Meaney, M., & Szyf, M. (2005) | References

Core Concept

The Interface Between Genes and Experience

The central insight of Meaney and Szyf's landmark paper is deceptively simple yet revolutionary: the genome is not a fixed blueprint but a responsive system that adapts to environmental input through chemical modifications. While the DNA sequence itself remains constant, the way genes are expressed—whether they are read strongly, weakly, or not at all—can be modified by experience. This occurs through epigenetics: chemical tags added to DNA or the proteins around which DNA wraps that control gene accessibility without changing the underlying code.

For decades, scientists assumed that gene expression patterns were either genetically determined or randomly established. Meaney and Szyf demonstrated something far more remarkable: that social experience—specifically, the quality of parental care—systematically programs how genes are expressed. The parent's behaviour becomes written into the child's biology through specific molecular mechanisms. This is not metaphor; it is molecular reality. The warmth or coldness of early caregiving modifies the chemical structure of chromatin (the DNA-protein complex) in ways that persist into adulthood, potentially across generations.

DNA Methylation as the Molecular Mechanism

The specific mechanism Meaney and Szyf identified is DNA methylation—the addition of methyl groups to cytosine bases in DNA. When methyl groups accumulate on a gene promoter (the region that controls when and how strongly a gene is read), they typically silence that gene by preventing transcription factors from binding. The gene remains present but inaccessible, like a book whose pages have been glued together.

In their studies with rats, they found that pups raised by mothers who showed low levels of nurturing behaviour (licking and grooming) developed increased methylation of the glucocorticoid receptor (GR) gene in the hippocampus. This region of the brain is crucial for shutting off the stress response—glucocorticoid receptors detect cortisol and signal that the stress response should wind down. With the GR gene silenced by methylation, fewer receptors are produced, and the stress response cannot properly terminate. The result is chronically elevated stress hormones, hypervigilance, and heightened anxiety—a biological state of perpetual alarm.

Conversely, pups raised by highly nurturing mothers showed reduced methylation of the GR gene, more abundant glucocorticoid receptors, and more moderate stress responses. Their biology was programmed for a world perceived as safe and responsive, where stress could be managed and contained.

Critical Periods and Developmental Windows

The paper emphasises that epigenetic programming occurs during specific developmental windows when the brain is maximally plastic and responsive to environmental input. In rats, the first week of life represents the critical period for GR gene methylation; in humans, this window likely extends through infancy and early childhood. During these periods, experience is not merely recorded—it is inscribed into the molecular structure of the developing organism.

This has profound implications for understanding developmental trauma. Adversity during critical periods does not just create bad memories or maladaptive beliefs; it programs the biological systems that will govern stress responses for life. The child whose early years are marked by neglect, unpredictability, or abuse develops a stress system calibrated for threat. This calibration becomes increasingly stable as development proceeds, like wet concrete hardening around whatever patterns have been impressed upon it.

However, Meaney and Szyf also emphasise that these patterns, while stable, are not immutable. Cross-fostering experiments demonstrated that pups born to low-nurturing mothers but raised by high-nurturing mothers developed the epigenetic profile—and the calm temperament—of their foster mothers. The biological inheritance could be overwritten by caregiving experience. This plasticity offers profound hope for intervention.

Reversibility and Therapeutic Implications

Perhaps the most important aspect of the paper for survivors is the demonstration that epigenetic modifications can be reversed. Using a drug called trichostatin A (a histone deacetylase inhibitor), the researchers were able to remove the methylation marks from adult animals who had been neglected as pups—and their stress responses normalised. What early experience had programmed, pharmacological intervention could reprogram.

This finding has massive implications for understanding healing from complex PTSD and developmental trauma. If the biological embedding of early adversity is reversible, then therapeutic change is not merely compensatory (learning to cope with permanent damage) but potentially restorative (actually modifying the underlying biological substrate). The same neuroplasticity that allowed harmful patterns to be written allows healing patterns to be inscribed.

For survivors of narcissistic abuse, this is genuinely hopeful news. Your chronic hypervigilance, your difficulty calming down, your exaggerated stress responses—these are not character flaws or permanent damage but biological adaptations that can be modified. The modification is not easy or quick; it likely requires sustained corrective experience at the relational level. But biology does not foreclose the possibility of change.

Original Context

The Scientific Landscape in 2005

When this paper appeared in 2005, the scientific understanding of gene-environment interaction was at a crossroads. The Human Genome Project had been completed just two years earlier, and there was widespread expectation that genetic determinism would explain most of human behaviour and disease. The epigenetics revolution was just beginning, and the idea that social experience could modify gene expression was still controversial in many quarters.

Meaney and Szyf's work challenged the reductionist view that genes were destiny. By demonstrating a specific molecular pathway from maternal behaviour to gene expression to lifelong stress reactivity, they provided concrete evidence that nurture could become nature—that the environment did not merely select among genetic predispositions but actively shaped how genes functioned. This paper helped establish what is now called "social epigenetics" or "behavioural epigenetics" as a legitimate field of scientific inquiry.

Building on Earlier Discoveries

This 2005 paper synthesised and extended the findings from the team's landmark 2004 paper in Nature Neuroscience (Weaver et al.), which had first demonstrated the methylation mechanism. While the 2004 paper presented the experimental evidence, the 2005 paper provided the broader theoretical framework—explaining what these findings meant for understanding development, stress, and the transmission of vulnerability across generations.

The research also built on decades of work in attachment theory and developmental psychology. John Bowlby had long argued that early relationships shape development, but the mechanisms remained mysterious. Harry Harlow's primate studies demonstrated that early deprivation had lasting effects, but again, the "how" was unclear. Meaney and Szyf's work provided the molecular mechanism that attachment theorists had lacked—the precise pathway from relationship to biology.

A Revolution in Understanding Intergenerational Transmission

Before this research, the intergenerational transmission of trauma and dysfunction was observed but poorly understood. Clinicians noted that children of traumatised parents often developed similar difficulties, but the mechanisms were assumed to be purely psychological—learned behaviour, unconscious identification, or family system dynamics. Meaney and Szyf demonstrated that the transmission could be biological: a parent's own epigenetic programming affects their caregiving capacity, which programs their offspring's epigenome, perpetuating the pattern.

This reframing had important implications for intervention. If transmission occurs through caregiving behaviour, then supporting parents' own healing and capacity for attunement becomes central to prevention. The research suggested that any nurturing relationship during critical periods might buffer the child's biological programming, even if the primary caregiver was compromised. Grandparents, teachers, therapists, and other consistent caregiving figures could potentially provide the epigenetic programming that builds resilience.

Implications for Human Health and Disease

While the original experiments were conducted in rats, subsequent research has confirmed that similar mechanisms operate in humans. McGowan et al. (2009) found increased GR gene methylation in the brains of adults who had experienced childhood abuse—the same pattern observed in neglected rat pups. Other studies have found similar epigenetic changes in blood cells of trauma survivors, suggesting these marks are present throughout the body.

The research has implications far beyond mental health. Adverse childhood experiences affect physical health across the lifespan, contributing to cardiovascular disease, autoimmune conditions, metabolic disorders, and shortened life expectancy. Meaney and Szyf's work suggests that these effects may be mediated partly through epigenetic programming—early adversity sets stress systems running hot, and chronic stress activation damages organs throughout the body over decades. Understanding this mechanism opens possibilities for targeted intervention at the biological level.

For Survivors

Understanding Why the Effects Feel So Deep

If you were raised by a narcissistic parent, you may have sensed that the damage goes deeper than memories or beliefs—that something about your fundamental biology was affected. Meaney and Szyf's research validates this intuition. Your parent's behaviour during your formative years didn't just create psychological patterns; it programmed how your stress-response genes function at the molecular level.

The hypervigilance that exhausts you, the difficulty truly relaxing, the exaggerated startle responses, the sense that you're always waiting for the other shoe to drop—these are not failures of will or character. They reflect a stress system that was epigenetically calibrated during development for an environment of chronic, unpredictable threat. Your amygdala learned to run hot because in your childhood, threat was everywhere. Your glucocorticoid receptors may have been silenced because the stress never stopped. Your biology adapted perfectly to the world you actually lived in—the tragedy is that adaptation now makes navigating a safer world more difficult.

Understanding the biological basis of your struggles can help reduce self-blame. You are not failing to "get over it" or "move on" because of weakness or self-indulgence. You are operating with a stress system that was built differently during construction, not damaged after completion. The modification is not superficial; it is written into the molecular structure of your cells. This is why cognitive insight—knowing intellectually that you are now safe—often fails to translate into felt safety. The knowledge lives in your prefrontal cortex, but the programming lives in your hippocampus and throughout your body.

The Reality of Body-Level Trauma

Many survivors describe trauma as living in their body, not just their mind. Meaney and Szyf's research explains why. The epigenetic changes they documented occur in cells throughout the brain and body, not just in memory systems. Your muscles carry the signature of early stress; your gut microbiome was shaped by stress hormones; your cardiovascular system was programmed for vigilance. When you feel that the trauma is "in your bones," you are describing biological reality.

This is why purely cognitive approaches to healing often feel insufficient. You can understand what happened, develop sophisticated frameworks for making sense of your family, identify the cognitive distortions caused by early experience—and still have a nervous system that reacts as if danger is ever-present. The insight lives in one neural system; the programming lives in another. Healing must address both levels.

Body-based approaches to trauma treatment—somatic experiencing, sensorimotor psychotherapy, EMDR, yoga, breathwork—work partly because they engage the body where the programming lives. Talking about trauma addresses the narrative level; working with the body addresses the epigenetic substrate. Both are necessary for deep healing.

Hope for Change Despite Deep Biological Embedding

The most important message of this research for survivors is that epigenetic modifications are not permanent. What experience has written, experience can rewrite. The same plasticity that allowed your stress system to be programmed for threat allows it to be reprogrammed for safety—with the right experiences over sufficient time.

Cross-fostering experiments proved that nurturing care could erase the epigenetic marks of early neglect. Pharmacological interventions demonstrated that adult brains retain the capacity for epigenetic modification. Emerging research suggests that psychotherapy can produce measurable changes in gene expression and possibly methylation patterns. While human translation of these findings continues, the principle is established: your biology is not your destiny.

This doesn't mean healing is easy or quick. The modifications were laid down during thousands of hours of early experience; they will likely require sustained corrective experience to modify. But "difficult" is different from "impossible." Each moment of genuine safety, each experience of attunement with a therapist or safe person, each time your nervous system learns that calm is possible contributes to reprogramming. You are not erasing years of damage overnight, but you are incrementally modifying the biological substrate of your stress responses. The brain that learned danger can learn safety—slowly, with repetition, through relationship.

Breaking Generational Cycles

If you are a parent or considering parenthood, this research offers both challenge and hope. The challenge: your own epigenetic programming affects your stress reactivity and emotional regulation, which affects your capacity to provide the consistent attunement your children's developing brains need. Parenting from a dysregulated nervous system is exponentially harder than parenting from a regulated one. The moments when your children most need calm presence may be exactly when your own programming floods you with stress hormones.

The hope: the research demonstrates unambiguously that it is your behaviour toward your children—not your history, not your genes—that programs their stress systems. If you can provide consistent, attuned care, even when it requires enormous effort, you are writing resilience into your children's biology. You don't have to be perfect; research suggests that healthy parent-child dyads are attuned only about 30% of the time. What matters is reliable repair, consistent overall presence, and your children's cumulative experience of being seen and responded to.

Getting support for your own healing is one of the most important things you can do for your children. Working with a therapist, building a support network, learning to regulate your own nervous system, understanding your triggers—these investments in yourself directly benefit your children by increasing your capacity to be present for them. The intergenerational cycle can be broken, but breaking it requires attending to your own biology as well as your parenting behaviours.

For Clinicians

Assessment Through a Developmental Lens

Meaney and Szyf's research requires clinicians to think developmentally about stress-related presentations. When patients present with chronic anxiety, hypervigilance, emotional dysregulation, or PTSD symptoms, assessment should map the timing of adverse experiences against developmental windows. Adversity during the period analogous to the rat "first week of life"—likely the first 2-3 years in humans—has different implications than later adversity because different brain systems were under construction.

Patients whose early childhood was marked by narcissistic parenting—with its characteristic emotional unavailability, unpredictable responsiveness, and chronic invalidation—may show the deepest epigenetic embedding of stress vulnerability. Their difficulties are not just about processing traumatic memories but about the foundational programming of stress physiology. This has implications for treatment planning: purely cognitive approaches may be insufficient; body-based and relational modalities may be essential; treatment may need to be longer and more intensive than standard protocols.

Assessment should include specific inquiry about early caregiving quality, not just the presence or absence of trauma. Was there consistent responsiveness to distress? Were there safe figures available? What was the overall emotional atmosphere of the home during the first years of life? These questions help identify patients whose presentations may reflect epigenetic embedding rather than discrete traumatic memories.

The Therapeutic Relationship as Intervention

If parental behaviour programs stress physiology through consistent relational experience, therapeutic relationships may operate through similar mechanisms. The consistent, attuned, boundaried presence of the therapist provides what Schore calls "psychobiological attunement"—the regulated co-presence that the patient's developing brain may have lacked. Over time, this experience may modify the biological substrate of stress reactivity.

This has implications for how clinicians conceptualise their role. The relationship is not merely the context for intervention (creating safety so techniques can be applied); it is the intervention. The therapist's regulated presence communicates safety to the patient's nervous system in ways that verbal reassurance cannot. The consistency of appointments, the reliability of the therapist's responsiveness, the repair of ruptures when they occur—these are not just good therapeutic practice but potentially epigenetic interventions.

Treatment intensity may need to match developmental depth. Standard outpatient therapy (weekly 50-minute sessions) may be insufficient for patients whose stress systems were programmed during early development. The original programming occurred through consistent experience over months; modification likely requires similar consistency. More frequent sessions, longer sessions, residential treatment, or therapeutic community approaches may be necessary for meaningful biological change.

Validating the Biological Reality of Trauma

Patients often struggle to find language for experiences that feel deeper than psychology—a sense that they are "wired differently" or "damaged at a cellular level." Meaney and Szyf's research allows clinicians to validate these intuitions: the patient is describing biological reality. The chronic hypervigilance, the difficulty trusting safety, the exaggerated stress responses are not character deficits but predictable outcomes of epigenetic programming.

This validation itself can be therapeutic. It reframes the patient's experience from personal failing to understandable consequence. It explains why insight alone hasn't resolved the difficulties—the programming lives below the level of language and belief. It provides a rationale for body-based approaches and sustained relational treatment. And it offers hope: what was programmed can be reprogrammed. The patient is not permanently broken; they are carrying adaptations that made sense developmentally and can be modified with the right experiences.

Pharmacological Augmentation

While Meaney and Szyf's reversal of epigenetic marks used a specific drug (trichostatin A) administered directly into the brain—not clinically practical—their findings suggest that pharmacological augmentation of psychotherapy may have biological rationale. Medications that enhance neuroplasticity, such as SSRIs (which increase brain-derived neurotrophic factor), may create neurobiological conditions more conducive to the relational learning that builds new patterns.

For patients with severe stress dysregulation that impedes engagement in therapy, stabilising medication may be necessary before meaningful therapeutic work can proceed. The goal is not to medicate away the problem but to create sufficient biological stability for the relational intervention to take hold. Understanding the epigenetic substrate helps clinicians frame medication as supporting, not replacing, the essential relational work of healing.

Broader Implications

Reframing the Nature-Nurture Debate

Meaney and Szyf's work dissolves the false dichotomy between nature and nurture. The genome is not a fixed blueprint that determines development independent of experience; nor is the organism a blank slate written upon by environment. Instead, genes and experience exist in continuous transaction, with experience shaping which genes are expressed through specific molecular mechanisms. Nature and nurture are not separate forces but interacting aspects of a single developmental process.

This reframing has implications for how we think about human potential and responsibility. We are neither genetically determined nor infinitely malleable. Biology creates predispositions and constraints, but experience shapes how those predispositions manifest. Early adversity programs vulnerability—but later experience can reprogram it. Understanding this dialectic allows for realistic assessment of what change requires and what change can achieve.

Intergenerational Trauma as Biological Transmission

The research provides a molecular mechanism for intergenerational trauma. A parent whose childhood was marked by neglect or abuse carries epigenetic modifications that affect their stress reactivity, emotional regulation, and capacity for attunement. These biological constraints make consistent, responsive caregiving harder—not impossible, but harder. Their caregiving behaviour then programs their offspring's epigenome, potentially transmitting vulnerability to the next generation.

Understanding this mechanism reveals intervention points. Supporting parents' own healing—through therapy, social support, stress reduction, and treating mental health conditions—may be as important as parenting education. The parent who achieves greater regulation can provide more regulated caregiving. Breaking the intergenerational cycle requires addressing the biology of the parent, not just their knowledge or intentions.

Public Health and Prevention

Viewing epigenetic programming through a public health lens transforms childhood adversity from an individual misfortune to a population-level crisis. The biological embedding of early stress affects health, behaviour, and functioning across the lifespan, contributing to chronic disease, mental illness, substance abuse, and reduced life expectancy. The costs cascade through healthcare systems, criminal justice systems, welfare systems, and lost economic productivity.

Investment in early childhood—supporting new parents, providing accessible mental health services, offering high-quality early education and childcare, preventing family violence—may represent one of the highest-return public health investments possible. Each child whose stress system is programmed for resilience rather than vulnerability represents reduced lifetime healthcare costs, increased workforce participation, and prevented transmission to the next generation.

Implications for Understanding Narcissistic Development

The epigenetic framework illuminates how narcissistic personality patterns may develop. The vigilance required to maintain the false self, the unpredictability of narcissistic parental mirroring, and the terror of empathic abandonment all constitute chronic stress during the critical period when the HPA axis is being calibrated. The resulting epigenetic profile—heightened stress reactivity, difficulty with emotional regulation, impaired capacity for genuine intimacy—underlies the narcissistic presentation.

This does not excuse narcissistic behaviour, but it explains its depth and resistance to change. The narcissist's characteristic patterns are not merely psychological defences but biologically embedded adaptations. Change would require sustained relational experience sufficient to modify the epigenetic substrate—a level of therapeutic intensity that most narcissists are not motivated to pursue because their defences protect them from the underlying vulnerability.

Workplace and Organisational Applications

Adults carrying the epigenetic signature of early adversity may struggle in environments that chronically activate their stress systems. The boss whose management style triggers vigilance, the performance review system that activates threat responses, the workplace competition that echoes early family dynamics—these can maintain or worsen biological programming laid down in childhood.

Organisations interested in employee wellbeing might consider how their cultures and practices affect those whose stress systems were calibrated by early adversity. Trauma-informed workplace design—emphasising psychological safety, predictability, transparent communication, and supportive management—may benefit not just individual employees but organisational performance by reducing the hidden costs of chronic stress activation.

Legal and Policy Considerations

The research has implications for how legal and child welfare systems understand behaviour and make decisions. If early caregiving programs stress-response systems through epigenetic mechanisms, adults raised in adverse conditions may genuinely have impaired stress regulation—a biological reality relevant to understanding behaviour without excusing it.

For child welfare systems, the research underscores the importance of stable placement during early childhood. Every move between caregivers disrupts the consistent relational experience needed for healthy epigenetic programming. Early, stable placement with nurturing caregivers may be more important than preserving biological family connections if the biological family cannot provide adequate care. The biological stakes of inconsistent early caregiving are now documented at the molecular level.

FAQs

Does this research mean my parent's behaviour permanently changed my DNA?

Not your DNA sequence—that remains unchanged—but how your genes are expressed. Think of it like a dimmer switch: the genetic code for the stress-response system remains intact, but epigenetic modifications determine how strongly that code is read. Meaney and Szyf showed that parental behaviour adds or removes chemical tags (methyl groups) on DNA that control whether stress-buffering genes are turned up or down. If you experienced neglect or abuse, these tags may have silenced genes that help shut off the stress response, leaving you with a system that runs chronically hot. But here's the crucial part: the study also demonstrated these tags can be modified. The same plasticity that allowed harmful patterns to be written allows healing patterns to be inscribed.

Why does it feel like my body remembers the trauma even when my mind doesn't?

Because epigenetic changes occur at the cellular level throughout your body, not just in memory systems. The modifications Meaney and Szyf documented affect the glucocorticoid receptor gene—which regulates stress hormones—in the hippocampus, but similar changes occur throughout the brain and body. Your muscles, gut, immune system, and cardiovascular system all carry epigenetic signatures of early experience. When survivors describe "body memories" or feeling that trauma lives in their flesh, they are describing biological reality. The experience was encoded not just in neural memory circuits but in the epigenetic programming of cells throughout your organism. This is why healing often requires body-based approaches—the memory isn't just in your mind.

If early experience programs stress responses, does that mean narcissists can't change because their biology is fixed?

No—and this is where the research offers both challenge and hope. While the epigenetic modifications are stable (they don't spontaneously reverse), they are not permanent. The study demonstrated that pharmacological intervention could remove the methylation marks and normalise stress responses in adult animals. For narcissists, this means the biological embedding of their early experience creates strong resistance to change but not impossibility. The challenge is that meaningful change would require sustained corrective experience at the relational level—the same kind of consistent, attuned caregiving that was missing in development. Most narcissists are not motivated to engage in this difficult work because their defences protect them from feeling the underlying vulnerability. But biology does not foreclose the possibility; psychology and motivation are the limiting factors.

How does this research explain the intergenerational transmission of narcissistic family patterns?

The research provides a molecular mechanism for a pattern clinicians have long observed: trauma and dysfunction transmitting across generations. A parent who experienced neglect carries epigenetic modifications that affect their stress reactivity and emotional regulation. These biological changes make it harder to provide the consistent, attuned caregiving that healthy child development requires. The parent's dysregulated nervous system cannot reliably offer the regulated presence that programs resilience in the child. As a result, their caregiving behaviour programs similar epigenetic modifications in their offspring. The child grows up, becomes a parent, and the cycle continues. Understanding this mechanism reveals intervention points: supporting parents' own healing may be as important as parenting education, and any nurturing relationship during critical periods may buffer the child's biological programming.

What does this mean for my own children—have I passed on my trauma?

This is one of the most important questions survivors ask, and the research offers genuine reassurance. While some epigenetic marks can transmit across generations, the Meaney and Szyf research emphasises that it is the quality of care the child receives—not the parent's history—that programs the child's stress system. Cross-fostering experiments proved this definitively: pups born to low-nurturing mothers but raised by high-nurturing mothers developed the calm phenotype of their foster mothers. If you are providing consistent, attuned care to your children—even if it requires tremendous effort because of your own history—you may be breaking the cycle at the biological level. Your children's epigenetic programming will reflect your behaviour toward them, not what was done to you.

How should clinicians use this research in treating survivors of childhood narcissistic abuse?

The research has several direct clinical implications. First, validate the biological reality of developmental trauma—when patients describe feeling "wired wrong" or "damaged at a cellular level," they are describing something real. Second, understand that treatment intensity matters: epigenetic marks were laid down through consistent patterns of caregiving over weeks and months, so modification likely requires sustained therapeutic exposure. Weekly 50-minute sessions may be insufficient for deeply programmed stress responses. Third, recognise the therapeutic relationship as a potential epigenetic intervention: if nurturing care programs resilience, consistent therapeutic attunement may serve a similar function. Fourth, consider body-based and regulatory approaches that address the physiological substrate of trauma, not just cognitive patterns. Finally, help patients understand that healing is biologically possible—they are not permanently marked—while setting realistic expectations about the time and consistency required.

Can therapy actually reverse these epigenetic changes, or is medication required?

This is an active research frontier, and early findings are encouraging for therapeutic intervention. While Meaney and Szyf used pharmacological agents (histone deacetylase inhibitors) to reverse epigenetic marks in their animal studies, subsequent research suggests that experience-based interventions may also modify methylation patterns. Studies have found that psychotherapy can produce measurable changes in gene expression and even DNA methylation in humans. The mechanism makes sense: if consistent relational experiences created the epigenetic marks, consistent new relational experiences might modify them. We don't yet have definitive evidence that therapy fully reverses the specific glucocorticoid receptor methylation, but we know that therapeutic relationships can alter cortisol patterns and stress reactivity. Whether these represent epigenetic reversal or other compensatory mechanisms, the clinical outcome—reduced stress vulnerability—appears achievable through relational intervention.

What specific aspects of parenting behaviour affect epigenetic programming?

In the rodent studies, the key behaviour was "licking and grooming"—the rodent equivalent of nurturing physical contact and attentive care. Pups who received more of this behaviour developed less methylation of the glucocorticoid receptor gene and more moderate stress responses. The human equivalents likely include consistent responsiveness to infant distress, affectionate physical contact, emotional attunement, and reliable presence. What appears to matter is not any single interaction but the cumulative pattern—thousands of moments of being seen, soothed, and responded to. For survivors of narcissistic parenting, the deficit is typically this consistent attunement: the narcissistic parent may provide occasional warmth but cannot sustain reliable responsiveness because their own needs take priority. The child's stress system calibrates to the unpredictability rather than the occasional good moments.

Environmental Programming of Stress Responses Through DNA Methylation: Life at the Interface Between a Dynamic Environment and a Fixed Genome

APA Citation