Beruflich Dokumente
Kultur Dokumente
2
(2)
= 24.92, p <.001). All fit indices are in the recommended range: (1) a non-significant
2
(
2
(3)
= 2.44, p >.05), (2) CFI, TLI and RNI values of 1, and (3) drop in the BIC greater than 10
indicating that the change in the BIC is significant at the .01 level (Raftery, 1995). Table 7
displays the regression, variance and covariance estimates of the final model. All regression
coefficients are significant, and show parameters size and sign consistent with theories on
maternal sensitivity.
Figure 1. Theoretical model of maternal sensitivity.
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42
Table 7. Parameter estimates of final measurement model (Model 3) for maternal sensitivity.
b SE P
Ainsworth sensitivity Sensitivity
1.17 .05 <.001 .97
MBQS Sensitivity
0.26 .01 <.001 .90
Ainsworth cooperation Sensitivity
1.00 - - .85
Ainsworth accessibility Sensitivity
1.09 .06 <.001 .88
Ainsworth acceptability Sensitivity
0.93 .04 <.001 .86
Covariances
Covariance E3 E4
-.27 .07 <.05
Covariance E3 E5
.13 .07 <.05
Variances
Sensitivity 2.7 .30 <.001
E1 0.2 .05 <.001
E2 0.0 .00 <.001
E3 1.1 .11 <.001
E4 0.9 .09 <.001
E5 0.8 .08 <.001
43
Figure 2. Final measurement model of maternal sensitivity.
Note: standardized estimates shown.
44
Measurement model of maternal depression.
A partial disaggregated model was estimated for maternal depression. This methodology
requires that the scale is unidimensional (Williams & Boyle, 2008) thus an exploratory factor
analysis was first conducted on the entire sample (N=501) to examine this assumption. Results
of the exploratory factor analysis indicated that the CES-D scale is indeed unidimensional (data
not shown). The 20 CES-D items were then grouped into parcels based on a correlation matrix
with the most correlated items grouped together. Table 8 displays the descriptive statistics and
psychometric properties of the parcels. Since the parcels demonstrated both skewness and
kurtosis, they were transformed into their square root. This transformation was successful in
correcting the skewness and kurtosis.
Figure 3 displays the measurement model for maternal depression. Model identification
required that all error terms (E1 to E3) have a fixed unit of measurement as well the regression
coefficients of parcel 1 and parcel 3 were set to 1. These constraints resulted in 5 unknown
parameters: 1 regression coefficient of the unfixed parcel 3, 4 variances (E1 to E3 and variance
term for the latent variable). The number of available data points is 6 (calculated as p(p+1)/2
where p is the number of observed variables). Since the number of estimated parameters (5) is
less than the number of available parameters (6), the t-rule is met indicating an identified
model.
As shown in Table 9, the theoretical model demonstrated good fit. All fit indices are in
the recommended range: (1) a non-significant chi-square (
2
(1)
= 1.03, p >.05), (2) CFI, TLI and
RNI values of .99, .99 and 1 respectively, and (3) the RMSEA value less than the .05 criteria and
associated p > .50. Table 10 displays the regression and variance estimates of the final model.
45
Table 8. Descriptive statistics and psychometric properties of the depression parcels.
N Min. Max. Mean SD Skewness Kurtosis Cronbach
alpha
Parcel 1
(No. of items = 11)
501 0 2.0 0.44 .36 1.1 1.3 .70
Parcel 1 square root
transformation
501 0 1.4 0.59 .30 -0.2 -0.3 -
Parcel 2
(No. of items = 4)
501 0 2.5 0.37 .5 1.6 2.2 .75
Parcel 2 square root
transformation
501 0 1.6 0.42 .44 0.5 -1.0 -
Parcel 3
(No. of items = 5)
501 0 2.6 0.62 .6 1.2 1.6 .67
Parcel 3 square root
transformation
501 0 1.6 .69 .37 -0.3 -0.2 -
46
Figure 3. Theoretical model for maternal depression.
Depression
Parcel 1
E1
1
1
Parcel 2
E2
1
Parcel 3
E3
1
1
Table 9. Goodness-of-fit indices for the depression measurement model.
2
df P CFI TLI RMSEA RMSEA P RNI
Theoretical model
1.03
1
0.32
0.99
0.99
0.01
0.56
1
47
Table 10. Parameter estimates of the final depression measurement model.
b SE p
Parcel 1 Depression
1 - - .75
Parcel 2 Depression
1.55 0.12 <.001 .80
Parcel 3 Depression
1 - - .60
Variances
Depression 0.05 .00 <.001
E1 0.04 .00 <.001
E2 0.07 .01 <.001
E3 0.09 .00 <.001
Mediation analysis.
Figure 4 displays the hypothesized model for the mediating role of mothers depression
and appraisal of infant temperament on the association between maternal sensitivity and
mothers early adversity and income. The model consists of three latent variables: Maternal
depression, Mothers appraisal of infant temperament and Maternal sensitivity. The
measurement models of maternal depression and maternal sensitivity are not discussed
further as these were described in detail in the respective sections. With regards to the latent
variable Mothers appraisal of infant temperament, three options were available for the
specification of this latent construct; these are discussed in detail under section Measurement
model for maternal depression. The second option was used for the specification of this
construct. Since mothers appraisal of infant temperament was assessed using a five-item scale
48
the latent variable was specified with a sole indicator which consisted of the mean of the five-
items. The variance of the latent construct was specified to a pre-determined value of 0.16
calculate using a reliability correction (calculated as (1-.67<Cronbach alpha of
scale>*.48<variance of scale>) (see Fig 4). Additionally, identification of this latent construct
required that the regression coefficient of the indicator be set to unity.
Last, a residual term (R1-R3) is associated with each latent factor; this represents error in
the prediction of the construct from the respective predictors (e.g. R1 represents error in the
prediction of Depression from the construct Early adversity and income).
The cumulative score of mothers early adversity was entered as an observed variable.
Likewise for mothers income, this construct was specified as an observed variable given that it
was assessed by a single question.
Based on existing theory, the following variables were entered as covariates of maternal
sensitivity: experience of prenatal difficulties, mothers education, mothers Canadian born
status, infant weight, number of children in the home, and single parent status. These control
variables were entered as observed measures with no measurement error. Only Canadian born
status and mothers education were found to relate to sensitivity therefore only these covariates
were retained in the model. A default of AMOS is to specify correlations among all observed
variables, hence the following covariances were specified: mothers education and the following:
Canadian born status income and early adversity, and two covariance terms between
Canadian born status and income and Canadian born status and early adversity.
The first step of the analysis was to achieve adequacy in model fit. As shown in Table
11, the theoretical model fit well as per the CFI, TLI and RNI values of .95 to .97. However, the
RMSEA values over .05 and the significant chi-square suggest misfit. Examination of the
49
parameter estimates indicated that the following pathways were not statistically significant and
therefore should be removed from the model. The non-significant pathway between Early
adversity Maternal sensitivity partially supports hypothesis 1 indicating that early adversity
does not directly influence maternal sensitivity but rather that the relationship is a mediated
association. The non-significant pathway between Depression Maternal sensitivity also
partially supports hypothesis 1 indicating that the association between depression and maternal
sensitivity is accounted for by mothers perceptions of their infants temperament. The non-
significant pathway of Early adversity Mothers appraisal of infant temperament suggests
that early adversity does not directly influence mothers perceptions of their infant as suggested
by alternate perspectives for the effects of early adversity on thought distortions (Gibb et al.,
2001; Gibb, Alloy, Abramson, & Marx, 2003; Kankin et al., 2001). Rather, as specified in
hypothesis 1, early adversity increases the risk of maternal depression which is in turn related to
mothers appraisal of infant temperament.
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51
Examination of the modification indices of the re-estimated model indicated that the
specification of four covariances would improve the fit of the model. It is noteworthy that the
only covariances specified were those justifiable based on shared measurement (i.e. where
mother reported on multiple measures). The covariances were specified one at a time and the
respective model re-estimated, the covariance included the following: (1) covariance among the
observed variable mothers education and the variance of depression parcel 1 (D1), (2)
covariance among the variance of depression parcel 3 (D3) and mothers income and
Canadian born status, and last (3) the covariance among the observed variable Canadian born
status and the residual term for the depression latent variable (RD1).
Specification of these covariances improved the fit of the final model, across the five
datasets, as shown in Table 11. The following fit indices are in the recommended range: (1) CFI,
TLI and RNI values of .95 to .97, (2) the RMSEA value equal to or less than the .05 criteria and
associated p > .50. The change in the BIC statistic clearly greater than 10 indicates that the
change in fit from the theoretical to the final model is significant at the .01 level (Raftery, 1995).
However, the chi-square remained significant (
2
(52)
= 99.64, p <.001). However, the chi-square
is sensitive to sample size and very trivial departures in fit produce large chi-squares in large
samples (Byrne, 2001). Further, the change in the chi-square (
2
(1)
= 67.50, p <.001) is
significant indicating that the final model is superior in fit than the theoretical model. Hence,
given the limitation of the chi-square due to the large sample size and that the other indices
suggest adequate fit, the final model is retained over the theoretical model.
Table 12 displays the parameter estimates for the final model. Evidence for hypothesis 1
and 2 was found. The model supports the two hypothesized indirect relationships for early
adversity (hypothesis 1) and low income (hypothesis 1). Mothers cumulative early adversity
52
and income are significantly related to mothers depression ( = .1, p < .001 and = -.40, p <
.0001 respectively) which is in turn positively related to mothers negative appraisal of the infant
temperament ( = .19, p < .0001) which is in turn negatively related to mothers sensitive
behavior toward their infant ( = -.11, p < .001). These indirect relationships are observed after
having controlled for significant covariates of maternal sensitivity including mothers education
( = .14, p < .05), and Canadian born status ( = .16, p < .01).
The second step of the analysis involved estimating confidence intervals to assess the
significance of the observed indirect effects. As shown in Table 13, the total indirect effect of
early adversity on sensitivity is -.003 (computed as multiplying the standardized parameter
estimates of early adversity on depression and that of depression on appraisal of temperament
and that of temperament appraisal on sensitivity (.13* .19 * -.11 = -.003). This effect is within
the estimated 95% lower and upper boundary indicating significance level of .05. Likewise, the
indirect effect of low income on maternal sensitivity is .008 (computed as multiplying the
standardized parameter estimates of low income on depression, depression on mothers negative
appraisal of infant temperament and the estimate of appraisal on sensitivity (-.40*.19*-.11=.008).
This effect is within the estimated 95% lower and upper boundary, indicating significance level
of .05. These significant indirect effects support hypothesis 1.
As specified in hypothesis 1, a direct association between income and sensitivity was also
found ( = .15, p < .01) even after accounting for incomes indirect effect on sensitivity and the
influence of mothers education. The total standardized effect (mediated and unmediated effect)
of mothers income on sensitivity is .16 (calculated as the sum of the direct effect and indirect
effect (.15 +.008=.16)). Low income also showed a direct relationship to maternal sensitivity
53
Figure 5 displays the final model, for simplicity the only coefficients displayed are those
that relate directly to the indirect and direct effects discussed above; all other coefficients (i.e.
variance and covariance terms) are displayed Table 12.
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55
Table 12. Parameter estimates of the final mediation model.
b SE
Depression Early adversity
0.03 0.01 0.13
Depression Income
-0.02 0.003 -0.40
Appraisal of infant temperament Depression
0.75 0.19 0.19
Sensitivity Income
0.06 0.02 0.15
Sensitivity Appraisal of infant temperament
-0.17 0.07 -0.11
Sensitivity Canadian born status
0.51 0.15 0.16
Sensitivity Mothers education
0.08 0.03 0.14
Covariances
Income Early adversity
-0.88 0.23
Early adversity
Mothers education
-0.71 0.15
Income
Mothers education
5.18 0.52
Canadian born status
Mothers education
0.15 0.06
Income
Canadian born status
0.65 0.09
Early adversity
Mother education
0.08 0.03
Variances
Income 16.28 1.02
RT1 0.74 0.06
Early adversity 1.63 0.10
Canadian born status 0.25 0.02
Mothers education 7.03 0.44
56
Table 12. Parameter estimates of the final mediation model, continued.
b SE
Variances
Rd1 0.05 0.01
T1 0.16 0.00
R1 2.20 0.20
a
p <.05
b
p <.01
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58
Table 13. Confidence intervals for the standardized indirect and direct effects of income on
sensitivity and for the standardized indirect effect of early adversity on sensitivity.
Parameter
estimate
95% lower
boundary
95% upper
boundary
Income standardized indirect effect .02 .001 .02
Income standardized total effect .16 .06 .26
Early adversity standardized indirect
effect
-.003 -.007 -.0002
Moderated mediation.
Neighborhood quality.
The model was first estimated across low versus high neighborhood conditions (relative
to the sample median) allowing the parameters of the indirect effect of early adversity and of
income to vary across the two groups. As shown in Table 14 (see Variant Model), this model
demonstrated adequate fit indices. Constraining the indirect pathways to be equal across the two
groups (see Invariant Model) resulted in a statistically significant change in the chi-square (
2
(5)
= 17.93, p <.01). Figure 6 and table 15 display the parameter estimates across levels of
neighborhood quality. The statistically significant change in the chi-square indicates that the two
groups are not equivalent on the constrained parameters. This partially supports hypothesis 2 that
the neighborhood quality would moderate the influence of early adversity and income on
sensitivity. It was further hypothesized that in low quality neighborhood the influence of early
adversity and low income would be exacerbated, while a high quality neighborhood would buffer
mothers from the influence of low income and early adversity. These hypotheses were
59
confirmed only for the association between income and sensitivity and early adversity and
depression.
In a context of poor neighborhood quality larger parameter estimates were found for the
following two pathways income sensitivity (= .16, p < .05 for low and = -.07, p >.05
for good quality), and early adversity depression (= .28, p < .05 for low and = .01, p >
.05 for good quality). This provides partial support for hypothesis 2 suggesting that low
neighborhood quality exacerbated the influence of income on maternal sensitivity and early
adversity on maternal depression. Conversely, in the context of good quality neighborhood, the
association between income and maternal sensitivity, and early adversity and depression was
reduced as indicated by the smaller magnitude of the respective parameters. This suggests that
living in a high quality neighborhood buffered mothers from the influence of early adversity on
maternal depression and income on maternal sensitivity.
Contrary to hypothesis 2, the neighborhood quality did not exacerbate the influence of
depression on mothers appraisal of infant temperament and the influence of mothers appraisals
on their maternal sensitivity. This is shown by the small change in parameter size across
neighborhood quality for the pathways depression mother appraisal of infant temperament
(= .17, p < .05 for low neighborhood quality and = .25, p < .05 for high neighborhood
quality) and the pathway mother appraisal of infant temperament sensitivity ( = -.11, p >
.05 for low neighborhood quality and = -.13, p < .05 for high neighborhood quality).
Contrary to hypothesis 2, a stronger association between income and depression was
found in the context of high neighborhood quality (= -.40, p < .05) rather than the hypothesized
effect of low neighborhood quality (= -.23, p < .05). As well, in high quality neighborhood
there is no evidence for a direct association between income and maternal sensitivity ( = -.07, p
60
> .05 for high neighborhood quality, ( = .16, p < .05 for low neighborhood quality). This
suggests that in high quality neighborhood the influence of income on maternal sensitivity is
completely mediated by mothers depression and appraisal of infant temperament, while in low
quality neighborhood there is evidence for both a direct and indirect association between income
and maternal sensitivity.
Last, the average level of maternal sensitivity across neighborhood quality was examined.
In low neighborhood quality the average level of sensitivity was -.27 (N=251) while in high
quality neighborhood the mean level of sensitivity was = .88 (N =250). This difference was
statistically significant (
2
(1, N=501)
= 24.43, p <.0001).
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62
Figure 6. Neighborhood quality moderates the association between maternal sensitivity, early
adversity and income.
a. Poor neighborhood quality
b. Good neighborhood quality.
* p <.05
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64
Discussion
The role of early adversity.
Mothers depression and mothers appraisals of infant temperament were found to
mediate the influence of mothers cumulative early adversity on maternal sensitivity. These
findings are consistent with life course theories which suggest that developmental history
influences subsequent parenting through aspects of parental functioning including parental
mental health (Belsky & Jaffee, 2006). The positive association found between early adversity
and maternal depression is consistent with research on the effects of early negative life events on
adult mental health (Brown & Harris, 1993; Rutter & Maughan, 1997). This research generally
shows that early adversity by ways of parental indifference, physical or sexual abuse (Brown &
Harris, 1993; Brown & Moran, 1994), and low quality parenting (Parker, 1981) is a risk factor
for adult depression including postpartum depression (Matthey et al., 2000; McLaren, Kuh,
Hardy, & Mishra, 2007).
Depression was found to relate to mothers negative appraisal of the infant, which in turn
completely accounted for the effects of the depression on mothers sensitivity. This finding is in
line with previous reports that have show that mothers with depression experience their infants as
more difficult (Edhborg, Selmyr, Lunsh, & Widstrom, 2000) and make more unfavorable
remarks of their children (Gordon, Burge, Hammen, Adrian, Jaeniecke, & Hiroto, D., 1989;
Nelson, Hammen, & Brennan, 2003). Although studies have examined the relationship between
maternal depression and the quality of the mother-child relationship (Murray & Cooper, 1997;
Nichd, 1999), and the significance of maternal depression with respect to mothers appraisal of
the child (Edhborg, et al., 2000; Gordon et al., 1989; Nelson, et al., 2003), to the best knowledge
65
of the author the present study is the first to show that mothers negative appraisals can account
for the effects of maternal depression on parenting quality.
Studies that have examined the associations between maternal depression and sensitivity
have documented inconsistent findings with some studies showing negative associations (Murray
& Cooper, 1997; Nichd, 1999) while others report no relationships (Pederson et al, 1990).
Findings from the present study add to this body of work demonstrating that the relationship
between mothers depression and their sensitivity is complex. Mothers perceptions of the child
serve as an important mechanism through which depression can influence the quality of early
mother-child interaction.
There is controversy as to whether depressed mothers provide biased or accurate
appraisals of the infant (e.g. see Cutrona & Troutman, 1986; Stein, Arteche, Lehtonen, Craske,
Harvey, Counsell, & Murray, 2010). The validity of mothers appraisals of infant temperament
was not assessed as there were no observers ratings of infant behavior. Therefore, it is possible
that the infants behavior was indeed difficult and that mothers provided valid assessments. This
would also be consistent with a genetic transmission of mental health problems from mother to
child. It is also possible that the association between mothers depression and mothers
appraisal of infant temperament represent a bidirectional relationship. For example, it may be
that the infants difficult behavior is a learned response from interacting with a non-contingent
depressed mother. The infant behavior may in turn feed-back to the mother who, due to the
demands of the depression, responds to the heightened infants bids with additional withdrawal.
Although the present study does not clarify the direction of causality between mothers
depression and their appraisal of the infant temperament, it is proposed that irrespective of their
validity and cause, mothers perceptions of their infant are nonetheless consequential to
66
sensitivity. The valence of parental beliefs on parenting is exemplified by research on parenting
self-efficacy. Parenting self-efficacy refers to parental beliefs and judgments about ones
competence in the parental role (Bandura, 1997). This construct has been regarded as a major
determinant of competent parenting (Jones & Prinz 2005). For example, parents who judge
themselves higher on parenting self-efficacy demonstrate more authoritative and consistent
parenting than parents with lower parenting self-efficacy (e.g. see Ardelt & Eccles, 2001). This
study extends this line of research by showing that mothers judgments of the infant explain
variance in maternal sensitivity. This implies that interventions aiming at improving mothers
sensitivity should be mindful of mothers perceptions of their infant, especially when maternal
depression is present.
The demonstrated mechanisms for the effects of early adversity on maternal sensitivity
are also consistent with attachment theory. This theory posits that parental attachment styles and
parental childhood experiences of having established and maintained healthy attachments are
influential for parental mental health (Bowlby, 1969, 1988; Marks & Ashleman, 2002). For
instance, Bifulco et al., (2004) reported an incremental increase in the risk of depression in
postpartum women as a function of insecure attachment style (marked, mild, none) with marked
insecurity showing the highest level of depression. Likewise, McMahon, Barnett, Kowalenko
and Tennant (2005) showed that, among new mothers, the effects of early adversity (i.e. low
maternal care) on 12 months postpartum depression were mediated by the mothers insecure
attachment.
Critical to attachment theory are the parents representations of early relationships which
are posited to shape mothers perceptions of themselves and others, including their children
(Bowlby, 1969). These representations, referred to as internal working models of attachment,
67
are cognitive-representational structures that shape what one can remember, feel or think about
early attachment and future attachment relationships (Slade & Cohen, 1996). Parental internal
working models shape the parental responses to the childs affect and attachment behaviors
(Slade & Cohen, 1996) which in turn influences the childs attachment to his or her parents
(Benoit & Parker, 1994; Fonagy, Steel, & Steele, 1991).
Mothers who are insecure with respect to their attachment representations rely on internal
working models that lack, distort or defensively exclude memory and affect of early relationships
(Slade & Cohen, 1996). Insecure mothers are either unable to see their own infants clearly, deny
or are overwhelmed by them, thereby directly influencing the infants own insecure attachment
(Slade & Cohen, 1996). From this perspective, maternal insensitivity to infants signals
originates from interaction patterns that allowed the mother to preserve felt security in her own
childhood relationships (Slade & Cohen, 1996). Felt security refers to the perception of the
sensitive availability of the attachment figure (West, Spreng, Rose, & Adam, 1999). Main and
Goldwyn (1995) argued that infant attachment behaviors such as crying, or approaching, may
threaten the parents felt security by interfering with the maintenance of an attachment state that
is comfortable for the parent (i.e. dismissing or preoccupied). Hence, insensitive responding to
infants signals allows the parent to protect themselves from experiences that may make them
feel vulnerable and unsafe, and to continue thinking about and experiencing relationships in a
manner that is most comfortable for them (Slade & Cohen, 1996).
The role of income.
With respect to mothers economic circumstances, family income was found to relate
directly to sensitivity, as well as indirectly through mothers depression and negative appraisal of
the infant. The direct association is consistent with findings showing that low income mothers
68
hold more authoritarian beliefs regarding parenting than higher income mothers (Martini, Root &
Jenkins, 2004; Dodge, Petit, & Bates, 1994) these beliefs have in turn been associated with
reduced responsivity (Maccoby & Martin, 1983). The indirect pathway is consistent with Conger
and colleagues (1994) family stress model which posits that familial socio-economic
circumstances influence child development through the negative influence on parental mental
health which subsequently compromises parenting quality. This proposed process has received
empirical support (see Conger, Patterson, & Ge, 1995; Conger et al., 1994). The present
findings suggest that the family stress model could be extended to include parental cognitions
about their children as a further proximal influence for the association between familial socio-
economic influences, parental mental health and parenting.
Moderated-mediation: the role of neighborhood quality.
The significance of early adversity and economic circumstances for mothers functioning
and sensitivity is further informed by the results of the moderated-mediation analyses. In low
quality neighborhoods, characterized by crime, poverty and disorder, early adversity was
associated with mothers depression; these findings are consistent with a cumulative risk model
(Rutter & Pickles, 1991) which posits that it is the accumulation of unfavorable conditions that
matters for ones functioning. In addition to coping with an adverse history, mothers that reside
in low quality neighborhoods are exposed to additional risk factors including poverty, violence,
feeling unsafe and limited access to resources. Furthermore, parents from disadvantaged
neighborhoods are more likely to have fewer social ties and to be isolated from formal and
informal networks (Coleman, 1988; Sampson & Groves, 1989; Ross, 2000). This isolation is
associated with compromised parenting, reduced child well-being (Coleman, 1994; Coleman &
Hoffer, 1987) and encourages an individualistic pattern of parenting where the adherence to
69
social norms, values and behaviors is diminished (Sampson, 1992; Sampson & Groves, 1989).
From an attachment perspective the combination of lack of supports and increased exposure to
risk factors evident in a context of low quality neighborhood, is particularly meaningful for
mothers with adverse histories. For mothers with adverse histories, low quality neighborhoods
may elicit a heightened level of fear which is likely to activate the attachment system (Bowlby,
1973). Mothers may use maladaptive coping strategies or may lack coping strategies altogether.
Hence, mothers with an adverse background may be especially vulnerable to the effect of a low
quality neighborhood and in addition lack the coping mechanisms to face the difficulties
presented by the neighborhood. The activation of the attachment system and inability to cope
may increase the risk of depression thereby facilitating the influence of early adversity on
sensitivity.
In contrast, in high quality neighborhoods, early adversity was not found to relate to
mothers depression. This suggests that characteristics of high quality neighborhoods may have
buffered mothers from the effect of early adversity. This is consistent with Belsky (1984)s
process model of parenting in which it is posited that parenting is a buffered system and that
aspects of the ecology may offer supports that will act in a compensatory way to repair the
negative effects of the early experience. Characteristics found among higher quality
neighborhoods that may assist mothers in compensating for a difficult history include greater
social ties, reduced alienation (Coleman, 1994; Coleman & Hoffer,1987) and overall lower level
of ecological stress (i.e. higher sense of safety) (e.g. see Caspi, Bolger, & Eckenrode, 1987).
Chronic exposure to ecological risks is troublesome for mothers. For instance, Caspi et al.,
(1987) found that relative to women living in safe neighborhoods, for those in unsafe
neighborhoods the effect of daily stress on depression lingered for longer period of time. Among
70
neighborhoods characterized by greater social ties and reduced isolation parenting becomes a
shared responsibility among the residents where there is a consensus on the adherence of shared
practices and norms (Steinberg, Darling, & Fletcher, 1995). For instance, child monitoring and
supervision is shared among neighbors (Coleman, 1994; Coleman, & Hoffer, 1987). This shared
responsibility and communal beliefs about parenting may assist mothers in overcoming their
adverse history by instilling in them feelings of support and providing them alternative ways of
viewing the world, themselves and their children and the task of parenting.
With respect to low family income, a stronger association between income and
depression was found in the context of high neighborhood quality rather than the hypothesized
effect of low neighborhood quality. As well, in high quality neighborhood there is no evidence
for a direct association between income and maternal sensitivity. This suggests that in high
quality neighborhood the influence of income on maternal sensitivity is completely mediated by
mothers depression and appraisal of infant temperament, while in low quality neighborhood
there is evidence for both a direct and indirect association between income and maternal
sensitivity. Mothers demographic data were examined in detail to better interpret these
findings. 42% of mothers from high quality neighborhoods reported working outside of the
home, relative to 19% of mothers from low quality neighborhoods. Residing in a higher quality
neighborhood may increase the families financial burden resulting in mothers needing to be
employed outside of the home. The increased financial demands and commitments outside of
the home may increase mothers risk of depression in turn accounting completely for the
influence of income on maternal sensitivity.
In low neighborhood quality, the direct association between income and sensitivity, after
accounting for incomes indirect effect, may represent left-over variance not accounted for by the
71
influence of income on maternal depression. This variance may be explained by low income
mothers beliefs and values regarding parenting. For example, low income mothers have been
shown to hold more authoritarian beliefs regarding parenting than higher income mothers
(Martini, Root & Jenkins, 2004; Dodge, Petit, & Bates, 1994). These beliefs in turn reduce
maternal responsivity (Maccoby & Martin, 1983).
Several limitations of the study are noteworthy. First, the findings illustrate only
correlational processes not causal, as the data were cross-sectional. Second, mothers provided
retrospective reports on their experiences of early adversity. Although retrospective accounts
may be biased due to recall limitations, the present measure of early adversity includes recall of
concrete events only in order to lessen bias. Recall of concrete experiences in childhood, such as
the experience of physical abuse, are remembered with less bias than recall of subjective
experiences such as reports of relationship quality (Prescott, Bank, & Reid, 2000). The exclusion
of families with infants born weighing less than 1500 gm may have favored the participation of
families from a higher socio-economic standing as birth weight is correlated with family socio-
economic status (SES; Crooks, 1995); this may limit the generalizability of the studys findings
to families of lower SES. Last, findings of moderated-mediation may represent selection
processes whereby mothers difficult childhood, depression and low family economic standing
may have constrained mothers to reside in poor quality neighborhoods while mothers with less
adverse histories and better economic circumstances supported their selection of a higher quality
neighborhood. It is noteworthy that neighborhood characteristics have been shown to influence
parental functioning even after accounting for the influence of selection factors (i.e. individual
characteristics such as depression; Ross, 2000). Strengths of the study include observed, multi-
method (Q-Sort and rating scales) measurement of maternal behavior and the neighborhood
72
(observations and census tract data), and the use of latent variables with multiple indicators in
Structural Equation Modeling which account for systematic and unsystematic measurement error
(Coffman & MacCallum, 2005).
Implications
The direct association between family income and sensitivity suggest that it is not enough
to consider the stress impact of low family income on parenting quality. Socioeconomic related
differences in parental beliefs, values and attitudes regarding childrearing may also explain
additional variance in maternal sensitivity; hence these factors should be considered when
aiming to improve parenting quality. Results from the moderated mediation analyses indicate
that neighborhood quality can buffer mothers from the effects of early adversity. The measure of
neighborhood employed in the present study examined objective aspects of the neighborhood
including evidence of loitering, crime, poverty and disorder. This suggests that maternal
sensitivity is also influence by factors that are distal to the mother and that interact with more
proximal influences (e.g. developmental history). Programs geared at creating safe communities
may assist mothers, especially those with a difficult background, in providing sensitive care to
their children. The finding that maternal depression operated completely through mothers
appraisal of infant temperament suggests that treatment programs should be mindful of mothers
cognitions about their child.
73
Study 2: Maternal Sensitivity, Early Adversity and the Arginine
Vasopressin 1a Receptor Gene (AVPR1A)
Introduction
Although much is known about the genetic underpinnings of animal parenting behavior
(e.g. see Perrigo, Belvin, Quindry, & Kadir, 1993) much less is known about the genetics of
human maternal behavior. The few existent studies suggest that genetics are indeed an important
source of influence. For instance, Spinath and O'Connor (2003) using a sample of 300 twin pairs
concordant for having children, found evidence of moderate genetic influence for over-
protectiveness, supportive/indulgent, and authoritarian parenting. Likewise, Losoya, Callor,
Rowe, and Goldsmith (1997) reported evidence of moderate genetic influence on
positive/supportive parenting. Furthermore, Kendler (1996) and Perusse, Neale, Heath, and
Eaves (1994) found that monozygotic twins parent more similarly than dizygotic twins, with
heritability estimates of approximately 38% for the provision of maternal warmth (Kendler,
1996).
There are discrepant findings however with regards to which dimensions of parenting are
influenced by genetics. For instance, Spinath and OConnor (2003) found that rejecting
parenting was attributable only to environmental factors. Likewise, Kendler (1996) found that
protective and authoritarian parenting was attributable only to environmental influence. In
contrast however, Perusse, Neale, Heath and Eaves (1994) found evidence of genetic influence
on all dimensions of parenting as measured by a shortened version of the Parental Bonding
Instrument (Parker, 1989) which assesses retrospective recall of how one was parented. Some of
74
these discrepancies are associated with differences in the methodology and informants employed
across studies (see Kendler, 1996).
To-date, no behavioral genetic studies have examined the influence of genetics on
maternal sensitivity. However, two molecular genetic studies have examined relations between
four genes and maternal sensitivity. In the first study, van Ijzendoorn, Bakermans-Kranenburg
and Mesman (2008) examined the association between maternal sensitivity and two dopamine-
related genes (Dopamine D4 Receptor (DRD4) and Catechol-O-Methyltransferase (COMT). No
association was found between maternal sensitivity and any of the COMT and DRD4 genotypes.
However, the authors found that mothers genotype moderated the effect of experience of stress
(daily hassles) on maternal sensitivity. The experience of daily hassles was associated with
lower maternal sensitivity in mothers with the combination of alleles COMT-val and DRD4-7R.
This combination of genes is hypothesized to lead to less efficient dopaminergic system
functioning. The highest level of maternal sensitivity was found among mothers with the same
combination of alleles but who experienced low levels of daily hassles. Thus the combination of
genes COMT-val and DRD4-7R increased mothers reactivity to both high and low stress
conditions. No association was found between daily hassles and sensitivity in mothers carriers
of different allele combinations.
In the second study, Bakermans-Kranenburg and van Ijzendoorn (2008) examined the
association between maternal sensitivity and the serotonin transporter (5-HTT) and oxytocin
receptor (OXTR) genes in a sample of 159 mother-child dyads. Lower sensitivity was observed
in mothers who were homozygous for the 5-HTT short alleles and for the OXTR G allele, versus
mothers with other genotypes. The short/short 5-HTT and the homozygous G/G OXTR
75
genotypes are hypothesized to correlate with less efficient serotonergic and oxytocin system
functioning (Bakermans-Kranenburg & van Ijzendoorn, 2008).
An additional gene that has been found to relate to parenting in animal research is the
Arginine Vasopressin 1a receptor gene (AVPR1A). Animal research provides strong evidence
that this gene is involved in parenting, as discuss below, yet to-date no study has examined its
possible association with human maternal behavior.
Relationship between AVPR1A and maternal behavior.
The neuropeptide arginine vasopressin (AVP) plays a role in social behavior (Kim, et al.,
2002) including maternal behavior (e.g. see Neumann, 2003). This peptide is largely synthesized
in the paraventricular and supraoptic nucleus of the hypothalamus (Wang, Liu, Young, & Insel,
2000) and acts through 3 distinct receptors (V1a, V1b and receptor 2) but with predominant
activity through the V1a receptors (Kim, et al., 2002; Young, 1999). Several lines of research
indicate that the vasopressin system contributes to maternal behavior. The vasopressin system is
activated around parturition and in lactation (for a review see Neumann, 2003). Central
administration of vasopressin induces maternal behavior in rats while vasopressin antagonist
suppresses the behavior (Pedersen, Caldwell, Walker, Ayers, & Mason, 1994). Recently Bosch
& Neumann (2008) found that these effects of central administration of vasopressin are mediated
by the V1a receptors and not due to the action of the closely related oxytocin receptors, as
previously suggested (Pedersen, et al., 1994).
The strongest evidence for the relationship between the vasopressin system and maternal
behavior comes from comparative studies of two arvicoline rodents: the prairie and montane
voles. These rodents differ in their organization of social behavior. The prairie vole is
monogamous, biparental and highly social, while the montane voles are promiscuous, minimally
76
social and solely maternal. The behavioral effects of central administration of vasopressin differ
significantly between the two types of voles, such that vasopressin administration stimulates
affiliative behavior in the prairie but not in the montane voles (Kendler & Greenspan, 2006).
Also, the distribution of the V1a receptors between the montane and prairie voles is almost non-
overlapping with the prairie vole showing higher density of receptors in reward pathways than
the montane voles (Insel, Wang, & Ferris, 1994). The dissimilarity in the V1a receptor binding
patterns is primarily due to differences in gene expression (Insel, et al., 1994). Despite these
differences, the AVPR1A receptor genes of the two voles are almost identical but with one
notable difference: the AVPR1A receptor gene of the monogamous, biparental prairie voles
shows an additional segment of DNA (microsatellite) in the promoter region of the gene (region
where transcription occurs); this additional segment has been shown to regulate gene expression
(Hammock, Lim, Nair, & Young, 2005).
Although humans do not have repeated sequences of DNA that are homologous to those
of the prairie voles other variants have been identified in humans in similar area of the gene as
the prairie voles. These markers include rs1042615, rs7298346 and RS3 and will be the focus of
the present study. Figure 7 displays the location of these variants on the AVPR1A gene. To the
best knowledge of the research has not yet examined whether human social behavior relates to
variants rs1042615 and rs7298346. rs7298346 is located upstream of the transcription start site,
while rs1042615 is located in exon 1. A few studies have shown relations between the
microsatellite RS3 and human social behaviors. The RS3 is a complex repeat of (CT)
4
-TT-
(CT)
8
-(GT)
n
325bp (base pairs) upstream of the transcription site with 16 different alleles in the
population. Walum et al., (2008) found that homozygosity for the RS3 allele 334 was found to
double the risk of marital crisis (as reported by spouse), threat of divorce and lower scores on
77
mens self-report of partner bonding compared those who carried no 334 allele. Likewise, there
is strong evidence of overtransmission in autism of the 334 and 340 alleles (Kim, et al., 2002).
Autism is also associated with variation in RS1 and RS3 microsatellite (Yirmia, Rosenberg,
Levi, Salomon, et al., 2006). These findings suggest that the associations between the AVPR1A
gene and animals social behaviors may generalize to humans with the RS3 alleles 334 and 340
conferring risk with respect to social behaviors. Given these findings it was hypothesized that
alleles 334 and 340 would relate to lower maternal sensitivity. Longer repeats (including alleles
334 and 340) of the RS3 microsatellite have also been shown to relate to overactivation of the
amygdala in response to fearful/angry face stimuli (Meyer-Lindenberg, et al., 2008). This further
supports the suggestion that variation in AVPR1A gene may relate to the organization of social
behaviors in humans. Hence, the association between maternal sensitivity and RS3 length was
also examined. It is noteworthy that Knafo et al. (2008) found that short alleles (308-325 bp)
conferred risk to altruistic behavior rather than long alleles (327 to 342 bp) but this latter study
has not been replicated.
Figure 7. Location of the RS3 microsatellite, rs7298346 and rs1042615 on the AVPR1A gene.
The variant rs1042615 was selected for study as the polymorphism tags for (or is
representative of) all other haplotypes on the gene. Haplotypes are combination of alleles at
particular locations on a chromosome that are transmitted together. Since the AVPR1A is a
highly conserved gene with most of its content showing high linkage disequilibrium (non-
78
random recombination of alleles and subsequent biased transmission of the combinations;
International Hapmap Project: Annotate Phased Haplotype Display), the inclusion of this variant
in the study increases confidence that most of the polymorphic content of the gene will be
accounted for. To the best knowledge of the author, research has not examined whether this
polymorphism relates to human social behavior. Given the lack of published empirical work on
this variant, no a priori hypotheses were specified with regards to which alleles and genotypes
might relate to maternal sensitivity.
Hence, the studys first objective was to examine whether maternal sensitivity is related
to variants of the AVPR1A gene. Furthermore, given several lines of evidence which suggest that
the AVPR1A gene might also relate to differential reactivity to environmental stress, the second
objective of the proposed study was to examine whether mothers AVPR1A genotype moderates
the effect of early adversity on mothers sensitivity.
AVPR1A and stress regulation.
Several lines of research suggest that variation in the AVPR1A gene may be associated
with individuals regulation of emotion and response to stress. Vasopressin and corticotrophin-
releasing hormone (CRH) are the primary hormones involved in the activation of the
hypothalamic-pituitary adrenal (HPA) axis, the neuroendocrine system mainly involved in stress
and emotion regulation. Dysregulation of the HPA axis has been associated with mood disorders
(Spencer & Hutchison, 1999). Likewise, variations in AVPR1A expression levels in the brain are
related to anxiety in mice (Murgatroyd, et al., 2004) and the prairie vole (Hammock, et al.,
2005). Positive correlations have been reported between variation in the AVPR1A gene and
AVPR1A gene expression in several areas of the hypothalamus and other areas of the limbic
system (Bosch & Neumann, 2008). Variation in the AVPR1A is also related to overactivation of
79
the amygdala in response to fearful face stimuli (Meyer-Lindenberg, et al., 2008). Given
vasopressins role in the activation of the HPA axis and that this peptide predominantly acts
through the V1a and receptors in the brain (Kim, et al., 2002) which are located throughout the
limbic system (Ebstein, et al., 2009) it has been suggested that variations in the AVPR1A gene
might relate to individuals stress reactivity (Ebstein, et al., 2009).
Hence, the second objective of the present study was to examine whether mothers
AVPR1A genotype moderates the relationship between mothers early adversity and maternal
sensitivity. Herein, the construct mothers early adversity is operationalized as a cumulative risk
score of various unfavorable conditions mothers experienced during childhood. A cumulative
score was used given evidence that single risk factors do not represent individuals experiences
adequately as risks cluster together. For example, Dong et al. (2004) demonstrated a high level of
interrelatedness among adverse childhood experiences (i.e. abuse, poverty, and parental mental
health and alcohol problems). Exposure to one risk such as parental alcohol abuse is associated
with an increased likelihood of exposure to other adverse events. Based on these findings it is
has been suggested that studies interested in the effects of early adversity on subsequent
functioning include measures of multiple adverse events as opposed to focusing on single
experiences (Dong, et al., 2004). This recommendation is consistent with studies examining the
impact of cumulative risks on mental health. The number of risks, rather than the nature of a
specific risk, is negatively associated with well-being including parenting (Dong, et al., 2004;
Masten, 2006; Rutter, 1979; Sameroff, 2000).
The risk factors included in the cumulative early adversity score have all been shown to
be associated with adult well-being; these include having been raised by a mother with low
education, who was a teen at the time of the first child, having experienced multiple parental
80
transitions, having experienced physical and sexual abuse, having witnessed physical and/or
verbal abuse, having been raised by parents who had problems with substance abuse (i.e. drugs
and alcohol) and mental health (e.g. see Dong, et al., 2004).
Since the present study is the first to examine the possible association between AVPR1A
gene and stress reactivity, no a priori hypotheses were specified on which AVPR1A genotypes
might moderate mothers response to early adversity. However, moderation was examined only
with regards to AVPR1A variants that showed relations to sensitivity. Analyses were performed
by covarying the influence of correlates of maternal sensitivity including maternal depression
(NICHD, 1999) and marital conflict (Grych, 2002).
Since allele frequencies differ across ethnicity (personal communication, Dr. Barr, 2009),
these frequencies were first examined. Ethnic groups that showed differences in allele
frequencies were omitted from the analyses to reduce the probability of confounding possible
genetic effects from cultural differences in parenting practices.
Method
The sample was drawn from wave two of the full sample of the Kids, Families and Places
Study which is an ongoing prospective study of newborns, older siblings and their families in
Toronto and Hamilton area. A total of 668 families with a newborn and an older sibling were
enlisted through the Public Health Units at wave one. Families were enlisted in the study if the
newborn was full term, the mother spoke enough English to engage in a conversation, and the
family had at least one other child under 16-years of age. A sub-sample of 501 families was
enlisted if they had a newborn and at least one child under the age of 4-years old (sibling). The
501 families were more intensively investigated including observations in the home of parents
81
and children, direct testing of children and DNA to allow for the investigation of broader
questions.
Of the 501 families, 397 participated in wave two of the study, of these 347 provided
cheek swabs for DNA extraction. Eight families subsequently dropped out of the study reducing
the sample to 339. For two families, the genetic material could not be matched to their
identifying information further reducing the available genetic sample to 337.
All of the participants were English speaking. The sample was representative of the
Toronto population with respect to race. Mothers were primarily Caucasian (66%), while 12%
were South Asian, 11% were Southeast Asian, and 5% of mothers endorsed Black as their race.
Likewise, Census data indicate that 57% of the population in 2006 was Caucasian, 13.5% were
South Asian, 14% were South East Asian, and 7% were Black (Statistics Canada, 2007). The
sample was higher in education and family income. For example, the sample median family
income was $85 000.00 to $95 000.00 while the Census 2006 data for Toronto indicated a
median income of $45 350.00.
Procedures.
Trained interviewers visited each familys residence for approximately two hours.
During the visit, mothers completed various standardized questionnaires, including
questionnaires that assessed their childhood experience and psychosocial functioning of their
parents. Mothers were videotaped interacting individually with their 18 month old child and at
least one of the infants sibling; mothers interacted individually with their children for 15
minutes. The interaction was divided in three segments, the first five minutes mothers and child
interacted without the use of a toy, then mothers engaged their child with a challenging task
which consisted of the child drawing a pattern from a spiral book. The last five-minute segment
82
involved mothers first reading a story to their child and then asking their child to give a brief
summary of the story.
Measures.
Genotyping. The markers rs10422615 and rs7298346 were found by searching for
confirmed polymorphisms in public databases (ABI database and the NCBI SNP database
(http://www.ncbi.nlm.nih.gov/SNP) and for pre-designed assays from Applied Biosystems (ABI,
Foster City, CA, USA, Assay-on-Demand by Applied Biosystems
C
r
s
7
2
9
8
3
4
6
(
C
_
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2
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0
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)
A
G
A
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A
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]
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G
C
T
T
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G
A
G
T
T
G
T
C
C
C
6
0
C
86
Cumulative Early Adversity: Variables consisting of the cumulative early adversity index
were drawn from the completed wave one data. Wave 1 data from the Kids, Families and Places
study were imputed using the PROC MI statement in SAS. Missing data on these variables were
imputed using multiple imputation. As described by Rubin (1996), the first step of multiple
imputation involves identifying all of the missing observations within a data set and then
generating a set of plausible values that can be used to replace the missing observations. This
step is then repeated multiple times to generate several complete data sets resulting in a more
accurate approximation of the parameter estimates and standard errors by accounting for
uncertainty regarding the accuracy of a single imputation (for a more detailed description of
these procedures see Allison, 2002; Horton & Kleinman, 2007; Horton & Lipsitz, 2001). This
resulted in five datasets with the imputed values. Variable comprising the cumulative early
adversity score were averaged across the five imputed data sets.
A cumulative indicator was created by summing mothers scores on the following risk
factors . Mothers were assigned a value of 1 on each variable if they experienced the respective
risk or 0 for no experience. Detailed description of the measures is provided in study 1.
1. Mothers mother had less than grade 8 education. Mothers reported on the level of
educational attainment of their own mother by answering six questions drawn from the
Ontario Child Health Study (Boyle, Offord, Racine, Sanford, et al., 1993).
2. Mothers mother was a teenager at time of first child. Mothers reported on the age of
their mother when the first child was born (source: Ontario Child Health Study; Boyle,
Offord, Racine, Sanford, et al., 1993). A code was created by assigning mothers a value
of 1 if their mother was under the age of 20, and a value of 0 if their mother was older
than 20-years of age.
87
3. Having been raised by one or both parents who suffered from mental illness, drug and/or
alcohol abuse (source: Ontario Child Health Study; Boyle, Offord, Racine, Sanford, et al.,
1993). Mothers reported on the presence of mental health disturbance and drug
and/alcohol abuse in their mother and father. As described in study 1, the possible scores
ranged from 0 to 6.
4. Having experienced physical and/or sexual abuse. Mothers reported on whether they
were ever sexually and/or physically abused during childhood. The possible score ranged
from 0 to 2 with 0 representing no experience of abuse, 1 representing either physical or
sexual abuse, and 2 indicating the experience of both physical and sexual abuse.
5. Having witnessed verbal and/or physical abuse. Mothers reported on whether they ever
witnessed verbal and/or physical abuse by answering two questions drawn from the
Ontario Child Health Study (Boyle, Offord, Racine, Sanford, et al., 1993):. Mothers were
assigned a value of 0 if they reported never witnessing verbal and/or physical abuse,
while a value of 1 was assigned to mothers with history of witnessing verbal and/or
physical abuse. Possible scores range from 0 to 2.
As described in study 1, since fewer than 3% of the sample endorsed 7 or more early
adversity risks, the variable was recoded so that risk levels 6 through 9 were recoded to 5 or
more risks.
Marital conflict. At wave two, mothers reported on the frequency and severity of
marital conflict with their spouse by answering two questions assessing minor and major
disagreements, drawn from Kerig (1996). As suggested by Kerig (1996) answers to the
88
question assessing major disagreements were weighted by multiplying the answer by a value
of two. The scores were then summed to create a total marital conflict frequency score;
higher numbers indicate greater frequency and severity of marital conflict.
Maternal depression. At wave two, mothers completed the Center for Epidemiological
Studies Depression Scale (Radloff, 1977). Mothers answered 20 questions (e.g. item 3: I felt
that I could not shake off the blues even with help from my family or friends) with response
options that range from 0 indicating no depression to 3 indicating high levels of depression.
The scores were summed to create a final depression score with a range from 0 to 60. Higher
scores indicate greater depression.
*Maternal Sensitivity. Maternal sensitivity was assessed from the 15-mimute videotaped
mother-child interaction using the Coding of Attachment-Related Parenting (CARP; Matias,
Scott & OConnor, 2006) and the Parent-Child Interaction System (PARCHISY; Deater-
Deckard, Pylas, & Petrill, 1997). The CARP is a global measure of parent-child interaction
quality that was derived from attachment theory and related assessments in young school-aged
children (Kochanska, 1997; Kochanska & Murray, 2000; Solomon & George, 1999; Thompson
& Raikes, 2003). Level and intensity were considered in deriving a score on a 7-point Likert
scale (1 = No evidence; 7 = Pervasive/extreme evidence). The system is based on attachment-
based interaction measures in infancy and young children (Ainsworth, Blehar, Waters, & Wall,
1978). Sensitive Responding measures the degree to which the parent displays awareness of the
child's needs and shows sensitivity to his/her signals, expresses warmth/support, supports the
child's autonomy, and demonstrates an ability to see things from the child's point of view.
Mutuality is a dyadic code and is compatible with the "goal-corrected partnership" notion in
attachment in toddlers and preschool- and school-aged children (Bowlby, 1982;
89
Kochanska, 1997; Kochanska & Murray, 2000). The scales demonstrated good stability over a
one-year period, with correlation estimates of .66 and .48 for Sensitivity and Mutuality,
respectively (Matias, 2006). Scores on the sensitive responding and mutuality scales have been
found to predict children's attachment narrative style as rated from a standard story stem
assessment and peer ratings of the child acceptance (Matias et al., submitted).
The PARCHISY is a global behavioural rating system that has been used widely to
examine naturalistic behaviours in a variety of populations (Brophy & Dunn, 2002; Corapci,
Radan, & Lozoff, 2006; Hughes & Ensor, 2005; Marks et al., 2006). The PARCHISY consists
of seven scales of parent behavior (positive and negative control, positive and negative affect,
responsiveness, on task behavior, and verbalisations) and seven categories of child behavior
(positive and negative affect, responsiveness, on task behavior, activity, noncompliance, and
verbalisations). For the purpose of this study only the positive control (use of praise,
explanations and open ended questions) scale was used. Assessments of mothers positive
control are associated with observed child difficult behavior (Deater-Deckard, 2000), concurrent
and future externalizing problems (Saltsman, 2008, Hughes & Ensor, 2007), and childrens
verbal ability and theory of mind (Hughes & Ensor, 2007).
For each five-minute task, coders provided ratings on a 7-point scale, with a score of one
indicating an absence of the constructs of interest (mutuality, sensitivity and positive control),
and a seven indicating an extreme amount of the constructs of interest. An expert coded 10% of
all coded data to ensure interrater reliability. When two coders were reliable with the expert,
10% of their data was compared to each other rather than to the expert. Reliability was checked
approximately every 10 families coded; discrepancies were resolved through discussion with the
ultimate decision made by the expert. For the 18-month old child, across the CARP and
90
PARCHISY scales, interrater reliability ranged from .75 to .96 with an average rating of .89; for
the older siblings interrater reliability ranged from .84 to .95 with an average rating of .89. First,
separate mean scores were computed across the three tasks on mutuality, sensitivity, and positive
control for each child. These scores were than averaged to create a final sensitivity score per
child. A family average was computed by taking the mean of the childrens total sensitivity
score.
Analysis
Missing Data.
Table 17 displays the frequency of missing data across the genetic markers and study
variables. The analyses were performed only on the families for whom genotypes were
available.
Table 17. Breakdown of available and missing data.
Variable Available N Maternal
depression
Marital
conflict
Early
adversity
Maternal
sensitivity
RS3 264 (22%) 260 (1.5%) 249 (6%) 264 (0%) 264 (0%)
rs1042615 320 (5%) 315 (4%) 301 (6%) 320 (0%) 320 (0%)
rs7298346 319 (5%) 314 (1.6%) 302 (5%) 319 (0%) 319 (0%)
Note: percentage of missing cases is indicated in brackets.
Hierarchical regression analysis.
Data were entered into separate hierarchical regressions to examine the associations
between maternal sensitivity and variation in the RS3 microsatellite and the markers rs1042625
and rs7298346. Hierarchical regression was used to (1) examine the amount of variance in
91
maternal sensitivity explained by genotype above and beyond the influence of covariates of
sensitivity (including maternal depression and marital conflict) and the experience of early
adversity, and (2) to examine the amount of variance explained by the interaction of genotype by
early adversity, after accounting for the main effects of covariates, early adversity and genotype.
In the first step of the regressions, the dichotomous codes for mothers genotypes were
entered. In the second step, covariates were entered to examine whether these explained
variance in sensitivity above and beyond mothers genotype. For genotypes showing
associations to sensitivity moderation was examined. First an interaction term was computed by
multiplying the variable early adversity with the respective dichotomous code representing the
genotype. This interaction term was entered in the last block of the regression.
Results
Normality.
The descriptive statistics of all study variables were examined for evidence of normality.
The distribution of the variable maternal depression showed skewness and kurtosis as indicated
by values greater than 1 on the respective statistics. The variable was transformed into its square
root. Since the results of the analysis were similar using the original versus the transformed
variable, the reported results are based on the original variable.
Marker: RS3 microsatellite.
Descriptive statistics.
In total 17 alleles were detected which is consistent with prior research (e.g. see Kim et
al., 2002). Table 18 displays the frequency of the detected alleles. Comparing the allele
frequencies in the present study with those from Kim et al., (2002) and comparing the length of
the primers used herein and in Kim et al., (2002) study it was determined that alleles 328 and 334
92
herein represent Kim et al., (2002) alleles 334 and 340, respectively. Given the low frequencies
of alleles 328 and 334, it was not possible to conduct the analyses at the allele level as the
infrequency would result in low statistical power. The low frequencies of the alleles would have
been further reduced by splitting the data set across ethnic groups. Analyses were performed at
the genotype level based on short versus long allele length; the long versus short category was
based on Knafo et al., (2008).
Table 19 displays the frequency of the RS3 genotypes across ethnicity. Mothers from
European background show the genotype long/long less frequently (34% for Europeans) than
South Asians (45%), Blacks (53%) and East/South Asian mothers (42%). As well, the
short/short genotype is observed less frequently in the South Asian and Black groups (6% and
7% respectively) than European (16%) and East/South Asian (16%). Given these differences,
the analyses were performed only on the European sample to avoid confounding possible genetic
effects with cultural differences in parenting practices.
93
Table 18. RS3 allele frequency.
Allele N Freq
310 8 0.015
316 2 0.004
318 1 0.002
320 2 0.004
322 34 0.064
324 51 0.096
326 110 0.206
328 118 0.221
330 73 0.137
332 65 0.122
334 18 0.034
336 3 0.006
338 24 0.045
340 17 0.032
342 5 0.009
344 2 0.004
346 1 0.002
Total 100
94
Table 19. RS3 genotype frequency across ethnicity.
Ethnicity Genotype Frequency Percent
1.00 European 1.00 short/short 27 16
2.00 short/long 87 50
3.00 long/long 58 34
Total 172 100.0
2.00 South Asian 1.00 short/short 2 6
2.00 short/long 17 49
3.00 long/long 15 45
Total 34 100.0
3.00 Black 1.00 short/short 1 7
2.00 short/long 6 40
3.00 long/long 8 53
Total 15 100.0
4.00 East/South Asian 1.00 short/short 5 16
2.00 short/long 13 42
3.00 long/long 13 42
Total 31 100.0
Grand total N 262*
*Note: Grand total does not equal 264 as 2 mothers identified themselves as
belonging to multiple ethnic groups.
95
Hierarchical regression analyses.
In relation to mothers homozygous for the short allele (S/S), mothers homozygous for the
long alleles (L/L) were significantly less sensitive (= -.31, p < .01, F(2, 162) = 5.08, p <.01).
No differences were found between mothers heterozygous for the long alleles (S/L) and those
homozygous for the short (S/S) alleles ( = -.10, p > .05). The long/long genotype explained
6% of the variance in sensitivity (R
2
= .06, adjusted R
2
= .05 ). The main effect of the long/long
genotype remained significant ( = -.32, p< .01) after accounting for theoretical covariates of
sensitivity including mothers depression, marital conflict and mothers early adversity. These
covariates were not significantly associated with sensitivity and did not explain additional
variance in sensitivity (R
2
change = .02, (F
change
(2, 160)=1.70, p >.05 for marital conflict and
depression, and for early adversity R
2
change = .004, (F
change
(1, 159)=0.69, p >.05) . Mothers
homozygous for the long alleles (L/L) were also significantly less sensitive than mothers
heterozygous for the long alleles (S/L), ( =-.21, p < .05, F(2, 162) = 5.08, p <.05).
Next, the moderating influence of the long/long genotype on the association between
early adversity and sensitivity was examined. Since mothers homozygous for the long alleles
were found to differ from mothers with the genotype long/short and those with the short/short,
the analysis was performed by entering only the code for the long/long genotype; hence, the
reference category is the short/long and short/short genotypes. As shown in Table 20, the
interaction term was significant and explained an additional 3% of the variance (R
2
change =
.025, (F
change
(1, 160)=4.39, p < .05). As shown in Fig. 8, in the context of low early adversity (-1
SD), mothers genotype is not related to lower sensitivity. However, in the context of high early
adversity (+1 SD) mothers homozygous for the long alleles (L/L) were less sensitive than those
with the genotype short/short and short/long. The effect size of the interaction is small
96
(calculated as f
2
= R
2
(final model)
- R
2
(model 1)
/ 1 - R
2
(final model)
= .102-.055 /1-.102 =.05) as
indicated by Cohens (1988) criteria of effect size of .02 and less than .15 indicating a small
effect.
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Figure 8. RS3 length moderates the association between early adversity and sensitivity.
* p < .05
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99
Marker: rs1042615.
Descriptive statistics.
Table 22 displays the frequency of the rs10422615 genotypes. As shown in Table 23,
notable differences in genotype frequencies are observed across ethnic groups. For example, the
genotype G/G is observed less frequently among East and South Asians (15%) relative to
Europeans (33%), South Asians (47%) and Blacks (77%). Given these differences, the analyses
were performed only on the European group to avoid confounding possible genetic effects from
cultural differences in parenting practices across the groups.
Table 22. Frequency of genotypes detected on rs10422615 marker.
Genotype N %
A/A 55 17
A/G 150 47
G/G 115 36
Total 320 100
100
Table 23. Genotype frequency of rs10422615 across ethnicity.
Ethnicity Genotype Frequency Percent
European A/A 38 18.2
A/G 102 48.8
G/G 69 33.0
Total 209 100.0
South Asian A/A 4 11.1
A/G 15 41.7
G/G 17 47.2
Total 36 100.0
Black A/G 4 23.5
G/G 13 76.5
Total 17 100.0
East/South Asian A/A 10 29.4
A/G 19 55.9
G/G 5 14.7
Total 34 100.0
Hierarchical regression analyses.
As shown in Table 24, no differences in sensitivity were found between mothers
homozygous for the G alleles (G/G) and those homozygous for the A alleles (A/A) ( = -.08, p >
.05) and mothers heterozygous for the G allele (A/G) , ( = .14, p > .05, F(2, 199)=1.61, p > .05).
101
Neither depression ( = -.08, p >.05) nor marital conflict ( = -.12, p >.05, F
change
(2,197)=2.4, p
>.05 ) were significantly associated with maternal sensitivity. Furthermore, in relation to
mothers heterozygous for the G allele (A/G), no significant differences were found between
mothers homozygous for the A allele (A/A) (= -.03, p > .05, F(2, 199)=1.61, p > .05; data not
shown in table form).
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103
Marker: rs7298346.
Descriptive statistics.
Table 25 displays the frequency of the rs7298346 genotypes. As shown in Table 26,
notable differences in genotype frequencies are observed across ethnic groups. For example,
relative to Blacks, the genotype A/A is observed less frequently among East and South Asians
(0%), South Asians (7.5%) and Europeans (2%). The genotype T/T is observed more frequently
among Europeans (77%) and East/South Asian (74%) relative to Blacks (37.5%) and South
Asians (52.5%). Given these differences, it was not possible to conduct the analyses across the
entire sample (irrespective of ethnicity) as this may have resulted in confounding possible
genetic effects from cultural differences in parenting practices across the groups. As well, since
the genotype A/A was detected in only 2% of the European sample it was also not possible to
compare levels of maternal sensitivity as a function of genotype. No further analyses with this
variant were conducted.
Table 25. Frequency of genotypes detected on rs7298346 marker.
rs7298346
Genotype N %
A/A 11 3
A/T 79 25
T/T 229 72
Total 319 100
104
Table 26. Genotype frequency of rs7298346 across ethnicity.
Ethnicity Genotype Frequency Percent
European A/A 4 2.0
A/T 43 21.0
T/T 158 77.0
Total 205 100.0
South Asian A/A 3 7.5
A/T 16 40.0
T/T 21 52.5
Total 40 100.0
Black A/A 4 25.0
A/T 6 37.5
T/T 6 37.5
Total 14 100.0
East/South Asian A/A 0 0
A/T 9 26.0
T/T 26 74.0
Total 35 100.0
105
Discussion
Results of this study suggest that variation in the AVPR1A gene relates to maternal
sensitivity and stress reactivity. Mothers homozygous for the long alleles of the RS3
microsatellite were rated by observers as significantly less sensitive than mothers homozygous
for the short alleles and those heterozygous for the long alleles. Previous studies have
documented biased transmission in Autism of allele 334 and 340 herein defined as long alleles
based on Knafo et al., (2008). These findings suggest that variation in RS3 length may be
associated with individuals ability to read and correctly interpret social and emotional cues and
to empathize with others. Remarkable impairments in these abilities are the hallmark feature of
Autism disorders. These abilities also constitute the foundation of maternal sensitivity, in this
study defined as mothers awareness and ability to correctly interpret subtle infants signals and
the prompt contingent response to infants cues. However, the mechanisms through which
variation in RS3 length relates to Autism and maternal sensitivity are unknown. Amygdala
activation has been proposed as a neural circuit possibly mediating the associations between
variation AVPR1A and the range of human social behavior afore-stated.
In humans, the peptide arginine vasopressin (AVP) binds to receptors located in the
amygdala (Whalen, Rauch, Etcoff, McInerney, Lee, Jenike, 1998). Lesions to the amygdala are
associated with social disinhibition (Adolphs, Gosselin, Buchanan, Tranel, Schyns, & Damaiso,
2005). Aggression is related to decreased amygdala activation, while increased activation is
related to social avoidance and phobia (Stein, Goldin, Sareen, Zorilla, & Brown, 2002). Fearful
stimuli strongly activate the amygdala, and lesions to the amygdala are associated with
impairments in recognition of fearful faces and social disinhibition (Adolphs, Gosselin,
106
Buchanan, Tranel, Schyns, & Damaiso, 2005). Individuals with Autism show impairments in
amygdala function (Dalton, Nacewicz, Johnstone Schaefer, Gernsbacher, Goldsmith, et al.,
2005). In healthy persons, longer repeats of the RS3 microsatellite relate to overactivation of the
amygdala in response to fearful/angry face stimuli (Meyer-Lindenberg, et al., 2008) These latter
findings coupled with the overtransmission of alleles 334 and 340 in Autism (Kim, 2002) herein
defined as long alleles, and the associations between Autism and RS3 microsatellite (Yirmia,
Rosenberg, Levi, Salomon, Shulman, Nemanov, L. et al., 2006) provide convergent evidence
that variation in the RS3 microsatellite may represent a diathesis for the organization of social
behavior and stress reactivity in humans.
The diathesis-stress model (Clark, Beck & Brown, 1992; Phelps, Belsky, & Crnic, 1998)
posits that negative outcomes result from the activation of an underlying diathesis by an
environmental insult. In the absence of the environmental insult the diathesis is not activated
bearing no consequences to the individuals functioning. In mice, chronic stress is associated
with increased expression of the peptide arginine vasopressin (AVP) and corticotrophin-releasing
hormone (CRH) (Merali, Hayley, McIntosh, Bdard, & Anistman, 2009) with the increased
expression showing endurance over time (Merali, Hayley, McIntosh, Bdard, & Anistman,
2009). Since AVP and CRH are the primary hormones involved in the activation of the
hypothalamic-pituitary adrenal (HPA) axis, it has been suggested that the increased expression of
these hormones may result in an heightened HPA response to subsequent demands (Merali et al.,
2009). In humans, longer repeats of the RS3 microsatellite are associated with higher
hippocampal mRNA levels (Knafo et al., 2008) suggesting an heightened expression of AVP.
The significant interaction found in this study between homozygosity for the long RS3
repeats and mothers early adversity is consistent with a diathesis-stress process. The lowest
107
levels of maternal sensitivity were found among mothers who experienced high levels of early
adversity and who carried the long/long RS3 genotype, relative to mothers with the short/short
and short/long genotype. In the context of low early adversity, no differences in maternal
sensitivity were found as a function of mothers genotype. Hence, length of RS3 bears
consequence to maternal sensitivity only in the context of high early adversity. Among mothers
who experienced high early adversity and who carry the long/long genotype, maternal
insensitivity may come about as a result of heightened level of stress reactivity which may
compromise mothers ability to successfully understand and meet the infants needs. Mothers
sensitivity may be further compromised by the possible difficulties in correctly interpreting the
infants cues, as suggested by the overtransmission of alleles 334 and 340 in Autism (Kim, 2002)
and impairments in correctly interpreting facial emotion associated with amygdala functioning
(Adolphs, Gosselin, Buchanan, Tranel, Schyns, & Damaiso, 2005).
Last, the study also examined whether variations in maternal sensitivity related to the
variant rs1042615. No associations were found. A trend toward statistical significance was
noted for less sensitivity among mothers homozygous for the G allele of the marker rs1042615,
relative to mothers with the genotype A/G and A/A. Given that single genes typically explain
less than 1% of the variance in human functioning (Ebstein, 2006), perhaps the study lacked
adequate statistical power to detect such small effects. A similar limitation is noteworthy for the
interaction between early adversity and homozygosity for the long alleles on the RS3. The effect
of this interaction is small (f
2
= .05) with the associated p value just at significance level. Last,
since the analyses were performed only on Europeans participants it is unknown whether the
results generalize to other ethnic populations. Splitting the sample across ethnic groups was not
possible given the small number of participants across ethnicity.
108
Strengths of the study include maternal behavior that was observed across reliable coders.
Maternal behavior was coded from naturalistic interactions using a normative sample, increasing
generalizability of results to normative patterns of mother-child interactions.
The measure of early adversity was based on mothers retrospective reports of their experiences
of early adversity. Although retrospective accounts may be biased due to recall limitations, the
present measure includes recall of concrete events only. Recall of concrete experiences in
childhood, such as the experience of physical abuse, are remembered with less bias than recall of
subjective experiences such as reports of relationship quality (Prescott, Bank, & Reid, 2000).
Last, the inclusion of three AVPR1A markers accounted for most of the variation of this small but
highly conserved gene.
The study results suggest that interventions aimed at improving mothers sensitivity
should be mindful of mothers ability to cope with stress and daily demands of child rearing.
Higher sensitivity is indeed associated with availability of support in mothers lives. In addition
to providing supports and/or in the context where such supports are lacking, such as the case
with new immigrants, interventions should also focus on providing mothers with adequate
coping skills to reduce the possible heightened state of stress reactivity. Last, given the
associations between variation in the AVPR1A, Autism and the ability to correctly decipher
emotions from faces, interventions should also be mindful of mothers capacity to correctly
identify the infants state and ability to choose a sensitive response strategy.
109
General discussion
The purpose of the present studies was to identify the underlying mechanisms that
explain how mothers early adversity relates to subsequent maternal sensitivity. Results from
these studies indicate that both proximal and distal factors are important source of influence and
that maternal sensitivity is determined by the interplay of these multiples factors. Proximal
mechanisms include mothers depression and their appraisal of their infant behavior. These two
mechanisms accounted for the association between early adversity and maternal sensitivity.
However, this relationship was not straightforward as shown by results of the moderated
mediation analyses. Quality of the neighborhood is a distal factor that was found to moderate the
influence of early adversity on maternal depression. High quality neighborhood protected
mothers from the influence of early adversity on maternal depression while a low quality
neighborhood exacerbated this association. These findings indicate that although early adversity
increases the risk of maternal depression thereby compromising maternal sensitivity, aspects of
the ecology in which mothers reside must also be considered when assessing the influence of
early adversity on subsequent maternal functioning. The implication of these findings is that
programs geared at prevention of compromised functioning across the life course should not only
consider the individual but also the wider ecology such as the neighborhood quality.
Results from study 1 also suggest that family income is also a very important source of
influence for maternal sensitivity. Some of this influence is accounted by the increased stress
that mothers from low income families feel resulting in increased feelings of depression and
more negative appraisals of infant temperament. However, family income also exerted a direct
influence on maternal sensitivity after accounting for the above-stated stress process. This
suggests that familys financial stress does not fully account for socioeconomic status (SES)
110
related differences in parenting practices. Parental beliefs, values and attitudes regarding child
rearing may be underlying factors of the direct relationship between family income and maternal
sensitivity. These possible influences should be better represented in theories on determinants of
parenting and parenting research.
A second proximal influence includes mothers genotype. Mothers homozygous for the
long alleles on the RS3 microsatellite were found to show lower levels of sensitivity relative to
mothers carriers of the long/short and short/short genotype. In humans, longer repeats of the RS3
microsatellite relate to overactivation of the amygdala in response to fearful/angry face stimuli
(Meyer-Lindenberg, et al., 2008). Amygdala activation has been proposed as a neural circuit
possibly mediating the associations between variation AVPR1A and a range of human affiliative
behavior (Meyer-Lindenberg, et al., 2008) and stress reactivity (Ebstein, et al., 2009). Results
from the moderation analyses indicate that the long repeats of the RS3 microsatellite increase the
risk of reduced sensitivity only when mothers experienced high levels of early adversity. These
findings highlight the importance of considering experiential factors alongside biological
predispositions when explaining variability in maternal behavior.
111
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Appendix A
Comparison of original and imputed data and percentage of missing data.
Original data Imputed data
N available
(Total N=501) % missing Mean SD Mean SD
Cumulative early adversity risk 501 0 2.09 1.28 2.09 1.28
MBQS 381 24 0.28 0.49 0.27 0.49
Ainsworth acceptance 381 24 6.27 1.74 6.29 1.74
Ainsworth accessibility 381 24 5.83 1.99 5.82 2.01
Ainsworth cooperation 381 24 5.57 1.9 5.59 1.9
Ainsworth sensitivity 381 24 5.4 1.96 5.42 1.98
Infant temperament 500 0.2 3.05 0.97 3.05 0.97
No. of children in the home 501 0 2.55 0.99 2.37 0.82
Family income 472 6 11.81 4.1 11.81 4.1
Infant weight (kilos and grams) 498 0.6 3.4 0.51 3.4 0.51
Mothers' education 500 0.2 15.12 2.7 15.27 2.7
Mothers' age 499 0.4 32.87 4.9 32.71 4.9
Maternal depression 493 1.6 9.45 7.3 9.46 7.27
Prenatal problems 500 0.2 0.08 0.11 0.08 0.11
Neighborhood quality 498 0.6 0 1 0 1
137
Appendix B
Change in maternal sensitivity measurement.
A switch in measurement of maternal behavior took place in study 2. Study 1 used the
Maternal Behavior Q-Sort (Pederson & Moran, 1995) a validated measure of maternal sensitivity
during the infancy period. Assessing maternal sensitivity with this measure yielded no significant
findings with mothers genotype. In study 2, maternal sensitivity was assessed with older
children (18 months of age to 6 years of age) and while mothers performed several tasks
independently with two of her children (the 18-month old infant and sibling closest in age).
Mothers assessments were averaged across the multiple children within the family. Observing
mothers interact separately with more than one child strengthens the quality of the measure as it
increases confidence that the assessment is that of mothers behavior and not an assessment of
the interaction pattern of a specific mother-child dyad. Thus, it was reasoned that the Time 2
assessment of sensitivity may have been a stronger measure of maternal behavior thus increasing
the likelihood of detecting the possible, albeit small, effect of the AVPR1A gene on mothers
behavior and stress reactivity.
Table 21. Correlations between time1 and time 2 maternal behavior measures.
MBQS AINSW.
ACCEPTANCE
AISNW.
ACCESSABILITY
AINSW.
COOPERATION
T1 SENSITIVITY
FACTOR SCORE
(WITH MBQS &
AINSWORTH)
T2 sensitivity
(CARP and
PARCHISY)
(N=377)
.21* .24* .25* .22* .26*
*p < .00001