Prenatal Major Depressive Disorder, Placenta Glucocorticoid and Serotonergic Signaling, and Infant Cortisol Response

被引:56
作者
Stroud, Laura R. [1 ,2 ,3 ]
Papandonatos, George D. [4 ]
Parade, Stephanie H. [1 ,5 ]
Salisbury, Amy L. [1 ,6 ,7 ]
Phipps, Maureen G. [7 ,8 ]
Lester, Barry M. [1 ,6 ,7 ]
Padbury, James F. [6 ,7 ]
Marsit, Carmen J. [9 ]
机构
[1] Brown Univ, Dept Psychiat & Human Behav, Warren Alpert Med Sch, Providence, RI 02912 USA
[2] Miriam Hosp, Ctr Behav Med, Providence, RI 02906 USA
[3] Miriam Hosp, Ctr Prevent Med, Providence, RI 02906 USA
[4] Brown Univ, Sch Publ Hlth, Dept Biostat, Providence, RI 02912 USA
[5] Bradley Hasbro Childrens Res Ctr, Providence, RI USA
[6] Brown Univ, Dept Pediat, Warren Alpert Med Sch, Providence, RI 02912 USA
[7] Women & Infants Hosp Rhode Isl, Providence, RI 02908 USA
[8] Brown Univ, Warren Alpert Med Sch, Dept Obstet & Gynecol, Providence, RI 02912 USA
[9] Emory Univ, Rollins Sch Publ Hlth, Dept Environm Hlth, Atlanta, GA 30322 USA
来源
PSYCHOSOMATIC MEDICINE | 2016年 / 78卷 / 09期
基金
美国国家卫生研究院;
关键词
depression; cortisol; HSD11B2; pregnancy; serotonin; infant; SLC6A4; stress; MATERNAL DEPRESSION; EPIGENETIC REGULATION; GENE-EXPRESSION; SEX-DIFFERENCES; AXIS FUNCTION; FETAL; STRESS; PREGNANCY; EXPOSURE; SYMPTOMS;
D O I
10.1097/PSY.0000000000000410
中图分类号
R749 [精神病学];
学科分类号
100205 ;
摘要
Objectives: Extending prior studies of prenatal adversity and depressive symptoms, we tested associations between maternal prenatal major depressive disorder (MDD) and infant cortisol regulation. Based on prior findings by our group, we also tested placenta glucocorticoid (HSD11B2 methylation) and serotonin (SLC6A4 gene expression) signaling as moderators of links between prenatal MDD and infant cortisol. Methods: Participants were 153 mother-infant pairs from a low-income, diverse sample (M [SD] age = 26[6] years). Repeated structured diagnostic interviews were used to identify mothers with (a) prenatal MDD, (b) preconception-only MDD, and (c) controls. Placenta samples were assayed for HSD11B2 methylation and SLC6A4 gene expression. Infant salivary cortisol response to a neurobehavioral examination was assessed at 1 month. Results: Daughters of prenatal MDD mothers had 51% higher baseline (ratio = 1.51; 95% confidence interval [CI] = 1.01-2.27; p = .045) and 64% higher stress responsive cortisol (ratio = 1.64; 95% CI = 1.05-2.56; p = .03) than daughters of controls and 75% higher stress-responsive cortisol (ratio = 1.75; 95% CI = 1.04-2.94; p = .04) than daughters of preconception-only MDD mothers. HSD11B2 methylation moderated links between prenatal MDD and baseline cortisol (p = .02), with 1% methylation decreases associated with 9% increased baseline cortisol in infants of prenatalMDD mothers (ratio = 1.09; 95% CI = 1.01-1.16). SLC6A4 expression moderated links between prenatal MDD and cortisol response among boys alone (p = .007), with 10-fold increases in expression associated with threefold increases in stress-responsive cortisol (ratio = 2.87; 95% CI = 1.39-5.93) in sons of control mothers. Conclusions: Results highlight specificity of associations between prenatal versus preconception MDD and cortisol regulation and the importance and complexity of placenta glucocorticoid and serotonergic pathways underlying the intergenerational transmission of risk from maternal adversity.
引用
收藏
页码:979 / 990
页数:12
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