Although early screening and intervention in Attention-Deficit/Hyperactivity Disorder (ADHD) have gained some ground in the past decade, this area has overall received very little research attention. The handful of studies on preschoolers who have already developed ADHD (4-6 years old) show treatment is feasible and (partly) effective. However, prevention of ADHD is a completely untouched research topic and children at risk of ADHD (i.e. before onset) rarely come to attention for clinical evaluation. Preventive intervention in very young children may, however, may yield the strongest effects. Hypothesis We hypothesize that Emotion Dysregulation (ED) -an emotion-driven dysregulated behavioral response- in infants and toddlers is an important causal factor for the subsequent onset of ADHD, and that it is amenable to change. Heritability estimates of ED are relatively low, in contrast to high heritability estimates for ADHD, suggesting an influential role of the environment. Indeed, parents provide the “emotion socialization environment” through which children’s emotion regulation strategies are learned, both by passive learning, i.e. by children observing parents’ own regulation strategies, and by active parental regulation of their young children’s emotions. However, ADHD runs in families, the majority of parents with ADHD have children at high risk of ADHD and ED is highly prevalent in adults with ADHD. Moreover, dysregulated emotional outbursts of the child easily elicit or worsen parental ED, and children with ED in turn have an increased sensitivity to parental ED. In these high-risk families, the learning environment for emotion regulation in children at risk can be improved, such that chronic cascades of mutually amplifying ED within parent-child interactions and a culmination towards onset of clinical ADHD can be prevented. Improving ED through parent-child interaction therapy (PCIT) is particularly promising for children at high risk for developing ADHD, as prior studies suggest that these children are very susceptible to parental use of emotion socialization practices – both supportive and non-supportive. Interventions cannot change the genetic liability of ADHD as it runs through families affected by ADHD, but can improve the circumstances for young offspring such that their liability will not unfold into the full extreme. Objectives Our overall aim is to identify the mechanisms leading to the onset of ADHD that are amenable to change, in order to prevent a full, clinical, onset of ADHD. WP1. Conduct an in-depth longitudinal cohort study in N=700 children spanning infancy (3 months) to first grade (6 years) capturing the early bio-psycho-social mechanisms leading to ADHD. This work will give detailed mechanistic insights in the causal processes leading to ADHD which we will translate into a screening tool aimed at the identification of infants and toddlers at high risk of ADHD. WP2. Conduct a proof-of-principle intervention study aimed at showing that interruption of the mutually amplifying ED cascades in ultra-high risk parent-child dyads (father-child and mother-child) through PCIT prevents the escalation towards ADHD in the child. If results are positive, this work will pave the way for implementing PCIT in secondary prevention and intervention care for vulnerable children at (ultra) high risk for ADHD. Method WP1. We include families from the general population and high- and ultra-high risk families. The population and high risk offspring cohorts (planned: N=500) are part of the already ongoing TRAILS-NEXT cohort (offspring from parents taking part in the TRAILS and TRAILS Clinical Cohort studies, respectively). Measurement is at 3 months 2.5y, 4.5y and 6y. A new ultra-high risk cohort (N=200) completely aligned with TRAILS-NEXT will be recruited. High risk is defined by at least one parent with childhood behavioral problems (before age 11) and ultra-high risk by presence of at least one parent with a current diagnosis of ADHD (adult-persistent ADHD is the most severe form of ADHD). Detailed on-site recorded live mother-child and father-child interactions and behavioral and physiological measures of ED (Autonomic Nervous System reactivity) in the child and parent are used to test the hypothesized culmination towards ADHD in the child. Implementation includes a screening tool for early detection of infants and toddlers at high risk for ADHD. WP2. An additional sample of children (n=80; age 2y-3.5y) meeting ultra-high risk criteria with clinical levels of ED will be randomized in a 1:1 ratio to either PCIT or observation only. Implementation includes training new PCIT therapists and appointing a national PCIT coordinator to stimulate PCIT in clinical practice. Client participation Patient representatives of the ADHD patient organisations (Balans and Impuls&Woortblind) and from the clinical centers strongly support this proposal and have agreed to give advice at every stage of the project.

Onderwerpen

Kenmerken

Projectnummer:
636340002
Looptijd: 53%
Looptijd: 53 %
2020
2028
Onderdeel van programma:
Gerelateerde subsidieronde:
Projectleider en penvoerder:
dr. C.A. Hartman
Verantwoordelijke organisatie:
Radboud Universitair Medisch Centrum