Adolescents’ Experiences of Distress and Well-Being during Intensive Mindfulness Practice: A Mixed-Methods Study

Objectives In recent years mindfulness has gone mainstream, reaching many adolescents through school programs and smartphone applications. Yet there is little empirical understanding of what mindfulness practice is like for adolescents. This mixed-methods study sought to capture adolescents’ lived experiences as they embarked on a period of intensive mindfulness practice. Methods Twenty-three self-selected youth (Mage = 16.68 years, SD = 1.55; 57% girls, 43% boys; 52% White, 13% African American, 4% Latino, 4% East Asian, and 26% Multiracial) participated in a six-day residential mindfulness retreat. Participants completed self-report surveys, open-ended daily diaries, and discussed their experiences in focus groups. Qualitative data were analyzed using a two-cycle coding process to categorize common patterns of adolescents’ experiences during mindfulness practice and quantitative data were examined for demographic subgroup differences. Results Adolescents reported an array of experiences of distress from cognitive (83% of adolescents; e.g., self-loathing and rumination), to emotional (87% of adolescents; e.g., sadness), to physical distress (44% of adolescents; e.g., physical pain) during mindfulness practice. They also described a range of well-being experiences from cognitive (87% of adolescents; e.g., self-inquiry and discovery), to emotional (65% of adolescents; e.g., acceptance), to social well-being (39% of adolescents; e.g., loving-kindness and connection). The frequency of experiences of distress and well-being reported were relatively balanced overall, yet girls and experienced meditators reported greater distress. Conclusions This study paints a descriptive picture of adolescents’ experiences during mindfulness practice and suggested that their experiences might reflect core developmental concerns. Implications for adolescent development and contemplative science are discussed

The Relationship Between Intelligence Mindset and Test Anxiety as Mediated by Effort Regulation

Test anxiety affects a sizable proportion of college students, especially in competitive STEM fields. Prior research has proposed interventions aimed at changing students’ implicit beliefs about intelligence (intelligence mindset) to help reduce students’ test anxiety, but results have been mixed and the mechanisms underlying this relationship are unclear. We propose that students’ beliefs about effort regulation may partially mediate the relationship between intelligence mindsets and test anxiety. We tested our model as an exploratory post-hoc analysis in a small sample of introductory physics students reporting psychological threat in a laboratory study. Effort regulation was measured as self-reported judgements of persistence in the face of difficulty and test anxiety was measured on a problem by problem basis during a laboratory physics assessment. Students’ intelligence mindset at pretest was a significant predictor of test anxiety at posttest, and this relationship was mediated by self-reported effort regulation. We discuss potential implications of these findings for mindset-based interventions aimed at reducing test anxiety

The Relationship Between Intelligence Mindset and Test Anxiety as Mediated by Effort Regulation

Test anxiety affects a sizable proportion of college students, especially in competitive STEM fields. Prior research has proposed interventions aimed at changing students’ implicit beliefs about intelligence (intelligence mindset) to help reduce students’ test anxiety, but results have been mixed and the mechanisms underlying this relationship are unclear. We propose that students’ beliefs about effort regulation may partially mediate the relationship between intelligence mindsets and test anxiety. We tested our model as an exploratory post-hoc analysis in a small sample of introductory physics students reporting psychological threat in a laboratory study. Effort regulation was measured as self-reported judgements of persistence in the face of difficulty and test anxiety was measured on a problem by problem basis during a laboratory physics assessment. Students’ intelligence mindset at pretest was a significant predictor of test anxiety at posttest, and this relationship was mediated by self-reported effort regulation. We discuss potential implications of these findings for mindset-based interventions aimed at reducing test anxiety

College Students’ Daily Mind Wandering is Related to Lower Social Well-Being

Objective. This study sought to examine how daily mind wandering is related to loneliness, felt connection to others, and school belonging among college students. Participants. Three samples (n = 209, n = 173, and n = 266) on two US campuses were recruited. Methods. Data were collected via ecological momentary assessment over the course of two academic quarters in one sample and an academic semester in two samples. Results. Social well-being declined throughout the academic term in all samples. Lower day-to-day mind wandering predicted lower loneliness at the next time point and was concurrently related to higher felt connection to others and higher school belonging. Thoughts about the past and future were associated with lower social well-being than present-focused thoughts. Conclusions. This research supports the proposition that promoting present-centered attention can benefit college students’ social well-being and alleviate feelings of loneliness and isolation that they often experience

Systems genomics in age-related macular degeneration

Genomic studies in age-related macular degeneration (AMD) have identified genetic variants that account for the majority of AMD risk. An important next step is to understand the functional consequences and downstream effects of the identified AMD-associated genetic variants. Instrumental for this next step are 'omics' technologies, which enable high-throughput characterization and quantification of biological molecules, and subsequent integration of genomics with these omics datasets, a field referred to as systems genomics.Single cell sequencing studies of the retina and choroid demonstrated that the majority of candidate AMD genes identified through genomic studies are expressed in non-neuronal cells, such as the retinal pigment epithelium (RPE), glia, myeloid and choroidal cells, highlighting that many different retinal and choroidal cell types contribute to the pathogenesis of AMD. Expression quantitative trait locus (eQTL) studies in retinal tissue have identified putative causal genes by demonstrating a genetic overlap between gene regulation and AMD risk. Linking genetic data to complement measurements in the systemic circulation has aided in understanding the effect of AMD-associated genetic variants in the complement system, and supports that protein QTL (pQTL) studies in plasma or serum samples may aid in understanding the effect of genetic variants and pinpointing causal genes in AMD. A recent epigenomic study fine-mapped AMD causal variants by determing regulatory regions in RPE cells differentiated from induced pluripotent stem cells (iPSC-RPE). Another approach that is being employed to pinpoint causal AMD genes is to produce synthetic DNA assemblons representing risk and protective haplotypes, which are then delivered to cellular or animal model systems.Pinpointing causal genes and understanding disease mechanisms is crucial for the next step towards clinical translation. Clinical trials targeting proteins encoded by the AMD-associated genomic loci C3, CFB, CFI, CFH, and ARMS2/HTRA1 are currently ongoing, and a phase III clinical trial for C3 inhibition recently showed a modest reduction of lesion growth in geographic atrophy. The EYERISK consortium recently developed a genetic test for AMD that allows genotyping of common and rare variants in AMD-associated genes. Polygenic risk scores (PRS) were applied to quantify AMD genetic risk, and may aid in predicting AMD progression.In conclusion, genomic studies represent a turning point in our exploration of AMD. The results of those studies now serve as a driving force for several clinical trials. Expanding to omics and systems genomics will further decipher function and causality from the associations that have been reported, and will enable the development of therapies that will lessen the burden of AMD

Systems genomics in age-related macular degeneration

Genomic studies in age-related macular degeneration (AMD) have identified genetic variants that account for the majority of AMD risk. An important next step is to understand the functional consequences and downstream effects of the identified AMD-associated genetic variants. Instrumental for this next step are ‘omics’ technologies, which enable high-throughput characterization and quantification of biological molecules, and subsequent integration of genomics with these omics datasets, a field referred to as systems genomics. Single cell sequencing studies of the retina and choroid demonstrated that the majority of candidate AMD genes identified through genomic studies are expressed in non-neuronal cells, such as the retinal pigment epithelium (RPE), glia, myeloid and choroidal cells, highlighting that many different retinal and choroidal cell types contribute to the pathogenesis of AMD. Expression quantitative trait locus (eQTL) studies in retinal tissue have identified putative causal genes by demonstrating a genetic overlap between gene regulation and AMD risk. Linking genetic data to complement measurements in the systemic circulation has aided in understanding the effect of AMD-associated genetic variants in the complement system, and supports that protein QTL (pQTL) studies in plasma or serum samples may aid in understanding the effect of genetic variants and pinpointing causal genes in AMD. A recent epigenomic study fine-mapped AMD causal variants by determing regulatory regions in RPE cells differentiated from induced pluripotent stem cells (iPSC-RPE). Another approach that is being employed to pinpoint causal AMD genes is to produce synthetic DNA assemblons representing risk and protective haplotypes, which are then delivered to cellular or animal model systems. Pinpointing causal genes and understanding disease mechanisms is crucial for the next step towards clinical translation. Clinical trials targeting proteins encoded by the AMD-associated genomic loci C3, CFB, CFI, CFH, and ARMS2/HTRA1 are currently ongoing, and a phase III clinical trial for C3 inhibition recently showed a modest reduction of lesion growth in geographic atrophy. The EYERISK consortium recently developed a genetic test for AMD that allows genotyping of common and rare variants in AMD-associated genes. Polygenic risk scores (PRS) were applied to quantify AMD genetic risk, and may aid in predicting AMD progression. In conclusion, genomic studies represent a turning point in our exploration of AMD. The results of those studies now serve as a driving force for several clinical trials. Expanding to omics and systems genomics will further decipher function and causality from the associations that have been reported, and will enable the development of therapies that will lessen the burden of AMD