The catecholamine neurotransmitter precursor tyrosine increases anger during exposure to severe psychological stress

Abstract

Rationale: Acute stress produces behavioral and physiological changes modulated by central catecholamines (CA). Stress increases CA activity, and depletion of CA stores reduces responses to stress. Increasing CA activity by administration of the dietary amino acid CA precursor tyrosine may increase responsiveness to stress. This study determined whether tyrosine enhances the ability of humans to respond to severe stress.

Methods: Severe psychological stress was generated during training at Survival, Evasion, Resistance, and Escape (SERE) School. The acute stressor consisted of two mock interrogations conducted during several days of simulated captivity. Seventy-eight healthy male and female military personnel participated in this double-blind, between-subjects study, in which they received either tyrosine (300 mg/kg, N = 36) or placebo (N = 36). Tyrosine (or placebo) was administered in food bars in two doses of 150 mg/kg each approximately 60 min before each mock interrogation. Mood (Profile of Mood States), saliva cortisol, and heart rate (HR) were assessed prior to stress exposure during a week of academic training preceding mock captivity and immediately following the mock interrogations.

Results: The severe stress produced robust effects on mood (i.e., increased tension, depression, anger, fatigue, vigor, and confusion; p < .001), cortisol, and HR (p < .001). Tyrosine increased anger (p = .002, ANOVA treatment condition by test session interaction) during stress but had no other effects.

Conclusion: Tyrosine did not alter most subjective or physiological responses to severe acute stress, but it increased ratings of anger. The modest increase in anger may be an adaptive emotional response in stressful environments.

Figures

Fig. 1

Changes in the six subscales of the POMS over the course of SERE training as a function of tyrosine vs. placebo administration. Tyrosine significantly increased the anger subscale at sessions 3 and 4 during the stressful captivity phase of SERE School. Session 1 was conducted prior to treatment administration during academic week, the low-stress portion of SERE School. Tyrosine or placebo was administered just prior to sessions 2 and 3 as shown by the arrows. Session 4 was conducted the following day. Significant effects of tyrosine compared to placebo on post-hoc testing at specific time points are indicated by a # (p < .03) or ## (p < .001). Significant changes on post-hoc testing when session 2, 3, or 4 was compared to session 1 (academic week-baseline) are indicated by * (p < .001)

Fig. 2

Cortisol levels (μg/dL) during academic week (session 1: A-morning, B-midday, and C-evening) and captivity (sessions 2, 3, 4). All session 1 samples (A, B, C) were obtained during baseline testing (pre-stress exposure). Sessions 2, 3, and 4 were conducted sequentially over the course of the captivity phase of SERE School. Session 2 was conducted midday immediately following the first interrogation. Session 3 was conducted immediately following the second interrogation. Session 4 was conducted in the morning when the captivity phase of SERE training was nearing completion. Due to substantial circadian variations in release of cortisol, statistical comparisons of captivity testing sessions were only conducted by comparing each session to the assessment session conducted at the equivalent time of day during academic week (*p < .001 on the within-subject factor of ANOVA)

Fig. 3

Mean HR (beats/min) during baseline testing conducted during the academic non-stressful portion of SERE School and peak heart rates during sessions 2 and 3 when interrogations were being conducted. On post-hoc testing, mean peak session 2 and session 3 HRs were significantly higher than baseline (*p < .001). Session 3 HR was significantly higher than Session 2 HR (#p = .008)