The Experience of the Tragic

At first, these episodes were rare, and my only strategy for coping was distraction. But the fear was more than just an emotion – it was an instinct, poisoning the mind. It lurked like a predator, waiting for the right moment. The older I became, the more clearly I sensed it.

By the time I turned twenty-one, this state had returned – this time consuming my entire consciousness. Thoughts of death became obsessive, crowding out everything else. Upon waking, I would immediately remember my mortality, and the horror would seize me. In search of comfort or answers, I turned to texts, read about near-death experiences, and explored philosophical theories. But the answers either seemed naive or proved useless. Any attempt to escape the thought of my demise crashed against the brutal clarity of its inevitability.

Two concepts are typically offered: either absolute nothingness after death, or traditional religious notions of an afterlife. Neither idea was acceptable to me. I lacked magical thinking, so religious beliefs offered no consolidation. And the prospect of complete annihilation inspired unspeakable dread. Eventually, I realized that the root of this horror was not fear of physical death or pain, but the fear of losing my self, the disappearance of consciousness.

I came to understand that my fear was not merely a fear of pain or the unknown. It was the terror of losing the I. The self-awareness I had taken as the essence of who I was turned out to be a shadow, doomed to vanish. I tried distracting myself with thoughts of the cosmos, but the grandeur of the stars only underscored my insignificance.

Comparing this experience to the Kübler-Ross model, I can confidently say that I went through the stages of denial, bargaining, and depression (Kübler-Ross, 2020). However, I did not experience the stage of anger. The final outcome of this inner order was acceptance. In that moment, I felt a sudden improvement in mood, bordering on euphoria.

One day, while walking home from work, reflecting on recent changes in my thinking, I passed a funeral supply store as I always did. Outside the shop stood a display of headstones visible to everyone passing by. And then I felt something strange. The sensation was unfamiliar – almost as if I were not the one walking, but merely an observer, watching myself from the outside, as though I were playing back a video in my mind. The world around me had subtly changed – the colors didn’t disappear entirely, but they seemed noticeably duller, as if reality had lost some of its saturation.

This state didn’t frighten me, even though I had never experienced anything like it before. I still felt everything around me, although my perception was somewhat distorted. Physically, I maintained full control over my body, but it felt different – almost automatic, as if my movements were being directed without conscious involvement.

It was depersonalization-derealization syndrome – as though I were viewing everything through glass or a screen. My body continued performing all necessary physiological functions, going to work, but my mind had fully turned inward, analyzing its surroundings. Looking at crowds of people, I thought about how brief their time was here, and how much attention they devoted to this world. I imagined skeletons with brains inside each of them, and how the outer shell to which they paid so much attention was utterly irrelevant. I remained in this state for more than a week. It didn’t particularly hinder me – though it unsettled me a bit – but I didn’t feel the same desperation to escape it as I had previously when trying to come to terms with death. Nor did I have the strength.

During those days, I persistently pondered the nature of reality. I was haunted by questions: Does only my consciousness exist? Can I be sure that others see and feel the same as I do? Or is this entire panorama nothing more than a façade woven by my perception? Like Sextus Empiricus, I grew skeptical of anything I could not verify. In the course of my reflections, science became a more reliable guide for me than philosophy. Philosophy offered abstract constructs, building castles of paradoxes in the air, but it gave me no solid ground to stand on. Science, by contrast, offered clarity and testability, transforming the fog of existential questions into more comprehensive patterns.

The state of depersonalization gradually faded, but it left a profound imprint. I realized that what I had called the “self” was not a unified entity, but a mere intersection of perceptions, memories, and fleeting impressions. This illusion of unity is a cunning product of evolution – not truth, but a convenient mask.

Becker’s models of “heroism” lost their power. The individual trying to cheat death now seemed to me not so much tragic as naive. All of Becker’s models of heroism had become irrelevant to me – except one, and even that was not directly related to death: the search for meaning in life and in the world at large.

The existential question of the meaning of being, despite the disappearance of the fear of death, did not vanish. It continued to torment me just as much as thoughts of finitude had before. All of this led me to understand that the fear of death cannot be the sole driver of human activity. In creating culture, systems of meaning, and value structures, human beings attempt to overcome not only the fear of death but many other existential challenges. Humans do not always seek heroism. Sometimes, they are motivated by entirely different factors – joy in the process itself or simple curiosity.

Becker’s “projects of immortality” can be viewed as unfalsifiable ideas, and this constitutes one of the central problems with his notion of heroism.

Like theological arguments for the existence of God or otherworldly forces, heroism projects are based on subjective belief and collective agreement. The problem is that neither heroism nor theological concepts can be confirmed or disproven using scientific methods. This makes them conceptually similar: both operate within the boundaries of human psychology and existential experience, but not within the domain of empirical science.

2.2 Devaluing Death, or The Problem of Suicide

The awareness of life’s finitude can give rise to various perceptual and behavioral anomalies. One such example is the belief held by some individuals that, since death is inevitable, life is therefore devoid of meaning, and that one may as well end one’s existence consciously rather than wait for a natural death. I maintain that such thoughts in themselves do not necessarily lead to action. While from both biological and philosophical perspectives it makes no essential difference whether one dies now or many years later – particularly in the absence of close relatives or children – what remains with us is the inner experience, which may be perceived as akin to observing a film or theatrical performance. We do not typically stop watching a film simply because we know it will eventually end. Nevertheless, as will be demonstrated below, the mere thought of suicide is insufficient for its implementation.

Suicide is an extraordinarily complex phenomenon, the emergence of which is conditioned by numerous factors. One key aspect is the biological mechanism involving inhibitory neurons that accumulate prediction errors and may lead to the conclusion that the future is invariably associated with inevitable suffering and lacks positive outcomes. Among the hypotheses under investigation is the assumption that certain individuals possess a genetic predisposition to suicidal behavior, which may be activated under specific circumstances. This means that the presence of certain genes or brain impairments can substantially increase the likelihood of suicide, even in the absence of overt pessimism or significant life difficulties.

It is important to stress that this hypothesis has not yet been definitively proven and remains the subject of ongoing research. Genetic predisposition is a significant, but by no means the sole, risk factor. Its influence is always interwoven with other psychological, social, and environmental conditions, forming a complex network of causes that lead to suicidal behavior.

In what follows, I shall treat suicide as a process that is genetically and deterministically conditioned. However, this is not to suggest that the genetic component constitutes an exhaustive account of the problem of suicide. The subject demands a more thorough and multidimensional analysis that includes a wide range of contributing factors, which lie beyond the scope of the present work.

Genetic Predisposition

In recent decades, scientific research has shown that genetics plays a significant role in susceptibility to depression and suicidal behavior. One of the key genes associated with suicide is the gene that encodes serotonin – a neurotransmitter that regulates mood and behavior. For example, the 5-HTTLPR gene, which is responsible for serotonin transport, has been linked to an increased risk of depression and suicidal tendencies. Individuals with a particular variant of this gene exhibit lower levels of serotonin, which may contribute to the development of depressive disorders and ultimately increase the risk of suicide.

Another important gene is MAOA (monoamine oxidase A). This gene also affects the levels of neurotransmitters such as serotonin and dopamine. Low MAOA activity is associated with a greater propensity toward aggression, impulsivity, and depression – all of which may contribute to suicidal tendencies. Such studies underscore that the presence of certain genetic variants may play a key role in a person’s decision to commit suicide under conditions of stress or crisis.

Brain Injury

In addition to genetic predisposition, brain injuries may also contribute to elevated suicide risk. Damage to specific areas of the brain – such as the prefrontal cortex and limbic system – can significantly alter emotional behavior and an individual’s capacity for self-regulation. For instance, individuals who have sustained traumatic brain injuries or strokes may experience changes in their self-perception and worldview, which increases the likelihood of depression and suicidal thoughts. Brain injuries may also affect serotonin levels and other neurotransmitters, promoting the development of depressive states and disturbances of emotional balance.

The Role of Medications

Medications that may increase suicidal tendencies play a crucial role in exploring the connections between biology, psyche, and behavior. Some drugs, despite their therapeutic properties, can produce serious side effects, including depression and suicidal ideation – especially among individuals with certain predispositions or psycho-emotional disorders.

One of the most well-known categories of drugs that heighten suicide risk is antidepressants. Selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine (Prozac) and sertraline (Zoloft), although widely used to treat depression, may in some cases exacerbate suicidal thoughts, particularly among adolescents and young adults during the initial stages of treatment. In 2004, the FDA issued a warning that antidepressants may increase the risk of suicidal ideation among youth. However, it is important to note that for some patients, antidepressants are effective, and the increased risk of suicidal ideation is more often linked to individual reactions to the drugs, initial instability of the condition, or insufficient medical supervision in the early weeks of therapy.

Another group of medications associated with increased risk of suicide is anticonvulsants, such as lamotrigine and valproate, used to treat epilepsy and psychiatric disorders. Studies have shown that these agents may increase suicidal tendencies, especially with long-term use. In 2008, the FDA added a warning about this risk to the packaging of medications such as lamotrigine, emphasizing the need for careful monitoring of patients’ psycho-emotional states.

Opioids – potent painkillers such as oxycodone and morphine – are also linked to elevated suicide risk. These substances alter the brain’s chemical balance, promoting depression and deteriorating emotional well-being, which may lead to suicidal tendencies, especially in cases of abuse or prolonged use.

In addition, psychotropic medications such as antipsychotics and benzodiazepines may also induce depression and suicidal ideation, particularly among individuals prone to psycho-emotional disorders. Certain antipsychotics, such as risperidone and quetiapine, may produce side effects that worsen mood and even provoke aggression. Benzodiazepines, including diazepam and Xanax, are often prescribed to reduce anxiety, but their prolonged use may also lead to depression and an increased risk of suicide.

No less dangerous is isotretinoin – a drug used to treat acne, widely known under the brand name Accutane. It has been reported to cause depression and suicidal ideation, as documented in numerous studies and FDA-issued warnings. Isotretinoin has been associated with psychiatric side effects, including depression and aggression, making it particularly risky when used during adolescence.

while many of these medications have important therapeutic properties, it is crucial to remain aware of their potential side effects, which may thus significantly increase the risk of suicidal tendencies. Careful monitoring of patients taking these drugs is essential to detect any changes in their psycho-emotional state and to prevent more serious outcomes.

Altered Brain Activity and Psychoactive Substances

Changes in brain activity are also directly related to the use of legal and illegal psychoactive substances, such as alcohol. Alcohol is one of the most accessible and widely consumed legal drugs in the world. Its use is associated with temporary alterations in brain activity, which may impair a person’s ability to regulate emotions and behavior. Chronic alcohol abuse is known to contribute to depression and other mental disorders, significantly increasing the likelihood of suicidal tendencies. Research indicates that individuals suffering from alcoholism exhibit substantially higher suicide rates than the general population. This is because alcohol suppresses central nervous system activity and intensifies feelings of hopelessness, which may lead to desperate decisions.

Neurochemical Mechanisms of Action

All of these substances act on neurotransmitters in the brain, such as serotonin, dopamine, and norepinephrine, which play a central role in mood and behavior. For example, alcohol enhances the activity of GABA (gamma-aminobutyric acid), producing relaxation and reduced anxiety. However, chronic alcohol consumption leads to decreased serotonin levels, which is associated with the onset of depression and increased suicide risk. Similar changes occur with other psychoactive substances, which may ultimately result in suicidal outcomes.

Social Context and Legality

The social dimension of legal drugs must not be overlooked. Despite their availability, these substances are often embedded within cultural and social stereotypes, which may in turn reinforce feelings of isolation and hopelessness in individuals already predisposed to depression and suicidal ideation. Moreover, societal pressure and stressors are related to the use of alcohol and tobacco may act as triggers for suicidal behavior.

Why People Without a Genetic Predisposition Do Not Commit Suicide

Studies show that individuals without such predispositions, despite facing existential dilemmas or depressive episodes, are less susceptible to suicide risk because their brain structure and neurochemical composition do not support the mechanisms leading to self-harm.

According to research in psychiatry and genetics, the absence of genetic risk factors or brain injuries may serve as an important safeguard against suicidal tendencies. Even in the presence of depression or life difficulties, such individuals are able to engage alternative stress-coping mechanisms that allow them to avoid suicide. Studies conducted in Sweden have demonstrated that among individuals with no family history of depression or suicide, the probability of suicide is significantly lower – even when they experience psychological challenges in life.

Family Studies and Suicidal Tendencies

Hereditary predisposition to suicidal tendencies is a crucial aspect substantiated by numerous studies in psychiatry and genetics. Some of the most compelling examples of hereditary suicidality are confirmed by family histories and hereditary factors that increase the risk of suicidal thoughts and behavior in descendants. The phenomenon whereby suicide becomes part of a family history may be linked to specific genetic and neurobiological factors that contribute to an elevated susceptibility to depression and suicidal inclinations.

One prominent example is a study conducted in Sweden that examined the role of family history in suicide cases. The analysis revealed that the risk of suicide is significantly higher in children whose parents had died by suicide. This finding supports the existence of a hereditary predisposition to suicidal behavior. Further studies have shown that if both parents suffer from depression or exhibit suicidal tendencies, the likelihood that their children will experience similar problems is markedly increased.

A study conducted in Norway also found that individuals with close relatives who had suffered from depression and suicidal tendencies demonstrated a heightened risk of developing depression and suicidal ideation later in life. Thus, the genetic component may predispose a person to more severe mental disorders, including depression, which is one of the leading factors contributing to suicide.

Methodological Considerations

Most studies of genetic and neurobiological predispositions to suicidal behavior are based on retrospective analyzes of correlations between the presence of certain genetic markers (or brain injuries) and completed suicides or suicide attempts. Such correlational studies cannot establish a strict causal relationship: we observe that a particular genetic variant appears more frequently among individuals who have died by suicide, but we cannot confidently assert that this variant was the cause.

More reliable conclusions require longitudinal cohort studies, in which selected groups of individuals undergo genetic, neuroimaging, and psychological testing long before the onset of suicidal thoughts or behavior, and are then observed over many years. Only such a multidisciplinary approach – combining psychology, neurobiology, and sociology – can reveal how genetic, psychological, and social factors interact, and which of these factors have a decisive influence.

It is also worth noting that many conclusions about the dangers of psychotropic medications are based on retrospective correlational data, which cannot definitively distinguish between the effects of the drug itself and the natural course of depression. For instance, during the initial stage of treatment with selective serotonin reuptake inhibitors (SSRIs), there is often an “activation phase” in which the patient regains enough energy to act before the depressive symptoms begin to recede. This creates a misleading impression of a “suicidogenic” effect of the medication. Moreover, patients prescribed antidepressants are often already in a more severe state, and comparing their suicide risk to that of the general population – without accounting for the depth of their depression – creates the illusion of a direct “antidepressants → suicide” link. Publication bias further exacerbates this effect: cases of suicidal outcomes during treatment are reported far more frequently in the literature than the numerous successful cases of recovery.

At the same time, there is compelling meta-analytic evidence – particularly the study by Kirsch et al. (2008) and subsequent reviews – which indicates the difference in efficacy between antidepressants and placebo is often clinically negligible, especially in cases of mild to moderate depression. These findings call into question the very “efficacy” of SSRIs as a class of drugs and underscore the need for prospective randomized studies with long-term monitoring of patients’ psycho-emotional states in order to determine whether the drug’s benefits truly exceed the natural course of the illness and the effects of placebo.

Ultimately, a proper assessment of the risks and benefits of any psychotropic medication is impossible without multidisciplinary monitoring, which must include genetic and neurobiological markers, psychosocial parameters, and access to crisis intervention services. Only a comprehensive approach can not only balance the therapeutic benefits and potential side effects of pharmacological treatments but also allow for timely adjustment of interventions, thereby minimizing adverse outcomes and reinforcing positive therapeutic effects.

For this reason, I cannot assert with certainty that suicide is solely a product of genetic predisposition – but I am confident in its significant influence on the fundamental question of life and its voluntary end.

Conclusion

If we consider genetics as one of the central risk factors for suicidal behavior, we are forced to rethink traditional philosophical reflections on the existential meaning of life: for many individuals, the question “is life worth living?” is not so much the result of deep personal reflection as it is a manifestation of physiological predispositions rooted in a specific set of genetic and neural mechanisms. However, even this biological perspective cannot be seen as exhaustive. The majority of existing studies, which are based on retrospective correlations, do not allow us to assert a direct causal link between genetic markers or traumatic brain injury and the act of suicide.

To reach more reliable conclusions, we need longitudinal cohort studies and prospective randomized trials in which psychosocial, neurobiological, and pharmacological factors are rigorously monitored over many years.

Although psychotherapeutic interventions can improve overall emotional well-being, they often fail to alter the vulnerability that stems from genetic predisposition. Even with high-quality support, individuals in high-risk groups continue to show elevated mortality rates. At the same time, the role of pharmacological treatment must neither be underestimated nor overstated. The effects of early-phase activation, publication bias, and the severity of patients’ initial mental states often create the illusion of a direct suicidogenic effect of antidepressants, whereas numerous meta-analyses reveal a clinically negligible difference between SSRIs and placebo in cases of mild to moderate depression.

Therefore, real suicide prevention must consist in a system where biological awareness is organically integrated with social policy and public health initiatives: regulation of access to psychoactive substances (including alcohol), improvement in quality of life, expansion of early intervention and crisis services, and the integration of psychological support tailored to individuals’ neurobiological profiles. Only such a comprehensive, multidisciplinary model – one that draws equally on philosophical reflection on the value of life, scientific knowledge about genetics and neurobiology, and practical strategies of social support – can reduce suicide risk and offer those standing on the edge not abstract questions, but concrete paths to survival.

3. Adaptation to meaninglessness

Acceptance of mortality, as discussed earlier, opens the door to an even deeper question: if existence is limited, how can one find meaning in a life devoid of inner purpose? This dilemma, intensified by the awareness of the chaotic nature of the world, forces the mind to seek ways to order and stabilize the perception of reality.

However, the problem of meaninglessness goes beyond simple logic. It affects the emotional and cognitive structures of a person, which often seek to compensate for the awareness of absurdity by creating subjective meanings. These adaptation strategies allow the gap between the finiteness of life and the desire for meaning to become not a catastrophe, but a new starting point.