Many children and even grandchildren of those who endure the trauma of war, genocide, rape, or parental abuse, say that, though they themselves did not witness the trauma, they feel it in their bones.
In 1975 Selma Fraiberg wrote, “In every nursery there are ghosts. They are visitors from the unremembered past of the parents.” When the interpersonal environment is happy, these “unfriendly and unbidden spirits are banished from the nursery and return to their subterranean dwelling place.”  Even when parental love is strong, these intruders may break through the “magic circle in an unguarded moment.” The child may not have experienced the traumatic event, but nonetheless re-experiences it through a parent’s unconscious reenactment. The parent’s touch, gesture, and tone inform daily interactions and communicate to the child the essence if not the particulars of the trauma.
For decades, Fraiberg’s model of inherited trauma, with some refinements , was the accepted model of the strange transmission of trauma from one generation to the next. I discovered a rich new seam of research while attending the World Economic Forum in Davos (2020) where Rachel Yehuda presented an overview of the genetic impacts of post-traumatic stress, adding yet another reason to the already long list of reasons why more reliable and effective treatments for this difficult to tackle condition are urgently needed. Yehuda, Director of Traumatic Stress Studies at the Mount Sinai School, highlighted therapies involving the use of MDMA, but what struck me was her meticulous discussion of how the trauma can be transmitted not only through subtle meanings embedded in a parent’s behavior or through the effects of a parent’s ability to conceptualize the child’s needs, but directly, insidiously through genes.
The idea that trauma takes hold in and changes our bodies is widely accepted. As Bessel van der Kolk says in his book on trauma, “the body keeps the score.” Yet the idea that trauma has a genetic legacy is highly controversial. But when a recent study followed descendants of Civil War prisoners and found their sons, from middle age on, were 10 percent more likely to die than their peers, and attributed this vulnerability to an epigenetic mechanism , critics saw a “malady in modern science” whereby the more sensational the claim, the lower the bar for supporting evidence. 
Such criticism does not do current research justice. Yehuda explores a range of studies, some in mice, but many in humans that show intergenerational transmission of trauma, some through the mother, some through the father.
Some examples she cites could perhaps be explained through Fraiberg’s model, where touch, mirroring, tone, and other behavior, account for the children’s severe psychiatric conditions. This includes Vivian Rakoff’s pivotal account of three children of Holocaust survivors who were so deeply disturbed, it was as though they themselves “had suffered the corrupting searing hell” . This “secondary traumatization” was also found in children of veterans of the Vietnam war. But when blunted cortisol activity was found in very young children of PTSD sufferers, it seemed more and more clear that, as Yehuda writes, “at least some ‘programmed’ epigenetic modifications may be established through gene… environments.” 
The epigenetic argument is that trauma leaves a chemical mark that influences how genes are expressed. The alteration in the mechanism translating the genetic code into functioning proteins is sometimes referred to as an on/off switch. Yehuda looks, broadly, at two very different routes to epigenetic effects. The first arises from the hormonal environment within the womb. This environment, impacted by maternal trauma, alters chemicals that impact gene transcription in the fetus. The womb environment also could explain findings that children born to mothers who, in their third trimester of pregnancy, were evacuated during the attack on the World Trade Center, were more reactive, or easily frightened by new experiences. Certain epigenetic changes are more likely to occur at specific stages of fetal development.
The second route to the intergenerational transmission of trauma occurs before conception, through changes in parental germ cells. Critics argue that this is implausible. How, they demand, could trauma impact an adult’s sperm or egg cells? In any case, the critics say, after conception, there is a process referred to as “rebooting” that strips away many chemical markers on the genes.
But there is strong evidence of cases where the “cleansing” or “rebooting” process is incomplete. Over a decade ago, descendants from parents and grandparents who endured the post-World War II famine in the Netherlands were found to carry a telltale chemical marker on their genes. This was then linked to high body mass in their offspring. The hypothesis is that starvation changed the genes of the children and grandchildren to ensure they were better at conserving calories. During a time of famine, such conservation would be beneficial. During a time of plenty, such conservation leads to obesity and its resulting hit to health. More recently, changes were also found in a specific gene of babies born to mothers who endured trauma in the Democratic Republic of Congo warzones.
Perhaps resistance to epigenetic explanations lies in its apparently pessimistic implication that the children of trauma victims are doomed by their genes. Yet what epigenetics teaches is that your genes do not hand you a fixed life script. If past experiences can cause generations of harm, subsequent good experiences can remedy at least some damage.
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