Introduction
Psychotic disorders have often been associated with social cognitive impairments [
1]. One of the domains of social cognition is facial emotion identification [
2], which refers to the ability to accurately identify emotional expressions from another person’s face. The ‘basic’ set of emotions (anger, disgust, fear, sadness, surprise and happiness) as proposed by Ekman and colleagues are each characterized by a distinct facial expression, physiology and evolutionary purpose [
3]. The ability to accurately recognize these emotions is crucial in facilitating emotional connections and communicating effectively with others. In psychotic disorders, recognition of positive expressions (happiness) is preserved and recognition of negative expressions (anger, fear, sadness and disgust) is impaired [
4‐
7], although some studies report impairments for both positive and negative emotions [
8].
Recent studies demonstrated that impairments in the identification of facial affect are not only found in chronic psychosis [
9], but also in first episode psychosis [
10], the ultra-high risk phase of psychosis [
11,
12], and in siblings [
13]. The evidence suggests that early impairment may show up for specific emotions, rather than as a general deficit [
10]. Deficits in facial emotion identification have been hypothesized to play a role in the development of psychotic experiences. To specify, facial emotion identification deficits could give rise to paranoia (an inability to understand others could feed negative interpretations [
5,
14]), delusions (an inability to correct faulty interpretations can cause and support delusional ideation [
15]), and potentially hallucinations (continuous erroneous interpretation of social situations and others can lead to social stress, hyper vigilance, and hallucinatory experiences [
16] (see also a review by [
17]). Overall, an impairment in facial emotion identification may be a trait vulnerability for psychosis, rather than a consequence of the disorder. It is important to investigate at which point facial emotion identification impairments can be ‘detected’ as to examine when early interventions may be possible and effective. Given that psychotic experiences are prevalent in samples of youth [
18‐
20], and may signify a precursor to psychotic disorders [
21], it is fruitful to examine whether reduced facial emotion identification in preadolescence is associated with psychotic experiences during adolescence.
Social cognitive impairments have been found to contribute to diminished social functioning in psychotic disorders [
22]. If deficits in facial emotion identification are present from childhood, this may already lead to problems in the development of socially competent behaviors and interactions. Given the importance of the family environment for children and adolescents’ functioning [
23], it is possible that children with poor facial emotion identification skills have more difficulty functioning in the family environment as well. For example, children with poor facial emotion identification skills may perceive parenting as more negative, either due to inaccurate identification of emotions of their parents, or due to an accurate perception of more rejective or overprotective parenting as a reaction to their lower social cognitive abilities. Therefore, if facial emotion identification abilities predict psychotic experiences throughout adolescence, it may be especially interesting to explore the possibility whether this association might be mediated, at least partially, by family functioning.
The family context has gained much attention in psychosis studies, mostly in more acute and chronic phases of illness [
24‐
30]. There is a strong indication that family factors such as expressed emotion [
24,
27], the family rearing environment [
25,
28] and family communication [
26,
30] are important predictors of the prognosis of psychosis once an individual has transitioned to a first psychotic episode. Several prospective studies have found that patients with family members who are high in expressed emotion (over-involvement, high criticism, and negative affective style) are at an increased risk of relapse in schizophrenia over a period of nine to 12 months [
24,
31]. Also in children with elevated mental health problems, parental styles (such as communication deviance, expressed emotion or affective style), significantly predicted schizophrenia spectrum disorders in adulthood in a 15 year prospective longitudinal study [
26], although it is important to note that this sample was limited in its size (n = 50). In the ultra-high risk phase of psychosis (before the first psychotic episode), family functioning (a positive warm environment) has been shown to be protective [
32,
33], both for reducing negative and disorganized symptoms, and improvement in functioning over a period of 3 [
32] and 6 [
33] months. Whether the family environment and parenting styles are predictive of the development and course of psychotic experiences (rather than a reaction towards clinical symptoms) during adolescence, remains understudied so far.
The aim of the current study is to examine whether a) facial emotion identification and b) family factors at preadolescence (age 11) predict psychotic experiences 5 years later during adolescence (age 16). We expect that both lower facial emotion identification abilities and more negative family functioning in preadolescence will predict a higher frequency of psychotic experiences at adolescence. If confirmed that facial emotion identification abilities are associated with psychotic experiences in adolescence, we will further explore whether functioning in the family environment (at least partially) mediates the relationship between facial emotion identification and psychotic experiences. Given that childhood mental health is associated with parenting behaviors at preadolescence [
34] and is likely to predict adult mental health, the current study will control for pre-adolescent mental health problems (internalizing and externalizing behaviors).
Discussion
Reduced social cognition has often been identified as a trait marker for psychosis, as it is compromised in early phases of psychosis [
10], as well as in siblings of individuals diagnosed with a psychotic disorder [
13]. We examined whether diminished facial emotion identification can be identified as a vulnerability marker for subsequent psychotic experiences in a young adolescent sample. The results did not confirm our hypothesis that facial emotion identification abilities at preadolescence were associated with psychotic experiences at adolescence. When examining a sub-sample of preadolescents scoring the lowest performance on the facial emotion identification task, we still found no vulnerability for psychotic experiences associated with impaired identification of facial affect in adolescence. In absence of an association, mediation by family factors was not explored. As a main effect, increased overprotective parenting at preadolescence was associated with a higher frequency of psychotic experiences as well as delusions in adolescence, after adjustment for preadolescent mental health. There was no indication that parenting stress, family functioning, and rejective and warm parenting were associated with psychotic experiences, indicating these factors may not pose a vulnerability for psychotic experiences.
In the broader adolescent population, when individuals are not recruited for their high risk status or previous episode of psychosis, facial emotion identification does not seem to be predictive of the development of psychotic experiences. Thus, it is possible that the association between facial emotion identification and psychotic experiences is not present in a large and relatively healthy sample. We speculated that perhaps this association would be detectable in a subgroup of adolescents with demonstrably lowered performance in facial emotion identification. However, a post hoc examination based on this subsample also showed no indication of a vulnerability for psychotic experiences over time. Although the reporting of psychotic experiences may increase the risk of developing a mental illness [
21,
64‐
66], the large majority of psychotic experiences are transient and benign during adolescence [
67]. Therefore, perhaps an impairment in facial emotion identification is not predictive of psychotic experiences in adolescence, but it may be predictive of clinical psychotic symptoms in young adulthood. This reasoning would be in line with findings of a recent study [
68] which reported that developmental cognitive deficits between infancy and adulthood are only found in those who develop a psychotic disorder, with only weak evidence for individuals who have psychotic experiences. The same might hold for the association between facial emotion identification abilities and family functioning, which perhaps becomes evident only at levels of actual impairment.
In the current study, perceived overprotective parenting at preadolescence was predictive of the frequency of psychotic experiences at adolescence, after controlling for early existing mental health problems. It should be noted first that we need to be cautious about the clinical relevance of this finding: the effect of overprotective parenting on the frequency of psychotic experiences was relatively small (denoted by the small, but significant correlation and regression coefficient). Second, we need to be cautious about the interpretation. It is possible that when parents overly protect their child, the child is less able to form its own coping mechanisms towards daily stressors. As a result, the child may be less resilient to negative events in life, rendering them more vulnerable to develop psychotic experiences and/or delusions. Another explanation may be that overprotection by the parent is a natural reaction towards a child that is more vulnerable, and requires extra support and care. The parent may sense that the child is sensitive towards certain experiences, and the overprotective parenting may then be an attempt of preventing negative outcomes. However, given that the association was corrected for preadolescent mental health problems, this explanation could be less likely. Overprotective parenting may be a trans-diagnostic risk factor, as previous studies have also found overprotective parenting to be predictive of substance abuse [
69,
70], anxiety [
71], and internalizing and externalizing problems [
72]. Such a risk factor may actually be genetically mediated, which leaves a third explanation that genetic background is causal in both overprotective parenting and in offspring liability to mental health problems. Future research should aim at furthering our understanding of the mechanisms shaping the association.
We expected that rejective parenting, parenting stress, lower family functioning and a lack of warm parenting would also predict psychotic experiences in adolescence, but we did not find evidence for this in the current study. It is possible that overprotective parenting is specifically relevant for the development of psychotic or internalizing problems, whereas rejective parenting may be more relevant for, for example, aggressive problems [
73]. An alternative explanation could be that the negative impact of family factors during preadolescence can be compensated with protective factors in adolescence, such as a strong social network of peers. Indeed, previous findings demonstrate that although negative parenting (specifically dominant and harsh parenting) is predictive of externalizing behaviors in adolescence, the association was attenuated by good quality friendships and peer group affiliation [
74]. In contrast, overprotective parenting often renders a child placid, cautious and sensitive [
75], making them less attractive to peers, and more often at risk of peer victimization [
76]. Future research could examine whether the protective effect of peer relationships on negative parenting in preadolescence is less strong (or perhaps not evident) for overprotected children.
This study has a number of limitations. The Facial Expressions Task (ANT [
39] is not suited to assess biases in facial emotion identification. An emotional bias is a qualitative deviation in emotional processing [
77], such as for example, the under-attribution of happiness when labelling neutral faces [
7]. Given that previous studies have found that emotional biases are present and important in psychosis [
78,
79] our study would have been more comprehensive to assess biases in addition to the ability to identify emotions per se. In addition, the inclusion of neutral faces would have yielded more information, as processing of neutral faces (a socially ambiguous stimulus) has reported to be abnormal in individuals with a psychotic disorder [
80]. A further limitation of our study is the lack of a control group of adolescents with clinical psychotic symptoms, as this would allow us to test our hypothesis that a facial emotion identification vulnerability may only be associated with clinical psychotic symptoms, rather than psychotic experiences more generally. In addition, having knowledge on the family history of mental health problems could shed more light on the potential presence of a genetic liability for both overprotective parenting and psychotic experiences. Last, in the ideal design, we would have assessed psychotic experience at age 11 (rather than general problem behavior), as well as emotion identification at age 16, which would have allowed us to examine concurrent associations that aid in the interpretation of our null findings across these 5 years.
This study also has a number of strengths. First, we used a longitudinal design to examine whether facial emotion identification and family factors would predict psychotic experiences in adolescence, where most studies utilize cross-sectional designs (or shorter follow-up periods) and examine these associations in older samples or in samples with individuals who already have psychotic experiences or symptoms, thus limiting the examination of cause-consequence associations. Second, our study has a large sample size and a follow-up period of 5 years. To the best of our knowledge, we were the first to examine in a longitudinal way whether preadolescent facial emotion identification abilities and family factors have the potential to predict psychotic experiences in adolescence.
The current study examined whether facial emotion identification and family factors at preadolescence (age 11) were predictive of psychotic experiences 5 years later at adolescence (age 16). Facial emotion identification at preadolescence was not associated with psychotic experiences at adolescence. This may suggest that a facial emotion recognition vulnerability for psychosis cannot be detected in early adolescence. Alternatively, it may only be evident in subgroups of individuals who ultimately develop a psychotic disorder, indicating that psychotic experiences in adolescence are still too mild or have little specificity for the subsequent psychotic disorder. Overprotective parenting at preadolescence predicted the frequency of both psychotic experiences and delusions, after adjusting for preadolescent mental health. Possibly, overprotective parenting at a young age results in a lack of self-reliance, autonomy or coping skills in adolescents, making them especially vulnerable to psychotic experiences as a reaction to life stressors. However, it could be that overprotection by parents is a natural reaction towards a child that is more vulnerable, and requires extra support and care. Likewise, overprotection by parents and their children’s vulnerability for psychotic experiences could have a shared background, for example, a shared genetic liability. Future research is needed to examine the mechanism behind the role of overprotective parenting on psychotic experiences during adolescence.
Summary
An impairment in facial emotion identification could signify a vulnerability for the development of psychosis. Family functioning may mediate the association between facial emotion identification and psychotic experiences. The current study examines whether facial emotion identification and family factors at preadolescence (age 11) predict psychotic experiences 5 years later during adolescence (age 16). Data was obtained from the epidemiological cohort TRAILS (TRacking Adolescents’ Individual Lives Survey; N = 2059). At preadolescence, a facial emotion identification test and three questionnaires to assess family functioning, perceived parenting styles and parenting stress, were administered. At adolescence, a questionnaire on psychotic experiences was administered. Data were analyzed using multiple linear regression models. Facial emotion identification at preadolescence was not associated with psychotic experiences at adolescence, and the mediational role of family functioning was therefore not further explored. Increased overprotective parenting at preadolescence was associated with a higher frequency of psychotic experiences and delusions at adolescence, while the other family factors (parenting stress, family functioning, and rejective and warm parenting) at preadolescence were not significantly associated with psychotic experiences at adolescence. While clinical symptoms in early and chronic psychosis have been associated with facial emotion identification deficits, this association was not present in the current adolescent cohort. Conversely, perceived overprotective parenting was prospectively associated with psychotic experiences, possibly either due to a vulnerability for psychosis, a natural reaction towards a vulnerable child, or a shared genetic liability in both parents and adolescents. Future research may examine the mechanism behind the role of overprotective parenting on psychotic experiences during adolescence.
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