Владислав Педдер – The Experience of the Tragic (страница 13)

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.