Cortisol awakening rise in middle-aged women in relation to psychological stress.
OBJECTIVE
The cortisol awakening rise (CAR) is defined as cortisol secretory activity in the first 45-60 min immediately post-awakening. It has been suggested that psychological factors may disrupt the normal awakening rise. Recent research has shown that psychological stress may influence the magnitude of the CAR, however the findings have been mixed. This study examined the impact of stress on the CAR and the diurnal mean in a sample of middle-aged women.


METHODS
One hundred and eighteen healthy female participants who reported experiencing high or low stress were recruited. Salivary cortisol levels were measured immediately upon awakening (at 0, 15, 30, and 45 min) and at 3, 6, 9 and 12 h on two consecutive days. A number of metabolic and inflammatory biomarkers were also assessed together with measures of mood disturbance and health behaviour.


RESULTS
The magnitude of the CAR, assessed by the area under the response curve (AURC) estimate, was significantly lower in the high stress group compared to the low stress group indicating that participants who experienced high stress secreted lower levels of cortisol. The effect was largely accounted for by differences 30 min after waking. The diurnal mean was also lower for the high stress group. Although participants in the high stress group had a slightly worse inflammatory profile, only low-density lipoprotein levels were found to be significantly higher, compared to the low stress group. Lifestyle indicators and mood were also found to be significantly poorer in the high stress group.


CONCLUSIONS
The results suggest that psychological stress may be associated with a smaller cortisol awakening rise, a lower diurnal mean, poor lifestyle choices and high levels of psychological distress. These findings may have broader implications for future health risk and for an individual's ability to cope with imminent daily stressors and demands.
O'Connor
D B
DB
Institute of Psychological Sciences, University of Leeds, Leeds, UK. d.b.o'connor@leeds.ac.uk
Hendrickx
H
H
Dadd
T
T
Elliman
T D
TD
Willis
T A
TA
Talbot
D
D
Mayes
A E
AE
Thethi
K
K
Powell
J
J
Dye
L
L
D000328:Adult; D000339:Affect / Q000502:physiology; D015415:Biomarkers / Q000378:metabolism; D002097:C-Reactive Protein / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D002940:Circadian Rhythm / Q000502:physiology; D015237:Dinoprost / Q000031:analogs & derivatives / Q000097:blood; D005260:Female; D015438:Health Behavior; D006801:Humans; D006854:Hydrocortisone / Q000378:metabolism*; D018836:Inflammation Mediators / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood; D008875:Middle Aged; D012307:Risk Factors; D012463:Saliva / Q000378:metabolism; D013315:Stress, Psychological / Q000378:metabolism*; D013997:Time Factors; D014280:Triglycerides / Q000097:blood; D014851:Wakefulness / Q000502:physiology
D015415:Biomarkers; D018836:Inflammation Mediators; D015850:Interleukin-6; D014280:Triglycerides; C075750:8-epi-prostaglandin F2alpha; D002097:C-Reactive Protein; D002784:Cholesterol; D015237:Dinoprost; D006854:Hydrocortisone