BIOLOGICAL RISK FACTORS AND CORRELATES OF YOUTH SUICIDE
Biological risk factors and correlates are arguably the most studied factors in suicide surveys and models. They provide a more comprehensive way to understand the behaviors and etiology related to suicide risk in individuals while presenting practical intervention techniques. These correlates are studied Molecules in Psychobiology Molecular regulation strategies for mood and thought are perhaps the biggest literature interests in biological correlates of suicide. Fluctuations in serotonin levels have long been suggested to be related to suicidal ideation and behavior. Since serotonin fluctuation has also been implicated in the etiology and clinical course of many mental disorders, this suggestion has received massive attention in the past decade. Researchers investigating a possible correlation between long-term mood disorders and suicidality risk compared the level of serotonin and its primary metabolite, 5-hydroxyindoleactic acid, in control groups and adults who had died by suicide. Preliminary evidence showed a link between increased suicidality score and reduced levels of serotonin and 5-hydroxyindoleactic acid. Although proposed many years ago, this relationship was established by many similar studies demonstrating how serotonergic abnormalities may prompt and hasten the transition from ideation to attempt in suicidal adults. In a 2002 study, Pandey et al. reported higher binding levels of serotonin receptors in the postmortem brains of people who died by suicide compared to those who did not. In addition to this discovery, Pandey’s studies also reveal distinct anatomical variations in the study groups. For instance, increased levels of serotonin receptor binding were more noticeable in the hippocampus and prefrontal cortex, regardless of differences in the nature of psychiatric diagnosis while alive (Verkhratsky et a., 2021). Literature reviews documenting the link between suicidality and molecules also present multiple study evidence suggesting a relationship between SIB and brain-derived neurotrophic factor (BDNF). This important protein is primarily responsible for neuronal proliferation and protection and is negatively impacted by stress and high-level serotonin receptor binding. At low levels, BDNF has also been linked with affective disorders. Although there is little evidence showing the link between suicidality score and BDNF levels, a 2008 study reported significantly low levels of BDNF protein expression in the prefrontal cortex of youth who died by suicide. In contrast to serotonin binding levels, the levels of BDNF expression in the hippocampus of youth who died by suicide were noticeably different from those seen in control groups (Ropret et al., 2021). In addition, lower levels of mRNA expression of BDNF were reported in both the hippocampus and the prefrontal cortex of youth who died by suicide compared to control groups. Genetic Predisposition A familial pattern in the severity of suicidal ideation and behavior is well established in psychiatry. As with the history of previous suicide attempts, studies have suggested a possible like between high suicidality scores and the heritable genes in a family (Lee et al., 2022). To provide more evidence in this regard, studies have looked beyond the well-known effects of peer-to-peer influence, contagion imitation, and environmental triggers. To explore the primary effect of familial transmission of genetic materials on suicidality, researchers look for evidence of suicidality patterns in close relatives and people related by birth. Early meta-analyses demonstrated how the suicide rates in monozygotic and dizygotic twins are significantly different. In large cohort studies, researchers found evidence suggesting that sex distribution may be a crucial factor when considering the link between suicidality score and the genetic components of suicide. The difference in the concordance rate in females and males is wider compared to the difference in the concordance rate in monozygotic and dizygotic twins (Edwards et al., 2021).
under three popular subdomains: Genes, molecules, and circuits. Although potential confounds such as mental disorders exist, the literature on biological correlates of suicide has been restricted to these subdomains.
These studies have received little attention due to the small sample size and the method of analysis. However, later studies investigating the same focus reestablished these initial findings and offered more insights. For instance, Salas- Magana et al. (2017) reported no confounding effect of age, sex distribution, patterns of protective factors, brain pH, or time until analysis and therapeutic management on the levels of BDNF protein expression in their subjects. These insights were consistent with studies examining the expression of BDNF in the adult population. Future direction in this regard will be on investigating possible links between the patterns of lower BDNF levels and their effect on the rate of transitioning from suicidal ideation to attempt in youth. These studies can provide templates and evidence for novel therapy in the management of suicidal youth. An emerging body of evidence also links proinflammatory markers with patterns of suicidality in youth. Tumor necrosis factor and interleukin-1 beta are the most studied proinflammatory markers in this regard. Researchers have found increased levels of these markers in the prefrontal cortexes of teenagers who died by suicide compared to a control group of those who did not. These levels were proven to be independent of other factors such as age, community interconnectedness, brain pH, therapy, and time before analysis (Chang et al., 2019). Similarly, tumor necrosis factor and c-reactive proteins were found to be elevated in teenagers and youth who had attempted suicide compared to those who had not. However, the distribution of c-reactive protein increase seems to be confounded by the method of suicide attempts. In an attempt to explain the expression of proinflammatory cytokines and suicidality scores, researchers have hypothesized that chronic early-life stress may be a primary link. Chronic early- life stress reduces cortisol levels, which in turn may negatively impact the body’s normal immune response. Subsequently, increased inflammation occurs, and the marker becomes distributed as established in the prefrontal cortexes. This hypothesis positions chronic early-life stress as a significant trigger of suicidal ideation and behavior in the youth population. In future investigations, researchers may probe further how the severity of stress directly affects proinflammatory cytokine distribution in the brain and how contextual factors such as sleep duration, quality of life, body fat mass, and mental disorders impact the link between SIB and proinflammatory cytokines. Compared with other factors that have been well detailed as a biological correlation of suicide in youth, genetic heritability has been relatively easy to study. However, it has been increasingly difficult to identify unique genetic variants of suicide-related outcomes in various genome-wide association studies. Only a few genetic markers of behavioral traits concerning some outcomes of suicide have been examined, with little evidence to convincingly prove a point. However, this is with the exemption of genetic markers for suicide risk as discussed concerning the serotonin binding system. It appears that genetic influences of heritable characters impact the outcomes of suicidal ideation and behavior through other biological correlates. This is in support of the popular hypothesis suggesting that genes influence suicidal behavior via multiple risk factors, including impulsivity and aggression. Point or cluster epigenetic alterations to genetic expression at the early stages of life could also predict suicidality behavior. Victims with a positive history of childhood abuse and exposure to media and peer-to-peer influences have
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