Alarm substances are airborne chemical signals, released by an individual into the environment, which communicate emotional stress between conspecifics. Here we tested whether humans, like other mammals, are able to detect emotional stress in others by chemosensory cues. Sweat samples collected from individuals undergoing an acute emotional stressor, with exercise as a control, were pooled and presented to a separate group of participants (blind to condition) during four experiments. In an fMRI experiment and its replication, we showed that scanned participants showed amygdala activation in response to samples obtained from donors undergoing an emotional, but not physical, stressor. An odor-discrimination experiment suggested the effect was primarily due to emotional, and not odor, differences between the two stimuli. A fourth experiment investigated behavioral effects, demonstrating that stress samples sharpened emotion-perception of ambiguous facial stimuli. Together, our findings suggest human chemosensory signaling of emotional stress, with neurobiological and behavioral effects.

This study investigated whether human chemosensory-stress cues affect neural activity related to the evaluation of emotional stimuli. Chemosensory stimuli were obtained from the sweat of 64 male donors during both stress (first-time skydive) and control (exercise) conditions, indistinguishable by odor. We then recorded event-related potentials (ERPs) from an unrelated group of 14 participants while they viewed faces morphed with neutral-to-angry expressions and inhaled nebulized stress and exercise sweat in counter-balanced blocks, blind to condition. Results for the control condition ERPs were consistent with previous findings: the late positive potential (LPP; 400-600 ms post stimulus) in response to faces was larger for threatening than both neutral and ambiguous faces. In contrast, the stress condition was associated with a heightened LPP across all facial expressions; relative to control, the LPP was increased for both ambiguous and neutral faces in the stress condition. These results suggest that stress sweat may impact electrocortical activity associated with attention to salient environmental cues, potentially increasing attentiveness to otherwise inconspicuous stimuli.

Despite the emergence of numerous clinical and non-clinical applications of bright light therapy (LT) in recent decades, the prevalence and severity of LT side effects have not yet been fully explicated. A few adverse LT effects—headache, eye strain, irritability, and nausea—have been consistently reported among depressed individuals and other psychiatric cohorts, but there exists little published evidence regarding LT side effects in non-clinical populations, who often undergo LT treatment of considerably briefer duration. Accordingly, in the present study we examined, in a randomized sample of healthy young adults, the acute side effects of exposure to a single 30-minute session of bright white light (10,000 lux) versus dim red light (< 500 lux). Across a broad range of potential side effects, repeated-measures analyses of variance revealed no significant group-by-time (Pre, Post) interactions. In other words, bright light exposure was not associated with a significantly higher incidence of any reported side effect than was the placebo control condition. Nevertheless, small but statistically significant increases in both eye strain and blurred vision were observed among both the LT and control groups. Overall, these results suggest that the relatively common occurrence of adverse side effects observed in the extant LT literature may not fully extend to non-clinical populations, especially for healthy young adults undergoing LT for a brief duration.

Lilienfeld (2007, Psychological treatments that cause harm. Perspectives on Psychological Science, 2, 53) identified a list of potentially harmful therapies (PHTs). Given concerns regarding the replicability of scientific findings, we conducted a meta-scientific review of Lilienfeld's PHTs to determine the evidential strength for harm. We evaluated the extent to which effects used as evidence of harm were as follows: (a) (in)correctly reported; (b) well-powered; (c) statistically significant at an inflated rate given their power; and (d) stronger compared with null effects of ineffectiveness or evidence of benefit, based on a Bayesian index of evidence. We found evidence of harm from some PHTs, though most metrics were ambiguous. To enhance provision of ethical and science-based care, a comprehensive reexamination of what constitutes evidence for claims of harm is necessary. Public Health Significance StatementPsychological interventions designed to help people sometimes inadvertently harm them instead. In our examination-incorporating more than 70 reports-of treatments previously identified as potentially harmful, we found that the clinical trials often provided weak scientific evidence and are therefore difficult to interpret. However, some interventions showed stronger evidence for harm and only grief therapy showed promise of benefit; as such, the remaining treatments we examined require more compelling, reproducible, and replicable evidence of benefit to justify continued clinical use.