Gene Expression in Response to Acute Stress
Conditions
Brief summary
Given the salient role of early-life adversity and the resulting biological embedding in disease risk, there is a critical need to understand the mechanisms operating at multiple levels of analysis in order to promote effective clinical treatments and intervention efforts for survivors. An example for such an effort could be to utilize models of dynamic cellular markers as individual-level factors to account for variation in intervention response and clinical outcomes. Results of this study will lead to new knowledge about specific gene expression pathways in response to stress, and whether the response is moderated by previous exposure to early adversity, shorter telomere length (a marker of cellular aging) and self-report mental-health measures. Thus, the long-term effects of this study will advance our understanding on stress-related transcriptomic changes that play a downstream role in disease susceptibility and accelerated aging, with the goal of targeting specific pathways and genes for potential intervention studies and pharmacological treatments to reverse the effects of exposure to early adversity. For example, considering high failure rates for depression treatments, and in order to tailor individual interventions, identifying objective changes in stress-induced gene expression may help to predict intervention efficacy in clinical and non-clinical settings, as seen, for example, in breast and leukemia cancers. Thus, findings will have a range of impacts for basic science, intervention studies and clinical practice that will influence treatments to match the specific cellular processes operating within an individual.
Interventions
BEHAVIORALBehavioral
Trier Social Stress Test
BEHAVIORALControl condition
In the no-stress control condition, participants will be instructed to sit in a room, read magazines, and to refrain from any stressful activities (e.g., cell-phone use will be restricted).
Sponsors
Penn State University
Study design
Allocation
RANDOMIZED
Intervention model
PARALLEL
Primary purpose
BASIC_SCIENCE
Masking
SINGLE (Investigator)
Eligibility
Sex/Gender
ALL
Age
18 Years to 25 Years
Healthy volunteers
Yes
Inclusion criteria
* Age 18-25 * Without significant medical illness or endocrine illness (for example, asthma, diabetes, thyroid disease or pituitary gland disorders) * Currently non-smokers * Not pregnant and had not given birth in the past year * Not using medication on a regular basis besides oral contraceptives to allow generalizability to adult women.
Exclusion criteria
* Recent infection or illness * Use of abused drugs * Immune disease, ascertained during the phone interview.
Design outcomes
Primary
| Measure | Time frame |
|---|---|
| Gene expression via RNAseq | Gene expression over 5 hours in response to stress or a no-stress condition |
Countries
United States
Outcome results
None listed