BES2004 Poster Presentations Neuroendocrinology and behaviour (25 abstracts)
1MRC Environmental Epidemiology Unit, University of Southampton, UK; 2Department of Public Health, University of Adelaide, South Australia; 3Department of Epidemiology and Public Health, University College London, UK; 4Department of Obstetrics and Gynaecology, University of Adelaide, South Australia.
Prenatal manipulations in animal models result in lifelong alterations in the stress responsivity of the hypothalamic-pituitary-adrenal axis (HPAA). While several human studies have found raised 0900h cortisol concentrations in low birthweight individuals, twenty-four hour cortisol profiles do not vary according to birthweight (a marker of adverse antenatal exposures). One explanation for this dichotomy is that 0900h cortisol concentration measured in a novel clinic setting may represent stress responsiveness rather than basal HPAA activity.
To examine this hypothesis, we measured salivary cortisol responses during a psychological stress test in a random sample of 98 men and 76 women aged 26.3 (0.4) years recruited from a well characterised birth cohort in Adelaide, South Australia. Full ethical approval and informed consent were obtained. The test comprised three tasks: a Stroop test, mirror drawing and a videotaped speech. The stress response was defined as the increment from the minimum pre stress value to the maximum post stress value on the study day. Further saliva samples were collected away from the clinic to provide baseline data from which the stress response could also be calculated. Associations between stress responses and size at birth were examined by correlation and multiple linear regression, correcting for potential confounders. Data are presented as median (interquartile range).
Responses on the study day differed significantly between men 2.1 (0.5-5.1) nanomoles per litre and women 0.5 (0.0-1.5) nanomoles per litre (p<0.001) and only 51% of men and 32% of women showed a clear salivary cortisol response to the tasks. There were no significant associations between stress responsiveness and size at birth in either sex.
This study highlighted the methodological difficulties of reliably stimulating the HPAA using psychological stress, but did not support the hypothesis that HPAA stress responses may be programmed in utero in humans.