Dataset Information

Depressed mood induction in early cigarette withdrawal is unaffected by acute monoamine precursor supplementation.

ABSTRACT: Background:Cigarette smoking is the leading preventable cause of death; however, quitting is difficult and early relapse is common. Dysphoric mood during early cigarette withdrawal is associated with relapse, and with the exception of bupropion and nortriptyline, few interventions have been developed to prevent this. During early cigarette withdrawal there is an elevation in the levels of monoamine oxidase-A (MAO-A), which removes monoamines excessively and induces oxidative stress and is implicated in creating sad mood. Hence, we conducted a randomized, placebo-controlled, double-blind crossover trial of a dietary supplement designed to counter the effects of elevated MAO-A levels on vulnerability to depressed mood. Methods:Twenty-one otherwise healthy cigarette smokers completed the protocol, receiving either active dietary supplement followed by washout and placebo or the same in reverse order. The dietary supplement was composed of monoamine precursors (2 g tryptophan, 10 g tyrosine) and blueberry antioxidants (blueberry juice with blueberry extract). Vulnerability to depressed mood was measured by the change in scores of depressed mood on the visual analog scale (VAS) following the sad mood induction paradigm (MIP). Results:There was a significant increase in VAS depressed mood scores after the sad MIP during supplement and placebo, but no difference between active and placebo conditions. There was also a significant increase in urge-to-smoke scores after sad MIP during supplement and placebo but no difference between active and placebo conditions. Reliability of the increase in VAS after MIP was very good. Conclusion:The dietary supplement had negligible effect on depressed mood, but sad MIP is a very reliable method that can be applied in future studies to assess other interventions for preventing dysphoric mood during early cigarette withdrawal.

SUBMITTER: Dowlati Y

PROVIDER: S-EPMC6352866 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Depressed mood induction in early cigarette withdrawal is unaffected by acute monoamine precursor supplementation.

Dowlati Yekta Y de Jesus Danilo R DR Selby Peter P Fan Ian I Meyer Jeffrey H JH

Neuropsychiatric disease and treatment 20190123

<h4>Background</h4>Cigarette smoking is the leading preventable cause of death; however, quitting is difficult and early relapse is common. Dysphoric mood during early cigarette withdrawal is associated with relapse, and with the exception of bupropion and nortriptyline, few interventions have been developed to prevent this. During early cigarette withdrawal there is an elevation in the levels of monoamine oxidase-A (MAO-A), which removes monoamines excessively and induces oxidative stress and i ...[more]

PMID: 30774343

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Project description:Inflammation plays a significant role in the pathophysiology of depression. However, not all individuals exposed to inflammatory challenge develop depression, and identifying those at risk is necessary to develop targeted monitoring, prevention, and treatment strategies. Within a randomized double-blind placebo-controlled study (n = 115), we examined whether leukocyte transcriptome profiles predicted inflammation-induced depressed mood in volunteers who received low-dose intravenous endotoxin (n = 58; aged 18-50). At baseline, transcription factor (TF) activities were assessed using genome-wide transcriptional profiling of peripheral blood mononuclear cells and promoter-based bioinformatic analyses. Then, participants were administered endotoxin. Self-reported depressed mood was assessed using the Profile of Mood States. Based on extant studies linking transcriptional profiles to depressive disorder, we examined whether post-endotoxin depressed mood is predicted by baseline activity of TFs related to immune activation, sympathetic activation, and glucocorticoid insensitivity: respectively, nuclear factor kappa B (NF-kB), cAMP response element-binding protein (CREB), and glucocorticoid receptor (GR). Twenty-one participants (36%) experienced an increase in depressed mood from baseline to 2 h post endotoxin, when depressive response peaks. Bioinformatics analyses controlling for age, sex, ethnicity, body mass index, and physical sickness response revealed that post-endotoxin depressed mood was predicted by increased baseline activity of TFs related to inflammation (NF-kB) and beta-adrenergic signaling (CREB) and by decreased activity of GR-related TFs (P's < 0.001). Inflammation-induced depressed mood is predicted by peripheral transcriptome profiles related to immune activation, sympathetic activation, and glucocorticoid insensitivity. With further replication, these stress-related molecular profiles could be used for a novel genomic approach for identifying individuals at high-risk for the inflammatory subtype of depression.

Project description:Inflammation has an important physiological influence on mood and behavior. Kynurenine metabolism is hypothesized to be a pathway linking inflammation and depressed mood, in part through the impact of kynurenine metabolites on glutamate neurotransmission in the central nervous system. This study evaluated whether the circulating concentrations of kynurenine and related compounds change acutely in response to an inflammatory challenge (endotoxin administration) in a human model of inflammation-induced depressed mood, and whether such metabolite changes relate to mood change. Adults (n = 115) were randomized to receive endotoxin or placebo. Mood (Profile of Mood States), plasma cytokine (interleukin-6, tumor necrosis factor-α) and metabolite (kynurenine, tryptophan, kynurenic acid, quinolinic acid) concentrations were repeatedly measured before the intervention, and at 2 and 6 h post-intervention. Linear mixed models were used to evaluate relationships between mood, kynurenine and related compounds, and cytokines. Kynurenine, kynurenic acid, and tryptophan (but not quinolinic acid) concentrations changed acutely (p's all <0.001) in response to endotoxin as compared to placebo. Neither kynurenine, kynurenic acid nor tryptophan concentrations were correlated at baseline with cytokine concentrations, but all three were significantly correlated with cytokine concentrations over time in response to endotoxin. Quinolinic acid concentrations were not correlated with cytokine concentrations either before or following endotoxin treatment. In those who received endotoxin, kynurenine (p = 0.049) and quinolinic acid (p = 0.03) positively correlated with depressed mood, although these findings would not survive correction for multiple testing. Changes in tryptophan and kynurenine pathway metabolites did not mediate the relationship between cytokines and depressed mood. Further work is necessary to clarify the pathways leading from inflammation to depressed mood in humans.

Dataset Information

Depressed mood induction in early cigarette withdrawal is unaffected by acute monoamine precursor supplementation.

Publications

Depressed mood induction in early cigarette withdrawal is unaffected by acute monoamine precursor supplementation.

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