The roles of dispositional flow, dispositional mindfulness, and self-compassion in the Objectification Theory Framework

Title from PDF of title page, viewed on August 23, 2016Dissertation advisor: Jacob M. MarszalekVitaIncludes bibliographical references (pages 202-229)Thesis (Ph.D.)--School of Education. University of Missouri--Kansas City, 2016Women are at greater risk than men for experiencing eating disorders, depression, and sexual dysfunction (American Psychological Association, 2007; Fredrickson & Roberts, 1997). Objectification theory (Fredrickson & Roberts, 1997) was proposed to explain one process through which sexist social experiences affect women’s mental health outcomes. Objectification theory posits that women are frequently treated as objects in Western society, and that they internalize this treatment such that they view themselves as objects. This selfobjectification affects their experience of themselves in the world, heightening body-related shame and appearance- and safety-related anxiety. It also makes it more difficult for women to feel connected with their bodies and to experience flow, a pleasant sensation of feeling absorbed in the present moment. Flow has a rich body of research dating back to at least 1975, when Csikszentmihalyi wrote about flow as experienced by chess players, dancers, rock climbers, and surgeons. Historically, however, objectification theory researchers have used measures of flow not grounded in Csikszentmihalyi’s multi-dimensional conceptualization. One purpose of the present study was to investigate the aspects of flow most relevant to objectification theory (i.e., concentration, control, and loss of selfconsciousness) using an appropriate, validated measure. A second purpose of the present study was to explore mindfulness and selfcompassion as potential moderators within the objectification theory framework. These strength-based practices have received recent attention for treatment of anxiety, depression, and other mental health concerns. We studied mindfulness and self-compassion at the trait level as a first step in exploring how these cultivatable strengths may buffer against the deleterious effects of objectification. The present study used a correlational design to explore relationships among objectification theory variables and hypothesized strength-based moderators. We sampled data obtained from 500 women recruited through three different methods who completed an online survey consisting of 11 different measures. Data were analyzed using structural equation modeling. Hypothesized moderated relationships were generally not supported, although most correlations were in the expected directions. Overall, results underscored the need to a) study flow within the objectification theory framework using a multi-dimensional conceptualization and b) develop strength-based interventions for treating women’s mental health concerns.Introduction -- Background and review of literature -- Research design and methodology -- Results -- Discussion -- Appendix A. Screening questions -- Appendix B. Demographic questionnaire -- Appendix C. The body surveillance subscale of the objectified body -- Appendix D. The body shame subscale of the objectified body consciousness scale -- Appendix E. The social appearance anxiety scale -- Appendix F. The dispositional flow scale-2 long form -- Appendix G. Measure of physical safety anxiety -- Appendix H. Measure of body responsiveness -- Appendix I. The eating attitudes test -- Appendix J. The center for epidemiologic studies depression scale-short form -- Appendix K. The female sexual function index -- Appendix L. The Freiburg mindfulness inventory-short form -- Appendix M. The self-compassion scale-short form -- Appendix N. AMOS proposed model of the mediating role of the three dimensions of flow in objectification theory -- Appendix O. AMOS retained model of the mediating role of the three dimensions of flow in objectiticaiton theory -- Appendix P. AMOS modified proposed model of the moderating role of dispositional mindefullness in objectification theory -- Appendix Q. AMOS retained model of the moderating role of dispositional mindefullness in objectification theory -- Appendix R. AMOS modified proposed model of the moderating role of self-compassion in objectification theory -- Appendix S. AMOS retained model of the moderating role of self-compassion in objectification theor

Contrasting influences of Drosophila white/mini-white on ethanol sensitivity in two different behavioral assays

Background The fruit fly Drosophila melanogaster has been used extensively to investigate genetic mechanisms of ethanol-related behaviors. Many past studies in flies, including studies from our laboratory, have manipulated gene expression using transposons carrying the genetic-phenotypic marker mini-white, a derivative of the endogenous gene white. Whether the mini-white transgenic marker or the endogenous white gene influence behavioral responses to acute ethanol exposure in flies has not been systematically investigated. Methods We manipulated mini-white and white expression via (i) transposons marked with mini-white, (ii) RNAi against mini-white and white and (iii) a null allele of white. We assessed ethanol sensitivity and tolerance using a previously described eRING assay (based on climbing in the presence of ethanol) and an assay based on ethanol-induced sedation. Results In eRING assays, ethanol-induced impairment of climbing correlated inversely with expression of the mini-white marker from a series of transposon insertions. Additionally, flies harboring a null allele of white or flies with RNAi-mediated knockdown of mini-white were significantly more sensitive to ethanol in eRING assays than controls expressing endogenous white or the mini-white marker. In contrast, ethanol sensitivity and rapid tolerance measured in the ethanol sedation assay were not affected by decreased expression of mini-white or endogenous white in flies. Conclusions Ethanol sensitivity measured in the eRING assay is noticeably influenced by white and mini-white, making eRING problematic for studies on ethanol-related behavior in Drosophila using transgenes marked with mini-white. In contrast, the ethanol sedation assay described here is a suitable behavioral paradigm for studies on ethanol sedation and rapid tolerance in Drosophila including those that use widely available transgenes marked with mini-white

Neuregulin-1 Regulates Cell Adhesion via an ErbB2/Phosphoinositide-3 Kinase/Akt-Dependent Pathway: Potential Implications for Schizophrenia and Cancer

Neuregulin-1 (NRG1) is a putative schizophrenia susceptibility gene involved extensively in central nervous system development as well as cancer invasion and metastasis. Using a B lymphoblast cell model, we previously demonstrated impairment in NRG1alpha-mediated migration in cells derived from patients with schizophrenia as well as effects of risk alleles in NRG1 and catechol-O-methyltransferase (COMT), a second gene implicated both in schizophrenia susceptibility and in cancer.Here, we examine cell adhesion, an essential component process of cell motility, using an integrin-mediated cell adhesion assay based on an interaction between ICAM-1 and the CD11a/CD18 integrin heterodimer expressed on lymphoblasts. In our assay, NRG1alpha induces lymphoblasts to assume varying levels of adhesion characterized by time-dependent fluctuations in the firmness of attachment. The maximum range of variation in adhesion over sixty minutes correlates strongly with NRG1alpha-induced migration (r(2) = 0.61). NRG1alpha-induced adhesion variation is blocked by erbB2, PI3K, and Akt inhibitors, but not by PLC, ROCK, MLCK, or MEK inhibitors, implicating the erbB2/PI3K/Akt1 signaling pathway in NRG1-stimulated, integrin-mediated cell adhesion. In cell lines from 20 patients with schizophrenia and 20 normal controls, cells from patients show a significant deficiency in the range of NRG1alpha-induced adhesion (p = 0.0002). In contrast, the response of patient-derived cells to phorbol myristate acetate is unimpaired. The COMT Val108/158Met genotype demonstrates a strong trend towards predicting the range of the NRG1alpha-induced adhesion response with risk homozygotes having decreased variation in cell adhesion even in normal subjects (p = 0.063).Our findings suggest that a mechanism of the NRG1 genetic association with schizophrenia may involve the molecular biology of cell adhesion

In the Laboratory and during Free-Flight: Old Honey Bees Reveal Learning and Extinction Deficits that Mirror Mammalian Functional Decline

Loss of brain function is one of the most negative and feared aspects of aging. Studies of invertebrates have taught us much about the physiology of aging and how this progression may be slowed. Yet, how aging affects complex brain functions, e.g., the ability to acquire new memory when previous experience is no longer valid, is an almost exclusive question of studies in humans and mammalian models. In these systems, age related cognitive disorders are assessed through composite paradigms that test different performance tasks in the same individual. Such studies could demonstrate that afflicted individuals show the loss of several and often-diverse memory faculties, and that performance usually varies more between aged individuals, as compared to conspecifics from younger groups. No comparable composite surveying approaches are established yet for invertebrate models in aging research. Here we test whether an insect can share patterns of decline similar to those that are commonly observed during mammalian brain aging. Using honey bees, we combine restrained learning with free-flight assays. We demonstrate that reduced olfactory learning performance correlates with a reduced ability to extinguish the spatial memory of an abandoned nest location (spatial memory extinction). Adding to this, we show that learning performance is more variable in old honey bees. Taken together, our findings point to generic features of brain aging and provide the prerequisites to model individual aspects of learning dysfunction with insect models

Characterization of lamin Mutation Phenotypes in Drosophila and Comparison to Human Laminopathies

Lamins are intermediate filament proteins that make up the nuclear lamina, a matrix underlying the nuclear membrane in all metazoan cells that is important for nuclear form and function. Vertebrate A-type lamins are expressed in differentiating cells, while B-type lamins are expressed ubiquitously. Drosophila has two lamin genes that are expressed in A- and B-type patterns, and it is assumed that similarly expressed lamins perform similar functions. However, Drosophila and vertebrate lamins are not orthologous, and their expression patterns evolved independently. It is therefore of interest to examine the effects of mutations in lamin genes. Mutations in the mammalian lamin A/C gene cause a range of diseases, collectively called laminopathies, that include muscular dystrophies and premature aging disorders. We compared the sequences of lamin genes from different species, and we have characterized larval and adult phenotypes in Drosophila bearing mutations in the lam gene that is expressed in the B-type pattern. Larvae move less and show subtle muscle defects, and surviving lam adults are flightless and walk like aged wild-type flies, suggesting that lam phenotypes might result from neuromuscular defects, premature aging, or both. The resemblance of Drosophila lam phenotypes to human laminopathies suggests that some lamin functions may be performed by differently expressed genes in flies and mammals. Such still-unknown functions thus would not be dependent on lamin gene expression pattern, suggesting the presence of other lamin functions that are expression dependent. Our results illustrate a complex interplay between lamin gene expression and function through evolution

Can We Develop Genetically Tractable Models to Assess Healthspan (Rather Than Life Span) in Animal Models?

Understanding healthspan is arguably the most relevant clinical, social, and economic feature of aging research. The model systems of worm, fly, and mouse are potentially powerful tools to achieve this aim. These models provide two unique approaches. The first is based on genetic screening for gain or loss of function mutations that ameliorate senescence. Genetic factors discovered by this process permit us to recognize causal and regulatory mechanisms of aging. A related screen looks for compounds that slow aging or act upon proteins that were initially identified from genetic analysis. The second research strategy uses manipulations of targeted genetic factors to test causal explanations for aging. These studies include transgenic organisms and genetic epistasis analysis. Overall, genetically driven research with model organisms is largely responsible for the breakthrough of aging biology in the past 15 years. Aging in these contexts, however, has been measured almost exclusively from cohort survival statistics such as life expectancy and age-specific mortality. This is for a good reason. Manipulated factors that extend life span are thought to unambiguously slow senescence and thus to reflect underlying causes of the aging process. But this approach is also common for a practical reason—healthspan is a poorly defined commodity in humans, let alone for genetic animal model systems. It was the consensus of the working session that making healthspan an operational metric would be an innovation needed for the genetic power of model systems to address this aspect of human aging

Genetic studies in Drosophila and humans support a model for the concerted function of CISD2, PPT1 and CLN3 in disease

Wolfram syndrome (WFS) is a progressive neurodegenerative disease characterized by diabetes insipidus, diabetes mellitus, optic atrophy, and deafness. WFS1 and WFS2 are caused by recessive mutations in the genes Wolfram Syndrome 1 (WFS1) and CDGSH iron sulfur domain 2 (CISD2), respectively. To explore the function of CISD2, we performed genetic studies in flies with altered expression of its Drosophila orthologue, cisd2. Surprisingly, flies with strong ubiquitous RNAi-mediated knockdown of cisd2 had no obvious signs of altered life span, stress resistance, locomotor behavior or several other phenotypes. We subsequently found in a targeted genetic screen, however, that altered function of cisd2 modified the effects of overexpressing the fly orthologues of two lysosomal storage disease genes, palmitoyl-protein thioesterase 1 (PPT1 in humans, Ppt1 in flies) and ceroid-lipofuscinosis, neuronal 3 (CLN3 in humans, cln3 in flies), on eye morphology in flies. We also found that cln3 modified the effects of overexpressing Ppt1 in the eye and that overexpression of cln3 interacted with a loss of function mutation in cisd2 to disrupt locomotor ability in flies. Follow-up multi-species bioinformatic analyses suggested that a gene network centered on CISD2, PPT1 and CLN3 might impact disease through altered carbohydrate metabolism, protein folding and endopeptidase activity. Human genetic studies indicated that copy number variants (duplications and deletions) including CLN3, and possibly another gene in the CISD2/PPT1/CLN3 network, are over-represented in individuals with developmental delay. Our studies indicate that cisd2, Ppt1 and cln3 function in concert in flies, suggesting that CISD2, PPT1 and CLN3 might also function coordinately in humans. Further, our studies raise the possibility that WFS2 and some lysosomal storage disorders might be influenced by common mechanisms and that the underlying genes might have previously unappreciated effects on developmental delay