ENDOCRINE BIOMARKERS OF SUICIDE RISK IN SCHIZOPHRENIA
Background
Suicide is one of the major causes of death in individuals with schizophrenia. Recent research has begun to explore biological biomarkers that may potentially determine which patients with schizophrenia have an increased risk of suicide. This could potentially offer clinical benefit through better risk assessment and, subsequently, tailored treatment options that can reduce mortality. There is substantial evidence that has investigated the association between inflammatory biomarkers and mechanisms involved with suicide in schizophrenia. However, there remains a lack of research investigating endocrine and metabolic biomarkers. Therefore, investigating the endocrine system for this purpose may shed light on both the pathophysiology of schizophrenia and the biological mechanisms that contribute to suicide risk among this population.
Methods
A PubMed search was conducted to find studies assessing endocrine or metabolic biomarkers related to suicidal ideation, suicide attempts, or suicide deaths in people with schizophrenia. From this search, 226 studies were found. The screening of titles yielded 31 studies, and after reviewing the abstracts of these 31 studies, 14 studies were found that were directly relevant to the chosen topic.
Results
The results showed that multiple endocrine systems appear to be dysfunctional in individuals with schizophrenia who exhibit suicidal behaviors. Endocrine Biomarkers included 1) alterations in hypothalamic-pituitary-adrenal (HPA) axis function were detected, with several studies demonstrating elevated baseline and post-dexamethasone cortisol levels in patients with prior or future suicide attempts, although findings regarding dexamethasone non-suppression were mixed, 2) thyroid axis hormone level abnormalities were also observed: suicidal ideation was associated with elevated free thyroxine levels, 3) gonadal axis abnormalities included lower testosterone levels in subgroups who died by violent suicide attempts, 4) reduced parietal cortical pregnenolone levels were reported post-mortem in patients with schizophrenia who had died by suicide. Of note, prolactin and BDNF levels were not associated with suicidality.
Discussion
These findings demonstrate that suicide in schizophrenia appears to be associated with dysfunction of multiple endocrine pathways. While the current research does not establish causality, the findings indicate biologically plausible pathways that require additional investigation and may lead to a re-evaluation of the relationships between endocrine function, psychosis pathophysiology, and suicide risk. Thus, endocrine markers may facilitate the early identification of high risk of suicide in patients with schizophrenia.