It is increasingly apparent that depressive disorders in children and adolescents are aetiologically as well as phenotypically heterogeneous. Behavioural genetic studies of twins have noted significant heritability rates of depressive symptoms; however, in some studies the common environment has around the same magnitude effect.(5,5 59 and 69 This lack of agreement between studies to date means that further studies, using larger sample sizes and including direct measurement of the shared and non-shared environments, are required.
A number of family studies have noted a significant increase in familial density of lifetime episodes of major affective disorder in first-degree relatives of child and adolescent probands with major depression compared with controls. (61) Family studies to date have been limited by sample size and ascertainment bias, being almost entirely confined to clinically referred populations.
One community-based study suggests that families with a high lifetime familial density of affective disorder increases the risk for recent undesirable life events in their offspring/62 This life-event prone mechanism may be one psychosocial consequence of an adverse familial environment, perhaps via impairments in parental care.
There is reasonably consistent evidence from clinical and community-based case-control studies that, as with adult depression, recent undesirable life events focused on the child and carrying a significant degree of negative impact are associated with the onset of an episode in children and adolescents. (6 6 65 and 66 Recent events occur, in the main, against a background of other more chronic or long-term family and peer group difficulties, which appear additive in their risk effects for onsets/666. and 68) The exact nature of the psychosocial mechanisms that result in onsets of first-episode depressions in young people remains unclear, but adverse social environments are known to lower self-esteem and increase the levels of depressive symptoms in adolescents. (69,Z9 However, negative cognitions in young children are not permanent internal constructs resistant to change, rather there is an active mutually interdependent system throughout the developing years between differing types of social experience, self-evaluation, and personal and social competency. (I1 Positive experiences may ameliorate previous adversities, and, equally, current undesirable experiences can increase the risk for depression in the absence of chronic difficulties. Further longitudinal research is required to determine if restitutions of self-percept (i.e. a return to a more positive sense of self) may be an important index of time it takes to recovery.
As well as negative cognitions, temperamental factors and, in particular, high stable levels of negative emotionality (defined as individuals who react intensely to environmental stimuli with irritability, tearfulness, mood change, but who also settle rapidly following a stimulus response) is a risk factor for major depression in adolescents/72 Higher emotionality levels may also be associated with the presence of latent negative cognitive schemas, (73) implying a link between two different types of affective-cognitive processes associated with depression in this age group.
Children with a high familial loading for major depression showed profiles of lower cortisol and higher prolactin levels following 5-hydroxy-L-tryptophan infusion similar to those of currently depressed children, both of which are significantly different from controls. (75> These early findings suggest that altered serotonergic regulation may precede first-episode early-onset depression in some cases. A loss of diurnal rhythm in selected adrenal steroids has also been noted in subjects at high risk for depression/51.) Both cortisol and dehydroepiandrosterone hypersecretion precede and predict the subsequent onset of major depression in high-risk subjects. (79 These abnormal steroid profiles are not a consequence of either current social adversities or negative cognitions or high emotionality. The associations between the genetic, social cognitive, and neurobiological factors prior to onset, during an episode, or following recovery are unknown.
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