Is the waning of passion and satisfaction in romantic relationships inevitable, or can the honeymoon period be sustained? The Hedonic Adaptation Prevention model, which describes the mechanisms by which people adapt to positive life changes, posits that hedonic adaptation is a powerful barrier to sustained relationship well-being and suggests how to thwart it. In this paper, we apply the model to a new area of study - namely, intimate relationships. We explore the practices, habits, and activities that can increase the number of positive events and emotions in relationships, boost their variety, lower a couple's entitled aspirations, and build their appreciation - all variables that can serve to slow adaptation and increase well-being. Additionally, we discuss types of romantic relationships (e.g. long-distance relationships and unhealthy relationships) that may be relatively less susceptible to hedonic adaptation. © 2013 Copyright Taylor and Francis Group, LLC.

Happiness seekers tend to focus on changing their life circumstances, such as buying a new house, switching jobs, or getting married. However, people have been found to adapt to both positive and negative life changes, such as marriage, job promotion, disability, and widowhood. This process-known as hedonic adaptation-can serve as a formidable barrier to achieving lasting happiness. The Hedonic Adaptation Prevention model outlines why people adapt to life changes and sheds light on how adaptation to favorable events can be forestalled and how adaptation to unfavorable events can be hastened. In this chapter, we focus on a positive change as the model's starting point, which is associated with an immediate boost in well-being and a gradual decline back to baseline. Individuals adapt to positive life changes due to increasing aspirations and declines in the number of positive events and emotions associated with the change. Fortunately, lasting happiness change is indeed possible, as adaptation can be slowed or arrested in a number of ways, such as feeling greater appreciation for the good things in life and introducing greater variety.

A functional analysis of prosociality considers how predispositions for prosocial behavior prompt, reinforce, and propagate kind behaviors in the real world. To examine the effects of practicing, receiving, and observing everyday prosociality-as well as the mechanisms underlying these effects-we randomly assigned employees in a Spanish corporate workplace (N = 111) to be Givers, Receivers, and Controls. Givers practiced 5 acts of kindness for a personalized list of Receivers over 4 weeks. We found that Givers and Receivers mutually benefited in well-being in both the short-term (e.g., on weekly measures of competence and autonomy) and the long-term (e.g., Receivers became happier after 2 months, and Givers became less depressed and more satisfied with their lives and jobs). In addition, Givers' prosocial acts inspired others to act: Receivers paid their acts of kindness forward with 278% more prosocial behaviors than Controls. Our results reveal that practicing everyday prosociality is both emotionally reinforcing and contagious (inspiring kindness and generating hedonic rewards in others) and that receiving everyday prosociality is an unequivocally positive experience (which may further reinforce Givers' actions). Prosociality's benefits shed light on its surprising ubiquity in humanity compared with our closest evolutionary cousins. (PsycINFO Database Record

Autoinflammatory disease and hyperinflammatory syndromes represent a growing number of diseases associated with inappropriately controlled inflammation in multiple organs. Systemic inflammation commonly results from dysregulated activation of innate immune cells, and therapeutic targeting of the IL-1β pathway has been used to ameliorate some of these diseases. Some hyperinflammatory syndromes, however, such as hemophagocytic lymphohistiocytosis and the newly classified proteasome disability syndromes, are refractory to such treatments, suggesting that other factors or environmental stressors may be contributing. In comparing two cytokine reporter mouse strains, we identify IFN-γ as a mediator of systemic autoinflammatory disease. Chronically elevated levels of IFN-γ resulted in progressive multiorgan inflammation and two copies of the mutant allele resulted in increased mortality accompanied by myeloproliferative disease. Disease was alleviated by genetic deletion of T-bet. These studies raise the possibility that therapeutics targeting the IFN-γ pathway might be effective in hyperinflammatory conditions refractory to IL-1β-targeted therapies.

Genetic and environmental influences on complex traits can change in response to developmental and environmental contexts. Here we explore the impact of a positive activity intervention on the genetic and environmental influences on well-being and mental health in a sample of 750 adolescent twins. Twins completed a 10-week online well-being intervention, consisting of kindness and gratitude tasks and matched control activities. The results showed significant improvements both in well-being and in internalizing symptoms in response to the intervention activities. We used multivariate twin analyses of repeated measures, tracking stability and change in genetic and environmental influences, to assess the impact of this environmental intervention on these variance components. The heritability of well-being remained high both before and after the intervention, and the same genetic effects were important at each stage, even as well-being increased. The overall magnitude of environmental influences was also stable across the intervention; however, different non-shared environmental influences emerged during the intervention. Our study highlights the value of exploring the innovations in non-shared environmental influences that could provide clues to the mechanisms behind improvements in well-being. The findings also emphasize that even traits strongly influenced by genetics, like well-being, are subject to change in response to environmental interventions.

Human positive transcription elongation factor b (P-TEFb) phosphorylates RNA polymerase II and regulatory proteins to trigger elongation of many gene transcripts. The HIV-1 Tat protein selectively recruits P-TEFb as part of a super elongation complex (SEC) organized on a flexible AFF1 or AFF4 scaffold. To understand this specificity and determine if scaffold binding alters P-TEFb conformation, we determined the structure of a tripartite complex containing the recognition regions of P-TEFb and AFF4. AFF4 meanders over the surface of the P-TEFb cyclin T1 (CycT1) subunit but makes no stable contacts with the CDK9 kinase subunit. Interface mutations reduced CycT1 binding and AFF4-dependent transcription. AFF4 is positioned to make unexpected direct contacts with HIV Tat, and Tat enhances P-TEFb affinity for AFF4. These studies define the mechanism of scaffold recognition by P-TEFb and reveal an unanticipated intersubunit pocket on the AFF4 SEC that potentially represents a target for therapeutic intervention against HIV/AIDS. DOI:http://dx.doi.org/10.7554/eLife.00327.001.

© 2014 Taylor & Francis Previous research has demonstrated a strong link between prosocial behavior – particularly autonomous prosocial behavior – and well-being. Little is known, however, about whether and how autonomy might be boosted in the context of everyday kindnesses. We tested the effect of supporting students’ autonomy on well-being gains from practicing acts of kindness in a six-week randomized experimental study in the United States and South Korea. As predicted, performing kind acts while receiving autonomy support led to greater improvements in well-being than performing kind acts without autonomy support or engaging in comparison activities (i.e. focusing on one’s academic work, with or without autonomy support). Notably, these well-being improvements were mediated by feelings of autonomy, competence, and relatedness. The current study is one of the first to demonstrate the causal effect of autonomous prosocial behavior on well-being, as well as the psychological mechanism (i.e. need satisfaction) explaining this effect.

The HIV-1 Tat protein stimulates viral gene expression by recruiting human transcription elongation complexes containing P-TEFb, AFF4, ELL2, and ENL or AF9 to the viral promoter, but the molecular organization of these complexes remains unknown. To establish the overall architecture of the HIV-1 Tat elongation complex, we mapped the binding sites that mediate complex assembly in vitro and in vivo. The AFF4 protein emerges as the central scaffold that recruits other factors through direct interactions with short hydrophobic regions along its structurally disordered axis. Direct binding partners CycT1, ELL2, and ENL or AF9 act as bridging components that link this complex to two major elongation factors, P-TEFb and the PAF complex. The unique scaffolding properties of AFF4 allow dynamic and flexible assembly of multiple elongation factors and connect the components not only to each other but also to a larger network of transcriptional regulators.