Adaptive and Maladaptive Aspects of Developmental Stress by Giovanni Laviola & Simone Macrì

Author:Giovanni Laviola & Simone Macrì
Language: eng
Format: epub
Publisher: Springer New York, New York, NY

6.4 Integration and Interpretation of Findings

The findings presented in this chapter highlight the potential effect of prenatal stress on various health outcomes, depending on the type of prenatal stress. We propose a psychobiological stress model that may be used to integrate and interpret these findings (Fig.6.1).

Fig.6.1Psychobiological stress model

Possible short-term effects of prenatal stress constitute birth outcomes (e.g., gestation length or birth weight) which in turn are known to be a risk factor for developing chronic diseases, such as cardiovascular diseases, hypertension, and diabetes (e.g., see review in Osmond and Barker 2000). Reviewing the literature revealed that various types of prenatal stress (all except for perceived stress and daily hassles 7) appear to be related to shortened gestation length or low birth weight. It is possible that this association is mediated by stress hormones. There is evidence that pCRH has regulating functions on gestation length, which is generally referred to as “placental clock” (McLean etal. 1995). Elevated pCRH during pregnancy may lead to the shortening of gestation length and may consequently increase the risk of preterm delivery, which in turn is often associated with low birth weight.

The majority of findings suggest that infants whose mothers experienced prenatal stress show augmented endocrine responses to a stress, e.g., increased cortisol levels when the HPA axis is challenged. Possible explanations for this pronounced HPA axis reactivity may be altered receptor sensitivity to glucocorticoids or impaired HPA axis feedback regulation. Some authors proposed that prenatal glucocorticoids may have a determining effect on the transcription of mineralocorticoid receptor (MR) and glucocorticoid receptor (GR) genes and thus on the receptor density in both brain and peripheral tissue, resulting in permanently altered tissue sensitivity to steroids (Welberg and Seckl 2001). While MRs appear to play a main part in the control of basal HPA axis activity, GRs are involved in the coordination of negative feedback regulation after stress. Thus, reduced GRs sensitivity may explain the augmented HPA axis reactivity in prenatally stressed infants (Cottrell and Seckl 2009).

We discussed the infants’ temperament and behavior as possible psychological outcomes of prenatal stress. The reviewed literature indicates that prenatal stress is associated with the infant’s distress (as indicated by startle reaction, fussiness) in response to novelty as well as behavioral problems (e.g., attention problems, aggressive/delinquent behavior, or anxiety/depression). These consequences of prenatal stress may be a result of prenatal programming. From an evolutionary point of view, prenatal programming prepares the unborn child for the expected environmental demands. Specifically, increased anxiety (precaution) or aggressive behavior may increase the survival changes in a stressful or dangerous environment. In accordance to this hypothesis, the reviewed studies suggest that prenatally stressed infants are more likely to show such behavior.

Prenatal stressors, particularly with high emotional value, such as traumas/major life events or maternal anxiety/depression during pregnancy, seem to have a negative impact on the infants’ mental or motor development. Specifically, children whose mothers experienced stress during pregnancy are more likely to show impairment in attention/concentration, verbal comprehension, reasoning, or memory performances, as well as difficulties in body control and gross and fine motor skills.

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