Emotion and Decision Making Lerner, Jennifer S; Li, Ye; Valdesolo, Piercarlo ...
Annual review of psychology,
2015-Jan-03, Volume:
66, Issue:
1
Journal Article
Peer reviewed
Open access
A revolution in the science of emotion has emerged in recent decades, with the potential to create a paradigm shift in decision theories. The research reveals that emotions constitute potent, ...pervasive, predictable, sometimes harmful and sometimes beneficial drivers of decision making. Across different domains, important regularities appear in the mechanisms through which emotions influence judgments and choices. We organize and analyze what has been learned from the past 35 years of work on emotion and decision making. In so doing, we propose the emotion-imbued choice model, which accounts for inputs from traditional rational choice theory and from newer emotion research, synthesizing scientific models.
Fear, Anger, and Risk Lerner, Jennifer S; Keltner, Dacher
Journal of personality and social psychology,
07/2001, Volume:
81, Issue:
1
Journal Article
Peer reviewed
Drawing on an appraisal-tendency framework (
J. S. Lerner & D. Keltner, 2000
), the authors predicted and found that fear and anger have opposite effects on risk perception. Whereas fearful people ...expressed pessimistic risk estimates and risk-averse choices, angry people expressed optimistic risk estimates and risk-seeking choices. These opposing patterns emerged for naturally occurring and experimentally induced fear and anger. Moreover, estimates of angry people more closely resembled those of happy people than those of fearful people. Consistent with predictions, appraisal tendencies accounted for these effects: Appraisals of certainty and control moderated and (in the case of control) mediated the emotion effects. As a complement to studies that link affective valence to judgment outcomes, the present studies highlight multiple benefits of studying specific emotions.
The Financial Costs of Sadness Lerner, Jennifer S.; Li, Ye; Weber, Elke U.
Psychological science,
01/2013, Volume:
24, Issue:
1
Journal Article
Peer reviewed
Open access
We hypothesized a phenomenon that we term myopic misery. According to our hypothesis, sadness increases impatience and creates a myopic focus on obtaining money immediately instead of later. This ...focus, in turn, increases intertemporal discount rates and thereby produces substantial financial costs. In three experiments, we randomly assigned participants to sad- and neutral-state conditions, and then offered intertemporal choices. Disgust served as a comparison condition in Experiments 1 and 2. Sadness significantly increased impatience: Relative to median neutral-state participants, median sad-state participants accepted 13% to 34% less money immediately to avoid waiting 3 months for payment. In Experiment 2, impatient thoughts mediated the effects. Experiment 3 revealed that sadness made people more present biased (i.e., wanting something immediately), but not globally more impatient. Disgusted participants were not more impatient than neutral participants, and that lack of difference implies that the same financial effects do not arise from all negative emotions. These results show that myopic misery is a robust and potentially harmful phenomenon.
Sadness and consumption Garg, Nitika; Lerner, Jennifer S.
Journal of consumer psychology,
January 2013, Volume:
23, Issue:
1
Journal Article
Peer reviewed
Sadness influences consumption, leading individuals to pay more to acquire new goods and to eat more unhealthy food than they would otherwise. These undesirable consumption effects of sadness can ...occur without awareness, thus representing more than just conscious attempts at “retail therapy.” In an experiment with real food consumption, the present paper examines the hypothesis that sadness' impact on consumption could be attenuated if the choice context counteracted appraisals of helplessness and enhanced a sense of individual control. Results revealed that: (1) sadness elevates self-reports of helplessness in response to the emotion-inducing situation, (2) helplessness mediates the sadness–consumption effect, and (3) inducing a sense of control (via choice) attenuates sadness' effect.
This article reviews the now extensive research literature addressing the impact of accountability on a wide range of social judgments and choices. It focuses on 4 issues: (a) What impact do various ...accountability ground rules have on thoughts, feelings, and action? (b) Under what conditions will accountability attenuate, have no effect on, or amplify cognitive biases? (c) Does accountability alter how people think or merely what people say they think? and (d) What goals do accountable decision makers seek to achieve? In addition, this review explores the broader implications of accountability research. It highlights the utility of treating thought as a process of internalized dialogue; the importance of documenting social and institutional boundary conditions on putative cognitive biases; and the potential to craft empirical answers to such applied problems as how to structure accountability relationships in organizations.
Maximal medical therapy (MMT) is the use of ≥3 classes of topical anti-glaucoma agents to achieve maximal intraocular pressure (IOP) reduction while minimizing adverse effects and compliance ...challenges.
To evaluate the additive IOP-lowering effect of twice-daily brinzolamide 1%/brimonidine 0.2% fixed-dose combination (BBFC) used adjunctively with once daily travoprost 0.004%/timolol 0.5% fixed-dose combination (TTFC) in patients with open-angle glaucoma (OAG)/ocular hypertension (OHT).
In this phase IV, double-masked study, patients on TTFC for ≥28 days, aged ≥18 years, with mean IOP ≥19 and ≤28 mmHg in at least 1 eye were randomized to receive BBFC+TTFC (n=67) or vehicle+TTFC (n=67) for 6 weeks. The primary endpoint was mean change in diurnal IOP from baseline (BL, averaged over 09:00 and 11:00) at Week 6.
The study was terminated prematurely due to recruitment challenges. BL mean IOP was similar in both groups (BBFC+TTFC: 21.6±1.78 mmHg; vehicle+TTFC: 21.8±1.90 mmHg). Mean change in diurnal IOP from BL at Week 6 was greater with BBFC+TTFC (-4.25 mmHg, 95% confidence interval CI: -4.7, -3.8) than with vehicle+TTFC (-2.11 mmHg, 95% CI: -2.6, -1.6, treatment difference, -2.15 mmHg (95% CI: -2.8, -1.5;
<0.001). Ocular adverse events (AEs) were reported in 11.9% of patients given BBFC+TTFC and 7.5% of patients given vehicle+TTFC. The AE with highest frequency was punctate keratitis (3%) in the BBFC+TTFC group; eye irritation (3%) in the vehicle+TTFC group.
BBFC+TTFC as MMT demonstrated clinically relevant and statistically significant reductions in mean diurnal IOP in patients with OAG/OHT. AEs were consistent with known safety profiles of individual medications.
The aim of this study was to elucidate the intracellular sources of oxidant species, the antioxidant response as well as the main signaling pathways involved in the regulation of the redox balance in ...the primary visual cortex of rats subjected to an experimental glaucoma model.
3-month female Wistar strain rats were operated under a microscope by cauterizing two of the episcleral veins in order to elevate the intraocular pressure (glaucoma group); the control group received a sham procedure. Seven days after surgery, the animals were sacrificed, the brains were carefully removed, and the primary visual cortex was dissected. NADPH oxidase (NOX) activity, as well as the inducible nitric oxide synthase (iNOS) expression, the enzymatic antioxidant defenses, the metabolism of glutathione, and the translocation of Nuclear factor-erythroid 2-related factor-2 (Nrf2) and Nuclear factor k-light-chain-enhancer of activated B cells (NF-κB) were assessed.
Compared to control, glaucoma group displayed an increase in NOX activity (147%, p < 0.05), leading to a rise in the steady state concentration of oxidant species. Specifically, NOX4 expression was higher (90%, p < 0.05), suggesting that it could be a source of H2O2. In addition, iNOS expression was increased in glaucoma (47%, p < 0.05), as a source of NO in the brain, induced by NF-κB translocation to the nucleus (48%, p < 0.01). An increase in primary antioxidant enzymes superoxide dismutase (40%, p < 0.01) and glutathione peroxidase (55%, p < 0.05) was observed as an adaptive response to reactive oxygen species (ROS) production. However, an alteration in glutathione metabolism was shown in glaucoma due to a decrease in its recycling (40%, p < 0.05) as well as in its de novo synthesis (53%, p < 0.05), leading to a decreased in reduced/oxidized glutathione ratio (55%, p < 0.001). Moreover, a lower expression of Nfr2 was shown in glaucoma (40%, p < 0.05), suggesting that the cell signaling pathway that regulates the antioxidant capacity is compromised. In this context, redox imbalance takes place, resulting in oxidative damage to both lipids (70%, p < 0.001) and proteins (140%, p < 0.001).
These results suggest that glaucoma damages not only eye structures but also brain visual targets such as the primary visual cortex. Redox imbalance takes place due to an enhancement in ROS and reactive nitrogen species production from different sources, such as NOX family and iNOS, respectively, in an onset where the antioxidant defenses are overwhelmed due to an impaired Nrf2 signaling, leading to oxidative damage to macromolecules.
•The primary visual cortex is target of oxidative damage and both lipids and proteins are vulnerable.•NOX4 is a source of ROS in glaucoma, contributing to the pro-oxidant environment.•Glaucoma alters brain GSH/GSSG ratio by impairment of GSH synthesis and recycling.•iNOS is a source of NO in glaucoma due to NF-kB translocation into the nucleus.•Nrf2 expression is decreased in glaucoma, compromising the cell antioxidant capacity.
Increasing evidence suggests that glaucoma affects the ocular surface. We aimed to investigate the cellular mechanisms underlying the glaucoma-associated corneal alterations in an animal model.
...Wistar rats underwent the cauterization of two episcleral veins of the left eye to elevate the intraocular pressure (ipsilateral, G-IL). Control animals received a sham procedure (C-IL). Contralateral eyes did not receive any procedure (G-CL or C-CL). Enzymes related to the redox status, oxidative damage to macromolecules, and inflammatory markers were assessed in corneal lysates.
Compared to C-IL, NOX4, NOX2, and iNOS expression was increased in G-IL (68%, p < 0.01; 247%, p < 0.01; and 200%, p < 0.001, respectively). We found an increase in SOD activity in G-IL (60%, p < 0.05). The GSH/GSSG ratio decreased in G-IL (80%, p < 0.05), with a decrease in GR activity (40%, p < 0.05). G-IL displayed oxidative (90%, p < 0.01) and nitrosative (40%, p < 0.05) protein damage, and enhanced lipid peroxidation (100%, p < 0.01). G-IL group showed an increased in CD45, CD68 and F4/80 expression (50%, p < 0.05; 190%, p < 0.001 and 110%, p < 0.05, respectively). G-CL displayed a higher expression of Nrf2 (60%, p < 0.001) and increased activity of SOD, CAT, and GPx (60%, p < 0.05; 90%, p < 0.01; and 50%, p < 0.05, respectively).
Glaucoma induces a redox imbalance in the ipsilateral cornea with an adaptive response of the contralateral one.
Our study provides a possible mechanism involving oxidative stress and inflammation that explains the corneal alterations observed in glaucoma. We demonstrate that these changes extend not only to the ipsilateral but also to the contralateral cornea.
•The cornea is a target of oxidative and nitrosative damage in glaucoma.•NOX family and iNOS are sources of ROS and RNS in the glaucomatous cornea.•The enzymatic and non-enzymatic antioxidant response is impaired in the glaucomatous cornea.•Inflammatory cells could also be a source of ROS in the glaucomatous cornea.•The contralateral cornea displays an adaptive response modulated by Nrf2.
As leaders ascend to more powerful positions in their groups, they face ever-increasing demands. As a result, there is a common perception that leaders have higher stress levels than nonleaders. ...However, if leaders also experience a heightened sense of control—a psychological factor known to have powerful stress-buffering effects—leadership should be associated with reduced stress levels. Using unique samples of real leaders, including military officers and government officials, we found that, compared with nonleaders, leaders had lower levels of the stress hormone cortisol and lower reports of anxiety (study 1). In study 2, leaders holding more powerful positions exhibited lower cortisol levels and less anxiety than leaders holding less powerful positions, a relationship explained significantly by their greater sense of control. Altogether, these findings reveal a clear relationship between leadership and stress, with leadership level being inversely related to stress.
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