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Benjamin D. Schalet

Bio: Benjamin D. Schalet is an academic researcher from Northwestern University. The author has contributed to research in topics: Item response theory & Medicine. The author has an hindex of 18, co-authored 45 publications receiving 2052 citations.


Papers
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Journal ArticleDOI
TL;DR: This work produced cross-walk tables linking 3 popular "legacy" depression instruments to the depression metric of the National Institutes of Health Patient-Reported Outcomes Measurement Information System (PROMIS; Cella et al., 2010).
Abstract: Interest in measuring patient-reported outcomes has increased dramatically in recent decades. This has simultaneously produced numerous assessment options and confusion. In the case of depressive symptoms, there are many commonly used options for measuring the same or a very similar concept. Public and professional reporting of scores can be confused by multiple scale ranges, normative levels, and clinical thresholds. A common reporting metric would have great value and can be achieved when similar instruments are administered to a single sample and then linked to each other to produce cross-walk score tables (e.g., Dorans, 2007; Kolen & Brennan, 2004). Using multiple procedures based on item response theory and equipercentile methods, we produced cross-walk tables linking 3 popular "legacy" depression instruments-the Center for Epidemiologic Studies Depression Scale (Radloff, 1977; N = 747), the Beck Depression Inventory-II (Beck, Steer, & Brown, 1996; N = 748), and the 9-item Patient Health Questionnaire (Kroenke, Spitzer, & Williams, 2001; N = 1,120)-to the depression metric of the National Institutes of Health (NIH) Patient-Reported Outcomes Measurement Information System (PROMIS; Cella et al., 2010). The PROMIS Depression metric is centered on the U.S. general population, matching the marginal distributions of gender, age, race, and education in the 2000 U.S. census (Liu et al., 2010). The linking relationships were evaluated by resampling small subsets and estimating confidence intervals for the differences between the observed and linked PROMIS scores; in addition, PROMIS cutoff scores for depression severity were estimated to correspond with those commonly used with the legacy measures. Our results allow clinicians and researchers to retrofit existing data of 3 popular depression measures to the PROMIS Depression metric and vice versa.

347 citations

Journal ArticleDOI
TL;DR: Paroxetine appears to have a specific pharmacological effect on personality that is distinct from its effect on depression, and this pattern would disconfirm the state effect hypothesis and support the notion that SSRIs' effects on personality go beyond and perhaps contribute to their antidepressant effects.
Abstract: Context High neuroticism is a personality risk factor that reflects much of the genetic vulnerability to major depressive disorder (MDD), and low extraversion may increase risk as well Both have been linked to the serotonin system Objectives To test whether patients with MDD taking selective serotonin reuptake inhibitors (SSRIs) report greater changes in neuroticism and extraversion than patients receiving inert placebo, and to examine the state effect hypothesis that self-reported personality change during SSRI treatment is merely a change of depression-related measurement bias Design A placebo-controlled trial Setting Research clinics Patients Adult patients with moderate to severe MDD randomized to receive paroxetine (n = 120), placebo (n = 60), or cognitive therapy (n = 60) Outcome Measures NEO Five-Factor Inventory and Hamilton Rating Scale for Depression Results Patients who took paroxetine reported greater personality change than placebo patients, even after controlling for depression improvement (neuroticism, P P = 002) The advantage of paroxetine over placebo in antidepressant efficacy was no longer significant after controlling for change in neuroticism ( P = 46) or extraversion ( P = 14) Patients taking paroxetine reported 68 times as much change on neuroticism and 35 times as much change on extraversion as placebo patients matched for depression improvement Although placebo patients exhibited substantial depression improvement (Hamilton Rating Scale for Depression score, −12 SD, P P = 08) or extraversion (008 SD, P = 50) Cognitive therapy produced greater personality change than placebo ( P ≤ 01); but its advantage on neuroticism was no longer significant after controlling for depression ( P = 14) Neuroticism reduction during treatment predicted lower relapse rates among paroxetine responders ( P = 003) but not among cognitive therapy responders ( P = 86) Conclusions Paroxetine appears to have a specific pharmacological effect on personality that is distinct from its effect on depression If replicated, this pattern would disconfirm the state effect hypothesis and instead support the notion that SSRIs' effects on personality go beyond and perhaps contribute to their antidepressant effects

344 citations

Journal ArticleDOI
TL;DR: Evidence is provided that the PROMIS negative affect scores are sensitive to change in intervention studies in which negative affect is expected to change and this results inform the estimation of meaningful change and enable comparative effectiveness research.

285 citations


Cited by
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Journal ArticleDOI

3,152 citations

Book ChapterDOI
19 Dec 2005

1,788 citations

01 Jan 2016
TL;DR: Dillman and Smyth as mentioned in this paper described the Tailored design method as a "tailored design methodology" and used it in their book "The Tailored Design Method: A Manual for Personalization".
Abstract: Resena de la obra de Don A. Dillman, Jolene D. Smyth y Leah Melani Christian: Internet, Phone, Mail and Mixed-Mode Surveys. The Tailored Design Method. New Jersey: John Wiley and Sons

1,467 citations

Journal ArticleDOI
TL;DR: A maladaptive personality trait model and corresponding instrument are developed as a step on the path toward helping users of DSM-5 assess traits that may or may not constitute a formal personality disorder.
Abstract: Background DSM-IV-TR suggests that clinicians should assess clinically relevant personality traits that do not necessarily constitute a formal personality disorder (PD), and should note these traits on Axis II, but DSM-IV-TR does not provide a trait model to guide the clinician. Our goal was to provide a provisional trait model and a preliminary corresponding assessment instrument, in our roles as members of the DSM-5 Personality and Personality Disorders Workgroup and workgroup advisors. Method An initial list of specific traits and domains (broader groups of traits) was derived from DSM-5 literature reviews and workgroup deliberations, with a focus on capturing maladaptive personality characteristics deemed clinically salient, including those related to the criteria for DSM-IV-TR PDs. The model and instrument were then developed iteratively using data from community samples of treatment-seeking participants. The analytic approach relied on tools of modern psychometrics (e.g. item response theory models). Results A total of 25 reliably measured core elements of personality description emerged that, together, delineate five broad domains of maladaptive personality variation: negative affect, detachment, antagonism, disinhibition, and psychoticism. Conclusions We developed a maladaptive personality trait model and corresponding instrument as a step on the path toward helping users of DSM-5 assess traits that may or may not constitute a formal PD. The inventory we developed is reprinted in its entirety in the Supplementary online material, with the goal of encouraging additional refinement and development by other investigators prior to the finalization of DSM-5. Continuing discussion should focus on various options for integrating personality traits into DSM-5.

1,322 citations

Journal ArticleDOI
TL;DR: Evidence is reported for the involvement of many systems in tobacco and alcohol use, including genes involved in nicotinic, dopaminergic, and glutamatergic neurotransmission, which provide a solid starting point to evaluate the effects of these loci in model organisms and more precise substance use measures.
Abstract: Tobacco and alcohol use are leading causes of mortality that influence risk for many complex diseases and disorders1. They are heritable2,3 and etiologically related4,5 behaviors that have been resistant to gene discovery efforts6–11. In sample sizes up to 1.2 million individuals, we discovered 566 genetic variants in 406 loci associated with multiple stages of tobacco use (initiation, cessation, and heaviness) as well as alcohol use, with 150 loci evidencing pleiotropic association. Smoking phenotypes were positively genetically correlated with many health conditions, whereas alcohol use was negatively correlated with these conditions, such that increased genetic risk for alcohol use is associated with lower disease risk. We report evidence for the involvement of many systems in tobacco and alcohol use, including genes involved in nicotinic, dopaminergic, and glutamatergic neurotransmission. The results provide a solid starting point to evaluate the effects of these loci in model organisms and more precise substance use measures.

1,082 citations