Cortisol rise in adolescence with psychosis
July 17, 2005
Below are some brief excerpts taken from my book-in-progress-cortisol levels rise during adolescence-concomitant with the onset of the psychoses-I think separation is a significant issue (invulnerabilitycloaking vulnerability, etc.).
Walker and Diforio (1997), after a review and meta-analysis of the research, concluded that schizophrenic patients evidence elevated cortisol at baseline. In addition symptom severity was correlated with plasma and saliva cortisol levels, and antipsychotic medications led to reductions in cortisol secretion. Several studies demonstrated that symptom exacerbations were preceded by increased cortisol levels. The latter suggests that the increase in anxiety results in, as opposed to being an effect of, psychotic symptom exacerbation. It is important to be aware that cortisol partially worsens symptomatology through its augmentation of dopamine. Both human and animal research studies have amply demonstrated that glucocorticoid administration increases dopamine activity. Another significant piece of this model is that there is a gradual rise in levels of saliva cortisol through childhood, with a prominent escalation in adolescence that correlates with pubertal maturation. Therefore there is an important relationship between the period when typical prodromal symptoms of schizophrenia emerge and the psychobiological increase in HPA activity Thus, the LHPA axis may play a crucial role in mediating the expression of the prodromal signs of schizophrenia.
Why Adolescence?
It is often during adolescence that prodromal symptoms and schizophrenic episodes are emergent.During this period there is a greater degree of cortical organization and functional efficiency, as well as increased activation of the LHPA (limbic-hypothalamic-pituitary-adrenal) axes. Myelination could result in increased excitatory glutamatergic inputs that are not disinhibited by GABAergic functioning due to dysfunction in the latter system (Benes 2000). Corcoran and colleagues (2003) suggested that cortisol may be neurotoxic to inhibitory GABAergic cells in the hippocampal formation.
For a psychological-developmental portrayal of the vulnerabilities initiating or exacerbating psychosis and schizophrenia during adolescence, especially the role of self and identity formation, see Chris Harrop and Peter Trower (2003)"Why does Schizophrenia Develop at Late Adolescence? A Cognitive-Developmental Approach to Psychosis," published by Wiley.
