EXPLORING PUBERTY HORMONES IN SUICIDALITY
Pubertal hormone production is regulated during the two stages of puberty: Adrenarche and gonadarche. Typically beginning at age 7 or 8, the adrenarche period is linked with the production of the hormones testosterone and dehydroepiandrosterone (DHEA). Gonadarche is triggered by the activation of the hypothalamic–pituitary–gonadal axis in a process that also increases the levels of luteinizing hormone and follicle-stimulating hormone. This period takes longer, lasting about five years and occurring earlier in males than in females. The corresponding increase in the levels of follicle- stimulating hormone and luteinizing hormone initiates the development of sex hormones in both genders (Osborn et al., 2021). Testosterone is predominantly produced by males, and estradiol is predominantly produced by females. Both hormones are principally responsible for the development of distinct sex characteristics in both genders. In the context of suicidal ideation and behavior at puberty, the sex hormones cross the blood–brain barrier, influencing brain development and contributing to the development of neuronal circuitry in the central nervous system. Testosterone and estradiol also exert a considerable effect on the various signaling pathways underlying the regulation of mood, cognition, and stress (Ankarberg- Lindgren et al., 2020). At this point, pubertal changes are linked with endocrine, neuronal, cognitive, and personal changes that last for the length of adolescence and adulthood. This period also represents a vulnerable psychobiological point during which suicidal ideation and behavior may emerge in youth. Although the production of sex hormones in both genders peaks at an age much earlier than 12, the prevalence rate of DHEA In pubertal adolescents, DHEA is the predominant steroid hormone serving principal functions, including providing a template for the production of sex steroids. Studies examining the effects of DHEA and its sulfate, DHEA-S, on SIB in adolescents have produced unclear results. However, a few themes are consistent with the results of these studies so far. A few of these studies suggest that an increasingly higher level of DHEA-S is consistent in male suicide attempters when compared to healthy non-suicidal controls. Also, early-life exposure to extreme social stressors, including bullying and child violence, appears to be negatively correlated with the ratio of cortisol to DHEA in adults. The presence of, or positive history of, an underlying mental illness at any stage of life also seems to correlate with suicidality score and DHEA levels in adults. In a study population of adults diagnosed with PTSD during an early stage of life, those with severe suicidality scores and who have attempted suicide present with significantly higher levels of DHEA compared with those without a history of PTSD in the same study population. In combat veterans, the ratio of DHEA to DHEA-S has been positively correlated with total adolescent aggression score and lifetime aggression score in those with a history of a suicide attempt (Sher et al., 2018). Although the primary social stressor in this study population is extreme violence, the SIB score in those with no history of suicide seems to be exceptionally low compared to suicide attempters. These observations open research inquiries on the multiple factors directly involved with pubertal hormone changes in the prevalence of SIB in the youth population. Controlling for other contributing factors, studies have consistently shown that increased levels of DHEA and DHEA-S may be associated with the risk of SIB in youth. These hormones exert multiple effects on the neurotransmitter complex, including mimicking the neurobiological effects of GABA receptors on genes widely distributed in the striatum, amygdala, and hippocampus. In medical conditions characterized by deficiencies in the normal metabolism of DHEA, the resulting
SIB in adolescents only begins to increase considerably after age 12. Logically, this means the increase in the prevalence of SIB at puberty does not entirely depend on the rise of endocrine changes during this period. Studies have shown that instead of a direct correlation, the organizational effect of these pubertal endocrine changes plays a more principal role in SIB prevalence. The organizational effects are described as occurring during sensitive developmental periods that initiate the course of sex-typical brain and behavioral phenotypes. Even in the absence of circulating pubertal hormones, these organizational effects remain active in both sexes. Evidence for this observation was provided by studies demonstrating how developmental processes such as neurogenesis and apoptosis that occur during the perinatal period as a result of rising levels of gonadal hormones also occur during puberty (Laube et al., 2020). In addition to hormone changes, puberty - through different influences on neuronal circuits - makes adolescence a vulnerable period for the onset of stress-related mental health complications. This influence is compounded by environmental triggers of suicide through the exposure of the adolescent to increased social stressors. There are also pieces of evidence suggesting that hormonal fluctuations during puberty exert an activation effect on neurotransmitters in an action that impacts the level of SIB risk, especially in adolescents with a neurobiological sensitivity to pubertal hormonal changes. To further understand the increased prevalence of SIB in pubertal adolescents, neurobiological studies have looked at the individual effects of the pubertal hormones on SIB. higher levels of DHEA may also contribute to the development of SIB in adults. This is the case in psychiatric conditions characterized by excessive stress that lead to the downregulation of neurosteroid biosynthesis, including the conversion of DHEA to GABAnergic metabolites (Pineles et al., 2018). The nature of DHEA in the brain structure and not just the neuronal circuitry alone is another interesting area of SIB in youth. Investigators have reported that higher levels of DHEA produced as a response to stress or due to abnormalities in neurosteroid biosynthesis are linked with structural changes in the brain anatomy, including larger hippocampal volumes and lower white matter organization in both sexes. A higher level of DHEA is also associated with increased functional connectivity between the amygdala and the ACC. This connectivity is also extended to other areas of the brain involved in processing information needed to understand social stimuli (Arendse et al., 2020). However, there is a gender twist to this observation. For instance, lower activation of regions responsible for processing information related to social stimuli as an association with high DHEA levels has been consistently reported in girls (Vijayakumar et al., 2019). As reported earlier, the results of studies investigating the link between DHEA levels and the prevalence of SIB in youth may be few and unclear; however, there are some themes that are consistent with these studies. Regardless of the protective factor or the nature of early-life social stressors, higher levels of DHEA appear to be consistently linked with both SIB in youth and the alteration of the brain’s structure and neuronal circuitry. In essence, these associations birth logical conclusions that DHEA may disrupt the development of emotional regulatory circuits in adolescents, prompting a corresponding increase in the risk of SIB in adolescents and adults. Subsequent exposure to interpersonal stress may increase the risk of SIB (Ho et al., 2022).
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