The purpose of this study was to investigate individual developmental pathways of repetitive NSSI (repNSSI) from adolescence into young adulthood, and potential adolescent predictors and young adult outcomes of these pathways. First, we considered how common different developmental pathways were, and we also explored if the prevalence rates of different pathways appeared to be influenced by the assumed tendency towards maintenance of repNSSI. Next, we focused on predicting three individual pathways of special relevance to our research questions: cessation before young adulthood vs. prolongation of stable adolescent repNSSI, and late onset of repNSSI in young adulthood. Finally, we explored the psychological adjustment in young adulthood of participants following these three developmental pathways.
Are stable repNSSI pathways more common than expected?
The mechanisms of NSSI maintenance, which were suggested for example in the model by Nock [
9], led us to assume that stable individual pathways would tend to occur
more often than they would without these mechanisms of maintenance. We explored this through analysing the observed frequencies of all conceivable individual developmental pathway of reporting repNSSI or not at three different age levels. We found that the
prolonged stability pathway, followed by the participants who reported stable repNSSI both in adolescence and in adulthood, was observed almost 12 times more often than would be expected by chance from an independence model. This finding gives a strong support for a tendency towards stability in repNSSI, even over the long developmental period when the adolescents become young adults. Importantly, however, the tendency towards stability in repNSSI did not preclude change to occur for most adolescents with stable repNSSI. Despite the strong tendency towards stability in repNSSI, adolescents with stable repNSSI were much more likely to cease their engagement in repNSSI after the adolescent years than to continue into young adulthood (7.2% vs. 4.0% in the longitudinal sample). The developmental pathway of cessation of stable adolescent repNSSI was also more common than expected by chance, although only twice as common.
Still, our data suggested that it was considerably more difficult to stop engaging in repNSSI when it had gained stability in adolescence than when it had not. Of the participants with full longitudinal data in the present study, 53 individuals showed stable repNSSI in adolescence; of these, 19 individuals (i.e., 35.8%) still engaged in repNSSI as young adults, whereas 34 individuals showed a cessation (i.e., 64.2%). When this is compared with the outcome for those participants who showed repNSSI only at one of the measurement points in adolescence the perspective changes. Seventy-two participants showed this kind of non-stable repNSSI in the present study; of these, only six individuals (i.e., 8.3%) still engaged in repNSSI as young adults, whereas 66 had stopped engaging in repNSSI (i.e., 91.7%). In summary, two thirds of the participants with a stable adolescent repNSSI did not continue to harm themselves repeatedly in young adulthood, which means that change was more common than not among these participants. Yet, the one-year stability in adolescence did involve a substantially increased risk of repNSSI in young adulthood as compared to the risk associated with repNSSI without stability in adolescence.
That so many adolescents with stable repNSSI had ceased their engagement in repNSSI may suggest some kind of spontaneous process. General developmental processes during adolescence and young adulthood may promote changes even in established problematic behaviours. One such process is the maturation of the brain. During adolescence, there are large structural and functional changes to brain regions implicated in the generation of emotions and in the regulation of emotions [
67]. Several researchers have argued that emotional control mechanisms are underdeveloped relative to their emotion generating counterpart in adolescence. This would to some extent account for the observed deficiencies in emotion regulation during adolescence and the adolescent affective and behavioural problems that may follow from these [
67].
Most individuals with stable adolescent repNSSI, who had stopped their repNSSI in young adulthood, identified themselves as women. Even prolonged stability in repNSSI was more common among women, but not significantly so. Previous prospective studies in the present project have suggested that, for girls, repNSSI and depressive symptoms may be involved in a “vicious cycle” that might contribute to the stabilization of existing problems. For example, Lundh et al. [
30] found not only that depressive symptoms at T1 were a risk factor for the development of repNSSI among girls one year later, but also that girls’ engagement in NSSI at T1 was a risk factor for increased depressive symptoms at T2. This bidirectional relationship was not found for boys. This type of mechanisms may have contributed to divergent developments of repNSSI between genders, at least in adolescence. To the extent that such bidirectional effects are at work, it is possible that they may contribute to what have been referred to in the literature as “chain reactions”, “snowball effects”, or “developmental cascades” (e.g., [
68]).
A
late onset of repNSSI among young adults who had not reported any repNSSI in adolescence was not a very common phenomenon (4.6%). Still our findings suggest that it was a real phenomenon, as it was identified in prospective data and at least not the result of a recall bias (as suggested by Gandhi et al. [
7]). The pattern was neither more nor less common than expected by chance. Nor was there a gender difference in late onset, which is at odds with the findings of Gandhi et al. [
7], who reported that the late onset peak was much sharper for women than for men. It should be noted, though, that our study focused on the onset of repetitive NSSI, and that some participants in our late-onset group had tested self-injurious behaviour sporadically already in adolescence.
The present study of individual developmental pathways of repNSSI also gave rise to another finding: 69.1% of the young persons in our study never reported repNSSI at any of the three time points, which means that as many as 30.9% of them
did. This would set a quite high lower boundary for the life-time prevalence of repNSSI among the young adults in our sample that is very concerning. This should not be interpreted in terms of a life-time prevalence of clinically significant non-suicidal self-injury, however. RepNSSI was operationalized in a way that partly resembles the suggested diagnosis of NSSI disorder in DSM-5 [
46], but there are crucial differences. Whereas repNSSI in the present study was defined in terms of the affirmation of at least five
instances of NSSI during the past 6 or 12 months, the corresponding DSM-5 criterion speaks of engagement in NSSI on 5 or more
days in the past year. For example, nothing precludes that participants in the present study who affirmed the presence of five instances of NSSI had engaged in all these NSSI behaviours on one and the same day. Furthermore, the DSM diagnosis also includes other criteria which refer to functional, motivational, and emotional aspects of NSSI. These aspects were not included in our operationalization of repNSSI. Therefore, the high lifetime prevalence of self-reported repNSSI in this study should not lead to any conclusions about the lifetime prevalence of clinically significant NSSI among young adults in the general population in Sweden. Still, the present operationalization of repNSSI may be valuable if it can contribute to new knowledge about the vicissitudes of NSSI during adolescence and onwards.
Can different developmental repNSSI pathways be predicted?
Previous research [
5,
26] has found that depression can predict onset of NSSI over shorter time periods. In a previous study of the present cohort [
30] we similarly found that depressive symptoms could predict onset of adolescent repNSSI over a 1-year interval. In the present study we wanted to see if adolescent depressive symptoms could also predict late onset of repNSSI over a 10-year interval. Although the effects were of medium size at both time points (
ORs 3.03 and 2.69, respectively), they were only nearly significant when adolescent sporadic NSSI was controlled for (T1:
p = .062; T2:
p = .069). Sporadic NSSI at T1 but not at T2 was a significant predictor. Based on these findings we would still suggest a continued consideration of adolescent depressive symptoms as potential risk factors of NSSI, not only in the short run but also over longer age periods. This is also consistent with the suggestion [
7] that late-onset of NSSI may be a delayed manifestation of untreated adolescent psychopathology.
Moreover, poor sleep – one of the symptoms included in the depression index we used – independently predicted late onset of repNSSI even when controlling for sporadic NSSI in adolescence, although only from T2 and with a low effect size (
OR 1.90). This finding to some extent resembles an earlier finding [
31] in our research project that poor sleep among the girls was a one year-predictor of onset (new cases of repNSSI) in adolescence. This means that the finding of poor sleep as a predictor of repNSSI was made for two non-overlapping groups in our project – girls with an onset of repNSSI in adolescence and participants with a late onset of repNSSI as reported in young adulthood. The number of participants with an onset of repNSSI in young adulthood was too low, however, for replicating the regression analyses separately for each gender. Still, these findings might be reason enough to suggest that poor sleep is a marker for problematic psychological health that does not necessarily show up in the self-assessment of depressive symptoms or of other psychological difficulties. In summary, this means that the findings concerning the prediction of new cases from our one-year follow-up of the cohort in adolescence were partly replicated in the 10-year follow-up in young adulthood.
On the other hand, we could not predict the prolongation of stable adolescent repNSSI into young adulthood. Why, then, were we not able to find any predictor of the prolongation? One possible explanation is that we did not include the relevant predictors. We chose to focus on the same risk factors that had proved successful in predicting new cases of repNSSI over one year in adolescence (i.e., general psychological difficulties, depressive symptoms, and poor sleep), but it has been argued that the risk factors for maintenance are different from those for onset [
8,
10]. Maybe the prolongation
versus cessation of NSSI is to be understood primarily in terms of the
functions of NSSI more than in terms of distal risk factors. Although the previous studies made in this area are mainly retrospective and suffer from contradictory findings, there is some evidence that intrapersonal functions of NSSI are associated with difficulties to stop engaging in NSSI [e.g.,
69,
70]. To achieve more clarity in this area there is a need for more prospective studies that investigate motives for cessation that young people think about and consider before actual cessation.
Our limited success in predicting developmental patterns regarding repNSSI should also be seen in the context of the rather weak findings from other research in this area. The authors of a meta-analysis of risk factors for NSSI [
8] concluded that few strong NSSI risk factors have been identified; this was so although most of the studies reviewed had considerably shorter follow-up lengths than our study. The difficulties of finding strong predictors of developmental patterns of repNSSI over a 10-year period might also be related to the period from adolescence to young adulthood being a period of much change in many areas in life simultaneously (leaving school, starting one’s work life or higher education, leaving home, finding a partner etc.). This might make it difficult to find single variables that can serve as predictors at the group level over such an extended period.
The difficulties we had to find predictors that differentiate between the two pathways with stable adolescent repNSSI but contrasting developments of repNSSI into young adulthood have parallels in previous pathway studies [
20‐
22]. Most risk factors identified in those studies differentiated between the low NSSI trajectory class, on the one hand, and the higher NSSI trajectory classes on the other. There were some exceptions, however, of risk factors that did differentiate between different pathways involving NSSI: negative attributional style [
20], family-related stress, peer victimization, and symptoms of depression and anxiety [
22]. Still, the predictions in those studies cover much shorter time periods.
What are the young adult outcomes of different repNSSI pathways?
Among the three pathway groups we chose to focus on in this study, the group with an onset of repNSSI in young adulthood appeared to fare the worst in young adulthood. This was evident both from their mean values in different psychological adjustment outcomes, and from the significant differences with the comparison group not reporting repNSSI during the 10-year period. The participants with a late repNSSI onset differed significantly from the No repNSSI pathway group in all positive and negative adjustment aspects considered, and the effect sizes were large. The Late-Onset group reported repNSSI behaviour for the first time at an age when most individuals with a stable adolescent repNSSI behaviour did not report this behaviour anymore. The social pressure against self-injurious behaviour probably is much increased in young adulthood and the threshold of an onset of this behaviour is probably much higher. In this perspective, it might be expected that it should take a more painful psychological situation for an individual to pass this threshold at that age. The repNSSI development of this group was partly predictable from symptom measures in adolescence (including sporadic NSSI at T1), however, which suggests that their poor psychological situation in young adulthood might have earlier roots.
The participants who had reported stable repNSSI only in adolescence, and had stopped their repNSSI in young adulthood, still reported significantly worse levels of stress symptoms, anxiety, and emotional dysregulation in young adulthood as compared to participants without repNSSI during the whole age period in question. These differences were large. This suggests that their overcoming the repNSSI behaviour represented a limited change in their symptom picture, leaving other impairments in their psychological adjustment. As concerns the group of participants whose repNSSI was prolonged into young adulthood, the disadvantages in comparison to the No RepNSSI group were large for most adjustment measures, but only the large difference in emotion dysregulation was significant. The low power in these comparisons constitutes a problem when it comes to evaluating the outcome in young adulthood of the prolonged repNSSI group. One possible explanation why the late onset group appeared to fare worse than this group is that the prolonged repNSSI group to some extent might have integrated the NSSI behavior into their coping strategies and/or identities in a way that the late onset group had not yet been able to do.
There were no significant differences between the three groups with different repNSSI pathways, which means that the conclusion that those with a late onset appeared to fare the worst is arguable. At the same time, the absence of significant differences cannot be interpreted as an absence of differences. The three groups were small, and the adjustment variation within the groups was rather large. Non-significant differences of medium effect sizes in the measures of positive adjustment as well as depression were found between the group with a late onset and the group with adolescence-limited stable repNSSI, which had the more positive outcome. As concerns the comparison between the adolescence-limited group and the prolongation group, however, most differences in negative adjustment were small: the participants in the adolescence-limited group did not differ much from the prolongation group in young adult symptoms of stress, anxiety, and depression.
Strengths and limitations
Two substantial strengths of the present study were the high response rate during adolescence, and the availability of ten-year follow up data in young adulthood. At the same time, the reduced response rate at the ten-year follow up represents an important limitation. This response rate, however, is comparable to the response rate in other similar studies (e.g., [
71,
72]).
Another limitation is that we only have three points of measurement, and that there is a 9-year time gap in our longitudinal sequence of data collections (that is, between T2 and T3), unfortunately during an important transition period in the lives of the participants. Additionally, the DSHI-9r asks about the presence of NSSI only during the past 6 months (at T1 and T2) or 12 months (at T3), whereas the time intervals between T1 and T2, and between T2 and T3, were longer than these periods of report; this means that we do not have any data on NSSI during 6 months after T1, and during an 8-year period after T2. It also means that the repNSSI assessments are not exactly comparable.
We merely used self-report measures of psychological difficulties in adolescence and young adulthood. Reports from parents, teachers, friends, and partners might have contributed with other perspectives on psychological difficulties among the participants. Further, the Strengths and Difficulties Questionnaire we used in the adolescent data collections may be questioned as to its ability to capture severe emotional and interpersonal problems in adolescence, because it does not include any questions about depression, shame, or self-hatred. And although the specially constructed Depression Index covered most of the criteria of major depression, as defined by the DSM-IV [
53], it did not cover the criteria of weight loss or weight gain, nor recurrent thoughts of death and suicide. This means that the depression index used in the present study does not do full justice to the psychiatric notion of major depression.
Finally, it should be noted that gender findings are limited by the use of only a binary conceptualization of gender. At T3 we did include the option to respond other than man or woman, but no one in the present longitudinal sample chose that alternative. It also remains to be seen to which extent the present findings are generalizable to other communities and cultures.