Title: The effect of maternal sensitivity on the intergenerational transmission of stress J. R. Rosetti
s1015117
Master Thesis Clinical Psychology Supervisor: M. S. Tollenaar
Institute of Psychology Universiteit Leiden 1-7-2017
2 Abstract
Maternal prenatal stress has been found to be a risk factor in offspring for adverse psychological, cognitive, and physical health outcomes, including higher hypothalamic-pituitary-adrenal(HPA)-axis activity, which can be indicative of a dysfunctional stress system. This has been referred to as intergenerational transmission of stress. Sensitive parenting can possibly serve as a buffer against the negative effects of the intergenerational transmission of stress. In this study, 94 mother-child pairs were followed from the 37th week of gestation to 6 years postpartum to examine whether it is possible to predict child cortisol reactivity (as an indicator of HPA-axis sensitivity) from prenatal stress, and if this link is moderated by maternal sensitivity. Prenatal stress was assessed with self-report measures of prenatal stress (Pregnancy Related Anxiety Questionnaire, State-Trait Anxiety Inventory) in conjunction with maternal prenatal cortisol. Child cortisol reactivity was assessed with the CREST protocol (Children’s Reactions to Evaluation Stress Test). Maternal sensitivity was observed 30 months postpartum and scored with the Erickson scales. Maternal prenatal anxiety
predicted the child cortisol reactivity in a positive trend, showing an association between a higher prenatal STAI score and higher child cortisol reactivity. Prenatal maternal cortisol predicted the child cortisol reactivity but, contrary to expectations, did so in a negative trend. Moderation was not significantly indicated, and transmission was not apparent when
considering concurrent maternal stress. Concurrent stress however, is not a probable mediator, but may rather be indicative of a related, underlying trait that influences the intergenerational transmission of stress.
3 Table of contents
Introduction ... 4
Stress ... 4
Intergenerational Transmission of Stress ... 5
Stress and Maternal Sensitivity ... 6
Method ... 6 Participants ... 6 Measures ... 7 Statistical Analysis ... 9 Results ... 9 Main analysis ... 10
Concurrent maternal stress ... 11
Discussion ... 12
4 The effect of maternal sensitivity on the intergenerational transmission of stress
Prenatal stress and its effects on mental and physical health in the offspring are of growing interest in both clinical and research settings (for reviews, see Glover, 2011; Lange, 2011; Weinstock, 2008).
Initially, studies were mainly focused on the effects of prenatal stress on pregnancy and fetal development, with birth outcomes being of main interest. Concerning the way prenatal stress may impact fetal development, many studies evaluated the effect of reported stress on low birthweight, and premature delivery. These two factors are some of the most frequent causes of perinatal mortality (Creasy, 1994), and are correlated with an increased frequency of adverse neurodevelopmental outcomes, such as decreased fetal brain growth and malformations in the cranial-neural crest (DiPietro, 2002). More recently, other long-term effects of prenatal stress on the child’s development have been examined. Maternal prenatal stress has been found to be a risk factor in offspring for other adverse effects, such as psychopathology, and abnormal emotional, and cognitive development (Graignic-Philippe, Dayan, Chokron, Jacquet, & Tordjman, 2014). The process through which this risk factor is conferred between generations has been referred to as the intergenerational transmission of stress.
Stress
When exposed to a stressor, organisms will express, and continue to express, a bio-behavioral response, for the duration of the stressor. To prepare the body for the flight-or-fight response, pupils dilate to allow more light through, muscles receive increased blood flow, and non-essential bodily functions are temporarily deactivated, among others (Yehuda, 2002). Cortisol (among other hormones), released by the hypothalamic-pituitary-adrenal-axis (HPA-axis) is essential for this response. Removal of the stressor results in a subsequent decrease of cortisol, as the body tries to restore homeostasis, returning to baseline functioning. Having the stress response activated for short periods of time does not result in long-lasting changes to the functioning of the HPA-axis, but more chronic stress (frequent activation) can exert effects which lead to a long lasting change. Prolonged, and frequent, exposure to stress can result in a dysregulation of the HPA-axis, making it more sensitive to future stressors, and subsequently leading to it being chronically activated, which may lead to higher baseline levels of cortisol, and higher levels in response to stress (McEwen, 2006). There is reason to believe this effect can be transferred from mother to child.
5 Intergenerational Transmission of Stress
Studies have demonstrated that the offspring of extremely stressed or traumatized parents are at higher risk for negative physical and psychological outcomes (Barker, 1998; Yehuda, Halligan, & Bierer, 2001). Several studies demonstrated this in instances where stress exposure occurred during pregnancy. For example, women who developed PTSD as a result of exposure to trauma during pregnancy – e. g. being present in The World Trade Centre on 9/11 - gave birth to offspring with higher indicated risk of developing Post Traumatic Stress Disorder (PTSD) (Yehuda et al, 2005). The Dutch Famine study (Barker, 1990, 1998) and others (Franklin et al., 2010; Gapp et al., 2014) have demonstrated that parental stress may be transmitted via the gestational uterine environment, early postnatal care, and gametes (Yehuda et al, 2005), thereby impacting the development of the offspring.
There have been some instances in which the parental stress even predated conception. For example, the adult offspring of Holocaust survivors were found to be more likely to develop various disorders such as depression, PTSD, and anxiety disorders (Yehuda, Bell, Bierer, &Schmeidler, 2008), even though World War II had already ended before the offspring were born.
Barker (1990, 1998) examined the offspring of women who suffered starvation during the Dutch famines. The author posited the then relatively novel notion that a change in offspring may be due to a biological change in the parent (due to stress or trauma). More recently, several studies (O'Connor et al, 2005; O'Connor, Bergman, Sarkar, & Glover, 2013; Gutteling, De Weerth, & Buitelaar, 2004; Gutteling, De Weerth, & Buitelaar, 2005) measured maternal prenatal stress and subsequent offspring basal HPA-axis activity – generally through the measurement of the concentration of cortisol – and found a positive association, meaning that higher levels of maternal prenatal stress are associated with a higher level of offspring basal HPA-axis activity, even after controlling for concurrent stress. Gitau, Cameron, Fisk, & Glover (1998) found cortisol to be able to access the gestating fetus, and even gametes. Later studies (e.g. Glover, 2011; Lange, 2011) generally posit that although the exact mechanisms involved in the intergenerational transmission of stress are still unknown, and likely to be numerous and complex, cortisol makes an appealing candidate for the aforementioned reason. Furthermore, cortisol affects gene transcription and could potentially alter the offspring epigenome, which in turn can affect brain development and the HPA-axis (Stahn, Lowenberg, Hommes, & Buttgereit, 2007). Given the negative effects of prenatal stress on the offspring (Beijers, Jansen, Riksen-Walraven, & de Weerth, 2010), the development, and
6 implementation of adequate interventions after maternal exposure to stress is important to mitigate the impact on offspring health.
Stress and Maternal Sensitivity
In line with the effects of prenatal stress, early life stress appears to lead to negative health outcomes in adulthood (Essex et al., 2011), such as atypical diurnal cortisol regulation; however, quality parenting (e.g. maternal sensitivity) may buffer this effect (Miller, Brody, Yu, & Chen, 2014). Recently, Farrell, Simpson, Carlson, Englund, and Sung (2016)
conducted a longitudinal study on the buffering effect of maternal sensitivity on negative health outcomes in adulthood, in light of early life stress in offspring. They found that
experiencing lower maternal sensitivity and higher stress resulted in negative health outcomes in adulthood. However, individuals who experienced higher stress, and had more sensitive mothers had equally positive health outcomes compared to those with a low-stress childhood and sensitive mothers. The authors suggest that the potential negative effect of early life stress on health outcome was fully buffered by maternal sensitivity. This finding is promising, given that it could lead to the development of interventions.
Although Farrell et al. (2016) focused on early life stress, the question now arises if sensitive parenting could possibly buffer the negative effects of prenatal stress on offspring health outcomes as well. The current study investigates this question. As described above, the hypothesis would be that the link between maternal prenatal stress and the offspring stress response is moderated by maternal sensitivity. In line with Farrell et al. (2016), it is expected that mothers with higher levels of prenatal stress would have given birth to offspring with greater cortisol reactivity, but that this intergenerational transmission of stress would be buffered if maternal sensitivity is high. Current findings could provide a stronger basis for the practical implementation of sensitivity interventions that can be indicated before childbirth in highly stressed mothers.
Method
Participants
The participants in this study were originally recruited as part of the BIBO (Basale Invloeden op de Baby Ontwikkeling; or in English: Basal Influences on Baby Development) study: an ongoing longitudinal study that follows 193 mothers and their children from pregnancy through their first years of life (Beijers, Jansen, Riksen-Walraven, & de Weerth, 2011; Tollenaar, Beijers, Jansen, Riksen-Walraven. & de Weerth, 2011). Inclusion criteria were: an
7 uncomplicated, singleton pregnancy, a clear understanding of the Dutch language, no drug use and no current physical or mental health problems, reflecting a healthy, non-clinical
population. Participants were healthy pregnant women living in the Netherlands, and were recruited with the cooperation of midwife clinics in the cities of Nijmegen, Arnhem and surrounding areas. At this moment, the BIBO study has delivered a wealth of information on the psychobiological development of children till age 8. The study is unique because of its start in pregnancy and the intensive multi-disciplinary assessments in the first years of life, including, but not limited to: mother-infant attachment, maternal social support, parenting stress, cortisol rhythms and reactivity in mothers and children, and maternal sensitivity. The study was approved by the Radboud University, Nijmegen, ethical committee for behavioral sciences and written informed consent was obtained from each participant at the time of enrolment and during subsequent sessions for their children.
Measures
For this study, the relevant variables are split into three prenatal stress measures, one child outcome measure, one moderator, and confounders. The prenatal stress measures comprise pregnancy-related anxiety, maternal anxiety, and maternal circadian cortisol; all measured in the 37th week of pregnancy. Infant cortisol reactivity functions as the child outcome measure; measured when the child was 6 years old. Maternal sensitivity is used as the moderator (measured when the child was two and a half years of age), and confounders comprise relevant demographics (sex, birth weight, maternal education level, smoking during
pregnancy, alcohol use during pregnancy, maternal age) and also concurrent maternal stress. Pregnancy-related anxiety. Pregnancy-related anxiety was measured using the abridged version of the Pregnancy Related Anxiety Questionnaire (PRAQ-R). Originally developed by Van den Bergh (1990), the abridged version consists of 34 items relating to pregnancy-related anxiety, and follows a three-factor model with the following three scales: fear of giving birth (PRAQ1) (Cronbach’s alpha between 0.79 and 0.83), fear of bearing a physically or mentally handicapped child (PRAQ2) (Cronbach’s alpha between 0.87 and 0.88), and concern about one’s appearance (Cronbach’s alpha between 0.78 and 0.83) (Huizink, Mulders, Robles de Medina, Visser, & Buitelaar, 2004). The individual items can be
answered with five different answers ranging from never true to always true. A higher score represents a higher level of pregnancy-related anxiety. The PRAQ-R was administered when the mother was 37 weeks pregnant. Scale 1 and 2 are measured.
8 Maternal Anxiety. Maternal anxiety was measured using the State-Trait Anxiety Inventory (STAI). The STAI differentiates between state anxiety and trait anxiety; the former being seen as a more temporary condition, and the latter being seen as a more permanent condition (Van der Ploeg, Defares, & Spielberger, 1981; Spielberger, 1983). The
questionnaire consists of 20 items, scored from 1 to 4, with higher numbers corresponding with higher agreement. The STAI has been validated (Cronbach alpha between 0.90 and 0.96) for use during pregnancy (Grant et al., 2008). The STAI was administered when the mother was 37 weeks pregnant, and when the child was 6 years old (i.e. concurrent anxiety).
Maternal circadian cortisol. At the 37th week of pregnancy, the mothers provided
salivary samples, in order to determine cortisol concentrations. Sampling took place over two consecutive days at awakening, 30 minutes after waking, 12:00, 16:00, and 21:00 hours. Subjects were instructed to refrain from brushing their teeth or eating 30 minutes prior to providing a sample, and to fill in a form recording waking times, exact sampling times, and eating times. Evening cortisol values are used in the analyses.
Maternal Sensitivity. Maternal sensitivity was measured by observation of play interaction between mother and child, and subsequently scored using the Erickson scales (Erickson, Sroufe, & Egeland, 1985). Maternal sensitivity was measured when the child was two and a half years of age. Mother-child interactions consisted of 12 minutes of semi-structured play with a set of toys that were somewhat difficult or challenging for the child or were aimed at eliciting positive interaction (every 3 or 4 minutes, toys were changed). Interrater reliability ranged from yielded Kappa values between .75 and .91.
Infant cortisol reactivity. Infant cortisol reactivity was measured at age 6 with six salivary samples taken from the children before, during, and following a paradigm developed by De Weerth, Zijlmans, Mack, and Beijers (2013) dubbed the Children’s Reactions to Evaluation Stress Test (CREST). The CREST consists of three tasks that children perform in front of a judge. The tasks are rigged so that the child partially fails. The goal of the paradigm is to elicit a stress response as the child anticipates to be evaluated poorly based on failed performance. The salivary samples are used to measure cortisol concentrations at baseline, in response to stress, and during recovery. Two samples measured baseline concentrations: one was taken just before the stress test and one 15 minutes after starting the stress test (after completion the tasks, but before the anticipated evaluation. Two samples were obtained 25 and 35 minutes after the beginning of the stress test (to assess reactivity). Lastly, two samples
9 obtained at 45 and 60 minutes after the beginning of the stress test were used as recovery measurements. For the current analyses, the difference between the highest of the reactivity measures, and the lowest of the baseline measure was used as an indication of overall cortisol reactivity to the stress associated with the anticipated negative evaluation.
Statistical Analysis
The goal of this study is to examine if the link between maternal prenatal stress and offspring stress (read: intergenerational transmission) can be moderated by sensitive parenting. To test this hypothesis, a moderated multiple regression (MMR) will be executed. Preliminary analyses will include correlation analysis and the testing of assumptions for multiple
regression. Pregnancy-related anxiety, maternal anxiety, and maternal circadian cortisol will be examined to determine the best predictor for use in MMR, as the independent variable. Infant cortisol reactivity will function as the dependent variable. Maternal sensitivity will serve as the moderator variable. Relevant confounders (sex, birth weight, maternal
educational level, smoking during pregnancy, alcohol use during pregnancy, maternal age, and concurrent maternal stress) will be controlled for in the analysis. Outliers were defined as values exceeding three standard deviations. It should be noted that due to potential problems with collinearity, the independent variables were centered by subtracting the individual values from the mean value; all other assumptions were met. SPSS version 22 was used, utilizing an alpha set at .05.
Results
The original sample size comprised 193 mother/child pairs. Predictably for longitudinal studies, there had been significant dropout, resulting in missing data. At age 6, 45 (23.3%) did not participate in the CREST protocol, leaving 146 mother/child pairs. Removing the
participants who had missing data for the relevant variables (not including confounders), 98 participants remained. Further removal of participants with outlying data in the cortisol reactivity measure left 94 participants with complete data (48.7% of the original sample).
Of the remaining 94 mothers, 55 (58.5%) had given birth to male offspring; 16 (17%) indicated having consumed at least some amount of alcohol during their pregnancy; and 75 (79.8%) reported having earned a college or university degree. The groups that were excluded from the analyses did not differ significantly from the final sample on any variables (ps > .05).
Descriptive statistics for the measures used in the analyses are presented in Table 1, as well as correlations between them. Child cortisol reactivity was significantly correlated with
10 maternal prenatal evening cortisol and the prenatal STAI score (p < .05 and p < .01,
respectively).
Smoking during pregnancy was omitted, because all remaining participants responded to not having smoked during pregnancy. Concurrent maternal stress is omitted in the initial analyses and descriptions, and discussed separately.
Main analysis
In a multiple regression analysis, maternal prenatal cortisol and the mother’s prenatal STAI score were found to be significant predictors of the child’s cortisol reactivity (beta = -.303 ;p = .004 and beta = .329 ;p = .003, respectively). Surprisingly, the coefficient for prenatal maternal cortisol is negative, indicating that higher levels of maternal cortisol predict a lower cortisol reactivity score in offspring, while the coefficient for the prenatal STAI score is positive, indicating that higher prenatal STAI scores predict a higher cortisol reactivity score in offspring. Adding the four independent variables on top of confounders to the model leads to a significant R² Change of .161 (F(5, 83) = 3.398, p = .008). Adding the moderator variable, and its four interaction terms, to the model leads to a nonsignificant R² Change of .051 (F(4, 79) = 1.372, p = .251).
All variables other than the maternal prenatal cortisol and the prenatal STAI score, including confounders, did not contribute significantly to the model, although the model itself was significant (F(14, 79) = 2.03, p = .026) with an R² of .264. Table 2 shows the regression results for the interaction between prenatal stress and maternal sensitivity, related to child cortisol reactivity.
Table 1
Correlations and Descriptive Statistics for Key Variables
Variable Mean SD 1 2 3 4 5 6 7 8 9 10
1. Sex - - -
2. Birth weight 3663.48 471.59 -.266** -
3. Maternal educational level - - .018 -.031 -
4. Alcohol consumption - - -.209* .024 .050 -
5. Maternal age 32.75 3.56 -.120 .025 .287** .194 -
6. Child cortisol reactivity 0.68 1.49 -.016 .062 -.124 .170 .024 -
7. PRAQ1 5.17 2.13 .065 -.078 .159 .020 .091 -.141 -
8. PRAQ2 8.74 3.16 .089 -.101 -.017 -.026 -.093 -.043 .244* -
9. Maternal cortisol 9.39 2.53 .073 -.090 .042 .125 .148 .263* .072 -.026 -
10. Prenatal STAI score 30.44 7.34 -.142 .082 .188 .004 .055 .278** .250* .065 .034 - 11. Maternal sensitivity 19.44 3.01 -.002 .000 .215* .009 -.111 .081 -.054 -.094 .064 .058 Note.* p < .05 ** p < .01; PRAQ1: subset “fear of giving birth”; PRAQ2: subset “fear of bearing a handicapped child”
11 Table 2
Regression Model Predicting Child Cortisol Reactivity At Age 6
Predictor B SE B β t p
(Constant) .367 2.054 .179 .858
1. Sex -.043 .327 -.014 -.130 .897
2. Birth weight .000 .000 .099 .968 .336
3. Maternal educational level -.150 .125 -.130 -1.206 .231 4. Alcohol consumption -.150 .409 .171 1.655 .102
5. Maternal age .677 .045 .011 .105 .916
6. PRAQ1 .003 .078 .004 .032 .974
7. PRAQ2 .031 .052 .066 .606 .546
8. Maternal cortisol -.179 .060 -.303 -2.967 .004 9. Prenatal STAI score .067 .022 .329 3.086 .003 10. Maternal sensitivity -.076 .052 -.153 -1.467 .146 11. PRAQ1 x Sensitivity -.035 .026 -.154 -1.368 .175 12. PRAQ2 x Sensitivity .033 .017 .216 1.989 .0501 13. Maternal cortisol x Sensitivity -.007 .025 -.029 -.266 .791 14. STAI x Sensitivity .006 .008 .086 .782 .437 Note. PRAQ1: subset “fear of giving birth”; PRAQ2: subset “fear of bearing a handicapped child”
Concurrent maternal stress
The measure for concurrent stress (maternal STAI score, 6 years postpartum) was completed by 57 participants. Inclusion of this measure results in the model becoming nonsignificant (F(14, 39) = 1.224, p = .295) with an R² of .315, without any significant predictors. This is achieved without a significant reduction in statistical power, and would seem to imply that the observed effects of prenatal stress on the child cortisol reactivity can be explained by
concurrent stress. Closer examination reveals concurrent maternal stress to have beta= -.349, p = .729. This seems to imply that although considering concurrent maternal stress results in the regression model becoming nonsignificant, it cannot be considering a mediating variable between prenatal maternal stress and the child’s cortisol reactivity.
12 Discussion
The aim of this study was to determine if the intergenerational transmission of stress could possibly be buffered by sensitive parenting. The first prediction was to find a positive association between maternal prenatal stress and the child’s cortisol response. The second prediction was that maternal sensitivity would moderate this intergenerational transmission of stress. To the author’s knowledge, the current study is the first to investigate potential
moderation of this association by maternal sensitivity. While we did find two significant predictors, i.e. the maternal prenatal anxiety and prenatal maternal evening cortisol, on the child’s cortisol reactivity, there was no moderating effect of sensitive parenting. Furthermore, taking concurrent stress into account results in the model becoming nonsignificant, with no significant predictors remaining.
Contrary to our prediction, maternal sensitivity did not seem to have a significant effect in buffering the intergenerational transmission of stress. Given the lack of previous research to provide a strong theoretical foundation for this particular association, we are hesitant to make strong conclusions as to why no moderation was indicated. One possibility is that the buffer effect reported in Farell et al. (2016) applies to early life stress, but not so much for prenatal stress. Unfortunately, no previous research is available that explores the differences between early life stress and prenatal stress, and how it relates to cortisol reactivity, so this possibility is very tentative.
As expected, maternal prenatal anxiety predicted the child cortisol reactivity in a positive trend, showing an association between a higher prenatal STAI score and higher child cortisol reactivity. No other studies have yet corroborated this finding for this particular age group, although Davis, Glynn, Waffarn and Sandman (2011) did find a positive association between prenatal maternal STAI scores and salivary cortisol in newborns. In contrast, Van den Bergh, Van Claster, Smits, Van Huffel, and Lagae (2008) found a negative association between the STAI and salivary cortisol in 14-15 year old offspring. Although cortisol
reactivity has been found to be relatively stable in youth (Hankin, Badanes, Smolen, & Young, 2015), no longitudinal studies have examined this stability over the period of more than two years. Without anteceding studies for this age group, it is difficult to draw strong conclusions on this finding, but this may indicate fluctuating effects of prenatal anxiety over time.
13 expectations, did so in a negative trend. This would seem to imply that mothers with higher levels of cortisol prenatally tend to have children who at age 6 show less cortisol reactivity. This finding conflicts with previous studies (Gutteling et al., 2004; 2005) that had determined a positive association between salivary cortisol measures, between mothers (prenatally) and their children ages 3-6 years old. There are several key differences between those studies and the current one. In Gutteling et al. (2004), prenatal stress measures were taken at 16 weeks of gestation and the stressful stimulus was a painful one (vaccine). In Gutteling et al. (2005), prenatal stress measures were also taken at 16 weeks of gestation and the stressful stimulus was much more complex (first day of school). Obel et al. (2005) found that salivary cortisol levels significantly increase from early to late pregnancy and conclude that their findings suggest that HPA-axis reactivity is dependent on the stage of pregnancy. It may be that the timing of prenatal stress influences child cortisol reactivity for this age group.
The results discussed above are dependent on concurrent stress not being taken into account. Given the notion that children with parents who exhibit high-stress behavior tend to exhibit it themselves as a result of learning (Eley et al., 2015), the question arises to what extent the stress response in this sample is “learned” from the parents. Furthermore, there exists the possibility of major life events occurring that may influence the families, in whole, or in part. Major life events such as divorce, death of a family member, and so on, can produce significant amounts of stress for the parties involved and may, directly or indirectly, affect cortisol responses (Karlén, Ludvigsson, Frostelli, Theodorsson, & Faresjö, 2011). Despite not being a probable mediator, the effect of concurrent maternal stress could possibly be indicative of its relation to a unknown variable that could account for the intergenerational transmission of prenatal stress in this study.
In summary, this study was able to predict child cortisol reactivity from maternal prenatal stress in a significant regression model, but did not manage to find any significant moderating effect of maternal sensitivity. Furthermore, one of the prenatal measures seemed to contribute negatively to the outcome measure, contrary to expectations. Moreover, taking concurrent maternal stress into account results in a nonsignificant model, implying that the effect of prenatal stress on child cortisol reactivity may be better explained by concurrent maternal stress. However, further investigation reveals concurrent maternal stress to not be a probable mediator; a related, unknown, underlying trait is a possible candidate that could account for transmission.
There are several caveats in this study to take into consideration. Firstly, a large portion of the total amount of participants had dropped out before the measurement of child
14 cortisol reactivity. This is to be expected of a longitudinal study, and although there were no significant differences between the final sample and the omitted group, there nevertheless exists the possibility of systematic differences in missing data.
Firstly, a large amount of time had passed between the measures. Prenatal measures were taken in the 37th week of gestation; sensitivity was measured 30 months postpartum; child cortisol reactivity was measured 6 years postpartum. Although there is some indication that maternal sensitivity is relatively stable in infancy (Bigelow et al., 2010), it would have been preferable for this study to have had it measured concurrently with the child cortisol reactivity.
Secondly, although concurrent maternal stress is controlled for, it is done with a single generalized measure, and it is unclear to what extent this influences the child cortisol
reactivity, or if specific aspects of stress are responsible. Furthermore, the precise nature of the mother/child relationship is not explored (e. g. to what extent does the mother express concern/stress in presence of her child). It would be advisable for future studies to further explore which aspects of concurrent maternal stress possibly influence child cortisol reactivity.
Thirdly, the role of the fathers has not been examined. There is a strong bias in studies reporting on sensitivity, attachment, and child outcomes to focus solely on the role of the mother. Studies examining the role of fathers in child development are vastly outnumbered, but there are indications that they can have significant influence on child development (Sarkadi, Kristiansson, Oberklaid, & Bremberg, 2008). It would be advisable for future studies to include measures of fathers.
Lastly, the current sample of participants were, compared to the general population (CBS, 2016), very highly educated. Higher levels of intelligence (particularly Emotional Intelligence) have been found to influence the cortisol response (Derksen, Kramer, & Katzko, 2002), and it is possible that this could have biased results (Mikolajczak, Roy, Luminet, Fillée, & De Timary, 2007).
In conclusion, this study is the first to examine the possible moderating role of maternal sensitivity in the intergenerational transmission of stress. Although there was indication of transmission, the exact nature of the finding contradicts previous research and goes against theoretical expectation. Moderation was not significantly indicated, and
transmission was not apparent when considering concurrent maternal stress. Concurrent stress however, is not a probable mediator, but may rather be indicative of a related, underlying trait that influences the intergenerational transmission of stress. Further research into this subject
15 should address the weaknesses of this study, including the role of fathers, emotional
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