Dose- and time-dependent increase in circulating anti-inflammatory and pro-resolving lipid mediators following eicosapentaenoic acid supplementation in patients with major depressive disorder and chronic inflammation.


Journal

Prostaglandins, leukotrienes, and essential fatty acids
ISSN: 1532-2823
Titre abrégé: Prostaglandins Leukot Essent Fatty Acids
Pays: Scotland
ID NLM: 8802730

Informations de publication

Date de publication:
01 2021
Historique:
received: 21 07 2020
revised: 23 11 2020
accepted: 24 11 2020
pubmed: 15 12 2020
medline: 3 6 2021
entrez: 14 12 2020
Statut: ppublish

Résumé

Eicosapentaenoic acid (EPA) supplementation is an effective treatment option in major depressive disorder (MDD) associated with chronic low-grade inflammation. EPA is the precursor of specialized pro-resolving lipid mediators (SPMs) termed resolvins (Rv), that serve important roles in the resolution of inflammation. The objective of this study was to assess the effects of different doses of EPA on plasma concentrations of EPA metabolites and SPMs in MDD patients. In a 2-site study, 61 MDD patients with body mass index >25 kg/m Plasma EPA and SPM concentrations did not change in the placebo group during 12 weeks of treatment. Plasma EPA and EPA-derived metabolites increased significantly and dose-dependently in all EPA supplementation arms. The increase in 18-hydroxyeicosapentaenoic acid (18-HEPE), the precursor of RvE1-3, was significantly greater with the 4 g/d EPA dose than the other doses from week 4 to 12. RvE1 was undetected in all treatment groups, while RvE2 was detected in half of the subjects both at baseline and after treatment, with dose-dependent increases. RvE3 was detected only after supplementation, dose-dependently. A significant reduction in plasma arachidonic acid (AA), relative to baseline, was observed in all EPA arms. This was in contrast with an increase in AA-derived SPM lipoxin B4 (LXB4) in the 4 g/d arm. Our results show a robust effect of EPA 4 g/d supplementation in increasing plasma EPA and 18-HEPE levels, associated with improved conversion to RvE2-3, and LXB4 levels.

Sections du résumé

BACKGROUND
Eicosapentaenoic acid (EPA) supplementation is an effective treatment option in major depressive disorder (MDD) associated with chronic low-grade inflammation. EPA is the precursor of specialized pro-resolving lipid mediators (SPMs) termed resolvins (Rv), that serve important roles in the resolution of inflammation. The objective of this study was to assess the effects of different doses of EPA on plasma concentrations of EPA metabolites and SPMs in MDD patients.
METHODS
In a 2-site study, 61 MDD patients with body mass index >25 kg/m
RESULTS
Plasma EPA and SPM concentrations did not change in the placebo group during 12 weeks of treatment. Plasma EPA and EPA-derived metabolites increased significantly and dose-dependently in all EPA supplementation arms. The increase in 18-hydroxyeicosapentaenoic acid (18-HEPE), the precursor of RvE1-3, was significantly greater with the 4 g/d EPA dose than the other doses from week 4 to 12. RvE1 was undetected in all treatment groups, while RvE2 was detected in half of the subjects both at baseline and after treatment, with dose-dependent increases. RvE3 was detected only after supplementation, dose-dependently. A significant reduction in plasma arachidonic acid (AA), relative to baseline, was observed in all EPA arms. This was in contrast with an increase in AA-derived SPM lipoxin B4 (LXB4) in the 4 g/d arm.
CONCLUSIONS
Our results show a robust effect of EPA 4 g/d supplementation in increasing plasma EPA and 18-HEPE levels, associated with improved conversion to RvE2-3, and LXB4 levels.

Identifiants

pubmed: 33316626
pii: S0952-3278(20)30177-0
doi: 10.1016/j.plefa.2020.102219
pmc: PMC7855824
mid: NIHMS1654304
pii:
doi:

Substances chimiques

Eicosapentaenoic Acid AAN7QOV9EA

Types de publication

Journal Article Randomized Controlled Trial Research Support, N.I.H., Extramural Research Support, U.S. Gov't, Non-P.H.S.

Langues

eng

Sous-ensembles de citation

IM

Pagination

102219

Subventions

Organisme : NCRR NIH HHS
ID : S10 RR027926
Pays : United States
Organisme : NCCIH NIH HHS
ID : UG3 AT008857
Pays : United States

Informations de copyright

Copyright © 2020 Elsevier Ltd. All rights reserved.

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Auteurs

Stefania Lamon-Fava (S)

Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA. Electronic address: stefania.lamon-fava@tufts.edu.

Jisun So (J)

Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA.

David Mischoulon (D)

Department of Psychiatry, Massachusetts General Hospital, Boston, MA.

Thomas R Ziegler (TR)

Department of Medicine, Emory University.

Boadie W Dunlop (BW)

Department of Psychiatry and Behavioral Sciences, Emory University, Atlanta, GA.

Becky Kinkead (B)

Department of Psychiatry and Behavioral Sciences, Emory University, Atlanta, GA.

Pamela J Schettler (PJ)

Department of Psychiatry and Behavioral Sciences, Emory University, Atlanta, GA.

Andrew A Nierenberg (AA)

Department of Psychiatry, Massachusetts General Hospital, Boston, MA.

Jennifer C Felger (JC)

Department of Psychiatry and Behavioral Sciences, Emory University, Atlanta, GA.

Krishna Rao Maddipati (KR)

Department of Pathology, Lipidomics Core Facility, Wayne State University, Detroit, MI.

Maurizio Fava (M)

Department of Psychiatry, Massachusetts General Hospital, Boston, MA.

Mark Hyman Rapaport (MH)

Department of Psychiatry and Behavioral Sciences, Emory University, Atlanta, GA.

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