Researcher ORCID Identifier

0009-0000-5869-1316

Graduation Year

2024

Date of Submission

4-2024

Document Type

Open Access Senior Thesis

Degree Name

Bachelor of Arts

Department

Neuroscience

Reader 1

Dr. Stacey Doan

Reader 2

Dr. Tessa Solomon-Lane

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Terms of Use for work posted in Scholarship@Claremont.

Rights Information

@2024 Keeley L LaRiviere

Abstract

Stress-motivated drinking is common among college students facing increased independence and novel stressors. Early life adversity (ELA) as well as individual variation in neuroendocrine stress signaling significantly increase risk for alcohol misuse. Research on the relationships between ELA and the physiological stress response system, suggest that a dampened stress response may mediate the relations between ELA and alcohol misuse. However, other research has suggested that rather than acting as mediator, stress reactivity may interact (moderate) the relations between ELA and alcohol misuse. This study examined the associations between ELA, cortisol reactivity to an acute stressor, and self-reported alcohol misuse in 449 undergraduates (Mage = 19.52, SD = 1.20; 55.9% female). We test cortisol reactivity as both a mediator and a moderator. Participants completed measures of ELA, alcohol misuse, and underwent the Trier Social Stress Task to index cortisol reactivity that was measured via salivary cortisol across 5 time points. Area under the curve with respect to ground was computed to get a measure of cortisol reactivity. Results showed a main effect of ELA predicting increased alcohol misuse (B = 0.120, p = .004), aligning with prior research. Contrary to expectations, mediation analysis did not support cortisol reactivity as the mechanism linking ELA to alcohol misuse. Moderation analysis revealed a significant interaction between ELA and cortisol reactivity (B = -0.07, p = .028). At low and moderate cortisol reactivity, higher ELA predicted greater alcohol misuse (p = .000 and p = .025, respectively). However, at high levels of cortisol reactivity, ELA was no longer associated with alcohol misuse (p = .346). Overall, findings indicate that while ELA increases risk for alcohol misuse, heightened cortisol reactivity may play a protective role, potentially by shaping cognitive appraisals of stressors across development. These results highlight the complex relationships between early adversity, neurobiological stress response systems, and health risk behaviors. Future research should further explore factors promoting resilience despite ELA as well as expand to other substances and populations of interest.

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