Genetic and environmental modulation of neurotrophic and anabolic stress response

Counterbalancing forces

Marcus K. Taylor, Jennifer Carpenter, Michael Stone, Lisa M. Hernandez, Mitchell J. Rauh, Heidemarie K. Laurent, Douglas A. Granger

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

The serotonin transporter genetic variant 5HTTLPR influences activation and feedback control of the hypothalamic-pituitary-adrenal axis, and has been shown to influence the effect of stressful life events on behavioral health. We recently reported that 5HTTLPR modulates cortisol response in healthy military men exposed to intense stress. Less is known of its combined effects with environmental factors in this context, or of its effect on neuroprotective stress responses. In this follow-up study, we examined the unique and combined effects of 5HTTLPR and prior trauma exposure on neuroprotective (salivary nerve growth factor [sNGF]), anabolic (dehydroepiandrosterone sulfate [DHEAS] and testosterone), and catabolic (cortisol) stress responses. Ninety-three healthy, active-duty military men were studied before, during, and 24. h after a stressful 12-day survival course. Distinct and interactive effects of 5HTTLPR long allele carriage [L] versus homozygous short allele carriage [SS]) and prior trauma exposure (low versus high) were evaluated, after which a priori group comparisons were performed between hypothesized high resilience (L/low) and low resilience (SS/high) groups. For sNGF, L/low produced the greatest sNGF throughout stress exposure while SS/high demonstrated the smallest; L/high and SS/low bisected these two extremes and were nearly identical to each other (i.e., SS/high. <. SS/low. =. L/high. <. L/low). Thus, 5HTTLPR and prior trauma exposure demonstrated counterbalancing (additive) forces. Similar patterns were found for DHEAS. To our knowledge, this study is the first to report counterbalancing genetic and environmental effects on novel biomarkers related to resilience in humans exposed to real-world stress. These findings have profound implications for health, performance and training in high-stress occupational settings.

Original languageEnglish (US)
Pages (from-to)1-8
Number of pages8
JournalPhysiology and Behavior
Volume151
DOIs
StatePublished - Nov 1 2015

Fingerprint

Nerve Growth Factor
Dehydroepiandrosterone Sulfate
Hydrocortisone
Wounds and Injuries
Alleles
Serotonin Plasma Membrane Transport Proteins
Health
Testosterone
Biomarkers
Survival
Modulation
Trauma
Resilience
Nerve

Keywords

  • Cortisol
  • Dehydroepiandrosterone sulfate
  • Genetics
  • Nerve growth factor
  • Serotonin transporter
  • Stress
  • Testosterone
  • Trauma

ASJC Scopus subject areas

  • Behavioral Neuroscience
  • Experimental and Cognitive Psychology
  • Philosophy

Cite this

Taylor, M. K., Carpenter, J., Stone, M., Hernandez, L. M., Rauh, M. J., Laurent, H. K., & Granger, D. A. (2015). Genetic and environmental modulation of neurotrophic and anabolic stress response: Counterbalancing forces. Physiology and Behavior, 151, 1-8. https://doi.org/10.1016/j.physbeh.2015.06.027

Genetic and environmental modulation of neurotrophic and anabolic stress response : Counterbalancing forces. / Taylor, Marcus K.; Carpenter, Jennifer; Stone, Michael; Hernandez, Lisa M.; Rauh, Mitchell J.; Laurent, Heidemarie K.; Granger, Douglas A.

In: Physiology and Behavior, Vol. 151, 01.11.2015, p. 1-8.

Research output: Contribution to journalArticle

Taylor, MK, Carpenter, J, Stone, M, Hernandez, LM, Rauh, MJ, Laurent, HK & Granger, DA 2015, 'Genetic and environmental modulation of neurotrophic and anabolic stress response: Counterbalancing forces', Physiology and Behavior, vol. 151, pp. 1-8. https://doi.org/10.1016/j.physbeh.2015.06.027
Taylor, Marcus K. ; Carpenter, Jennifer ; Stone, Michael ; Hernandez, Lisa M. ; Rauh, Mitchell J. ; Laurent, Heidemarie K. ; Granger, Douglas A. / Genetic and environmental modulation of neurotrophic and anabolic stress response : Counterbalancing forces. In: Physiology and Behavior. 2015 ; Vol. 151. pp. 1-8.
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