Parental posttraumatic stress disorder as a vulnerability factor for low cortisol trait in offspring of holocaust survivors.
BACKGROUND
Lower cortisol levels in posttraumatic stress disorder (PTSD) may reflect a preexisting vulnerability associated with developing the disorder after trauma exposure. Because offspring of trauma survivors with PTSD have a greater prevalence of PTSD after their own life events than offspring of trauma survivors without PTSD and offspring of nonexposed persons, examination of patterns of basal cortisol secretion in such offspring provides an opportunity to test this hypothesis.


OBJECTIVE
To characterize the patterns of basal cortisol secretion in offspring of Holocaust survivors with and without parental PTSD and children of nonexposed parents.


METHODS
Cortisol secretion was measured every 30 minutes for 24 hours. The raw hormonal data were subjected to a chronobiological analysis by applying single-oscillator and multioscillator cosinor analyses, a nonlinear least squares curve-fitting program, to determine circadian and ultradian regulatory dynamics.


METHODS
The study was conducted under controlled conditions at the General Clinical Research Center at the Mount Sinai School of Medicine.


METHODS
Twenty-three Holocaust offspring with parental PTSD and 10 without parental PTSD were compared with 16 children of nonexposed parents. No participant had PTSD.


METHODS
Mean cortisol levels during the 24-hour cycle and other chronobiological parameters (amplitude, acrophase, circadian quotient, and goodness-of-fit coefficient) derived from single-oscillator and multioscillator models.


RESULTS
Offspring with parental PTSD displayed lower mean cortisol levels, reflected by the circadian mesor and reduced cortisol amplitude, compared with offspring without parental PTSD and children of nonexposed parents. This effect seemed to be specifically related to the presence of maternal PTSD.


CONCLUSIONS
Low cortisol levels and other chronobiological alterations in offspring are associated with the risk factor of maternal PTSD, raising the possibility that these alterations are acquired via glucocorticoid programming either from in utero exposures or in response to maternal behaviors early in life.
Yehuda
Rachel
R
Traumatic Stress Studies Program, Department of Psychiatry, Mount Sinai School of Medicine and James J. Peters Veterans Affairs Medical Center, Bronx, NY, USA. rachel.yehuda@va.gov
Teicher
Martin H
MH
Seckl
Jonathan R
JR
Grossman
Robert A
RA
Morris
Adam
A
Bierer
Linda M
LM
D000204:Activity Cycles; D032721:Adult Children; D002648:Child; D016241:Child of Impaired Parents / Q000523:psychology / Q000706:statistics & numerical data*; D002909:Chronobiology Phenomena; D002940:Circadian Rhythm; D004198:Disease Susceptibility / Q000453:epidemiology* / Q000523:psychology; D005260:Female; D017767:Holocaust / Q000523:psychology*; D006801:Humans; D006854:Hydrocortisone / Q000097:blood*; D008016:Life Change Events; D008297:Male; D008875:Middle Aged; D015233:Models, Statistical; D009035:Mothers / Q000523:psychology / Q000706:statistics & numerical data; D010290:Parents / Q000523:psychology*; D015995:Prevalence; D012307:Risk Factors; D013313:Stress Disorders, Post-Traumatic / Q000097:blood* / Q000453:epidemiology* / Q000523:psychology; D017741:Survivors / Q000523:psychology / Q000706:statistics & numerical data*
D006854:Hydrocortisone