Professor Zoltan Sarnyai said it was the first meta-analysis study to compare the level of cortisol in a waking patient’s body with the stage of schizophrenia they are suffering.
Dr Sarnyai said it means doctors may be able to eventually identify those who will develop full-blown psychosis from amongst those who present with early stages of the disease.
"Only some 20 to 30 per cent of individuals who are at high-risk of developing psychosis due to their clinical presentation or family history actually do so. Identifying those people early is where the cortisol measurement comes in.
“Biomarkers are very few and far between in psychiatry, so even though a huge amount of work is still needed, this could become a valuable technique,” said Dr Sarnyai.
Full Research Paper available for download here:
http://linkinghub.elsevier.com.sci-hub.cc/retrieve/pii/S0149-7634(16)30054-9
Full story here:
Pubmed Summary:
Introduction to Paper:
Neuroendocrine abnormalities are a commonly observed feature in patients with schizophrenia
and are thought to interact with the multifactorial etiology of the disorder. One of the most
consistently reported neuroendocrine findings in schizophrenia is elevation of plasma and saliva
cortisol levels (Girshkin et al., 2014; Ryan et al., 2004), an important observation as cortisol is both a
marker and mediator of the body’s multisystem response to stress (McEwen and Stellar, 1993).
Cortisol is the hormonal endpoint of the hypothalamic-pituitary-adrenal (HPA) axis and a powerful
glucocorticoid with multiple effects on brain and body. As such, cortisol interacts with multiple target
tissues including immune cells, metabolic organs and brain areas with high density of glucocorticoid
receptors (GR) including the prefrontal cortex and limbic circuitry (Arnsten, 2009; Lupien et al.,
2009).
Consequently, exposure to excessive cortisol can contribute to neurodevelopmental insults and
in the context of contemporary frameworks of psychosis onset it is thought to be relevant for onset
and progression of psychosis (Walker and Diforio, 1997). However, the role of cortisol in
schizophrenia pathophysiology from early risk states to chronic schizophrenia remains mostly
unclear.
Aberrations in stress processing in patients with schizophrenia that potentially lead to increased
cortisol release and over time to dysregulations of the HPA axis are thought to explain the
hypercortisolemia found in cross-sectional studies (McEwen, 1998). Lower stress threshold in
response to a stressful stimulus and prolonged activation of the limbic system have been observed in
patients (Castro et al., 2015).
The neuroendocrine response to laboratory stress on the other hand is
blunted in patients with schizophrenia (Ciufolini et al., 2014) and dexamethasone suppression is
reduced, indicating impaired negative feedback mechanisms (Thompson et al., 2007). Moreover,
brain areas with inhibitory function on the HPA-axis such as the hippocampus are commonly found to
be reduced in volume. Furthermore, increased volume of the pituitary gland has been observed in
patients with schizophrenia (Aiello et al., 2012; Garner et al., 2005; Witthaus et al., 2009).