Daisuke Nishi1, Kuan-Pin Su2, Kentaro Usuda3, Jane Pei-Chen Chang4, Kei Hamazaki5, Tamaki Ishima6, Yo Sano7, Hiroe Ito8, Keiich Isaka8, Yoshiyuki Tachibana9, Shinji Tanigaki10, Tomo Suzuki11, Kenji Hashimoto6, Yutaka J Matsuoka12. 1. Department of Obstetrics and Gynecology, Tokyo Medical University, Tokyo, Japan; Department of Mental Health, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan; Department of Mental Health Policy, National Institute of Mental Health, National Center of Neurology and Psychiatry, Tokyo, Japan. Electronic address: d-nishi@umin.ac.jp. 2. Department of Psychiatry & Mind-Body Interface Laboratory (MBI-Lab), China Medical University Hospital, Taichung, Taiwan; Department of Psychological Medicine, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK. Electronic address: cobolsu@gmail.com. 3. Department of Obstetrics and Gynecology, Tokyo Medical University, Tokyo, Japan; Department of Mental Health Policy, National Institute of Mental Health, National Center of Neurology and Psychiatry, Tokyo, Japan. 4. Department of Psychiatry & Mind-Body Interface Laboratory (MBI-Lab), China Medical University Hospital, Taichung, Taiwan; Department of Psychological Medicine, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK. 5. Department of Public Health, Faculty of Medicine, University of Toyama, Toyama, Japan. 6. Division of Clinical Neuroscience, Chiba University Center for Forensic Mental Health, Chiba, Japan. 7. Toda Chuo Women's Hospital, Saitama, Japan. 8. Department of Obstetrics and Gynecology, Tokyo Medical University, Tokyo, Japan. 9. Division of Infant and Toddler Mental Health, Department of Psychosocial Medicine, Japan. 10. Center for Maternal-Fetal, Neonatal and Reproductive Medicine, National Center for Child Health and Development, Tokyo, Japan; Department of Obstetrics and Gynecology, Kyorin University School of Medicine, Tokyo, Japan. 11. Center for Maternal-Fetal, Neonatal and Reproductive Medicine, National Center for Child Health and Development, Tokyo, Japan. 12. Department of Obstetrics and Gynecology, Tokyo Medical University, Tokyo, Japan; Division of Health Care Research, Center for Public Health Sciences, National Cancer Center Japan, Tokyo, Japan.
Abstract
BACKGROUND:Omega-3 polyunsaturated fatty acids (PUFAs) reduce depressive symptoms through an anti-inflammatory effect, and injection of both omega-3 PUFAs and estradiol (E2) induces antidepressant-like effects in rats by regulating the expression of inflammatory cytokines. The aims of this study were to examine the association of increased E2 during pregnancy with depressive symptoms and with inflammatory cytokines in women who were and were not supplemented with omega-3 PUFAs. METHODS:Pregnant women with Edinburgh Postnatal Depression Scale scores ≥9 were recruited at 12-24 weeks of gestation. The participants were randomly assigned to receive 1800 mg omega-3 fatty acids (containing 1206 mg eicosapentaenoic acid [EPA]) or placebo for 12 weeks. E2, omega-3 PUFAs, high-sensitivity C-reactive protein, interleukin-6, andadiponectin were measured at baseline and at the 12-week follow-up. Multivariable regression analyses were conducted to examine the association of the changes of E2 and omega-3 PUFAs with the changes in depressive symptoms and with the changes of inflammatory cytokines at follow-up by intervention group. RESULTS: Of the 108 participants in the trial, 100 (92.6%) completed the follow-up assessment including blood sampling. Multivariable regression analyses revealed that the increase of EPA and E2 was significantly associated with a decrease in depressive symptoms among the participants assigned to the omega-3 group, but not among those assigned to the placebo group. Neither E2 nor any PUFAs were associated with a change in inflammatory cytokines. CONCLUSION: Supplementation with EPA and increased levels of E2 during pregnancy might function together to alleviate antenatal depression through a mechanism other than anti-inflammation.
RCT Entities:
BACKGROUND:Omega-3 polyunsaturated fatty acids (PUFAs) reduce depressive symptoms through an anti-inflammatory effect, and injection of both omega-3 PUFAs and estradiol (E2) induces antidepressant-like effects in rats by regulating the expression of inflammatory cytokines. The aims of this study were to examine the association of increased E2 during pregnancy with depressive symptoms and with inflammatory cytokines in women who were and were not supplemented with omega-3 PUFAs. METHODS: Pregnant women with Edinburgh Postnatal Depression Scale scores ≥9 were recruited at 12-24 weeks of gestation. The participants were randomly assigned to receive 1800 mg omega-3 fatty acids (containing 1206 mg eicosapentaenoic acid [EPA]) or placebo for 12 weeks. E2, omega-3 PUFAs, high-sensitivity C-reactive protein, interleukin-6, and adiponectin were measured at baseline and at the 12-week follow-up. Multivariable regression analyses were conducted to examine the association of the changes of E2 and omega-3PUFAs with the changes in depressive symptoms and with the changes of inflammatory cytokines at follow-up by intervention group. RESULTS: Of the 108 participants in the trial, 100 (92.6%) completed the follow-up assessment including blood sampling. Multivariable regression analyses revealed that the increase of EPA and E2 was significantly associated with a decrease in depressive symptoms among the participants assigned to the omega-3 group, but not among those assigned to the placebo group. Neither E2 nor any PUFAs were associated with a change in inflammatory cytokines. CONCLUSION: Supplementation with EPA and increased levels of E2 during pregnancy might function together to alleviate antenatal depression through a mechanism other than anti-inflammation.