اضطراب مادر صفت، ناراحتی عاطفی و کورتیزول بزاق در دوران بارداری
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|33354||2010||7 صفحه PDF||سفارش دهید||6596 کلمه|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Biological Psychology, Volume 83, Issue 3, March 2010, Pages 169–175
Animal models suggest that stress-induced hormonal changes in the mother during pregnancy lead to enduring changes in the fetus and empirical links between prenatal maternal stress and negative child development have been discerned repeatedly in human studies. But the role of heritable personality traits has received little attention in the latter work. The goal of the current study was to investigate the relationship between maternal personality, psychological measures of maternal distress and maternal salivary cortisol during pregnancy. Maternal reports of personality (16 PF) and stress-related psychological measures (depression, pregnancy-related anxiety, perceived stress, negative life events) as well as salivary cortisol samples of 66 healthy pregnant women were collected in early and late pregnancy. Maternal trait anxiety proved related to all stress-related psychological measures and high anxiety predicted low baseline cortisol awakening levels in early pregnancy. Maternal trait anxiety is related to both psychological and biological stress measures during pregnancy.
A growing body of evidence links maternal emotional distress during pregnancy with negative child functioning in the behavioral, emotional, and cognitive domain (for review of the literature see: Huizink et al., 2004, Ruiz and Avant, 2005, Van den Bergh et al., 2005b and Rice et al., 2007). Prenatal programming of fetal stress reactivity is the most often suggested mechanism responsible for this association. More specifically, the fetal programming hypothesis suggests that elevated levels of maternal cortisol in response to psychological or physical stressors produce permanent alterations of the hypothalamic–pituitary–adrenal (HPA) axis of the developing fetus (Barker, 1998 and Egliston et al., 2007). Consequently, such elevated stress reactivity – an individual physiological trait expected to extend across childhood into adult life (Kofman, 2002, Huizink et al., 2004 and Weinstock, 2005) – contributes to negative child development (Van den Bergh et al., 2005b). Because experimental studies with animals prove generally consistent with such prenatal programming, it is assumed that the same mechanisms operate in humans. While animal studies allow for the experimental induction of stress across randomized groups and thus afford precise control of stress exposure and other important variables, human studies on prenatal stress effects are generally limited by being observational. Due to this methodological constraint, the discerned relationship between prenatal stress and child development in human studies could be an artifact of enduring maternal personality traits, reflective of underlying heritable mechanisms given the highly heritable nature of personality (Jang et al., 1996), influencing not only maternal reports of stress during pregnancy but also the child's postnatal functioning by means of shared genes. Thus, enduring personality characteristics of mothers may account for the putative causal – and compromising – influence of prenatal stress on children's development. It is not difficult to imagine, in fact, that personality traits specifically related to stress reactivity and sensitivity (e.g., neuroticism, trait anxiety) may influence a pregnant woman's reporting and/or experiencing of prenatal stress (e.g., cortisol reactivity). If this is so, it would compromise any causal interpretation of associations linking prenatal stress with postnatal child well-being. Thus, the purpose of the research reported herein is to explore links between stress-related personality traits of pregnant women and measures of their prenatal stress, including cortisol levels. It is predicted that neuroticism/trait anxiety would be reflected in both psychological and physiological measures of prenatal stress. Neuroticism, reflecting proclivities to experience negative affect (Costa and McCrae, 1992), to arouse quickly when stimulated and inhibit slowly, and to appraise events as stressful (Widiger et al., 1984), is one personality trait often associated with response to stress (Costa and McCrae, 1992). Behavior-genetic studies reveal it to be 40–50% heritable (Plomin et al., 1994, Jang et al., 1996 and Eaves et al., 1999). Many studies chronicle links between neuroticism and psychological distress and emotional disorders (Bolger and Schilling, 1991, Kendler et al., 1993, Engelhard et al., 2006 and Hettema et al., 2006). Empirical evidence also chronicles links between neuroticism and biological stress response in humans, such that high neuroticism is associated with dysregulated autonomic nervous system functioning (e.g., lower heart rate variability, see Riese et al., 2006) and altered HPA axis functioning. Highly neurotic individuals manifest a blunted cortisol response when exposed to stress (Oswald et al., 2006), a higher range of dose-dependent cortisol response after the application of naloxone, an opioid receptor antagonist (Mangold and Wand, 2006), and enhanced early morning cortisol levels 30 min after awakening (Portella et al., 2005). As it turns out, neuroticism also proves related to exposure to stressful situations, with individuals scoring high on neuroticism experiencing more stressful life events than do those scoring low (Bolger and Zuckerman, 1995 and Kendler et al., 2003). Considered together, findings such as those just summarized raise the very real possibility that maternal personality traits contribute to the phenomenological and biological experience of stress during pregnancy. Indeed, it seems eminently plausible that maternal personality may influence (1) self-reported psychological stress measures (e.g., depression, anxiety), (2) biological measures of stress (e.g., cortisol levels), and even (3) exposure and reaction to stressful situations and experiences (e.g., negative life events, natural disasters). Surprisingly, personality measures, apart from a study by Mohler et al. (2006), have generally not been included in research on prenatal programming via prenatal maternal distress, though several well designed studies have controlled for postnatal anxiety and depression, two fundamental facets of neuroticism, in attempt to distinguish emotional stress experienced during fetal life and postnatal exposure (e.g., Huizink et al., 2002, O’Connor et al., 2003, Davis et al., 2004 and Van den Bergh et al., 2005a). What such research designs cannot due, however, is disentangle putative effects of prenatal stress from maternal personality characteristics such as neuroticism which may influence both the predictors and outcomes of prenatal programming studies. Given this background, the main objective of the work reported herein was to investigate the relationship between maternal personality, psychological measures of distress, and maternal salivary cortisol, all measured during pregnancy. To this end, we analyzed data from a prospective longitudinal study (see Rieger et al., 2004 and Wurmser et al., 2006) in which personality, several measures of psychological distress, and the cortisol awakening response were assessed in healthy women both in early and late pregnancy. This work is thus conceptualized as a first step in exploring, eventually, the role of personality, measured prenatally, in accounting for effects of prenatal stress on child well being. Based on the preceding analysis, we expected maternal personality – specifically trait anxiety (i.e., neuroticism) – to be positively related to maternal self-report measures commonly used in the research of prenatal stress effects (perceived stress, depression, pregnancy anxiety, and negative life events) and with maternal cortisol levels of the cortisol awakening response during pregnancy.
نتیجه گیری انگلیسی
Despite the study's limitations the results of the present study suggest that subjective measures of psychological distress and cortisol levels during pregnancy are related to maternal trait anxiety scores. Maternal prenatal stress has been defined and assessed differently across studies on the effects of maternal stress on child development with measures used ranging from single or multiple subjective psychometric state and/or trait measures to biological correlates of stress (e.g., salivary cortisol levels). While a small number of studies were able to use exposure to a natural disaster as a more objective measure of stress (Glynn et al., 2001, Laplante et al., 2004 and Huizink et al., 2008), and a few studies assessed maternal levels of salivary cortisol (Huizink et al., 2002, Buitelaar et al., 2003, de Weerth et al., 2003 and Davis et al., 2007), most other studies relied on self-reported psychological measures (e.g., state and trait anxiety, pregnancy-related anxiety, depression, perceived stress, stressful life events, and daily hassles). Based on the significant correlations between maternal trait anxiety and self-reported distress and the implied association between maternal trait anxiety and cortisol levels reported in this study, the question arises as to what extent measures of stress generally used in studies on prenatal stress effects are able to capture stress responses during pregnancy that are independent from mothers inherent disposition to respond more or less to stressful experiences. This distinction between state and trait is of crucial importance considering the significant heritable compound of neuroticism (Plomin et al., 1994, Jang et al., 1996 and Eaves et al., 1999). Given that women scoring high on trait anxiety/neuroticism – as a function of their genetic make-up – are more likely to give birth to children that tend to exhibit similar personality traits, associations between mothers’ reported stress exposure during pregnancy and offspring's stress reactivity may be confounded by shared genes. However, maternal trait anxiety/neuroticism may have a number of effects over and above genetics: (1) the enhanced stress reactivity of women with high trait anxiety/neuroticism may amplify the biological mechanisms of fetal programming (e.g., higher cortisol levels), (2) the greater number of stressful life events individuals with high trait anxiety/neuroticism typically experience may affect the child both pre- and postnatally, and (3) maternal personality may define a large amount of the postnatal environment's quality (e.g., parenting, marital quality). In conclusion, the present study suggests that maternal trait anxiety is reflected in self-reported maternal stress measures and in maternal cortisol levels and that it predicts exposure to negative life events during pregnancy. It may, therefore, be advisable to include measures of maternal trait anxiety/neuroticism in studies investigating effects of maternal stress during pregnancy on child development.