Table 2.

Exposure to war and subsequent inherited epigenetics to offspring.

Study details	Outcome
Yehuda et al. (121); Holocaust survivors (n = 32), adult offspring (n = 22), control parents (n = 8), their offspring (n = 9).	Correlation of increased methylation of FKBP5 in Holocaust survivors vs. decreased methylation in their offspring.
Yehuda et al. (122); adult offspring of Holocaust survivors (n = 211), demographically comparable Jewish controls (n = 73); subdivided on parental lifetime PTSD status.	Overall higher prevalence of mood, anxiety disorders, substance abuse and lifetime PTSD seen in Holocaust survivors' offspring. Maternal PTSD made a larger contribution to PTSD risk in offspring.
Yehuda et al. (76); adult offspring of Holocaust survivors (n = 35), healthy comparison controls (n = 15); PTSD and parental PTSD status; 24-h urinary cortisol levels measured.	Significant association of low cortisol with PTSD in parents and lifetime PTSD in individuals. Lowest cortisol seen in offspring with lifetime and parental PTSD.
Yehuda et al. (123); adult offspring of Holocaust survivors with parental PTSD (n = 13), adult offspring of Holocaust survivors without parental PTSD (n = 12); controls (n = 16); blood cortisol after dexamethasone suppression.	Increased suppression of cortisol via dexamethasone administration predominantly linked to status of parental PTSD.
Yahyavi et al. (79); veterans with PTSD (n = 41), their offspring (n = 41), veterans without PTSD (n = 43), their offspring (n = 43); afternoon serum cortisol recorded.	Offspring of veterans with PTSD showed decreased cortisol, only when groups arranged to show PTSD history. No changes to adrenaline or noradrenaline.
Yehuda et al. (124); women pregnant and present in World Trade Center attack (11 September 2001) (n = 38) and 1-year-old babies; salivary cortisol samples.	Significantly lower levels of cortisol in mothers with PTSD and their babies; most significant in babies when exposed during third trimester.
Yehuda et al. (125); adult offspring of Holocaust survivors (n = 39) with parental and/or lifetime PTSD, healthy comparison controls (n = 15); urinary cortisol.	Both parents must be affected with PTSD for offspring association with lower cortisol. Significant negative correlation seen for severity of parental PTSD accounting for offspring urinary cortisol, as well as offspring PTSD and said levels. No effect on age or gender.
Yehuda et al. (126); adult offspring of Holocaust survivors with parental PTSD (n = 23), 10 comparison controls with non-exposed parents (n = 10); blood cortisol. No participant had PTSD.	Lower mean and amplitude of cortisol in offspring with parental PTSD vs. without, and offspring of non-exposed parents. Associated sex-specific (maternal PTSD) risk factor.
Yehuda et al. (127); prevalence of PTSD and other psychiatric diagnoses in adult offspring of Holocaust survivors (n = 100), comparison controls (n = 44). Recruited from clinical and non-clinical populations.	Adult offspring of Holocaust survivors show increased prevalence of PTSD and psychiatric diagnoses (depression, anxiety, substance abuse, eating disorders).
Yehuda et al. (128); adult Holocaust survivors (n = 22) and their 22 offspring (n = 22).	Increased likelihood of development of PTSD in offspring with traumatic events if parents had PTSD.
Perroud (103); 25 women and offspring exposed to Tutsi genocide vs. 25 non-exposed women and children of the same ethnicity.	Higher peripheral blood methylation in the exon 1F promoter of NR3C1 in mothers and offspring (methylation higher in NR3C2 in mothers) and reduced cortisol levels in mother and child.
Costa et al. (120); children born after the US Civil War (1861–1865) to survivors of Confederate POW camps; children (n = 2,342) of no-exchange period ex-POWs (n = 732), children (n = 2,416) of exchange-period ex-POWs (n = 715), children (n = 15,145) of non-POW veterans (n = 4,920). All born after 1866, surviving to age 45 years.	Sex-specific impacts from father to son; no impact seen on daughters. Sons born post-war to POWs who endured prison during the no-exchange period were 11% more likely to die early vs. non-POW sons and 9% more than sons of exchange-period POWs. Within families, sons of no-exchange ex-POW fathers born after the war died at 2.23 times the rate of those born before the war.
Solomon et al. (129); Israeli combat participants in 1982 Lebanon war, offspring of Holocaust survivors (n = 44), offspring of non-Holocaust survivor parents (n = 52). PTSD inventory scores taken from questionnaires.	Higher rates of PTSD in the Holocaust survivor children cohort, 1–3 years after participation in the Lebanon war. Suggested that recovery from PTSD was also slower in veterans with Holocaust survivor parents.
Mulligan et al. (130); women from the Democratic Republic of Congo who had experienced war and violence in 2010 (n = 25). Whole blood and umbilical cord blood samples.	Methylation of NR3C1 in new-born infants correlated with increased severity of war stress. Also decreased birthweight correlated with increased NR3C1 methylation.

POW, prisoner of war; PTSD, post-traumatic stress disorder.

This includes study details and descriptive outcomes including both alterations to genes, as well as physiological effects.