You may inherit your mother’s eyes or your father’s curly hair, but can trauma also be passed down through generations? Even if you never personally experience famine, natural disaster, or war, emerging research suggests that your body may still carry biological imprints of the traumatic events your parents endured.
So how does it all work? The story begins decades ago in the notes of a psychiatrist.
From the Beginning
After the horrific events of World War II, Dr. Vivian Rakoff began encountering patients experiencing severe psychological challenges and seeking psychiatric treatment. One commonality was noted between his patients: they were all children of holocaust survivors. Despite never living through the war themselves, Dr. Vivian Rakoff remarked, “It would almost be easier to believe they, rather than their parents, had suffered the corrupting searing hell”. Later, further studies found similar psychological problems in the offspring of Vietnam veterans. Headaches, tearfulness, and feelings of helplessness are all symptoms that were termed “secondary traumatization” by the author of these studies. The lack of a biological explanation for their difficulties led to an increase in neurobiology and endocrinology research.
The Missing Key: The HPA Axis
Although you have probably never heard of the hypothalamic-pituitary-adrenal (HPA) axis, humans utilize it every day. Whenever you are stressed about an exam, running late for a bus, or even fighting off a bear, your internal alarm, the HPA axis, is set off. First, the hypothalamus in the brain senses something stressful, a stimulus: a test, a missed bus, or a bear. Then it rings the alarm, sending down CRH (corticotropin-releasing hormone) to the pituitary gland.As an endocrine gland, the pituitary gland secretes and regulates hormones. When CRH is released, it signals the pituitary gland to secrete ACTH into the bloodstream. Travelling through the body, ACTH (adrenocorticotropic hormone) reaches the adrenal gland above the kidney. The chain of reaction triggers the final boss of the alarm system, cortisol. Finally rushing through your bloodstream, cortisol can sharpen focus, pump up blood, and fuel you with energy. By raising blood sugar, muscles gain the energy to run quickly, and by increasing blood pressure, the heart begins to pump extra hard to improve alertness. These physiological responses all prepare the body in the face of demanding situations.
When the Alarm Malfunctions
When the internal alarm malfunctions, also called HPA axis dysregulation, instead of warning you about a bear, you’re warned about everything else. An example is the body constantly firing a signal to run away when no life-threatening events are present. However, HPA axis dysregulation could also be the polar opposite: instead of always ringing the alarm, the body may barely react to stressors. For example, if you were to encounter a bear in the woods, your system could not activate the physiological response needed to defend yourself or run away.
Both these types of HPA axis dysregulation can be problematic. An overstimulated HPA axis can cause immune diseases, obesity, and cardiovascular issues. One such case is hypercortisolism–an excess exposure to cortisol produced by the HPA axis. Due to the nature of cortisol’s immunosuppressiveness, the surplus of cortisol can impair important tissues responsible for immune cell production and damage cytokine regulations, which sustain inflammatory responses.
On the other hand, forms of understimulation of the HPA axis can lead to autoimmune diseases, chronic fatigue, and mood disorders. Low cortisol states cause immune system up-regulation, which results in an increased production of pro-inflammatory cytokines. Left unchecked, these signal proteins induce fatigue, impaired cognition, and depressed mood.
As a crucial component of the body’s stress-response system, the dysregulation of the HPA axis profoundly affects immune functions, signaling pathways, and other physiological and psychological well-being.
The Womb’s First Warning Sign
On the island of Galápagos, researchers followed 24 mothers throughout their pregnancy and measured the cortisol levels of both the mother and their infants. Mothers with HPA axis dysregulation tend to exhibit elevated cortisol levels, so the study analyzed its effect on fetal development, especially the HSD11B2 gene (11β-hydroxysteroid dehydrogenase type 2). Within the placenta, the HSD11B2 enzyme functions as a protective buffer by catalyzing the conversion of active cortisol to its inert form, cortisone. However, under prolonged stress, this defense can weaken, resulting in a greater fetal exposure to the maternal cortisol. The deterioration occurs through a type of epigenetic (environmental) modification known as DNA methylation. Rather than changing the gene sequence itself, epigenetic changes regulate whether the body can access and express genetic information. Increased methylation reduces transcription on a certain gene, limiting the production of the desired protein. In this case, the HSD11B2 gene is where the methylation occurs. Data from the study reveal that high maternal cortisol is associated with low expression of HSD11B2, clarifying the link between stress and high HSD11B2 methylation. This diminished gene expression, however, can be consequential to the baby. With less HSD11B2 enzyme to inactivate maternal cortisol, the study found an elevated infant cortisol level, a sign of HPA axis dysregulation. Through the mechanism of the HSD11B2 gene, scientists observe how the mother’s stress is transferred to the baby, physically altering their system for managing pressure.
A Lasting Impact: What happens to these children of individuals with trauma?
Researchers at the Medical University of South Carolina investigated the effects of maternal PTSD (post-traumatic stress disorder) on their youth offspring, especially examining how the children respond to acute stressors. The 366 youth participants were asked to perform a series of stress-inducing challenges that engaged the HPA axis. These tasks involved threats of social rejection and evaluation, as well as anticipatory and processive stress. During the experiment, five saliva samples were collected to characterize the children’s cortisol reactivity profiles. The offspring of mothers with PTSD were significantly lower than those of the control group. This “blunted reactivity profile” matches descriptions of HPA axis dysregulation, where the body does not produce enough cortisol in the face of a demanding task. Results from the study show parental HPA axis dysregulation affecting their children’s stress response system. Although never experiencing their parents’ “trauma”, these children’s bodies inherited their stress reaction.
Into Adulthood
After studying infants and teenagers, researchers question whether the effects of parental trauma can last into one’s adulthood.This question was explored through a historical case study known as the Dutch Hunger Winter, a severe famine that occurred in the Netherlands after Nazi Germany blocked food supplies. During this period, daily food rations dropped dramatically, reaching as low as 370 calories per person, with especially severe consequences for pregnant mothers. In 2008, 60 children who were conceived during a famine, now adults, participated in a study by Dr. Bastiaan T Heijmans. Dr Heijmans and his team analyzed the epigenetic changes of these adults with IGF2 (insulin-like growth factor II), a well-characterized epigenetically regulated loci. A locus (or loci) refers to a specific location on a gene. For IGF2, the gene is maternally imprinted, meaning the maternal copy is silenced and only the paternal copy is expressed. This imprinting occurs through the IGF2 differentially methylated region (DMR), where low methylation allows both copies of the gene to be expressed.
IGF2 plays a key role in human growth and development, and its methylation pattern remains relatively stable into middle age, making it useful for detecting the long-term effects of early environmental exposure. In four of the five IGF2 DMR sites studied, individuals exposed during the periconceptional period showed significantly lower methylation compared to their same-sex siblings. This effect was not observed in individuals exposed later in gestation (for at least ten weeks), including those born during or shortly after the famine. The extreme case study of the Dutch Hunger Winter reveals how trauma is passed down from generation through epigenetic modifications.
The Future
The science of intergenerational trauma extends beyond measuring cortisol levels and doing stress tests; it reshapes our understanding of mental disorders, disease risk, and public health. Stress profiles of youth not only link maternal PTSD to children’s stress response, but also serve as early biomarkers for PTSD detection and intervention. Likewise, the effort in maternal HPA axis dysregulation creates opportunities for more responsive prenatal care during pregnancy, helping to identify and reduce risk factors in the process. The evaluation of traumatic events like Dutch Hunger Winter allows scientists to study their impact on next generations and develop support on a larger and more public scale. Furthermore, the association of stress and HPA dysregulation can shine light on communities in need: veterans, first responders, trauma survivors, and families living in impoverished environments. Understanding the biological pathways linking parent to child can provide targeted support for these families.
Intergenerational trauma research gains insight into complex mechanisms that link us to our parents. It tells stories of adversity and of resilience. By addressing the biological mechanism of our emotional systems, we improve our understanding of individuals and of ourselves.
References
Ancharoff, M. R., J. F. Munroe, and L. M. Fisher. “The Legacy of Combat Trauma: Clinical Implications of Intergenerational Transmission.” International Handbook of Multigenerational Legacies of Trauma, edited by Yael Danieli, Plenum Press, 1998, pp. 257–276. https://doi.org/10.1007/978-1-4757-5567-1_17.
Danielson, C. K., et al. “Youth Offspring of Mothers with Posttraumatic Stress Disorder Have Altered Stress Reactivity in Response to a Laboratory Stressor.” Psychoneuroendocrinology, vol. 53, Mar. 2015, pp. 170–178. https://doi.org/10.1016/j.psyneuen.2015.01.001.
de Zwarte, Ingrid. “Introduction.” The Hunger Winter: Fighting Famine in the Occupied Netherlands, 1944–1945, Cambridge University Press, 2020, pp. 1–16.
Dunlavey, Christopher J. “Introduction to the Hypothalamic-Pituitary-Adrenal Axis: Healthy and Dysregulated Stress Responses, Developmental Stress and Neurodegeneration.” Journal of Undergraduate Neuroscience Education, vol. 16, no. 2, 15 June 2018, pp. R59–R60.
Guilliams, Thomas G., and Lenard Edwards. “Chronic Stress and the HPA Axis: Clinical Assessment and Therapeutic Considerations.” Volume 9, no. 2, 2010.
Heijmans, Bastiaan T., et al. “Persistent Epigenetic Differences Associated with Prenatal Exposure to Famine in Humans.” Proceedings of the National Academy of Sciences of the United States of America, vol. 105, no. 44, 4 Nov. 2008, pp. 17046–17049. https://doi.org/10.1073/pnas.0806560105.
Jahnke, J. R., et al. “Maternal Stress, Placental 11β-Hydroxysteroid Dehydrogenase Type 2, and Infant HPA Axis Development in Humans: Psychosocial and Physiological Pathways.” Placenta, vol. 104, 15 Jan. 2021, pp. 179–187. https://doi.org/10.1016/j.placenta.2020.12.008.
Live to Create Photography. “Anxiety.” Flickr, 9 Jan. 2014, https://www.flickr.com/photos/91752758@N07/12040481414.
Lu, Yoyo. 17 Dec. 2025.
Nunez, S. G., et al. “Chronic Stress and Autoimmunity: The Role of HPA Axis and Cortisol Dysregulation.” International Journal of Molecular Sciences, vol. 26, no. 20, 2025. https://doi.org/10.3390/ijms26209994.
Rakoff, Victor. “A Long Term Effect of the Concentration Camp Experience.” Viewpoints, 1966.
sinclair.sharon28. “IMG_5914” Flickr, 6 May. 2015, https://www.flickr.com/photos/128745475@N07/17360676006.
