There’s lots of talk these days about the transgenerational transmission of trauma (TTT).  Some of it focuses on epigenetic changes in the chemical environment of the genes that make people more or less susceptible to trauma.  I find this topic incredibly complicated and difficult to understand.  I’ll try to explain it the best I can, but the reader should be clear that as far as PTSD is concerned, the epigenetic transmission of trauma is still up in the air, a hypothesis with no established empirical (scientific) basis.  As two of the leading researchers put it in the Journal of Traumatic Stress,

There have been no empirical demonstrations of epigenetic modifications per se in association with PTSD or PTSD risk. (Yehuda and Bierer, p. 430)

This reality has done little to dampen speculation, including that of Yehuda and Bierer, as we shall see.  I’m not sure if this is bad or good.  Mostly I think it’s irrelevant.

Genetic transmission of vulnerability to trauma

There seems to be little doubt that there is a genetic component to vulnerability to stress. 

Family and twin studies have found that risk for PTSD is associated with an underlying genetic vulnerability and that more than 30% of the variance associated with PTSD is related to a heritable component. (Kellerman, p. 33)

This claim, by the way, is not benign.  It means that the dose/response curve insisted upon by Judith Herman (p. 57) is wrong. (The dose/response curve states that the degree of traumatization is almost completely dependent on how much trauma a person is subjected to, how early, and how long.  Individual variability doesn’t count.)  Indeed, the genetic claim challenges the argument behind the establishment of the diagnosis of PTSD at the time of the Vietnam War: that it is the result of putting normal people in abnormal situations.   Instead, the genetic claim says that some soldiers were less resistant to stress than others.  It’s not a big step from that proposition to one that says that the victim of PTSD is responsible for his or her condition.  Certainly this is the way some scientists write.

What is epigenetic transmission?

Genes are embedded in chains of DNA.  The chain of DNA is wrapped around a core of proteins, called histones.  For years, biologists thought that this core was little more than a scaffold for the genes.  More recently, biologists have come to see these histones as switches that turn the gene on or off.  The gene expresses itself, or not, under the influence of histones, and histones, unlike the DNA, are subject to environmental changes. 

Darwin taught us that it takes many generations for a genome to evolve, but researchers have found that it takes only the addition of a methyl group to change an epigenome. A methyl group is a basic unit in organic chemistry: one carbon atom attached to three hydrogen atoms. When a methyl group attaches to a specific spot on a gene — a process called DNA methylation — it can change the gene’s expression, turning it off or on, dampening it or making it louder. (Cloud)

And what causes DNA methylation?  One key factor is environmental stress.  (Meaney)

Of rats and men

Rats are important in the study of epigenetics.  It’s easy to confuse them with people.  In a well-known and well-regarded study, rat mothers were removed from their home cage, where they were held by a researcher for fifteen minutes a day.  The result was better rat mothers, who devoted more time to licking and grooming their pups compared to mothers who had not been handled. 

As an apparent result, the pups of the meticulous mothers had lower levels of cortisol in adulthood than the pups of the non-handled mothers.  Cortisol is considered a stress hormone.  More cortisol, more stress.  This study exemplifies epigenetic transmission of an ability to withstand stress.  Without changing the genes of the mother, but only the chemical reaction that turns genes on and off, the pups were born with and maintained an ability to resist stress, as measured by cortisol levels (Cook). 

This is shown by the persistence of both lower cortisol levels and greater grooming in the third generation of female pups.  Why this isn’t just a case of learning (good rat mothers teach their female pups to be good mothers) is revealed by the increased activity of a gene involved in cortisol regulation in both mother and pups (Francis et al.). 

Applying this study to the children of Holocaust survivors, Yehuda and Bierer turned to studies that show that children of survivors with PTSD rate their parents as more overprotective than the children of survivors not suffering from PTSD.  Survivor parents with PTSD had difficulty separating from their children, resulting in less secure attachments, and less secure children.   

Thus, Holocaust survivor offspring report childhood histories that are not incompatible with having had mothers who excessively “licked and groomed,” but unlike rodents, this cohort can articulate the subjective emotional consequences of such behaviors (p. 431)

Good thing these kids could talk or they might have been licked to death.

One little problem

The problem is that the children of over-protective parents had lower levels of the stress hormone cortisol than the children of the “normal” parents, just the opposite of what one sees with the well-groomed rat pups.  Only now this low level of cortisol is bad, not good, because “mounting a cortisol response to a stressor is an adaptive response.”  (p. 430) 

At this point we have left the realm of science.  Whereas a high level of cortisol is a widely accepted indicator of stress, here a low level indicates an inability to handle stress.  High or low, it seems that any result would confirm the epigenetic transmission of trauma.  Yehuda and Bierer published their paper in The Journal of Traumatic Stress, the most prestigious journal in the field.  It’s something to worry about. 

Rat studies have become the gold standard of research in this area.  The National Institutes of Mental Health (NIMH) will no longer fund studies based on the DSM, the Diagnostic and Statistical Manual of Mental Disorders, published by the American Psychiatric Association.   NIMH refuses to do so because the DSM is a categorization of symptoms.  NIMH wants studies at the genetic, cellular, and molecular level.  And research follows funding, not vice-versa. 

How it might work

In an admittedly speculative work, Kellerman wonders if the children and grandchildren might actually inherit the unconscious mind of the parent.

How can a repressed memory be passed on from one person to another? Can a child really “inherit” the unconscious mind of a parent? (p. 33)

His conclusion is more subtle than his question.  What children may epigenetically inherit (though there is as yet no evidence) is a vulnerability to stress, making them more sensitive to the traumatic experiences of their parents. 

Because of their neurobiological susceptibility to stress, children of Holocaust survivors may thus easily imagine the physical suffering of their parents and almost “remember” the hunger, the frozen limbs, the smell of burned bodies and the sounds that made them scared. (p. 34)

Though it is the actual family relationships that matter, the “pre-traumatized” children of Holocaust survivors may pick up on more subtle cues of parental distress.  Or they may simply be more disturbed by parental accounts of the Holocaust than other children.  Here a virtue, sensibility to the suffering of others, becomes a vice.  As it may if the parents’ trauma overwhelms the child’s own developmental needs.  

If this is how it might work, what difference does it make?

As yet there is no evidence that epigenetic transmission plays a role in the transgenerational transmission of trauma in humans.  Nevertheless, Kellerman at least suggests a plausible method by which it might.  The question is what difference does it make.  Some children are more sensitive than others.  Some traumatized parents are better able to contain their anxiety than others. 

The work that families afflicted by trauma need to do to raise healthy children is the same relational work that needs to be done in any case, above all encouraging the children to develop lives of their own.  Helen Epstein’s Children of the Holocaust, written long before the rise of epigenetics, discusses how experts and discussion groups among children of survivors help.  What does epigenetics add?  Science and money I suppose. 

It’s not the gene, it’s the meme

In a study of ethnic differences in response to Hurricane Andrew in 1992, at that time the deadliest hurricane in United States history, S. Malan-Müller et al. posit that differences “in the prevalence of PTSD between Hispanics, non-Hispanic blacks, and Caucasian groups” might be explained by “changes in DNA methylation.”  They also consider that these differences might contribute to differences in “treatment-seeking behaviours.” 

It’s not impossible, but in this study, as in so many studies like this, chemical differences in the epigenome of different ethnic groups become causal, rather than themselves being caused by social factors such as systemic racism, cultural practices, and the fact that poor people live in more vulnerable structures.  It’s interesting to study how racism might affect the epigenome.  It’s more important, at least at this point, to study the effects of racism on ways of life. In other words, it’s not the gene, it’s the meme.* 

* A meme is the smallest unit of cultural expression.  No one agrees how small, or how to define it.

References

C. J. Cook, Patterns of weaning and adult response to stress. In Physiology & Behavior (1999), vol. 67: 803–808.

John Cloud, Why your DNA isn’t your destiny.  Time Magazine, January 6, 2010.  http://www.time.com/time/printout/0,8816,1952313,00.html

Helen Epstein, Children of the Holocaust.  Plunkett Lake Press, 2010. [orig. 1979]

E. Francis, J. Diorio, D. Liu, and M. J. Meaney, Nongenomic transmission across generations of maternal behavior and stress responses in the rat. Science (1999), vol. 286: 1155–1158

Judith Herman, Trauma and Recovery.  New York: Basic Books, 1997.  

Natan P. F. Kellermann, Epigenetic transmission of Holocaust trauma: can nightmares be inherited?  Israel Journal of Psychiatry and Related Sciences (2013), vol. 50: 33-39.

S. Malan-Müller, S. Seedat, and S. M. J. Hemmings, Understanding posttraumatic stress disorder: insights from the methylome. Genes, Brain, and Behavior (28 November 2013).  http://onlinelibrary.wiley.com/doi/10.1111/gbb.12102/pdf

J. Meaney and M. Szyf, Environmental programming of stress responses through DNA methylation: life at the interface between a dynamic environment and a fixed genome. Dialogues in Clinical Neuroscience (2005), vol. 7: 103-123.

Rachel Yehuda and Linda Bierer, The relevance of epigenetics to PTSD: implications for the DSM-V. Journal of Traumatic Stress (2009), vol. 22 (5): 427–434.