Handbook of Well-Being

It is a pleasure to bring to you the eHandbook of Subjective Well-Being, the science of when and why people experience and evaluate their lives in positive ways, including aspects such as positive feelings, life satisfaction, and optimism. There are chapters in this eHandbook on the philosophy and history of well-being, as well as reviews of empirical research on the ways to assess well-being, the circumstances that predict it, the outcomes that it produces, the societal policies that enhance it, and many other social, biological, and cultural processes that help us understand why some people are happy and satisfied with their lives, while others are not. There are also chapters on theories of well-being, such as the baseline or set-point models. We believe that Open publication is the wave of the future (Jhangiani & Biswas-Diener, 2017). Therefore, we are presenting the handbook in an electronic format so that it is widely available to everyone around the world. The handbook is entirely open and free – anyone can read and use it without cost. This is important to us as we desire to lower knowledge barriers for individuals and communities, especially because it provides access to students, educators, and scholars who do not have substantial financial resources. We are not certain if this is the first free and open handbook in the behavioral sciences, but hopefully it will not be the last. In the past the prohibitive price of many handbooks have made them available only to scholars or institutions in wealthy nations, and this is unfortunate. We believe scientific scholarship should be available to all. The field of subjective well-being has grown at rapid pace over the last several decades, and many discoveries have been made. When Ed Diener began his research within the field in 1981 there were about 130 studies published that year on the topic, as shown using a Google Scholar search on “subjective well-being.” Eighteen years later when Shigehiro Oishi earned his Ph.D. in 2000 there were 1,640 publications that year on the topic, and when Louis Tay was awarded a Ph.D. in 2011 there were 10,400 publications about subjective well-being. Finally, in 2016 there were 18,300 publications – in that single year alone! In other words, during the time that Diener has been studying the topic, scholarship on subjective well-being has grown over 100-fold! It is not merely the number of published studies that has grown, but there have been enormous leaps forward in our understanding. In the 1980s, there were questions about the reliability and validity of subjective well-being assessments, and the components that underlie it. One notable advance is our understanding and measurement of well-being. We now know a great deal about the validity of self-report measures, as well as the core evaluative and affective components that make up subjective well-being. Further, scholars have a much greater understanding of the processes by which people report their subjective well-being, and various biases or artifacts that may influence these reports. In 1982 many studies were focused on demographic factors such as income, sex, and age that were correlated with subjective well-being. By 2016 we understood much more about temperament and other internal factors that influence happiness, as well as some of the outcomes in behavior that subjective well-being helps produce (e.g., income, performance, physical health, longevity). In the 1980s, researchers assumed that people adapt to almost any life event, and that different life events only have a short-term effect on subjective well-being. A number of large-scale longitudinal studies later showed that that is not the case. By now we know what kinds of life events affect our subjective well-being, how much, and for roughly how long. In the 1980s researchers believed that economic growth would not increase the happiness of a given nation. Now we know when economic growth tends to increase the happiness of a given nation. Additionally, we know much more about the biology of subjective well-being, and an enormous amount more about culture and well-being, a field that was almost nonexistent in 1982. With the advent of positive psychology, we are also beginning to examine practices and interventions that can raise subjective well-being. Given the broad interest in subjective well-being in multiple fields like psychology, economics, political science, and sociology, there have been important developments made toward understanding how societies differ in well-being. This understanding led to the development of national accounts of well-being – societies using well-being measures to help inform policy deliberations. This advance changes the focus of governments away from a narrow emphasis on economic development to a broader view which sees government policies as designed to raise human well-being. We were fortunate to have so many leading scholars of subjective well-being and related topics contribute to this volume. We might be slightly biased but most of the chapters in this eHandbook are truly superb. Not only do they provide a broad coverage of a large number of areas, but many of the chapters present new ways of thinking about these areas. Below is a brief overview of each of the sections in this volume: In Section 1 we begin the volume with chapters on philosophical, historical, and religious thinking on well-being through the ages. Next, we cover the methods and measures used in the scientific study of well-being. Section 2 is devoted to theories of well-being such as the top-down theory, activity theory, goal theory, self-determination theory, and evolutionary theory. Section 3 covers the personality, genetics, hormones, and neuroscience of well-being. Then, demographic factors such as age, gender, race, religion, and marital status are discussed. Section 4 is devoted to how domains of life – such as work, finance, close relationships, and leisure – are related to overall subjective well-being. Section 5 covers the various outcomes of subjective well-being, ranging from work outcomes, to cognitive outcomes, to health, and finally relationship outcomes. Section 6 covers interventions to increase subjective well-being. Finally, Section 7 is devoted to cultural, geographical, and historical variations in subjective well-being. This eHandbook presents the most up-to-date and comprehensive understanding of subjective well-being – and it is freely available to all! The editors would like to extend their thanks to several individuals who have been critical to the success of the handbook. First, our gratitude is immense toward Chris Wiese, Keya Biswas-Diener, and Danielle Geerling, who organized and kept the entire venture on track. Their hard work and organizational skills were wonderful, and the book would not have been possible without them. Second, we extend our thanks to the Diener Education Fund, a charitable organization devoted to education that in part made this project possible. In particular we express deep gratitude to Mary Alice and Frank Diener. Not only did their help make this eHandbook possible, but their lives stood as shining examples of the way to pursue well-being!https://digitalcommons.unomaha.edu/psychfacbooks/1008/thumbnail.jp

Feeding Cues and Injected Nutrients Induce Acute Expression of Multiple Clock Genes in the Mouse Liver

The circadian clock is closely associated with energy metabolism. The liver clock can rapidly adapt to a new feeding cycle within a few days, whereas the lung clock is gradually entrained over one week. However, the mechanism underlying tissue-specific clock resetting is not fully understood. To characterize the rapid response to feeding cues in the liver clock, we examined the effects of a single time-delayed feeding on circadian rhythms in the liver and lungs of Per2::Luc reporter knockin mice. After adapting to a night-time restricted feeding schedule, the mice were fed according to a 4, 8, or 13 h delayed schedule on the last day. The phase of the liver clock was delayed in all groups with delayed feeding, whereas the lung clock remained unaffected. We then examined the acute response of clock and metabolism-related genes in the liver using focused DNA-microarrays. Clock mutant mice were bred under constant light to attenuate the endogenous circadian rhythm, and gene expression profiles were determined during 24 h of fasting followed by 8 h of feeding. Per2 and Dec1 were significantly increased within 1 h of feeding. Real-time RT-PCR analysis revealed a similarly acute response in hepatic clock gene expression caused by feeding wild type mice after an overnight fast. In addition to Per2 and Dec1, the expression of Per1 increased, and that of Rev-erbα decreased in the liver within 1 h of feeding after fasting, whereas none of these clock genes were affected in the lung. Moreover, an intraperitoneal injection of glucose combined with amino acids, but not either alone, reproduced a similar hepatic response. Our findings show that multiple clock genes respond to nutritional cues within 1 h in the liver but not in the lung

A proposal for a coordinated effort for the determination of brainwide neuroanatomical connectivity in model organisms at a mesoscopic scale

In this era of complete genomes, our knowledge of neuroanatomical circuitry remains surprisingly sparse. Such knowledge is however critical both for basic and clinical research into brain function. Here we advocate for a concerted effort to fill this gap, through systematic, experimental mapping of neural circuits at a mesoscopic scale of resolution suitable for comprehensive, brain-wide coverage, using injections of tracers or viral vectors. We detail the scientific and medical rationale and briefly review existing knowledge and experimental techniques. We define a set of desiderata, including brain-wide coverage; validated and extensible experimental techniques suitable for standardization and automation; centralized, open access data repository; compatibility with existing resources, and tractability with current informatics technology. We discuss a hypothetical but tractable plan for mouse, additional efforts for the macaque, and technique development for human. We estimate that the mouse connectivity project could be completed within five years with a comparatively modest budget.Comment: 41 page

A Novel RNAi Lethality Rescue Screen to Identify Regulators of Adipogenesis

Adipogenesis, the differentiation of fibroblast-like mesenchymal stem cells into mature adipocytes, is tightly regulated by a complex cascade of transcription factors, including the nuclear receptor Peroxisome proliferator activator receptor γ (PPARγ). RNAi-mediated knock down libraries may present an atractive method for the identification of additional adipogenic factors. However, using in vitro adipogenesis model systems for high-throughput screening with siRNA libraries is limited since (i) differentiation is not homogeneous, but results in mixed cell populations, and (ii) the expression levels (and activity) of adipogenic regulators is highly dynamic during differentiation, indicating that the timing of RNAi-mediated knock down during differentiation may be extremely critical. Here we report a proof-of-principle for a novel RNAi screening method to identify regulators of adipogenesis that is based on lethality rescue rather than differentiation, using microRNA expression driven by a PPARγ responsive RNA polymerase II promoter. We validated this novel method through screening of a dedicated deubiquitinase knock down library, resulting in the identification of UCHL3 as an essential deubiquitinase in adipogenesis. This system therefore enables the identification of novel genes regulating PPARγ-mediated adipogenesis in a high-throughput setting

Multiple Roles for the Non-Coding RNA SRA in Regulation of Adipogenesis and Insulin Sensitivity

Peroxisome proliferator-activated receptor-γ (PPARγ) is a master transcriptional regulator of adipogenesis. Hence, the identification of PPARγ coactivators should help reveal mechanisms controlling gene expression in adipose tissue development and physiology. We show that the non-coding RNA, Steroid receptor RNA Activator (SRA), associates with PPARγ and coactivates PPARγ-dependent reporter gene expression. Overexpression of SRA in ST2 mesenchymal precursor cells promotes their differentiation into adipocytes. Conversely, knockdown of endogenous SRA inhibits 3T3-L1 preadipocyte differentiation. Microarray analysis reveals hundreds of SRA-responsive genes in adipocytes, including genes involved in the cell cycle, and insulin and TNFα signaling pathways. Some functions of SRA may involve mechanisms other than coactivation of PPARγ. SRA in adipocytes increases both glucose uptake and phosphorylation of Akt and FOXO1 in response to insulin. SRA promotes S-phase entry during mitotic clonal expansion, decreases expression of the cyclin-dependent kinase inhibitors p21Cip1 and p27Kip1, and increases phosphorylation of Cdk1/Cdc2. SRA also inhibits the expression of adipocyte-related inflammatory genes and TNFα-induced phosphorylation of c-Jun NH2-terminal kinase. In conclusion, SRA enhances adipogenesis and adipocyte function through multiple pathways

Partner in fat metabolism: role of KLFs in fat burning and reproductive behavior

The abnormalities caused by excess fat accumulation can result in pathological conditions which are linked to several interrelated diseases, such as cardiovascular disease and obesity. This set of conditions, known as metabolic syndrome, is a global pandemic of enormous medical, economic, and social concern affecting a significant portion of the world’s population. Although genetics, physiology and environmental components play a major role in the onset of disease caused by excessive fat accumulation, little is known about how or to what extent each of these factors contributes to it. The worm, Caenorhabditis elegans offers an opportunity to study disease related to metabolic disorder in a developmental system that provides anatomical and genomic simplicity relative to the vertebrate animals and is an excellent eukaryotic genetic model which enable us to answer the questions concerning fat accumulation which remain unresolved. The stored triglycerides (TG) provide the primary source of energy during periods of food deficiency. In nature, lipid stored as TGs are hydrolyzed into fatty acids which are broken down through β-oxidation to yield acetyl-CoA. Our recent study suggests that a member of C. elegans Krüppel-like factor, klf-3 regulates lipid metabolism by promoting FA β-oxidation and in parallel may contribute in normal reproduction and fecundity. Genetic and epigenetic factors that influence this pathway may have considerable impact on fat related diseases in human. Increasing number of studies suggest the role of mammalian KLFs in adipogenesis. This functional conservation should guide our further effort to explore C. elegans as a legitimate model system for studying the role of KLFs in many pathway components of lipid metabolism

Srebf1a is a key regulator of transcriptional control for adipogenesis

Adipogenesis is regulated by a complex cascade of transcriptional factors, but little is known about the early events that regulate the adipogenic program. Here, we report the role of the srebf1a gene in the differentiation of fibroblastic 3T3-F442A cells. We found that expression of srebf1a depended on GSK3β activity and that GSK3β activity was necessary for C/EBPβ phosphorylation at Thr188. Knockdown of srebf1a inhibited the adipogenic program because it blocked the expression of genes encoding PPARγ2, C/EBPα, SREBP1c and even FABP4, demonstrating that SREBP1a activation is upstream of these three essential adipogenic transcription factors. Kinetic analysis during differentiation illustrated that the order of expression of adipogenic genes was the following: cebpb, srebf1a, pparg2, cebpa, srebp1c and fabp4. Our data suggest that srebf1a acts as an essential link between the GSK3β-C/EBPβ signaling axis and the beginning of the adipogenic transcriptional cascade

Multimodal surface-based morphometry reveals diffuse cortical atrophy in traumatic brain injury.

<p>Abstract</p> <p>Background</p> <p>Patients with traumatic brain injury (TBI) often present with significant cognitive deficits without corresponding evidence of cortical damage on neuroradiological examinations. One explanation for this puzzling observation is that the diffuse cortical abnormalities that characterize TBI are difficult to detect with standard imaging procedures. Here we investigated a patient with severe TBI-related cognitive impairments whose scan was interpreted as normal by a board-certified radiologist in order to determine if quantitative neuroimaging could detect cortical abnormalities not evident with standard neuroimaging procedures.</p> <p>Methods</p> <p>Cortical abnormalities were quantified using multimodal surfaced-based morphometry (MSBM) that statistically combined information from high-resolution structural MRI and diffusion tensor imaging (DTI). Normal values of cortical anatomy and cortical and pericortical DTI properties were quantified in a population of 43 healthy control subjects. Corresponding measures from the patient were obtained in two independent imaging sessions. These data were quantified using both the average values for each lobe and the measurements from each point on the cortical surface. The results were statistically analyzed as z-scores from the mean with a p < 0.05 criterion, corrected for multiple comparisons. False positive rates were verified by comparing the data from each control subject with the data from the remaining control population using identical statistical procedures.</p> <p>Results</p> <p>The TBI patient showed significant regional abnormalities in cortical thickness, gray matter diffusivity and pericortical white matter integrity that replicated across imaging sessions. Consistent with the patient's impaired performance on neuropsychological tests of executive function, cortical abnormalities were most pronounced in the frontal lobes.</p> <p>Conclusions</p> <p>MSBM is a promising tool for detecting subtle cortical abnormalities with high sensitivity and selectivity. MSBM may be particularly useful in evaluating cortical structure in TBI and other neurological conditions that produce diffuse abnormalities in both cortical structure and tissue properties.</p

Personality profiles of cultures: aggregate personality traits

Personality profiles of cultures can be operationalized as the mean trait levels of culture members. College students from 51 cultures rated an individual from their country whom they knew well (N = 12, 156). Aggregate scores on Revised NEO Personality Inventory scales generalized across age and gender groups, approximated the individual-level Five-Factor Model, and correlated with aggregate self-report personality scores and other culture-level variables. Results were not attributable to national differences in economic development or to acquiescence. Geographical differences in scale variances and mean levels were replicated, with Europeans and Americans generally scoring higher in Extraversion than Asians and Africans. Findings support the rough scalar equivalence of NEO-PI-R factors and facets across cultures, and suggest that aggregate personality profiles provide insight into cultural differences

Measurement of the Ratio of b Quark Production Cross Sections in Antiproton-Proton Collisions at 630 GeV and 1800 GeV

We report a measurement of the ratio of the bottom quark production cross section in antiproton-proton collisions at 630 GeV to 1800 GeV using bottom quarks with transverse momenta greater than 10.75 GeV identified through their semileptonic decays and long lifetimes. The measured ratio sigma(630)/sigma(1800) = 0.171 +/- .024 +/- .012 is in good agreement with next-to-leading order (NLO) quantum chromodynamics (QCD)