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Discuss research suggesting that maternal stress and depression affect foetal development.

Discuss research suggesting that maternal stress and depression affect foetal development.

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An essay for the 2012 Undergraduate Awards (International Programme) Competition by Katrin Hulme. Originally submitted for Child Health at Durham University, with lecturer Dr Nadja Reissland in the category of Psychology
An essay for the 2012 Undergraduate Awards (International Programme) Competition by Katrin Hulme. Originally submitted for Child Health at Durham University, with lecturer Dr Nadja Reissland in the category of Psychology

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Published by: Undergraduate Awards on Aug 31, 2012
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 Discuss research suggesting that maternal stress and depression affect foetal  development.
AbstractAs Barker (2001) describes in his study of 
foetal and infant origins of adult disease(specifically addressing the consequences of limited nutrient supply),
the foetus is known tobe affected by the external biological substances it is exposed to during the gestational period(such as nutrients, tobacco and alcohol) because the placenta and umbilical cord enable themto pass from mother to child, regardless of whether they are necessary or unfavourable for the
child’s development in the uterus. However, as Barker (2001) reports, it is not just the in
-uterine development that is affected. Future adult health is also thought to be determined by
‘programming’ of the baby’s biological and regulatory systems during gestation,
with faultyprogramming in response to adverse environmental circumstances contributing to healthproblems such as diabetes and coronary heart disease in later life.Recently, research additionally suggests that it is not only the biological substancesthe baby is exposed to which influence this programming process, but also maternalemotionality in response to the stressors present in her external environment that may impactth
e foetus’ development. These psychological variables, are, in comparison to the physical
substance variables mentioned above, very difficult to amend because people cannot altertheir feelings as they could their diet for example. They are, however, readily identifiablewith the mental healthcare infrastructure, which already exists to cater for the generalpopulation, able to be adapted and utilised for the care of pregnant women. Given thenegative effects that psychological variables reportedly have on
a foetus’ development (such
as decreased growth and birth weight) and the adverse implications for future health, it isvital that, if research does in fact indicate that negative maternal emotionality can affect the
child’s development
harmfully, the upmost should be done to minimise it.Thus, this essay aimed to critically analyse the existing research surrounding thistopic by conducting a review of the literature surrounding two emotional states that arefrequently addressed and well documented as occurring during pregnancy; stress anddepression, to ascertain whether defective foetal development could be a consequence of maternal psychological ill-being and additionally
investigate how the mother’s
state is able to affect the baby’s
2It must be noted that mood comorbidity is a problematic and confounding variablebecause stress and depression are sometimes discussed as separate emotional entities, butmore often addressed as interlinking psychological phenomena, along with anxiety, whichcannot (or have not) been individually defined. This inconsistency needs to be rectified,
maybe through utilising ‘emotional stress’ as an umbrella term. Furthermore, clarification
and consistency is also required with regard to the timing of the heightened emotional stressduring the pregnancy.Overall, research does tend to consistently report detrimental findings though.Maladaptive programming occurs in response to negative maternal emotionality dueneurotransmitters, specifically cortisol and catecholamines, underpinning psychologicalemotionality. Thus, neurological chemical imbalances and neural structural defects arise asconsequences of mothers reacting to emotional stressors, impacting negatively on foetaldevelopment and growth.EssayThe pre-natal period is one of rapid development for the foetus with organ systemmaturation and bodily growth being susceptible to changes in the sensitive uterineenvironment (Davis & Sandman, 2010). Sontag (1941) was one of the first to suggest that
women’s emotionality during pregnancy could affect this environment, thus affecting the
gestation and development of their unborn babies. As part of this emotionality, stress anddepression have been shown to be maternal affective states which affect foetal development.The literature tends to address these 2 states separately (Davis & Sandman, 2010; Field,2011), so I will do the same. Firstly, this essay will discuss research into the biologicalmechanism which enables maternal stress to affect the foetus, before investigating theknowledge gained from animal studies. The adverse effects on foetal growth will beacknowledged, before contemplating whether the timing of exposure is of importance.Secondly, research debating the affective pathway for depression will be addressed and someof the adverse effects of depression on the foetus will be introduced. Finally, this essay willhighlight the confounding problem of mood comorbidity on research findings, especiallywhen investigating maternal depression.Research studies have focused on one particular physiological pathway which allowsthe maternal emotional state to affect the foetus
’ development
; the glucorticoid pathway
3(Field, Diego & Hernandez-Reif, 2006). Glucocorticoids (primarily known as cortisol inhumans) are secreted in response to emotional stressors, a process controlled by thehypothalamic-pituitary-adrenal (HPA) axis, a stress-hormone regulation system (Engelmann,Landgraf & Wotjak, 2004). The corticotrophin-releasing hormone (CRH), which causescortisol secretion, is part of a positive feedback loop in pregnant mothers, with placentallevels of CRH
increasing in parallel with the mothers’ adrenal cortisol levels (Ellman et al.,
2008). This presence of placental CRH causes the foetal cortisol levels to increase becausethe CRH is able to diffuse through the placenta and, once there, stimulate foetal cortisolsecretion (Gitau et al., 2001). The existence of this pathway was illustrated by Gitau, Fisk andGlover (2004) who used intrauterine vein transfusions to demonstrate the association betweenelevated maternal and foetal cortisol levels, as well as to identify the placenta as the likelyregion which these hormones cross from the maternal to the foetal environment.Animal studies have been utilised to investigate the effects of maternal stress on foetaldevelopment, such as Barbazanges et al.
(1996) study which involved restraining orinjecting glucocorticoids into pregnant rats to induce stress. They found that the offspring hadfewer corticosoid receptors in their hippocampus (Moberg & Mench, 2001). Consequently
the brain’s ability to
modulate future glucocorticoid-induced stress responses was reduced(Yehuda & Mostofosky, 2006). These fin
dings suggest that the pregnant mother’s HPA axisresponse to stress results in ‘prenatal programming’ of the offspring’s brain and
neuroendocrine system (Matthews, 2000) and present an initial indication as to how maternalstress may affect foetal central nervous system development. However, because animalgestation periods do not match those of humans and neurological differences exist betweenspecies, the use of animal research in generalising findings to the human foetus isquestionable (Charil, 2010). An experiment by Clancy, Finlay, Darlington & Anand, (2007)has successfully paired gestational time points and neurological developmental stagesbetween rat and human embryos, which suggests certain comparisons can be made.Nevertheless,
research findings undoubtedly give a better indication of the effects of maternal stress on
foetus development.The majority of research in human foetuses tends to focus on the physicallymeasurable attributes of development, such as the significant correlations between maternalexposure to stress and foetal growth that have been identified (Mulder et al., 2002; Rondo etal., 2003). Once socio-demographic and distress variation was taken into account, it was

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