Acute Stress Reaction
Background
Section titled “Background”Acute stress reaction, often referred to as acute stress disorder (ASD), is a transient psychological and physiological response that can occur immediately following exposure to an exceptionally severe or traumatic stressor. It is characterized by a range of symptoms, including intense anxiety, emotional numbing, detachment, a reduced awareness of surroundings, derealization, and depersonalization. These reactions typically manifest within hours or days of the traumatic event and generally resolve within one month.
Biological Basis
Section titled “Biological Basis”Genetic factors are understood to influence an individual’s susceptibility to developing an acute stress reaction. Research in genomics has begun to identify specific genetic variants associated with this condition. For instance, a genome-wide association study (GWAS) identified the variantrs577242570 as significantly associated with acute stress reaction. This variant showed an odds ratio (OR) of 2.33 (95% CI: 1.77–3.08) with a p-value of 4.56 × 10−8, suggesting that individuals carrying this variant may have a substantially increased likelihood of experiencing an acute stress reaction.[1] Understanding such genetic underpinnings can contribute to a more comprehensive view of the biological mechanisms involved in stress response.
Clinical Relevance
Section titled “Clinical Relevance”The clinical relevance of acute stress reaction lies in its potential to cause significant distress and impair daily functioning. Symptoms can be debilitating, affecting an individual’s ability to work, maintain relationships, and engage in routine activities. Early identification and intervention are crucial, as acute stress reaction can sometimes precede the development of more chronic stress-related disorders, such as post-traumatic stress disorder (PTSD). Effective management often involves psychological first aid, trauma-focused cognitive behavioral therapy, and supportive care to mitigate symptoms and prevent long-term complications.
Social Importance
Section titled “Social Importance”Acute stress reaction carries considerable social importance due to its impact on individuals and communities, particularly following large-scale traumatic events like natural disasters, accidents, or acts of violence. The prevalence of these reactions can place a significant burden on public health systems and social support networks. Addressing acute stress reaction is vital for community resilience, enabling affected individuals to recover and reintegrate into society. Awareness and understanding of this condition help to reduce stigma, encourage help-seeking behaviors, and foster a supportive environment for those experiencing the immediate aftermath of trauma.
Methodological and Statistical Constraints
Section titled “Methodological and Statistical Constraints”Genetic studies on acute stress reaction, like many complex traits, face inherent methodological and statistical limitations that impact the scope and generalizability of findings. A significant challenge lies in achieving adequate statistical power, especially for detecting genetic associations that follow non-additive inheritance models. For instance, power calculations reveal that an additive test might require substantially larger sample sizes (e.g., over 370,000 individuals forrs201654520 and over 188,000 for rs77704739 ) to detect recessive associations that could be identified with much smaller cohorts (e.g., 21,021 and 67,611 individuals, respectively) when using a recessive model.[1] This suggests that many significant non-additive variants, which could explain a substantial portion of genetic architecture, may be missed if only additive models are employed or if sample sizes are insufficient, thereby leading to an incomplete understanding of the trait’s genetic basis.[1]Furthermore, the predictive power of genetic models is often directly correlated with cohort size, emphasizing the critical need for large-scale datasets to enhance the robustness and accuracy of findings.[2]Beyond sample size, study design choices and analytical approaches can introduce biases and affect the interpretation of results. For example, clinical cohorts, while beneficial for longitudinal follow-up, may inadvertently include individuals at pre-disease stages classified as controls, which can dilute observed genetic effects.[1] Rigorous quality control measures, such as adjusting for principal components (PCA) and employing stringent P-value thresholds (e.g., <5 × 10−8), are crucial to minimize the influence of factors like pronounced linkage disequilibrium that can lead to an overestimation of genetic effects.[2] Despite these efforts, novel genetic associations, particularly those identified through less commonly used non-additive models, often require future validation and follow-up analysis to confirm their significance and clinical relevance.[1]
Ancestral Diversity and Generalizability
Section titled “Ancestral Diversity and Generalizability”A pervasive limitation in genetic research, including studies of acute stress reaction, is the significant underrepresentation of non-European populations in genome-wide association studies (GWAS). This bias profoundly affects the generalizability of findings, as unique genetic risk factors for diseases are predominantly influenced by an individual’s ancestry.[2] Relying heavily on genetic data from a single ancestry, such as European populations (e.g., studies using European ancestry individuals), risks exacerbating health disparities and limits the identification of rare variants that may be more common or have different minor allele frequencies in other populations.[1], [2] The genetic architecture of diseases and traits can vary substantially across different ancestral groups, meaning that genetic associations and polygenic risk scores (PRS) derived from one population may not accurately predict risk in another. For instance, a variant like rs6546932 in the SELENOIgene demonstrated a notable discrepancy in effect size between the Taiwanese Han population (OR=1.58) and the UK Biobank (OR=1.21), highlighting the necessity of considering ancestry-specific genetic architectures when developing and applying PRS models.[2] Studies predominantly focused on populations like the Taiwanese Han, while valuable for specific groups, must be interpreted with caution regarding their applicability to broader global populations, especially those with different predominant ancestral lineages or mixed descents.[2]
Phenotypic Complexity and Environmental Confounders
Section titled “Phenotypic Complexity and Environmental Confounders”The interpretation of genetic findings for acute stress reaction is further complicated by the complex nature of the phenotype itself and the influential role of environmental factors. Many complex diseases and traits, including reactions to stress, arise from an intricate interplay of multiple genes and significant environmental influences, rather than being driven by single genetic variants.[2] While polygenic risk scores offer a powerful approach to summarize cumulative genetic effects and can theoretically incorporate environmental factors, precisely capturing and integrating these diverse environmental exposures remains a considerable challenge in current models.[2]Furthermore, the definition and of acute stress reaction as a phenotype can be prone to variability. Relying on electronic medical records and classifications like PheCode, while enabling large-scale analysis, may introduce heterogeneity or misclassification if diagnostic criteria are not uniformly applied or if the records lack detailed contextual information.[2] This phenotypic complexity, combined with the often unmeasured or unquantified environmental confounders, contributes to the phenomenon of “missing heritability,” where only a small fraction of the estimated heritability for complex diseases is currently explained by identified genetic variants.[1] A comprehensive understanding therefore necessitates future research that more thoroughly accounts for gene-environment interactions and refined phenotypic characterization.
Variants
Section titled “Variants”Genetic variations play a crucial role in shaping an individual’s susceptibility and response to acute stress. Among these, the single nucleotide polymorphism (SNP)rs577242570 has been identified with a significant association with acute reaction to stress. This variant, located on chromosome 18, is linked to an odds ratio of 2.33, indicating that individuals carrying the associated allele have more than double the odds of experiencing an acute stress reaction compared to those without it, with a strong statistical significance (p = 4.56 × 10−8).[1] The variant is situated near LIN28AP1 and CACYBPP2, both of which are pseudogenes. Pseudogenes are typically non-coding DNA sequences that resemble functional genes but have lost their protein-coding ability; however, they can exert regulatory effects on their functional counterparts or other genes, potentially influencing the complex physiological cascade that constitutes an acute stress response.
The functional genes related to these pseudogenes, LIN28A (or LIN28B) and CACYBP, are involved in fundamental cellular processes that are often modulated during stress. LIN28 proteins are RNA-binding proteins that regulate microRNA processing and mRNA translation, critical for development, metabolism, and stem cell function. Dysregulation of LIN28 pathways has been implicated in various stress-related conditions. Similarly, Calcybin (CACYBP) participates in the ubiquitin-proteasome system and cytoskeletal organization, processes that are essential for cellular adaptation and survival under stressful conditions. The pseudogenes LIN28AP1 and CACYBPP2 may act as competitive endogenous RNAs (ceRNAs) or through other non-coding mechanisms, subtly fine-tuning the expression levels or stability of their respective functional genes, thereby modulating the intricate molecular pathways involved in acute stress reactions.
Another variant, rs149368821 , is associated with the genes YBX1P1 and LINC02290. YBX1P1 is a pseudogene of YBX1 (Y-Box Binding Protein 1), a highly conserved protein involved in critical cellular functions such as DNA replication and repair, transcription, and mRNA processing and translation. YBX1 is known to be a key player in cellular responses to various stressors, including oxidative stress and heat shock. LINC02290 is a long intergenic non-coding RNA (lncRNA), a class of RNA molecules increasingly recognized for their diverse regulatory roles in gene expression, chromatin remodeling, and cellular differentiation. LncRNAs can significantly impact an individual’s biological response to stress by modulating the expression of genes involved in neuronal plasticity, inflammation, and metabolic regulation, thereby contributing to the overall physiological and psychological response to acute stressors.
Key Variants
Section titled “Key Variants”| RS ID | Gene | Related Traits |
|---|---|---|
| rs577242570 | LIN28AP1 - CACYBPP2 | acute stress reaction |
| rs149368821 | YBX1P1 - LINC02290 | acute stress reaction |
Conceptualization and Standardized Nomenclature
Section titled “Conceptualization and Standardized Nomenclature”In large-scale genetic research, “acute reaction to stress” is primarily conceptualized as a distinct phenotype identified through standardized systems, rather than a detailed clinical description of its symptomatology.[1] This approach relies on the systematic curation of vast electronic medical record (EMR) data to ensure consistency across study cohorts, transforming diverse medical histories into meaningful, interpretable phenotypes suitable for genetic analysis.[1] Phenotype curation tools, such as the PHEnome Scan ANalysis Tool (PHESANT), are specifically employed to process and recode complex health data from sources like the UK Biobank.[1]The operational definition of diseases, including acute stress reaction, often involves the utilization of International Classification of Diseases (ICD) codes, specifically ICD-9-CM and ICD-10-CM, which are then mapped to a more granular system known as PheCodes.[2]PheCodes serve as a standardized vocabulary, consolidating various diagnostic codes into specific disease categories, thereby facilitating large-scale phenome-wide association studies (PheWAS).[2] This systematic conversion ensures that complex clinical diagnoses from patient records are uniformly translated into research-ready phenotypes for robust analysis.
Classification and Diagnostic Approach
Section titled “Classification and Diagnostic Approach”Within genetic studies, acute stress reaction is classified as a distinct disease entity using the PheCode criteria, which represent a nosological system for organizing medical diagnoses.[2] For robust case ascertainment in such studies, a diagnosis is typically established based on the consistent application of PheCode criteria on multiple distinct occasions, often requiring at least three instances, to increase diagnostic certainty and minimize misclassification.[2] This categorical approach delineates individuals into “case” and “control” groups, enabling the identification of genetic variants associated with the presence or absence of the condition.[2] This methodology underscores a research-centric diagnostic criterion, where the presence of the condition is defined by its PheCode designation derived from EMRs, rather than an active clinical assessment based on symptom presentation.[2]
Genetic Associations and Risk
Section titled “Genetic Associations and Risk”Genetic studies have begun to identify specific variants associated with an increased susceptibility to acute stress reaction, offering a approach beyond clinical symptomology.[1] For instance, the variant rs577242570 has been found to be significantly associated with acute reaction to stress.[1] The presence of this variant is linked to an elevated odds ratio of 2.33 (95% CI, 1.77–3.08), indicating its role as a potential genetic marker for the condition.[1] This genetic association contributes to a broader understanding of polygenic risk, where multiple genetic factors collectively influence an individual’s predisposition to complex diseases.[2] While rs577242570 highlights a specific locus, the integration of such findings into polygenic risk scores (PRS) could offer a more comprehensive of an individual’s genetic liability, potentially serving as a predictive tool for risk assessment in the future.[2] Such advancements move towards a dimensional understanding of risk, even if the primary diagnostic categorization remains binary in these genetic epidemiology studies.
Genetic Predisposition
Section titled “Genetic Predisposition”Genetic factors play a significant role in an individual’s susceptibility to acute stress reaction. Research has identified specific genetic variants, such as*rs577242570 *on chromosome 184,407,101, which is significantly associated with acute stress reaction, exhibiting an odds ratio of 2.33.[1] This indicates that individuals carrying certain alleles may have a substantially increased risk of experiencing this condition. The genetic architecture of such complex diseases often involves polygenic risk, where numerous genetic variants, each with a small effect, cumulatively contribute to an individual’s overall predisposition.
Beyond simple additive models, non-additive genetic associations, including dominant, recessive, and heterodominant models, are also crucial in understanding disease etiology. These non-additive genetic effects can reveal associations that might be missed by standard additive analyses, providing a more comprehensive view of genetic risk.[1]Furthermore, the effectiveness of polygenic risk prediction models emphasizes the importance of considering ancestry-specific genetic architectures, as genetic backgrounds can significantly influence disease associations across different populations.[2]
Environmental and Lifestyle Factors
Section titled “Environmental and Lifestyle Factors”Environmental and lifestyle elements are important contributors to the manifestation of acute stress reaction, often interacting with genetic predispositions. Lifestyle choices such as exercise, diet, alcohol consumption, and smoking are recognized as environmental factors that can influence the risk profiles for polygenic diseases and can enhance the accuracy of predictive models when included.[2] These factors can modulate physiological stress responses and overall resilience to acute stressors.
Moreover, demographic variables like age and sex are consistently found to be significant influences on disease prevalence and risk. The prevalence of many complex diseases, including acute stress reaction, typically increases with age, and incorporating age into predictive models consistently improves their accuracy.[2] This highlights how an individual’s life stage and biological sex can modify their vulnerability to developing acute stress reactions in response to triggering events.
Gene-Environment Interactions and Age-Related Influences
Section titled “Gene-Environment Interactions and Age-Related Influences”The development of acute stress reaction is often a result of intricate gene-environment interactions, where an individual’s genetic makeup influences how they respond to environmental triggers. While specific gene-environment interactions for acute stress reaction are not explicitly detailed, studies on polygenic diseases broadly demonstrate that environmental factors can significantly modify the expression and impact of genetic risks.[2] This suggests that genetic predispositions for stress reactivity may only manifest under certain environmental conditions or in the presence of specific stressors.
Acute stress reaction is categorized among age-related complex diseases, indicating that the aging process itself and its associated physiological changes can play a role in altering an individual’s susceptibility or the severity of their reaction.[1] The cumulative effect of life experiences, coupled with age-related biological changes, can influence the body’s capacity to cope with acute stress, potentially exacerbating reactions in genetically predisposed individuals.
Genetic Predisposition and Variation
Section titled “Genetic Predisposition and Variation”The acute stress reaction, like many complex human traits, is influenced by its genetic architecture, which contributes to individual differences in susceptibility and response. Through large-scale genome-wide association studies (GWAS), specific genetic variants have been identified as being significantly associated with this reaction. For instance, the single nucleotide polymorphism (SNP)rs577242570 has been linked to acute stress reaction, demonstrating a notable odds ratio that highlights its potential role in modulating an individual’s predisposition to this condition.[1] Such findings underscore the importance of genetic mechanisms, where variations in DNA sequences can alter gene functions or regulatory elements, thereby contributing to the diverse range of stress responses observed across populations.[2] These genetic insights contribute to understanding the broader genetic landscape of complex diseases and traits. The analysis of these variants, including their minor allele frequencies and effect sizes, helps to build models that predict risk and inform personalized medicine approaches. While specific epigenetic modifications or detailed gene expression patterns directly linked to rs577242570 for acute stress reaction are not detailed, the general framework of genetic research aims to uncover how such genetic differences influence the dynamic regulation of gene activity, ultimately shaping an individual’s biological response to stressors.[1]
Molecular Pathways
Section titled “Molecular Pathways”Understanding the molecular pathways involved in acute stress reaction begins with investigating how genetic variants translate into functional changes. Genetic associations are often explored through techniques like expression quantitative trait loci (eQTL) analysis, which investigates how specific single nucleotide polymorphisms (SNPs) impact gene expression levels. By utilizing resources such as the eQTLGen Consortium and GTEx portal, researchers can identify if a variant likers577242570 influences the transcription of nearby genes, thereby affecting crucial signaling pathways and metabolic processes.[1] This detailed molecular analysis helps to map out the cascade of biochemical events that are initiated or altered in response to stress, providing insights into the regulatory networks that govern the body’s physiological responses.[1]
Cellular Functions and Key Biomolecules
Section titled “Cellular Functions and Key Biomolecules”Functional characterization builds upon molecular insights to elucidate how genetic variations impact cellular functions and the roles of key biomolecules. This involves identifying critical proteins, enzymes, receptors, and transcription factors whose activity or abundance might be altered by a genetic variant such as rs577242570 . These biomolecules are integral to the intricate cellular machinery that mediates the body’s response to stress, influencing everything from neurotransmitter release to hormonal regulation.[1] Changes in receptor sensitivity or enzyme kinetics due to genetic differences could profoundly influence cellular signaling and the overall cellular response, ultimately contributing to the manifestation of acute stress reactions by disrupting normal cellular homeostasis.[1]
Systemic Responses and Homeostatic Disruption
Section titled “Systemic Responses and Homeostatic Disruption”The acute stress reaction involves a complex interplay of various tissues and organs, leading to systemic consequences that temporarily disrupt normal homeostatic balance. While specific details on organ-level effects or disease mechanisms directly attributable tors577242570 , stress responses generally engage multiple physiological systems, including the nervous, endocrine, and immune systems. Genetic predispositions can influence the intensity and duration of these systemic reactions, affecting how well an individual’s body can mount compensatory responses to restore equilibrium.[1] Research into complex diseases highlights how genetic variants can impact homeostatic disruptions, such as those related to blood pressure regulation, metabolic processes, or immune system modulation. The broader context of age-related complex diseases, which often have genetic underpinnings, suggests that variants influencing stress responses could also have long-term implications for health. Understanding these tissue interactions and systemic consequences is vital for a comprehensive view of how acute stress reactions are regulated and how genetic factors contribute to individual variations in these critical physiological processes.[1]
Ethical Implications of Genetic Information and Disclosure
Section titled “Ethical Implications of Genetic Information and Disclosure”The identification of genetic variants, such as rs577242570 associated with acute stress reaction, introduces complex ethical considerations regarding genetic testing. While such testing could potentially offer insights into an individual’s predisposition, it raises questions about the appropriate scope and utility of disclosing such sensitive information. Ensuring robust informed consent is paramount, requiring clear communication about the potential implications, limitations, and future uses of genetic data, especially given the long-term storage and analysis of samples as seen in large cohorts (.[1] ).
Privacy concerns are central to genetic research. Studies emphasize the importance of patient confidentiality, with personal medical details being encrypted and used exclusively for research purposes (.[2]). However, the aggregation of large-scale genetic and health records, even when anonymized, carries inherent risks of re-identification and potential misuse, necessitating stringent data protection measures. Furthermore, the specter of genetic discrimination in areas like employment or insurance based on predispositions to conditions such as acute stress reaction highlights the need for strong legal and ethical safeguards to protect individuals from adverse consequences.
Social Equity and Access to Genetic Insights
Section titled “Social Equity and Access to Genetic Insights”The potential for genetic predispositions to acute stress reaction raises concerns about social stigma, which could adversely affect individuals’ psychological well-being and willingness to seek support. Moreover, significant health disparities exist within genetic research, as evidenced by the underrepresentation of non-European populations, which can lead to “suboptimal outcomes” when genetic models are applied across diverse ethnic groups (.[2] ). This creates an ethical imperative to ensure that genetic insights and subsequent interventions are equally applicable and accessible to all, irrespective of ancestry.
Socioeconomic factors and cultural considerations profoundly influence both the uptake and interpretation of genetic information. Disparities in access to advanced genetic counseling and testing can exacerbate existing health inequities, especially for vulnerable populations who may already face multiple barriers to care. Achieving health equity requires careful resource allocation and culturally sensitive approaches to integrate genetic findings into healthcare systems globally, ensuring that the benefits of personalized medicine for conditions like acute stress reaction do not disproportionately favor certain groups.
Governance, Data Protection, and Research Ethics
Section titled “Governance, Data Protection, and Research Ethics”The growing integration of genetic insights into understanding conditions like acute stress reaction necessitates comprehensive policy and regulatory frameworks. These frameworks must govern the ethical conduct of genetic testing, ensuring its clinical validity and utility, and protecting individuals from potential harms. Robust data protection mechanisms are essential for safeguarding the vast repositories of genetic and phenotypic data collected in research, such as those from the China Medical University Hospital or UK Biobank, to prevent unauthorized access and maintain public trust (.[1] ).
Ethical research practices, guided by institutional review boards, are fundamental to responsible genetic studies, including those exploring acute stress reaction (.[2] ). This involves not only meticulous informed consent but also addressing the equitable representation of diverse populations in research to avoid perpetuating biases in scientific understanding. As genetic discoveries translate into clinical applications, clear clinical guidelines are crucial to ensure that healthcare providers use genetic information responsibly and effectively, promoting consistent, high-quality, and ethical care while navigating the complexities of personalized medicine.
Frequently Asked Questions About Acute Stress Reaction
Section titled “Frequently Asked Questions About Acute Stress Reaction”These questions address the most important and specific aspects of acute stress reaction based on current genetic research.
1. Why do I react so strongly to bad news, but others seem fine?
Section titled “1. Why do I react so strongly to bad news, but others seem fine?”There’s a genetic component to how people react to severe stress. Some individuals carry specific genetic variations that make them more susceptible to intense reactions; for instance, the variant rs577242570 has been linked to a substantially increased likelihood. This means even with similar experiences, your biological makeup can lead to a stronger physiological and psychological response. It’s not about being “weak,” but about differing genetic predispositions.
2. Is it true that my family history makes me more likely to freak out after trauma?
Section titled “2. Is it true that my family history makes me more likely to freak out after trauma?”Yes, genetic factors inherited from your family can influence your susceptibility to acute stress reactions. If close relatives have experienced similar intense responses to trauma, you might have inherited some of those genetic predispositions. Research is identifying specific genetic variants associated with this increased likelihood, suggesting a biological basis for family patterns.
3. My friend and I went through the same thing; why am I struggling more?
Section titled “3. My friend and I went through the same thing; why am I struggling more?”Even when exposed to the exact same traumatic event, individuals can have very different reactions due to their unique genetic makeup. You might carry specific genetic variants, like rs577242570 , that increase your susceptibility to a more pronounced acute stress reaction. This means your biological response to the stressor is inherently different, leading to a more intense experience for you.
4. Could my ethnic background affect how I deal with a sudden shock?
Section titled “4. Could my ethnic background affect how I deal with a sudden shock?”Yes, your ancestral background can play a role in how you respond to traumatic stress. Genetic risk factors and the overall genetic architecture of traits can vary significantly across different ethnic groups. For example, a variant like rs6546932 can have different effect sizes depending on ancestry, meaning your background can influence your unique genetic predisposition.
5. If I have a really tough reaction, does that mean I’ll get PTSD?
Section titled “5. If I have a really tough reaction, does that mean I’ll get PTSD?”Not necessarily, but having an acute stress reaction can sometimes precede the development of PTSD. While it increases your risk, it doesn’t guarantee a long-term condition. Early identification and intervention through psychological first aid or trauma-focused therapy are crucial to mitigate symptoms and prevent the progression to more chronic disorders like PTSD.
6. Is my intense stress reaction “all in my head” or something real?
Section titled “6. Is my intense stress reaction “all in my head” or something real?”It’s definitely something real, with a clear biological basis. Acute stress reaction is a recognized psychological and physiological response, influenced by genetic factors. Research has identified specific genetic variants, likers577242570 , that are significantly associated with this condition, showing it’s not simply a matter of willpower but an inherent biological susceptibility.
7. Could a DNA test tell me if I’m prone to extreme stress reactions?
Section titled “7. Could a DNA test tell me if I’m prone to extreme stress reactions?”While research is ongoing, genetic studies are identifying specific variants linked to acute stress reaction, such asrs577242570 which has an odds ratio of 2.33. In the future, DNA tests might offer insights into your genetic susceptibility. However, the genetic architecture is complex, and many factors beyond single variants contribute, so current tests might not provide a complete picture.
8. If my immediate reaction is bad, can I still prevent long-term problems?
Section titled “8. If my immediate reaction is bad, can I still prevent long-term problems?”Absolutely. Early identification and intervention are crucial for managing acute stress reactions and preventing long-term complications like PTSD. Engaging in psychological first aid, trauma-focused cognitive behavioral therapy, and supportive care can significantly help mitigate symptoms. These interventions can help you process the trauma and build resilience, regardless of your initial genetic predisposition.
9. Why does this sudden stress make it hard for me to do daily things?
Section titled “9. Why does this sudden stress make it hard for me to do daily things?”Acute stress reaction is characterized by debilitating symptoms like intense anxiety, emotional numbing, and detachment that significantly impair daily functioning. These reactions are a natural, though intense, response to severe trauma, and they can temporarily affect your ability to work, maintain relationships, and engage in routine activities. It’s a recognized and impactful condition.
10. Do some people just naturally have a higher “stress threshold”?
Section titled “10. Do some people just naturally have a higher “stress threshold”?”Yes, people do have varying innate susceptibilities to stress reactions, partly due to their genetics. Some individuals carry genetic variants that make them more resilient, while others, like those with the rs577242570 variant, may have a substantially increased likelihood (OR 2.33) of experiencing an acute stress reaction. This means their biological “threshold” for an intense response can indeed differ.
This FAQ was automatically generated based on current genetic research and may be updated as new information becomes available.
Disclaimer: This information is for educational purposes only and should not be used as a substitute for professional medical advice. Always consult with a healthcare provider for personalized medical guidance.
References
Section titled “References”[1] Guindo-Martinez M et al. The impact of non-additive genetic associations on age-related complex diseases. Nat Commun. 2021 Apr 23;12(1):2436. PMID: 33893285
[2] Liu, T. Y., et al. “Diversity and longitudinal records: Genetic architecture of disease associations and polygenic risk in the Taiwanese Han population.”Sci Adv, 2024.