Investigating the impact of endocrine-disrupting compounds on antepartum mental health at the Nexus of genetic insights and maternal-fetal outcomes: A prospective study

IF 4.1 2区 医学 Q1 PSYCHIATRY General hospital psychiatry Pub Date : 2025-03-13 DOI:10.1016/j.genhosppsych.2025.03.009
S. Aishwarya , V.M. Vinodhini , P. Renuka , R. Arul Saravanan , M. Anuradha , T. Gomathi , V. Amuthavalli
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Abstract

Background

Antepartum depression arises from hormonal, environmental, and genetic factors. Endocrine-disrupting compounds (EDCs) disrupt the endocrine system, increasing vulnerability to depressive symptoms. Genetic variations, particularly in estrogen receptor (ER) pathways, are linked to peripartum depression, with EDCs exposure exacerbating these effects by further disrupting estrogen pathways. Additionally, EDCs exposure in antepartum women is associated with adverse maternal and fetal outcomes. Hence, study aims to evaluate the relationship between EDCs and genetic polymorphisms with antepartum depressive symptoms and assess the impact of EDCs and antepartum depressive symptoms on maternal and fetal outcomes.

Materials and methods

We conducted a prospective cohort study to evaluate depressive symptoms during pregnancy in 400 women between 28 and 40 weeks of gestation, utilizing the Edinburgh Postnatal Depression Scale (EPDS). Women with elevated EPDS scores and matched controls were assessed for urinary bisphenol A and methylparaben levels, along with ER1 gene polymorphism using Tetra-ARMS PCR. The cohort group was followed to document maternal-fetal outcomes, with statistical analyses performed using SPSS.

Results

Twenty-three percent of antepartum women exhibited depressive symptoms. A linear regression analysis indicated that a one-unit increase in log bisphenol A levels corresponded to a 1.1-point increase in EPDS-measured depressive symptom scores. ER1 polymorphisms (A/A and T/A genotypes) and the frequency of the A allele correlate with an increased risk of experiencing antepartum depressive symptoms. Elevated EPDS scores correlated with pregnancy-induced hypertension, anemia, hypothyroidism, and fetal distress. Notably, bisphenol A and methylparaben levels were higher in homozygous genotypes, with bisphenol A linked to maternal anemia, hypothyroidism, and fetal distress, while methylparaben was associated with maternal anemia and fetal distress.

Conclusion

Nearly a quarter of antepartum women displayed depressive symptoms, correlating with elevated endocrine disruptor levels. Higher bisphenol A and methylparaben levels were observed in individuals with mutant genotypes, indicating gene-environment interactions with antepartum depressive symptoms. The observed association of EDCs with maternal anemia, hypothyroidism, and fetal distress highlights the possible effect of EDC on maternal and fetal health.
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背景产后抑郁症源于荷尔蒙、环境和遗传因素。干扰内分泌的化合物(EDCs)会扰乱内分泌系统,增加抑郁症状的易感性。遗传变异,尤其是雌激素受体(ER)通路的遗传变异与围产期抑郁症有关,而暴露于 EDCs 会进一步干扰雌激素通路,从而加剧这些影响。此外,产前妇女接触 EDCs 与孕产妇和胎儿的不良结局有关。因此,本研究旨在评估 EDCs 和遗传多态性与产前抑郁症状之间的关系,并评估 EDCs 和产前抑郁症状对孕产妇和胎儿预后的影响。材料与方法我们利用爱丁堡产后抑郁量表(EPDS)对 400 名妊娠 28 周至 40 周的妇女进行了前瞻性队列研究,以评估其孕期抑郁症状。对 EPDS 评分升高的妇女和匹配的对照组进行了尿液中双酚 A 和对羟基苯甲酸甲酯水平的评估,并使用 Tetra-ARMS PCR 对 ER1 基因多态性进行了评估。结果23%的产前妇女表现出抑郁症状。线性回归分析表明,双酚 A 对数水平每增加一个单位,EPDS 测量的抑郁症状评分就会增加 1.1 分。ER1多态性(A/A和T/A基因型)和A等位基因的频率与出现产前抑郁症状的风险增加有关。EPDS 分数升高与妊娠诱发的高血压、贫血、甲状腺功能减退和胎儿窘迫有关。值得注意的是,同型基因型中的双酚 A 和苯甲酸甲酯水平较高,其中双酚 A 与孕产妇贫血、甲状腺功能减退和胎儿窘迫有关,而苯甲酸甲酯则与孕产妇贫血和胎儿窘迫有关。在突变基因型的个体中观察到双酚 A 和苯甲酸甲酯水平较高,这表明基因与环境之间存在着产前抑郁症状的相互作用。观察到的 EDC 与孕产妇贫血、甲状腺机能减退和胎儿窘迫之间的关联,凸显了 EDC 对孕产妇和胎儿健康可能产生的影响。
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来源期刊
General hospital psychiatry
General hospital psychiatry 医学-精神病学
CiteScore
9.60
自引率
2.90%
发文量
125
审稿时长
20 days
期刊介绍: General Hospital Psychiatry explores the many linkages among psychiatry, medicine, and primary care. In emphasizing a biopsychosocial approach to illness and health, the journal provides a forum for professionals with clinical, academic, and research interests in psychiatry''s role in the mainstream of medicine.
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