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Hello, my name is Sebastian Torres-Antuna and in this Podcast I will be talking about a global mental health problem whose discussion is extremely important for the well-being of society. The subject of my podcast will be on the topic of suicide or more accurately, I’m going to be discussing the concept of suicide prevention. During this podcast, my intent is to able to give you some insight into the neurobiology behind suicidal behavior. A brief glimpse into one of the prevailing mental illnesses associated with the act. And finally, an overview of some of the treatment and prevention options that are in current use as well as being considered for the use to further prevent suicide and suicidal behavior. As you will notice throughout the podcast I will reference several academic articles or studies done on suicidal behavior which I found to be extremely useful in helping me understand the concept as accurately as possible. <\/p>\n\n\n\n
*five-seconds of silence*<\/strong><\/p>\n\n\n\nNow, the first question we should ask ourselves while on this topic, is how does suicide impact our society? Who is at risk? According to the World Health Organization, close to 800,000 people die by suicide each year. With the majority of suicides, that is 79% of suicides, occurring in low-and-middle-income countries, which is where 84% of the world\u2019s population lives. These statistics show us how significant a public health problem suicide is in our society. Its effects are felt in all aspects of daily life. Causing serious emotional, physical, and economic impacts to our society. Suicide is also one of the main causes of death of people between the ages of 10 to 24, with it being the third leading cause of death of 15 to 19-year-olds, for both sexes. <\/p>\n\n\n\n
A 2017 study by Velez-Perez and colleagues on the incidence of suicidality among university students in Puerto Rico, found that approximately one in ten students participating in the study claimed to have attempted suicide with a slightly smaller proportion of them expressing that they have had suicidal ideation in the previous calendar year. A significant number of the participants with ideation reported having attempted suicide at some point in their life.<\/p>\n\n\n\n
Now to be clear, two major observations that must be reconciled in a model of suicidal behavior as stated by Mann & Risk (2020) in their article \u201ca brain-centric model of suicidal behavior\u201d says only a minority of psychiatric patients make suicide attempts, and the presence or absence of suicidal behavior is not simply determined by the presence of a psychiatric illness or the overall severity of illness. Suicidal ideation is much more prevalent than suicidal behavior, and it often does not progress to suicidal behavior. <\/p>\n\n\n\n
In their article, Mann & Risk also provides us with what they term the \u201cStress-diathesis model of suicidal behavior\u201d which is a term they give to the interaction of internal and external stressors with the traits that form a diathesis for suicide risk. The article goes on to say that suicide behavior is moderated by a set of psychopathological and cognitive traits that are different from the psychopathology of associated psychiatric illnesses. <\/p>\n\n\n\n
The stress-diathesis model depicts suicidal behavior as a consequence of an interaction between acute stressors or proximal risk factors and a diathesis or distal factors. It also refers to a set of suicide-related traits that moderate the likelihood of suicidal behavior in response to stressors. Some of the identified suicide-related, risk-moderating traits are: <\/p>\n\n\n\n
1. Excessive subjective distress when depressed and attentional bias towards negative stimuli, this has been linked to familial transmission of suicidal behavior and encompasses hopelessness and subjective depression, which are more severe in depressed suicide attempters compared to depressed non-attempters. <\/p>\n\n\n\n
2. altered decision-making involving less delayed discounting and less executive control resulting in impulsive-aggressive tendencies and favoring acting on emotions. The article calls this decision making multifaceted, which includes impaired probabilistic learning assessed by monetary reward and punishments, risky decision tendency under uncertainty, and a bias for active responding when escaping an aversive state<\/p>\n\n\n\n
3. An array of neuropsychological abnormalities, including learning difficulties, cognitive rigidity, and memory problems, ergo, suicide attempters exhibit less language fluency and learning. <\/p>\n\n\n\n
And finally, social distortions. Suicide risk is increased by cognitive distortions related to social reward and inclusion. <\/p>\n\n\n\n
Even insomnia has been recently associated with suicide and suicidality independent of well-established risk factors for suicide, such as depression and hopelessness. Insomnia is now listed, alongside other sleep disturbances such as nightmares as one of the top warning signs by the Substance Abuse and Mental Health Services Administration. A more detailed analysis of insomnia and how it can be related to suicide can be found in an article, written by Hamilton & Buysse in 2019, the article is called \u201cReducing Suicidality through Insomnia Treatment: Critical Next Steps in Suicide Prevention.\u201d<\/p>\n\n\n\n
Another major observation from the same model by Mann & Risk, is that suicidal behavior is found in many psychiatric disorders and not just in mood and borderline personality disorders. Although, an elevated risk of committing suicide has been more correlated with depression, especially major depression disorder, than any other mental illness. It is the most prevalent mental health condition related to suicide and suicide attempts. Major depressive disorder is a remarkably common and severe psychiatric disorder. It has been associated with high levels of morbidity and mortality. Patients with major depression disorder prone to several comorbid psychiatric conditions, including PTSD, anxiety disorders, OCD, and substance use disorders. It is also prone to several comorbid medical conditions, including cardiovascular disease, diabetes, stroke, and even cancer. Now coupled with the risk of suicide, it results in a shortened life expectancy than the average person without this type of mental health diagnosis. A South Korean study, conducted in 2011, of postmortem suicide victims found that approximately 60% suffered from major depression disorder and other mood disorders. <\/p>\n\n\n\n
A 2001 article named \u201cDepression and Suicide\u201d by Takahashi referenced a table for risk factors associated to patients suffering to depression. Now, even though this table was written in 1974, I believe there are a lot of risk factors that are still prevalent to this day. This includes signs of suicide risk and selection of means, which includes prior history of attempted suicide or implication of suicide, family history of suicide, verbal threats of suicide, concrete disclosures as to preparation and implementation of suicide, an unnaturally calm behavior after having been in an unstable state and dreams of self-destruction. More specific symptoms include severe anxiety, irritability; persistent insomnia; uncontrollable aggressiveness; initial, convalescent, and mixed stages of depression; age periods associated with biological crisis which include adolescence, pregnancy, puerperium and climacterium; severe self-guilt feelings; an incurable illness or hypochondriacal delusion, or concomitant alcohol dependency. And finally, it mentions environmental factors, including a broken family, loss of someone or something important, occupational, and financial difficulties, failure to carry out tasks or reach life goals, and loss of religious affiliations.<\/p>\n<\/div>\n\n\n\n
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Takahashi\u2019s article also tells us that when an alcohol dependence is concomitant with depression, it increases the rate of suicide. And that many who attempt suicide are under the influence of alcohol even where the diagnostic criteria for alcoholism is not met.<\/p>\n\n\n\n
And a 2010 study by Cabra, the article identifies risk factors for children and adolescents. In children, the personality of the parents are a suicidal risk factor, because in cases of suffering a disorder of the same, such as antisocial or emotionally instability, the upbringing would be mediated by these traits. In the same way, parents with psychiatric illnesses, such as maternal depression, alcoholism, or schizophrenia, are predisposing factors in their children. A dysfunctional home in which there are frequent arguments between parents and other members, associated with physical or psychological abuse or a home without rules, can predispose to a suicidal act. Nemeroff (2020) also states that there is a vast body of evidence that poverty, as one form of child mistreatment, is associated with poor health outcomes and with increases in both major medical and psychiatric disorders, and, not surprisingly, suicide rates. <\/p>\n\n\n\n
For adolescents, among the risk factors described are the presence of mental disorders, especially major depression, bipolar disorder, or psychosis, abuse of psychoactive substances, family history of suicide, sexual abuse, delinquency, parental divorce, poor interpersonal relationships, and a history of family abuse.<\/p>\n\n\n\n
*five-seconds of silence*<\/strong><\/p>\n\n\n\nNow I would like to talk about the neurobiology of suicidal behavior, beginning with the genetics of Suicide. <\/p>\n\n\n\n
An article called \u201cInsights into Suicide and Depression\u201d written in 2020 by Kalin references an article by Docherty et al. (2020) in which new genetic leads from a genome-wide association study or a GWAS identified 22 genes potentially related to suicide death with a heritability, this was based on single-nucleotide polymorphisms, of 25%. The study also found that a number of the implicated genes overlapped with genes associated with schizophrenia and bipolar disorder. A polygenic risk scores (PRSs) computed from the suicide GWAS data was predictive of suicide in an independent sample. But another article by Mann & Rizk mentions that there can be as many as 40 genes associated with suicidal behavior, independently of psychiatric diagnoses. And that further combining GWASs with transcriptome data reveals suicide-related genes associated with inflammation, the hypothalamic-pituitary-adrenal (HPA) axis, GABA, which is the \u0194-aminobutyric acid, and glutamate transmission, and finally, neurogenesis.<\/p>\n\n\n\n
In another article called \u201cPredicting suicide\u201d by David Goldman, he also references Docherty et. al and is able to continue with the premise of how to predict suicide as the article clearly mentions. Now in the article, he said that the identification of genes that are significantly associated with suicide, and the implication of a much larger number of other genes in the genomic statistical threshold, was what enabled Docherty et al. to derive a polygenic risk score accounting for a substantial portion of the risk of suicide. The GWAS study done by Dochety et. al, was of more than 3,400 suicide victims from the state of Utah and several times that number of ethnically matched comparison subjects from outside the state, and although more studies on the genetics of suicide need to be done, a hypothesis that Goldman mentions is \u201ca hypothesis that never dies\u201d is that depletions of brain serotonin and, as reflected in low levels of the metabolite 5-HIAA (or 5-Hydroxyindoleacetic acid, which is the main metabolite of serotonin) in Cerebrospinal fluid, serotonin receptor binding potential, as well as serotonin itself, predict suicide. Goldman concludes with the ability of geneticists to capture increasing portions of the heritability of suicide may enable psychiatrists to better help people at risk, combining genetic predictors of innate (trait) vulnerability with such state and trait measures.<\/p>\n\n\n\n
Continuing with another article on the genetics of suicide called \u201cThe Promise and Limits of Suicide Genetics\u201d by Lopes & McMahon (2019) tells us that in people with bipolar disorder, suicide attempts were associated in a small but significant way with a common genetic marker on chromosome 4, although even when this marker does not immediately implicate any particular gene, the marker was also associated with genome-wide significance in a meta-analysis of suicide attempts in mood disorder, suggesting that bipolar disorder and major depression have something in common. In references to an article by Mullins et al (2019), PSR analysis showed that genetic risk for major depression increases risk for suicide attempts in people with major depression. However, results also showed that genetic risk for major depression also increased risk for suicide in people diagnosed with bipolar disorder or schizophrenia. <\/p>\n\n\n\n
Continuing forward, I want to talk about an explanatory model for suicidal acts written by Carballo et al. (2008), in which he references Gottesman & Gould, 2003, which talks about endophenotypes, which are \u201cmeasurable components along the pathway between disease and distal genotype\u201d. These can be characteristics that often accompany psychiatric illness including abnormal neurophysiological, biochemical, endocrinological, neuroanatomical, cognitive, and neuropsychological findings. In Carballo\u2019s model, the endophenotypic models for suicide behavior are deemed clinical, neurochemical, and neuroendocrine. <\/p>\n\n\n\n
The clinical endophenotypes include impulsivity, aggression, neuroticism, and hopelessness which can also be regarded as intermediary phenotypes, which can possibly predispose individuals to suicidal behavior.<\/p>\n\n\n\n
Beginning with Impulsivity it\u2019s a personality trait or cognitive style that can be characterized by disinhibition and a tendency to act quickly on urges or in response to stimuli. An association between impulsivity and suicidal\/self-destructive behaviors has been reported in various adult psychiatric populations<\/p>\n\n\n\n
Continuing, pessimism has also been implicated in suicidal behavior. With studies showing that compared to non-attempters, suicide attempters tend to experience more pessimism as reflected in more suicidal ideation, fewer perceived reasons for living in response to illness or social adversity, and higher subjective ratings of the severity of depression and hopelessness. <\/p>\n\n\n\n
Elevated neuroticism has also been linked to negative affect and may constitute a vulnerability factor for suicidal behavior. Carballo references Roy (2002) when he mentions that differences in neuroticism scores between those with and without a family history of suicide which were significant when personal histories of suicide attempts were taken into account, with patients with a positive family history for suicide and who had themselves attempted suicide having had higher neuroticism scores. <\/p>\n\n\n\n
Another clinical endophenotype is hopelessness, which can be associated with suicidal behavior. Pollock and Williams (2004) propose that suicidal behavior is associated more with hopelessness than with the severity of depression. And hopelessness was the principal predictor of suicidality in a study conducted among schizophrenic patients. <\/p>\n<\/div>\n\n\n\n
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Now moving on to the neurochemicals endophenotypes, we first begin with serotonin, which has long been known to be involved in emotional and cognitive functions including suicidal behavior. Cerebrospinal fluid (CSF) concentrations of major serotonin metabolite 5 hydroxyindoleacetic acid (or 5-HIAA) are reported to reflect central nervous system serotonergic function. Of note, low CSF 5-HIAA has been associated with impulsive, externally directed aggression which has been observed in impulsive murderers and arsonists compared to non-impulsive murderers and control subjects. The relationship between impulsivity and reduced serotonergic function has led to the hypothesis that this function supports a restraint mechanism and a deficiency in serotonergic function results in greater impulsivity and aggression including self-directed aggression of suicidal behavior. <\/p>\n\n\n\n
Another endophenotype is Norepinephrine. The catecolaminergic dysfunction has been hypothesized to play a role in suicide based the observation of a high concentration of norepinephrine (or NE) with decreased alpha2-adrenergic bindings which has been observed in the prefrontal cortex of suicide victims. <\/p>\n\n\n\n
The last neurochemical endophenotype is Dopamine. The dopaminergic system is abnormal in depression; increased concentrations of dopamine have been associated with aggressive behavior and suggest that increased dopamine concentrations may be related to violent suicide attempts or completions. In terms of neuroticism, studies have shown associations between the dopaminergic system and neuroticism. Striatal dopamine D2 receptor may be a significant predictor of neuroticism scores. <\/p>\n\n\n\n
Finally in the last endophenotype of Carballo\u2019s model, which are neuroendocrine endophenotypes. We focus more on the Hypothalamic-Pituitary-Adrenal Axis, or the HPA axis, now, this is a neuroendocrine system that regulates the body\u2019s response to stress and has complex interactions with brain serotonergic, noradrenergic, and dopaminergic systems. Stress results in the release of the corticotrophin releasing hormone (CRH). Now, some studies indicate that suicidal behavior may be associated with hyperactivity of the HPA axis. These studies indicate higher cortisol levels after dexamethasone suppression (this is a clinical measure of HPA axis hyperactivity) and this hyperactivity at baseline levels may increase the risk of eventual suicide by as much as 14-fold. This according to two studies conducted in 1988 and 2001. The 1988 study was Brown, Ebert, Goyer et al., and the 2001 study, Coryell & Schlesser. <\/p>\n\n\n\n
Continuing with neurobiological correlates of suicide risk-related diathesis traits, as found in Mann & Rizk\u2019s article, which tells us that neuroimaging studies have found five main features of dysfunctional neural circuitry, starting with a relationship of enhanced negative affective and self-referential processing networks to suicidal ideation that may also underlie excessive subjective distress (these include the ventromedial prefrontal cortex, the medial orbitofrontal cortex , rostral anterior cingulate cortex, the insula, and the ventral striatum); two, structural and functional deficits in the dorsomedial prefrontal cortex, dorsolateral prefrontal cortex, the ventrolateral prefrontal cortex, and the dorsal anterior cingulate cortex that correlate with severity of subjective depression and contribute to less top-down control over ventromedial prefrontal cortex regions, which results in impaired decision making and, in turn, suicidal behavior; three, differential activation of the medial orbitofrontal cortex to pleasant versus negative facial expressions, which could be related to excessive distress and social distortions; four, serotonergic release deficits in the ventral prefrontal cortex and anterior cingulate cortex are more prominent in high-lethality suicidal behavior and suicide death; and finally, abnormalities of glutamate and opioid systems may affect memory, learning, and reward mechanisms.<\/p>\n\n\n\n
In terms of Neurotrophic and Apoptotic Pathways, brain-derived neurotrophic factor (or BDNF) regulates neuron survival, plasticity, and synaptic function as well as plays an integral role in differentiation during development and is affected by stress as well as associated with major depression and suicidal behavior. With expression of BDNF and BDNF receptor tyrosine kinase B genes being lower in suicide decedents, and plasma BDNF levels being low in suicide attempters which could be reflecting a systemic genomic effect on BDNF expression.<\/p>\n\n\n\n
Neuroinflammation can also be found to be related to suicide risk, with peripheral inflammatory biomarkers linked to this risk including elevated C-reactive protein, neutrophil-to-lymphocyte ratio, proinflammatory interleukins, cytokines that regulate the immune response, tumor necrosis factor-alfa, tissue growth factor b1 , and vascular endothelial growth factor as well as low levels of the anti-inflammatory Interleukin-2, Interleukin-4, and interferon-gamma in suicidal individuals (generally suicide attempters). Mann & Rizk\u2019s article also refers that activated microglia, which is the primary immune response cells in the brain, and brain translocator protein found in mitochondria of activated glial cells are linked to suicide risk, independently of the presence of psychiatric disorders. Finally, greater suicidal ideation severity has been found to be associated with higher C-reactive protein, Interleukin-6, and Interleukin-10 levels and with activated microglia-related alterations of the tryptophan-kynurenine pathway. This suggests that regulation of inflammatory pathways may change with level of suicidal ideation and therefore risk. However, more longitudinal studies are needed to determine whether fluctuating suicide risk correlates with severity of inflammation, this is due to a recent study that reports no association between suicidal ideation severity and cytokine pathway marker mRNA expression.<\/p>\n\n\n\n
Now to conclude this talk about the neurobiology of suicide, I will give a clinical description of Depression. Forbes (2020) tells us that depression is a developmental disorder that can occur as early as the preschool years, with adolescence being a vulnerability period for it. <\/p>\n\n\n\n
In the article, Forbes references Rappaport et al. (2020) whose study showed that cumulative and current depression were associated with different patterns of frontostriatal response during adolescence. In addition, the developmental point at which depression was experienced appeared to influence the regions exhibiting disruption: while depression during early childhood was related to low responding in the dorsal striatum, ventral striatum, and rostral anterior cingulate cortex, depression during adolescence was related to low responding in the nucleus accumbens. <\/p>\n\n\n\n
Nemeroff (2020) identifies the risk of major depressive disorder being characterized by a combination of ill-defined genetic and environmental factors, including a higher prevalence in the female gender, a history of childhood mistreatment, and family history of the illness, as well as more recent stressors. <\/p>\n\n\n\n
There are remarkably high levels of a bidirectional comorbidity of major depression with other psychiatric illnesses including PTSD, syndromal anxiety disorders, OCD, and substance abuse disorders and even medical illnesses, where there is a documented relatively low treatment response in depressed patients with comorbid medical disorders, which coupled with suicide, is the primary cause of premature mortality in patients with major depression. <\/p>\n\n\n\n
Depression is a uniquely human con<\/p>\n\n\n\n
dition. It does not occur naturally in any other species in the same longitudinal nature, including its recurrent course.<\/p>\n\n\n\n
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Now that I\u2019ve explained to you who is at risk for suicide and how suicidal behavior could have its roots come from a neurobiological origin, let\u2019s continue with how we can prevent suicide. <\/p>\n\n\n\n
In terms of novel approaches of suicide prevention, Mann & Rizk suggest some of these approaches. One of them is training primary care providers target internal stressors in the management of major depressive episodes which have been shown to prevent suicide, however, it has not been shown to prospectively influence risk of suicidal behavior when taking into the account external stressors. <\/p>\n\n\n\n
Mann & Rizk also suggest two types of therapies: Pharmacotherapy and Psychotherapy. With Pharmacotherapy, they reference lithium and clozapine which have effects on the internal stressors of depression and acute psychosis. Intravenous ketamine being a rapidly acting treatment that robustly reduces depressive symptoms and suicidal ideation in hours instead of weeks. They also mention Intranasal ketamine (or esketamine) which shows promise as an anti\u2013suicidal ideation treatment and is less invasive, but its absorption is more erratic, and, like intravenous ketamine, must be administered in medical settings. and Psychotherapy. Most studied the cognitive-behavioral therapy (CBT) and dialectical behavior therapy, which both can prevent suicide attempts. CBT works by improving the capacities for cognitive regulation of emotion, it\u2019s been associated with decreased activity in the amygdala-associated negative emotional reactivity and enhanced activity of the emotion regulation network. Dialectical behavior therapy prevents suicidal behavior via problem-solving and stress management or elements of the diathesis such as dampening amygdala reactivity to negative emotions. <\/p>\n\n\n\n
Previously, I mentioned two pharmacotherapies: Ketamine & Esketamine, which I also found additional articles in order to better explain how these medications work. In a study by Parikh & Walkup (2021), they reference Dwyer et al.\u2019s study of a randomized cross-over trial of single-dose ketamine compared with midazolam for the treatment of refractory depression in adolescents. The study\u2019s results when measured with the Montgomery-\u00c5sberg Depression Rating Scale (or MADRS) 24 hours after infusion, showed that ketamine had a significant greater effect than midazolam in reducing depressive symptoms. In another study, Canuso et al. (2018) conducted a proof-of-concept study on the efficacy and safety of intranasal esketamine for rapid reduction of depression in suicidality in high-risk patients, the preliminary results of this study indicate that intranasal esketamine compared with placebo, given in addition to comprehensive standard-of-care treatment, may result in significantly rapid improvement in depressive symptoms, including some measures of suicidal ideation, among depressed patients at imminent risk for suicide. <\/p>\n\n\n\n
Another approach mentioned by Mann & Risk, are Brief Interventions and Active Postdischarge Outreach in the Emergency Department or From Inpatient Units. This is because after seeking help for suicidal thoughts or low-lethality suicide attempts in the emergency department, discharged patients have an elevated suicide attempt rate. Suicide prediction models based on computational analyses of electronic health records could help identify individuals with a higher-risk for suicide at time of discharge, these individuals would be the most likely to potentially benefit most from intensive treatment and follow-up. There already exists, some brief, inexpensive psychological and educational interventions for use for individuals that are presenting to the emergency department with acute suicidal crisis. These interventions are also easy to implement, and don\u2019t require much staff resources. They seek to project a helpful option for a patient in crisis to help them overcome the social cognitive distortion that the social network is more hostile than helpful.<\/p>\n\n\n\n
Continuing by another study by Kalin (2020), in which references The Treatment for Adolescents with Depression study and The Child\/Adolescent Anxiety Multimodal Study whose results highlight the efficacy of relatively short-term interventions and point to the need for treatments that can fundamentally affect childhood developmental trajectories that will enable initial interventions to have long-lasting positive effects. <\/p>\n\n\n\n
One final novel approach by Mann & Rizk is the restriction of Lethal Means, this works because it seeks to make access to the most popular high-lethality methods more difficult. It takes advantage of two key observations. One, the acute risk of acting on suicidal thoughts is brief, and second, the flexibility of the suicidal person in changing from one method to another is surprisingly limited. Studies of survivors of suicide attempts have indicated that most attempts are the result of a rash decision to act that was made minutes earlier, even if the method of suicide was planned months or years head ahead. <\/p>\n\n\n\n
Now, one last addition from the Mann & Rizk article of \u201cA brain-centric model of suicidal behavior\u201d, let\u2019s move our attention to what they refer as the Future of Research and Suicide Prevention. They first refer suicide in a possibility as a distinct mental disorder. This is due to the prevailing evidence that suggests that suicide could be considered a moderately heritable independently of the heritability of major psychiatric disorders, and as I have shown you through various articles, there those exist a number of neurobiological abnormalities that could prove that monitoring genes associated to the risk of suicide is a possibility. Now speaking of monitoring, another suggestion made by Mann & Rizk on the future of research is Real-Time Monitoring of Acute Suicidal Crisis. In the article, suicidal ideation, which is usually preceded and may even represent a risk of an imminent suicide attempt, can go unrecognized by even the most systematic periodic evaluation of outpatients. A reference to a 2020 article revealed that around 60% of individuals denying suicidal ideation on a weekly basis through self-report measures reported that they were having suicidal thoughts while using an ecological momentary assessment (or EMA) technology that delivered questions on their smartphones six times a day over the same 1-week period. Combining this EMA-collected real-time data on suicidal thoughts and behavior with what is known as \u201cpassive sensing,\u201d which collects data from individuals\u2019 smartphones, allows examination of the very short-term risk factors of suicide in multiple domains. And this is helpful because the wide availability of smartphones can allow accumulation of massive amounts of personal level data that may lead to identification of a, what the article references to a \u201cphonotype\u201d or \u201cscreenotype\u201d. Another technique that the Mann & Rizk article references is the Implicit Cognitions and Neuroimaging for Suicide Risk Detection. Neural decoding is an approach where machine-learning methods have been used to identify the neural activity pattern involved in the mental representation of a deceased loved one and to track unconscious deceased-related thinking. fMRI-measured neural representation of mental concept representations differentiates suicidal ideators from suicide attempters and healthy control subjects. The possible identification of a neural signature of suicidal ideation could be a biomarker for suicide risk even when suicidal ideation is denied or unrecognized. <\/p>\n<\/div>\n\n\n\n
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An article by Auerbach et. al (2021) references Vidal-Ribas and colleagues, in a challenging study of identifying possible biological markers that confer risk for suicidal behaviors in preadolescent youths. The strongest neural correlate discovered was an association between suicidal thoughts and behaviors and decreased thickness of the superior temporal gyrus. <\/p>\n\n\n\n
The last approach in terms of research and suicide prevention in the Mann & Rizk article talks medication and neuromodulation. Mann & Rizk suggest the use of buprenorphine, a medication used primarily for relapse prevention in opioid use disorder, this, the buprenorphine also has antidepressant effects when used for both its intended use and for depression that has been found to be treatment resistant. By addressing both opioid relapse and comorbid depression and suicidality, it could be further evaluated if it\u2019s a possible way to reduce suicide risk via opioid overdose. <\/p>\n\n\n\n
In terms of neuromodulation, there have been preliminaries studies have also indicated a decrease of suicidal ideation following treatment with rTMS or repetitive transcranial magnetic stimulation. Also, the role of inflammation in the pathogenesis of depression and suicidal behavior suggests use of anti-inflammatory drugs for depressive symptoms and suicidal ideation. Even though, none have shown to improve suicidal ideation, minocycline has been able to decrease microglial activation in the Prefrontal cortex & depressive and anxiety-like traits in animals so it may reduce depressive symptoms. <\/p>\n\n\n\n
A study by Hamilton & Buysse (2019) references McCall et al. whose REST-IT study, that is R-E-S-T-dash-I-T study which examined controlled-release zolpidem relative to placebo serves as a benchmark for future studies conducting randomized controlled trials of suicidality with outpatients. This study also saw reductions in insomnia, depression, and suicidality, which supports the utility of targeting insomnia in suicide prevention efforts. <\/p>\n\n\n\n
The Mann & Rizk article also told us that no drugs targeting HPA axis dysregulation have been evaluated for the use of preventing suicide. The glucocorticoid receptor antagonist mifepristone and cortisol synthesis inhibitors such as metyrapone and ketoconazole have not shown distinct benefit for depression but may warrant testing in suicidal individuals with glucocorticoid hypofunction.<\/p>\n\n\n\n
*5-seconds of silence*<\/strong><\/p>\n\n\n\nIn closing, I hope you’ve enjoyed this podcast. And that by giving you a brief glimpse, and believe it or not, this has been a brief glimpse into all the research that has been done and is being done on suicide prevention. And that you’ve seen how suicidal behavior is a real risk that prevails at all ages for both men and women. It’s a phenomenon that involves various biological and psychosocial factors, and although there is a lot of ongoing studies related to identifying its most prevalent biological risk factors as well as treatments, there is still a growing need for further research to successfully develop effective suicide prevention methods that would help decrease global suicide rates. As I said in the beginning, close to 800,000 people die each year from committing suicide. It’s not a problem that can be ignored. Thanks for listening and I hope you have a nice day.<\/p>\n<\/div>\n\n\n\n
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Title: Suicide prevention: a brief introduction to suicidal behavior, the neurobiology behind, and the treatments used to prevent it By Sebastian Torres Antuna Sebastian Torres Antuna University of Puerto Rico, Rio Piedras CampusFaculty: Natural ScienceBaccalaureate: Biology Year: 4th Transcript Hello, my name is Sebastian Torres-Antuna and in this Podcast I will be talking about a … <\/p>\n
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