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The neurobiology of suicide

(2014) LANCET PSYCHIATRY. 1(1). p.63-72
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Abstract
The stress-diathesis model posits that suicide is the result of an interaction between state-dependent (environmental) stressors and a trait-like diathesis or susceptibility to suicidal behaviour, independent of psychiatric disorders. Findings from post-mortem studies of the brain and from genomic and in-vivo neuroimaging studies indicate a biological basis for this diathesis, indicating the importance of neurobiological screening and interventions, in addition to cognitive and mood interventions, in the prevention of suicide. Early-life adversity and epigenetic mechanisms might explain some of the link between suicide risk and brain circuitry and neurochemistry abnormalities. Results from a range of studies using diverse designs and post-mortem and in-vivo techniques show impairments of the serotonin neurotransmitter system and the hypothalamic-pituitary-adrenal axis stress-response system in the diathesis for suicidal behaviour. These impairments manifest as impaired cognitive control of mood, pessimism, reactive aggressive traits, impaired problem solving, over-reactivity to negative social signs, excessive emotional pain, and suicidal ideation, leading to suicidal behaviour. Biomarkers related to the diathesis might help to inform risk-assessment procedures and treatment choice in the prevention of suicide.
Keywords
MAJOR DEPRESSIVE DISORDER, WHITE-MATTER HYPERINTENSITIES, POSITRON-EMISSION-TOMOGRAPHY, TRANSPORTER BINDING-CAPACITY, CORPUS-CALLOSUM AREA, LATE-LIFE DEPRESSION, SEROTONIN TRANSPORTER, MOOD, DISORDERS, ANTIDEPRESSANT TREATMENT, PREFRONTAL CORTEX

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Citation

Please use this url to cite or link to this publication:

Chicago
Van Heeringen, Cornelis, and J John Mann. 2014. “The Neurobiology of Suicide.” Lancet Psychiatry 1 (1): 63–72.
APA
Van Heeringen, C., & Mann, J. J. (2014). The neurobiology of suicide. LANCET PSYCHIATRY, 1(1), 63–72.
Vancouver
1.
Van Heeringen C, Mann JJ. The neurobiology of suicide. LANCET PSYCHIATRY. 2014;1(1):63–72.
MLA
Van Heeringen, Cornelis, and J John Mann. “The Neurobiology of Suicide.” LANCET PSYCHIATRY 1.1 (2014): 63–72. Print.
@article{8573374,
  abstract     = {The stress-diathesis model posits that suicide is the result of an interaction between state-dependent (environmental) stressors and a trait-like diathesis or susceptibility to suicidal behaviour, independent of psychiatric disorders. Findings from post-mortem studies of the brain and from genomic and in-vivo neuroimaging studies indicate a biological basis for this diathesis, indicating the importance of neurobiological screening and interventions, in addition to cognitive and mood interventions, in the prevention of suicide. Early-life adversity and epigenetic mechanisms might explain some of the link between suicide risk and brain circuitry and neurochemistry abnormalities. Results from a range of studies using diverse designs and post-mortem and in-vivo techniques show impairments of the serotonin neurotransmitter system and the hypothalamic-pituitary-adrenal axis stress-response system in the diathesis for suicidal behaviour. These impairments manifest as impaired cognitive control of mood, pessimism, reactive aggressive traits, impaired problem solving, over-reactivity to negative social signs, excessive emotional pain, and suicidal ideation, leading to suicidal behaviour. Biomarkers related to the diathesis might help to inform risk-assessment procedures and treatment choice in the prevention of suicide.},
  author       = {Van Heeringen, Cornelis and Mann, J John},
  issn         = {2215-0374},
  journal      = {LANCET PSYCHIATRY},
  keyword      = {MAJOR DEPRESSIVE DISORDER,WHITE-MATTER HYPERINTENSITIES,POSITRON-EMISSION-TOMOGRAPHY,TRANSPORTER BINDING-CAPACITY,CORPUS-CALLOSUM AREA,LATE-LIFE DEPRESSION,SEROTONIN TRANSPORTER,MOOD,DISORDERS,ANTIDEPRESSANT TREATMENT,PREFRONTAL CORTEX},
  language     = {eng},
  number       = {1},
  pages        = {63--72},
  title        = {The neurobiology of suicide},
  url          = {http://dx.doi.org/10.1016/S2215-0366(14)70220-2},
  volume       = {1},
  year         = {2014},
}

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