This paper was written to complement the talk, Unseen Scars: The Neurobiology of Trauma, presented at a meeting of the National Crime Victims Bar Association in Scottsdale, AZ, July 2014.

Walter E.B. Sipe, MD
Assistant Clinical Professor of Psychiatry and Pediatrics
University of California, San Francisco

Unseen Scars: The Neurobiology of Trauma

“Traumatic events of the earliest years … are not lost but, like a child's footprints in wet cement, are often preserved lifelong. Time does not heal the wounds … time conceals them. They are not lost; they are embodied.” —Vince Felitti, forward to Lanius et al.(1)


The Mind-Body Split

The profound impact of overwhelming trauma has long been recognized: modern day soldiers with what is now called PTSD hear the echoes of their experience in the ancient Greek tragedies of Sophocles. But only recently has there been an emerging understanding of how what we see outwardly as the behavioral and psychological effects of trauma, are a reflection of alterations at the level of hormones, nerve cells, and even our genes. Despite the fact that neuroscience tells us that mood, behavior, and social interactions are products of specific (albeit still incompletely defined) neural networks, we still speak in the 17th century language of Rene Descartes, where our physical selves are somehow distinct from our mind. This artificial distinction is reified in our tax code: psychological damages are taxed when physical damages are not.

Intention of this Talk

There are extensive book length reviews on the topic of trauma and its effects,(1,2) and more articles are published every month. The intention of this talk is to provide a brief overview of some of the ways in which overwhelming stress and trauma can have lifelong consequences on emotional and physical health, and the current research suggesting how the lasting psychological impact of exposure to trauma in childhood might be accompanied by equally enduring changes at the molecular level.(3) By examining alterations in several important domains—coping and the stress response; childhood and adult attachment; learning and memory; and cellular aging—participants will have a better sense of how observable social, occupational, and medical dysfunction in traumatized individuals may reflect damages of fundamental biological processes.

Stress & Trauma

Stress as biologic universal

To be human is to be exposed to stress and adversity. Over 60 years ago the pioneering endocrinologist Hans Selye recognized the essential nature of an organism’s ability to maintain balance in the face of threat: "Anything that causes stress endangers life, unless it is met by adequate adaptive responses; conversely, anything that endangers life causes stress and adaptive responses. Adaptability and resistance to stress [resilience] are fundamental prerequisites for life, and every vital organ and function participates in them.”(4) So fundamental is this process of stress, adaptation, and expanded resilience that almost anyone on a jury will recognize some version of it in their own life: for example, a weight lifter who adds a little more weight to the bar every time, or in lessons learned from “The School of Hard Knocks.” Indeed, research bears out the notion that early life exposure to stressful experiences that are challenging but not overwhelming, leads to improved coping in adulthood with challenges such as spousal loss, illness, and major accidents.(5) This phenomenon—stress inoculation—is likely due to expanded regulation of emotional centers of the brain by the prefrontal cortex.(6)

The inverted U

Yet if manageable amounts of stress enhance functional capacity, it is also NOT the case that “What does not kill me, makes me stronger.”(7) Lifting weights in the gym will yield a very different result than will trying to catch a falling piano. Similarly, when stress becomes overwhelming and exceeds an individual’s coping capacity, as in the case of trauma, the system will still adapt in some way, prioritizing survival at expense of future health. The impact of stress on an individual takes the shape of an inverted U. At very low levels of stress, there is no impetus for performance or adaptation. As stress increases, more resources are called upon, and up until a point (which varies for every individual) adaptation will leave them more resilient and able to more adequately tolerate subsequent stressors. Once the adaptive capacity is exceeded, performance breaks down and any additional stress becomes a trauma in the sense I am using the word: a stressor that induces a negative adaptation. We will go on to explore how these negative adaptations play out at the neurobiological level.

The ACE Study: Childhood Adversity and Lifelong Health

Before looking at specific systems, it is useful to have a broader context of just how pervasive and enduring the effects of early abuse and stressful experience can be. The Adverse Childhood Experiences (ACE) study includes data from over 17,000 individuals receiving primary care services in a major U.S. city.(8,9) Each participant was asked to fill out a brief questionnaire regarding a number of adverse experiences, including neglect, abuse, and family chaos, that may have occurred during the first 18 years of life. For every health outcome examined, there was a direct relationship with the burden of adverse experiences. This includes increased rates of psychiatric issues, poor social function, and problematic substance use. The findings were just as striking for medical illness, and perhaps even more provocative. There is a strong association between childhood adversity and greater prevalence of liver disease, chronic obstructive pulmonary disease, autoimmune issues, and coronary artery disease (the leading cause of death in the United States). This relationship between adverse experience and disease persists independent of risk factors such as smoking or alcohol use. This relationship between childhood trauma and health is anything but trivial. Analysis of the current data set suggests that, all other factors equal, individuals with a high burden of adverse experiences have a lifespan almost two decades shorter than those without reported trauma.(10)

Cortisol and Stress Regulation

Critical to our ability to manage our response to stress are the adrenal hormones cortisol and adrenaline, as well as the sympathetic nervous system. Release of these peripheral hormones is largely mediated by the release of corticotrophin releasing factor (CRF) in our brain. When we are subjected to a potential threat—emotional or physical—CRF activates the sympathetic nervous system, and the blood stream is flooded with cortisol and adrenaline, leading to increased physical arousal, attention, and vigilance. CRF also activates neurons involved in behavioral and emotional response to stress.(11) In the short term this response, while uncomfortable, leads to improved mental performance and ability to deal with physical challenge. (This is the crest of the inverted U). Negative feedback from these hormones back to the brain shuts down the response, and in a healthy system leads to a self-limited, acute stress response. Victims of trauma, however, have a profoundly altered stress response system. With severe stress during a critical period, there appears to be a lifelong increase in CRF levels(12) and these changes are the result of programing occurring at the level of individual genes.(13) In essence, traumatic events and environments shift what is ideally a system designed to cope with short-term stress into a chronically “ON” state, with profound consequences on mood, anxiety and physical health.

Depression, anxiety, and physical health

Women with a history of child abuse are four times more likely to develop depression compared to non-abused women, and the magnitude of abuse is correlated with the severity of depression.(14) Depressed individuals demonstrate a variety of dysfunctions in the CRF-cortisol system, and these changes may be a biologically distinguishable subtype of depression as a function of early trauma exposure.(12) Chronic activation of the stress axis by CRF also alters expression of certain serotonin receptors in the brain, also contributing to the onset of anxiety and depression.(15)

Individuals with PTSD and a history of child abuse appear to have a toxic combination of abnormally low baseline levels of cortisol while at the same time having a hyperactive response to everyday stress, thereby perpetuating the chronic stress response.(16) Indeed, poor resilience to later life stresses may be one of the most important hidden damages of early trauma. For example, data from combat veterans points to early childhood abuse / adversity as a significant risk factor for developing combat-related PTSD (even if there were not prior obvious symptoms of PTSD related to the early trauma itself).(17)

Chronic dysregulation of the stress response is not simply a matter of psychological well-being. Individuals with chronic stress have poor ability to mobilize white blood cells during surgery and subsequently demonstrate poor healing compared to individuals who can mount an appropriate acute stress response.(18) In addition, poor regulation of stress responses may contribute to alterations in insulin sensitivity (hence obesity), bone metabolism, and acquired immune responses.(19)

The Attachment System and Oxytocin

As social animals, our attachment system—the way in which we seek out and maintain connection with other human beings—is fundamental to life. One can barely function in society, let alone develop meaningful friendships and romantic partnerships, or raise children, without the ability to establish social bonds and regulate emotional behaviors. At the center of this capacity is the hormone, oxytocin, which is released during every imaginable form of pleasant social contact.(20)

Impaired trust and stress-regulation

In almost every social mammal studied, oxytocin has been found to be critical for expression of social behaviors, and it plays a seminal role in mediating complex social interactions such as affiliation, attachment, maternal behavior, trust and aggression.(21) Experiments demonstrate that oxytocin delivered as a nasal spray measurably increases trust and willingness to take social risks (of exactly the sort that underlie economic exchanges).(22) With actions far more complex than being a general “love hormone,” oxytocin specifically appears to modulate cooperation and a sense of group belonging.(23)

Oxytocin also is essential for regulation of stress and fear: oxytocin acts directly to reduce activity in the brain’s “threat center,” the amygdala.(24) At a behavioral level, one of the ways that a human being regulates stress is to connect closely with another person. When an upset child runs into the arms of a parent, something more fundamental than simple reassurance is taking place. The caring parent is literally helping regulate the child’s nervous system. While these care seeking behaviors become more sophisticated in adulthood, the ability to confide and receive support from a valued friend, family member, or lover, is nonetheless an important mechanism by which we regulate stress. The oxytocin response appears to be both necessary to initiate these contacts (one can only approach someone when trust is greater than fear), as well as a product of this connection.

Children exposed to early neglect have lower levels of oxytocin and other attachment related hormones, even several years removed from the deprived environment.(25) Even as adults, the fluid surrounding the brain of adult survivors of abuse or neglect have lower levels of oxytocin, which correlates with the severity and duration of the abuse, as well as current anxiety ratings.(21) In addition, emotional abuse is especially predictive of lower oxytocin level. Therefore, when victims of trauma, particularly those incidents that involve a violation by a family member or an otherwise trusted figure, speak of having “trust issues,” they may be speaking of a profound biological deficit in their capacity to manage all variety of interpersonal interactions.

Decreased sexual sensation in women

For adults, some of the most important attachment dynamics play out in sexual intimacy. Not surprisingly, oxytocin levels increase significantly after orgasm,(26) and sexual problems are rife in victims of sexual abuse. In a striking brain imaging study, women who were exposed to childhood sexual abuse actually had a reduction in the size of their brain area associated with processing genital sensations. This suggests a specific protective brain adaptation that may shield a child from the sensory processing of the specific abusive experience at the cost of sexual dysfunction later in life.(27)

Learning and Memory: Hippocampus and Amygdala

Much ink has been spilled on the topic of trauma and memory, so what follows is necessarily limited to primarily illustrate how psychological observations have a cellular basis.

Under conventional wisdom, when the average person speaks of “remembering,” they typically are referring to the sense of having a conscious recollection of a series of words, images, and sensations of something distinct that happened in the past, much like watching an internal video. Brain scientists, however, recognize several different types of memory.(28) Explicit memory is that portion of memory that is associated with the conscious sense of recollection. It can be further divided into episodic memory—the distinct sense of recollection of a self and events, in place and time, and—narrative / sematic memory—heavily language based aspect of memory that includes “facts” but also the story that we put together to put episodic memories in context. There is also implicit memory. When triggered, implicit memory has a sense of experiential immediacy devoid of subjective sense of recall or “remembering.” In trauma, a classic example would be a sexual assault victim who becomes uneasy and panicked in a dark parking garage, even without any thought of the past assault. And all these different types of memory involve interconnected but still distinct brain circuits.

Moderate levels of stress enhance memory

To again revisit the inverted U, it has long been recognized that memory functions best at moderate level of stress, and that this phenomenon is related to the function of stress hormones and neurotransmitters on the hippocampus.(29) Episodic memory requires focal attention for formation and the hippocampus is the part of the brain essential for ongoing storage. Up to a certain point, increasing arousal of the amygdala (the brain region that activates under conditions of high emotional content) facilitates the hippocampus to encode environmental and sensory information. This is part of the reason why major events such as a first kiss, a graduation, or a scary experience live so easily in memory, and why a potential juror may have the thought, “If something like THAT happened to ME I would certainly have remembered it.” Most people who have not suffered severe stress or trauma will extrapolate from their own experience and not take into account the other side of the U.

Traumatic stress impairs memory

But as the level of amygdala activity increases from novelty, past mild anxiety, to abject terror, the enhancing function on the hippocampus peaks, after which overwhelming amygdala activation actually inhibits formation and retrieval of episodic memories. So the result can be absent sense of distinct events in place and time, combined with fragmented implicit sensory impression that are very powerful.(2) Not only the magnitude of the stress impacts memory function, but also the duration of the stress response. During stress responses that last on the order of minutes, the stress hormone CRH actually primes connections between nerve cells in the hippocampus—the cellular process generally believed to underlie learning and memory. As the exposure to CRH extends to hours, the opposite process occurs, and hippocampal nerves begin to experience decreased function. As stress becomes chronic over days, weeks and beyond (see stress regulation, above) the structural changes become more pronounced.(30) Indeed the majority of brain imaging studies in PTSD demonstrate that the volume of the hippocampus is reduced.(31) And from a functional perspective, traumatized youth have lower hippocampal activation,(32) indicating that learning and memory for all types of information—not just that of traumatic nature—may be impaired.

Given the central role that the hippocampus plays in storage and retrieval of episodic memories, it is striking to note that when researchers examined hippocampal brain tissue from men with a history of childhood trauma they discovered widespread alterations in over 350 promoters—regions of DNA that control the expression of individual genes.(33) Follow-up studies also show changes in multiple genes in the same brain region of an individual completing suicide.(34)

There is overwhelming clinical evidence of recovered memories,(29) consistent with our current understanding of memory function,(35) but a definitive neuroscience account of how recovered memory events occur remains to be established. However, there are compelling accounts emerging of how memory suppression may be mediated by frontal lobe regulation of the hippocampus.(36)

Telomeres: The Ultimate Biological Clock

An increasing area of interest in medical science is the role of telomeres—they were the subject of a Nobel Prize in 2009. Telomeres can be thought of as the aglets of our genetic material (an aglet being the plastic tip that prevents your shoelaces from unraveling). Every time a cell divides and replicates its DNA, a small piece from the end of the strand does not get copied. If there were not some buffer between the end of a chromosome and the region of activity, very soon important genetic information would get lost as the chromosome “unraveled.” Telomeres are this buffer and the longer they are, the better they fill this function.

Telomeres shorten with age, and shorter telomeres have been associated with increased incidence of age-associated diseases and poor survival.(37) In this way, telomeres can also be thought of as the ultimate “biological clock”.(38) However, the rate of telomere shortening can be dramatically impacted by specific lifestyle factors, with consequent impact on the speed of aging and disease onset. One clear association with shorter telomeres is ongoing stress. In one study conducted at UCSF, women with the highest levels of perceived stress had telomeres shorter on average by the equivalent of at least one decade of additional aging compared to low stress women.(39)

Early adversity and premature aging

In addition to current chronic stress, other studies have demonstrated shorter telomeres in subjects with childhood exposure to trauma, neglect, and maltreatment that are independent of any current demographic factors.(3,40) And the impact of dealing with a chronic current stressor was magnified in individuals with past childhood adversity, who demonstrated more pronounced telomere shortening and higher markers of systemic inflammation. These authors suggest that shortened telomeres due to childhood adversity could lead to a 7- to 15-year difference in life span.(41) Linking these finding back to the results from the ACE study, a picture emerges of a whole set of hidden damages that reveal themselves at the end of life in the form of premature senescence, early onset of chronic disease, and shortened life spans.


When is a stress a trauma

One pitfall in defining psychological trauma is attempting to quantify what particular level of stressful insult (e.g., what degree of threat, what level of inappropriate touching, etc.) constitutes a “trauma.” Yet we do not do this for physical injuries: if an injured patient has broken a bone, we generally do not quibble about how many pounds of force the limb suffered. Similarly, myriad variables such as age, social support, temperament, and genetic factors will impact an individual’s resilience to any particular set of external stressors. Ultimately any experience on the right side of the inverted U can set in motion biological processes that leave “molecular scars” down to the level of our very genes.

Damages: From biology to behavior

Translating findings from the world of medicine and science—where understanding is a constantly unfolding process that rarely yields facile cause and effect explanations—to the exigencies of the courtroom will always be a challenge. But in the case of traumatic stress, the link between fundamental biological changes and real world damages grows increasingly stronger:

  • Alterations in the stress regulation system involving cortisol and related hormones become risk factors for subsequent depression, anxiety disorders, and physical illness. Decreased resilience to later life stressors may limit the range of employment options, and lead to destructive coping techniques such as drugs and excessive alcohol use, and actually increase the risk of developing PTSD to later stressors.(42)
  • Disruptions of the attachment system, of which oxytocin is central, may lead to lifelong deficits in effectively managing social interactions, and lead to the sorts of deficits observed in the ACE study: sexual dysfunction, multiple marriages, and serious job problems.
  • Wide ranging impacts on the hippocampus, amygdala, and other elements of the memory system can produce distressing phenomena ranging from intrusive and repetitive sensory and emotional flashbacks, to incoherent or inaccessible episodic memories. The neurologic basis of recovered memories continues to be defined.
  • Early childhood trauma is associated with shorter telomeres, which are associated with earlier onset of the wide range of diseases of senescence. Given that trauma survivors may also be more susceptive to chronic stress via mechanisms described above—further impacting telomere length—the ultimate impact may be one to two decades of shortened life span and disease related disability.

  1. Lanius RA, Vermetten E, Pain C. The impact of early life trauma on health and disease: the hidden epidemic. Cambridge, UK ; New York: Cambridge University Press; 2010.
  2. Van der Kolk BA, McFarlane AC, Weisæth L. Traumatic stress: The effects of overwhelming experience on mind, body, and society: The Guilford Press; 1996.
  3. O'Donovan A, Epel E, Lin J, Wolkowitz O, Cohen B, Maguen S, et al. Childhood trauma associated with short leukocyte telomere length in posttraumatic stress disorder. Biological psychiatry. 2011;70(5):465-71.
  4. Selye H. Stress and the general adaptation syndrome. British Medical Journal. 1950;1(4667):1383.
  5. Lyons DM, Parker KJ, Katz M, Schatzberg AF. Developmental cascades linking stress inoculation, arousal regulation, and resilience. Frontiers in behavioral neuroscience. 2009;3.
  6. Lyons DM, Parker KJ, Schatzberg AF. Animal models of early life stress: implications for understanding resilience. Developmental psychobiology. 2010;52(7):616-24.
  7. Nietzsche F. Twilight of the Idols. 1889.
  8. Anda RF, Felitti VJ, Bremner JD, Walker JD, Whitfield C, Perry BD, et al. The enduring effects of abuse and related adverse experiences in childhood. A convergence of evidence from neurobiology and epidemiology. Eur Arch Psychiatry Clin Neurosci. 2006;256(3):174-86.
  9. Felitti VJ, Anda RF. The relationship of adverse childhood experiences to adult medical disease, psychiatric disorders and sexual behavior: implications for healthcare. In: Lanius RA, Vermetten E, Pain C, editors. The impact of early life trauma on health and disease : the hidden epidemic. Cambridge, UK ; New York: Cambridge University Press; 2010. p. xvii, 315 p.
  10. Brown DW, Anda RF, Tiemeier H, Felitti VJ, Edwards VJ, Croft JB, et al. Adverse childhood experiences and the risk of premature mortality. American journal of preventive medicine. 2009;37(5):389.
  11. LeDoux JE. Emotion circuits in the brain. Annual review of neuroscience. 2000;23(1):155-84.
  12. Heim C, Newport DJ, Mletzko T, Miller AH, Nemeroff CB. The link between childhood trauma and depression: insights from HPA axis studies in humans. Psychoneuroendocrinology. 2008;33(6):693-710.
  13. Murgatroyd C, Spengler D. Epigenetics of early child development. Frontiers in psychiatry / Frontiers Research Foundation. 2011;2:16.
  14. Mullen P, Martin JL, Anderson JC, Romans SE, Herbison G. The long-term impact of the physical, emotional, and sexual abuse of children: a community study. Child abuse & neglect. 1996;20(1):7-21.
  15. Leonard B. The HPA and immune axes in stress: the involvement of the serotonergic system. European psychiatry: the journal of the Association of European Psychiatrists. 2005;20:S302.
  16. LaPrairie JL, Heim CM, Nemeroff CB. The neuroendocrine effects of early life traum. In: Lanius RA, Vermetten E, Pain C, editors. The impact of early life trauma on health and disease : the hidden epidemic. Cambridge, UK ; New York: Cambridge University Press; 2010. p. xvii, 315 p.
  17. Van Voorhees EE, Dedert EA, Calhoun PS, Brancu M, Runnals J, Beckham JC. Childhood trauma exposure in Iraq and Afghanistan war era veterans: implications for posttraumatic stress disorder symptoms and adult functional social support. Child Abuse Negl. 2012;36(5):423-32.
  18. Gouin J-P, Kiecolt-Glaser JK. The impact of psychological stress on wound healing: methods and mechanisms. Immunology and allergy clinics of North America. 2011;31(1):81.
  19. Raison CL, Miller AH. When not enough is too much: the role of insufficient glucocorticoid signaling in the pathophysiology of stress-related disorders. The American journal of psychiatry. 2003;160(9):1554-65.
  20. Olff M. Bonding after trauma: on the role of social support and the oxytocin system in traumatic stress. European journal of psychotraumatology. 2012;3.
  21. Heim C, Young LJ, Newport DJ, Mletzko T, Miller AH, Nemeroff CB. Lower CSF oxytocin concentrations in women with a history of childhood abuse. Molecular psychiatry. 2009;14(10):954-8.
  22. Kosfeld M, Heinrichs M, Zak PJ, Fischbacher U, Fehr E. Oxytocin increases trust in humans. Nature. 2005;435(7042):673-6.
  23. De Dreu CK. Oxytocin modulates cooperation within and competition between groups: an integrative review and research agenda. Horm Behav. 2012;61(3):419-28.
  24. Kirsch P, Esslinger C, Chen Q, Mier D, Lis S, Siddhanti S, et al. Oxytocin modulates neural circuitry for social cognition and fear in humans. The Journal of neuroscience: the official journal of the Society for Neuroscience. 2005;25(49):11489-93.
  25. Wismer Fries AB, Ziegler TE, Kurian JR, Jacoris S, Pollak SD. Early experience in humans is associated with changes in neuropeptides critical for regulating social behavior. Proceedings of the National Academy of Sciences of the United States of America. 2005;102(47):17237-40.
  26. Blaicher W, Gruber D, Bieglmayer C, Blaicher A, Knogler W, Huber J. The role of oxytocin in relation to female sexual arousal. Gynecologic and Obstetric Investigation. 1999;47(2):125-6.
  27. Heim CM, Mayberg HS, Mletzko T, Nemeroff CB, Pruessner JC. Decreased cortical representation of genital somatosensory field after childhood sexual abuse. The American journal of psychiatry. 2013;170(6):616-23.
  28. Siegel DJ. The developing mind: Toward a neurobiology of interpersonal experience: Guilford Press; 1999.
  29. Dalenberg C. Recovered memory and the Daubert criteria: recovered memory as professionally tested, peer reviewed, and accepted in the relevant scientific community. Trauma, violence & abuse. 2006;7(4):274-310.
  30. Maras PM, Baram TZ. Sculpting the hippocampus from within: stress, spines, and CRH. Trends in neurosciences. 2012;35(5):315-24.
  31. Teicher MH, Rabi K, Sheu Y-S, Seraphin SB, Andersen SL, Anderson C, et al. Neurobiology of childhood trauma and adversity. The impact of early life trauma on health and disease: The hidden epidemic. 2010:112-22.
  32. Carrión VG, Haas BW, Garrett A, Song S, Reiss AL. Reduced hippocampal activity in youth with posttraumatic stress symptoms: an fMRI study. Journal of pediatric psychology. 2010;35(5):559-69.
  33. Labonte B, Suderman M, Maussion G, Navaro L, Yerko V, Mahar I, et al. Genome-wide epigenetic regulation by early-life trauma. Archives of general psychiatry. 2012;69(7):722-31.
  34. Labonte B, Suderman M, Maussion G, Lopez JP, Navarro-Sanchez L, Yerko V, et al. Genome-wide methylation changes in the brains of suicide completers. The American journal of psychiatry. 2013;170(5):511-20.
  35. Brewin CR. A theoretical framework for understanding recovered memory experiences. Nebraska Symposium on Motivation Nebraska Symposium on Motivation. 2012;58:149-73.
  36. Anderson MC, Huddleston E. Towards a cognitive and neurobiological model of motivated forgetting. Nebraska Symposium on Motivation Nebraska Symposium on Motivation. 2012;58:53-120.
  37. Shammas MA. Telomeres, lifestyle, cancer, and aging. Current opinion in clinical nutrition and metabolic care. 2011;14(1):28-34.
  38. von Zglinicki T. Telomeres and replicative senescence: Is it only length that counts? Cancer Lett. 2001;168(2):111-6.
  39. Epel ES, Blackburn EH, Lin J, Dhabhar FS, Adler NE, Morrow JD, et al. Accelerated telomere shortening in response to life stress. Proceedings of the National Academy of Sciences of the United States of America. 2004;101(49):17312-5.
  40. Tyrka AR, Price LH, Kao HT, Porton B, Marsella SA, Carpenter LL. Childhood maltreatment and telomere shortening: preliminary support for an effect of early stress on cellular aging. Biological psychiatry. 2010;67(6):531-4.
  41. Kiecolt-Glaser JK, Gouin JP, Weng NP, Malarkey WB, Beversdorf DQ, Glaser R. Childhood adversity heightens the impact of later-life caregiving stress on telomere length and inflammation. Psychosomatic medicine. 2011;73(1):16-22.
  42. Yehuda R, Flory JD, Pratchett LC, Buxbaum J, Ising M, Holsboer F. Putative biological mechanisms for the association between early life adversity and the subsequent development of PTSD. Psychopharmacology. 2010;212(3):405-17.
Show Footnotes...