Date of Award

8-2026

Document Type

Dissertation

Degree Name

Doctor of Philosophy (PhD)

Department

Food, Nutrition, and Culinary Science

Committee Chair/Advisor

Geetha Thangiah

Committee Member

Ramesh Jeganathan

Committee Member

Hannah Wilson

Committee Member

Sarah Griffin

Abstract

Childhood obesity is a major public health concern because it increases the risk of lifelong health problems, including diabetes, cardiovascular disease, stroke, and certain cancers. Healthy diet and regular physical activity are well-established behaviors that support metabolic health, yet there are still underexplored lifestyle factors contributing to childhood obesity rates in this country. Growing evidence suggests that sleep habits, especially when children go to bed, may also play an important role. However, the biological processes that connect sleep behaviors to obesity risk in children are not fully understood.

This dissertation explores how sleep timing may influence children’s health by shaping biological signals that regulate metabolism, growth, and inflammation. A key focus is epigenetics, which refers to chemical modifications that affect how genes are turned “on” or “off” without altering the DNA sequence itself. One common epigenetic process is DNA methylation, which involves small chemical tags attaching to DNA, influencing a genes responsiveness within the epigenomic landscape, thus having a potential impact on the health and longevity of an individual. These changes in genetic expression can be influenced by everyday experiences, such as sleep patterns, dietary patterns, exercise, environmental stressors, and pollutants to name a few, and may help explain how these behaviors become biologically embedded early in life.

First, a comprehensive review of the scientific literature summarizes current knowledge on sleep, epigenetics, and childhood obesity. This review highlights important gaps, particularly the lack of research examining sleep-related biological pathways in children. Next, an epigenome-wise analysis was conducted to identify DNA methylation patterns associated with bedtime in school-aged children. This analysis revealed widespread differences in gene regulation between children with earlier versus later bedtimes, involving genes related to circadian rhythms, brain development metabolism, and stress response.

Building on these findings, targeted analyses focused on two specific genes, ABCG2 and CDH4, to better understand how sleep timing relates to body fat measurements and metabolic risk in youth. Children with later bedtimes showed higher methylation of ABCG2 and lower methylation of CDH4, patterns that were linked to higher body mass index and central adiposity. These results suggest that sleep timing is associated with distinct biological changes that may increase obesity risk.

Finally, this dissertation examined DNA methylation-based protein proxies measured from saliva to capture broader biological processes related to obesity. Several protein signals associated with inflammation, blood vessel development, and metabolism were linked to children’s body size, and some of these associations were influenced by socioeconomic factors such as maternal education and annual household income.

Overall, this work demonstrates that when children sleep, not just how long, may shape early biological pathways linked to obesity. By integrating sleep behaviors, molecular biology, and social context, this research provides new insight into how childhood health risks develop and highlights opportunities for early, noninvasive prevention strategies.

Author ORCID Identifier

https://orcid.org/0009-0009-5867-5231

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Available for download on Tuesday, August 31, 2027

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