Tailored Inhibitory Control Training to Reverse EA-linked Deficits in Mid-life
Tailored Inhibitory Control Training to Reverse EA-linked Deficits in Mid-life
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.
Inclusion Criteria:

 -  Age 35-55

 -  Experience of early adversity (EA) before age 18 (EA is be defined as a score of 4 or
 higher on the Adverse Childhood Experiences (ACEs) questionnaire [Felitti, Anda,
 Nordenberg, Williamson, Spitz, Edwards, et al., 1998])

 -  IC difficulties such as disinhibited alcohol use, tobacco use, or food intake during
 adulthood. IC difficulties will be self-reported based on questions from the
 self-control questionnaire (Tangney, Baumeister, & Boone, 2004) modified to be
 specific to alcohol, tobacco, and energy-dense food intake (e.g., "I am self-indulgent
 with unhealthy food at times", "I refuse alcohol when offered") using a 4-point
 Likert-style scale.

 Exclusion Criteria:

 -  Individuals over age 55 will be excluded because of established functional and
 structural neural changes that begin to escalate at that time (Good, Johnsrude,
 Ashburner, Henson, Friston, & Frackowiak, 2001; Grady, Springer, Hongwanishkul,
 McIntosh, & Winocur, 2006)

 -  Given the high rates of morbidity for such disorders among people with high EA, we
 will not exclude based on past diagnoses for any of those disorders or based on
 current drug and alcohol use. However, we will exclude individuals who do not pass a
 urine toxicology screen during either of the functional magnetic resonance imaging
 (fMRI) sessions to ensure that the neuroimaging data are as homogeneous and reliable
 as possible.

 -  Participants who cannot undergo an MRI scan will be excluded; contraindications
 include metal implants (e.g., braces, pins) or metal fragments, pacemakers or other
 electronic medical implants, claustrophobia, pregnancy, and weight greater than 550
 lbs.

 Beyond these criteria, participants will be recruited without exclusions based on gender,
 race, or ethnicity, so our sample will reflect the diversity in the local population (Lane
 County, Oregon) with regard to gender, race, and ethnicity.