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The essence of the neurobiology of suicidal behavior is that a specific vulnerability to suicidal behavior is mediated by an underlying genetic predisposition interacting with environmental stressors and probable epigenetic factors throughout the lifespan to modify the function of neuronal circuits, thus rendering an individual more likely to engage in a suicidal act.
This chapter will introduce the methods by which the behaviors and models discussed in the previous two chapters are studied. This chapter will thus provide the reader with a foundation of neuroscience techniques from which they can build upon with information in the remainder of the book. These techniques address (epi-)genetics and functional neuro-anatomy.
Neuroscience approaches to the study and understanding of suicidal behavior may differ somewhat from those targeting other behavioral issues. As suicide appears to be a unique human behavior, there is a lack of animal models. However, much information is available from postmortem studies of brain tissue, in which brain characteristics of suicide victims are compared to those of individuals who died from other causes. Postmortem studies are sometimes accompanied by psychological autopsies, which are standardized interviews with individuals who were in close contact with the deceased, covering a wide range of health- and personality-related issues.
A particular case of a suicide attempt by a young girl has inspired a career, that has resulted in this book. This chapter describes the story of the girl, and indicates why and how neuroscientific studies may contribute to the prevention of suicidal behavior by means of an overview of the chapters in this book.
Computational neuroscience uses formal models of brain function to characterize the mechanisms behind behavioral problems. The production of false beliefs and their behavioral consequences are a central issue in such models. Hopelessness and suicidal thoughts are examples of such false beliefs that commonly lead to suicidal behavior as a consequence. In normal everyday life, people update their beliefs based on what they perceive: bottom-up sensory inputs are compared with top-down beliefs, and mismatches are signaled as prediction errors. Neurobiological correlates of belief updating are increasingly demonstrated. Cortical activations as demonstrated in functional neuroimaging studies, such as those reported in Chapter 6, thus reflect the production of prediction errors that signal a mismatch between beliefs and perceptual information. These errors can be minimized in several ways: beliefs can be updated, or sensory input can be minimized by withdrawal into oneself or escape from this world. If something goes wrong in this process of belief updating, false beliefs may develop and persist despite perceptual proof of the opposite. This chapter will describe a predictive coding model of suicidal behavior, in which findings from neurocognitive, neuroimaging, and neurobiological studies can be integrated. This model leads to a new understanding of suicide and, consequently, to new approaches to prevention.
Children who have experienced sexual or physical abuse during childhood are at increased risk of suicidal behavior in adulthood, independent of other factors such as depression. Recent neurobiological studies target the mechanisms that link childhood abuse and suicidal behavior in adulthood. How does early-life adversity influence behavioral reactions to stressors much later in life to such an extent that people take their own lives? It is now becoming clear that early-life adversity increases the risk of suicide by influencing the development of stable emotional, behavioral and cognitive characteristics that confer a specific vulnerability. There is now considerable evidence that changes in the expression of particular genes constitute the molecular basis of this vulnerability. This chapter will review recent findings from genetic studies of suicidal behavior, with a particular focus on epigenetic regulation of the hypothalamic–pituitary–adrenal axis and other systems involved in responses to stress and on transcriptional changes in association with early-life adversity. It appears that such changes may become manifest as cognitive impairments that are commonly found in association with suicidal behavior, and that may be due to structural and functional alterations in the brain.
Nearly one million people take their own lives each year world-wide - however, contrary to popular belief, suicide can be prevented. While suicide is commonly thought to be an understandable reaction to severe stress, it is actually an abnormal reaction to regular situations. Something more than unbearable stress is needed to explain suicide, and neuroscience shows what this is, how it is caused and how it can be treated. Professor Kees van Heeringen describes findings from neuroscientific research on suicide, using various approaches from population genetics to brain imaging. Compelling evidence is reviewed that shows how and why genetic characteristics or early traumatic experiences may lead to a specific predisposition that makes people vulnerable to triggering life events. Neuroscientific studies are yielding results that provide insight into how the risk of suicide may develop; ultimately demonstrating how suicide can be prevented.
This chapter provides an introduction to the book by providing a basic understanding of suicidal behavior. It first provides the reader a general knowledge of the epidemiological, clinical, and behavioral presentations of suicidal behaviors. In many situations, acts of nonfatal suicidal behavior will precede lethal suicidal behavior, and a suicidal process with clear implications for prevention is commonly found. The multiple causes of suicidal behaviors will be discussed, and it will become clear that each suicide results from a complex convergence of many possible sociocultural and neurobiological (e.g. genetic) factors. In spite of the unique characteristics of each suicide in terms of personal features and social circumstances, many such suicides can be understood as the consequence of an interaction between stressors and a specific vulnerability to suicidal behavior. Stressors may include problems in relational, professional, or financial areas, or consequences of psychiatric disorders such as depression that may precipitate suicidal behavior in vulnerable individuals. It is particularly with regard to this vulnerability that neuroscience studies have contributed substantially to our insights, and thus provide opportunities for prevention and treatment.
Although there are many pathways to suicide, studies in the domains of neuropsychology, cognitive psychology, neurobiology, and clinical psychiatry provide increasing evidence in support of a stress–diathesis model of suicidal behavior. While depression is the common final pathway to suicidal behavior, the vast majority of depressed individuals neither attempt nor complete suicide. It appears that a diathesis to suicidal behavior differentiates depressed individuals who will kill themselves from other depressed patients. The diathesis may be due to (epi-)genetic effects and childhood adversity, and is reflected by a distinct biological, psychological and clinical profile. This chapter will first review stress-diathesis models of suicidal behavior, ranging from cognitive models such as the “cry of pain” model to a neurobiological model in which deficient decision-making and its neural basis are central issues. Second, implications for treatment and prevention will be discussed. The identification of diathetic traits can be expected to facilitate early recognition of suicide risk. Vulnerability traits are open to modification early in life, and interventions during sensitive periods of development may have durable effects on vulnerability and resilience. The antisuicidal effects of drugs such as lithium and clozapine may well exert such effects via neurobiological components of the diathesis such as the serotonergic neurotransmission system.
In addition to neurocognitive studies, neuroimaging techniques provide a unique opportunity to study brain characteristics. Structural imaging studies clearly demonstrate volumetric differences in particular brain areas between individuals with a history of nonfatal suicidal behavior and those without such a history. Functional imaging studies show a reduced prefrontal perfusion or metabolism and a blunted increase in activation when challenged in the brains of individuals with a history of suicide attempts. Moreover, impairment of the prefrontal serotonergic system in association with suicidal behavior is demonstrated in a number of studies. Recent structural and functional imaging studies show changes in cortical and subcortical areas and their connections in association with suicidal behavior and risk factors such as mental pain, hopelessness, and impulsivity. The global picture that emerges from these studies reflects the involvement of a particular circuit in the development of suicidal behavior, the so-called frontothalamic network.
In addition to suicide prediction, neuroscience can be expected to contribute in a unique and substantial way to the treatment of suicide risk. For psychotropic drugs such as lithium and clozapine a specific antisuicidal effect has been demonstrated, independent of effects on associated psychiatric disorders. The results from studies with ketamine are promising as they indicate a rapid and sustained relief of suicidal thoughts. Neurostimulation and neuromodulation provide new approaches to treatment, with a substantial impact on suicide risk. Novel pharmacological compounds targeting the vulnerability to suicidal behavior include drugs that affect the stress-response system and neuroprotective factors.
Limitations in our capacity to predict the occurrence of suicidal behavior constitute a major problem in the prevention of suicide. Due to their extremely limited predictive value, ratings scales and clinical measures are not available for practical use. This is an area in which neuroscience can be expected to contribute substantially via the identification of biomarkers using genetic and brain imaging techniques. Recent studies using genetic approaches suggest the existence of specific biomarkers that can be detected in the blood. In addition, findings from neuroimaging and neuropsychological studies indicate functional impairments with increasing specificity in association with suicidal behavior. Biomarkers can be expected to contribute substantially to the devlopment of accurate prediction in the context of personalized medicine.
The core question in suicide prevention is: why does a person in a particular situation take their own life, while another person in the same situation would react in a different way? This chapter investigates to what extent and in which way neurocognitive studies may contribute to finding an answer to this question. The term 'neurocognitive' refers to the study of the relationship between the brain and behavior by utilizing specialized tests that have been designed to evaluate a wide variety of behavioral, cognitive and emotional domains. Thus, neurocognitive studies contribute to understanding how behavioral decisions following exposure to particular environmental stimuli relate to changes in brain functions. Such studies offer a great opportunity to measure and quantify cognitive functions, emotional states and behavioral repertoires through standardized questionnaires and testing. From such neurocognitive data, inferences are made regarding brain function and the localization of brain dysfunctions based on patterns of cognitive strengths and weaknesses. As conclusions from neuropsychological assessments are necessarily inferential, findings from neuropsychological investigations are commonly combined with those from neuroimaging (see next chapter) in order to fully understand the relationship between behavioral phenomena and changes in brain functions.
Results from a range of studies using diverse designs and both postmortem and in-vivo techniques show impairments in the serotonin neurotransmitter system and the hypothalamic–pituitary–adrenal (HPA) axis stress-response system in the vulnerability to suicidal behaviour. The involvement of serotonin in the development of suicidal behavior is well known since the 1970s when low levels of serotonin metabolites in the cerebrospinal fluid of suicide attempters were demonstrated. This involvement has been confirmed in numerous subsequent postmortem and in-vivo neuroimaging studies. For example, molecular imaging studies have localized lower binding to the serotonin transporter in areas of the brain, such as the ventromedial prefrontal cortex, which are known to be involved in decision-making processes. Serotonergic impairments may also manifest as impaired cognitive control of mood, pessimism, impaired problem solving, increased reactivity to negative social signs, excessive emotional pain, and suicidal ideation, leading to suicidal behavior.