Anxiety disorders often onset in adolescence and continue into adulthood. Multiple factors contribute to anxiety disorder development, such as parent emotional availability (EA) and adolescent anxiety sensitivity (AS). Previous research determined attachment is a similar construct to EA, and attachment is related to anxiety disorders. Moreover, EA is a more specific construct than attachment that can be targeted in therapy. It has been determined that adolescent attachment to parental figures contributes to anxiety, with AS mediating this relationship. The present research sought to determine if AS is one mechanism underlying the relationship between parent EA and adolescent anxiety, while exploring the moderating roles of parent and adolescent gender. In a Midwestern sample (13–19 years old), this study examined adolescent AS as a mediator of the relationship between perceived parent EA and adolescent anxiety, and gender as a potential moderator. Self-report data were collected from adolescents via Qualtrics. The findings supported the mechanism of adolescent AS as a mediator between perceived parent EA and adolescent anxiety. As AS emerges during adolescence, it is a pertinent treatment target for youth anxiety. Furthermore, this study underscores the significance of parent and adolescent gender and parental EA as treatment targets for adolescent anxiety. While targeting adolescent AS and enhancing parental EA can be beneficial for both male and female adolescents, focusing on parental EA may offer greater benefits for male adolescents. In sum, these findings can increase the efficacy of current parenting programs and further increase treatment outcomes for youth and families.
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Introduction
Anxiety disorders are one of the most common mental health disorders among children and adolescents (Costello et al., 2005). Epidemiological studies have estimated the prevalence of adolescent anxiety disorders to be between 10% and 31.9% (Merikangas et al., 2010) with a mean age of onset of any anxiety disorder of 11 years of age (Kessler et al., 2005). Anxiety disorders are also highly comorbid with other psychiatric disorders such as major depressive disorder and substance use disorder, as over 51% of adolescents with anxiety disorders are also diagnosed with other mental health disorders (Essau, 2003).
Adolescent anxiety disorders increased by 20% from 2007 to 2012, and the number of adolescents diagnosed has been increasing every year (Data Resource Center for Child & Adolescent Health, 2020). Notably, the COVID-19 pandemic exacerbated the mental health crisis, with 37% of high school students reporting poor mental health and 44% reporting persistent hopelessness or sadness (CDC, 2022). Adolescent anxiety is also a cause for concern because it leads to more adverse psychosocial outcomes including poor coping skills, unemployment, chronic stress, and other issues in later adulthood (Essau et al., 2014). Untreated anxiety disorders in adolescence often lead to chronic anxiety disorders and physical health concerns in adulthood (Essau et al., 2014).
Anxiety disorders often begin to develop in adolescence when there are many changes in cognition, perception, and autonomy. One factor developing in adolescence is anxiety sensitivity (AS), which is also known as “the fear of fear” (Reiss et al., 1986). Anxiety sensitivity is a vulnerability factor for anxiety referring to one perceiving anxiety-related symptoms to cause harmful consequences which in turn increases the experience of anxiety (Muris et al., 2008). AS contributes to the severity and maintenance of anxiety disorders, as individuals who have high levels of AS are more likely to interpret their internal sensations as catastrophic (e.g., an individual notices their heart beating and thinks they are having a heart attack). This attribution of physical concerns caused by AS is strongly related to the maintenance and development of generalized worry and anxiety (Knapp et al., 2016). This vulnerability is created because high AS levels create a feedback loop, where an environmental cue stimulates the nervous system, which produces a sensation. An individual with high levels of AS will begin to fixate on this sensation, which will raise anxiety levels. After this process occurs a few times, the individual will begin to fear the sensation as much as the environmental cue (Silverman et al., 2003). As such, AS is a critical target in adolescence as this time is when it develops (e.g., Knapp et al., 2020; Mattis & Ollendick, 1997a, 1997b).
Environmental factors also tend to predict child anxiety, with parenting being one of the most influential environmental factors (Degnan et al., 2010). Parents influence the development of anxiety disorders since children learn by watching and attach to their caregivers. One such construct influencing child development is parent emotional availability (EA). Parent EA is defined by parental support and acceptance of their children’s negative and positive behaviors, with parents who display more EA tending to have children that display healthier functioning and normative psychosocial outcomes (Lee & Gotlib, 1991).
The existing research has not investigated the associations between parent EA and the adolescent AS on adolescent anxiety, which can potentially be targeted to promote change. As such, the goal of the current study is to examine the relationships between adolescent AS and parental EA in the context of adolescent anxiety.
AS has roots in childhood but tends to develop more during adolescence (Mattis & Ollendick, 1997a), making it a critical target for adolescents. Mattis and Ollendick (1997a) conducted a study and their findings aligned with the hypothesis that children recognize and respond to internal cues differently than adolescents. Youth cognitive capacities seem to underlie AS, with adolescents being able to attribute their anxious thoughts or feelings to internal cues as they have more sophisticated reasoning (Weems et al., 2021). Thus, AS represents a viable target in the treatment of anxiety disorders in adolescents.
Development and Definition of Emotional Availability
Parenting and the parent–child relationship impact child and adolescent emotional and behavioral functioning. The construct of parent emotional availability (EA), which is defined by parents supporting and accepting their children’s negative and positive behaviors, tends to impact the relationship between parents and children. Specifically, parents with more EA tend to have better adjusted children which leads to healthier functioning and psychosocial outcomes (Lee & Gotlib, 1991). EA has been conceptualized in accordance with different theoretical perspectives. The construct of EA has roots in attachment theory, and it has been conceptualized as an overlapping construct to attachment but with more of an emphasis on how a parent both attends to their child’s emotional needs and displays their own emotions (Easterbrooks & Biringen, 2000). As EA is similar to attachment and both constructs have lasting effects on psychopathology, it is important to consider Bowlby’s (1969) statement that how infants emotionally attach to their caregivers will impact healthy development, with parents who are responsive and reliable having more securely attached children. Parents who attach securely to their offspring have met the emotional needs of their offspring, which leads to better social and emotional outcomes. Conversely, parents who form anxious, avoidant, or insecure attachments with their offspring have not met their children’s needs which will lead to them having social or emotional difficulties. Additionally, Ainsworth and Bell (1970) further described attachment as being heightened or diminished by environmental or biological factors. These factors impacting EA and attachment became the basis for a research-oriented description of EA. Parental warmth, or empathy, is part of EA, and fathers with anxiety tend to be perceived as less warm which can cause conflict and lead to less secure attachment with offspring (Bögels & Phares, 2008). While researchers have not extensively examined the relationship between father’s EA and child functioning, Ducharme et al. (2002) found mothers and fathers attach similarly to adolescents. They found parent–child relationships and parent EA tends to be relatively stable throughout development (Lum & Phares, 2005). Parents who display more EA tend to have children who function adaptively, while parents with less EA tend to have children with maladaptive functioning (Lee & Gotlib, 1991). Broadly, parents who have discussions about emotions, engage in supportive responses to their children’s emotions, and model a positive family emotional climate tend to have children who show greater abilities to manage emotions successfully (Eisenberg et al., 1998; Morris et al., 2007).
Gender and Psychopathology
Youth Gender and Psychopathology
Youth gender is another factor influencing the development of anxiety disorders in adolescence. Specifically, epidemiological meta-analyses determined that between the ages of 13 to 18 years old, of the 32% of adolescents with anxiety disorders, females were more at risk than males (Kessler et al., 2005). There is a gender-specific differential sensitivity with female offspring being more likely to develop anxiety disorders (Merikangas et al., 1999). While female offspring may be more likely to develop anxiety disorders, parenting behaviors can influence the disorders. Ranney et al. (2021) found maternal and paternal anxiety to be associated with adolescent anxiety more strongly for female offspring. There are also gender differences related to AS, such that adolescent girls experience more physical and social concerns than adolescent boys (Walsh et al., 2004; Wright et al., 2010). Additionally, youth gender may moderate the association between parent and child AS, as Graham and Weems (2015) found a positive association between female offspring and parent AS and a negative association between male offspring and parent AS.
Parent Gender and Psychopathology
Parent gender may also impact the relationship between EA, AS, and anxiety. In a sample of adults, AS mediated the relationship between gender and anxious and depressive symptoms (Norr et al., 2015). Additionally, Deacon et al. (2003) found that women had higher levels of AS. However, for parents specifically, one study found paternal, but not maternal, AS to be associated with offspring AS and psychopathology (East et al., 2007) while Lum and Phares (2005) found adolescents’ feelings toward their mothers was a stronger indicator of their emotional and behavioral functioning than their feelings toward their fathers. In general, both maternal and paternal EA and AS impact adolescent social and emotional functioning, but adolescent gender may impact the direction and strength of these relationships.
Parenting and Adolescent Internal Factors
Parent EA and Youth AS
The literature on parenting and parenting practices relating to youth anxiety has been well researched, while the literature on individual parenting behaviors and youth behaviors has suggested important areas for future research. Specifically, Scher and Stein (2003) conducted early research on youth AS as a mediator between specific parenting behaviors and adolescent anxiety. They found adolescents who perceive their parents to be more negative have higher levels of AS and anxious symptomatology. Watt et al. (2005) expanded upon this research and found individuals who reported insecure attachment to their parents also reported higher levels of AS. Viana and Rabian (2008) found that perceptions of alienation from mothers was associated with higher AS even when worry and GAD were controlled. Erözkan (2011) found parent attachment styles to be highly correlated with adolescent AS, and he later examined the relationship between adolescent AS and parenting styles. This study found adolescents who perceive their parents to be authoritarian tend to have higher AS than adolescents who perceive their parents to be more democratic (Erözkan, 2012). According to research on parenting styles, parents who are authoritarian tend to be less warm, while parents who are more authoritative tend to be warmer (Baumrind, 1966). As warm parents tend to display more EA, it can be hypothesized that parents with EA tend to have children with lower AS. As AS develops from genetics, stressful life events, and parenting (Boswell et al., 2013; Coppola et al., 2018), it is also relevant to see how AS may impact the relationship between attachment and anxiety.
AS and EA as Protective Factors
There are a variety of risk and resilience factors in the development of anxiety disorders. One factor promoting resilience is secure early parental attachment, which increases autonomy and decreases avoidance (Bögels & Phares, 2008). However, an insecure parental attachment lacking in parent EA can be a risk factor as it can lead to emotion dysregulation and anxiety for the youth (Morris et al., 2007). Similarly, a factor that can mitigate or exacerbate the risk for developing an anxiety disorder is AS, with higher levels of AS leading to higher levels of anxiety and lower levels of AS leading to lower levels of anxiety (Muris et al., 2008). AS and parenting factors together can be resilience factors, as it has also been determined that positive parenting styles contribute to lower levels of AS in offspring (Graham & Weems, 2015).
The previous research has focused on attachment or parenting styles in relation to AS and youth anxiety. While this research has identified these broad associations, it has not identified the mechanism underlying parent EA and youth anxiety. The previous research suggests the psychosocial factor of adolescent AS may be the mechanism. Additionally, it is important to identify parent EA, and not attachment, as a predictor for youth anxiety as it is a specific construct that can be a treatment target in therapy. The literature also lacks or has conflicting findings on how parent and adolescent gender interact with these variables (e.g., East et al., 2007; Lum & Phares, 2005). Further information on how gender interacts with these variables can specify who would most benefit from therapeutic interventions targeting EA and AS in treating anxiety disorders.
Study Rationale
Previous research has established youth AS as a mediator between parenting behaviors or characteristics and youth anxiety (e.g., Drake & Kearney, 2008; Scher & Stein, 2003). There has also been a link established between parent attachment styles and adolescent AS, with adolescents who have warmer parents displaying less anxiety and lower AS (Erözkan, 2011). While attachment styles have been studied in relation to adolescent AS and anxiety, EA specifically has not been studied with adolescent AS and anxiety. Attachment and EA are similar constructs, but EA is a potentially more clinically relevant construct as it is more behaviorally specific than attachment and can be targeted in therapy. Furthermore, enriching our understanding of the risk factors for adolescent anxiety can help us create more effective and beneficial prevention and intervention programs. For these reasons, we addressed this literature gap to examine the relationships between parent EA, adolescent AS, and adolescent anxiety.
Current Study Hypotheses
To examine the relationships between parent EA, adolescent AS, and adolescent anxiety, survey data were collected from adolescents. The adolescents were between the ages of 13 and 19 years of age, and they were either current high school students enrolled in a college class or current students in their first year of college. In this survey, demographic data were collected, and a variety of measures were administered. The measures used in this study included the Lum Emotional Availability of Parents (LEAP; Lum & Phares, 2005), Revised Childhood Anxiety Sensitivity Index (CASI-R; Muris et al., 2008), and the Revised Children’s Anxiety and Depression Scale (RCADS; Ebesutani et al., 2012). The LEAP was used to determine how adolescents perceive their parent’s EA. The CASI-R is a revised measure used to assess adolescent anxiety sensitivity. To measure adolescent anxiety, a shortened version of the RCADS was used.
As previous research has found that parents who display more EA have children who are able to better manage their emotions (Morris et al., 2007), we hypothesized (H1) parent EA will be negatively associated with anxiety symptoms. We then hypothesized (H2) adolescent AS will be positively associated with anxiety symptoms, because AS is positively associated with levels of anxious symptomatology (Boswell et al., 2013; Muris et al., 2008). Offspring who are securely attached to their parents have less AS (Graham & Weems, 2015), which led to the hypothesis (H3) parent EA will be negatively associated with adolescent AS. It has been determined that AS is a mediator for parenting behaviors and adolescent anxiety (Drake & Kearney, 2008; Scher & Stein, 2003), so we predicted (H4) adolescent AS will mediate the relationship between parent EA and adolescent anxiety, and this model will be examined twice, the first time with paternal EA as the predictor and the second time with maternal EA as the predictor. While females are more likely than males to develop anxiety disorders (Merikangas et al., 1999), parent and adolescent gender can influence the relationships between EA, AS, and anxiety. Paternal, but not maternal, AS was found to be associated with offspring psychopathology and AS (East et al., 2007), and attachment to mothers was found to be a stronger indicator of emotional functioning than attachment to fathers (Lum & Phares, 2005). Thus, we hypothesized that in the aforementioned mediation models gender will be an exploratory variable and we predict (H5) either maternal or paternal EA will have a stronger direct effect on adolescent anxiety as adolescents may attach differently to their mothers and fathers and (H6) adolescent gender will moderate the relationship between parent EA and adolescent AS.
To test these hypotheses, a correlation matrix, mediation models, and a moderated mediation model were run with the variables of parent and adolescent gender, parent EA, adolescent AS, and adolescent anxious symptomatology in a nonclinical sample. In the models, there were direct paths from parental EA to adolescent anxiety symptoms. Adolescent AS was a proposed mediator between parental EA and adolescent anxiety. In one of the models, adolescent gender was a proposed moderator between parental EA and adolescent AS.
Method
Participants
Online survey self-report data were collected from adolescents using SONA Systems at a Midwestern university as part of a larger study (Table 1). For adolescents under the age of 18 years old, their mothers or fathers provided consent prior to participation in the SONA study which was completed on the Qualtrics platform. A Monte Carlo power analysis for indirect effects was conducted in R (R Core Team, 2021) to determine statistical power (Schoemann et al., 2017). It was determined that a sample of at least 140 participants was needed to detect indirect effects.
Table 1
Descriptive statistics
Demographics
Item
# of Participants
Percentage
Participants
Total participants
237
-
Eligible participants
164
-
Ineligible participants
73
-
Age
13 years old
1
0.6%
14 years old
7
4.3%
15 years old
6
3.7%
16 years old
26
15.9%
17 years old
82
50%
18 years old
15
9.1%
19 years old
24
14.6%
Gender
Male
34
20.7%
Female
113
79.3%
Ethnicity
White
115
70.1%
Black
14
8.5%
South Asian
9
5.5%
Latinx
5
3%
Middle Eastern
8
4.9%
Multiracial
10
6.1%
Other
3
1.8%
Grade
6th grade
1
0.6%
7th grade
1
0.6%
8th grade
1
0.6%
9th grade
7
4.3%
10th grade
11
6.7%
11th grade
48
29.3%
12th
68
41.5%
College
27
16.5%
Family income
Above $150,000
35
21.3%
$100,000–150,000
33
20.1%
$75,000–100,000
35
21.3%
$50,000–75,000
21
12.8%
$25,000–50,000
21
16.5%
Below $25,000
13
7.9%
Living arrangement
Mom & dad together
107
65.2%
Mostly/only with mom
28
17.1%
Mostly/only with dad
7
4.3%
Neither mom or dad
14
8.5%
Equal time mom & dad, different houses
8
4.9%
Measures
The construct of parent EA was measured using the LEAP (Lum & Phares, 2005). The LEAP is a 15-item, youth self-report measure which assesses adolescents’ perceptions of their mother’s and father’s emotional availability (EA) separately. Adolescents were asked to rate their parent’s behavior on a Likert scale ranging from 1 to 6, with 1 meaning Never and 6 meaning Always. Some of the sample items related to parent behaviors are: “Is available to talk at any time” and “Consoles me when I am upset”. Both mother (α = 0.98) and father (α = 0.98) forms displayed good internal consistency and test–retest reliability (p < 0.001) (Lum & Phares, 2005). Youth self-report correlated significantly with both mother’s and father’s self-report (r = 0.42, p < 0.0001; r = 0.63, p < 0.0001) (Lum & Phares, 2005). Overall, the LEAP is a reliable and valid measure assessing adolescent perception of both mother and father emotional availability.
The moderating construct of adolescent anxiety sensitivity was measured using the CASI-R (Muris et al., 2008). The CASI-R is a 31-item, youth self-report measure which assesses for the fear of anxiety-related sensations in the body that are interpreted as having possibly harmful psychological, social, or somatic consequences. Sample items include: “It scares me when my heart beats fast” and “It is important for me not to appear nervous”. Each item on the CASI-R is scored on a 3-point Likert scale, with 0 meaning Not True and 2 meaning Very True. The items can be summed for a general AS score, with higher scores indicating greater AS. Certain items can also be summed to create the following subscales: Fear of Cardiovascular Symptoms (α = 0.88), Fear of Respiratory Symptoms (α = 0.88), Fear of Cognitive Dyscontrol (α = 0.81), and Fear of Publicly Observable Anxiety Reactions (α = 0.85) (Muris et al., 2008). (Francis et al., 2019a, 2019b). The CASI-R also has good internal consistency (α = 0.90), good reliability (α > 0.70), and convergent validity (r = 0.29, 0.38, 0.47 with significance at α = 0.05, 0.01, and 0.001) in adolescent samples (Francis et al., 2019a, 2019b).
The shortened version of the RCADS was used to measure the construct of adolescent anxiety (Ebesutani et al., 2012). Items from the original 47-item RCADS were used to create this measure (Chorpita et al., 2000). Adolescents were asked to select one of the four words (Never, Sometimes, Often, Always) to show how often something happens to them. Some of the items include: “I worry what other people think of me” and “I suddenly become dizzy or faint when there is no reason for this”. This measure is a 25-item, youth self-report measure for symptoms of anxiety and depression. This measure was chosen because it has better psychometric properties than other youth anxiety measures (Piqueras et al., 2017). The RCADS has sufficient internal consistency (α = 0.82), structural validity (CFI = 0.98), criterion validity (AUC = 0.79), and test–retest reliability (ICC = 0.73; Klaufus et al., 2020).
Procedure
The procedures were first be approved by the university’s Institutional Review Board. The survey was then constructed via the Qualtrics platform. After approval, the adolescents were then recruited through SONA, where they could choose to take a variety of surveys for class credit. The population surveyed were high school students or first year college students who were enrolled in an Introductory Psychology course at the university. When the students under the age of 18 years old began the course at the beginning of the semester, they received a parental permission form that their parents signed to allow them to take SONA surveys. Once the parental permission form is returned, the students under the age of 18 years provided assent and students ages 18 to 19 years old provided consent via a link to SONA Systems which allowed them to participate if they were eligible and willing. Eligibility for the survey included parental consent and adolescent assent for 13–17 years old or adolescent consent for 18 to 19 years old, and for the adolescents to be between the ages of 13 to 19 years old. The survey was then completed via Qualtrics, LLC. The adolescents were not compensated for survey completion, but they were awarded course credit.
Analyses
Prior to any analyses, the data were cleaned. First, it was determined if there were any outliers or missing values. Participants who started the survey but did not begin the survey were removed from the dataset. Individuals outside the age range or who did not report having maternal or paternal figures were excluded from the data set. Next, frequencies were determined to figure out how many times the data values occurred in the set. Finally, descriptive statistics were conducted to determine the demographics of the data set. Alongside this, bivariate correlations were run to determine the strength and relationships present between the variables.
After the preliminary analyses were completed, the main analyses were run. Mediation and moderated mediation models were run via PROCESS macro (Hayes, 2013) for SPSS. Cocor (Diedenhofen & Musch, 2015) was used to conduct statistical comparisons between correlations. To test H1, H2, and H3 bivariate correlations were run for all participants. To test H4 and H5, PROCESS model 4 was run twice, and the independent variable was first maternal EA and then paternal EA, the mediator was adolescent AS, and the dependent variable was adolescent anxiety. To test H6, PROCESS model 7 was used, with the independent variable as parent EA, the mediator as adolescent AS, the dependent variable as adolescent anxiety, and the moderator as adolescent gender.
Results
All data were analyzed with IBM SPSS Statistics 29, and mediation and moderated mediation analyses were run with PROCESS 4.2. Participants were excluded if they did not answer at least 50% of each measure. However, all participants either completed nearly 100% or 0% of the measures for the survey. Of the participants that completed 0%, they were screened out of the study due to ineligibility. The most common reason participants were excluded is because they were outside of the age range. When asked to identify their parental figures, some participants (n = 9) identified non-biological parents (either step or adoptive parents). They were included in the dataset as the research questions did not specify that parents must be biological. Thus, no steps were taken regarding missing data as the sample contained the appropriate number of participants after some cases were excluded. Descriptive statistics were obtained for all variables of interest (Table 1). The variables were approximately normally distributed (skew <|1.00|; kurtosis <|2.00|) and there were no concerns with collinearity (VIF < 2).
Internal Consistency
In the study, internal consistency reliability coefficients for all measures were assessed (Table 2). For all measures, the Cronbach’s α ranged from 0.94 to 0.98, which is in the excellent range (George & Mallery, 2003).
Table 2
Internal consistency
Measure
# of items
Cronbach’s α
LEAP Maternal
15
0.94
LEAP Paternal
15
0.97
RCADS
25
0.98
CASI-R
31
0.95
Correlations
Pearson correlations were examined for the variables of interest (Fig. 1–3; Table 3). In accordance with the first hypothesis, parent EA was negatively associated with adolescent anxiety. Specifically, both maternal (r(164) = −0.40, p < 0.01) and paternal (r(164) = −0.32, p < 0.01) EA had significant, moderate correlations with adolescent anxiety symptomatology. However, the difference between the correlations for maternal and paternal EA did not differ significantly (z = −1.07, p = 0.29) (Diedenhofen & Musch, 2015). In accordance with the second hypothesis, adolescent AS was significantly, strongly positively correlated (r(164) = 0.71, p < 0.01) with adolescent anxiety symptomatology. In accordance with the third hypothesis, parent EA was negatively associated with adolescent AS. Specifically, maternal EA had a significant, moderate correlation (r(164) = −0.38, p < 0.01) with adolescent AS and paternal EA had a significant, small correlation r(164) = −0.25, p < 0.01) with adolescent AS. However, the difference between the correlations for maternal and paternal EA did not differ significantly (z = −1.78, p = 0.07) (Diedenhofen & Musch, 2015). These findings support the first three hypotheses.
Fig. 1
Simple slopes for maternal EA
Table 3
Correlations
Maternal EA
Paternal EA
Adolescent Anxiety
Adolescent AS
Maternal EA
-
0.51**
−0.40**
−0.38**
Paternal EA
Adolescent AS
0.51**
−0.38**
-
−0.25**
−0.32**
−0.71**
−0.25**
-
Mean
Std. Deviation
71.64
17.56
60.50
23.70
11.98
7.20
51.97
14.3
Cronbach’s Alpha
0.97
0.98
0.94
0.95
** Correlation is significant at the 0.01 level (2-tailed)
×
Simple Mediation
To investigate the fourth and fifth hypotheses assessing for adolescent AS as a mediator between parental EA and adolescent anxiety, simple mediation analyses were conducted using PROCESS model 4 (Table 4). Before analyses were run, it was determined that the data met the assumptions for a mediation analysis. The variables were continuous, the dependent and independent variables had linear relationships, there were no concerns with collinearity, and there were no outliers.
Table 4
Simple mediation analyses
Predictor
indirect
direct
t
R2
R2change
Fchange
p
CI
Maternal EA (X)
−0.06
−5.18
0.38
0.14
26.84
0.00
−0.43, −0.19
Adoles. AS (M)
−0.10
11.25
0.73
0.53
90.10
0.00
0.27, 0.34
Paternal EA (X)
−0.05
−3.26
0.25
0.06
10.62
0.00
−0.24, −0.06
Adoles. AS (M)
−0.05
11.97
0.72
0.53
89.14
0.00
0.28, 0.39
For both mediation analyses, the outcome variable was adolescent anxiety, and the mediator variable was adolescent AS. For the first model, the predictor variable was maternal EA and for the second model the predictor variable was paternal EA. It was determined that approximately 14% of the variance in adolescent anxiety was accounted for by the predictor of maternal EA (b = −0.06, R2 = 0.14, F(1,164) = 26.84, p = 0.01). Additionally, it was determined that adolescent AS had a significant impact on adolescent anxiety (b = 0.33, t = 11.25, p = 0.00). The direct effect was significantly different from zero (b = −0.06, SE = 0.02, 95% CI = −0.11, −0.01) and indicates maternal EA predicts adolescent anxiety. The indirect effect coefficient was significantly different from zero (b = −0.10, SE = 0.02, 95% CI = −0.15, −0.06), which suggests the mediator of adolescent AS partially explained why maternal EA was associated with adolescent anxiety. The standardized effect (b = −0.16) suggested a small effect for adolescent AS as a mediator between maternal EA and adolescent anxiety, which supported the fourth hypothesis.
It was determined that approximately 6% of the variance in adolescent anxiety was accounted for by the predictor of paternal EA (b = −0.05, R2 = 0.06, F(1,164) = 10.62, p = 0.001). Additionally, it was determined that adolescent AS had a significant impact on adolescent anxiety (b = 0.34, t = 11.97, p = 0.00). The direct effect was significantly different from zero (b = −0.05, SE = 0.02, 95% CI = −0.08, −0.01) and indicates paternal EA predicts adolescent anxiety. The indirect effect coefficient was significantly different from zero (b = −0.05, SE = 0.02, 95% CI = −0.08, −0.02), which suggests the mediator of adolescent AS partially explained why paternal EA was associated with adolescent anxiety. The standardized effect (b = −0.10) suggested a small effect for adolescent AS as a mediator between paternal EA and adolescent anxiety.
For both models, adolescent AS was a negative mediator of the relationship between parent EA and adolescent anxiety, which supported the fourth hypothesis. In regard to the fifth hypothesis, it was not supported as both paternal and maternal EA had significant direct effects on adolescent anxiety.
Moderated Mediation
To investigate the sixth hypothesis, two moderated mediation analyses were conducted using PROCESS model 7 (Table 5), and Aiken and West (1991) were referenced for the interpretation of these results. Before analyses were run, it was determined that the data met the assumptions for a mediation analysis. For both mediation analyses, the outcome variable was adolescent anxiety, the moderator was adolescent gender, and the mediator variable was adolescent AS. For the first model, the predictor variable was maternal EA and for the second model the predictor variable was paternal EA. Adolescent gender was the moderator between parental EA and adolescent AS.
Table 5
Moderated mediation analysis with maternaL EA as X
Effect
SE
t
p
95% CI Lower
Adolescent AS
Constant
63.49
7.81
8.13
< 0.001
48.07, 78.92
Maternal EA
−0.05
0.12
−0.44
0.66
−0.30, 0.19
Gender
8.71
5.26
1.66
0.10
−1.69, 19.10
Int_1
−0.21
0.09
−2.36
0.02
−0.38, −0.03
Conditional Effects
Female
−0.26
0.06
−4.22
< 0.001
−0.38, −0.14
Male
−0.47
0.09
−5.25
< 0.001
−0.65, −0.29
Adolescent Anxiety
Constant
−0.96
2.73
−0.35
0.73
−6.35, 4.44
Maternal EA
−0.06
0.02
−2.52
0.01
−0.12, −0.01
Adolescent AS
0.33
0.03
11.25
< 0.001
0.27, 0.39
Direct and Indirect Effects
Direct
−0.06
0.02
−2.52
0.01
−0.12, −0.01
Indirect Female
−0.09
0.02
−0.13, −0.04
Indirect Male
−0.16
0.05
−0.31, −0.10
Index of Moderated Mediation
Gender
−0.07
0.05
−0.23, −0.02
R2change
F
p
X*W
0.03
5.54
0.02
When maternal EA was the predictor, adolescent AS was the outcome variable, and adolescent gender was the moderator it was determined maternal EA did not have a significant impact on adolescent AS (b = −0.05, t = −0.44, p = 0.66). Adolescent gender also did not have a significant impact on adolescent AS (b = 8.71, t = 1.66, p = 0.10). However, the interaction between maternal EA and adolescent gender had a significant impact on adolescent AS (b = −0.21, t = −2.36, p = 0.02). When maternal EA was the predictor, adolescent AS was the mediator, and adolescent anxiety was the outcome variable, maternal EA had a significant impact on adolescent anxiety (b = −0.06, t = −2.52, p = 0.01) and adolescent AS had a significant impact on adolescent anxiety (b = 0.33, t = 11.25, p = 0.00). The moderated mediation was significant for both females (b = −0.09, 95% CI = −0.13, −0.04) and males (b = −0.16, 95% CI = −0.31, −0.10), and as maternal emotional availability increased adolescent anxiety sensitivity levels decreased, and the effect was more pronounced for male adolescents (Fig. 1). Thus, the overall hypothesis for the model was supported as the indirect effect of maternal EA on adolescent anxiety through adolescent AS was moderated by adolescent gender (b = −0.07, 95% CI = −0.23, −0.02).
When paternal EA was the predictor, adolescent AS was the outcome variable, and adolescent gender was the moderator, it was determined paternal EA did not have a significant impact on adolescent AS (b = 0.03, t = 0.29, p = 0.77). Adolescent gender also did not have a significant impact on adolescent AS (b = 3.23, t = 0.97, p = 0.34). However, the interaction between paternal EA and adolescent gender had a significant impact on adolescent AS (b = −0.14, t = −2.01, p = 0.04). When paternal EA was the predictor, adolescent AS was the mediator, and adolescent anxiety was the outcome variable, paternal EA had a significant impact on adolescent anxiety (b = −0.05, t = −2.77, p = 0.01) and adolescent AS had a significant impact on adolescent anxiety (b = 0.34, t = 11.97, p = 0.00). The moderated mediation was significant for both females (b = −0.04, 95% CI = −0.07, −0.004) and males (b = −0.08, 95% CI = −0.18, −0.04), and as paternal emotional availability increased adolescent anxiety sensitivity levels decreased, and the effect was more pronounced for male adolescents (Fig. 2). Thus, the overall hypothesis for the model was supported as the indirect effect of paternal EA on adolescent anxiety through adolescent AS was moderated by adolescent gender (b = −0.05, 95% CI = −0.15, −0.01).
Fig. 2
Simple slopes for paternal EA
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Purpose of Study
The purpose of this study was to examine the relationships between adolescent anxiety sensitivity and parental emotional availability in the context of adolescent anxiety. Previous research has determined AS and EA influence one another, with parents who are warm and positive having more EA and offspring who tend to report lower levels of AS (Graham & Weems, 2015); likewise, individuals with insecure attachments to their parents tend to have higher levels of AS (Weems et al., 2002). However, previous research has not examined adolescent AS as the mechanism mediating the relationship the relationship parent EA and youth anxiety. Additionally, parent EA has been rarely studied in the context of youth anxiety, whereas the broader constructs of attachment and parenting styles have often been studied in relation to youth anxiety. Researchers have also found both parent and adolescent gender to influence this relationship, yet the findings have yielded equivocal results (East et al., 2007; Lum & Phares, 2005). Thus, the gaps in the literature led to the current study which provided information on the roles of gender, parent EA, and adolescent AS in the expression of anxiety. This study found both adolescent and parent traits and behaviors can predict levels of anxiety. Further, this study found adolescent AS does mediate the relationship between parent EA and adolescent anxiety, but there is no difference in parent gender on this relationship. Additionally, the interaction between paternal EA and adolescent gender had a significant impact on adolescent AS. The specific findings and implications will be further discussed.
Aims and Implications
The current study had multiple aims. The first hypothesis was that parent EA would be negatively associated with anxiety symptoms. It was observed that parent EA was negatively, moderately correlated with anxiety symptoms. However, there was not a significant difference between correlations for maternal and paternal EA and youth anxiety symptoms. In the literature, as EA is a newer, less researched construct, identifying the relationship between parental EA and adolescent anxiety has important implications for current and future research. Specifically, parental EA can be targeted in family therapy whereas attachment is more difficult to target. Additionally, either maternal or paternal EA can be effectively targeted in treatment to assist in the reduction of adolescent anxiety.
For the second hypothesis, it was hypothesized that adolescent AS would be positively associated with anxiety symptoms. After analyses were conducted, it was determined that adolescent AS was significantly, strongly positively correlated with adolescent anxious symptomatology. This finding supported previous research, and further contributed to the replicability of AS as a construct strongly associated with anxious symptomatology.
The third hypothesis assessed for parent EA being negatively associated with adolescent AS. In accordance with our third hypothesis, parent EA was negatively associated with adolescent AS. Specifically, maternal EA had a significant, moderate correlation with adolescent AS and paternal EA had a significant, small correlation with adolescent AS. However, there was not a significant difference between the correlations of maternal and paternal EA and adolescent AS. This finding was important as the majority of previous research on parenting and adolescent AS has only assessed the relationship between certain behaviors, parenting styles, or the broader construct of attachment which are difficult to target in treatment. Additionally, this finding was important because the previous literature had unclear findings related to parent gender and adolescent anxiety. As both paternal and maternal EA are related to adolescent anxiety, either parent can partake in treatment and it will be efficacious.
In the fourth hypothesis, we hypothesized adolescent AS would mediate the relationship between parent EA and adolescent anxiety. For the fifth exploratory hypothesis, the influence of parent gender in this model was examined. The fourth hypothesis supported adolescent AS as the mechanism mediating the relationship the relationship parent EA and youth anxiety. Our fifth hypothesis was not supported, as there were not significant differences observed between maternal and paternal EA as a predictor of adolescent anxiety. However, this implies that targeting paternal or maternal EA is equally effective in the treatment of adolescent anxiety. This finding also has implications for the creation of prevention and intervention programs for adolescent anxiety. The most empirically supported parenting programs involve cognitive, developmental, and behavioral theories, and the proposed programs that can be modified using the constructs in this study is discussed below.
For the sixth hypothesis, a moderated mediation model was tested, with adolescent AS mediating the relationship between parent EA and adolescent anxiety, and adolescent gender moderating the relationship between parental EA and adolescent AS. The hypothesis was supported, as the indirect effect of paternal and maternal EA on adolescent anxiety through adolescent AS was moderated by adolescent gender. Specifically, as parental EA increased, adolescent AS decreased. The direction of this effect was present for both male and female adolescents, but the effect was more pronounced for male adolescents. Thus, parental EA is more effective at lowering male adolescent AS than female adolescent AS. Therefore, these findings support targeting both parent EA and adolescent AS to treat adolescent anxiety; while these treatment targets can be beneficial for both adolescent males and females, targeting parent EA can be more beneficial for male adolescents.
Limitations and Future Directions
There are several limitations of the current study that future work should address. First, the present study relied only on self-report data from adolescents, which can be a fallible method as it introduces the possibility of biased responses as individuals will report on their subjective experiences. Second, parent reports were not obtained. Parent reports could have provided a more comprehensive view of the respondents, which could have increased the reliability of responses. Third, the participants were high school students who were in college classes, which is a potentially biased sample as the students were encouraged to take surveys for class credit. Additionally, the sample primarily consisted of white female adolescents. The limitations in the demographics may impact the generalizability of these findings, and future studies would benefit from a more diverse sample collected from the community. Also, since the sample was comprised of students, the population is non-clinical and caution must be used when generalizing the finding to a clinical population. Fourth, formal diagnoses for anxiety disorders could have been obtained or the longer version of the RCADS could have been used to assess for different anxiety subtypes. Fifth, the study utilized a cross sectional design which only provides data at one time point, which is also in line with much of the current research on AS development and parenting. Additionally, mediational analyses were used in this study and as such the findings cannot be casual as assumptions were made about the temporal sequencing of the variables. Sixth, confounding variables such as individual factors, risk factors, and others may have influenced the relationship between the variables. In the future, researchers may utilize more rigorous measures to explore or control for confounding variables.
Conclusion
The present study provided researchers and clinicians with information on the relationships between parental EA, adolescent AS, and adolescent anxiety. The findings supported the mechanism of adolescent AS as a mediator between parent EA and adolescent anxiety. Further, this study also provided evidence for the importance of parental and adolescent gender in the development and treatment of anxiety disorders. As anxiety disorders tend to onset around the age of 11 years old (Kessler et al., 2005), and the prevalence of anxiety disorders in youth has increased greatly in current years (CDC, 2022), it is vital to understand the mechanisms underlying anxiety disorder development in adolescence. Further, understanding how gender can influence the development of anxiety disorders can assist clinicians and researchers in developing programs that are most beneficial for specific groups (i.e., mothers and daughters, fathers and daughters, mothers and sons, fathers and sons). This study additionally supports AS as a mechanism to be targeted to treat anxiety disorders, and this may also be generalizable to the treatment of other disorders in which AS is a factor as it is a transdiagnostic construct (Chorpita & Lilienfeld, 1999). As AS has been targeted to treat panic disorders, it can also be relevant a treatment target for youth anxiety as AS develops in adolescence. Moreover, parental EA can also be targeted in therapy. These findings suggest that if both adolescent AS and parental EA are targeted in family therapy, adolescent anxiety may decrease.
Future researchers can use this information to develop more specific therapy modalities targeting both of these mechanisms at the same time to prevent or treat adolescent anxiety. Previously developed efficacious programs support the wellbeing of youth and the reduction of behavioral issues have utilized empirical research for their creation. Some of these well-known programs include elements of observational learning (such as behavior modeling) include the Triple P Positive Learning Program (Triple P; Sanders, 2012), Parent Management Training – Oregon Model (Forgatch & Patterson, 2010), Parent Child Interaction Therapy (Fernandez & Eyberg, 2009), and the Incredible Years Program (Webster-Stratton, 1998). Most of these programs focus on positive parenting approaches, and Triple P has had widespread, effective results (Sanders et al., 2014). These results suggested that Triple P was effective for promoting short term, positive changes to children’s functioning, parenting adjustment and satisfaction, and parent/family relationships. Programs like Triple P can be even more effective in reducing youth anxiety by incorporating interventions increasing parent EA and decrease youth AS. Additionally, programs can be modified for specific youth and parent genders to increase their efficacy. In sum, beneficial parenting programs exist and can be strengthened by the current literature to further increase treatment outcomes for children and families.
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