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The effects of tryptophan enhancement and depletion on plasma catecholamine levels in healthy individuals

Boyle, Stephen H., PhD1; Brummett, Beverly H., PhD1; Kuhn, Cynthia M., PhD2; Barefoot, John C., PhD1; Siegler, Ilene C., PhD, MPH1; Williams, Redford B., MD1; Georgiades, Anastasia, PhD1

doi: 10.1097/PSY.0000000000000637
Original Article: PDF Only

Objective Central nervous system (CNS) serotonin (5-HT) exerts both excitatory and inhibitory effects on the sympathetic nervous system (SNS) in animals. In this study, we examine the effects of tryptophan enhancement and depletion on plasma catecholamine levels in humans.

Methods The total sample consisted of 164 healthy men and women who were tested over 2 days. Seventy-nine participants were randomized to a tryptophan enhancement condition and eighty-five to a tryptophan depletion condition. Both protocols consisted of a “sham-day” followed by an “active-day”. Blood samples for assessment of plasma norepinephrine and epinephrine levels were collected prior and post tryptophan enhancement/depletion. Data were analyzed using general linear models. Separate analyses were conducted for each study arm and for each measure.

Results In the depletion condition, both epinephrine (F(5,330) = 2.69, p = .021) and norepinephrine (F(5,335) = 2.79, p =.018) showed small increases on active vs ‘sham’ depletion days. There were also significant day X time interactions for epinephrine (F(3,171) = 39.32, p < .0001) and norepinephrine (F(3,195) = 31.09, p < .0001) levels in the enhancement arm. Tryptophan infusion resulted in a marked increase in epinephrine (Premean =23.92±12.23 vs. Postmean =81.57±62.36) and decrease in norepinephrine (Premean =257.2±106.11 vs. Postmean =177.04±87.15 ) whereas levels of both catecholamines were stable on the “sham-day”.

Conclusions CNS 5-HT exerts both inhibitory and excitatory effects on SNS activity in humans, potentially due to stimulation of CNS 5-HT receptors that have shown to have inhibitory (5-HT1A) and excitatory (5-HT1A and/or 5-HT2) SNS effects in animal models.

1Department of Psychiatry and Behavioral Sciences, Duke University School of Medicine, Durham, N.C., 27710, USA

2Department of Pharmacology and Cancer Biology, Duke University Medical Center, USA

Corresponding author: Stephen H. Boyle, Box 2969 Duke University School of Medicine, Durham, North Carolina, 27710. Phone: (919) 668-3647, email:

Conflicts of Interest and Source of Funding: No conflicts of Interest declared. This research was supported by the by National Heart, Lung, and Blood Institutes grant P01 HL036587.

Copyright © 2018 by American Psychosomatic Society
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