The main finding of this study was that the SOC scale appears to be an inverse measure of persistent and generalized symptoms of anxiety and depression. The SOC scale and self-assessed symptoms of anxiety and depression showed high correlations and multiple regression models showed that symptoms of anxiety and depression explained a major part of the SOC variance in both the non-clinical and clinical samples. The SOC scale and measures of anxiety and depression showed similar patterns of correlations to health-related parameters in both non-clinical and clinical samples of adolescent girls, similar to what has been shown in adults . Multivariate analyses failed to isolate SOC as a separate construct distinct from measures of anxiety and depression. As the SOC items pertaining to the putative categories of meaningfulness, manageability and comprehensibility showed high covariance, the multivariate analyses failed to identify these as separate clusters. Previous factor analyses of SOC items in samples of Swedish students show similar results .
Regarding temporal stability, the highest correlations between the first and the repeated measurements six months later, were found for SOC followed by BDI, BAI, SDQ-em. This may be explained by the fact that the BDI and BAI ask about symptoms during the last two weeks. BDI and BAI may thus capture mood swings and shorter episodes of major depressive disorder and situational anxiety on top of more persistent depressive symptoms and generalized anxiety. Contradictory to the salutogenic theory  the low quartile of the SOC score in the non-clinical sample showed higher temporal stability than the high quartile (data not shown). The data failed to support that the SOC-scale is more stable at the high end of the continuum. A limitation of this investigation was the lack of repeated measures of the clinical sample, which would have given information of temporal stability in the very low end of the SOC continuum.
The extended hierarchical cluster analyses, that included all the items of SOC, BDI, BAI, SDQ-em, revealed that BAI and SDQ-em items that assessed symptoms of severe anxiety and physiological reactions of fear clearly separated themselves from the BDI and SOC items. It thus appeared as if BAI did not capture the type of anxiety typical for GAD or generalized SAD. The generalized type of anxiety was better identified by the SOC-scale. The results of the hierarchical cluster analyses cannot be regarded as evidence, but aid an alternative interpretation of SOC. The superior sensitivity of the SOC scale for caseness of emotional disorders in adolescent females described in our previous work  may be explained by the fact that the SOC scale covers symptoms congruent with the DSM-IV criteria for MDD, dysthymic disorder, GAD and generalized SAD.
The question of item-overlap between SOC and measures of anxiety and depression has previously been suggested  since meaninglessness/hopelessness is one of the cardinal symptoms of major depressive disorder. Furthermore, when suffering from MDD or generalized anxiety the cognitive function and social drive decrease leading to a diminished comprehensibility and manageability. In other psychiatric disorders such as ADHD, conduct disorder or situational anxiety this is not necessarily the case. However, comorbidity is common in this age group and depressive and anxious problems in combination with ADHD, conduct disorder or situational anxiety may explain a possible decrease of SOC and also the poorer outcome related to low SOC reported for ADHD .
In adolescence, a decline in social engagement can be the result of different trajectories. For example, depressive and anxious symptoms may co-exist and develop simultaneously to disorders of depression and anxiety. Alternatively, a primary diagnosis of SAD or GAD may lead to secondary depressive symptom. Finally, as often the case, primary MDD or dysthymic disorder generate secondary social problems. The differential diagnosing of MDD, GAD and SAD is specifically difficult in adolescence, since the diagnoses are highly co-morbid . Genetic studies even indicate that depression and anxiety disorders may share a genetically determined neurobiological component [48, 49]. Comorbidity tends to generate higher severity scores in adolescent girls  and comorbidity of GAD and MDD, is related to an increase of overall mortality in adults . Adolescents with comorbidity of generalized anxiety and depression thus need to be identified and prioritized for treatment and deserve also more attention in future research.
The SOC-scores showed higher correlations to the awakening response of saliva cortisol compared to the psychiatric self-assessment scales in both samples. Due to the great loss of cortisol samples especially in the clinical sample this data is unsecure, nevertheless the finding is in line with our hypothesis that SOC but not BDI and BAI measures generalized anxiety, since in adolescents, persistent anxiety, but not current or situational anxiety, is associated with increase of the awakening response of saliva cortisol .
Earlier population-based and clinical studies have shown that a decrease of HRV is present both in anxiety and depression [52–54], although the correlation of HRV and SOC-score is not previously shown. In line with previous discussion the correlation between HRV and SOC support that autonomous regulation is impaired in adolescent girls with MDD, dysthymic disorder, GAD or generalized SAD.
The loss of SOC data (11 cases in the non-clinical sample) was due to incomplete forms from one of the schools at the first measurement and can be considered a random error. When omitting the subjects with incomplete forms the rest of the sample showed a strong correlation to the measures of anxiety and depression. The correlation was similar in repeated measures six months later when the full sample was included. The mean SOC score from the subjects from measurement 1 (mean 137.1 SD 26.9) and from the measurement 2 (mean 138.1 SD 27.5) were similar. Hence, the impact of this data loss did not seem to affect the conclusion. The loss of HRV data was due to registration artifacts caused by body movements was also random and should not have affected the conclusions.
The loss of salivary cortisol on the contrary must be regarded as a non-random error since it was more frequent in the clinical sample (non clinical 20/66 and in the clinical 38/73) creating an asymmetric loss in the samples. The loss of cortisol data may be linked to the depressed mood of the patients. However, the primary aim of including the salivary cortisol in table 1 was to compare the correlation between AUC-b cortisol and SOC, BDI, BAI and SDQ-em respectively.