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Numerous studies have questioned the reliability and validity of borderline personality disorder's (BPD) categorical conceptualization. DSM-5 Section III's alternative trait-based model of BPD may better capture borderline pathology, but aspects of its validity should be further established. Thus, the authors examined whether a latent BPD factor derived from Section III traits exhibits (1) familial aggregation among siblings and (2) association with constructs related to borderline pathology. The authors also tested whether gender moderated associations. A total of 498 community-recruited adults completed the Personality Inventory for DSM-5, a behavioral assessment of risk-taking, and reported their history of childhood maltreatment, substance use, nonsuicidal self-injury, and suicidal ideation. Familial aggregation was assessed among 232 sibling pairs. Siblings' BPD scores were significantly correlated and most external validators were significantly associated with BPD, with the exception of risk-taking. Results did not vary by gender. Findings further support the construct validity of Section III's BPD trait profile.

Low perceived distress tolerance (DT), a trait-like individual difference factor reflecting one’s perceived ability to withstand aversive affective states, has been linked with current internalizing and substance use disorders (SUD). However, perceived DT has not been systematically evaluated as a familial, transdiagnostic vulnerability factor for internalizing and SUDs. The current study tested whether perceived DT runs in families and whether it is reduced among individuals with vs. without remitted internalizing/SUD psychopathology. Perceived DT and internalizing/SUD disorders were measured in 638 individuals (nested within 256 families). Analyses also adjusted for the effects of neuroticism to test whether DT was a specific vulnerability factor independent of temperamental negative affect. Analyses revealed that perceived DT was lower in individuals with remitted distress (i.e., major depression, generalized anxiety disorder, post-traumatic stress disorder) but not fear disorders (i.e., panic disorder, social anxiety disorder, specific phobia, obsessive-compulsive spectrum disorders) relative to healthy controls, and the effect of distress-misery disorder history remained significant when adjusting for neuroticism. Perceived DT was not significantly different among individuals with vs. without a remitted SUD disorder. There were no effects for comorbid SUD and distress-misery disorders. Finally, perceived DT was also significantly correlated within families, suggesting that it runs in families. Overall, results suggest that independent of neuroticism, low perceived DT is a familial vulnerability for distress (but not fear or substance use) disorders.

Non-suicidal self-injury is a risk factor for suicidal behavior, particularly in females. Two prominent theories of suicide suggest that habituation to the psychophysiological aversiveness of NSSI is a mechanism by which NSSI exposure may lead to increased risk for suicide. Several laboratory studies examining the relationship between physiological habituation and suicide attempt history have yielded mixed results, potentially due to their use of broad measures of physiological arousal and/or focus on specific psychopathologies. However, no studies have examined the association between the time course (e.g., habituation, initial reactivity) of responding to aversiveness and NSSI, which may help to elucidate psychophysiological mechanisms of NSSI. Therefore, we examined habituation and initial reactivity to aversiveness (indexed by the time course of acoustic startle reflex, a well-validated measure of defensive responding) in three groups of young adult females – those with a history of NSSI, psychiatric controls matched on potential confounds (e.g., psychopathology, trauma history, demographics), and healthy controls. Results indicated that individuals with a history of NSSI exhibited blunted initial reactivity and marginally slower habituation to aversiveness relative to the two control groups. The NSSI group’s insensitivity to aversiveness may reflect prior psychophysiological habituation, and may be a mechanism through which prior NSSI exposure leads to increased risk for suicidal behavior.

Affect dynamics reflect individual differences in how emotional information is processed, and may provide insights into how depressive episodes develop. To extend prior studies that examined affect dynamics in currently depressed individuals, the present study tested in 68 non-depressed young adults whether three well-established risk factors for major depressive disorder (MDD) – (a) past episodes of MDD, (b) family history of MDD, and (c) reduced neurophysiological responses to reward – predicted mean levels, instability, or inertia (i.e., inflexibility) of positive affect (PA) and/or negative affect (NA). Momentary PA and NA were assessed up to 6 times per day for 14 days (mean number of surveys completed = 45.89). MDD history and family history of MDD were assessed via semi-structured interview, and neurophysiological responses to reward were indexed using the Reward Positivity, an event-related potential related to depression. After adjusting for current depressive symptoms, results indicated that (a) past episodes of MDD predicted higher mean levels of NA, (b) family history of MDD predicted greater PA inertia, and (c) blunted reactivity to reward predicted greater NA inertia. Collectively, these results suggest that elevated mean levels of NA and inflexibility of PA and NA may be potential mechanisms that confer risk for depression.

The clinical presentation of anxiety may differ between Hispanics/Latinx (H/L) and non-H/L, although findings on ethnic differences in self-reported anxiety symptoms have been mixed. Fewer studies have focused on ethnic differences in quick and relatively automatic laboratory-assessed indicators of anxiety symptoms, which have the potential to be more objective indicators than self-report. Therefore, the present study examined ethnic differences in two laboratory-assessed indicators of threat sensitivity (an important transdiagnostic mechanism of anxiety): attentional bias to threat and electromyography startle reactivity to threat. White H/L (n = 117) and White non-H/L (n = 168) adults who were matched on demographics and lifetime psychopathology (including anxiety) completed a dot-probe task to assess attentional bias to threat and the No-Predictable-Unpredictable threat (NPU) task to assess startle reactivity to threat. Results indicated that H/L displayed less Slow Orientation(RB) (β = −0.27, p = 0.032, R(2)(β*) = 0.02), and increased Slow Disengagement(RB) (β = 0.31, p = 0.016, R(2)(β*) = 0.02) compared to non-H/L. H/L exhibited blunted overall startle compared to non-H/L (β = −0.30, p = 0.014, R(2)(β*) = 0.02), but groups did not differ in startle reactivity to either predictable or unpredictable threat. In summary, H/L and non-H/L may differ in their experience and presentation of anxiety symptoms and such differences may vary across indicators of sensitivity to threat.

Studies suggest that individuals with alcohol use disorder (AUD) display abnormal neural error-processing, measured via the error-related negativity (ERN). The nature of the error-related abnormalities in AUD is unclear, however, as prior research has yielded discrepant findings. In addition, no study to date has attempted to characterize the dispositional nature of the ERN in AUD and directly test to what extent ERN amplitude reflects a risk factor, disease marker, and/or scar of AUD psychopathology. The current study compared ERN amplitude across 244 adult volunteers in the following five groups: 1) current AUD (n = 39), 2) AUD in remission (n = 60), 3) at-risk for AUD (n = 43), 4) psychiatric controls with comparable rates of internalizing psychopathology as the AUD groups (n = 53), and 5) healthy controls with no lifetime history of psychopathology (n = 49). Risk for AUD was defined as a positive, first-degree family history. All participants completed a well-validated flanker task, designed to robustly elicit the ERN, during continuous electroencephalographic (EEG) data collection. Results indicated that individuals with current AUD displayed smaller ERNs compared with individuals at-risk for AUD, with AUD in remission, psychiatric controls, and healthy controls. There were no differences amongst any of the other groups. This suggests that a blunted ERN may be concomitant with current AUD psychopathology and relatedly, a novel neurobiological AUD treatment target and/or objective marker of AUD disease status.