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The Effects of Tryptophan Enhancement and Depletion on Plasma Catecholamine Levels in Healthy Individuals

Boyle, Stephen H., PhD; Brummett, Beverly H., PhD; Kuhn, Cynthia M., PhD; Barefoot, John C., PhD; Siegler, Ilene C., PhD, MPH; Williams, Redford B., MD; Georgiades, Anastasia, PhD

doi: 10.1097/PSY.0000000000000637
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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 for 2 days. Seventy-nine participants were randomized to a tryptophan enhancement condition and 85 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 before and after 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 versus “sham” depletion days. There were also significant day by 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) versus Postmean = 81.57 (62.36)) and decrease in norepinephrine (Premean = 257.2 (106.11) versus 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.

From the Department of Psychiatry and Behavioral Sciences (Boyle, Brummett, Barefoot, Siegler, Williams, Georgiades), Duke University School of Medicine, Durham, North Carolina; and Department of Pharmacology and Cancer Biology (Kuhn), Duke University Medical Center, Durham, North Carolina.

Address correspondence to Stephen H. Boyle, PhD, Duke University School of Medicine, Box 2969, Durham, North Carolina, 27710. E-mail: shboyle@duke.edu

Supplemental Content

Received for publication December 21, 2017; revision received July 26, 2018.

Copyright © 2019 by American Psychosomatic Society
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