Friday, March 6, 2020

After Aesop's fable, the “sour-grape effect”: A systematic tendency to downplay the value of unattainable goals and rewards

Greener grass or sour grapes? How people value future goals after initial failure. Hallgeir Sjåstad, Roy F. Baumeister. Michael Ent. Journal of Experimental Social Psychology, Volume 88, May 2020, 103965.

Abstract: Across six experiments (N = 1304), people dealt with failure by dismissing the value of future goals. Participants were randomly assigned to receive good or poor feedback on a practice trial of a cognitive test (Studies 1–3, 5–6) or their academic performance (Study 4). Those who received poor (vs. good) feedback predicted that they would feel less happy about a future top performance. However, when all participants received a top score on the actual test they became equally happy, regardless of initial feedback. That is, initial failure made people underestimate how good it would feel to succeed in the future. Inspired by Aesop's fable of the fox and the grapes, we term this phenomenon the “sour-grape effect”: A systematic tendency to downplay the value of unattainable goals and rewards. Mediation analyses suggest that the low happiness predictions were a self-protective maneuver, indicated by apparent denial of the personal and future relevance of their performance. Moderation analysis showed that people high in achievement motivation constituted the main exception, as they predicted (correctly) that a big improvement would bring them joy. In a final and high-powered experiment, the effect generalized from predicted happiness to predicted pride and gratitude. Crucially, the sour-grape effect was found repeatedly across two different countries (USA and Norway) and multiple settings (lab, field, online), including two pre-registered replications. In line with the principle of “adaptive preferences” from philosophy and cognitive dissonance theory from psychology, the results suggest that what people want is restricted by what they can get.

Keywords: GoalsHappinessCognitive dissonanceSour grapesAffective forecasting

Local sleep and wakefulness & insomnia disorder:Wake-like activations (‘islands of wakefulness’) can occur during both major sleep stages (NREM & REM)

Local sleep and wakefulness—the concept and its potential for the understanding and treatment of insomnia disorder. Lina Stålesen Ramfjord, Elisabeth Hertenstein, Kristoffer Fehér, Christian Mikutta, Carlotta Louisa Schneider, Christoph Nissen & Jonathan Gabriel Maier. Somnologie, March 6 2020.

Abstract: In ancient mythology, sleep was often regarded as an inactive state, close to death. Research in the past century has, however, demonstrated that the brain is highly active and oscillates through well-defined stages during sleep. Yet it is only over the past decade that accumulating evidence has shown that sleep and wake processes can occur simultaneously, localized in distinct areas of the brain. The aim of this article is to review relevant aspects of the shift from global to local concepts of sleep–wake regulation and to further translate this perspective to the clinical problem of insomnia. Animal and human studies show that local wake-like activations (‘islands of wakefulness’) can occur during both major sleep stages, i.e. non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. Preliminary evidence suggests that higher levels of local wake-like activity, not captured in standard polysomnographic recordings, might underlie the perception of disrupted sleep or even wakefulness during polysomnographic epochs of sleep in patients with chronic insomnia. To further decipher the neural mechanisms, advanced techniques of high-density electroencephalography (hdEEG) and non-invasive brain stimulation techniques can be applied. Furthermore translating the concept of local sleep and wakefulness to the prevalent health problem of chronic insomnia might help to reduce the current mismatch between subjective sleep–wake perception and standard recordings, and might inform the development of new treatments.

Substantial mobility in & out of poverty: 41 pct of those in poverty in 2007 were out of poverty in the following year; however, many of those who are poor spend multiple years in poverty or escape poverty only to fall back into it

Presence and Persistence of Poverty in U.S. Tax Data. Jeff Larrimore, Jacob Mortenson, David Splinter. Feb 2020.

Abstract: This paper presents new estimates of the level and persistence of poverty among U.S. households since the Great Recession. We build new annual household data files using U.S. income tax filings between 2007 and 2018. These data, which are constructed for the population of U.S. residents, allow us to track individuals over time and measure how tax policies affect poverty trends. Using an after-tax household income measure, we estimate that over 4 in 10 people spent at least one year in poverty between 2007 and 2018. Those that experienced at least one year of poverty spent an average of one-fourth of the 12-year period in poverty. There is substantial mobility in and out of poverty. For example, 41 percent of those in poverty in 2007 were out of poverty in the following year. However, many of those who are poor spend multiple years in poverty or escape poverty only to fall back into it. Of those who were in poverty in 2007, one-third are in poverty for at least half of the years through 2018. We also document substantial heterogeneity in these trends by age: younger individuals experience higher rates of poverty but less persistence; older individuals experience lower rates of poverty but more persistence.

New Frontiers in Irritability Research—From Cradle to Grave and Bench to Bedside

New Frontiers in Irritability Research—From Cradle to Grave and Bench to Bedside. Neir Eshel, Ellen Leibenluft. JAMA Psychiatry. 2020;77(3):227-228, December 4, 2019. doi:10.1001/jamapsychiatry.2019.3686

We all know what it’s like to be irritable. Our partners walk on eggshells around us. The slightest trigger sets us off. If there’s a punching bag nearby, it had better watch out. Irritability, defined as a low threshold for experiencing frustration or anger, is common. In the right context, irritability can be adaptive, motivating us to overcome barriers or dominate our environment. When prolonged or disproportionate, however, irritability can be counterproductive, causing us to waste our energy on maladaptive behavior.

In recent years, there has been an increase in research on irritability in childhood, with an emerging literature on its neurobiology, genetics, and epidemiology.1 There is even a new diagnosis focused on this symptom, disruptive mood dysregulation disorder (DMDD). However, there is a dearth of irritability research in adults. This is regrettable, because irritability is an important clinical symptom in multiple mental illnesses throughout the life span. From depression to posttraumatic stress disorder, dementia to premenstrual dysphoric disorder, traumatic brain injury to borderline personality disorder, irritability is associated with extensive burdens on individuals, their families, and the general public.

In this Viewpoint we suggest that studying the brain basis for irritability across development and disorder could have substantial clinical benefits. Furthermore, we propose that irritability, like addiction or anxiety, is an evolutionarily conserved focus ready for translational neuroscience.

Diagnosis and Treatment Across the Life Span

Despite its clinical toll, there are few evidence-based treatments for irritability. The only US Food and Drug Administration–approved medications for irritability are risperidone and aripiprazole, which are approved only in the context of autism and are associated with adverse effects that limit their utility. Stimulants, serotonin reuptake inhibitors, and variants of cognitive behavioral therapy and parent management training show promise for different populations, but overall there is a shortage of options, leading many health care professionals to try off-label drug cocktails with unclear efficacy. This situation results in part from our primitive understanding of the phenomenology and brain mechanisms of irritability throughout the life span.
An emerging body of work focuses on measuring irritability in children and adolescents, determining comorbid disorders, and tracking related functional impairment.1 Multiple studies, for example, report that chronically irritable youth are at elevated risk for suicidality, depression, and anxiety in adulthood.2,3 But what are the clinical characteristics and longitudinal course of irritability in adults? Irritability diminishes from toddlerhood through school age, but does it continue to decrease monotonically with age into adulthood? What about the end of life? Irritability and aggression are common in patients with neurodegenerative disorders, but are these symptoms similar to those in a child with DMDD? There has been limited systematic study of irritability in adulthood, and studies that mention irritability in adulthood operationalize the construct in different ways. One study counted 21 definitions and 11 measures of irritability in the psychiatric literature, all of which overlapped with anger and aggression.4 This lack of clarity diminishes our ability to identify biomarkers or track treatment success. Even studies that use childhood irritability to predict adult impairment do not typically measure irritability in adults, thereby obscuring the natural history of irritability as a symptom.5 For the field to progress, it will be crucial to establish standard definitions and measurements spanning childhood through adulthood.
Beyond phenomenology, we need to identify brain signatures associated with the emergence, recurrence, and remission of irritability across the life span and during treatment. Irritability is a prototypical transdiagnostic symptom, but it remains unclear to what extent its brain mechanisms overlap across disorders. For example, in children, data suggest that the brain mechanisms mediating irritability in DMDD, anxiety disorders, and attention-deficit/hyperactivity disorder are similar but differ from those mediating irritability in childhood bipolar disorder.1,6 The frequency of irritable outbursts appears to diminish in step with the maturity of prefrontal regions during childhood.1 Could degeneration in the same structures predict reemergence of irritable outbursts in patients with dementia? Could developmental differences in these regions increase the likelihood of irritability when individuals are sleep deprived or intoxicated later in adolescence or adulthood? Only through fine-grained neuroscientific studies can we disentangle what is unique to the symptom (ie, irritability) and to the disorder (eg, bipolar disorder vs DMDD vs dementia), and develop treatments tailored to an individual’s brain pathology.
Translational Neuroscience and Irritability

In addition to their clinical relevance, neuroscientific studies of irritability can address fundamental questions about brain dysfunction and recovery. Over the past 2 decades, studies have revealed the circuits underlying reward processing, and in particular prediction error, the mismatch between expected and actual reward.7 The neuroscience of aggression has also advanced through the discovery of cells in the amygdala and hypothalamus that form a final common pathway for aggressive behavior.8 Irritability and the concept of frustrative nonreward can tie these 2 fields together.
Frustrative nonreward is the behavioral and emotional state that occurs in response to a negative prediction error, ie, the failure to receive an expected reward. In the classic study by Azrin et al,9 pigeons were trained to peck a key for food reward. After pigeons learned the task, the experimenters removed the reward; then when the pigeons pecked, nothing happened. For the next several minutes, there were 2 changes in the pigeons’ behavior. First, they pecked the key at a higher rate. Second, they became unusually aggressive, damaging the cage and attacking another pigeon nearby. In other words, a negative prediction error led to a state of frustration, which then induced increased motor activity and aggression. Such responses to frustration have been replicated in many species, including chimpanzees, cockerels, salmon, and human children and adults.10 Frustrative nonreward therefore provides an evolutionarily conserved behavioral association between prediction error and aggression. Apart from studies in children,1,6 however, little has been done to probe the neural circuits of frustrative nonreward or of irritability, which can be defined as a low threshold for experiencing frustrative nonreward.
We know, for example, that negative prediction errors cause phasic decreases in dopamine neuron firing, which help mediate learning by reducing the valuation of a stimulus. Does this dip in dopamine level also increase the likelihood of aggression and if so how? The same optogenetic techniques that have demonstrated a causal role for dopamine prediction errors in reward learning could be used to test their role in aggressive behavior. Likewise, multiple nodes in the reward circuit encode the value of environmental stimuli. Could these values modulate the propensity for aggression? Environments of plenty, for instance, may protect against aggressive outbursts, because if there is always more reward available, the missing out factor may not be salient. Conversely, scarcity could make individuals more likely to be aggressive, because if there are few rewards to be had, achieving dominance may be necessary for survival.
Exploring the bidirectional associations between the reward processing and aggression circuits would help us understand state changes in the brain and how environmental context determines our behavior. At the same time, understanding these circuits will lay the groundwork for mechanism-based treatments for irritability.
The neuroscience of irritability is in its infancy and research has focused almost exclusively on children. We now have an opportunity to expand this field to adults, across disorders, and to animal models for more precise mechanistic studies. Through better measurement, careful experimental design, input from theorists and computational psychiatrists, and coordinated efforts across experts in multiple disorders, we can guide the field to maturity.

Reduction of Facebook use longitudinally increased life satisfaction, enhanced the level of physical activity, & reduced depressive symptoms and smoking behavior

Less Facebook use – More well-being and a healthier lifestyle? An experimental intervention study. Julia Brailovskaia et al. Computers in Human Behavior, March 6 2020, 106332.

• Experimental reduction of Facebook use longitudinally increased life satisfaction.
• Reduction of Facebook use longitudinally enhanced the level of physical activity.
• Reduction of Facebook use longitudinally reduced depressive symptoms and smoking behavior.
• Less time spent on Facebook leads to more well-being and a healthier lifestyle.

Abstract: Use of the social platform Facebook belongs to daily life, but may impair subjective well-being. The present experimental study investigated the potential beneficial impact of reduction of daily Facebook use. Participants were Facebook users from Germany. While the experimental group (N = 140; Mage(SDage) = 24.15 (5.06)) reduced its Facebook use for 20 min daily for two weeks, the control group (N = 146; Mage(SDage) = 25.39 (6.69)) used Facebook as usual. Variables of Facebook use, life satisfaction, depressive symptoms, physical activity and smoking behavior were assessed via online surveys at five measurement time points (pre-measurement, day 0 = T1; between-measurement, day 7 = T2; post-measurement, day 15 = T3; follow-up 1, one month after post-measurement = T4; follow-up 2, three months after post-measurement = T5). The intervention reduced active and passive Facebook use, Facebook use intensity, and the level of Facebook Addiction Disorder. Life satisfaction significantly increased, and depressive symptoms significantly decreased. Moreover, frequency of physical activity such as jogging or cycling significantly increased, and number of daily smoked cigarettes decreased. Effects remained stable during follow-up (three months). Thus, less time spent on Facebook leads to more well-being and a healthier lifestyle.