ASU Scholarship Showcase

In this study, we examine how development status and water scarcity shape people's perceptions of "hard path" and "soft path" water solutions. Based on ethnographic research conducted in four semi-rural/peri-urban sites (in Bolivia, Fiji, New Zealand, and the US), we use content analysis to conduct statistical and thematic comparisons of interview data. Our results indicate clear differences associated with development status and, to a lesser extent, water scarcity. People in the two less developed sites were more likely to suggest hard path solutions, less likely to suggest soft path solutions, and more likely to see no path to solutions than people in the more developed sites. Thematically, people in the two less developed sites envisioned solutions that involve small-scale water infrastructure and decentralized, community-based solutions, while people in the more developed sites envisioned solutions that involve large-scale infrastructure and centralized, regulatory water solutions. People in the two water-scarce sites were less likely to suggest soft path solutions and more likely to see no path to solutions (but no more likely to suggest hard path solutions) than people in the water-rich sites. Thematically, people in the two water-rich sites seemed to perceive a wider array of unrealized potential soft path solutions than those in the water-scarce sites. On balance, our findings are encouraging in that they indicate that people are receptive to soft path solutions in a range of sites, even those with limited financial or water resources. Our research points to the need for more studies that investigate the social feasibility of soft path water solutions, particularly in sites with significant financial and natural resource constraints.

Background: Weight-related stigma is reported frequently by higher body-weight patients in healthcare settings. Bariatric surgery triggers profound weight loss. This weight loss may therefore alleviate patients' experiences of weight-related stigma within healthcare settings. In non-clinical settings, weight-related stigma is associated with weight-inducing eating patterns. Dietary adherence is a major challenge after bariatric surgery.

Objectives: (1) Evaluate the relationship between weight-related stigma and post-surgical dietary adherence; (2) understand if weight loss reduces weight-related stigma, thereby improving post-surgical dietary adherence; and (3) explore provider and patient perspectives on adherence and stigma in healthcare settings.

Design: This mixed methods study contrasts survey responses from 300 postoperative bariatric patients with ethnographic data based on interviews with 35 patients and extensive multi-year participant-observation within a clinic setting. The survey measured experiences of weight-related stigma, including from healthcare professionals, on the Interpersonal Sources of Weight Stigma scale and internalized stigma based on the Weight Bias Internalization Scale. Dietary adherence measures included patient self-reports, non-disordered eating patterns reported on the Disordered Eating after Bariatric Surgery scale, and food frequencies. Regression was used to assess the relationships among post-surgical stigma, dietary adherence, and weight loss. Qualitative analyses consisted of thematic analysis.

Results: The quantitative data show that internalized stigma and general experiences of weight-related stigma predict worse dietary adherence, even after weight is lost. The qualitative data show patients did not generally recognize this connection, and health professionals explained it as poor patient compliance.
Conclusion: Reducing perceptions of weight-related stigma in healthcare settings and weight bias internalization could enhance dietary adherence, regardless of time since patient's weight-loss surgery.

Background: Multiple studies show that obesity and depression tend to cluster in women. An “appearance concern” pathway has been proposed as one basic explanation of why higher weights might lead to depression. The transition to motherhood is a life phase in which women’s body image, weight, and depressive risk are in flux, with average weight increasing overall during this period. Examination of how these factors interact from pre- to post-pregnancy provides a means to test how body image plays a key role, as proposed, in causally shaping women’s depressive risk.

Methods: Tracking 39,915 pregnant women in the Norwegian Mother and Child (MoBA) Cohort Study forward 36 months after their deliveries, we test the moderating and mediating effects of body image concerns on the emergence of new mothers’ depressive symptoms by using a binary logistic regression model with a discrete-time event history approach and mediation analysis with bootstrapping.

Results: For women with high pre-pregnancy body mass index (BMI), weight gain heightens their depressive symptoms over time. Body image concerns mediate the association between weight gain and the development of depressive symptoms regardless of weight status. However, the mediation effect is more evident for women with higher pre-pregnancy BMI. Conversely, better body image is highly protective against the transition to mild or more severe depressive symptoms among new mothers, but only for women who were not classified as obese prior to their pregnancies.

Conclusions: These findings support a role for body image concerns in the etiology of depressive symptoms during the transition to motherhood. The findings suggest body image interventions before or during pregnancy could help reduce risks of depression in the early postpartum period and well beyond.

Food and water shortages are two of the greatest challenges facing humans in the coming century. While our theoretical understanding of how humans become vulnerable to and cope with hunger is relatively well developed, anthropological research on parallel problems in the water domain is limited. By carefully considering well-established propositions derived from the food literature against what is known about water, our goal in this essay is to advance identifying, theorizing, and testing a broader anthropology of resource insecurity. Our analysis focuses on (1) the causes of resource insecurity at the community level, (2) “coping” responses to resource insecurity at the household level, and (3) the effect of insecurity on emotional well-being and mental health at the individual level. Based on our findings, we argue that human experiences of food and water insecurity are sufficiently similar to facilitate a broader theory of resource insecurity, including in how households and individuals cope. There are also important differences between food and water insecurity, including the role of structural factors (such as markets) in creating community-level vulnerabilities. These suggest food and water insecurity may also produce household struggles and individual suffering along independent pathways.

The impact of undergraduate research experiences (UREs) is supported by evidence from physical and life science fields, especially when student-apprentices work in traditional laboratories. Within social sciences specifically, some excellent student outcomes associated with UREs adhere to non–lab-based modalities like course-based research experiences (CUREs). Here, the authors evaluate the laboratory-based undergraduate research experiences (LUREs) as a potentially valuable approach for incorporating social science undergraduates in research. Using comparative analysis of survey data from students completing three types of social science-based UREs (n = 235), individual research experiences (IREs), CUREs, or LUREs, students perceived gains overall regardless of the type of experience, with some indication that LUREs are the most effective.

Although insulin resistance in skeletal muscle is well-characterized, the role of circulating whole blood in the metabolic syndrome phenotype is not well understood. We set out to test the hypothesis that genes involved in inflammation, insulin signaling and mitochondrial function would be altered in expression in the whole blood of individuals with metabolic syndrome. We further wanted to examine whether similar relationships that we have found previously in skeletal muscle exist in peripheral whole blood cells. All subjects (n=184) were Latino descent from the Arizona Insulin Resistance registry. Subjects were classified based on the metabolic syndrome phenotype according to the National Cholesterol Education Program’s Adult Treatment Panel III. Of the 184 Latino subjects in the study, 74 were classified with the metabolic syndrome and 110 were without. Whole blood gene expression profiling was performed using the Agilent 4x44K Whole Human Genome Microarray. Whole blood microarray analysis identified 1,432 probes that were altered in expression ≥1.2 fold and P<0.05 after Benjamini-Hochberg in the metabolic syndrome subjects. KEGG pathway analysis revealed significant enrichment for pathways including ribosome, oxidative phosphorylation and MAPK signaling (all Benjamini-Hochberg P<0.05). Whole blood mRNA expression changes observed in the microarray data were confirmed by quantitative RT-PCR. Transcription factor binding motif enrichment analysis revealed E2F1, ELK1, NF-kappaB, STAT1 and STAT3 significantly enriched after Bonferroni correction (all P<0.05). The results of the present study demonstrate that whole blood is a useful tissue for studying the metabolic syndrome and its underlying insulin resistance although the relationship between blood and skeletal muscle differs.

Many population centers in the American West rely on water from the Colorado River Basin, which has faced shortages in recent years that are anticipated to be exacerbated by climate change. Shortages to urban water supplies related to climate change will not be limited to cities dependent on the Colorado River. Considering this, addressing sustainable water governance is timely and critical for cities, states, and regions facing supply shortages and pollution problems. Engaging in sustainability transitions of these hydro-social systems will increase the ability of such systems to meet the water needs of urban communities. In this paper, we identify historical transitions in water governance and examine their context for three sites in the Colorado River Basin (Denver, Colorado, Las Vegas, Nevada, and Phoenix, Arizona) to provide insight for intentional transitions towards sustainable, or “water sensitive” cities. The comparative historical approach employed allows us to more fully understand differences in present-day water governance decisions between the sites, identify past catalysts for transitions, and recognize emerging patterns and opportunities that may impact current and future water governance in the Colorado River Basin and beyond.

Type 2 diabetes (T2D) is a complex metabolic disease that is more prevalent in ethnic groups such as Mexican Americans, and is strongly associated with the risk factors obesity and insulin resistance. The goal of this study was to perform whole genome gene expression profiling in adipose tissue to detect common patterns of gene regulation associated with obesity and insulin resistance. We used phenotypic and genotypic data from 308 Mexican American participants from the Veterans Administration Genetic Epidemiology Study (VAGES). Basal fasting RNA was extracted from adipose tissue biopsies from a subset of 75 unrelated individuals, and gene expression data generated on the Illumina BeadArray platform. The number of gene probes with significant expression above baseline was approximately 31,000. We performed multiple regression analysis of all probes with 15 metabolic traits. Adipose tissue had 3,012 genes significantly associated with the traits of interest (false discovery rate, FDR ≤ 0.05). The significance of gene expression changes was used to select 52 genes with significant (FDR ≤ 10^-4) gene expression changes across multiple traits. Gene sets/Pathways analysis identified one gene, alcohol dehydrogenase 1B (ADH1B) that was significantly enriched (P < 10^-60) as a prime candidate for involvement in multiple relevant metabolic pathways. Illumina BeadChip derived ADH1B expression data was consistent with quantitative real time PCR data. We observed significant inverse correlations with waist circumference (2.8 x 10[superscript -9]), BMI (5.4 x 10^-6), and fasting plasma insulin (P < 0.001). These findings are consistent with a central role for ADH1B in obesity and insulin resistance and provide evidence for a novel genetic regulatory mechanism for human metabolic diseases related to these traits.

Our previous studies show reduced abundance of the β-subunit of mitochondrial H+-ATP synthase (β-F1-ATPase) in skeletal muscle of obese individuals. The β-F1-ATPase forms the catalytic core of the ATP synthase, and it is critical for ATP production in muscle. The mechanism(s) impairing β-F1-ATPase metabolism in obesity, however, are not completely understood. First, we studied total muscle protein synthesis and the translation efficiency of β-F1-ATPase in obese (BMI, 36±1 kg/m²) and lean (BMI, 22±1 kg/m²) subjects. Both total protein synthesis (0.044±0.006 vs 0.066±0.006%·h^-1) and translation efficiency of β-F1-ATPase (0.0031±0.0007 vs 0.0073±0.0004) were lower in muscle from the obese subjects when compared to the lean controls (P<0.05). We then evaluated these same responses in a primary cell culture model, and tested the specific hypothesis that circulating non-esterified fatty acids (NEFA) in obesity play a role in the responses observed in humans. The findings on total protein synthesis and translation efficiency of β-F1-ATPase in primary myotubes cultured from a lean subject, and after exposure to NEFA extracted from serum of an obese subject, were similar to those obtained in humans. Among candidate microRNAs (i.e., non-coding RNAs regulating gene expression), we identified miR-127-5p in preventing the production of β-F1-ATPase. Muscle expression of miR-127-5p negatively correlated with β-F1-ATPase protein translation efficiency in humans (r = – 0.6744; P<0.01), and could be modeled in vitro by prolonged exposure of primary myotubes derived from the lean subject to NEFA extracted from the obese subject. On the other hand, locked nucleic acid inhibitor synthesized to target miR-127-5p significantly increased β-F1-ATPase translation efficiency in myotubes (0.6±0.1 vs 1.3±0.3, in control vs exposure to 50 nM inhibitor; P<0.05). Our experiments implicate circulating NEFA in obesity in suppressing muscle protein metabolism, and establish impaired β-F1-ATPase translation as an important consequence of obesity.

Background: Obesity is a metabolic disease caused by environmental and genetic factors. However, the epigenetic mechanisms of obesity are incompletely understood. The aim of our study was to investigate the role of skeletal muscle DNA methylation in combination with transcriptomic changes in obesity.

Results: Muscle biopsies were obtained basally from lean (n = 12; BMI = 23.4 ± 0.7 kg/m[superscript 2]) and obese (n = 10; BMI = 32.9 ± 0.7 kg/m[superscript 2]) participants in combination with euglycemic-hyperinsulinemic clamps to assess insulin sensitivity. We performed reduced representation bisulfite sequencing (RRBS) next-generation methylation and microarray analyses on DNA and RNA isolated from vastus lateralis muscle biopsies. There were 13,130 differentially methylated cytosines (DMC; uncorrected P < 0.05) that were altered in the promoter and untranslated (5' and 3'UTR) regions in the obese versus lean analysis. Microarray analysis revealed 99 probes that were significantly (corrected P < 0.05) altered. Of these, 12 genes (encompassing 22 methylation sites) demonstrated a negative relationship between gene expression and DNA methylation. Specifically, sorbin and SH3 domain containing 3 (SORBS3) which codes for the adapter protein vinexin was significantly decreased in gene expression (fold change −1.9) and had nine DMCs that were significantly increased in methylation in obesity (methylation differences ranged from 5.0 to 24.4 %). Moreover, differentially methylated region (DMR) analysis identified a region in the 5'UTR (Chr.8:22,423,530–22,423,569) of SORBS3 that was increased in methylation by 11.2 % in the obese group. The negative relationship observed between DNA methylation and gene expression for SORBS3 was validated by a site-specific sequencing approach, pyrosequencing, and qRT-PCR. Additionally, we performed transcription factor binding analysis and identified a number of transcription factors whose binding to the differentially methylated sites or region may contribute to obesity.

Conclusions: These results demonstrate that obesity alters the epigenome through DNA methylation and highlights novel transcriptomic changes in SORBS3 in skeletal muscle.