How is "Biological Response to Acute Stress" encoded by the genome?
Many people feel stress when they encounter unfamiliar or unexpected events, or they feel threatened. On the other hand acute stress is different then chronic stress. What happens in our bodies when we feel acute stress? How does our body respond?
Individuals vary widely in their psychological, behavioral, and biological responses to acute stress, with the sympathetic nervous system and hypothalamic–pituitary–adrenal axis (HPA) as primary mediators. One of the most well-characterized elements of the biological stress response is a rise in cortisol levels 20–30 minutes following stressor exposure, with a subsequent return to baseline. Many factors, including genetic variation, influence the magnitude and duration of this response, leading to substantial individual differences. Lower or higher than expected cortisol responses may have unfavorable effects on health and well-being later in life. Lower than expected cortisol responses may reflect early-life adversity or co-occurring internalizing conditions, such as anxiety, impacting health and disease risk. Higher than expected cortisol levels in response to acute stress also reflect dysregulated emotional and physical states, which also impacts health.
Because variability in the cortisol response to stress has a broad impact on health, identifying factors contributing to this variability is important for designing an optimal treatment for individuals. Most studies of the cortisol stress response, including those in children, often rely on lab-based standardized stress tasks.
However, these tests might not consistently generate stress responses in young children. Therefore, this study aimed to identify genetic variants associated with the cortisol stress response in the clinical setting.
Children 4–10 years old who were scheduled for procedures requiring the relatively painful insertion of a peripheral intravenous (IV), were enrolled. Following IV insertion, children provided saliva samples to evaluate the cortisol response as a biological measure of distress. Saliva samples were also collected at home on a non-stressful day as a control comparison. Genes selected for analysis included those potentially associated with children’s pain, distress, and anxiety in response to peripheral IV insertion as well as those known to be or potentially relevant to the cortisol stress response. After quality control, 86 SNPs in 34 genes were analyzed. Association analysis of child genotype (n=326) identified that four single-nucleotide polymorphisms (SNPs), including rs1176744 in the 5-hydroxytryptamine receptor 3B gene (HTR3B) and rs8030107 in the neurotrophic receptor tyrosine kinase 3 gene (NTRK3), were associated with the cortisol stress response. Children with the rare allele (G) at rs1176744 (HTR3B) experienced a lower cortisol stress response. In the opposite direction, children having the rare allele (T) at rs8030107 (NTRK3) experienced a greater mean cortisol stress response.
Although there are some limitations, including the modest study sample size for a analysis and the absence of an independent replication population, this study focuses on a naturally occurring stressor in childrens population. This research also supports prior work evaluating the response to standardized, lab-based stressors. This analysis provides preliminary evidence for genes and pathways potentially important in cortisol response to an acute stressor in children and could guide future analyses. Read more about the study here:
https://www.ncbi.nlm.nih.gov/pubmed/30700110
Are you interested in learning more about your genetic tendency for cortisol response to an acute stressor? You can login to your Genomelink dashboard to see this new genetic trait.
