Symposium 12: Integrating Behavioral Genetic Approaches to the Study of Physical Activity and Health

Symposium Overview:

Behavior genetic approaches utilize advanced quantitative methods to estimate the extent to which genetic and environmental factors contribute to individual differences. This empirical approach can help us gain a deeper insight into how genetic and environmental influences shape health behaviors and risk for disease. Being informed about the heritability of a phenotype is useful as it informs us about how much effort should be invested into manipulating salient features of an environment, and for whom this effort is best invested in. Thus, findings from behavioral genetic studies frequently emphasize the need for tailored approaches for health promotion and encourage clinicians to recognize that individuals respond differently to the same environmental interventions due to their genetic predispositions. Importantly, a strong genetic influence on a phenotype does not mean that genetics solely determine the outcome – there is still significant potential for change. However, high heritability indicates that individuals will react to the same environment in varying degrees and ways based on their genetic predisposition. The ability to account for genetic factors is crucial when developing prevention and intervention programs as it allows clinicians to identify individuals at greatest risk for maladaptive health outcomes, as well as those with the greatest potential to benefit from prevention and intervention efforts.

The presentations in this symposium outline empirical findings from three separate twin studies, which each integrate behavior genetic approaches to investigate the role of physical activity in association with a variety of health outcomes. The first presenter will highlight findings from the Colorado Adoption/Twin Study of Lifespan Behavioral Development and Cognitive Aging (CATSLife) study on the differential influence of vigorous exercise on cardiovascular and metabolic disease biomarkers. The second presenter will discuss findings from five twin studies which highlight the importance of physical fitness for decreasing dementia risk after adjusting for genetic and shared-environmental confounding. The third presenter will provide insights from the Arizona Twin Project on the genetic and environmental contributions to physical activity, diet, and adiposity, as well as the underlying latent liability of adiposity indicators. Each of the presentations integrates behavior genetic approaches in unique ways, including co-twin analyses, leveraging genetic similarities and shared environments, and utilizing quantitative twin modeling to estimate the respective contribution of genetic and environmental influences on health outcomes.

The overarching goal of this symposium is to highlight the utility of integrating behavior genetic approaches to physical activity and health research. By presenting three unique applications of behavior genetics in health research from three separate cohorts of twins, we aim to generate a deeper insight into how physical activity and behavioral health interventions may best serve individuals at greatest risk for maladaptive health outcomes as well as those with the greatest potential to reap positive outcomes from prevention and intervention efforts.

Abstract 1: Health Benefits of Engaging in More Vigorous than Moderate Intensity Exercise

Authors: Ryan Bruellman1, Shandell Pahlen2,4, Jarrod M. Ellingson3,4, Robin P. Corley4, Sally J. Wadsworth4, Ilana J. Bennett1,2, Chandra A. Reynolds1,2,4

Affiliations:
1. Genetics, Genomics and Bioinformatics, University of California Riverside, Riverside, California
2. Department of Psychology, University of California Riverside, Riverside, California
3. Department of Psychiatry, Anschutz Medical Campus, University of Colorado, Denver, Colorado
4. Institute for Behavioral Genetics and Department of Psychology and Neuroscience, University of Colorado, Boulder, Colorado

Regular exercise is a powerful behavioral prescription that can prevent or slow diseases, including those linked to poor cardiovascular and metabolic health. The United States Department of Health and Human Services recommends at least 150 minutes of moderate intensity or 75 minutes of vigorous intensity exercise per week. These recommendations imply that the health benefits of two minutes of moderate intensity exercise are comparable to one minute of vigorous intensity exercise. We sought to evaluate the effect of this exercise intensity ratio on cardiovascular and metabolic disease biomarkers using a quasi-experimental approach in twins and siblings from the Colorado Adoption/Twin Study of Lifespan behavioral development and cognitive aging (CATSLife; N=1,327, Age range=28-51 years). Measures included baseline exercise, biomarker data, and fitness tracker data from the ongoing follow-up wave that started six years after baseline (N=618). Specifically, we compared the influence of moderate and vigorous exercise on cardiovascular and metabolic biomarkers while considering sedentary behavior at each wave. Whereas both exercise intensities partly mitigated sedentary behavior on biomarker outcomes, higher levels of vigorous exercise (e.g., Waist to Hip Ratio, B=-0.005, CI=-0.006, -0.005) outweighed moderate exercise (e.g., Waist to Hip Ratio, B=-0.002, CI=-0.003, -0.001) for some outcomes, particularly metabolic biomarkers of visceral fat. Cotwin analysis of active monozygotic twin pairs that differed in exercise intensity further supported the greater metabolic and cardiovascular health benefits of vigorous exercise over moderate exercise beyond the 2:1 ratio established by current guidelines. For example, twins that performed 10 more minutes a day of vigorous exercise showed improved cardiovascular health (e.g., total cholesterol to high-density lipoprotein (TC/HDL) approximately 0.35 lower and Waist to Hip Ratio was 0.02 lower) compared to their cotwin. A comparable (based on the 2:1 time ratio) 20 more minutes a day of moderate exercise did not find equivalent results (e.g., TC/HDL ratio was 0.38 higher, Waist to Hip Ratio was largely unchanged as it was only 0.01 lower). Our findings emphasize, for those past young adulthood, the differential influence of vigorous exercise on health indicators and the need for public health messaging to prioritize this type of exercise.

Abstract 2: Title: Physical fitness is associated with dementia risk after adjusting for genetic and environmental confounds.
Authors: Matthew J. D. Pilgrim1, Elina Sillanpää2,3, Christopher R. Beam1

Affiliations:
1. Department of Psychology, University of Southern California, Los Angeles, USA
2. Faculty of Sport and Health Sciences, University of Jyväskylä, Finland
3. Central Finland Wellbeing Services County, Jyväskylä, Finland

Introduction: Epidemiological studies have found that higher levels of physical activity, and better physical fitness, like structured exercise, are associated with lower dementia risk. Results from a small number of randomized controlled physical activity interventions and dementia risk are mixed, raising the question about whether physical activity and fitness are causally related to dementia risk. Recent genetically informed studies have suggested that physical activity may be an indicator of a generally healthy phenotype rather than causally associated with disease risk. In the current study, we use a large multi-national older adult twin sample to test the association between a latent variable measure of physical fitness and dementia risk that statistically adjusts for genetic and shared environmental sources of confounding. We test the hypothesis that twins lower on physical fitness had a greater risk of dementia risk compared to their co-twins who scored higher on physical fitness.

Methods: Our sample includes 4,061 individual twins (NMZ = 1,699, NDZ = 2,362) between ages thirty-two and ninety-eight (M = 68.0, SD = 10.2) from five twin studies of aging conducted in Sweden, Australia, and the United States. The physical fitness of each twin was estimated as a latent factor accounting for common variance across multiple health and activity measures. Dementia risk was measured as common variance across memory ability, non-memory cognitive ability, and functional status. We then leveraged the genetic similarity and shared developmental environments of twin pairs to test the association between physical fitness and dementia risk after controlling for genetic and environmental sources of confounding.

Results and Conclusion: Physical fitness and dementia risk were both moderately heritable. Bivariate twin models revealed a statistically significant association between latent physical fitness and dementia risk after adjusting for genetic and shared-environmental confounding. This finding aligns with the hypothesized causal association between physical fitness and dementia risk and supports the notion that interventions to increase physical fitness may be one mechanism help to reduce dementia risk.

Abstract 3: Genetic and Environmental Contributions to Physical Activity, Dietary Intake, and Adiposity: Insights from the Arizona Twin Project
Authors: Eva M. Bartsch1, Sierra Clifford1, Gianna Rea-Sandin2, Mary C. Davis1, Leah D. Doane1, Kathryn Lemery-Chalfant1

Affiliations:
1. Department of Psychology, Arizona State University, Tempe, Arizona, USA
2. Department of Psychology, University of Minnesota, Minneapolis, USA

Background: High levels of adiposity are associated with the development of a variety of health risk factors, and childhood levels of adiposity exhibit a notable propensity to persist into adulthood. Understanding the etiology of adiposity in youth is crucial for developing effective prevention efforts targeting rising obesity rates for at-risk youth. Empirical studies consistently demonstrated high heritability estimates for adiposity in youth, and the obesogenic environment theory posits that physical activity and dietary intake are important predictors of high adiposity. However, little is known about the extent to which commonly used adiposity indicators are related for genetic and environmental reasons, and the genetic and environmental contributions to objectively measured physical activity and dietary intake remain largely unexplored during middle childhood and the transition to early adolescence.

Objective: We utilized behavior genetic analyses to clarify the etiological underpinnings of adiposity, physical activity, and dietary intake in youth. Our first aim was to examine the genetic and environmental covariance among body mass index (BMI), percent body fat, and waist circumference. We compared two quantitative behavior genetic models, the independent pathway and common pathway models, to examine whether there is an underlying latent liability of adiposity indicators. Our second aim was to investigate the genetic and environmental contributions to moderate-to-vigorous activity (MVPA), sedentary behavior (SB), and dietary intake, and their associations with adiposity.

Methods: A diverse community sample of twins from the Arizona Twin Project6 were followed longitudinally at ages 8, 9, 10, and 11 (subsample N=254-436 pairs [146 pairs at age 11 due to COVID-19 shutdowns]; monozygotic (MZ)=29.5%-31.8%, same-sex dizygotic (ssDZ)=35.7%-39.8%, opposite-sex dizygotic (osDZ)=28.4%-33.5%; female=47.8%-49.9%; Non-Hispanic white=51.9%-59.5%, Hispanic=26.6-29.5%; age 8 MBMI=16.76). Indicators of adiposity (i.e., BMI, percent body fat, and waist circumference) were assessed by trained research assistants during annual home visits. Children’s diet was assessed at age 8 via individual daily 24-hour recall food diaries completed by their primary caregiver over three consecutive weekdays and was coded into 7 nutrient classes. Daily physical activity levels were measured at age 8 using a wrist-based accelerometer in a free-living standard environment for seven consecutive days and were coded for MVPA and SB based on previously validated acceleration counts.

Results: The ACE model is a multigroup structural equation model that uses the observed variances and covariances of phenotypes in MZ and DZ twins to estimate three latent factors: A (additive genetic influences), C (shared environmental influences), and E (non-shared environmental influences). Using OpenMx for biometric twin modeling, covarying age and sex, we found that the common pathway model yielded the most parsimonious fit for adiposity (8 years: χ2(4)=2.61, p=.624; 9 years: χ2(4)=5.46, p=.243; 10 years: χ2(4)=1.60, p=.809; 11 years: χ2(4)=0.77, p=.942), indicating that covariance between indicators was best represented by a single highly heritable common latent factor (broad h2=80%-93%, C=0%-10%, E=7%-12%). This common factor explained 97-98% of the variance in BMI regardless of age, whereas indicator-specific genetic and environmental influences explained 10%-17% of the remaining variance in the other indicators. Variation in MVPA and SB was explained by genetic and unique environmental factors. Over 80% of the variance in sugar, vegetable, and fruit consumption was due to the shared environment, such as availability in the home. In contrast, protein, carbohydrate, fat, and fiber consumption were moderately heritable. SB predicted higher adiposity concurrently but not longitudinally, whereas MVPA did not significantly predict adiposity at any age. Greater fiber intake predicted greater adiposity at ages 8, 9, and 11, whereas carbohydrate intake predicted greater adiposity at ages 8 and 10. Average levels of health behaviors were not correlated highly enough with adiposity to parse genetic and environmental covariance (rs<0.2).

Discussion: Our findings suggest that a common latent factor of BMI, percent body fat, and waist circumference is highly heritable and best represents the underlying construct of adiposity in a community sample of twin children. In addition, MVPA and SB were moderately heritable. Sugar, vegetable, and fruit consumption were mainly influenced by shared environmental influences, whereas protein, carbohydrate, fat, and fiber consumption were influenced by both genetic and mainly shared environmental factors. This suggests unique etiologies for the consumption of different macronutrients such as that genetic factors may influence children’s requirements for certain sources of nutritional energy, whereas consumption of sugar, fruits, and vegetables may depend on availability. Both physical activity and dietary intake demonstrated no shared etiology with adiposity in this community sample at this age. Our findings suggest that the obesogenic environment theory should be revised to consider individual differences and genetic influences. Our findings demonstrate that youth react to the same environment in varying degrees and ways, making one-size-fits-all prevention and intervention efforts inadequate for reducing youth’s vulnerability to health contexts.

Chair - Eva Bartsch M.A.  Student
Arizona State University

Presenter - Matthew Pilgrim M.Sc  Student
University of Southern California

Presenter - Ryan Bruellman M.Sc  Student
University of California Riverside

Presenter - Eva Bartsch M.A.  Student
Arizona State University

Discussant - Savannah Ostner M.A.  Student
Arizona State University

Symposium Overview:

Behavior genetic approaches utilize advanced quantitative methods to estimate the extent to which genetic and environmental factors contribute to individual differences. This empirical approach can help us gain a deeper insight into how genetic and environmental influences shape health behaviors and risk for disease. Being informed about the heritability of a phenotype is useful as it informs us about how much effort should be invested into manipulating salient features of an environment, and for whom this effort is best invested in. Thus, findings from behavioral genetic studies frequently emphasize the need for tailored approaches for health promotion and encourage clinicians to recognize that individuals respond differently to the same environmental interventions due to their genetic predispositions. Importantly, a strong genetic influence on a phenotype does not mean that genetics solely determine the outcome – there is still significant potential for change. However, high heritability indicates that individuals will react to the same environment in varying degrees and ways based on their genetic predisposition. The ability to account for genetic factors is crucial when developing prevention and intervention programs as it allows clinicians to identify individuals at greatest risk for maladaptive health outcomes, as well as those with the greatest potential to benefit from prevention and intervention efforts.

The presentations in this symposium outline empirical findings from three separate twin studies, which each integrate behavior genetic approaches to investigate the role of physical activity in association with a variety of health outcomes. The first presenter will highlight findings from the Colorado Adoption/Twin Study of Lifespan Behavioral Development and Cognitive Aging (CATSLife) study on the differential influence of vigorous exercise on cardiovascular and metabolic disease biomarkers. The second presenter will discuss findings from five twin studies which highlight the importance of physical fitness for decreasing dementia risk after adjusting for genetic and shared-environmental confounding. The third presenter will provide insights from the Arizona Twin Project on the genetic and environmental contributions to physical activity, diet, and adiposity, as well as the underlying latent liability of adiposity indicators. Each of the presentations integrates behavior genetic approaches in unique ways, including co-twin analyses, leveraging genetic similarities and shared environments, and utilizing quantitative twin modeling to estimate the respective contribution of genetic and environmental influences on health outcomes.

The overarching goal of this symposium is to highlight the utility of integrating behavior genetic approaches to physical activity and health research. By presenting three unique applications of behavior genetics in health research from three separate cohorts of twins, we aim to generate a deeper insight into how physical activity and behavioral health interventions may best serve individuals at greatest risk for maladaptive health outcomes as well as those with the greatest potential to reap positive outcomes from prevention and intervention efforts.

Abstract 1: Health Benefits of Engaging in More Vigorous than Moderate Intensity Exercise

Authors: Ryan Bruellman1, Shandell Pahlen2,4, Jarrod M. Ellingson3,4, Robin P. Corley4, Sally J. Wadsworth4, Ilana J. Bennett1,2, Chandra A. Reynolds1,2,4

Affiliations:
1. Genetics, Genomics and Bioinformatics, University of California Riverside, Riverside, California
2. Department of Psychology, University of California Riverside, Riverside, California
3. Department of Psychiatry, Anschutz Medical Campus, University of Colorado, Denver, Colorado
4. Institute for Behavioral Genetics and Department of Psychology and Neuroscience, University of Colorado, Boulder, Colorado

Regular exercise is a powerful behavioral prescription that can prevent or slow diseases, including those linked to poor cardiovascular and metabolic health. The United States Department of Health and Human Services recommends at least 150 minutes of moderate intensity or 75 minutes of vigorous intensity exercise per week. These recommendations imply that the health benefits of two minutes of moderate intensity exercise are comparable to one minute of vigorous intensity exercise. We sought to evaluate the effect of this exercise intensity ratio on cardiovascular and metabolic disease biomarkers using a quasi-experimental approach in twins and siblings from the Colorado Adoption/Twin Study of Lifespan behavioral development and cognitive aging (CATSLife; N=1,327, Age range=28-51 years). Measures included baseline exercise, biomarker data, and fitness tracker data from the ongoing follow-up wave that started six years after baseline (N=618). Specifically, we compared the influence of moderate and vigorous exercise on cardiovascular and metabolic biomarkers while considering sedentary behavior at each wave. Whereas both exercise intensities partly mitigated sedentary behavior on biomarker outcomes, higher levels of vigorous exercise (e.g., Waist to Hip Ratio, B=-0.005, CI=-0.006, -0.005) outweighed moderate exercise (e.g., Waist to Hip Ratio, B=-0.002, CI=-0.003, -0.001) for some outcomes, particularly metabolic biomarkers of visceral fat. Cotwin analysis of active monozygotic twin pairs that differed in exercise intensity further supported the greater metabolic and cardiovascular health benefits of vigorous exercise over moderate exercise beyond the 2:1 ratio established by current guidelines. For example, twins that performed 10 more minutes a day of vigorous exercise showed improved cardiovascular health (e.g., total cholesterol to high-density lipoprotein (TC/HDL) approximately 0.35 lower and Waist to Hip Ratio was 0.02 lower) compared to their cotwin. A comparable (based on the 2:1 time ratio) 20 more minutes a day of moderate exercise did not find equivalent results (e.g., TC/HDL ratio was 0.38 higher, Waist to Hip Ratio was largely unchanged as it was only 0.01 lower). Our findings emphasize, for those past young adulthood, the differential influence of vigorous exercise on health indicators and the need for public health messaging to prioritize this type of exercise.

Abstract 2: Title: Physical fitness is associated with dementia risk after adjusting for genetic and environmental confounds.
Authors: Matthew J. D. Pilgrim1, Elina Sillanpää2,3, Christopher R. Beam1

Affiliations:
1. Department of Psychology, University of Southern California, Los Angeles, USA
2. Faculty of Sport and Health Sciences, University of Jyväskylä, Finland
3. Central Finland Wellbeing Services County, Jyväskylä, Finland

Introduction: Epidemiological studies have found that higher levels of physical activity, and better physical fitness, like structured exercise, are associated with lower dementia risk. Results from a small number of randomized controlled physical activity interventions and dementia risk are mixed, raising the question about whether physical activity and fitness are causally related to dementia risk. Recent genetically informed studies have suggested that physical activity may be an indicator of a generally healthy phenotype rather than causally associated with disease risk. In the current study, we use a large multi-national older adult twin sample to test the association between a latent variable measure of physical fitness and dementia risk that statistically adjusts for genetic and shared environmental sources of confounding. We test the hypothesis that twins lower on physical fitness had a greater risk of dementia risk compared to their co-twins who scored higher on physical fitness.

Methods: Our sample includes 4,061 individual twins (NMZ = 1,699, NDZ = 2,362) between ages thirty-two and ninety-eight (M = 68.0, SD = 10.2) from five twin studies of aging conducted in Sweden, Australia, and the United States. The physical fitness of each twin was estimated as a latent factor accounting for common variance across multiple health and activity measures. Dementia risk was measured as common variance across memory ability, non-memory cognitive ability, and functional status. We then leveraged the genetic similarity and shared developmental environments of twin pairs to test the association between physical fitness and dementia risk after controlling for genetic and environmental sources of confounding.

Results and Conclusion: Physical fitness and dementia risk were both moderately heritable. Bivariate twin models revealed a statistically significant association between latent physical fitness and dementia risk after adjusting for genetic and shared-environmental confounding. This finding aligns with the hypothesized causal association between physical fitness and dementia risk and supports the notion that interventions to increase physical fitness may be one mechanism help to reduce dementia risk.

Abstract 3: Genetic and Environmental Contributions to Physical Activity, Dietary Intake, and Adiposity: Insights from the Arizona Twin Project
Authors: Eva M. Bartsch1, Sierra Clifford1, Gianna Rea-Sandin2, Mary C. Davis1, Leah D. Doane1, Kathryn Lemery-Chalfant1

Affiliations:
1. Department of Psychology, Arizona State University, Tempe, Arizona, USA
2. Department of Psychology, University of Minnesota, Minneapolis, USA

Background: High levels of adiposity are associated with the development of a variety of health risk factors, and childhood levels of adiposity exhibit a notable propensity to persist into adulthood. Understanding the etiology of adiposity in youth is crucial for developing effective prevention efforts targeting rising obesity rates for at-risk youth. Empirical studies consistently demonstrated high heritability estimates for adiposity in youth, and the obesogenic environment theory posits that physical activity and dietary intake are important predictors of high adiposity. However, little is known about the extent to which commonly used adiposity indicators are related for genetic and environmental reasons, and the genetic and environmental contributions to objectively measured physical activity and dietary intake remain largely unexplored during middle childhood and the transition to early adolescence.

Objective: We utilized behavior genetic analyses to clarify the etiological underpinnings of adiposity, physical activity, and dietary intake in youth. Our first aim was to examine the genetic and environmental covariance among body mass index (BMI), percent body fat, and waist circumference. We compared two quantitative behavior genetic models, the independent pathway and common pathway models, to examine whether there is an underlying latent liability of adiposity indicators. Our second aim was to investigate the genetic and environmental contributions to moderate-to-vigorous activity (MVPA), sedentary behavior (SB), and dietary intake, and their associations with adiposity.

Methods: A diverse community sample of twins from the Arizona Twin Project6 were followed longitudinally at ages 8, 9, 10, and 11 (subsample N=254-436 pairs [146 pairs at age 11 due to COVID-19 shutdowns]; monozygotic (MZ)=29.5%-31.8%, same-sex dizygotic (ssDZ)=35.7%-39.8%, opposite-sex dizygotic (osDZ)=28.4%-33.5%; female=47.8%-49.9%; Non-Hispanic white=51.9%-59.5%, Hispanic=26.6-29.5%; age 8 MBMI=16.76). Indicators of adiposity (i.e., BMI, percent body fat, and waist circumference) were assessed by trained research assistants during annual home visits. Children’s diet was assessed at age 8 via individual daily 24-hour recall food diaries completed by their primary caregiver over three consecutive weekdays and was coded into 7 nutrient classes. Daily physical activity levels were measured at age 8 using a wrist-based accelerometer in a free-living standard environment for seven consecutive days and were coded for MVPA and SB based on previously validated acceleration counts.

Results: The ACE model is a multigroup structural equation model that uses the observed variances and covariances of phenotypes in MZ and DZ twins to estimate three latent factors: A (additive genetic influences), C (shared environmental influences), and E (non-shared environmental influences). Using OpenMx for biometric twin modeling, covarying age and sex, we found that the common pathway model yielded the most parsimonious fit for adiposity (8 years: χ2(4)=2.61, p=.624; 9 years: χ2(4)=5.46, p=.243; 10 years: χ2(4)=1.60, p=.809; 11 years: χ2(4)=0.77, p=.942), indicating that covariance between indicators was best represented by a single highly heritable common latent factor (broad h2=80%-93%, C=0%-10%, E=7%-12%). This common factor explained 97-98% of the variance in BMI regardless of age, whereas indicator-specific genetic and environmental influences explained 10%-17% of the remaining variance in the other indicators. Variation in MVPA and SB was explained by genetic and unique environmental factors. Over 80% of the variance in sugar, vegetable, and fruit consumption was due to the shared environment, such as availability in the home. In contrast, protein, carbohydrate, fat, and fiber consumption were moderately heritable. SB predicted higher adiposity concurrently but not longitudinally, whereas MVPA did not significantly predict adiposity at any age. Greater fiber intake predicted greater adiposity at ages 8, 9, and 11, whereas carbohydrate intake predicted greater adiposity at ages 8 and 10. Average levels of health behaviors were not correlated highly enough with adiposity to parse genetic and environmental covariance (rs<0.2).

Discussion: Our findings suggest that a common latent factor of BMI, percent body fat, and waist circumference is highly heritable and best represents the underlying construct of adiposity in a community sample of twin children. In addition, MVPA and SB were moderately heritable. Sugar, vegetable, and fruit consumption were mainly influenced by shared environmental influences, whereas protein, carbohydrate, fat, and fiber consumption were influenced by both genetic and mainly shared environmental factors. This suggests unique etiologies for the consumption of different macronutrients such as that genetic factors may influence children’s requirements for certain sources of nutritional energy, whereas consumption of sugar, fruits, and vegetables may depend on availability. Both physical activity and dietary intake demonstrated no shared etiology with adiposity in this community sample at this age. Our findings suggest that the obesogenic environment theory should be revised to consider individual differences and genetic influences. Our findings demonstrate that youth react to the same environment in varying degrees and ways, making one-size-fits-all prevention and intervention efforts inadequate for reducing youth’s vulnerability to health contexts.

Chair - Eva Bartsch, M.A.,
Arizona State University

Presenter - Matthew Pilgrim, M.Sc,
University of Southern California

Presenter - Ryan Bruellman, M.Sc,
University of California Riverside

Presenter - Eva Bartsch, M.A. ,
Arizona State University

Discussant - Savannah G. Ostner, MA, MA,
Arizona State University