Introduction
One of the well-examined features of anxiety disorders (ADs) is that they tend to ‘run in families’ and are transmitted from parents to children [
1]. So far, evidence is available that this can partly (30–40%) be attributed to biological/genetic markers [
2]. However, a recent study in a large sample of children of twins found evidence for direct environmental transmission of ADs from the parent to the child, which could imply that parental anxiety shapes the way for a parenting style that contributes to the development of ADs in children [
3]. One of these parenting styles is over-controlling behavior, which limits children’s autonomy, and could maintain their inhibition and anxiety. Moreover, children’s anxious behavior could also evoke parents' over-controlling parenting behavior in order to prevent distress in their child [
4]. In addition, parents’ anxious behavior and expressed anxiety could also promote and maintain child anxiety through modeling, i.e. catastrophizing and over-attribution of threat [
1,
4,
5]. Together this shows that the development and maintenance of ADs in children are a result of genetic, environmental and parenting factors.
In order to inform our understanding of the etiology, prevention and treatment of child ADs, it is important to know to what extent parents of children with ADs have ADs themselves. It has been shown that children with ADs did less well in treatment when their mothers had ADs [
6], and CBT for children with AD is less effective when parents have an AD themselves [
7]. Numerous studies have examined the familial risk of ADs; however, most used a top-down approach (i.e., examining the presence of ADs in the offspring of parents with ADs) [
2,
8,
9]. Another way to examine transmission of ADs is to use a bottom-up approach: evaluating the presence of ADs in parents of children that are diagnosed with ADs.
Bottom-up studies have shown increased rates of ADs in parents of children referred with ADs compared to parents of typically developing children, with lifetime prevalence rates ranging between 46 and 83% in mothers, and between 30 and 45% in fathers [
10‐
13], compared to 15–38% in parents of typically developing children. While these initial studies were valuable in terms of examining the associations between child and parental ADs, it should also be noted that some of these studies included participants diagnosed with DSM-III disorders [
13,
14], had low father participation and/or did not use a diagnostic instrument to assess fathers’ clinical status [
10,
11,
13], or lacked a control group [
11]. In addition, an important aspect that was not addressed in these studies is the prevalence of ADs in siblings.
To determine familial transmission of ADs and to understand the mechanisms behind it, it is important to include the whole family. Recently, fathers are more often included in child anxiety research, and it has been suggested that fathers’ ADs contribute differently to the development of child anxiety than mothers, for example father’s role in physical play may be affected more by his own anxiety (disorders) than mother’s role of caring [
15,
16]. Nevertheless, associations between mother–child ADs seem to be stronger than father-child ADs, with odds ratios of lifetime ADs found between 3.40 and 4.44 for mothers and odds ratios between 2.33 and 3.17 for fathers [
10,
12]. However, Last et al. [
14] found twice as many ADs in fathers and brothers (male relatives combined) of children with ADs than in control children, and no difference in mothers’ prevalence, but note that father participation was low in the group of children with ADs (38%). To conclude, the relative risks of mothers versus fathers of children referred with ADs being affected by own ADs need to be established in studies in which no more fathers are missing than mothers, in order to draw valid conclusions, as missing fathers are likely to be systematically missing (e.g., because of divorce, anxiety disorders, or busy in the outside world [
16]).
Next to the increased prevalence of ADs in mothers and fathers, siblings of children with mental health problems are at risk of developing psychopathology themselves [
17]. However, it is unclear whether they develop an AD more often than siblings of typically developing children. Only a few studies examined the prevalence of ADs in siblings of anxious children [
14,
18‐
20]. The study of Dia and Harrington [
18] showed that 12% of siblings of children with ADs had a (mostly mother-reported) diagnosis of AD, but this study did not include a control group and two other studies examining anxiety in siblings lacked a DSM-based diagnostic assessment [
19,
20]. One study did use a control group and a diagnostic instrument (but based on DSM-III), and found that siblings of children with ADs were about twice as likely to have ADs as siblings of typically developing children [
14].
In addition to the intergenerational transmission of ADs, it is interesting to examine to what extent there is diagnostic specificity in this transmission. Diagnostic specificity suggests that children of anxious parents are at greater risk of developing the same AD as their parents, because their parents, next to heritability aspects [
2], model or communicate their specific anxieties to their children [
12]. A better understanding of the specificity of the transmission of ADs could inform child treatment or preventive interventions. In previous studies, some evidence has been found for specificity of social anxiety disorder (SAD), separation anxiety disorder and panic disorder between child and mother, but not between child and father [
10,
12]. Otherwise, strong associations have been found between parental social phobia and social phobia in their adolescent children (odds ratio = 4.7; [
21]). In addition, specificity in siblings was found for agoraphobia and social phobia [
20], although those ADs were not measured with a diagnostic instrument but based on clinical judgment. In contrast, other studies did not find evidence for specificity, thus providing support for a transmission of anxiety in general and not for specific ADs, which implies that ADs have shared etiology [
3,
10]. Thus, only few studies have studied specificity of ADs between family members and those studies that did, found contrasting results.
Finally, considering the comorbidity between ADs and depressive disorders [
22], parents of children with ADs may be more likely to have depressive disorders than parents of children without ADs. Bottom-up studies have found mixed results, as Cooper et al. [
10] found that children with ADs were more likely to have mothers with current and lifetime depressive disorder than children without anxiety disorders, whereas Last et al. [
14] and Hughes et al. [
12] did not find that parents of children with ADs were at increased risk for lifetime mood disorders. In addition, stronger associations have been found between ADs in children and parents than between ADs in children and depressive disorders in parents [
8]. Moreover, it remains unclear whether children with ADs have an elevated risk of having parents with depressive disorder, or that this is mainly due to an elevated risk of ADs in parents with comorbid depressive disorder [
23]. Thus, it is important to consider comorbid depressive disorder in parents when examining ADs in parents of children with ADs.
The main aim of the current study was to examine the transmission of ADs in the family using a bottom-up approach, in order to understand to what extent children with ADs grow up with parents and siblings with ADs. Establishing the risk for ADs in mothers, fathers, and siblings of referred children with ADs is important for our understanding of the etiology, prevention, and treatment of child ADs. In this study, we examined the association between ADs in a clinically referred sample of children with ADs, their mothers, fathers, and siblings, using diagnostic interviews, and we compared these rates to a control group of typically developing children. We hypothesized that mothers, fathers, and siblings of children with ADs would be more likely to have ADs than families of typically developing children. Additionally, given that parental depression has been associated with the development of child ADs, we examined the association between depressive disorder in parents of children with AD and parents of children in the control group. Finally, we examined specificity of transmission, i.e. whether a specific AD in the child (e.g., SAD) would be associated with the same AD (SAD) in the parent or not; and familial risk of specific ADs, i.e. whether children with a specific AD (e.g., SAD) would be more likely to have parent(s) and/or siblings with any AD, compared to children with other ADs.
Discussion
The aims of the current study were to examine whether (I) children with ADs referred to community mental health care centers were more likely to have mothers, fathers, and siblings with ADs than typically developing children, and (II) children with specific ADs were more likely to have parents and siblings with the same AD (specificity) and/or parents and siblings with any AD (familial risk). Regarding (I), as compared to controls, children with ADs were respectively two and three times more likely to have at least one parent with lifetime and current ADs; two-and-a-half times more likely to have a mother with current ADs; nearly three times more likely to have a father with lifetime ADs, and—although borderline significant—four times more likely to have fathers with current ADs. Children with ADs were not more likely to have siblings with ADs. Regarding (II), specificity was found for mother–child SAD, all fathers with lifetime SAD had children with SAD, and all siblings with SAD were siblings from children who had SAD. In addition, specificity was found for mother–child GAD. At the same time, there were indications of a familial risk for some child ADs: (1) children with SAD were nearly three times more likely to have fathers with lifetime AD, and (2) children with GAD were two-and-a-half times more likely to have mothers with lifetime AD, compared to children with other ADs. Each of these findings is discussed in more detail below.
In line with our hypothesis and previous research [
10,
12], we found that children with ADs were more likely to have mothers and fathers with ADs than controls. Results of the current study showed comparable sizes of odds ratios for mothers and fathers, whereas previous research mainly found stronger associations for internalizing problems between mother–child than for father–child [
10,
36]. Therefore, our findings could suggest that both mothers and fathers are important to consider when assessing transmission of ADs in families. Moreover, we have found no heightened prevalence of depressive disorder in mothers and fathers of children with ADs compared to controls, which adds to the evidence that ADs are running in families. In contrast to our hypothesis, we did not find that siblings of children with ADs were more likely to have ADs which could be explained by the child susceptibility hypothesis. That is, some children, who are genetically susceptible for the development of an AD, because of an anxious temperament, are more likely to be affected by the consequences of living in a family with parental ADs than siblings who are not genetically-burdened, based on gene-environment interaction [
37,
38]. In addition, anxious parents may be differentially susceptible for the anxious temperament of their child (for example experiencing the child as highly vulnerable), and consequently treat their anxious child different from their non-anxious children, for example by overprotecting their anxious child, which could influence parents’ risk of developing pervasive ADs [
3]. Another, methodological, explanation for the lack of heightened risk of ADs in siblings of children with ADs, is the elevated prevalence of ADs in siblings of both groups (26.2% in the AD-group and 31.6% in the control group) when compared to the general prevalence of childhood AD (8.3–27%, [
26]), as well as when compared to previous studies on siblings of children with AD (21.7%, [
14]; 12%, [
18]). It is remarkable that these rates are this high, and they are higher than would be expected in this sample. One explanation could be that the siblings that were interested in participating in our study were more familiar with anxiety symptoms. Moreover, the siblings of the control group were younger and consisted of more girls compared to the group of children with ADs, which could have affected prevalence rates [
26]. Larger child and sibling samples are needed, as well as full participation of siblings to prevent systematic missing data, in order to examine the prevalence of ADs in siblings.
Strong evidence was found for the specificity of mother–child SAD, and for an elevated risk of SAD in fathers and siblings of children with SAD. These findings are interesting as they suggest that something specific is happening with the (familial) transmission of SAD. Next to heritability of an inhibited temperament (although only moderately, [
39]), it could be that mothers and fathers of children with SAD are lacking certain social skills, which are modeled to the children and thus leading to childhood SAD. Previous studies have found that mother–child SAD is related [
12], but the finding that all fathers of children with SAD have SAD themselves is interesting. This could be explained by the finding that socially anxious fathers show less challenging parenting behavior, which is a risk factor for the child developing social anxiety [
40]. This indicates that fathers do have a different role in the development of ADs in their offspring than mothers (as suggested by Bögels and Phares [
15]), and that father’s role may be particularly important for children with SAD [
16,
41]. Interestingly, there are indications that children with SAD respond less well to treatment [
42]. This could be related to the finding that SAD runs in the family and perhaps SAD needs a more family oriented treatment approach than other ADs. In sum, it seems that SAD runs in the family, and as SAD is the most common AD [
43], more research towards the mechanisms of family transmission of SAD in specific is necessary.
Next to SAD, specificity was found for mother–child GAD, that is, children with GAD were more likely to have mothers with lifetime GAD than children with other ADs. This is interesting as previous research suggested that avoidance in GAD is less observable and therefore less easily transmitted through modeling [
12]. Thus, it seems that GAD is transmitted through another mechanism, and it has been proposed that mothers transmit the cognitive styles associated with GAD, for example that worry helps to cope with uncertainty [
44]. Next to this environmental transmission of GAD, it could be that genetic transmission of a certain trait or physiological marker is more important in GAD than in other ADs [
2]. Furthermore, the specificity of both mother–child SAD and GAD could indicate a shared etiology or trans-diagnostic perspective, for example the tendency to worry that is present in both disorders [
45]. Nevertheless, we cannot rule out that there are specific or common pathways in the transmission of SAD and GAD between mothers and children and vice versa. These effects should be examined bi-directionally in order to understand which mechanisms account for the specificity and to understand to what extent the worrying child affects maternal worry and maternal feelings of uncertainty.
Finally, we have found indications of a more familial risk of certain ADs, because children with GAD were more likely to have mothers with ADs, whereas children with SAD were more likely to have fathers with ADs, compared to children with other ADs. It could be that the mechanisms of transmission from father to child are different from transmission from mother to child, and/or that mothers and fathers respond differently to an anxious subtype in the child, i.e. a child with GAD evokes more anxiety in the mother while a child with SAD evokes more anxiety in the father. Previous studies have shown that fathers of socially anxious children show less emotional warmth and more rejection [
41] and this relation is likely to be bi-directional, i.e. fathers show less warmth because their child is socially anxious and/or their child becomes more socially insecure because fathers show less warmth and more rejection [
15]. Concerning GAD, it could be that mothers of children with GAD are transmitting their anxious thoughts and behaviors through specific and non-specific pathways (see Aktar, Nikolic, and Bögels [
44] for a review of the literature), and/or that mothers of children with GAD feel more anxious when their child is worrying and expressing uncertainty. Experimental studies need to be carried out in order to understand the mechanisms behind the transmission of SAD and GAD between father, mother and child, as well as the direction of effects (parent to child, child to parent or both). Next to the possibility of a different transmission from mother and father to the child, the child’s gender could also play a role in the transmission of ADs. It has been found that rates of ADs between mothers and daughters were higher than between fathers and sons [
14]. However, a more recent study did not find gender effects between sons and daughters [
46]. Thus, in order to get a better understanding of the transmission of ADs, future studies should not only consider the specificity of ADs for mothers and fathers, but also whether this differs between daughters and sons.
As with all studies, the current study is not without limitations. First, although the clinical sample size was large, not all odds ratios could be calculated. This study provided important information (i.e. no SAD fathers had children without SAD), but this issue should be examined further, for example by including a larger sample of children with SAD. Second, due to the large amount of children meeting criteria for several ADs, the interpretation of the current findings concerning the specific disorders is somewhat limited. Thus, in order to improve internal validity, only children with a single AD should participate; however, this will limit the generalizability to the field of child and adolescent psychiatry where comorbidity is the rule rather than the exception [
26]. Third, the design of this bottom-up study only examined children with ADs and not children with other types of psychopathology, which limits the findings of specificity only to this AD sample, and it would be interesting to compare these rates to parents of children with other disorders. Fourth, the control group included children that met criteria for an AD, which raises the question whether this is a true control group. We have decided to keep the children with ADs in the control group, in order to support the external validity of our study. Nevertheless, the control group was smaller than the group of children with ADs, and it could be that the control group is less representative due to the recruitment through newspaper advertisements. Finally, the study design does not allow conclusions about the mechanisms that are underneath the observed transmission of anxiety (i.e. genetic and/or environment), nor about the direction of transmission.
Despite its limitations, this study represents a comprehensive evaluation of prevalence of ADs and specificity in mothers, fathers, and siblings of children referred with ADs. The study was one of the first to systematically include fathers and siblings, which adds to the existing knowledge of ADs running in families. Another strong point is that this study used structured diagnostic interviews for all family members and combined child and parent report for the child diagnoses. We have found that children with ADs are over twice as likely to have mothers and/or fathers with lifetime and/or current ADs. We have also found evidence for specificity of SAD and specificity of mother–child GAD. It has been shown that children of parents with ADs do less well in treatment than children of parents without ADs [
7], and, in specific, children of mothers with SAD tend to do poorly compared to children of mothers without ADs [
10]. In addition, this study showed that fathers and siblings of children with SAD reported high rates of SAD themselves. Siblings of children with ADs usually are not included in treatment and research (compared to siblings of children with special needs [
17]), but it may be important to screen them for ADs as well and to consider involving them in treatment. Finally, treatment of SAD in children has been mentioned as least effective compared to other ADs [
42]. Possibly, treatment of childhood SAD is less effective because parents’ SAD functions as a maintaining factor and parents are for example not able to facilitate social exposures because they lack certain social skills. Thus, it should be examined whether parents will also change when their child is treated or vice versa, especially regarding SAD.