Abstract
The relationship between metabolic health and brain function is typically studied in older adults, often after cognitive decline has already begun. But what if metabolic dysfunction — obesity, insulin resistance — is already altering how the brain processes information in young, otherwise healthy adults? If so, the neural consequences of metabolic risk may begin decades before dementia onset, and metabolic interventions in young adulthood could have neuroprotective benefits that compound over a lifetime.
This project investigated exactly that question, using neuroelectrophysiology and neuroimaging to examine how metabolic factors modulate neural processing and memory function in young adults. Two studies explored complementary aspects of this relationship.
The first study examined how obesity and insulin resistance affect the neural processing of emotional visual stimuli. The key finding was that metabolic dysfunction altered neural responses to unpleasant stimuli — but not pleasant ones — suggesting a valence-specific effect. This means that metabolic risk does not globally impair neural processing; rather, it selectively disrupts how the brain handles negatively valenced information, which has implications for emotional regulation and decision-making. This work was published in Brain Sciences (2026).
The second study asked whether adiposity and insulin resistance moderate the link between neuroelectrophysiology and working and episodic memory. The answer was yes — but only in males. In young adult males, metabolic risk factors significantly moderated the associations between neural electrical activity and memory performance, while no such moderation was observed in females. This sex-specific vulnerability suggests that the neural consequences of metabolic dysfunction may follow different pathways in men and women, with implications for personalized risk assessment. This study appeared in Physiology & Behavior (2023).
Together, these findings establish that the neural impact of metabolic dysfunction is not a late-life phenomenon — it is already measurable in young adults, it is selective in its effects, and it differs by sex. This reframes the timeline for prevention and opens new questions about whether early metabolic intervention could preserve neural function decades before dementia risk becomes clinically apparent.