Risk Factors For Depression in Children, Onset and Recurrence

Risk Factors For Depression in Children, Onset and Recurrence. There are several suspected risk factors can trigger the development of depressive disorders. These risk factors may explain the onset and recurrence of depressive disorders in children.

Genetic
Twin studies demonstrate that depressive disorders symptoms have a greater concordance among monozygotic than among dizygotic twins, and a heritability of around 40-65%, with higher estimates of heritability in adolescent vs. prepubertal children. Both bottom-up and top-down family studies have shown a 2-4 fold increased risk of depressive disorders in first-degree relatives. Twin studies suggest a greater genetic component in adolescent vs. pre-pubertal onset depressive disorders, supportive of the view that very early onset depressive disorders may often be a response to a chaotic environment.

There is evidence that liability to depressive disorders is co transmitted along with anxiety symptoms, with a heritability of 61-65%. Genes that influence the risk of anxiety may in turn lead to a higher rate of post pubertal depressive disorders by increasing sensitivity to life events, and also by increasing the likelihood of exposure to depressogenic life events. This formulation is consistent with the results of longitudinal studies, as well as with evidence that stressful life events and genetic diatheses (e.g., shorter allelic form of the serotonin transporter) interact to result in early-onset depressive disorders.

Cognitive Factors
Individuals with depressive disorders have been shown to have a negative view of self, future, and the world. No depressed individuals with these biases are more likely than those without these biases to develop depressive disorders symptomatology when confronted with stressful life events. Cognitive distortions are associated with depressive disorders in both prepubertal children and adolescents, but only in adolescents is there some evidence that the distortions persist after the episode resolves. Depressed youth also exhibit performance-based disruptions in cognitive processes, such as greater difficulty than controls in remembering fearful faces, difficulty in inhibiting negative affect in response to distressing stimuli, and more global and less specific recall in tests of categorical autobiographical memory.

Familial/Environmental Risk Factors
Twin studies show that the effect of shared environment is at least as potent as are heritable factors. Parental depressive disorders may exert its deleterious effect on child mood disorder not only through genetic mechanisms, but also via modeling of cognitive distortions, and through either passive and withdrawn or hostile interactions. Family environmental risk factors for child depressive disorders, such as parental criminality, parental substance abuse, lack of family cohesion, and parent-child discord, may be most relevant in the absence of a family history of depressive disorders. However, in some studies, family discord and expressed emotion interact with a depressive disorders diathesis to predict onset and recurrencese. Greater chronicity and severity of maternal depressive disorders has been related to greater liability for child cognitive distortions and parent child conflict, both of which increase liability and persistence for child depressive disorders symptoms. Longitudinal studies show reciprocal interrelationships between maternal and child interpersonal difficulties, child behavior symptoms, cognitive distortions, and depressive disorders outcome.

Neglect and child maltreatment increases the risk not only for depressive disorders, but also for substance abuse, disruptive disorder, posttraumatic stress disorder, and suicide attempt. The deleterious effects are strongest for more severe and chronic abuse, such as sexual abuse resulting in intercourse. Abuse may be associated with an earlier age of onset of depressive disorders. The effects of abuse may be long lasting, resulting in a lower rate of response to treatment and a higher risk for recurrent depressive disorders. However, it is difficult to isolate the effects of abuse from the other interrelated adverse aspects of parental functioning and home environment such as parental mood disorder, substance abuse, and criminality; lower education and income; marital discord; and association with deviant peers. The relationship between depressive disorders and abuse is much stronger in the presence of other family-genetic risk factors such as a family history of depressive disorders or the short form of the serotonin transporter gene.

Bereavement due to the loss of a sibling, parent, or close friend is associated with an increased risk for depressive disorders, especially if there is a positive family history for mood disorder.
Connection to family and to school, parental behavioral and academic expectations, and nondeviant peer group are all protective against several key health risk behaviors, including depressive disorders and suicidality.

Neuroendocrine
Provocative challenges that are putative measures of noradrenergic and serotonergic neurotransmission find differences in depressed children, both during episode and recovery, and in nondepressed children at high risk for depressive disorders. This pattern of finding suggests that these changes may be trait markers for early-onset depressive disorders. However, similar neuroendocrine responses to provocative serotonergic challenge may be found in those with adverse or abusive home environments, and with high levels of aggression.

Sleep
Subjective sleep complaints are a very prominent component of early-onset depressive disorders, although subjective complaints and objective observations of sleep in a sleep laboratory are not closely correlated. Increased cortisol secretion at the time of sleep onset may be related to adolescent depressive disorders. Decreased REM latency and increased latency of sleep onset were found more often in adolescents compared to prepubertal depressed children, and may be associated with greater severity, onset, and recurrence, although these findings may emerge only after a strict sleep/wake schedule has been imposed. Decreased sleep efficiency and delayed sleep onset have been reported to be associated with depressive episode persistence and recurrence.

Neuroimaging Studies
Structural imaging studies of adult subjects with early-onset, familial depressive disorders as well as in adolescents with depressive disorders have found reduced volume of the left subgenual prefrontal cortex. Preliminary studies of female adolescent depressed twins suggest that this structural difference is genetically transmitted and may partially mediate the heritability of depressive disorders. Steingard et al. reported decreased prefrontal cortex and increased third and fourth ventricular volume in depressed adolescents, although these findings may be a marker for the effects of chronicity. MacMillan reported an increased pituitary and amygdala: hippocampal ratio size in depressed subjects compared to nondepressed controls, with amygdala: hippocampal ratio size correlated with the severity of anxiety symptoms. In line with these findings, Thomas and colleagues found, in response to fearful faces, increased amygdala activation in anxious children, and decreased amygdala activation in depressive disorders in children.