Maternal, not paternal, PTSD is related to increased risk for PTSD in offspring of Holocaust survivors

Yehuda, Rachel; Bell, Amanda; Bierer, Linda M.; Schmeidler, James

doi:10.1016/j.jpsychires.2008.01.002

Cited by 293 publications

(254 citation statements)

References 49 publications

Supporting

Mentioning

232

Contrasting

Unclassified

Order By: Relevance

“…This hypothesis was supported by data demonstrating that parental, and specifically maternal, PTSD associated with lower cortisol levels in offspring (Yehuda et al, 2000). Importantly, these same offspring were found to be at higher risk for PTSD (Yehuda et al, 2008). The idea that low cortisol levels may be related to PTSD vulnerability, potentially due to the presence of parental PTSD acting as a risk factor, was bolstered by additional studies that replicated low cortisol findings in offspring, even when accounting for offspring's own traumatization and PTSD (Yehuda et al, , 2007.…”

Section: Neuroendocrinementioning

confidence: 77%

“…Studies investigating offspring effects of paternal stress may be instrumental in determining whether paternal effects are unique from maternal effects, as well as whether combined effects of maternal and paternal stress are additive. In studies of Holocaust survivor offspring, maternal, not paternal, PTSD has an effect on offspring PTSD; however, paternal PTSD moderates the effect of maternal PTSD in that the effect of the mother's PTSD is greater in the presence of paternal PTSD (Yehuda et al, 2008). Studies that account for stress in both mothers and fathers will enable researchers to more thoroughly interpret effects in offspring.…”

Section: Methodological Problemsmentioning

confidence: 99%

“…Studies demonstrating a particularly potent effect of maternal PTSD on offspring PTSD prompted a reanalysis of data to determine gender effects. Studies examining an effect of parent gender observed differential effects of maternal and paternal PTSD on both GR sensitivity and vulnerability to psychiatric disorders (Yehuda et al, 2008;Lehrner et al, 2014). Observed changes in offspring GR sensitivity may stem from parent gender-specific methylation changes to NR3C1, the gene that encodes GR.…”

Section: Epigeneticsmentioning

confidence: 99%

“…This has been demonstrated in instances where exposure predated conception or exposure occurred during pregnancy, supporting the idea that transmission can occur via gametes and/or the fetus. For example, adult offspring of Holocaust survivors were shown to be at greater risk for the development of PTSD, depression, and anxiety disorders (Yehuda et al, 2008). This was true, even though in all cases offspring were born after World War II.…”

Section: Clinical Observations and Significancementioning

confidence: 99%

See 3 more Smart Citations

Intergenerational Transmission of Stress in Humans

Bowers

Yehuda

2015

Neuropsychopharmacol

Self Cite

409

269

View full text Add to dashboard Cite

The hypothesis that offspring are affected by parental trauma or stress exposure, first noted anecdotally, is now supported empirically by data from Holocaust survivor offspring cohorts and other populations. These findings have been extended to less extreme forms of stress, where differential physical, behavioral, and cognitive outcomes are observed in affected offspring. Parental stress-mediated effects in offspring could be explained by genetics or social learning theory. Alternatively, biological variations stemming from stress exposure in parents could more directly have an impact on offspring, a concept we refer to here as 'intergenerational transmission', via changes to gametes and the gestational uterine environment. We further extend this definition to include the transmission of stress to offspring via early postnatal care, as animal studies demonstrate the importance of early maternal care of pups in affecting offsprings' long-term behavioral changes. Here, we review clinical observations in offspring, noting that offspring of stress-or trauma-exposed parents may be at greater risk for physical, behavioral, and cognitive problems, as well as psychopathology. Furthermore, we review findings concerning offspring biological correlates of parental stress, in particular, offspring neuroendocrine, epigenetic, and neuroanatomical changes, in an attempt to determine the extent of parental stress effects. Although understanding the etiology of effects in offspring is currently impeded by methodological constraints, and limitations in our knowledge, we summarize current information and conclude by presenting hypotheses that have been prompted by recent studies in the field.

show abstract

Section: Neuroendocrinementioning

confidence: 77%

Section: Methodological Problemsmentioning

confidence: 99%

Section: Epigeneticsmentioning

confidence: 99%

Section: Clinical Observations and Significancementioning

confidence: 99%

See 2 more Smart Citations

Intergenerational Transmission of Stress in Humans

Bowers

Yehuda

2015

Neuropsychopharmacol

Self Cite

409

269

View full text Add to dashboard Cite

show abstract

“…Recent studies have demonstrated a higher prevalence of depression and anxiety disorders in descendants of holocaust survivors than in a control population (Yehuda et al, 2008). Furthermore, the lifetime risk for posttraumatic stress disorder (PTSD) in the offspring depends on the presence of maternal and, to a lesser extent, paternal PTSD.…”

Section: Stressmentioning

confidence: 99%

Epigenetic Inheritance of Disease and Disease Risk

Bohacek

Mansuy

2012

Neuropsychopharmacol

151

View full text Add to dashboard Cite

Epigenetic marks in an organism can be altered by environmental factors throughout life. Although changes in the epigenetic code can be positive, some are associated with severe diseases, in particular, cancer and neuropsychiatric disorders. Recent evidence has indicated that certain epigenetic marks can be inherited, and reshape developmental and cellular features over generations. This review examines the challenging possibility that epigenetic changes induced by environmental factors can contribute to some of the inheritance of disease and disease risk. This concept has immense implications for the understanding of biological functions and disease etiology, and provides potential novel strategies for diagnosis and treatment. Examples of epigenetic inheritance relevant to human disease, such as the detrimental effects of traumatic stress or drug/toxic exposure on brain functions, are reviewed. Different possible routes of transmission of epigenetic information involving the germline or germline-independent transfer are discussed, and different mechanisms for the maintenance and transmission of epigenetic information like chromatin remodeling and small noncoding RNAs are considered. Future research directions and remaining major challenges in this field are also outlined. Finally, the adaptive value of epigenetic inheritance, and the cost and benefit of allowing acquired epigenetic marks to persist across generations is critically evaluated.

show abstract