Search

Background: Individuals seeking treatment for mental health conditions often explore multiple therapeutic modalities before finding one that is beneficial. Early identification of individuals likely to respond to a particular psychotherapy modality may substantially decrease this burden. Objective: The current study tested novel variables as potential predictors of response to psychotherapy for public speaking anxiety (PSA). Specifically, the current study (1) evaluated whether responsivity to a laboratory-based analogue intervention for acceptance and commitment therapy (ACT) predicted subsequent treatment response to an actual ACT-based intervention, and (2) evaluated whether frontal brain activity (frontal asymmetry; bilateral activity) at baseline or (3) in anticipation of public speaking predicted subsequent treatment response. Participants: A total of 48 individuals with PSA completed all study components. Methods: Participants completed a public speaking task prior to and following receipt of a brief ACT-based analogue intervention. In association with each public speaking task, neurophysiological measurements, including frontal brain activity measured by electroencephalography (EEG) and heart rate (HR), were collected. Analogue intervention responsivity was considered based on residualized change in self-reported anxiety and openness to anxiety, neurophysiological measurement (EEG; HR), behavioral ratings of speech performance, and an analogue responsivity composite factor. Participants subsequently received a 2.5 hour ACT treatment over two days. A final public speaking task was completed and psychological, physiological (HR), and behavioral ratings were collected as primary measures of treatment outcome, along with a composite treatment outcome factor. Results: The analogue responsivity composite factor predicted ACT treatment outcome on several measures, with greater analogue intervention symptom improvement associated with greater subsequent ACT treatment symptom improvement on most measures. Individual analogue responsivity variables generally did not predict ACT treatment responsivity. Greater right-frontal asymmetry at baseline and in anticipation of a public speaking task trended towards an association with greater symptom improvement over treatment across several outcome measures. Greater bilateral frontal activity – a measure associated with self-reported mindfulness at baseline – significantly predicted greater symptom improvement over treatment across several outcome measures; higher mindfulness at baseline also predicted greater symptom improvement across several outcome measures. Implications: Findings suggest that an individual's response to an analogue intervention, or a small 'dose' of psychotherapy, may inform their response to a longer course of psychotherapy, particularly in ACT for PSA. Individuals with greater bilateral frontal activity and (to a lesser degree) individuals with greater right-frontal asymmetry may experience greater symptom reduction in an ACT-based treatment for PSA. Future studies should evaluate whether any of these variables (analogue responsivity; frontal brain activity) differentially predict response to two or more different psychotherapies in a quest towards personalized medicine. Future research should also evaluate whether interventions designed to increase baseline mindfulness (e.g., meditation training) prior to a course of ACT for PSA, or a similar intervention, improves treatment efficacy.

Objective: Anorexia nervosa (AN) is a debilitating illness and is highly resistant to treatment. Prior research in AN has emphasized the importance of low absolute body weight, but emerging research suggests the importance of also considering low body weight relative to an individual's highest past weight (weight suppression; WS). Leptin is a hormone produced by adipose tissue that increases in proportion to body fat. Prior research has identified a relationship between BMI and leptin, while the potential relationship with WS is less well established. Research also suggests that individuals with AN display cognitive impairments on a range of neuropsychological tests. The interpretation of such impairments is complicated by the potential for starvation and low body weight to influence performance. Additionally, there is reason to suspect that weight status variables (BMI, WS) and/or leptin may be related to cognitive performance. Therefore the goals of the present study are: (1) to evaluate the relationship between weight status variables and leptin; (2) to evaluate the relationship between weight status variables and cognitive performance; (3) to evaluate the relationship between leptin and cognitive performance. These relationships were evaluated twice, once when patients were first admitted and again after they gained weight to reach 90% of their ideal body weight. Participants: Data were collected from 64 women with AN at an inpatient eating disorder treatment facility; a subsample of 33 of these women also provided blood samples for leptin assay. Methods: Data were collected at two time points: at admission and soon after weight restoration. At each time point, participants completed a series of neuropsychological tests (including measures of memory, cognitive flexibility and spatial reasoning), blood was collected for leptin assay, and weight status variables (including BMI and WS) were calculated. Results: (1) At admission, both weight status variables were associated with leptin; higher WS and lower BMI were independently associated with lower leptin level. Following weight restoration, the WS/leptin relation held whereas the BMI/leptin relation did not. (2) At admission and following weight restoration, weight status variables were mostly unrelated to performance on cognitive tasks, with the exception of performance on one memory task. (3) At admission and following weight restoration, leptin was mostly unrelated to performance on cognitive tasks, although a non-significant association with spatial reasoning task performance emerged. Conclusions: Leptin appears to be a marker not only of current body fat levels but also of the discrepancy between past highest weight and current weight. These findings suggest that the body may be defending against weight loss from a previous highest level, not just from a medically healthy body mass. Thus, weight gain to a minimally healthy level may not be sufficient to restore leptin to normal levels. Findings also suggest that weight status and leptin do not have a robust influence on the specific cognitive tasks considered in the current study. Notably, cognitive task performance was not impaired among AN individuals in the current study as compared to data from a normative sample, potentially influencing this finding. Future studies should evaluate whether other domains of cognitive performance are related to weight status and/or leptin to continue to clarify whether neurocognitive abnormalities identified in AN are weight-related and/or more integral to the specific psychopathology associated with the disorder.