Diurnal Rhythms of Plasma Cortisol, Beta-Endorphin and Prolactin, and Cerebrospinal Fluid Amine Metabolite Levels before Suicide

Dent, Robert; Ghadirian, Missagh; Kusalic, Maria; Young, Simon N.

doi:10.1159/000118299

Cited by 9 publications

(2 citation statements)

References 10 publications

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“…In other words, the hypothalamic–pituitary–adrenal (HPA) stress system (CRH, ACTH) and opioid systems (beta-endorphins) are closely related ( 41 ). This is not surprising, given that ACTH and β-endorphins are derived from the same precursor, pro-opiomelanocortin (POMC) ( 42 , 43 ). In sum, opioid and dopaminergic systems, and HPA axis, which interact in the forebrain ( 31 , 32 ) and can be activated either by psychoactive drugs or by behaviors ( 44 ), are probably involved in the development of an addiction to self-harming behaviors (Figure 2 ).…”

Section: Resultsmentioning

confidence: 99%

The Addictive Model of Self-Harming (Non-suicidal and Suicidal) Behavior

et al. 2016

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IntroductionBehavioral addictions such as gambling, sun-tanning, shopping, Internet use, work, exercise, or even love and sex are frequent, and share many characteristics and common neurobiological and genetic underpinnings with substance addictions (i.e., tolerance, withdrawal, and relapse). Recent literature suggests that both non-suicidal self-injury (NSSI) and suicidal behavior (SB) can also be conceptualized as addictions. The major aim of this mini review is to review the literature and explore the neurobiological and psychological mechanisms underlying the addiction to self-harming behaviors.MethodThis is a narrative review. The authors performed literature searches in PubMed and Google for suicidal behavior, self-harming, addiction, and “major repeaters.” Given the scarce literature on the topic, a subset of the most closely related studies was selected. The authors also focused on three empirical studies testing the hypothesis that major repeaters (individuals with ≥5 lifetime suicide attempts) represent a distinctive suicidal phenotype and are the individuals at risk of developing an addiction to SB.ResultsThe authors reviewed the concept of behavioral addictions and major repeaters, current empirical evidence testing concerning whether or not NSSI and SB can be understood as “addictions,” and the putative mechanisms underlying them.ConclusionOur review suggests that both NSSI and SB can be conceptualized as addictions. This is relevant because if some individual’s self-harming behaviors are better conceptualized as an addiction, treatment approaches could be tailored to this addiction.

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Section: Resultsmentioning

confidence: 99%

The Addictive Model of Self-Harming (Non-suicidal and Suicidal) Behavior

et al. 2016

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“…Mancini und Brown [113] fanden keine Unterschiede hinsichtlich Urin-und Serum-Werten bei suizidalen Patienten. In einem Fallbericht beschrieben Dent et al [114] einem Suizidversuch vorausgehende niedrige Kortisol-Spiegel im Plasma.…”

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Neurobiologische Korrelate suizidalen Verhaltens

Brunner

Bronisch

1999

Fortschr Neurol Psychiatr

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Studies in postmortem brain tissue from suicide victims show a presynaptic serotonergic deficit resulting in compensatory upregulation of postsynaptic 5-HT2 receptors in the prefrontal cortex. Reduced levels of cerebrospinal fluid (CSF) 5-hydroxyindoleacetic acid, the major serotonin metabolite, are associated with violent suicide attempts independent of psychiatric diagnosis and predict future suicide attempts and suicide completion, consistent with the notion of a biochemical trait. Neuroendocrine challenge tests, platelet studies and a polymorphism in the gene for tryptophan hydroxylase, the rate-limiting enzyme in the biosynthesis of serotonin, suggest that serotonergic activity may be reduced. This serotonergic abnormality might be related to the vulnerability or diathesis for suicidal behaviour by predisposing individuals to impulsive and autoaggressive behaviour. The hypothesis of hyperactivity of the hypothalamic pituitary adrenal axis (HPA) is supported by the postmortem findings of increased CSF corticotropin releasing hormone (CRH) concentrations and reduced CRH receptor binding sites in the frontal cortex of suicide victims (interpreted as downregulation following CRH hypersecretion) and dexamethasone nonsuppression in suicide attempters. Animal studies and in vitro experiments indicate that the HPA system modulates serotonergic activity. It is hypothesized that the serotonergic alterations potentially result from dysregulation of the HPA system. Data from epidemiological and clinical studies demonstrate that low levels of cholesterol are associated with increased suicide risk. In neuronal membranes cholesterol modulates presynaptic and postsynaptic serotonergic neurotransmission. In monkeys dietary cholesterol lowering inhibits central serotonergic activity and predisposes the animals to impulsive and aggressive behaviour. It is speculated that dysregulation of the HPA system and disordered cholesterol metabolism could enhance the serotonergic deficit, thus contributing to a neurobiological vulnerability or diathesis for impulsive and autoaggressive behaviour.

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