ECE2009 Poster Presentations Neuroendocrinology, Pituitary and Behaviour (74 abstracts)
University of Sussex, Brighton, UK.
Previous studies suggest that individuals characterized by high trait hostility may be more sensitive to stress and that this may contribute to their greater vulnerability to alcohol abuse. To characterize the stress reactivity of hostile individuals and to evaluate the possibility that serotonergic dysfunction may underlie their susceptibility to stress, we examined the effects of acute dietary tryptophan enhancement and stress on mood and physiological reactivity in low (LoH) and high hostile (HiH) heavy social drinkers.
Thirty-four LoH and thirty-three HiH heavy social drinkers received either tryptophan-enriched or control diet and underwent a stress-induction procedure. Trait differences between the two hostile groups were explored using personality, anxiety and depression questionnaires. Mood and salivary cortisol levels (CORT) were measured before and after tryptophan diet and after stress-induction. Heart rate (HR) was measured during stress-induction.
HiHs compared to LoHs were characterized by greater trait anxiety and depression and reported more stress exposure over the past month. They also experienced more negative mood throughout the testing session. Stress increased CORT, HR and negative mood in most participants. Compared to LoHs, HiH individuals displayed a higher CORT increase and lower HR as well as a tendency to report more anger in response to stress. Tryptophan manipulation did not modulate any of the subjective and physiological effects of stress.
Among heavy drinkers HiHs show greater reactivity to stress as measured by CORT and negative mood but lower heart rate response. Dissociation between cardiovascular and hypothalamopituitaryadrenocrotical axis (HPA) response to stress suggests that HiH heavy drinkers may indeed be at a greater risk of HPA-related disorders such as depression and alcohol abuse but not at a greater risk of cardiovascular problems. The present data do not support the hypothesis that the greater sensitivity of HiH individuals to stress may be due to a serotonergic dysfunction.