GENETICS AND TRAUMA

Psychogenetics is a broad field that examines the (seemingly invisible yet fundamental) interplay between genes and the imprints left by lived experiences: sometimes unpleasant, other times pleasant, but always impactful.

Each individual responds differently to trauma; while some find themselves trapped in their wounds and scars, others appear to possess an extraordinary capacity for resilience (whether innate or acquired), as if they were equipped with a "biological key" that enables them to overcome even the most disruptive emotional storms.

Behind this diversity lies the complexity of genetic predisposition. The response to trauma is never entirely random.

Various studies reveal that psychological vulnerability in human beings depends on a range of gene variants that determine their biological response to stressful events; some individuals are naturally more inclined to develop mental disorders such as PTSD (Post-Traumatic Stress Disorder), while others seem to “evade” its devastating effects, demonstrating a certain resistance.

This points to a subtle balance between the foundations provided by genetics and the environmental ability

to “write a story.”

Among the phenomena involved, it is important to refer to the so-called DNA methylation, which could even

be considered a kind of “alchemy of trauma.”

It is a process that involves the modification of gene expression without altering the sequence itself, and it represents one of the mechanisms by which the body records its past.

Every psychic upheaval leaves a trace on the cells, altering gene activity and changing the way the organism responds to new challenges. This epigenetic mechanism allows us to understand how traumas not only leave a mark, but can (often profoundly) transform one’s biological predispositions since DNA is not a static entity, but rather a palimpsest that rewrites its expression through life events.

The clinical implications of these discoveries are noteworthy, as they allow us to adopt a new perspective on the treatment of psychological disorders one that acknowledges the need for each therapeutic path to be tailored not only to the individual’s personal history, but also to their genetic makeup which, if adequately analysed and understood, can provide a multitude of insights useful not only for healing and recovery, but also for prevention and advancement.

Through my work, I have had the opportunity to observe and experience how the application of targeted therapies (integrating pharmacological and psychotherapeutic approaches that directly engage with epigenetic mechanisms)makes it possible to design more effective and personalised treatments.

Further Insights and Clarifications

In the methylation process, methyl groups (-CH₃) are added to specific DNA bases; typically cytosines, one of its four fundamental components (nitrogenous bases).

As previously mentioned, this addition does not alter the DNA sequence, but changes gene expression; in practice, when a cytosine is methylated, it can inhibit the activity of a specific gene, making it either partially active or completely silent.

This occurs thanks to enzymes known as DNA methyltransferases, and it happens particularly in certain regions

of the DNA, such as gene promoters, which are crucial for activating or deactivating genes; essentially a kind of molecular “switch.”

This mechanism is closely linked to environmental factors and others such as stress and lifestyle, and it therefore significantly affects the psycho-biological response of living beings.

It is one of the reasons why trauma can “write” on DNA, leaving a trail that may persist over time.

So, is it something negative that should be counteracted? Absolutely not.

We are referring to a natural and essential system that constantly occurs within the body.

It doesn’t take place only as a result of external factors and traumatic events, but is part of the body’s innate regulatory process. It is necessary for proper cellular function and genomic stability.

During embryonic development, for instance, it determines cellular differentiation.

It is also essential for X chromosome inactivation in females, so that only one of the two X chromosomes

is active in each cell.

Problems arise when methylation becomes dysregulated; it can be either excessive or insufficient in specific areas. When it is excessive, it can silence protective genes, such as those that regulate the stress response (like FKBP5, which balances the reaction to cortisol, and BDNF). When insufficient, it may anomalously activate genes that should remain silent. This dysregulation is frequently implicated in conditions and disorders such as PTSD, depression, and certain forms of cancer.

Balance, once again, plays a central role and shows how the same physiological-functional process can take on opposing connotations if disrupted.

Recent studies have enabled us to identify several genetic polymorphisms involved in responses to stress and emotional regulation; specific alleles can increase vulnerability to developing multiple psychopathologies.

Gene variants of COMT (catechol-O-methyltransferase) and MAOA (monoamine oxidase A) can predispose individuals to greater emotional reactivity.

There are also alternative versions that, conversely, activate genetic resilience mechanisms that endow individuals with the ability to overcome trauma without developing permanent psychological disorders.

By promoting neuroplasticity, they encourage more adaptive responses.

Such is the case of the BDNF gene (Brain-Derived Neurotrophic Factor), already mentioned, which is particularly relevant here, as it is involved in neuronal growth and survival; increased expression enhances psychological recovery. Genes like OXTR, which encodes the oxytocin receptor, also play a crucial role in the formation of emotional bonds and social behaviour.

(Polymorphisms, in general, perform a key function in inducing the susceptibility of organic responses to both endogenous and exogenous stimuli. Therefore, identifying an individual’s specific polymorphisms enables clinicians to evaluate or estimate their specific risk increase.

SNPs (Single Nucleotide Polymorphisms), for instance, may influence various biological processes: leading, depending on the case, to greater or lesser production of a given protein than the norm; or altering the efficiency of the proteins produced, which may become dysfunctional or more prone to instability.

Some of these SNPs can influence the way drugs are metabolised; sensitivity to food and skin intolerances; predisposition to rheumatic, neurological, metabolic, and cardiovascular diseases.

Others affect the tissues’ ability to use glucose appropriately, with inevitable metabolic consequences.

A further group contributes to the effectiveness of substances involved in the body’s defence processes against oxidative damage [mediated by the so-called “free radicals,” if produced excessively] and/or inflammatory activity.)

Epigenetic plasticity, which allows for the flexibility of gene expression in response to the environment, is fundamental to understanding how biology and context interact.

Exposure to positive experiences is more likely to foster flexibility, thereby enhancing adaptive capacity.

Traumatic experiences, on the other hand, can alter methylation patterns of genes related to these abilities.

Research has also revealed that therapeutic interventions themselves can modify such patterns, highlighting

the transient nature of epigenetic reprogramming.

- 𝐷𝑟. 𝑉𝑎𝑙𝑒𝑟𝑖𝑎 𝐺ℎ𝑖𝑠𝑢

𝑆𝑝𝑒𝑐𝑖𝑎𝑙𝑖𝑠𝑡 𝑖𝑛 𝑃𝑠𝑦𝑐ℎ𝑜-𝐺𝑒𝑛𝑒𝑡𝑖𝑐𝑠