Transmitting PTSD From Generation to Generation

Table of Contents

by Heidi Hanson

artist, writer, trauma survivor

Stewart Canter
Article author – Stewart Canter

I’m excited to introduce a guest blogger to my blog. Stewart Canter is a seasoned psychologist specializing in trauma treatment. Stewart and his wife Lelia run Operation Pegasus, a nonprofit organization located near Asheville, North Carolina. Operation Pegasus uses Trauma Resiliency Model (TRM) in conjunction with equine assisted therapy to help people recover fromΒ  traumatic life experiences.

I’ve been volunteering with Operation Pegasus for four months now. The Operation Pegasus horse stables are located on the side of a valley in the mountains. In the fall it was like a fairytale, with sheep dotting the fields at the bottom of the other side of the valley, and colorful rust, yellow and green trees covering the mountaintops that reach high into the sky in every direction.

So without further ado, here is “Transmitting PTSD From Generation to Generation,” by Stewart Canter.

Transmitting PTSD From Generation to Generation
Vulnerability to PTSD can be passed biologically from parent to child. Operation Pegasus offers this public health information for the benefit of communities, employers, families, and individuals.

It’s pretty easy to see how an overwhelmingly stressful, life threatening event can impact many biological systems of the body. This type of experience activates the reptilian brain, floods the system with stress hormones and creates changes in functioning – changes that in some develop into Posttraumatic Stress Disorder (PTSD).

But what about a traumatic event that happened to your mother, or to your great grandmother? Could that event from long ago that impacted the biology of your ancestor show up in your body today? And what about a trauma you experienced? Could it show up biologically in your great great grandchildren?

Well, the answer appears to be yes.

Researchers have shown that vulnerability to posttraumatic stress can be passed down biologically from one generation to the next. These findings provide scientific explanations for how PTSD extends beyond the individual, reaching into family lineages, ultimately impacting entire communities and the larger society.

One common finding among all the studies presented here, is that low cortisol levels in the body chemistry make us more vulnerable to developing posttraumatic stress symptoms. Cortisol, which is the hormone linked to management of stress and trauma, can be depleted in the mother due to exposure to traumatic events such as 9/11, the Holocaust, domestic violence or emotional abuse, poverty, housing, financial and food insecurity. The mother, through this exposure to extreme stress, burns through her cortisol reserves and significantly increases her vulnerability to developing PTSD.

This increased vulnerability is biologically transmissible during pregnancy through hormonal (chemical) and genetic means to her child. The child may then grow up to be biologically less able to cope with stress and trauma. Their own biology will be more predisposed to being overwhelmed by feelings of anxiety, fear and stress, and if confronted with a traumatic experience, they will have a significantly higher likelihood of developing PTSD.

The Research…

Groups of research studies were carried out that examined:

  • Children of parents who had experienced the Holocaust
  • Children of mothers who survived the World Trade Center attack
  • Infants whose mothers had a history of early-life sexual and physical abuse
  • Comparing biological impacts from mother versus father... In one study, researchers aimed to find out if the impact of a mother’s traumatic experiences was more significant than that of the father’s.

Being Vulnerable to PTSD is Key to Developing PTSD

One of these studies (focusing on lineages containing holocaust survivors) shows that there are two essential elements that play a role in developing PTSD. The first is a severe traumatic event. The second is personal vulnerability.1

If a person is not vulnerable, even a severe trauma may not result in PTSD. However, a person who is vulnerable will likely develop posttraumatic stress symptoms when exposed to a traumatic event that is not usually severe enough to trigger PTSD.2,3 So, the obvious question is, β€œWhat things make us vulnerable to developing PTSD?”

Two Types of Vulnerability to Trauma – Psychological Versus Biological…

Our vulnerability is shaped by two major causative factors. One is psychological vulnerability which refers to personality traits such as strength of ego, beliefs and coping strategies. The other is biological vulnerability which refers to internal biological systems such as the autonomic nervous system, hormonal patterns and neurotransmitter patterns.4 The group of studies referenced here that examine the generational impact of trauma focus on the biological category of factors. 5-7

The Importance of Cortisol – A Biological Marker of Vulnerability to PTSD

One of the core biological features that contributes to the transmission of PTSD vulnerability to offspring is cortisol.8,9

Cortisol is a hormone produced in the adrenal glands. It is often called β€œthe stress hormone” but may be more accurately thought of as the “anti-stress hormone” because cortisol actually helps counteract the biological effects of stress.

CortisolΒ has many functions. Cortisol reduces the duration of emotional distress. It increases the availability of the body’s fuel supply (carbohydrate, fat and glucose) which is needed to respond to stress. It promotes proper functioning of the immune system and helps create memories of emotional events that should be avoided in the future. Cortisol levels can be affected by many conditions, such as physical or emotional stress, strenuous activity, infection or injury.10-12

If our cortisol reserve is low due to being used up when handling previous stressful events, then subsequent stressful events have a greater biological impact on us. Thus, low cortisol levels make us more vulnerable to developing posttraumatic stress symptoms.13,14

What does this mean in terms of transmitting PTSD from one generation to the next?

When mothers who were Holocaust survivors had PTSD and low cortisol levels, the low cortisol levels were significantly associated with lifetime PTSD vulnerability in their biological children (both first and second generations). These children had lower cortisol levels than children with PTSD whose mothers did not have PTSD.15 It was also found that greater severity of PTSD symptoms in parents correlated with greater severity of PTSD symptoms in children.16

Childhood Trauma…

The role of childhood trauma was also examined in this group. The adult children of Holocaust survivors reported high levels of childhood trauma, particularly emotional abuse and neglect.17 Their cortisol levels were lower than in those without a history of emotional abuse.

It was also found that traumatized parents are more likely to express improper (abusive or neglecting) behavior toward their offspring during a critical developmental window, and that such behavior may have long-lived effects on cortisol regulation in the offspring.18

Hence, the experience of childhood trauma could be a key factor in the biological transmission of PTSD vulnerability from parent to child.19

The World Trade Center Attack…

The attack on the World Trade Center in New York City also allowed researchers to study the relationship between PTSD in mothers and PTSD in their infant offspring.

Cortisol levels were measured in infants and their mothers who had been directly exposed to the World Trade Center attack during pregnancy. At nine months old, the levels of cortisol in the infants of women with PTSD were significantly lower than in those infants whose mothers had not developed PTSD.

Interestingly, lower cortisol levels were most apparent in babies born to mothers with PTSD who were exposed to the World Trade Center attack in their third trimesters. The authors also suggested that exposure to traumatic experience during pregnancy is a stronger vulnerability factor than abusive parenting.20

Early-Life Sexual and Physical Abuse (of Mothers)

A similar study was conducted that found that infants whose mothers had a history of early-life sexual and physical abuse showed significantly lower baseline cortisol levels and therefore greater vulnerability to developing PTSD.21

Other similar studies have indicated that PTSD in mothers may be due to their genetics. The mother’s genetics can be altered by early life sexual and physical abuse. Those genetic alterations can account for the low cortisol levels in the mother, which can be transmitted to her offspring.22

Fortunately, other studies show that even if the mother has PTSD, and her offspring has low levels of cortisol, it does not mean that her offspring will certainly develop PTSD.23

The Unique Role of the Mother

Another study was aimed at determining if the biological transmission of vulnerability to PTSD by the mother was more significant than transmission by the father. In this study, 284 communities recruited participants to identify their lifetime traumatic experiences and their psychiatric diagnoses. The analysis demonstrated that offspring who had fathers with PTSD (and mothers who did not have PTSD) were not significantly different from offspring with fathers who did not have PTSD.

The same study also found that offspring who have both parents with PTSD had low cortisol levels similar to offspring with only a mother with PTSD. The authors hypothesize that these findings provide evidence that PTSD in mothers may contribute in a unique (biological) manner to decreased cortisol levels in her offspring.24

How Does it Happen? Chemical Programming of the Fetal Brain and Altered Gene Expression

We have looked at biological evidence that vulnerability to PTSD can be transmitted from one generation to the next. A couple of studies explain how low cortisol levels can be transmitted biologically in a couple of ways:

  1. Exposure of the fetus to the mother’s body chemistry that has been altered by her exposure to traumatic experiences during pregnancy may program the stress response pattern in the fetus’ brain (increasing its vulnerability to PTSD).25 (Note that her altered body chemistry may have been transferred to her from her own mother.)
  2. Vulnerability may occur due to changes to the mother’s and fetus’ gene expression. Gene expression is “the flow of genetic information from gene to protein; the process, or the regulation of the process, by which the effects of a gene are manifested; the manifestation of a heritable trait in an individual carrying the gene or genes that determine it.”26 Severe environmental stressors are associated with gene expression that results in lower cortisol levels and therefore increased vulnerability to developing PTSD.27

As mentioned before, although there is evidence that both parents may contribute to vulnerability to PTSD in their offspring, the mother has a unique role in that contribution. This could be because of how chemical programming and gene expression are passed through the biology of pregnancy.28

More Research Needed

The studies referenced in this article had some limitations. The authors who presented this research noted the limitations of their studies as the following:

  • Limited sample sizes in many of the studies
  • Most samples comprised a specific type of patients with a particular trauma, namely, Jewish victims of the Holocaust.
  • Not every subject exposed to early-life or in utero stressors developed PTSD

The authors also note that these findings should be studied in more detail in other types of trauma with different severities and other populations with a variety of genetic backgrounds. Survivors of the tsunami in Southeast Asia and of the earthquakes of Tabas (Iran), Japan, Pakistan, and Turkey seem to be reasonable cases for further investigation.

Conclusion

Certainly more research is needed, but even based on just what we know now, there are many potential implications. One traumatic event appears to affect not just one person but potentially many generations, which means that one traumatic experience can potentially result in hundreds of years of psychological impairment. Future generations could be directly and personally impacted by current events such as wars, natural and manmade disasters, economic depressions, unemployment, and major dislocations. Other traumatic events are more personal and private for families and individuals. These include various types of rejection such as abuse, abandonment, deceit, disappointment, humiliation, and betrayal of trust. Accidents, assaults, multiple medical procedures, and difficult childbirth experiences are further examples of other types of traumatic events.

People who are born with biological vulnerability to trauma could experience disabling problems in the life cycle such as difficulty with employment, relationships, and feelings of well being. There is also a financial cost to society, as people who suffer from PTSD may have a greaterΒ need for government services.

The study of the transmission of PTSD from generation to generation could lead to more personal insight into one’s own individual case, greater understanding from healing professionals, employers, educators, law enforcement, as well as scientific advances, such as the ability to scientifically measure the impact of trauma to individuals (including service-related PTSD disability determination for military service members), families, and society over time.

References

The study was conducted by two universities; first is the Mazandaran University of Medical Sciences in Sari, Iran. The other is the Medical University of the Americas, Charlestown, Saint Kitts and Nevis (in the Caribbean). The article is titled A review on the evidence of transgenerational transmission of posttraumatic stress disorder vulnerability. The researchers are Seyyed Taha Yahyavi,1 Mehran Zarghami,1 Urvashi Marwah2.

1. Perkonigg A, Kessler RC, Storz S, Wittchen HU. Traumatic events and posttraumatic stress disorder in the community: Prevalence, risk factors, and comorbidity. Acta Psychiatr Scand. 2000;101:46-59.

2. Davidson JR, Stein DJ, Shalev AY, Yehuda R. Post-traumatic stress disorder: acquisition, recognition, course, and treatment. J Neuropsychiatry Clin Neurosci. 2004;16:135-47.

3. McFarlane AC. Posttraumatic stress disorder: a model of the longitudinal course and the role of risk factors. J Clin Psychiatry. 2000;61:15-20.

4. Yehuda R, Bierer LM. Transgenerational transmission of cortisol and PTSD risk. Prog Brain Res. 2008;167:121-35.

5. Yehuda R, Bierer LM. Transgenerational transmission of cortisol and PTSD risk. Prog Brain Res. 2008;167:121-35.

6. Yehuda R, Schmeidler J, Giller EL Jr, Siever LJ, Binder-Brynes K. Relationship between posttraumatic stress disorder characteristics of Holocaust survivors and their adult offspring. Am J Psychiatry, 1998;155:841-3.

7. Yehuda R, Schmeidler J, Wainberg M, Binder-Brynes K, Duvdevani T. Vulnerability to posttraumatic stress disorder in adult offspring of Holocaust survivors. Am J Psychiatry. 1998;155:1163-71.

8. Mason JW, Giller EL, Kosten TR, Ostroff RB, Podd L. Urinary freecortisol levels in posttraumatic stress disorder patients. J Nerv Ment Dis. 1986;174:145-9.

9. Boscarino J A. Posttraumatic stress disorder, exposure to combat, and lower plasma cortisol among Vietnam veterans – findings and clinical implications. J Consult Clin Psychol. 1996;64:191-201.

10. Kennedy, Ron.Β “Cortisol (Hydrocortisone)”. The Doctors’ Medical Library.

11. de Quervain DJ, Roozendaal B, McGaugh JL; Roozendaal; McGaugh (August 1998). “Stress and glucocorticoids impair retrieval of long-term spatial memory”.Β NatureΒ 394(6695): 787–90.Β doi:10.1038/29542.Β PMIDΒ 9723618.

12. Yehuda R. Current status of cortisol findings in post-traumatic stress disorder. Psychiatr Clin North Am. 2002;25:341-68.

13. Resnick HS, Yehuda R, Pitman RK, Foy DW. Effect of previous trauma on acute plasma cortisol level following rape. Am J Psychiatry. 1995;152:1675-7.

14. Delahanty DL, Raimonde AJ, Spoonster E, Cullado M. Injury severity, prior trauma history, urinary cortisol levels, and acute PTSD in motor vehicle accident victims. J Anxiety Disord. 2003;17:149-64.

15. Yehuda R, Bierer LM, Schmeidler J, Aferiat DH, Breslau I, Dolan S. Low cortisol and risk for PTSD in adult offspring of holocaust survivors. Am J Psychiatry. 2000;157:1252-9.

16. Yehuda R, Halligan SL, Bierer LM. Cortisol levels in adult offspring of Holocaust survivors: relation to PTSD symptom severity in the parent and child. Psychoneuroendocrinology. 2002;27:171-80.

17. Yehuda R, Halligan SL, Grossman R. Childhood trauma and risk for PTSD: relationship to intergenerational effects of trauma, parental PTSD, and cortisol excretion. Dev Psychopathol. 2001;13:733-53.

18. Yehuda R, Bierer LM. The relevance of epigenetics to PTSD: implications for the DSM-V. J Trauma Stress. 2009;22:427-34.

19. Gunnar MR, Vazquez DM. Low cortisol and a flattening of expected daytime rhythm: potential indices of risk in human development. Dev Psychopathol. 2001;13:515-38.

20. Yehuda R, Engel SM, Brand SR, Seckl J, Marcus SM, Berkowitz GS. Transgenerational effects of posttraumatic stress disorder in babies of mothers exposed to the World Trade Center attacks during pregnancy. J Clin Endocrinol Metab. 2005;90:4115-8.

21. Brand SR, Brennan PA, Newport DJ, Smith AK, Weiss T, Stowe ZN. The impact of maternal childhood abuse on maternal and infant HPA axis function in the postpartum period. Psychoneuroendocrinology. 2010;35:686-93.

22. Bartels M, Van den Berg M, Sluyter F, Boomsma DI, de Geus EJ. Heritability of cortisol levels: review and simultaneous analysis of twin studies. Psychoneuroendocrinology. 2003;28:121-37.

23. Yehuda R, Teicher MH, Seckl JR, Grossman RA, Morris A, Bierer LM. Parental posttraumatic stress disorder as a vulnerability factor for low cortisol trait in offspring of holocaust survivors. Arch Gen Psychiatry. 2007;64:1040-8.

24. Yehuda R, Bell A, Bierer LM, Schmeidler J. Maternal, not paternal, PTSD is related to increased risk for PTSD in offspring of Holocaust survivors. J Psychiatr Res. 2008;42:1104-11.

25. Seckl JR. Prenatal glucocorticoids and long-term programming. Eur J Endocrinol. 004;151:U49-62.

26. Gene expression. (n.d.) Mosby’s Medical Dictionary, 8th edition. (2009). Retrieved January 19 2015 from http://medical-dictionary.thefreedictionary.com/gene+expression

27. Yehuda R, Bierer LM. The relevance of epigenetics to PTSD: implications for the DSM-V. J Trauma Stress. 2009;22:427-34.

28. Maurel MC, Kanellopoulos-Langevin C. Heredity — Venturing beyond genetics. Biol Reprod. 2008;79:2-8.

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