Elliot Berkman, UO Psychology. Late adolescents are particularly likely to engage in risky behaviors (RBs) such as drug use, unsafe sex, and other antisocial behaviors when they are with peers. RBs are associated with problematic outcomes (e.g., academic underachievement, physical injury, STDs, and unwanted pregnancies), and can mark the beginning or escalation of life course trajectories towards long-term physical and mental health difficulties (e.g., addictions, depressive disorders, and other forms of pathology). An underlying causal factor shared by many RBs in adolescence and early adulthood is behavioral disinhibition. Behavioral disinhibition occurs when an individual is unable to recruit adequate inhibitory control (IC), a domain general neurocognitive ability that is amenable to change with focused intervention in children, adolescents, and young adults. The first Aim of the proposed study is to evaluate the feasibility of an intervention to reduce peer-linked RBs by increasing IC in a sample of at-risk adolescents. Furthermore, peer-associated RBs and their sequelae are particularly pronounced among individuals with high levels of early adversity (EA), and EA is associated with IC deficits throughout childhood and adolscence. The second Aim of the proposed study is to understand the effects of EA on IC and the mechansims through which those effects might be remediated with intervention. This aim will be achieved by comparing groups with high and low levels of EA in terms of their underlying neural systems for IC and how those systems respond differently to intervention.
Elliot Berkman, UO Psychology. The proposed research is a series of randomized experiments to quantify the economic value of sociality. Sociality is manipulated using an existing socialization game (Study 1) and through a minimal groups induction (Study 2), and then economic decisions are measured using a set of validated economic choice games (e.g., Prisoner’s Dilemma, Welfare Game) when played against in- and out-group members. These decisions and their accompanying neural activity will be compared to each other and to decisions made when playing against computers (non-sociality control).
Elliot Berkman, UO Psychology. Eating energy-dense foods when one is not hungry is a contributor to obesity and overweight, which are risk factors for a range of cancer-promoting foods. The goal of this project is to reduce cancer risk by improving cognitive self-regulation of cravings for cancer-promoting foods. We focus on craving of cancer-promoting foods as one proximal determinant of their consumption. Craving consists of a subjective sense of wanting to eat a food, a motivation to seek out the food, and recurrent or intrusive thoughts related to the food. Considerable research shows that craving is a strong predictor of eating, even in the absence of hunger. Thus, enhancing a simple, low-cost and easily disseminated tool to reduce craving for cancer-promoting foods would meaningfully advance the goal of cancer prevention. Studies from affective science and social neuroscience have identified cognitive self-regulation strategies that are effective in reducing craving and their associated neural systems. This work has focused mostly on craving for other appetitive stimuli (e.g., drug cues), and has only begun to study regulation of food craving. Recent results from our laboratory validated four strategies that are effective in reducing cravings for ED foods. This work relies upon self-reports of craving, which provide an empirical starting point but do not demonstrate the validity of the strategies on their own. Thus, the goals of the proposed project are to provide additional support for the effectiveness of cognitive self-regulation of food cravings using other measures beyond self-report, and to validate a theoretically grounded means to further increase the efficacy of those strategies—strategy choice. These goals will be accomplished in the context of a single longitudinal study. Obese and overweight participants, who have increased risk of developing cancer, will be randomly assigned to choose their own regulation strategy or to be assigned to one. Their self-reported cravings and brain activity will be recorded while they alternately view images of ED foods and regulate their responses to those foods. These data will be used to examine the effects of strategy choice on food regulation success (measured by changes in self-reported craving and brain activity). Immediately after the scan and then again 6 months later, participants will monitor their real-life consumption of a personally-craved ED food and report the number of servings they consume 4 times per day via text message. The difference in number of servings consumed between the two groups will provide a behavioral measure of the efficacy of strategy choice on eating. Also, brain activity in key regions during food reactivity and regulation will be used to predict intake. Psychological theory and previous neuroscience data suggest that brain activity, particularly in the ventromedial prefrontal cortex, will account for ED food intake above and beyond self-report, and will mediate the effect of strategy choice on intake.
Elliot Berkman, UO Psychology. 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 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.
Anita Christie, UO Human Physiology. Muscle fatigue, defined as an activity-induced decline in the force producing capability of the muscle, has been the focus of study for several decades. While age-related differences in muscle fatigue are often reported, the mechanisms leading to these differences have not been elucidated. Recent studies of fatigue in young men suggest that sensory feedback from the working muscles plays a critical role in the development of fatigue. These results, however, have not been extended to older populations. Through a unique combination of techniques, including measures of central nervous system output, via indwelling electromyography, and muscle metabolism, via magnetic resonance spectroscopy, we are studying the role of sensory feedback during fatigue in young and older individuals. This study will fill a critical gap in our mechanistic understanding of age-related differences in muscle fatigue and provide novel information regarding the role of sensory feedback in muscle function with advanced age.
Phan Luu, Electrical Geodesics, Inc. EGI is currently developing a dense-array EEG system that can be used to acquire the EEG simultaneously with fMRI data acquisition. The goals are to develop an EEG system that 1) is safe to operate with the MRI environment, 2) does not distort the MRI data and 3) accurately captures the MRI's gradient pulses in the EEG recordings. If these goals can be accomplished, this MRI-compatible EEG system will advance both basic and clinical research by allowing investigators to leverage the spatial accuracy of MRI and temporal resolution of EEG to understand brain functions.
Jenn Pfeifer and Phil Fisher, UO Psychology. Adolescence is widely understood to be a time of both increased risk-taking behavior and heightened sensitivity to social contexts. Adolescent risk-taking has significant implications for long-term health outcomes, and adolescents may be particularly vulnerable to social context effects on decision-making. The impact of social context on decision-making may be especially relevant for adolescents who have experienced high levels of early adversity, including those in the child welfare system. A growing literature connects adolescent risk-taking with brain development, specifically with the varying courses of functional maturation in regions such as the prefrontal cortex and subcortical limbic systems. This project aims to better understand the interactions between risk-taking and social contexts in early adolescence (across the spectrum of experiences with early adversity) using a driving simulation task that includes both behavioral and neuroimaging assessments of risk-taking across key social contexts. It will also characterize longitudinal associations between neural and behavioral measures of risk-taking behavior assessed in the laboratory, and concurrent or subsequent health-risking behaviors, including drug use and high-risk sexual behavior. In other words, the study will use estimates of brain functioning and connectivity during risk-taking across social contexts as predictors of real-world outcomes impacting teenagers.
Eric Stice, Oregon Research Institute. This study, funded by the National Institute of Mental Health, aims to examine: 1) differences in the neural circuitry related to food reward between adolescents at high risk for weight gain and low-risk adolescents; 2) the effects of abnormalities in the neural circuitry related to food reward to future weight gain and obesity onset; and 3) changes in food reward after obesity onset.