the role of parental bonding in depression
DESCRIPTION
The Role of Parental Bonding in DepressionTRANSCRIPT
ORIGINAL ARTICLE
Unique and Shared Aspects of Affective Symptomatology:The Role of Parental Bonding in Depression and AnxietySymptom Profiles
Tiffany M. Meites • Rick E. Ingram •
Greg J. Siegle
Published online: 22 December 2011
� Springer Science+Business Media, LLC 2011
Abstract Prior research has found an association
between parental bonding and depression and anxiety.
Specifically, low levels of care and high levels of over-
protection have been associated with increased risk for
developing depression and anxiety. However little research
has explored the relationship between factors of parental
bonding and specific aspects of depression and anxiety.
The present study investigated these relationships in a
sample of undergraduate students (n = 680) who reported
a range of affective symptomatology. Lower levels of
maternal care were associated with negative beliefs about
the self, negative interactions with others and fatigue;
lower levels of maternal and paternal care were associated
with generalized fear. Maternal overprotection was asso-
ciated with physical symptoms of anxiety and a fear of
dying, whereas paternal overprotection was a significant
predictor of negative beliefs about the self and difficulty
maintaining steadiness when anxious. These findings
highlight the importance of understanding the role of par-
enting in the development of vulnerability to affective
symptomatology.
Keywords Depression � Anxiety � Bonding � Parenting �Attachment � Cognitive vulnerability
Introduction
An extensive body of theory and research has suggested
that early life stressors may play a critical role in creating
cognitive vulnerability to anxiety and depression (Petchel
and Pizzagalli 2011). For example, Beck’s original cogni-
tive model of depression highlighted the importance of
developmentally based cognitive factors in depression
(1967). The theory stated that, ‘‘In childhood and adoles-
cence, the depression-prone individual becomes sensitized
to certain types of life situations…when a person is sub-
jected to situations reminiscent of the original traumatic
experiences, he may then become depressed (p. 278; Beck
1967). A wealth of empirical data have supported this idea
for depression (see Ingram et al. 2011 for review). Like-
wise, theory and data suggest that early negative life events
contribute to the development of vulnerability to anxiety
disorders in adulthood (Malcarne et al. 2010). It appears
clear that childhood adversity plays a critical role in the
development of depression and anxiety.
Parental bonding processes are associated with child-
hood adversity and are broadly linked to ideas about
attachment processes. Although a number of parenting
behaviors can affect bonding, the core features of parental
bonding are frequently conceptualized as the multidimen-
sional constructs of care (warmth and nurturance) and
protection (an appropriate level of concern for safety and
security). Adequate bonding with key caregivers along the
lines of care and protection is assumed to provide the
necessary psychological foundation for healthy functioning
in adulthood. Conversely, disrupted parental bonding, often
defined as lower levels of care (rejection and neglect) and
overprotection (controlling and intrusive behaviors), has
been linked with the development of psychopathology
(Enns et al. 2002). In particular, deficits in parental
T. M. Meites � R. E. Ingram (&)
Department of Psychology, University of Kansas, Lawrence,
KS 66045, USA
e-mail: [email protected]
T. M. Meites
e-mail: [email protected]
G. J. Siegle
University of Pittsburgh School of Medicine, Pittsburgh,
PA, USA
e-mail: [email protected]
123
Cogn Ther Res (2012) 36:173–181
DOI 10.1007/s10608-011-9426-3
bonding have been found to predict both depression and
anxiety (e.g., Blatt and Homann 1992; Grotmol et al. 2010;
Lima et al. 2010).
Although depression and anxiety are conceptualized as
distinct disorders, there is considerable overlap between the
two. In the categorical framework of the Diagnostic and
Statistical Manual of Mental Disorders-IV-Text Revision,
depression and anxiety can co-exist and thus be comorbid
(DSM-IV-TR; American Psychiatric Association 2000).
Some estimates suggest that as many as half of those
diagnosed with major depressive disorder also suffer from
an anxiety disorder (e.g., Hirschfeld 2001; Kessler et al.
2003). Such comorbidity complicates efforts to understand
how variables such as deficits in parental bonding may
contribute to the development of these affective states,
particularly since anxiety has emerged as a significant
predictor of the development of depression (Olino et al.
2010; Wittchen et al. 2003) and because high levels of
one syndrome are correlated with high levels of the other
(Ingram 1990).
Although depression and anxiety are viewed as separate
affective syndromes with unique factors, they are none-
theless characterized by factors that are common to each
disorder (e.g., Ahrens and Haaga 1993; Cropley and
MacLeod 2003; MacLeod et al. 1997; Reardon and
Williams 2007). For example, evidence derived from the
tripartite model of depression and anxiety suggests that
they differ on features such as anhedonia, physiological
reactivity (e.g., Watson et al. 1995a, b), and level of
positive affect (e.g., Williams et al. 2004), but that both
conditions involve a high level of negative affect. Addi-
tionally, even though depression and anxiety are nosolog-
ically distinct syndromes within the DSM-IV-TR, their
diagnostic symptoms overlap; specifically fatigue, con-
centration problems, and sleep difficulties are criteria for
both categories.
The overlap of depression and anxiety has implications
for understanding the role of parental bonding in the
development of these syndromes. Despite empirical evi-
dence linking parental bonding variables with depressive
and anxious states, the exact nature of this relationship
remains unclear. Although data have shown that parental
bonding is related to the global states of depression and
anxiety, it is unclear if they have varying relationships with
the different patterns of symptoms. Similarly it is unknown
whether the core features of parental bonding (i.e., care and
overprotection) are associated with distinct affective fac-
tors. A number of studies have suggested that a lack of care
and heightened overprotection are associated with psy-
chopathology in general (Blatt and Homann 1992;
Gladstone and Parker 2005; Ingram et al. 1998; Lima et al.
2010; Rapee 1997), but with few exceptions, it has yet to
be determined whether these dimensions are uniquely
associated with the features of depressed or anxious states.
Moreover, lack of care and heightened overprotection can
characterize either or both maternal or paternal behaviors;
maternal and paternal bonding may act independently and
may be associated with a unique set of affective factors. To
date, however, there is little evidence as to whether these
specific parent behaviors are associated with the unique
elements of depressive and anxious states. Exploration of
these relationships may yield evidence with significant
implications for understanding the development of the
distinct features of affective states.
One consideration when exploring these relationships is
identifying the appropriate samples to study. Diagnosti-
cally assessed samples of individuals with affective disor-
ders are obviously important in this regard, but the high
degree of comorbidity between patients with substantial
degrees of symptomatology also makes disentangling var-
ious features both difficult and possibly misleading (Ingram
1990). An alternate strategy is to test these questions in
nonclinical samples with a range of affective symptom-
atology, which may permit the distinct features of anxiety
and depression to be more clearly distinguishable. More-
over, as long as the commonly recognized affective fea-
tures of depression and anxiety exist in these samples, this
strategy may yield insights into how parental bonding is
related to the important features of depressive and anxious
disorders.
Given these considerations, the present study sought to
examine the association between dimensions of parental
bonding and the distinct features of depressive and anxious
symptoms. Because relationships of depressive and anx-
ious symptoms cannot be evaluated in participants who do
not report any symptoms, analyses were confined to those
reported at least some symptomatology on both measures.
We then examined the association between these factors
and scores on measures of maternal and paternal care and
overprotection. In order to examine this issue, a sample of
undergraduates was administered the Beck Anxiety
Inventory (BAI; Beck and Steer 1990), the Beck Depres-
sion Inventory (BDI; Beck and Steer 1993) and the
Parental Bonding Instrument (Parker et al. 1979).
To derive depressive and anxious symptoms profiles,
factor analyses were conducted on the BDI and on the BAI.
Prior research has suggested that the BDI and the BAI are
comprised of individual sub-factors (e.g., Osman et al.
1997; Shafer 2006) but it is important to note that dis-
crepancies have arisen as to the number of factors each
measure contains. Helm and Boward (2003) reported a
two-factor structure for the BDI whereas other studies have
reported only a single factor (e.g., Welch et al. 1990), a
four factor structure (Bennett et al. 1997), or a three factor
structure (Byrne and Baron 1993). Similar findings have
been reported for the BAI, with some evidence for a four
174 Cogn Ther Res (2012) 36:173–181
123
factor model with two higher order factors (Osman et al.
1997) and other evidence suggesting a two-factor model
(Chapman et al. 2009). Because no definitive factor
structure has been identified for either the BDI or BAI, and
because this study sought to maximize the descriptiveness
of symptoms when exploring relations between parenting
and symptomatology, exploratory factor analyses were
conducted.
Method
Participants and Procedure
Participants received credit in partial completion of a
course requirement and completed the measures in mass
testing procedure. Nine hundred sixty-two participants
initially completed the study, but because the present study
sought to explore the relation between anxiety and
depressive symptoms and parental bonding, participants
who did not endorse any symptoms on the BDI and the
BAI were excluded from analyses. The final sample con-
sisted of 680 participants, with women comprising 73.9%
of the final sample. The mean BDI score of the sample was
14.51, with individual scores ranging from 1 to 59. The
mean BAI score of the sample was 8.43, with individual
scores ranging from 1 to 58. Descriptive data for the
sample are presented in Table 1.
Measures
Parental Bonding
The Parental Bonding Instrument (PBI; Parker et al. 1979)
is a self-report questionnaire that measures parenting atti-
tudes and behaviors (i.e., caring and overprotection) from
the first 16 years of life. Participants rate each parent on
two four-point Likert subscales: a 12-item caring subscale
and a 13-item overprotection subscale. Higher scores on
the care scales represent more positive parental behavior,
whereas higher scores on the overprotection scales indicate
less positive parental behavior (e.g., more parental intru-
siveness). Although the PBI is a retrospective measure,
several studies have established that the PBI has adequate
reliability and validity (Brewin et al. 1993; Parker et al.
1979; Parker 1989), as well as temporal stability (Wilhelm
et al. 2005). In the present study, all four subscales had
adequate internal consistency, such that the Maternal and
Paternal Care subscales had Chronbach’s a = 0.91 and
a = 0.93 respectively, while the Maternal and Paternal
Protection subscales had Chronbach’s a = 0.87 and
a = 0.86 respectively.
Depressive Symptomatology
The BDI (Beck and Steer 1993) was used to assess current
depressive symptomatology. The BDI is a widely used
21-item self-report inventory that measures a range of
depressive symptoms. Each item is rated on a 0–3 scale
with total scores ranging from 0 to 63; higher scores are
assumed to reflect increased levels of depressive symp-
tomatology. Research has demonstrated that the BDI has
acceptable reliability and validity (e.g., Beck et al. 1988).
In the present study, the BDI had adequate internal con-
sistency, Chronbach’s a = 0.87.
Anxious Symptomatology
The BAI (Beck and Steer 1990) is a 21-item self-report
questionnaire that parallels the BDI in structure and scoring
(e.g., a 0–3 scale). It assesses the presence and severity of a
variety of symptoms associated with anxiety, with higher
scores indicating higher levels of anxiety. The BAI has
adequate reliability and validity (Steer and Beck 1997).
The BDI had adequate internal consistency, Chronbach’s
a = 0.89.
Results
Analyses
Principal components factor analyses with varimax rotation
were conducted on the individual items to identify the
underlying factor structure. Items were considered to load
onto a specific factor if their loading was larger than 0.400.
However, if items cross-loaded on more than one factor,
item content was reviewed and the items were assigned to
the factor most representative of that content. Composite
Table 1 Demographic information for the present sample
Mean (SE) Minimum Maximum
Age 18.44 (0.05) 16.25 33.75
BAI 8.43 (0.27) 1.00 58.00
BDI 14.51 (0.36) 1.00 59.00
PBIMC 27.62 (0.28) 0.00 36.00
PBIMP 14.10 (0.30) 0.00 38.00
PBIFC 22.45 (0.36) 0.00 36.00
PBIFP 12.81 (0.30) 0.00 37.00
BAI beck anxiety inventory, BDI beck depression inventory, PBIMCparental bonding instrument maternal care, PBIMP parental bonding
instrument maternal overprotection, PBIFC parental bonding instru-
ment paternal care, PBIFP parental bonding instrument paternal
overprotection
Cogn Ther Res (2012) 36:173–181 175
123
scores were created for each identified factor by summing
the scores of items on that factor. To assess the relation
between these factors and parental bonding, multiple
regression analyses were used. Parental bonding factors
(maternal and paternal care and overprotection) were
entered simultaneously in multiple regression analyses to
predict the factors identified from the BDI and the BAI. All
analyses were conducted using PASW 18.0 software.
Missing Data
Because less than one percent of data were missing, a
single imputation was conducted to estimate missing data.
Prior research suggests that one imputation is sufficient to
reduce error estimates when there is less than 1% of
missing data (Fichman and Cummings 2003). All further
analyses were conducted on the data set including this
imputation.
Factor Analyses
Factor analyses conducted independently on the BDI and
BAI together and separately suggested the same underlying
factor structure; results presented here represent separate
factor analyses for each measure. Primary factor structures
were not reduced to secondary factor structures in order to
provide greater specificity in analyses. A four factor structure
provided the best fit for the BDI data, explaining 46.38% of
total variance. These factors were identified as: negative
feelings about the self (e.g., ‘‘I feel sad;’’ explaining 18.54%
of the total variance; eigenvalue = 6.25), negative interac-
tions with others (e.g., ‘‘I am less interested in other people
than I used to be;’’ explaining 12.62% of the total variance;
eigenvalue = 1.33), sleep difficulties and fatigue (e.g., ‘‘I
don’t sleep as well as I used to;’’ explaining 7.24% of the total
variance; eigenvalue = 1.14), and weight related concerns
(e.g., ‘‘My appetite is not as good as it used to be;’’ explaining
8.00% of the total variance; eigenvalue = 1.02). Seven
items had loadings greater than 0.300 on two factors; items
were assigned to specific factors based on thematic content.
Factor loadings are presented in Table 2.
For the BAI, a four factor structure was identified as
providing the best fit, explaining 51% of the total variance.
These four factors were conceptually defined as general
fear (e.g., ‘‘Fear of the worst happening;’’ explaining
15.41% of the total variance; eigenvalue = 6.97)., physical
symptoms (e.g., ‘‘Numbness or tingling;’’ explaining
11.63% of the total variance; eigenvalue = 1.29), lack of
steadiness (e.g., ‘‘Dizzy or lightheaded;’’ explaining
14.41% of the total variance; eigenvalue = 1.49), and fear
of dying (e.g., ‘‘Fear of dying;’’ explaining 9.85% of the
total variance; eigenvalue = 1.03). Information on these
factors is presented in Table 3.
Parental Bonding and Depressive Symptoms
Significant associations for parental bonding and depres-
sive and anxious symptom factors are reported in Table 4.
Approximately 10.3% of total variance for participants’
negative feelings about the self factor was explained by
parental bonding. Maternal care and paternal overprotec-
tion were significant predictors, such that lower levels of
maternal care, b = -0.253, t(675) = -6.005, P \ 0.01,
and higher levels of paternal overprotection, b = 0.089,
t(675) = 2.03, P = 0.042, were associated with higher
levels of self-related negativity.
Similarly, 7.2% of the total variability in the negative
beliefs about interactions with others factor was explained by
Table 2 Component matrix for the BDI
Item Self Neg.
interactions
Weight
concerns
Fatigue
1 0.389
2 0.559
3 0.735
4 0.593
5 0.684
6 0.565
7 0.692
8 0.527
9 0.504
10 0.394
11 0.333
12 0.651
13 0.546
14 0.589
15 0.534
16 0.769
17 0.447
18 0.655
19 0.707
20 0.357
21 0.453
Loadings are reported from the rotated component matrix. Self (‘‘I do
not feel sad;’’ ‘‘I am not particularly discouraged about the future;’’ ‘‘I
do not feel like a failure;’’ ‘‘I don’t feel particularly guilty;’’ ‘‘I don’t
feel I am being punished;’’ ‘‘I don’t feel disappointed in myself;’’ ‘‘I
don’t feel any worse than anybody else;’’ ‘‘I don’t have any thoughts
of killing myself;’’ ‘‘I make decisions about as well as I ever could;’’
‘‘I can work about as well as before.’’). Negative interactions (‘‘I get
as much satisfaction out of things as I used to;’’ ‘‘I am no more
irritated now than I ever am;’’ ‘‘I have not lost interest in other
people;’’ ‘‘I don’t feel I look any worse than I used to;’’ ‘‘I am more
worried about my health than usual;’’ ‘‘I have not noticed any recent
changes in my interest in sex’’). Weight concerns (‘‘My appetite is no
worse than usual;’’ ‘‘I haven’t lost much weight, if any, lately’’).
Fatigue (‘‘I don’t cry any more than usual;’’ ‘‘I can sleep as well as
usual;’’ ‘‘I don’t get more tired than usual’’)
176 Cogn Ther Res (2012) 36:173–181
123
parental bonding. Maternal and paternal care were signifi-
cant predictors, with lower levels of maternal, b = -0.194,
t(675) = -4.52, P \ 0.01, and paternal, b = -0.105,
t(675) = -2.544, P = 0.011, care associated with higher
levels of negative beliefs about interactions with others.
For fatigue, 2.5% of the total variability was explained
by parental bonding, indicating that lower levels of
maternal care were significantly associated with higher
levels of fatigue, b = -0.088, t(675) = -2.01,
P = 0.045. Approximately 1.8% of total variability in
weight-related symptoms was explained by parental
bonding; however none of the components of parental
bonding were significant predictors.
Parental Bonding and Anxiety Symptoms
Results of the multiple regression analysis using general
fear as the dependent variable suggested that approxi-
mately 2.4% of variability in fear was explained by
parental bonding. Of the four components of maternal
bonding, only maternal care was a significant predictor of
fear, b = -0.098, t(675) = -2.218, P = 0.027, such that
as maternal care decreased, participant fear increased. For
participants’ reported physical symptoms of fear, parental
bonding explained approximately 1.0% of the total vari-
ability; however none of the parental bonding factors were
a significant predictor of participants’ reported physical
symptoms of fear.
For lack of steadiness, 3.4% of the total variability was
accounted for by parental bonding, with parental bonding
factors nonsignificant predictors of this construct. Finally
parental bonding explained approximately 3.9% of the total
variability for fear of dying. Maternal overprotection was
the only significant predictor, such that higher levels of
maternal overprotection were associated with increased
fears of dying, b = 0.151, t(675) = 3.235, P \ 0.01.
Discussion
Previous research has examined the overall association
between PBI factors and depression and anxiety and found
that PBI factors are correlated with both depression and
anxiety. In the current study, we examined more specific
associations between parenting behaviors and depressive
and anxious symptoms. Regression analyses suggested that
participants’ reported parental bonding was significantly
associated with several symptom patterns identified from
the BDI and BAI. In particular, lower levels of maternal
care were associated with negative self-beliefs, negative
interactions with others, fatigue, and generalized fear;
lower levels of paternal care were also related to negative
interactions with others. Maternal overprotection was
associated with a fear of dying, whereas paternal over-
protection was associated with negative beliefs. Weight-
related issues in depression and autonomic nervous system
activity and lack of steadiness in anxiety were not signifi-
cantly associated with any dimension of parental bonding.
Table 3 Component matrix for the BAI
Item General
fear
Lack of
steadiness
Physical
fear
Fear of
dying
1 0.554
2 0.560
3 0.606
4 0.647
5 0.728
6 0.518
7 0.520
8 0.549
9 0.626
10 0.589
11 0.615
12 0.656
13 0.697
14 0.528
15 0.487
16 0.723
17 0.697
18 0.411
19 0.522
20 0.726
21 0.759
All loadings are reported from the rotated component matrix. General
fear (‘‘Unable to relax;’’ ‘‘Fear of the worst happening;’’ ‘‘Terrified;’’
‘‘Nervous;’’ ‘‘Fear of losing control;’’ ‘‘Scared.’’). Steadiness
(‘‘Numbness or tingling;’’ ‘‘Wobbliness in legs;’’ ‘‘Dizzy or light-
headed;’’ ‘‘Unsteady;’’ ‘‘Hands trembling;’’ ‘‘Shaky’’). Physical fear
(‘‘Feeling hot;’’ ‘‘Heart pounding or racing;’’ ‘‘Indigestion/discomfort
in abdomen;’’ ‘‘Face flushed;’’ ‘‘Sweating (not due to heat)’’). Fear of
Dying (‘‘Feeling of choking;’’ ‘‘Difficulty breathing;’’ ‘‘Fear of
dying;’’ ‘‘Faint’’)
Table 4 Standardized significant beta coefficients for parental
bonding and identified factors of anxiety and depressive symptoms
BDI
negative
self
Negative
interactions
Fatigue BAI
general
fear
Dying
fear
Maternal care -0.25 -0.19 -0.09 -0.10
Maternal
overprotection
0.15
Paternal care -0.11
Paternal
overprotection
0.09
Cogn Ther Res (2012) 36:173–181 177
123
Clearly parenting behaviors do not account for all the
variance in these affective factors; the present pattern of
findings brings into sharper relief the broader links that
have been found between parenting and depression and
anxiety. When the overall relationship is decomposed into
separate factors, unique relationships were obtained
between maternal and paternal parenting behaviors and
aspects of depressive and anxious symptoms. Thus
depressive and anxious syndromes are not simply related to
parenting but also to particular parenting patterns, at least
for some aspects of these syndromes. As such, these data
provide clues about how specific types of parenting may be
related to particular aspects of these affective states, with
implications for understanding some of the causal factors
associated with the development of depression and anxiety.
The pattern of findings may also have implications for
understanding some of the causal factors associated with
the development of depression and anxiety. For example,
results indicated that deficits in maternal care were asso-
ciated with more self-related negative cognitions and more
negative cognitions about interactions with others. These
results are broadly consistent with prior research showing a
unique association between maternal care and cognitive
vulnerability to depressive symptoms, including finding an
attention bias for negative stimuli in individuals with lower
reported levels of maternal care (Ingram and Ritter 2000).
The current results are also consistent with findings of
elevated levels of automatic negative thoughts in individ-
uals with lower levels of maternal bonding (Ingram et al.
2001). Parental bonding deficits may thus influence the
way children (and later on adults) process information from
the world (McGinn et al. 2005; Ingram et al. 2004); an
individual with perceived low levels of maternal care may
begin to assume that she is unlovable and unworthy of
others’ care and consideration. With repeated exposure to
similar patterns of parental caregiving, these thoughts may
be consolidated into schemas, much in the same way as
posited by Beck’s (1967) cognitive theory of depression.
These negative schemas may then be translated into cog-
nitive vulnerabilities; parental bonding may function as a
mediating factor in the development of anxiety and
depression through the emergence of these schemas.
Alternatively, parental bonding may mediate the rela-
tionship between stressful life events and the development
of depression or anxiety through coping styles. For exam-
ple, positive levels of maternal bonding have been asso-
ciated with increased use of problem-solving coping
strategies and decreased use of emotion-focused coping
strategies (Matheson et al. 2005). Inasmuch as emotion-
focused coping strategies have been associated with
increased risk of developing depression or anxiety (e.g.,
Matheson et al.), it seems likely that poor maternal bonding
may result in the development of less adaptive coping
strategies and increased risk for poor psychological health.
Together these findings suggest that maternal bonding may
be particularly important in the development of both cog-
nitive vulnerability and coping strategies.
Deficits in maternal care were also associated with sleep
difficulties/fatigue and generalized fear. These specific
factors are not typically addressed in theories pertaining to
parenting and affective distress, and thus the processes
underlying the relationship been maternal care deficits and
these problems are unclear. If deficits in maternal care
result in the development of negative cognitive schemas,
however, poor maternal care may indirectly affect sleep.
That is, sleep difficulties can be driven by cognitive pro-
cesses, and to the extent that a process like rumination
takes place, difficulty sleeping may occur and consequently
cause fatigue. Failure to use problem-solving coping
strategies may also perpetuate rumination and continued
sleep and energy problems. Likewise, when considering
anxiety and maternal care deficits, individuals whose
mothers are perceived as rejecting and neglectful may be
more prone to experience heightened fearfulness when
anxiety is provoked, lacking maternal comfort and direc-
tion in developing strategies for managing anxiety.
Whereas a comforting mother might reduce fears, an
individual whose mother is critical and lacking in warmth
may develop a schema of the world as a fearful place with
regular and uncontrollable negative events; this schema
may become prominent when stressful events occur,
resulting in heightened and persistent anxiety.
Although deficits in maternal care were associated with
the greatest number of affective factors, maternal over-
protection was associated with a heightened fear of dying.
Some of the items that children with overprotective
mothers were more likely to endorse included feeling of
choking and difficulty breathing. Parents who are over-
protective of their children seem likely to manage problems
themselves and not permit children to explore solutions to
concerns, providing an invalidating message of incompe-
tence. By sending the message that children are incapable
of handling problems themselves and excessively limiting
the development of control over their lives, an overpro-
tective mother may send create a fertile climate for
developing schemas of incompetence and low self-efficacy,
both of which may increase and perpetuate anxiety.
Even though maternal behaviors may be particularly
virulent in certain facets of depression and anxiety, pater-
nal behaviors may also play an important role, albeit a
different one. Specifically, higher levels of paternal over-
protection were associated with a more negative view of
the self. An overprotective/intrusive father may be likely to
convey the message that the world is a dangerous place and
that the child is unable to manage these concerns inde-
pendently. Likewise, an intrusive father may play a role in
178 Cogn Ther Res (2012) 36:173–181
123
creating negative self-views; to the extent that fathers’
intrusiveness inhibits the child’s ability to develop an
independent view of the self, the child is likely to develop a
schema of disappointment, failure and guilt, all aspects of
the ‘‘negative view of self’’ factor. Interestingly, the neg-
ative view of self was associated with paternal overpro-
tection but not with deficits in paternal care. Hence,
although mothers and fathers both play a role in creating a
negative sense of the self, the specific pathways may differ:
criticalness for mothers and intrusiveness for fathers.
Similarly, the association between care and negative
interactions with others involves deficits in both maternal
and paternal care. Parental care likely plays the same role
in the development of negative interactions with others that
maternal care does.
Inasmuch as the data show that mothers and fathers play
related but unique roles in certain dimensions of depression
and anxiety, it seems likely that the combination of dys-
functional parenting may be particularly troublesome for
children’s cognitive and emotional development. Further,
although the effects of parenting can be examined sepa-
rately, they likely interact to produce the vulnerability. For
example, is a father’s overprotection interpreted as criti-
cism when the other parent is in fact critical or neglectful?
If so, a child with a critical mother might be primed to
develop negative views of the self that are potentiated by
an intrusive father. Moreover, to the extent that both a lack
of maternal care and controlling paternal behavior broad-
ens and strengthens negative self-schemas, individuals
raised with these parenting styles may be at particular risk
for developing affective symptoms in the face of stress. Of
course, a father and mother who are both critical and
lacking in warmth would create a poor care-giving envi-
ronment; it is perhaps not surprising that these factors were
related to negative interactions with others in this study.
Caregivers who are critical and rejecting have been long
thought to shape the development of a generalized schema
that others who will also be critical and rejecting (e.g.,
Bowlby 1980). This may be particularly the case when both
caregivers exhibit these behaviors; interactions with others
are viewed through the lens of the child’s interactions with
caregivers.
Although deficits in care and excesses in protection for
both mothers and fathers appear to create considerable
difficulties for the individual, a greater number of, and
stronger, relationships with the depression and anxiety
factors were observed for maternal parenting factors. Such
findings are broadly in line with data previously reported
data showing that maternal care deficits are specifically
linked to negative self-schemas (e.g., Ingram et al. 2001;
Ingram and Ritter 2000). As such, maternal care may play a
particularly significant role in the development of schemas,
likely due in part to unique factors associated with mothers.
It seems likely that mothers in most families play the pri-
mary role in care giving. Accordingly, levels of maternal
bonding may reflect the relative time spent with a primary
caregiver. With more exposure to maternal care, partici-
pants’ schemas may be more reflective of their interactions
with their mothers. Alternatively, there may be additional
social expectations of mothers that are less prevalent for
fathers (e.g., taking on a nurturing, caring role); violations
of these expectations may be more unexpected for the child
and result in broad reappraisal of the situation. Disrupted
maternal bonding may thus result in more pervasive cog-
nitive biases and vulnerability to symptoms than disrupted
paternal bonding.
The present study suggested that parental bonding may
play a particularly important role in some symptoms of
anxiety and depression. However several limitations should
be acknowledged. The factor analytic strategy used may
have overfactored the BAI and BDI, resulting in additional
factors that are not well explained by parental bonding. To
some extent, this may have been unavoidable, because
these factors are conceptually related and are highly cor-
related with each other (see Table 5). Additionally, the
present study sought to maximize descriptiveness of factors
in order to identify relations between subtle differences in
symptomatology and parental bonding. Although visual
Table 5 Correlations between
BDI and BAI factors
** P \ 0.01
Self Negative
interactions
Weight
concerns
Fatigue General
fear
Physical
fear
Fear of
dying
Negative
interactions
0.62**
Weight concerns 0.35** 0.27**
Fatigue 0.52** 0.46** 0.30**
General fear 0.42** 0.33** 0.13** 0.37**
Physical fear 0.19** 0.18** 0.11** 0.22** 0.56**
Fear of dying 0.26** 0.21** 0.24** 0.26** 0.52** 0.50**
Lack of
steadiness
0.31** 0.24** 0.27** 0.31** 0.59** 0.57** 0.61**
Cogn Ther Res (2012) 36:173–181 179
123
analysis of the scree plot might suggest a two-factor
solution for each inventory, the factors selected each
explain a minimum of 7% of the total variance. Each factor
had face validity, such that items loading on each factor
were conceptually related. Given theoretical basis for
maintaining those factors and the relatedness of items on
each factor, as well as the desire for greater specificity of
these analyses, these factors were not evaluated for a sec-
ond order structure. The finding of a four factor structure
for these inventories is consistent with prior research on the
BDI (e.g., Bennett et al. 1997; Shafer 2006) and BAI (e.g.,
Osman et al. 1997). However, given that prior research has
failed to find consistent factor structures for these inven-
tories, replication of the present factor structure and find-
ings is recommended.
Additionally, the PBI is a retrospective self-report
inventory and even though data support its reliability and
validity, causal conclusions between maternal and paternal
factors and patterns of affective symptomatology cannot be
drawn. For instance, rather than deficits in maternal care
creating a negative self-schema, it may be that those indi-
viduals who were inclined to endorse a more negative self
view attributed these deficits in maternal care and are
attributing blame to their mother retrospectively. Although
such a possibility cannot be discounted, two factors argue
against this interpretation. First, specific deficits in maternal
care tend to be consistently linked to negative self-views
across studies, including one which assessed maternal
bonding several weeks before assessment of other factors
(Ingram and Ritter 2000). Second, if blaming after the fact
was occurring, a broader pattern of negative bias might be
seen across all factors of affective symptomatology. Instead,
a unique pattern of relationships between parenting factors
and facets of depression and anxiety was observed and the
only overlap was the association between maternal and
paternal care deficit and negative interactions with others.
In sum, the present study provides evidence linking
parental bonding with anxious and depressive symptom-
atology. Aspects of parental bonding were stronger pre-
dictors of cognitive symptomatology than physiological
symptomatology. Maternal care predicted the most factors
and was significantly associated with four of the eight
factors of affective symptomatology, suggesting a unique
role for maternal care in these symptoms. Future studies
should consider which aspects of symptomatology are of
interest when exploring parental bonding and vulnerability
to anxiety and depression. Additionally, this study suggests
that examining common factors between anxious and
depressive symptomatology is a viable method for under-
standing the development of vulnerability to these disor-
ders. Such an approach, particularly when conducted with a
nonclinical population with a range of symptomatology,
may yield additional information on the relation between
the disorders. Commonalities between individuals with
these disorders and with subclinical features may also be
elucidated using this method. Understanding this relation-
ship may provide greater insight into the importance of
early life events in the development of cognitive vulnera-
bility to anxiety and depression.
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