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Human Genetics
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Human Genetics
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Biomedical Science
Abstract
Background: The projected worldwide population of people aged 65 and over is anticipated to hit 1.6 billion by 2050. Frailty, marked by increased susceptibility to adverse health outcomes, mortality, and decreased health-related quality of life (HrQoL), poses significant challenges to an aging population. The Frailty Index (FI), is the ratio of the number of accumulated health deficits to the total number of deficits considered, is used to predict frailty.
Methods: Utilizing data from the Mexican American Family Study, we investigated the heritability and gene-environment (GxE) interactions influencing frailty in 1,029 Mexican American participants. We calculated the FI using 34 variables, including phenotypes, social determinants of health, medical history, and metabolism-related behaviors. Environmental factors included dietary, physical activity, socioeconomic, and dichotomous disease variables. We employed a linear mixed model approach to estimate heritability, and to investigate GxE interactions, incorporating dichotomous and continuous environmental measures. Statistical analysis utilized likelihood-based estimation and hypothesis testing.
Results: The FI demonstrated moderate heritability (h²=0.36, p=6.2×10-12). We found significant GxE interactions across six discrete “environments” (obesity, hypertriglyceridemia, low high-density lipoprotein, impaired fasting glucose test, diabetes, and hypertension) and nine continuous measures of dietary environment (polyunsaturated fat, carbohydrates, calories, monounsaturated fat, fiber, protein, saturated fat, and cholesterol). Between-environment genetic correlation analysis suggested distinct gene sets influencing frailty under different conditions, with significant genetic contributors (inflammation and diet) to frailty.
Conclusion: The study investigates the heritability and GxE in frailty, showing how lifestyle and environment can affect gene expression and contribute to frailty. The findings highlight the importance of considering heritability and GxE interactions in frailty research and advocates for future exploration of specific genes and mechanisms involved in frailty development and progression.
Presentation Type
Poster
Recommended Citation
Garcia-Rodriguez, Natasha; Diego, Vincent P.; Almeida, Marcio; Galan, Jacob; Laston, Sandra; Curran, Joanne E.; Howard, Tom; Manusov, Eron; Blangero, John; and Williams-Blangero, Sarah, "Investigating the determinants of frailty: The intersection of genetics and environment in Mexican Americans from South Texas" (2024). Research Colloquium. 63.
https://scholarworks.utrgv.edu/colloquium/2024/posters/63
Included in
Investigating the determinants of frailty: The intersection of genetics and environment in Mexican Americans from South Texas
Background: The projected worldwide population of people aged 65 and over is anticipated to hit 1.6 billion by 2050. Frailty, marked by increased susceptibility to adverse health outcomes, mortality, and decreased health-related quality of life (HrQoL), poses significant challenges to an aging population. The Frailty Index (FI), is the ratio of the number of accumulated health deficits to the total number of deficits considered, is used to predict frailty.
Methods: Utilizing data from the Mexican American Family Study, we investigated the heritability and gene-environment (GxE) interactions influencing frailty in 1,029 Mexican American participants. We calculated the FI using 34 variables, including phenotypes, social determinants of health, medical history, and metabolism-related behaviors. Environmental factors included dietary, physical activity, socioeconomic, and dichotomous disease variables. We employed a linear mixed model approach to estimate heritability, and to investigate GxE interactions, incorporating dichotomous and continuous environmental measures. Statistical analysis utilized likelihood-based estimation and hypothesis testing.
Results: The FI demonstrated moderate heritability (h²=0.36, p=6.2×10-12). We found significant GxE interactions across six discrete “environments” (obesity, hypertriglyceridemia, low high-density lipoprotein, impaired fasting glucose test, diabetes, and hypertension) and nine continuous measures of dietary environment (polyunsaturated fat, carbohydrates, calories, monounsaturated fat, fiber, protein, saturated fat, and cholesterol). Between-environment genetic correlation analysis suggested distinct gene sets influencing frailty under different conditions, with significant genetic contributors (inflammation and diet) to frailty.
Conclusion: The study investigates the heritability and GxE in frailty, showing how lifestyle and environment can affect gene expression and contribute to frailty. The findings highlight the importance of considering heritability and GxE interactions in frailty research and advocates for future exploration of specific genes and mechanisms involved in frailty development and progression.