Introduction
Attention-deficit/hyperactivity disorder (ADHD) is one of the most commonly diagnosed disorders of childhood [
1]. Although on average ADHD symptoms decline after childhood, the course of symptoms differs between individuals (e.g., [
2‐
4]). The course of ADHD symptoms is explained by genetic and environmental influences [
5,
6], including family functioning (e.g., [
7,
8]). It is well-documented, although based on predominantly cross-sectional studies, that ADHD symptoms and adverse family circumstances may co-occur (e.g., [
9‐
13]). Longitudinal studies, which provide more compelling evidence of cause–effect relations, have shown in (pre-)school aged boys that a less optimal family environment predicted higher ADHD levels [
14]. In addition, in 4-year-old boys, a negative home atmosphere was significantly associated with ADHD symptoms 2.5 years later [
15], but it is unknown whether this association holds for adolescents. Furthermore, little is known about the role of a positive environment in the course of ADHD symptoms, despite evidence that individuals living in a supporting environment generally tend to have better developmental outcomes across adolescence [
16,
17]. One longitudinal study found that higher levels of parental involvement predicted reduced symptoms of ADHD symptoms in young children [
18]. In school age boys, a more optimal family environment predicted lower ADHD symptoms [
19,
20]. In recent years, there has been more attention for (prospective) associations between ADHD symptoms and family functioning, but those studies often focused on parental ADHD symptoms rather than the broader family environment (e.g., [
21,
22]). Prospective associations between adolescents’ ADHD symptoms and the socio-emotional quality of family functioning, which we here refer to as the family climate, are an understudied topic.
The school environment another important environmental factor that may be related to ADHD symptoms over time, has received little research attention, despite the fact that adolescents spent substantial amounts of time at school. In general, it is well known that classroom quality is influential in reducing ADHD symptoms by behavioral school interventions [
23], but it is also possible that a negative classroom environment might exacerbating adolescents’ risk for elevated ADHD symptoms. It has frequently been reported that individuals with ADHD are more often rejected [
24] or bullied by their peers than typically developing adolescents [
25,
26], which may have negative effects on development. Conversely, friendships may play an important protective role against negative psychosocial outcomes for individuals with ADHD [
27]. Apart from peers in the classroom, teachers make a crucial contribution to adolescents’ academic and social-emotional outcomes [
28,
29], and this may well hold for ADHD symptoms as well. However, students with ADHD exhibit a variety of behaviors in the classroom that may disrupt teaching, increase teacher’s experience of stress, and may stand in the way of a supporting school climate [
30]. Taken together, these studies suggest that the school climate, here defined as the extent of experienced security and comfort at school by the adolescent, may also affect the ADHD symptom course across adolescence.
Individuals differ in the extent to which they are influenced by the environment. The differential susceptibility theory states that some individuals are sensitive to negative and positive environments [
31,
32]. The dopamine D4 receptor gene (
DRD4) is proposed as one of the genetic susceptibility variants [
33]. In the present study, we investigated whether this gene functions as a moderator of the effect of the family and school climate on ADHD symptoms across adolescent development. Gene–environment interaction (G × E) studies have shown that individuals carrying the
DRD4 7-repeat are more vulnerable to negative environments and may also benefit more from supportive environments [
34,
35]. In relation to the family environment, young children with the
DRD4 7-repeat allele have been shown to be more sensitive to both positive and negative aspects of parenting [
33,
35]. Another study, focusing on negative family influences, showed that children’s
DRD4 variants moderated the association between parental inconsistent discipline and the children’s ADHD [
36]. In relation to the school environment, genetic moderation studies with the
DRD4 genotype have examined the influence of peers and teachers in promoting positive development. For example, children with the
DRD4 7-repeat allele who experienced little to no peer victimization had lower levels of externalizing behaviors compared to when they experienced high amounts of peer victimization [
37]. However, in a previous TRacking Adolescents’ Individual Lives Survey (TRAILS) study, in relation to delinquency,
DRD4 7-repeat allele carriers were less sensitive to the effects of both peer victimization and social well-being [
38]. A similar effect has been found for the association between teacher–student dissatisfaction and rule-breaking behaviors which was stronger for adolescents without the 7-repeat
DRD4 non-long carriers [
39]. Together these findings suggest that the prospective associations between family and school climate and ADHD studied here may be moderated by
DRD4 genotype.
Within the framework of differential susceptibility theory, it is also relevant to investigate another plasticity gene, the
5-
HTTLPR genotype [
34]. Individuals who are S-allele carriers were found to be more vulnerable to negative environments, but also profited more from a positive environment compared to L-allele homozygotes [
40]. One cross-sectional study in youth aged 6–17 years showed that family conflict predicted increased inattention symptoms, whereas family cohesion predicted decreased inattention symptoms, but only for adolescents homozygous for the S-allele [
41]. Furthermore, only in S-allele carriers, caregiver-reported peer problems at age 4 predicted ADHD symptoms two years later [
42]. This literature thus suggests that the
5-
HTTLPR genotype might moderate associations between ADHD symptoms and both the family and school climate.
The present study investigated whether longitudinal bidirectional associations between the family and school climate, and ADHD symptoms across adolescent development (mean ages 11, 13.5, and 16 years) is moderated by the
DRD4 and/or
5-
HTTLPR. Using the Random Intercept Cross-Lagged Path Model (RI-CLPM), we aimed to distinguish between-person differences (i.e., between stable trait levels) from within-person (causal) processes over time (i.e., in change over time [
43,
44]). By partialling out between- and within-person variance, more adequate inferences can be drawn regarding within-person (causal) processes in development [
44], compared to conventional cross-lagged path models [
45,
43]. That is, on one hand, genetic moderation may take place on the stable associations of ADHD symptoms with both family and school climate capturing the entire period of adolescence between ages 11 and 16 (i.e., moderation at the between-person level). On the other hand, genetic moderation may take place at the within-person level, where the application of the RI-CLPM allows for determining genetic moderation is present in within causal-person processes of ADHD influencing the family and school climate or vice versa during adolescence. The latter captures the dynamic interplay between genes and environment on developmental change over the life course [
46], which we examined here during adolescence.
In line with most G × E research, we expected that
DRD4 7-repeat carriers and
5-
HTTLPR S-allele homozygotes would be more sensitive to the effects of a more favorable family and school climate as indicated by a reduction of ADHD symptoms. Vice versa, we expected also that adolescents with these genetic variants would have higher ADHD symptoms across adolescence in less favorable family and school climates. However, the previous G × E research has been mainly cross section in nature (e.g., [
33,
35,
37,
39]) and, furthermore, has not focused on within person change dynamics. Using the RI-CLPM model, we expected G × E effects on both the between-person level and the within-person level.
Discussion
The current study examined whether bidirectional associations between ADHD symptoms and the family and school climate were moderated by the plasticity genes DRD4 and 5-HTTLPR across adolescence (mean ages 11, 13.5, and 16 years) in a large pooled population and clinic-referred sample. We did not find genetic moderation by the DRD4 or 5-HTTLPR genotype, neither at the between-person nor the within-person level. Independent from the DRD4 and 5-HTTLPR genotype, we found important trait associations (i.e., between-person level) between ADHD and the family and school climate which indicated that adolescents with higher stable ADHD symptom levels lived in a less favorable family climate, and experienced a less favorable school climate across adolescence. Moreover, our results suggest causal effects between ADHD symptoms and the family climate (i.e., within-person level). That is, ADHD symptoms at age 11 predicted a less favorable family climate at the age of 13.5, while ADHD symptoms at age 13.5 predicted a more favorable family climate at age 16. No evidence was found for family climate altering ADHD symptoms over time, nor for change processes between ADHD and school climate at the within-person level.
Using an advanced methodological approach that separates between-person differences from within-person processes, we found that ADHD symptoms and family climate were predominantly associated at the between-person level (i.e., the stable trait) compared to the within-person level. The link between ADHD symptoms and a less favorable family climate is consistent with previous literature [
11,
12,
63], but does not inform us about the within-person changes that may take place during adolescence. Based on our findings between ADHD symptoms and family climate on the within-person level (i.e., in change over time) we found some evidence on prospective change in the link between ADHD symptoms and the family climate across adolescence. The findings that relate to change yielded two important conclusions about possible causal processes between ADHD symptoms and family climate. First, we found evidence, in line with the results of the between-person level, that ADHD symptoms at age 11 prospectively predicted a lower family climate at age 13.5. On top of the stable characteristics between ADHD symptoms and family climate at the between-person level, high ADHD symptom levels predicted an even worse family climate 2.5 years later. However, the converse held later in adolescence, such that ADHD symptoms at age 13.5 predicted a more favorable family climate at age 16 years. This latter finding may at first glance seem unexpected, given that previous literature showed lower quality of family life among older youth, and high caregiver strain in families with ADHD [
64]. It has to be kept in mind, however, that little is known about within person change processes, and that we also confirm this negative association between ADHD symptoms and family climate as being consistently present. There are two possible explanations for the unexpected finding which may be driven by those with or without ADHD symptoms. One explanation is that this finding might be a result of normative adolescent development, as adolescents spent less time at home [
65] resulting in less parenting strain especially in families with ADHD. A second explanation again related to normative development would be that the positive effect of ADHD on family climate in the later phase of adolescence is in particular driven by the typically developing part of the sample without ADHD symptoms. That is, parents of adolescents without ADHD, at the most intense period of puberty when hormonal changes contribute to greater mood disruptions [
66], may see the family climate as changing for worse. This in contrast with parents of children with ADHD who have been exposed to difficult behavior for a long time may actually during puberty not experience any surplus change for worse. Although our findings clearly need replication, and the explanations offered for our findings are currently speculative, they illustrate that, by distinguishing stable traits (i.e., between-person level) from change processes that occur between adolescents and their families (i.e., within-person level [
43,
44]), more valid estimates of dynamic processes between the individual and his or her environment can be obtained. Future studies, using larger numbers of adolescents with and without ADHD are required to investigate to which extent effects (if replicated) are explained by ADHD or non ADHD individuals.
The second important finding related to processes over time is that we did not find evidence for possible causal effects of family climate on ADHD symptoms. That is, worsening of family climate did not increase ADHD symptoms or, conversely, improvement in family climate did not lead to reductions in ADHD symptoms. This contrasts with the suggestion of Johnston and Mash [
67] that negative family relations might influence the continuation of ADHD symptoms, or, with findings from a meta-analysis of Coates et al. [
68], showing the attenuation of ADHD following parent training intervention. But again, the existing literature has so far documented between person associations without disentangling the stable status quo from the change processes. These findings from the literature may thus be consistent with our stable findings that positive family climate co-occurs with less ADHD symptoms (or negative family environment with more ADHD symptoms). Alternatively, our null-finding may reflect the observational study design with large time lags of 2–3 years between measurements. Positive changes in the family climate may be more likely and, therefore, more easily detected, following treatment interventions A second alternative explanation is that the parenting environment, which is part of the family climate, is more critical in childhood than in adolescence [
69]. It is, therefore, possible that the family climate influences ADHD symptoms especially at younger ages than examined here. Overall, our findings should be replicated.
Our finding of higher stable ADHD symptoms correlated with a less positive school climate across adolescence at the between-person level is in line with previous studies documenting an association between a good school climate and fewer student- and teacher reported internalizing and externalizing problems [
70,
71,
72 in press]. However, there were no directional effects on the within-person level between ADHD symptom levels and the school climate in our study. While this may indicate that the two are not causally linked across adolescence, an alternative explanation for not finding these cross-lagged dynamical effects in the current study may lie in the large time lag, which might not capture reciprocal person- environment change. That is, it is to be expected that, compared to the family environment, there is a multitude of changes during two measurement waves, including changing peers and teachers. In light of these constantly changing circumstances in the adolescent’s life outside the family environment, the absence of effects may indicate that the school climate is too distal and has changed too much to be of influence 2–3 years later. Vice versa, adolescence is a phase of considerable change in ADHD symptoms. The impulsive ADHD symptoms at for example age 11 may have receded at age 13.5 and may play no role in the renewed school environment at age 13.5. We recommend that causal effects of a positive school environment on ADHD symptoms be studied at smaller time intervals.
In contrast to previous studies (e.g., [
33,
34]), adolescents with the
DRD4 7-repeat or being homozygous for the S-allele of the
5-
HTTLPR were not more responsive to the family or school environment in a ‘for better and worse’ manner. Thus, our study found no support for the differential susceptibility hypothesis. Previous studies on differential susceptibility have focused mostly on differences between individuals rather than the processes of change as they take place within the lives of an individual (i.e., within-person level), and have not applied the RI-CLPM model which separates these two levels. Thus, in so far as our data would show support for differential susceptibility, based on the literature we did expect this to become apparent at the between- subject level, while potential effects at the within-subject level would be novel. We had hoped that our developmental perspective would elucidate conflicting results especially about the ‘risk’ variant of the
DRD4 genotype [
37‐
39]. The absence of G × E effects could be due to the lack of power despite a relatively large sample size of almost 2000 participants. It could also be argued that the absence of G × E associations between ADHD symptoms and both family and school climate indicates these associations do not exist. There is a strong publication bias towards positive findings in the G × E literature [
73], which might result in the absence of comparable (i.e., null-finding) published G × E studies.
Strengths and limitations
A strength of this study was the use of a large, longitudinal dataset and the application of an advanced methodological approach that separates between-person (i.e., stable trait levels) and within-person (i.e., causal processes) associations, providing clear evidence for links between ADHD symptoms and both family and school climate independent from the
DRD4 and
5-
HTTLPR genotypes across adolescent development. Some limitations should be taken into account when interpreting the current findings. First, assessment of the family climate as reported by parents does not necessarily inform us how adolescents themselves experienced the family climate. Another disadvantage of relying on parent reports of the family climate is that method variance may in part explain the associations with ADHD symptom levels (as these were also rated by the parents). However, it has been found that parent-reports of the home environment are well in line with child-reports [
74]. Nevertheless, future research could benefit from self-ratings of both the family and school climate and the assessment of ADHD symptoms by at least two independent evaluators in different contexts. Second, the rating of the school climate was a compound measure of items relating to peers and teachers. This may have concealed parts of the effects (peers and teachers may not be equally important to adolescents). We also cannot be certain about the extent in which Positive Illusory Bias may have been involved in our school climate rating, despite our selection of the least subjective items. Third, adolescents are embedded in multiple other contexts than the family and school (e.g., sports team) that might affect ADHD symptoms across adolescence and which need to be included in future research. Fourth, while we controlled for ADHD medication, for a better understanding of causal processes at the within-person level other factors that are subjective to change (e.g., time spent outside home) should be incorporated as covariates in future investigations. Finally, it should be noted that present findings on the full spectrum of ADHD symptoms in adolescents may not generalize to clinical samples selected for being diagnosed with ADHD, or to other age groups.