THE EPIGENETIC SCARS OF MODERN LIFE: INTERTWINING STRESS, TECHNOSTRESS, AND HEALTH IN THE CONTEMPORARY WORLD

Liviu Poenaru, PhD & Stefania Ubaldi, PhD, MD

June 22, 2025

ABSTRACT

Context and Problematics
In today’s hyperconnected world, chronic stress is no longer confined to traditional psychosocial stressors; it has expanded into the digital sphere through phenomena such as technostress, information overload, and the collapse of work–life boundaries. Recent advances in epigenetics underscore how persistent stress—both biological and psychological—can leave molecular traces on the genome, influencing health across the lifespan and even transgenerationally. Yet, the specific epigenetic effects of digital stressors remain underexplored. The convergence of psychosocial stress and technostress represents a profound challenge for understanding the new biological burdens imposed by contemporary lifestyles. These forms of stress may act synergistically to disrupt physiological regulation and accelerate biological aging, but their epigenetic imprint is still insufficiently mapped and rarely integrated into mental health frameworks.

Aims
This work aims to examine the biological embedding of chronic psychosocial and technostress by evaluating their impact on epigenetic mechanisms, especially DNA methylation, histone modification, and telomere length. It also seeks to establish whether digital stressors such as techno-overload, techno-invasion, and information fatigue are plausible modulators of the epigenome, akin to more established stressors like trauma and low socioeconomic status. Furthermore, the study explores the differential vulnerability of populations—particularly older adults, remote workers, and youth—who are increasingly exposed to digital stress environments, and evaluates the role of protective factors such as mindfulness and organizational health practices.

Method
This is a comprehensive interdisciplinary review synthesizing data from neuroscience, psychology, public health, and molecular biology. Over 150 peer-reviewed articles and systematic reviews were analyzed, covering topics such as stress physiology, psychoneuroimmunology, epigenetic regulation, technostress typologies, and mental health outcomes. The review includes recent studies on biomarkers such as cortisol, inflammatory cytokines, C-reactive protein, and epigenetic clocks. Particular attention was given to longitudinal studies, controlled interventions (e.g., mindfulness, digital detox), and mechanistic models linking stress exposure to molecular changes.

Results
Technostress consistently correlates with burnout, depression, anxiety, and reduced well-being. Physiological studies demonstrate dysregulation of the HPA axis, elevated sympathetic activity, and emerging links with altered cortisol levels and inflammatory responses. Although direct studies on epigenetic effects are limited, converging evidence from high-tech work environments, sleep disruption, and cognitive overload points to plausible epigenetic mechanisms. Data from the PROAGEING study and recent findings on digital strain in youth and aging populations suggest associations between technostress and biological aging markers, such as telomere shortening and differential methylation in stress-related genes (e.g., NR3C1, BDNF). Protective interventions, including mindfulness and supportive organizational structures, show promise in mitigating both psychological and physiological damage.

Interpretations
The findings strongly support the view that technostress is not merely a psychological or ergonomic inconvenience, but a biologically active stressor capable of interacting with core regulatory systems and potentially shaping gene expression through epigenetic pathways. Modern stress must now be reconceptualized to include digital exposures as a critical determinant of health. This shift has significant implications for public health, occupational medicine, and preventive strategies targeting the root causes of stress-related illness. The study calls for an urgent expansion of epigenetic research frameworks to incorporate digital lifestyle variables and to treat technostress as a core component of environmental risk.

1. Introduction: the converging streams of modern stress, technology, and epigenetic regulation

The contemporary human experience is increasingly characterized by a confluence of pervasive stressors, many of which are amplified or directly generated by the ubiquitous presence of technology. This exploration aims to dissect the intricate relationships between epigenetics, a field illuminating how environmental factors modulate gene expression without altering the DNA sequence itself; stress, in its myriad forms; and the burgeoning phenomenon of technostress. The central objective is to analyze their interplay and delineate the profound implications for human health in the modern world, drawing upon an extensive body of research.

The escalating prevalence of both general life stressors—ranging from psychosocial challenges and environmental toxins to metabolic disturbances—and the pervasive integration of digital technologies into nearly every facet of existence forms a critical backdrop to this analysis. While the scientific community has robustly documented the capacity of diverse stressors to imprint upon the epigenome, thereby influencing health trajectories, the specific epigenetic impact of technostress remains a frontier of active and pressing investigation.

The modern individual navigates a unique stress landscape, where technology frequently acts as both a direct source of stress and a powerful mediator of other stressors. This "always-on" culture, characterized by information overload and the relentless pace of technological change, necessitates a deeper understanding of its biological, and specifically epigenetic, consequences. Such an understanding is paramount for developing effective public health strategies and interventions tailored to the realities of the 21st century.

Our analysis will first lay the foundational principles of epigenetic regulation, detailing key mechanisms such as DNA methylation, histone modifications, non-coding RNA activity, and telomere dynamics. Subsequently, it will explore the documented impacts of various stressors on these epigenetic mechanisms and their associated health outcomes. The nature and consequences of technostress will then be defined and examined. Following this, a critical analysis will correlate the domains of general stress, technostress, and epigenetic alterations, highlighting both established links and areas requiring further research. Finally, we will contextualize these findings within the broader milieu of contemporary stressors and discuss pathways toward resilience, intervention, and future research imperatives.

2. Method

The comparative analysis of the two PubMed corpora—one focusing on epigenetics and stress, the other on technostress and stress—was conducted using a mixed-methods approach that integrates quantitative lexical analysis, topic modeling, and interdisciplinary interpretation. Each corpus was built using targeted PubMed E-utilities queries: "epigenetics AND stress" for the biomedical dimension and "technostress AND stress" for the psychosocial dimension. Titles and abstracts were extracted and formatted as CSV files with PMID, Title, and Abstract fields. Texts were preprocessed through lowercasing, punctuation and stopword removal, and lemmatization to standardize the lexical input. Frequency and TF-IDF analyses were used to map the dominant lexical fields, while co-occurrence analysis helped reveal recurrent conceptual pairs within each dataset.

To move beyond lexical patterns, topic modeling was applied using Latent Dirichlet Allocation (LDA) to extract recurring semantic structures and dominant conceptual axes within each corpus. These probabilistic clusters allowed for a thematic segmentation of the abstracts and revealed how each domain structures its discourse on stress. Dimensionality reduction techniques such as PCA or t-SNE were used to project these thematic clusters into visual spaces, complemented by unsupervised clustering methods like K-means and DBSCAN to assess semantic cohesion. Co-occurrence networks were also generated using graph-theoretical models to highlight central terms—such as DNA methylation or digital overload—and to identify thematic hubs and bridges across articles.

In a final interpretive phase, the analysis drew from multiple disciplinary perspectives including neuroscience, occupational health, clinical psychology, and digital sociology. This allowed for a critical comparison of the conceptual infrastructures shaping how stress is defined, studied, and explained in each field. While the epigenetic corpus emphasized molecular mechanisms (e.g., DNA methylation of genes like NR3C1 or SLC6A4), the technostress corpus highlighted digital labor stressors like information overload and techno-invasion. These divergences and latent convergences were assessed to explore whether technostress, despite its psychosocial framing, might share biological pathways with chronic stress—a hypothesis not yet explored in the literature but emerging here as a promising direction for future research. Overall, this method enabled a synthetic biopsychosocial interpretation of stress across domains.

3. Foundations of epigenetic control: modulators of gene expression and health

Epigenetic mechanisms are pivotal in orchestrating gene expression patterns that are fundamental to development, cellular differentiation, and responsiveness to environmental cues. These mechanisms, which do not alter the underlying DNA sequence, provide a vital interface between an individual's genome and their environment, including exposure to stress. Understanding these foundations is essential to appreciate how stressors, including those emanating from the technological environment, can sculpt long-term health and disease trajectories.

3.1. DNA methylation and epigenetic clocks

DNA methylation is one of the most extensively studied epigenetic modifications, involving the addition of a methyl group to a cytosine residue, predominantly within cytosine-phosphate-guanine (CpG) dinucleotides.1This process is catalyzed by DNA methyltransferases (DNMTs) and can be reversed by demethylases (Jones & Takai, 2001; Portela & Esteller, 2010). Generally, methylation in promoter regions of genes is associated with transcriptional repression or gene silencing, as it can impede the binding of transcription factors or recruit methyl-CpG-binding proteins that promote a condensed chromatin state. Aberrant DNA methylation patterns, characterized by either hypermethylation (increased methylation) or hypomethylation (decreased methylation) at specific genomic loci, are deeply implicated in the pathogenesis of a wide array of human diseases. For instance, increased promoter methylation leading to the silencing of tumor suppressor genes is a hallmark of many cancers (Esteller, 2008). Similarly, dysregulated DNA methylation contributes to neurodegenerative disorders like Alzheimer's and Parkinson's diseases, and plays a role in cardiovascular conditions, potentially through mechanisms like endothelial dysfunction and inflammation associated with gestational diabetes mellitus (GDM).

Building upon the understanding of DNA methylation's role in aging and disease, researchers have developed "epigenetic clocks." These are algorithms that use DNA methylation levels at specific CpG sites across the genome to estimate biological age. Deviations between epigenetic age and chronological age can indicate accelerated or decelerated aging. Epigenetic age acceleration (EAA), where epigenetic age is greater than chronological age, has been linked to various stressors and adverse health outcomes (Horvath & Raj, 2018; Galkin et al., 2020). Different clocks, such as PhenoAge, GrimAge2, DunedinPACE, and measures like DNAmTL (DNA methylation-based telomere length), have been developed and associated with cumulative stress, psychosocial factors, and clinical conditions (Levine et al., 2018; Lu et al., 2019). In patients with early-onset psychosis, accelerated epigenetic age—measured by Wu’s clock—was significantly associated with chronological age (PedBE clock), global functioning, psychiatric admissions (DNAmTL), and years of schooling (Levine’s clock) (Montiel et al., 2023).

3.2. Histone modifications

Histones are proteins around which DNA is wrapped, forming chromatin. Post-translational modifications of these histone proteins, such as acetylation, methylation, phosphorylation, and ubiquitination, constitute another major layer of epigenetic regulation (Kouzarides, 2007). These modifications occur primarily on the N-terminal tails of histones and can alter chromatin structure, making DNA more or less accessible to the transcriptional machinery, thereby activating or repressing gene expression. For instance, histone acetylation, mediated by histone acetyltransferases (HATs), generally neutralizes the positive charge of lysine residues, leading to a more open chromatin structure and transcriptional activation. Conversely, histone deacetylases (HDACs) remove acetyl groups, promoting chromatin condensation and gene silencing. Similarly, histone methylation can be activating or repressive depending on the specific lysine or arginine residue methylated and the number of methyl groups added.

The "histone code" hypothesis posits that specific combinations of histone modifications are read by other proteins to bring about distinct downstream events.1 Dysregulation of histone modifications is implicated in human diseases, including neurodegenerative conditions where HDAC inhibitors are being explored as therapeutic agents 1, and in age-related macular degeneration (AMD), where histone acetylation influences angiogenesis and inflammation.1 In plants, histone modifications are crucial for development and orchestrating responses to various stresses (Strahl & Allis, 2000). For example, the multiprotein complex HOS15-PWR-HDA9 plays a well-documented role in regulating the acetylation status of histone H3 at target genes during plant development and in response to environmental stresses, thereby facilitating appropriate gene expression or repression (Ali, Zareen, & Yun, 2025).

3.3. The role of non-coding RNAs (ncRNAs)

Non-coding RNAs (ncRNAs) are RNA molecules that are not translated into proteins but have significant regulatory functions in the cell. They are broadly classified based on their size and function, with microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and tRNA-derived small RNAs (tsRNAs) being prominent examples relevant to stress and epigenetic regulation (Anastasiadou, Jacob, & Slack, 2018).

MicroRNAs (miRNAs) are small (typically 20-24 nucleotides) ncRNAs that primarily regulate gene expression post-transcriptionally by binding to complementary sequences in messenger RNAs (mRNAs), leading to mRNA degradation or translational repression (Bartel, 2009). miRNAs are increasingly recognized as sensitive biomarkers of environmental exposures and are involved in a multitude of biological processes, including inflammation, oxidative stress, apoptosis, and DNA repair (Letelier et al., 2023). Dysregulation of specific miRNAs has been linked to various diseases. For instance, altered expression of miRNAs like miR-34a, miR-140, miR-455-3p, and miR-1273g-3p is implicated in mitochondrial dysfunction and the pathology of Alzheimer's disease. Exposure to environmental hazards can induce changes in miRNA profiles, contributing to disease development (Seyedaghamiri et al., 2025; Kumar & Reddy, 2018).

Long non-coding RNAs (lncRNAs) are a diverse class of ncRNAs longer than 200 nucleotides. They can regulate gene expression through various mechanisms, including chromatin remodeling, transcriptional interference, and post-transcriptional processing. Their functions are still being extensively explored, but evidence points to their involvement in plant stress responses, development, and metabolism. In humans, lncRNAs are implicated in the epigenetic regulation of diseases like chronic kidney disease (CKD) (He & Li, 2025; Chen, Zhu, & Kaufmann, 2020).

tRNA-derived small RNAs (tsRNAs) are a newer class of ncRNAs generated from the cleavage of transfer RNAs (tRNAs). They are categorized into tRNA-derived stress-induced RNAs (tiRNAs; 29-50 nt) and tRNA-derived fragments (tRFs; 14-40 nt).1 These molecules are emerging as important regulators in response to abiotic stress in plants, influencing stress signaling pathways and epigenetic modifications. They can modulate gene expression at transcriptional, post-transcriptional, and translational levels (Martinez, Choudury, & Slotkin, 2017).

3.4. Telomeres as markers of cellular aging and stress

Telomeres are specialized nucleoprotein structures at the ends of eukaryotic chromosomes, vital for maintaining genomic stability by protecting chromosome ends from degradation and fusion (Blackburn, 2001). Due to the "end-replication problem," telomeres naturally shorten with each cell division. Thus, telomere length (TL) is widely regarded as a biomarker of cellular aging (Harley, Futcher, & Greider, 1990). Critically short telomeres can trigger cellular senescence or apoptosis (d'Adda di Fagagna et al., 2003).

Various factors, notably oxidative stress and chronic inflammation, can accelerate the rate of telomere shortening (von Zglinicki, 2002). Shorter telomere length has been associated with an increased risk for a range of age-related diseases, as well as increased morbidity and mortality (Cawthon et al., 2003). The enzyme telomerase can elongate telomeres, but its activity is tightly regulated and often low in most somatic cells. Stress-induced telomere damage is considered an important pathway through which chronic psychological stress can lead to disease (Epel et al., 2004).

These diverse epigenetic mechanisms—DNA methylation, histone modifications, non-coding RNA activities, and telomere dynamics—do not operate in isolation. Instead, they form a complex, interconnected regulatory network. Stressors, whether psychological, environmental, or physiological, can impact multiple mechanisms simultaneously or sequentially. This can lead to a cascade of changes in gene expression that ultimately underpin the development and progression of various health conditions. The research frequently highlights the co-occurrence of alterations in several epigenetic mechanisms in response to a single stressor or in the context of a specific disease. Neurodegenerative diseases involve aberrant DNA methylation, histone modifications, and dysregulated non-coding RNAs. This interconnectedness underscores the holistic nature of the epigenome's response to environmental perturbations and is critical for understanding the comprehensive impact of stress on health.

4. Stress and the epigenome: documented impacts of diverse stressors

The epigenome serves as a dynamic interface between an individual's genetic makeup and their environment, translating experiences, particularly stressful ones, into lasting alterations in gene activity. A substantial body of research demonstrates that various forms of stress—ranging from acute psychosocial challenges to chronic environmental exposures and internal physiological imbalances like oxidative stress—can induce specific and often enduring epigenetic modifications. These modifications, in turn, are increasingly linked to a wide spectrum of health consequences, influencing susceptibility to disease and the overall aging process.

4.1. Psychosocial stress and epigenetic signatures

Psychosocial stressors, encompassing a wide range of adverse experiences from early life through adulthood, exert a profound influence on epigenetic landscapes.

Cumulative life stress: The burden of lifelong cumulative stressors, aggregated across multiple domains such as work, relationships, and finances, has been associated with epigenetic age acceleration (EAA) (Zannas et al., 2015). Notably, one study utilizing data from the Midlife in the United States (MIDUS) Genomics Project found that higher levels of cumulative stressors were significantly linked to EAA, as measured by the GrimAge2 epigenetic clock, particularly among individuals with lower levels of psychological well-being or higher neuroticism (Cha et al., 2025). Conversely, EAA in individuals with higher psychological well-being or lower neuroticism was not significantly impacted by cumulative stress levels, highlighting the moderating role of psychological assets and vulnerabilities.

Early-life adversity (ELA): Experiences of adversity during critical developmental periods, such as childhood abuse, neglect, or significant household dysfunction, are particularly potent in shaping long-term health trajectories (Tyrka et al., 2012). Epigenetic modifications, especially DNA methylation, are proposed as key mechanisms mediating these enduring effects. ELA has been linked to altered epigenetic aging and an increased risk for later-life mortality, morbidity, and various diseases (Jovanovic et al., 2017). A consistent finding in this area involves altered DNA methylation of the NR3C1 gene, which encodes the glucocorticoid receptor crucial for stress hormone regulation. Maltreatment and ELA have been robustly associated with changes in NR3C1 methylation, particularly in exon 1F (Turecki & Meaney, 2016; Perroud et al., 2011).

Trauma and post-traumatic stress disorder (PTSD): Severe traumatic experiences can leave lasting epigenetic marks. Studies on intimate partner violence (IPV), a severe form of trauma, point to epigenetic modifications as one of the molecular mechanisms underlying the development of stress-related disorders in victims (Radtke et al., 2011). In animal models of PTSD, exposure to stressors like foot shocks has been shown to induce significant alterations in N6-methyladenosine (m6A) RNA methylation in the ventral hippocampus, a brain region critical for stress and emotional regulation (Engel et al., 2018). Deep brain stimulation (DBS) of the basolateral amygdala, a potential treatment for PTSD, was found to reverse some of these aberrant methylation changes, suggesting a dynamic interplay between stress, epigenetic marks, and therapeutic interventions (Ma et al., 2025).

Social stress & discrimination: Chronic social stressors, including experiences of racial discrimination, are increasingly recognized for their biological toll. Research indicates that such experiences are associated with accelerated biological aging, as measured by various DNA methylation-based epigenetic clocks like PhenoAge, GrimAge, and DunedinPACE. One study found that among African American mothers who did not seek social support, experiences of racial discrimination were linked to an older PhenoAge; however, social support seeking appeared to mitigate this risk (Nyembwe, 2025). Social discrimination, as a form of chronic psychological stress, also has a complex relationship with telomere length. While direct associations are mixed, discrimination may interact with other factors such as depressive symptoms, acculturation processes, and coping mechanisms (like not discussing discrimination experiences) to contribute to telomere shortening (Chae, 2016).

4.2. Oxidative stress, inflammation, and their epigenetic consequences

Physiological stressors, particularly oxidative stress and chronic inflammation, are potent drivers of epigenetic change and are implicated in numerous pathological conditions.

Oxidative Stress: Oxidative stress arises from an imbalance between the production of reactive oxygen species (ROS) and the body's antioxidant defense capacity. This imbalance can damage cellular components, including DNA, and is a well-established inducer of epigenetic alterations (Shin et al., 2011). The oxidative DNA lesion 8-hydroxy-2'-deoxyguanosine (8-OHdG) can disrupt DNA methylation patterns, histone modifications, and the function of small non-coding RNAs, particularly in sensitive contexts like sperm development, thereby influencing fertilization and offspring health (Valavanidis et al., 2009; Aitken & De Iuliis, 2010). Oxidative stress is a common mechanistic thread in various conditions linked to epigenetic changes, including gestational diabetes mellitus (GDM) (Ruchat et al., 2013), cardiovascular diseases programmed by intrauterine growth restriction (IUGR) (Gheorghe et al., 2010), chronic kidney disease (CKD) where it contributes to mitochondrial dysfunction and fibrosis (Dounousi et al., 2006). In neurodegenerative diseases, oxidative stress exacerbates neuronal damage and has been shown to influence the epigenetic regulation of genes involved in neuroprotection (García-Giménez et al., 2017). Environmental pollutants can trigger oxidative stress by activating pathways like the aryl hydrocarbon receptor (AhR)/cytochrome P450 family 1 (CYP1) cascade, which in turn leads to epigenetic modifications (aberrant DNA methylation, histone alterations, miRNA dysregulation) that contribute to metabolic disorders such as diabetes mellitus (Hou et al., 2012).

Inflammation: Chronic inflammation, often intertwined with oxidative stress, is another major driver of epigenetic dysregulation and is a hallmark of aging—commonly referred to as "inflammaging"—as well as many chronic diseases (Franceschi et al., 2018). There is growing evidence that paternal exposure to infection or inflammation can lead to epigenetic reprogramming in offspring, potentially priming their immune systems in early life (Gapp et al., 2014). In neurodegenerative conditions like Alzheimer’s disease (AD) and Parkinson’s disease (PD), inflammatory pathways are significantly dysregulated, with transcription factors such as NF-κB1 playing a central role in modulating both pro-inflammatory and neuroprotective processes, often through epigenetic interactions (Glass et al., 2010). Systemic chronic low-grade inflammation, often measured by biomarkers like C-reactive protein (CRP), has been robustly associated with widespread DNA methylation signatures at numerous CpG sites across the genome. These inflammation-linked methylation patterns are, in turn, associated with an increased risk for complex diseases, including cardiometabolic and neuropsychiatric disorders (Ligthart et al., 2016).

4.3. Key biological pathways mediating stress-induced epigenetic changes

The translation of stressful experiences into epigenetic modifications is mediated by several interconnected biological systems.

Hypothalamic-Pituitary-Adrenal (HPA) Axis: The HPA axis is the body's central stress response system. Chronic stress leads to its dysregulation, resulting in altered patterns of cortisol secretion. Cortisol, a glucocorticoid hormone, can cross the blood-brain barrier and bind to glucocorticoid receptors (GRs) in various tissues, including the brain. This binding can directly or indirectly influence the activity of epigenetic modifying enzymes, leading to changes in DNA methylation and histone modifications at specific gene loci (Zannas & West, 2014). For example, prenatal stress-induced HPA axis dysregulation in the mother can lead to altered cortisol exposure for the fetus, a key mechanism driving epigenetic modifications in the developing offspring with long-term consequences for behavior, cognition, and psychopathology (Palma-Gudiel et al., 2015; Braithwaite et al., 2017). The methylation status of the NR3C1 gene, which encodes the glucocorticoid receptor, is itself a well-established target of stress-induced epigenetic modification, creating a potential feedback loop that can perpetuate HPA axis dysfunction (Turecki & Meaney, 2016).

Sympathetic nervous system (SNS): The SNS is the other major arm of the physiological stress response, responsible for the rapid "fight-or-flight" reaction, mediated by catecholamines like adrenaline and noradrenaline. Chronic activation of the SNS, often occurring alongside HPA axis dysregulation, can also contribute to the milieu of cellular changes that influence epigenetic programming—for instance, by promoting inflammation or oxidative stress (Powell et al., 2013).

Immune system modulation: Stress has profound effects on the immune system, often leading to a state of chronic low-grade inflammation. Immune cells release cytokines and other inflammatory mediators that can directly influence cellular processes, including the activity of epigenetic enzymes. This stress-induced immune dysregulation and subsequent inflammation are critical pathways through which stressors like social discrimination or paternal infection can drive epigenetic changes, impacting both the individual and potentially future generations (Cowan, Callaghan, & Richardson, 2013).

Diverse stressors, therefore, appear to converge upon the epigenome. Whether originating from psychosocial trauma in early life, the cumulative burden of adult stressors, exposure to environmental toxins, or internal physiological states like oxidative stress and chronic inflammation, these adverse exposures often recruit common biological pathways—most notably HPA axis dysregulation and immune system activation. These pathways, in turn, orchestrate changes in DNA methylation, histone modifications, and non-coding RNA profiles. The epigenome thus acts as a biological ledger, recording these experiences and translating them into altered gene expression programs that can predispose individuals to a wide spectrum of diseases, from mental health disorders to cardiovascular disease and cancer. This convergence suggests a fundamental role for epigenetic mechanisms in mediating the long-term impact of stress on human health.

5. Technostress: defining the digital age's unique burden

In an era increasingly dominated by digital technologies, a novel form of stress has emerged, termed "technostress." This phenomenon, born from our complex interactions with Information and Communication Technologies (ICTs), represents a significant and growing concern for individual well-being and organizational health. Understanding its definition, primary creators, and its psychological and physiological impacts is crucial for contextualizing its potential role in the broader landscape of modern stressors that may influence epigenetic pathways.

5.1. Defining technostress

Technostress is broadly defined as an unhealthy condition, a state of stress, or a negative psychological response induced by the use of, introduction to, or threat of information and communication technologies (ICTs), particularly in the workplace, or more generally, the difficulty in coping with these technologies (Tarafdar et al., 2007). It is recognized as a psychosocial phenomenon where the demands associated with technology use exceed an individual's adaptive capacities, leading to detrimental health effects and a strain on their ability to function effectively (La Torre et al., 2019). This stress can manifest when individuals struggle to adapt to new technologies or when existing technologies create overwhelming demands.

5.2. Creators of technostress (techno-stressors)

Research has identified several distinct factors, often referred to as "techno-stressors" or "technostress creators," that contribute to the experience of technostress (Tarafdar et al., 2007) These include:

Techno-overload: This refers to situations where technology forces individuals to work faster, handle more information, or manage an excessive workload, leading to feelings of being overwhelmed. It is a common experience for employees in various sectors, including healthcare and IT.
Techno-invasion: This describes the blurring of boundaries between work and personal life due to the pervasive nature of ICTs, leading to a sense of constant connectivity and the feeling that technology is encroaching upon one's private time and space. This is a significant issue for remote workers and those who use technology extensively for communication.
Techno-complexity: This arises from the difficulty individuals experience in understanding and effectively using complex technologies, leading to feelings of inadequacy and frustration. This is particularly relevant for older workers or those less familiar with new digital tools.
Techno-insecurity: This involves the fear that one's job skills are becoming obsolete due to technological advancements, or concerns about job loss to automation. It can also encompass anxieties related to data privacy and security in the digital realm.
Techno-uncertainty: This stems from the continuous and rapid changes and updates in technology, creating a sense of instability and uncertainty about future skill requirements and the relevance of current technological knowledge.
Work interruptions & multitasking: Frequent disruptions caused by notifications, alerts, and the expectation of immediate responses, coupled with the demand to handle multiple digital tasks simultaneously, are significant stressors.
Information overload: Distinct from techno-overload (which relates to workload), this refers to being inundated with an excessive volume of information from digital sources, making it difficult to process, prioritize, and act upon.
Lack of technical support & unreliability: Insufficient assistance when encountering technological problems, or technology that frequently malfunctions or does not perform as expected, leads to frustration and stress.
Other specific stressors: Additional stressors identified in specific contexts include digital visibility (the pressure of being constantly seen online), comparison pressure (feeling compelled to compare oneself to others via digital platforms), and permanent monitoring (the sense of being constantly watched or tracked through technology). Schedule overload, perceived uselessness of technology, and a feeling of compulsion to use technology have also been noted.

5.3. Psychological correlates of technostress

The psychological toll of technostress is well-documented across various populations and occupational contexts. La Torre et al. (2019) highlight general impacts such as reduced job and life satisfaction, diminished productivity, and associations with psychological or behavioral disturbances. More specifically, Borle et al. (2021) have shown that technostress is positively associated with a range of adverse mental health outcomes:

Burnout: This is one of the most consistently reported consequences of technostress. Studies involving nurses, general practitioners, bank employees, dermatologists, university faculty, and other workers have demonstrated a significant positive association between various technostress creators and increased symptoms of burnout, such as emotional exhaustion, mental distance from work (cynicism), and reduced personal accomplishment.
Anxiety: Technostress is significantly linked to heightened levels of anxiety. This has been observed in university students adapting to technology-enhanced learning, remote workers during the COVID-19 pandemic, and employees experiencing telepressure (the urge to respond quickly to electronic messages).
Depression: Some research also indicates an association between technostress and depressive symptoms, particularly when mediated by factors like burnout or in vulnerable populations such as university students.
Reduced job satisfaction: A negative correlation between technostress and job satisfaction has been found among professionals like general practitioners, dentists, and hospital physicians, indicating that technology-related stress can diminish overall contentment with one's work.
Mental fatigue and decreased psychological well-being: Technostress contributes to mental fatigue, especially in demanding contexts like teleworking, and can lead to a general decline in psychological well-being, manifesting as frustration, lower confidence, and self-doubt.
Work-privacy conflict: The techno-invasion aspect of technostress, characterized by constant accessibility, significantly contributes to conflict between work responsibilities and private life, hindering recovery and regeneration.
Reduced work engagement: Technostress can diminish employees' enthusiasm and dedication to their work, leading to decreased work engagement.

5.4. Physiological correlates of technostress

Beyond psychological effects, technostress has also been linked to measurable physiological stress responses, suggesting a biological embedding of this modern stressor.

Hypothalamic-Pituitary-Adrenal (HPA) axis activity (cortisol): Evidence regarding HPA axis involvement in technostress is emerging. A prospective study by Kaltenegger et al. (2024) involving hospital employees found that higher baseline levels of technostress—particularly work interruptions, multitasking, and information overload—were negatively associated with hair cortisol concentrations (HCC) six months later. This suggests not a classic hyperactivation of the stress response, but rather a potential blunting or dysregulation of the HPA axis over time. In a complementary study among Egyptian university staff, Kasemy et al. (2022) found that most technostress subscales were significantly correlated with elevated blood cortisol levels, reinforcing the association between sustained ICT-related stress and physiological stress responses.
Sympathetic Nervous System (SNS) activation: Technostress triggers physiological stress responses via SNS activation. In experimental settings, multitasking and work interruptions consistently elevate salivary alpha-amylase (sAA)—a reliable marker of sympathetic nervous system activity—indicating acute stress effects from digital task overload (Becker et al., 2022). Additionally, unexpected technology behaviors, such as system delays during decision-making tasks, have been shown to alter physiological arousal: they decrease skin conductance levels and produce curvilinear changes in heart rate (BPM) and heart rate variability (HRV), reflecting complex stress responses to digital unpredictability (Korosec-Serfaty et al., 2022).
Inflammation (C-Reactive Protein - CRP): The direct link between technostress and systemic inflammation remains inconclusive. A cross-sectional study among university hospital employees (Kaltenegger, 2023) found no significant association between various technostressors (e.g., information overload, work interruptions) and high-sensitivity C-reactive protein (hs‑CRP) levels, although these stressors were associated with burnout symptoms—which themselves can involve inflammatory pathways. In a prospective follow-up study by Kaltenegger et al. (2024), baseline technostress was again not significantly linked to CRP levels at six months; however, the researchers noted reciprocal effects between CRP and hair cortisol concentrations (HCC), indicating complex interplay between inflammatory and HPA-axis markers.
Musculoskeletal pain: While not a direct measure of core stress systems, musculoskeletal disorders (MSDs) frequently arise from prolonged ICT use—especially due to static postures and repetitive movements—and can amplify stress effects. A recent cross-sectional study of bank employees found that those with MSDs experienced significantly higher levels of technostress-induced burnout, illustrating how physical strain can moderate the relationship between technostress and psychological outcomes (Kutlutürk Yıkılmaz et al., 2024).

Technostress is clearly not a singular, ill-defined discomfort but rather a multifaceted syndrome resulting from a range of specific, identifiable technology-related pressures. Such pressures elicit well-characterized psychological responses, including burnout and anxiety, and are increasingly associated with physiological stress activation, particularly through the HPA axis and the sympathetic nervous system. The reactivity profiles observed in technostress contexts closely resemble those linked to other well-established chronic stressors. This convergence is significant, as it provides compelling grounds to hypothesize that technostress—like long-term psychosocial adversity—may induce lasting epigenetic modifications, thus establishing a plausible mechanistic pathway from the digital environment to enduring health consequences. By precisely mapping the sources and manifestations of technostress, researchers can better understand how various dimensions of human-technology interaction contribute to pathogenic processes.

6. Bridging the divide: correlating technostress with epigenetic alterations

The connection between technostress and epigenetic modifications, while an area of emerging direct investigation, can be substantially inferred from the well-established links between chronic psychosocial stress, its physiological sequelae, and epigenetic changes. Technostress, with its documented capacity to induce chronic psychological distress and perturb physiological stress systems, stands as a prime candidate for influencing the epigenome.

6.1. Technostress as a chronic psychosocial stressor: inferring epigenetic impact

The spectrum of psychological outcomes associated with technostress—such as persistent burnout, chronic anxiety, and depressive symptoms—closely mirrors the profiles observed in individuals experiencing various forms of chronic psychosocial stress (Borle et al., 2021). Likewise, physiological responses linked to technostress—namely HPA axis dysregulation (as reflected in altered cortisol levels), heightened sympathetic nervous system (SNS) activation, and the potential for increased inflammation and oxidative stress—are well-established features of the body’s response to enduring stressors (Kaltenegger et al., 2024).

Given that chronic stress from various sources is a well-established modulator of epigenetic mechanisms—including DNA methylation, histone modifications, non-coding RNA expression, and telomere attrition—it is highly plausible that technostress, by inducing similar sustained stress states, contributes to epigenetic alterations. Burnout, one of the central psychological consequences of technostress, has already been linked to changes in DNA methylation. A systematic review by Bakusic et al. (2017) reported associations between work-related stress and altered methylation patterns in genes such as SLC6A4 (serotonin transporter), BDNF (brain-derived neurotrophic factor), NR3C1, and TH, providing evidence for epigenetic changes in burnout and depression.

Because technostress is a major contributor to burnout in modern workplaces (Borle et al., 2021), it likely plays a role in shaping epigenetic signatures through this pathway. Moreover, the physiological mechanisms engaged by technostress—particularly HPA axis dysregulation and SNS overactivation—are precisely those known to influence the activity of epigenetic enzymes like DNMTs and HDACs, thereby further supporting the plausibility of a technostress–epigenetics pathway.

6.2. Emerging research: direct investigations into technostress and epigenetic markers

While much of the connection is currently inferential, direct research is beginning to explore the biological embedding of technostress, including studies that incorporate biomarkers relevant to epigenetic pathways.

A pivotal ongoing investigation into the biological embedding of work-related stressors is the PROAGEING study, a longitudinal, multidisciplinary cohort study of aging workers (aged 50+) in Italy. The study explores the complex interplay between workability, cognitive functioning, sleep quality, and psychosocial risk factors—including technostress—in relation to biological aging. Approximately 1,000 participants are being enrolled, with molecular assessments of biological age (telomere length and DNA methylation profiles) conducted on a subset of 500 individuals. By tracking technostress exposure alongside these epigenetic markers over time, PROAGEING is uniquely positioned to determine whether digital-era stressors contribute to accelerated aging via epigenetic pathways. Its findings are expected to significantly advance our understanding of how contemporary psychosocial and digital work demands shape long-term health at the molecular level (Bonzini et al., 2023).

Another relevant piece of research (already mentioned earlier) is a prospective cohort study that assessed the associations between technostress (specifically work interruptions, multitasking, and information overload), general work stress, burnout symptoms, hair cortisol concentration (HCC) as a marker of HPA axis activity, and C-reactive protein (CRP) as an indicator of systemic inflammation in hospital employees over a six-month period (Kaltenegger et al., 2024). This study found that baseline technostress was negatively associated with HCC at follow-up, suggesting dysregulation of the HPA axis—one of the key biological pathways involved in stress adaptation and epigenetic modification. Although the study did not directly assess DNA methylation or histone modifications, the observed HPA axis alterations linked to technostress support the plausibility of epigenetic consequences. Additionally, burnout symptoms and HCC both increased during the follow-up, underscoring the chronic stress burden experienced by employees in highly digitalized work environments.

6.3. Indirect links: screen time, information overload, circadian disruption, and epigenetic effects

Several components or consequences of technostress have been independently linked to epigenetic changes, providing indirect support for the technostress-epigenetics connection.

Screen time: Excessive screen time is an inherent aspect of many technostress-inducing scenarios. Research in children highlights the broader role of sedentary behavior in health outcomes: a Spanish cohort found higher sedentary time at age 4 correlated with 3.9% shorter leukocyte telomere length and a greater telomere rank decrease between ages 4 and 8, suggesting early-life physical inactivity undermines cellular longevity (Prieto‑Botella et al., 2023). In adults, the Make Better Choices 2 (MBC2) trial—a 9‑month randomized intervention—deliberately decreased leisure screen time along with promoting healthier eating and exercise. This intervention produced significant epigenome-wide DNA methylation changes in blood, notably in genes involved in cell cycle regulation and carcinogenesis (e.g., PI3K/AKT, Wnt/β‑catenin, p53 pathways) (Hibler et al., 2019).
Information overload: As a prominent technostressor, information overload creates significant cognitive and psychological strain. While direct epigenetic studies on "information overload" per se are sparse, the concept is closely related to cognitive workload and stress. Some research in broader contexts has linked factors related to information processing and depression (a potential outcome of chronic overload) with epigenetic mechanisms, such as DNA methylation of the NR3C1 gene (Palma-Gudiel et al., 2015). The cognitive burden imposed by information overload likely engages stress pathways known to affect the epigenome.
Circadian disruption: The “always-on” nature of modern technology—especially through techno-invasion, such as responding to work-related messages at night—can significantly disrupt circadian rhythms. Evening exposure to blue light from screens is a well-established suppressor of melatonin, interfering with natural sleep-wake cycles (Gooley et al., 2011). Disruptions to circadian rhythms, such as those seen in night shift workers, have been associated with epigenetic changes, including widespread DNA methylation differences in genes involved in biological timing and immune regulation. Bhatti et al. (2015) identified over 16,000 differentially methylated loci in night shift workers, including core circadian genes like PER3 and CSNK1E. Animal models also support this link: mice exposed to dim light at night before conception exhibited altered immune function in their offspring, suggesting that even brief light exposure can trigger heritable biological changes potentially mediated by epigenetic mechanisms (Cissé et al., 2020). Together, these findings suggest that circadian disruption induced by digital technostress may result in epigenetic modifications, contributing to long-term health risks.
Mental workload: High mental workload is a core component of techno-overload and techno-complexity. Although direct research linking mental workload to epigenetic changes in technostress is currently limited, sustained cognitive effort and related psychological stress are known to engage physiological stress systems—HPA axis, SNS activation—that have well-established epigenetic consequences. A comprehensive review by Dee et al. (2023) across diverse stress paradigms (acute, chronic, early-life, traumatic) found consistent DNA methylation alterations in stress-related genes like NR3C1, BDNF, and SLC6A4, demonstrating how cognitive burden and emotional stress can trigger epigenetic reprogramming. These findings support the hypothesis that persistent mental workload inherent in high digital task demands may similarly result in epigenetic modifications via stress mechanism engagement.

The causal chain linking technostress to epigenetic modifications and subsequent health outcomes can be inferred as follows: specific technostressors (e.g., overload, invasion, interruptions) lead to the chronic activation of physiological stress pathways, primarily the HPA axis and the SNS. This, in turn, can promote systemic conditions such as chronic low-grade inflammation and increased oxidative stress. These biological states are known to directly influence epigenetic machinery, resulting in alterations to DNA methylation profiles, histone modification patterns, dysregulation of non-coding RNA expression, and accelerated telomere attrition. Over time, these epigenetic modifications can lead to stable changes in gene expression programs that underpin the development of adverse long-term health outcomes, including accelerated biological aging, mental health disorders, cardiovascular disease, and other chronic conditions. The PROAGEING study mentioned before is designed to empirically test several links within this hypothesized chain.

However, a significant challenge lies in identifying specific epigenetic signatures that are uniquely attributable to technostress, as distinct from general work stress or other life stressors. Research on psychological stress has shown that while biological pathways—such as stress response, brain development, and immunity—are consistently implicated across diverse stress exposures, the reproducibility of DNA methylation changes at individual CpG sites is often poor (Zhang & Liu, 2022; Klengel & Binder, 2015). Technostress rarely occurs in isolation; it frequently coexists with, and is exacerbated by, other workplace demands (e.g., high workload, low job control) and personal life stressors (Tarafdar et al., 2007). Furthermore, individual factors—including genetic predispositions, stress history, coping strategies, and psychological resilience—strongly modulate epigenetic responses. For instance, resilience has been found to buffer against epigenetic age acceleration (Zhang et al., 2024). Therefore, disentangling the unique epigenetic contribution of technostress requires longitudinal study designs, large and diverse cohorts, and integrative analyses of multiple interacting variables.

7. The contemporary milieu: amplification of stress and its epigenetic toll

The stressors examined in this report, particularly technostress, do not operate in isolation. They are embedded within a complex contemporary environment characterized by unique societal, economic, and lifestyle pressures. This milieu can amplify the intensity and chronicity of stress exposures, potentially leading to a greater cumulative epigenetic burden and an increased susceptibility to adverse health outcomes.

7.1. The "always-on" culture and chronic connectivity

A defining feature of modern life is the expectation of constant availability and responsiveness, largely facilitated by digital technologies. This "always-on" culture, fueled by smartphones, email, and instant messaging platforms, directly contributes to techno-invasion, where the boundaries between work and personal life become increasingly blurred (Tarafdar et al., 2007). Such chronic connectivity can prevent adequate psychological detachment from work, leading to a sustained state of low-grade stress. This continuous, albeit sometimes subtle, activation of the HPA axis and sympathetic nervous system may maintain an internal physiological environment—and consequently, an epigenetic state—that is conducive to the development or exacerbation of stress-related diseases. The inability to "switch off" can impair crucial recovery processes, including sleep, which itself has implications for epigenetic regulation and overall health.

7.2. Information overload and cognitive burden

The digital age has unleashed an unprecedented deluge of information. Individuals are constantly bombarded with data, notifications, and communication, leading to techno-overload and significant information overload. The cognitive demand of processing this vast amount of information—often while multitasking—imposes a substantial burden. Empirical research confirms that digital stress induces cognitive overload, particularly in individuals already experiencing high levels of stress, thereby impairing attention, memory, and even innovation capacity (Vanni, Syvänen, & Viteli, 2024). This chronic cognitive strain and associated mental fatigue act as potent stressors, likely engaging physiological systems that influence epigenetic regulation. For example, methylation changes in the BDNF gene, which plays a critical role in neuronal plasticity and mental health, have been directly linked to psychological stress (Fuchikami et al., 2010). These findings suggest that the mental burden imposed by information overload in digital environments could contribute to epigenetic alterations with long-term consequences for brain function and well-being.

7.3. The aging workforce and digital adaptation

Demographic shifts are leading to an increasingly aging workforce in many industrialized nations. Older workers often face unique challenges in adapting to rapidly evolving digital technologies in the workplace, potentially experiencing higher levels of techno-complexity and techno-insecurity (Tarafdar et al., 2007). This demographic is simultaneously undergoing natural age-related epigenetic changes, including alterations in DNA methylation patterns and telomere shortening, both of which are recognized hallmarks of biological aging. The added burden of technostress could interact with these intrinsic aging processes, potentially accelerating epigenetic aging and increasing vulnerability to age-related diseases. The PROAGEING study already mentioned earlier, a longitudinal investigation of workers aged 50 and older, is specifically designed to examine these dynamics by assessing technostress exposure alongside biological aging markers such as telomere length and DNA methylation (Bonzini et al., 2023). This research is poised to provide critical insights into how digital stress may amplify the molecular processes of aging.

7.4. Interplay with other modern stressors

Technostress often co-occurs and interacts with a host of other stressors prevalent in contemporary society:

Work intensification: While digital tools can enhance efficiency, they are also frequently used to increase work demands, pace, and expectations for productivity, contributing to overall job strain.
Job insecurity: The fear of job displacement due to automation or the need for constant reskilling in response to technological advancements (techno-insecurity) exacerbates economic anxieties and financial stress, which are themselves potent stressors with epigenetic consequences.
Social isolation vs. hyper-connectivity: Modern society presents a paradox of being hyper-connected digitally yet potentially more socially isolated in meaningful ways. Problematic or excessive use of social media, a specific form of technology engagement, can induce its own stressors [e.g., fear of missing out (FoMO), social comparison, cyberbullying], leading to mental health issues. Both perceived social isolation and the stress from negative online social interactions are psychosocial stressors with the potential to influence epigenetic pathways.
Environmental exposures and lifestyle factors: The impact of technostress does not occur in a biological vacuum. Exposure to environmental pollutants (which can induce epigenetic changes and oxidative stress), dietary habits, and levels of physical activity (often reduced by prolonged screen time and sedentary behavior) can all interact with the biological responses to technostress, collectively modulating the epigenetic landscape and influencing overall health risk.

7.5. Cumulative stress burden and epigenetic load

The concept of “cumulative life stress” suggests that the aggregate burden of stressors experienced throughout an individual's life contributes to their overall risk for adverse health outcomes, partly through mechanisms like epigenetic age acceleration. Technostress, given its pervasive and often chronic nature, undoubtedly contributes significantly to this cumulative stress load in modern society. The combined effect of ongoing technostress coupled with other contemporary pressures (e.g., economic instability, societal pressures, environmental concerns) likely results in a more substantial and widespread "epigenetic scar" than would be predicted by examining any single stressor in isolation. This compounded epigenetic burden may play a role in the rising prevalence of chronic non-communicable diseases, including mental health disorders, cardiovascular conditions, and metabolic syndromes.

The interaction between technostress and other modern stressors implies a synergistic detriment. Each stressor can independently activate shared biological pathways such as the HPA axis, the sympathetic nervous system, inflammatory cascades, and oxidative stress responses. When an individual is simultaneously grappling with high techno-invasion, demanding work deadlines, financial uncertainty, and perhaps suboptimal lifestyle factors, these pathways are likely to be under sustained and multifaceted assault. This convergence suggests that epigenetic machinery is being influenced from multiple directions, potentially resulting in more profound, widespread, and resilient epigenetic dysregulation than would occur from a single stressor. The cumulative stress model, which posits that the accumulation of stress exposures accelerates epigenetic aging, supports the idea that the overall burden of stress—including a significant contribution from technostress—shapes our biological and health trajectories in the modern world (Zhang et al., 2024; Klengel & Binder, 2015).

8. Mitigation, intervention, and future research imperatives

Addressing the multifaceted challenges posed by stress, particularly technostress, and its potential epigenetic consequences requires a multi-pronged approach encompassing individual coping strategies, organizational changes, and targeted research initiatives. The dynamic nature of the epigenome offers a window of opportunity for interventions aimed at mitigating adverse effects and fostering resilience.

8.1. Addressing technostress: individual and organizational strategies

A growing body of research highlights various strategies that can be employed at both individual and organizational levels to manage and reduce technostress.

Individual strategies:

Individuals can adopt several practices to buffer the negative impacts of technology use. Mindfulness has emerged as a promising strategy, with research showing its potential to reduce technostress and improve job-related outcomes. For example, a qualitative study found that mindfulness practices—such as attention regulation, emotional awareness, and acceptance—help employees manage digital demands and foster greater satisfaction in their work environments (Ioannou, 2023). Additionally, e-work self-efficacy, or the belief in one's ability to effectively perform remote work using digital tools, has been shown to act as a protective factor. It buffers the negative effects of techno-stressors on outcomes such as burnout and psychological well-being, especially among remote workers during the pandemic (Consiglio et al., 2023). These findings highlight the importance of developing personal coping strategies like mindfulness and digital self-efficacy to mitigate the harmful psychological impacts of constant connectivity and digital demands.

Organizational strategies:

Organizations play a vital role in creating environments that minimize technostress. By providing adequate technical support and training, organizations help employees feel competent with ICTs, reducing stress associated with techno-complexity and techno-unreliability (Tarafdar et al., 2007). Health-oriented leadership, in which supervisors prioritize employee well-being and model healthy digital behaviors, serves as a valuable resource for mitigating technostress (Ioannou, 2023). Ensuring user-friendly technology design and reliable systems further alleviates stressors related to system malfunction and complexity. Supportive work environments and high-quality leader-member exchange have been shown to protect against the negative effects of technostress on engagement and innovation (Consiglio et al., 2023). Implementing clear policies on digital communication, including expectations around work hours and the right to disconnect, directly addresses issues of techno-invasion and techno-overload. While flexible work arrangements can enhance autonomy and well-being, organizations should balance these with strategies to prevent digital exhaustion and encourage healthy detachment.

8.2. Potential for modulating epigenetic responses to stress

Encouragingly, research suggests that epigenetic marks are not immutable and can be influenced by positive behavioral changes and interventions.

Psychobehavioral interventions such as mindfulness-based stress reduction (MBSR), cognitive behavioral therapy (CBT), and yoga are gaining attention for their potential to modulate DNA methylation. A recent scoping review found that although many studies are underpowered, several reported significant changes in DNA methylation following such interventions, especially in genes related to stress and inflammation (Zhang et al., 2024). Specifically, yoga practice has been associated with the downregulation of pro-inflammatory genes (e.g., IL-6, TNF-α, NF-κB) and the upregulation of anti-inflammatory and immune-regulatory genes (e.g., TGF-β, FoxP3), along with increased expression of genes involved in DNA repair (e.g., OGG1) and evidence of reduced TNF methylation (Harkess et al., 2017). These findings suggest that mind–body practices may exert their health benefits, at least in part, by influencing gene expression through epigenetic pathways.

Inherent psychological factors can also serve as buffers. Individuals with high psychological well-being or low levels of neuroticism appear to be more resilient to the epigenetic age acceleration effects associated with cumulative life stressors. This underscores the importance of fostering psychological resilience.

While more pharmacological in nature, the potential to reverse epigenetic dysregulation in conditions such as neurodegenerative diseases using HDAC inhibitors and DNMT inhibitors offers a compelling proof-of-concept: epigenetic marks are not static and can be therapeutically targeted. This insight highlights the plasticity of the epigenome and supports the broader notion that targeted interventions—whether pharmacological or behavioral—may help mitigate stress-related epigenetic alterations (Honer et al., 2024). Although distinct from psychosocial approaches, these findings reinforce the possibility of restoring epigenetic balance across diverse contexts of disease and stress exposure.

The epigenome, therefore, should not be viewed as merely a passive recipient of stress-induced damage. It is a dynamic system that responds to both adverse and beneficial inputs. Interventions that effectively reduce stress, enhance coping mechanisms, or improve overall well-being may actively contribute to reshaping epigenetic patterns in a health-promoting direction. This offers a molecular basis for understanding resilience and recovery, suggesting that positive lifestyle changes and supportive environments can indeed "get under the skin" to foster better health at a fundamental biological level.

8.3. Identifying knowledge gaps and charting the course for future inquiry

Despite significant advances, several knowledge gaps remain in understanding the complex interplay between technostress, general stress, and epigenetics. Future research should prioritize:

Direct technostress-epigenetics research: There is a pressing need for more longitudinal studies, akin to the PROAGEING study, that directly measure specific techno-stressors alongside a comprehensive panel of epigenetic markers (DNA methylation at candidate genes and genome-wide, histone modifications, ncRNA profiles, and telomere dynamics) in diverse human populations. Such studies should track changes over time to establish causality.
Biomarker development: A significant gap is the limited use of objective biological markers in technostress research. Future work should aim to identify and validate robust epigenetic signatures that can serve as reliable biomarkers of technostress burden, susceptibility, and the success of interventions. This includes moving beyond self-report measures of stress.
Mechanistic studies: Elucidating the precise molecular pathways that link specific categories of techno-stressors (e.g., how techno-overload versus techno-invasion differentially impacts HPA axis responsivity and downstream epigenetic targets) is fundamental for understanding the nuances of these relationships.
Interaction effects: Investigating the interactive epigenetic effects of technostress with other critical lifestyle factors (such as diet, physical activity, sleep quality – all of which have their own epigenetic implications) and co-occurring environmental exposures (e.g., pollutants) will provide a more holistic understanding of cumulative risk.
Vulnerable populations: Research should focus on populations that may be particularly vulnerable to the adverse effects of technostress, such as older workers navigating digital transitions, healthcare professionals working in highly digitized environments, and young people whose neurodevelopmental and epigenetic programming may be especially sensitive to chronic digital stressors.
Intervention efficacy on biological markers: The effectiveness of interventions (behavioral, organizational, technological design improvements) needs to be rigorously evaluated not only based on perceived stress reduction but also on their ability to modulate underlying biological markers, including epigenetic changes and physiological stress responses.

9. Conclusion

The evidence synthesized in this report compellingly demonstrates that stress, in its diverse manifestations, is a potent modulator of the human epigenome. From the enduring impacts of early-life adversity and chronic psychosocial challenges to the physiological toll of oxidative stress and inflammation, stressors can induce significant and often lasting epigenetic modifications. These alterations—encompassing changes in DNA methylation, histone modifications, non-coding RNA expression, and telomere dynamics—occur through well-defined biological pathways, primarily involving the hypothalamic-pituitary-adrenal (HPA) axis, the sympathetic nervous system (SNS), and the immune system. Crucially, these epigenetic changes are not benign; they are increasingly linked to a wide array of adverse health outcomes, contributing substantially to the global burden of chronic diseases, including mental illnesses, cardiovascular disorders, metabolic conditions, and accelerated aging.

A key assertion of this analysis is that technostress—the stress arising from interaction with and adaptation to information and communication technologies—must be recognized as a significant and pervasive chronic psychosocial stressor in the contemporary world. It is not merely a fleeting annoyance or a minor inconvenience but a complex phenomenon with clearly documented adverse psychological effects (e.g., burnout, anxiety, depression) and measurable physiological stress responses (e.g., HPA axis and SNS activation, increased cortisol). Given that these responses mirror those elicited by other well-established chronic stressors known to impact the epigenome, there is a strong inferential basis, supported by emerging direct research such as the PROAGEING study (see above), to conclude that technostress has the potential for significant long-term epigenetic impact. Specific facets of the digital experience, such as excessive screen time, information overload, and circadian disruption due to chronic connectivity, have already been independently linked to epigenetic alterations like telomere shortening and changes in DNA methylation.

It is vital to adopt a holistic perspective, recognizing that technostress rarely occurs in isolation. It interacts with and is often amplified by other modern stressors, including work intensification, economic uncertainties, social pressures, and environmental exposures. This cumulative and interactive burden of stress likely leads to a compounded impact on the epigenome, potentially accelerating the onset and progression of chronic conditions more than any single stressor studied alone.

The dynamic and potentially reversible nature of some epigenetic modifications offers hope. Proactive strategies at individual, organizational, and societal levels are essential to mitigate technostress and its downstream consequences. This includes fostering individual resilience through practices like mindfulness and effective coping, implementing organizational changes that promote healthier work environments and technology use (e.g., better training, support, user-centric design, clear boundaries), and encouraging the design of technologies that prioritize user well-being. Interventions that successfully reduce stress and improve coping have shown promise in modulating epigenetic marks related to stress and inflammation.

Looking forward, a concerted interdisciplinary research effort is paramount. This research must continue to unravel the specific epigenetic signatures of technostress, identify vulnerable populations, develop robust biomarkers, and evaluate the efficacy of interventions in normalizing stress-induced epigenetic changes. Just as public health initiatives have historically promoted physical hygiene to combat infectious diseases, there is an emerging imperative to cultivate a form of "epigenetic hygiene" for the digital age. This entails fostering practices, policies, and technological environments that minimize detrimental epigenetic programming resulting from chronic stressors, prominently including technostress. By understanding and addressing the epigenetic consequences of our profound and ever-increasing engagement with technology, society can aspire to build a healthier, more resilient future in an increasingly digital world.

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THE EPIGENETIC SCARS OF MODERN LIFE: INTERTWINING STRESS, TECHNOSTRESS, AND HEALTH IN THE CONTEMPORARY WORLD

3.1. DNA methylation and epigenetic clocks

YOU CAN SPEND YOUR LIFE MEASURING THE DIMENSIONS OF YOUR PRISON

YOU CAN SPEND
YOUR LIFE
MEASURING
THE DIMENSIONS
OF YOUR PRISON