Early adversity and psychiatric symptoms – a prospective study on Ethiopian mothers and their children

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Abstract

Background

Maternal exposure to adversity during the perinatal period has been associated with increased susceptibility for psychiatric symptoms in the offspring. The aim of this study was to investigate a possible developmental effect of maternal perinatal stressors on emotional and behavioural symptoms in the offspring in a developing country.

Methods

We followed an Ethiopian birth cohort ( N = 358), assessing intimate partner violence (IPV) and maternal psychiatric symptoms during the perinatal period and at follow-up 10 years later, as a proxy for adversity, and maternal ratings on the Child Behavior Checklist (CBCL) 10 years later as the outcome.

Results

Among the women, exposure to IPV was common (60.6%) during the perinatal period and predicted IPV (29.9% of the mothers) at follow-up ( ρ = 0.132; p = 0.012). There was also an association between maternal psychiatric symptoms at the two time points ( ρ = 0.136; p = 0.010) and between maternal symptoms and IPV. Current maternal symptoms of anxiety and depression ( β = 0.057; p < 0.001), but not during the perinatal period, were associated with child CBCL-scores.

Conclusion

Our findings do not support the hypothesis that early adversity increase susceptibility for psychiatric symptoms. However, the findings emphasize the public health problem of IPV in this population, adding to the women’s mental health problem.

Related collections

Most cited references 20

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Prevalence and determinants of common perinatal mental disorders in women in low- and lower-middle-income countries: a systematic review.

Jane Fisher, Meena Cabral de Mello, Vikram Patel … (2012)

To review the evidence about the prevalence and determinants of non-psychotic common perinatal mental disorders (CPMDs) in World Bank categorized low- and lower-middle-income countries. Major databases were searched systematically for English-language publications on the prevalence of non-psychotic CPMDs and on their risk factors and determinants. All study designs were included. Thirteen papers covering 17 low- and lower-middle-income countries provided findings for pregnant women, and 34, for women who had just given birth. Data on disorders in the antenatal period were available for 9 (8%) countries, and on disorders in the postnatal period, for 17 (15%). Weighted mean prevalence was 15.6% (95% confidence interval, CI: 15.4-15.9) antenatally and 19.8% (19.5-20.0) postnatally. Risk factors were: socioeconomic disadvantage (odds ratio [OR] range: 2.1-13.2); unintended pregnancy (1.6-8.8); being younger (2.1-5.4); being unmarried (3.4-5.8); lacking intimate partner empathy and support (2.0-9.4); having hostile in-laws (2.1-4.4); experiencing intimate partner violence (2.11-6.75); having insufficient emotional and practical support (2.8-6.1); in some settings, giving birth to a female (1.8-2.6), and having a history of mental health problems (5.1-5.6). Protective factors were: having more education (relative risk: 0.5; P = 0.03); having a permanent job (OR: 0.64; 95% CI: 0.4-1.0); being of the ethnic majority (OR: 0.2; 95% CI: 0.1-0.8) and having a kind, trustworthy intimate partner (OR: 0.52; 95% CI: 0.3-0.9). CPMDs are more prevalent in low- and lower-middle-income countries, particularly among poorer women with gender-based risks or a psychiatric history.

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Fetal Origins of Mental Health: The Developmental Origins of Health and Disease Hypothesis.

Kieran O'Donnell, Michael Meaney (2017)

The quality of fetal growth and development predicts the risk for a range of noncommunicable, chronic illnesses. These observations form the basis of the "developmental origins of health and disease" hypothesis, which suggests that the intrauterine signals that compromise fetal growth also act to "program" tissue differentiation in a manner that predisposes to later illness. Fetal growth also predicts the risk for later psychopathology. These findings parallel studies showing that antenatal maternal emotional well-being likewise predicts the risk for later psychopathology. Taken together, these findings form the basis for integrative models of fetal neurodevelopment, which propose that antenatal maternal adversity operates through the biological pathways associated with fetal growth to program neurodevelopment. The authors review the literature and find little support for such integrated models. Maternal anxiety, depression, and stress all influence neurodevelopment but show modest, weak, or no associations with known stress mediators (e.g., glucocorticoids) or with fetal growth. Rather, compromised fetal development appears to establish a "meta-plastic" state that increases sensitivity to postnatal influences. There also remain serious concerns that observational studies associating either fetal growth or maternal mental health with neurodevelopmental outcomes fail to account for underlying genetic factors. Finally, while the observed relation between fetal growth and adult health has garnered considerable attention, the clinical relevance of these associations remains to be determined. There are both considerable promise and important challenges for future studies of the fetal origins of mental health.

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Prenatal stress and brain development.

Arnaud Charil, David P Laplante, Cathy Vaillancourt … (2010)

Prenatal stress (PS) has been linked to abnormal cognitive, behavioral and psychosocial outcomes in both animals and humans. Animal studies have clearly demonstrated PS effects on the offspring's brain, however, while it has been speculated that PS most likely affects the brains of exposed human fetuses as well, no study has to date examined this possibility prospectively using an independent stressor (i.e., a stressful event that the pregnant woman has no control over, such as a natural disaster). The aim of this review is to summarize the existing animal literature by focusing on specific brain regions that have been shown to be affected by PS both macroscopically and microscopically. These regions include the hippocampus, amygdala, corpus callosum, anterior commissure, cerebral cortex, cerebellum and hypothalamus. We first discuss the mechanisms by which the effects of PS might occur. In particular, we show that maternal and fetal hypothalamic-pituitary-adrenal (HPA) axes, and the placenta, are the most likely candidates for these mechanisms. We see that, although animal studies have obvious advantages over human studies, the integration of findings in animals and the transfer of these findings to human populations remains a complex issue. Finally, we show how it is possible to circumvent these challenges by studying the effects of PS on brain development directly in humans, by taking advantage of natural or man-made disasters and assessing the impact and consequences of such stressful events on pregnant women and their offspring prospectively. Copyright © 2010 Elsevier B.V. All rights reserved.

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Author and article information

Contributors

Johan Isaksson:

ORCID: http://orcid.org/0000-0003-1033-2618

+46-186112540 , johan.isaksson@neuro.uu.se

Negussie Deyessa: negdaysun@gmail.com

Yemane Berhane: yemaneberhane@gmail.com

Ulf Högberg: ulf.hogberg@kbh.uu.se

Journal

Journal ID (nlm-ta): BMC Psychiatry

Journal ID (iso-abbrev): BMC Psychiatry

Title: BMC Psychiatry

Publisher: BioMed Central (London )

ISSN (Electronic): 1471-244X

Publication date (Electronic): 11 October 2017

Publication date PMC-release: 11 October 2017

Publication date Collection: 2017

Volume: 17

Electronic Location Identifier: 344

Affiliations

[1 ]ISNI 0000 0004 1936 9457, GRID grid.8993.b, Department of Neuroscience, Child and Adolescent Psychiatry Unit, , Uppsala University, ; Uppsala, Sweden

[2 ]ISNI 0000 0004 1937 0626, GRID grid.4714.6, Department of Women’s and Children’s Health, Paediatric Neuropsychiatry Unit, , Centre for Neurodevelopmental Disorders at Karolinska Institutet (KIND), Karolinska Institutet, ; Stockholm, Sweden

[3 ]ISNI 0000 0001 1250 5688, GRID grid.7123.7, Department of Preventive Medicine, School of Public Health, , Addis Ababa University, ; Addis Ababa, Ethiopia

[4 ]GRID grid.458355.a, Addis Continental Institute of Public Health, ; Addis Ababa, Ethiopia

[5 ]ISNI 0000 0004 1936 9457, GRID grid.8993.b, Department of Women’s and children’s health, , Uppsala University, ; Uppsala, Sweden

Author information

Johan Isaksson http://orcid.org/0000-0003-1033-2618

Article

Publisher ID: 1500

DOI: 10.1186/s12888-017-1500-2

PMC ID: 5637326

PubMed ID: 29020947

SO-VID: 3d62a44c-a86b-42e5-93e3-1587dce74e11

License:

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.