When it comes to the pursuit of happiness, popular culture encourages a focus on oneself. By contrast, substantial evidence suggests that what consistently makes people happy is focusing prosocially on others. In the current study, we contrasted the mood- and well-being-boosting effects of prosocial behavior (i.e., doing acts of kindness for others or for the world) and self-oriented behavior (i.e., doing acts of kindness for oneself) in a 6-week longitudinal experiment. Across a diverse sample of participants (N = 473), we found that the 2 types of prosocial behavior led to greater increases in psychological flourishing than did self-focused and neutral behavior. In addition, we provide evidence for mechanisms explaining the relative improvements in flourishing among those prompted to do acts of kindness-namely, increases in positive emotions and decreases in negative emotions. Those assigned to engage in self-focused behavior did not report improved psychological flourishing, positive emotions, or negative emotions relative to controls. The results of this study contribute to a growing literature supporting the benefits of prosocial behavior and challenge the popular perception that focusing on oneself is an optimal strategy to boost one's mood. People striving for happiness may be tempted to treat themselves. Our results, however, suggest that they may be more successful if they opt to treat someone else instead. (PsycINFO Database Record

Loneliness, or perceived social isolation, may be evident in any group-living species, although its assessment in nonhumans provides some measurement challenges. It is well-known that loneliness in humans confers significant risk for morbidity and mortality, although mechanisms remain unclear. The authors describe a naturally-occurring model of loneliness in adult male rhesus monkeys that shows many parallels with the phenomenon in humans. Lonely monkeys (those that display high frequencies of social initiations but low frequencies of complex interaction) show elevated sympathetic nervous system activity and down regulated Type I interferon responses. Analysis of data from simian immunodeficiency virus-infected monkeys indicates that these physiological changes have functional consequences. Use of this animal model can help identify mechanisms by which loneliness impacts health.

Oxytocin appears to be centrally involved in socioemotional functioning, and is hypothesized to be relevant to the severe disruption in close relationships characteristic of borderline personality pathology. We examined whether a polymorphism of the oxytocin receptor gene (OXTR rs53576) interacts with quality of family functioning to predict borderline personality disorder (BPD) symptomatology in a sample of youth at age 20. A total of 385 youth from a longitudinal study of offspring of depressed or nondepressed mothers who were well characterized with respect to their family conditions and BPD symptomatology provided DNA for genotyping. Analyses revealed a significant moderation of the link between early family quality and later BPD symptoms by OXTR rs53576, and the pattern was consistent with differential susceptibility (plasticity). Whereas A-allele carriers had high levels of BPD symptoms under negative family conditions and low levels under positive conditions, GG homozygotes had average levels of BPD symptoms regardless of their family quality.

The "widowhood effect" (i.e., morbidity/mortality in recently bereaved spouses) may be related to changes in immune function, but little is known about the impact of bereavement on gene transcription in immune cells. This study examined how Complicated Grief and Non-complicated Grief responses to bereavement differentially affect leukocyte gene expression. Genome-wide transcriptional profiling and bioinformatic analyses were completed on 63 older adults. Thirty-six of them had lost their spouse/partner on average 2years ago, and 27 were nonbereaved, married controls. Twelve of the bereaved participants met criteria for Complicated Grief. Compared to nonbereaved controls, bereavement (both Complicated Grief and Non-complicated Grief) was associated with upregulated expression of genes involved in general immunologic activation and a selective downregulation of genes involved in B lymphocyte responses. However, Complicated Grief and Non-complicated Grief differed markedly in their expression of Type I interferon-related transcripts, with Non-complicated Grief subjects showing substantial upregulation relative to nonbereaved controls and Complicated Grief subjects showing substantial downregulation. Bereavement significantly modulates immune function gene expression. The magnitude of bereavement-related distress (i.e., Complicated Grief vs. Non-complicated Grief) is linked to differential patterns of transcription factor activation and gene expression involved in innate antiviral responses. These findings provide a molecular framework for understanding the health effects of bereavement, as well as new insights into the particular gene modules that are most sensitive to the individual's psychological response to loss.

Objective

Prosocial behavior has been linked to improved physical health, but the biological mechanisms involved remain unclear. This study tested whether a 4-week kindness intervention could reduce expression of a stress-related immune response gene signature known as the Conserved Transcriptional Response to Adversity (CTRA).

Methods

In a diverse sample of community adults (N = 182), study participants were randomly assigned to perform 3 kind acts for other people, to perform 3 kind acts for themselves, or to list daily activities (control), on one day per week over 4 weeks. CTRA gene expression was measured by RNA sequencing of dried blood spots (DBS) collected at baseline and 5 weeks later (1 week after completing study assignments). Participants' descriptions of their kind acts were coded for protocol adherence and act content.

Results

Participants who were randomized to perform kind acts for others showed significant reductions in CTRA gene expression relative to controls. Participants who were randomized to perform kind acts for themselves also showed significant reductions in CTRA gene expression relative to controls, but this pattern emerged only for those who failed to perform the requested self-kind acts (protocol non-adherent). Those who fully adhered to the self-kindness protocol showed no change in CTRA gene expression and did not differ from controls. Act content analyses implicated self-stress-reducing behavior in the paradoxical effects of self-kindness and the physical presence of others in the effects of prosocial behavior.

Conclusions

Prosocial engagement-doing something kind for others rather than oneself-reduces CTRA gene expression. The nature of kind acts and their intended recipient plays a key role in shaping the genomic impact of kindness.

© 2015 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved. Despite an extensive body of reported information about peripheral and central mechanisms involved in the pathophysiology of IBS symptoms, no comprehensive disease model has emerged that would guide the development of novel, effective therapies. In this Review, we will first describe novel insights into some key components of brain–gut interactions, starting with the emerging findings of distinct functional and structural brain signatures of IBS. We will then point out emerging correlations between these brain networks and genomic, gastrointestinal, immune and gut-microbiome-related parameters. We will incorporate this new information, as well as the reported extensive literature on various peripheral mechanisms, into a systems-based disease model of IBS, and discuss the implications of such a model for improved understanding of the disorder, and for the development of more-effective treatment approaches in the future.

Social relationships endow health and fitness benefits, but considerable variation exists in the extent to which individuals form and maintain salutary social relationships. The mental and physical health effects of social bonds are more strongly related to perceived isolation (loneliness) than to objective social network characteristics. We sought to develop an animal model to facilitate the experimental analysis of the development of, and the behavioral and biological consequences of, loneliness. In Study 1, using a population-based sample of older adults, we examined how loneliness was influenced both by social network size and by the extent to which individuals believed that their daily social interactions reflected their own choice. Results revealed three distinct clusters of individuals: (i) individuals with large networks who believed they had high choice were lowest in loneliness, (ii) individuals with small social networks who believed they had low choice were highest in loneliness, and (iii) the remaining two groups were intermediate and equivalent in loneliness. In Study 2, a similar three-group structure was identified in two separate samples of adult male rhesus monkeys (Macaca mulatta) living in large social groups: (i) those high in sociability who had complex social interaction with a broad range of social partners (putatively low in loneliness), (ii) those low in sociability who showed tentative interactions with certain classes of social partners (putatively high in loneliness), and (iii) those low in sociability who interacted overall at low levels with a broad range of social partners (putatively low or intermediate in loneliness). This taxonomy in monkeys was validated in subsequent experimental social probe studies. These results suggest that, in highly social nonhuman primate species, some animals may show a mismatch between social interest and social attainment that could serve as a useful animal model for experimental and mechanistic studies of loneliness.

To define the cellular mechanisms of up-regulated inflammatory gene expression and down-regulated antiviral response in people experiencing perceived social isolation (loneliness), we conducted integrative analyses of leukocyte gene regulation in humans and rhesus macaques. Five longitudinal leukocyte transcriptome surveys in 141 older adults showed up-regulation of the sympathetic nervous system (SNS), monocyte population expansion, and up-regulation of the leukocyte conserved transcriptional response to adversity (CTRA). Mechanistic analyses in a macaque model of perceived social isolation confirmed CTRA activation and identified selective up-regulation of the CD14(++)/CD16(-) classical monocyte transcriptome, functional glucocorticoid desensitization, down-regulation of Type I and II interferons, and impaired response to infection by simian immunodeficiency virus (SIV). These analyses identify neuroendocrine-related alterations in myeloid cell population dynamics as a key mediator of CTRA transcriptome skewing, which may both propagate perceived social isolation and contribute to its associated health risks.

Psychosocial stress can affect inflammatory processes that have important consequences for cancer outcomes and the behavioral side effects of cancer treatment. To date, however, little is known about the upstream neural processes that may link psychosocial stressors and inflammation in cancer patients and survivors. To address this issue, 15 women who had been diagnosed with early-stage breast cancer and completed cancer treatment and 15 age- and ethnicity-matched women with no cancer history were recruited for a neuroimaging study. Participants provided a blood sample for levels of circulating inflammatory markers (CRP and IL-6), underwent an fMRI scan in which they completed a threat reactivity task designed to elicit activity in the amygdala, and reported their levels of perceived social attachment/support. There were no significant differences between cancer survivors and controls in levels of CRP or IL-6, in amygdala reactivity to the socially threatening images, or in levels of perceived social support. However, results showed a strong, positive correlation between CRP concentration and left amygdala reactivity in the survivor group that was not apparent in controls. Higher levels of social support in the survivor group were also associated with reduced amygdala reactivity and CRP. These data suggest the possibility of a stronger "neural-immune pipeline" among breast cancer survivors, such that peripheral inflammation is more strongly associated with neural activity in threat-related brain regions.

High conflict and low warmth in families may contribute to immune cells developing a tendency to respond to threats with exaggerated inflammation that is insensitive to inhibitory signaling. We tested associations between family environments and expression of genes bearing response elements for transcription factors that regulate inflammation: nuclear factor kappa B (NF-κB) and glucocorticoid receptor. The overall sample (47 families) completed interviews, questionnaires, and 8-week daily diary assessments of conflict and warmth, which were used to create composite family conflict and warmth scores. The diaries assessed upper respiratory infection (URI) symptoms, and URI episodes were clinically verified. Leukocyte RNA was extracted from whole blood samples provided by a subsample of 42 children (8-13 years of age) and 73 parents. In children, higher conflict and lower warmth were related to greater expression of genes bearing response elements for the proinflammatory transcription factor NF-κB, and more severe URI symptoms. In parents, higher conflict and lower warmth were also related to greater NF-κB-associated gene expression. Monocytes and dendritic cells were implicated as primary cellular sources of differential gene expression in the sample. Consistent with existing conceptual frameworks, stressful family environments were related to a proinflammatory phenotype at the level of the circulating leukocyte transcriptome.