Researcher ORCID Identifier

0009-0003-7829-9145

Graduation Year

2026

Date of Submission

4-2026

Document Type

Open Access Senior Thesis

Degree Name

Bachelor of Arts

Department

Biology

Reader 1

Diana Williams

Reader 2

Kyle Jay

Rights Information

2026 Calvin G Miller

Abstract

Food insecurity affects nearly 48 million Americans and 318 million people worldwide, with very low food security disrupting normal eating habits through “feast-or-famine” episodes characterized by cycles of food overconsumption followed by restriction. This dietary pattern alters dopamine signaling within the mesocorticolimbic system — brain circuitry intimately linked to reward processing. This system includes the ventral tegmental area (VTA) and prefrontal cortex (PFC). Overstimulation can be promoted through sporadic high-fat, high-sugar diet (HFHSD) exposure, promoting dopamine neuron architecture alterations and binge-eating behavior. Adolescence represents a vulnerable window, as mesocorticolimbic dopamine projections undergo maturation during this period. Though evidence links food insecurity to reward system dysregulation and eating disorder risk, the effect of intermittent palatable food access during adolescence on the VTA to PFC dopamine development remains unknown. Adolescent rats were assigned to intermittent HFHSD access (INT), continuous HFHSD access (HFHS), or standard show (CHOW) groups. INT rats exhibited a sawtooth intake pattern — escalating on HFHSD access days and dropping on post-access chow-only days (p< 0.05). CHOW and HFHS rats maintained stable intake, indicating that intermittent access (IA) rather than diet composition drove the feast-or-famine phenotype. This binge-restriction cycle was accompanied by reduced body weight gain in INT rats relative to CHOW controls by IA Day 6 (p< 0.05), despite access to calorie-dense food, suggesting post-access hypophagia offsets binge intake — a trend not observed in adult rats. These findings establish a behaviorally validated adolescent model of food unpredictability and provide the foundation for subsequent neurobiological analysis of mesocortical dopamine development.

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