Insufficient inhibitory control is one pathway through which early adversity is related to a range of problems including excessive alcohol use, tobacco use, and unhealthy eating. The proposed research leverages a neurally informed model of inhibitory control and how it can be improved to test the efficacy of a person-centered inhibitory control intervention in a sample of mid-life individuals with early adversity. The knowledge obtained by this study could be scaled into a flexible, low-cost, and wide-ranging intervention to remediate some of the effects of early adversity on inhibitory control and thus a number of prevalent health risking behaviors.
Early adversity (EA) in humans is a major contributing factor to a range of deleterious physical and mental health outcomes extending through adulthood such as depression and anxiety, obesity and heart disease, and premature death. In addition to detracting significantly from individual well being and quality of life, these conditions also consume considerable resources from federal, state, and community organizations. The mechanisms through which EA exerts its effects on these outcomes are increasingly well understood, and include neurocognitive pathways related to executive function. An intervention that can successfully target, engage with, and alter the functioning of one or more of these mechanisms would be a promising way of mitigating the impact of EA on deleterious outcomes later in life. The proposed research focuses on one such pathway-deficits in inhibitory control (IC)-and tests the feasibility and efficacy of an intervention to increase functioning in that pathway in a sample of individuals who experienced EA. The intervention is grounded in a neurally informed model of change that specifies deficits in IC as an underlying causal factor common to several health-risking behaviors (HRBs). These IC deficits emerge during development as a result of a range of EA, and, critically, can be remediated in mid-life through targeted intervention. Research from our laboratory has validated an intervention that can increase IC performance and alter its underlying neural systems in young adults (Berkman, Kahn, \& Merchant, 2014). The next step in this program of research, proposed here, is to test the efficacy of that intervention in a sample of mid-life individuals who have experienced EA and the extent to which our intervention generalizes to HRBs that are prevalent in that sample. The first Aim is to test whether the intervention alters the IC system in tasks both similar to and dissimilar from the training task in terms of both behavioral performance and neural functioning. The second Aim is to test whether alterations in the functioning of the underlying neural systems mediate the effect of the intervention on performance and disinhibition-related HRBs. The two Aims will be accomplished within the context of a single randomized controlled trial (RCT) with two arms (IC training vs. active control) and pre-post measurements of IC performance, IC neural systems, and HRBs. All participants (N = 110) come to the lab for an initial assessment of behavioral / neural measures of IC and HRBs, among other measures. Then, participants are randomly assigned to receive a Person-Centered Inhibitory Control (PeCIC) training or active control training, every other day for 3-4 weeks. The PeCIC systematically pairs IC engagement with alcohol, tobacco, and/or energy-dense food cues, depending on each participant's reports of disinhibited behavior in those domains. The active control task uses personalized cues and response time tasks but does not involve IC. Finally, participants return to the laboratory for an endpoint assessment where all baseline measures are repeated. The two Aims will be robustly tested in a series of analyses comparing the behavioral and neural change from pre- to postintervention between the groups.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
PREVENTION
Masking
SINGLE
Enrollment
103
A brief, computer-based, multisession training aimed at increasing the connection between environmental risk cues (e.g., cigarettes) and engagement of the brain network for inhibitory control.
A brief computer-based, multisession training aimed at training behavioral responses to personalized environmental risk cues (e.g., cigarettes) that does not engage the inhibitory control network of the brain.
University of Oregon, Social and Affective Neuroscience Laboratory
Eugene, Oregon, United States
Inhibitory control performance, Task 1
Performance on a standard inhibitory control task (Stop-Signal) with personal risk cues
Time frame: 1 month
Inhibitory control performance, Task 2
Performance on a standard inhibitory control task (Go/No-Go) with personal risk cues
Time frame: 1 month
Inhibitory control neural activity
Early ("proactive") engagement of the inferior frontal gyrus and dorsal anterior cingulate cortex during the inhibitory control tasks
Time frame: 1 month
Far transfer to a task related to inhibitory control, Behavioral marker
Performance on a standard risky-behavior task (Balloon Analogue Risk task)
Time frame: 1 month
Far transfer to a task related to inhibitory control, Neural marker
Neural activity during a standard risky-behavior task (Balloon Analogue Risk task)
Time frame: 1 month
Health-risking behavior
Standard self-report questions regarding health-risking behavior related to inhibitory control (e.g., cigarette smoking, excessive alcohol intake, illicit drug use and prescription drug misuse, and excessive energy intake)
Time frame: 1 month, 3 months
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