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Apart from altering the eggs and sperm that encapsulate our genetic inheritance, sometimes decades before conception, trauma also seems to influence the uterine environment. Meticulous studies of the offspring of women who were pregnant during the Dutch Famine—a six-month period during World War II when the Nazis blocked the food supply to the Netherlands, causing widespread starvation—provided an early indication of in utero effects. Researchers discovered that the combined effects of extreme stress and nutritional deprivation, such as deficits in metabolism and susceptibility to cardiovascular illness, depended on the trimester of exposure.
The 9/11 babies were also impacted in the womb, with those in the third trimester having significantly lower cortisol levels. What this condition meant for their future development I sadly never found out. At the wellness visit, mothers who had PTSD (and low cortisol) were more likely to report that their nine-month-olds were unusually anxious and afraid of strangers. But we didn’t get the funding to follow the babies into adulthood.
How might the uterine environment leave a trauma trace in the offspring? Our work on Holocaust survivors and their adult children provided some clues. The story is again complicated, and it involves an enzyme known as 11-beta-hydroxysteroid dehydrogenase type 2 (11β-HSD2). Holocaust survivors had lower levels of the enzyme than those who hadn’t lived through the Holocaust—and such effects were particularly pronounced in those who were the youngest during World War II. The enzyme is normally concentrated in the liver, kidneys and brain. Under conditions of food deprivation, however, the body can lower levels of 11β-HSD2 to increase metabolic fuel in the interest of promoting survival. In adults, the enzyme level will return to what it was when there is no more starvation, but in children, the level may remain low. Our findings suggested that 11β-HSD2 levels might have been altered during childhood when Holocaust survivors were exposed to long periods of malnourishment; the change persisted well into old age.
In the children of women who were Holocaust survivors, however, we saw quite the opposite: 11β-HSD2 levels were higher than in Jewish control subjects. The result might seem contradictory, but there is a logic to it. During pregnancy, 11β-HSD2 also acts in the placenta, protecting the fetus from exposure to circulating maternal cortisol, which can be toxic to the developing brain. The enzyme, which is particularly active in the third trimester, converts maternal cortisol into an inactive form, creating a kind of chemical shield in the placenta that protects the fetus from the hormone’s harmful effects. The high levels of this enzyme in the offspring of Holocaust survivors may thus reflect an adaptation, an effort to protect the fetus from the lowered 11β-HSD2 levels in their mothers.
All of this means that offspring are not always passive recipients of their parents’ scars. Just as a parent was able to survive trauma by means of biological adaptations, offspring can sometimes adapt to the biological impact of their parents’ trauma.
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