Ovarian Hormones (Estradiol and Progesterone) At puberty, the ovarian hormones estradiol and progesterone and their metabolites fluctuate cyclically in girls, which dictates the method and level of expression of sexual characteristics. Studies that briefly controlled hormone conditions in women with affective symptoms in whom suicide risks are also elevated compared to control groups provided a valid template for investigating the possible link between ovarian hormones and the development of SIB. Preliminary findings in this regard suggest that neurobiological sensitivity to hormonal changes in girls at puberty may explain certain clinical phenomena, including suicidal ideation and behavior (Nolan et al., 2022). In a recent study, researchers demonstrated how the cyclical hormone changes in adult women may play important roles in acute risks of suicidal ideation, planning, and attempts in subjects with high sensitivity to hormone changes. This sensitivity and the accompanying cyclical hormone changes are also reported to be consistent with the onset of puberty in females. Typically, adolescent females have a pronounced neurobiological sensitivity to hormonal changes and experiences of heightened exposure to social stressors – in addition to hormonal fluctuations during puberty – may be important to the study of SIB. This complex combination of factors may exacerbate and complicate emotion regulation and impulse control circuits of the central nervous system. This connection is so important that nearly all studies measuring the risk of SIB in young women typically assess changes in the levels of progesterone and estradiol during different phases of the menstrual cycle over the study period. The results of these studies have, however, been too inconsistent to reach a consensus on the link between ovarian hormone levels and the risk of SIB in young women. Some studies have reported an inverse relationship between the two, with low or declining levels of estradiol and progesterone linked to a higher risk of suicide attempts and more severe suicidal ideation. Others have reported a contrasting Testosterone Androgens, as is the case for ovarian hormones in females, have received significant attention in the study of SIB in adolescent males. Testosterone levels are associated with the level of the expression of aggression, competition, tolerance, appetitive behavior, and some other social behaviors linked with suicidal ideation and behavior. In males, testosterone is considered the most androgenic hormone produced by the adrenal cortex and is responsible for multiple principal roles in behavior modulation and the regulation of biological responses to social stressors. There is strong research evidence backing up the trait-like levels of testosterone and its reliable within-person stability. Compared to adolescent females, the reliable trait-like levels of testosterone in males have facilitated advanced discoveries in the hormonal associations of SIB in males. Testosterone has been linked to suicide risk factors in males, specifically with the incidence of suicide attempts in this population. The link, once explored, provided a stronger link between testosterone and SIB in males than any other pubertal hormone. Although the reports on this link as related to the levels of testosterone have been consistent, the explanations proposed for this relationship have been mixed thus far. A leading theory is testosterone’s biological activity of modulating emotion-related impulsivity and impulsive aggression, which are traits consistently reported in the onset and development of suicidal ideation in male adolescents. Studies that explore the administration of testosterone and the subsequent assessment of behavioral change have reported reliable effects of this hormone on socially motivated behaviors, including the display of aggression and exerting dominance. This result is consistent with the results of multiple studies investigating the association between changes in the levels of endogenous testosterone and corresponding changes in social interactions and social status-seeking behavior in adolescent males. Testosterone levels also correlate closely with social
proportional relationship. Another study also reported no significant difference in the ovarian hormonal levels of women with or without clinical indications of depression, with or without suicidal ideation and behavior. These inconsistencies prompted the development of different study models aimed at eliminating the multiple single-point difference responsible for these inconsistencies. Neurobiological sensitivities to the fluctuations in ovarian hormone levels provided a conclusive context for SIB in puberty – a period when these fluctuations are more likely to happen. Neurobiological sensitivities eliminate the need for measuring between-person differences in levels of ovarian hormones and the effect on SIB. Both between-person and within-person variabilities also seem to be dependent on multiple factors, including diurnal effects, cycle lengths, diet, anovulation, and family medical history. In a bid to better explain the link between ovarian hormone levels and the development of SIB in adolescent women, researchers have attempted to explain the effect of these hormones on the brain as it relates to the development and onset of suicide indicators in this population. There is strong clinical evidence suggesting that estrogen receptors are expressed in significant quantities in regions of the brain primarily involved in social cognition and social rejection. These regions include the amygdala and the hippocampus (Sheppard et al., 2019). In considerably higher quantities, estradiol has been demonstrated to show resting-state functional connectivity in regions responsible for processing salient information. Also, during periods of relatively high estradiol levels in naturally cycling women, large hippocampal gray matter volumes have been reported. Since these ovarian cycles have significant effects on the region of the brain implicated in the onset of SIB, understanding the basic neural circuitry involved in this relationship can help scientists better explore new interventions for the management of SIB. dominance behavior. Hence, testosterone reportedly acts as a principal biological modulator of the behavioral response to social stressors and events associated with the loss of social dominance and status in males. These social stressors and events readily precipitate behavioral patterns and observations consistent with the onset and development of suicidality. Testosterone also appears to double as a driver of heightened sensitivity to social context as it relates to status and dominance, leading to significant impulse control and emotion dysregulation. Consequently, it may elevate the risk of suicidal ideation and attempt. In adult males, elevated levels of testosterone have also been reported to be linked with psychological states and traits associated with suicide risk, depression, and impulsive aggression. Compared to same-sex suicide attempters, there are multiple reports of higher testosterone levels in both male and female suicide attempters. Underlying medical conditions, when present, also seems to have a significant relationship with the link between testosterone levels and suicidality severity. Adolescent females with a history of bipolar disorder and suicide attempts had higher levels of testosterone when compared to control groups of non-attempters with no underlying mental disorders. Evidence of a possible related brain circuit and mechanisms through which testosterone modulates the risk of suicidal ideation and behavior have been weak. Since aromatization readily converts testosterone to estradiol, measuring the specific effects of testosterone on brain circuits modulating suicidal behavior has been difficult (Shay et al., 2018). However, a few pathways through which testosterone may modulate this behavior have been studied. For instance, by altering dopaminergic neurotransmissions, testosterone may modulate mood and cognition. This is evidenced by the differences in dopamine density, transporter binding capacity,
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