This study examined the acute immunological effects of two laboratory stressors, expected to evoke distinct patterns of cardiac autonomic activity; namely an “active coping” time-paced memory test, and a “passive coping” stressful video showing surgical operations. We measured salivary S-IgA, IgA-subclasses (IgA1, IgA2), and secretory component (SC). SC is responsible for the transport of S-IgA across the epithelium, and thus a rate-determining step in S-IgA secretion. Thirty-two male undergraduates were subjected to both stressors and a control video (a didactic television program). The memory test induced a typical “fight-flight” response, characterized by increases in heart rate and blood pressure in association with a decrease in cardiac preejection period (PEP) and vagal tone. The surgical video produced a “conservation-withdrawal”-like response, characterized by an enhanced vagal tone, a decrease in heart rate, and a moderate sympathetic coactivation (as indicated by a shortened PEP and an increased systolic pressure). The memory test induced an increase in the concentration and, to a lesser extent, in the output of S-IgA, IgA], and SC. The output of IgA2 was not significantly affected. For the surgical video, a different pattern emerged: During stressor exposure S-IgA remained unaffected, against the background of a small increase in SC output. However, 10 min after the surgical video S-IgA levels had decreased. This decrease in S-IgA was paralleled by a decrease in IgA1, but not IgA2. We conclude that acute stress can have both enhancing and suppressive effects on secretory immunity, the IgA1 subclass in particular. The mechanisms that underlie these divergent responses may include stressor-specific patterns of autonomic activation.

In a longitudinal study of Dutch adolescent and young adult twins, their parents and their siblings, questionnaire data were collected on depression, anxiety and correlated personality traits, such as neuroticism. Data were collected by mailed surveys in 1991, 1993, 1995 and 1997. A total of 13,717 individuals from 3344 families were included in the study. To localise quantitative trait loci (QTLs) involved in anxiety and depression, the survey data were used to select the most informative families for a genome-wide search. For each individual a genetic factor score was computed, based on a genetic multivariate analysis of anxiety, depression, neuroticism and somatic anxiety. A family was selected if at least two siblings (or DZ twins) had extreme factor scores. Both discordant (high-low) and concordant (high-high and low-low) pairs were included in the selected sample. Once an extreme sibling pair was selected, all family members (parents and additional siblings of the selected pair) who had at least once returned a questionnaire booklet were asked to provide a DNA sample. In total, 2724 individuals from 563 families (1007 parents and 1717 offspring) were approached and 1975 individuals from 479 families (643 patients and 1332 offspring) complied by returning a buccal swab for DNA isolation. All offspring from selected families were asked to participate in a psychiatric interview and in a 24-hour ambulatory assessment of cardiovascular parameters and cortisol. The interview consisted of the WHO-Composite International Diagnostic Interview and was administered to 1253 offspring. In this paper we describe the genetic-epidemiological analyses of the survey data on anxiety, somatic anxiety, neuroticism and depression. We detail how these data were used to select families for the QTL study and discuss strategies that may help elucidate the molecular pathways leading from genes to anxious depression.

Background
Although mental stress is commonly considered to be an important trigger factor for migraine, experimental evidence for this belief is yet lacking.
Objective
To study the temporal relationship between changes in stress-related parameters (both subjective and objective) and the onset of a migraine attack.
Methods
This was a prospective, ambulatory study in 17 migraine patients. We assessed changes in perceived stress and objective biological measures for stress (saliva cortisol, heart rate average [HRA], and heart rate variability [low-frequency power and high-frequency power]) over 4 days prior to the onset of spontaneous migraine attacks. Analyses were repeated for subgroups of patients according to whether or not they felt their migraine to be triggered by stress.
Results
There were no significant temporal changes over time for the whole group in perceived stress (p=0.50), morning cortisol (p=0.73), evening cortisol (p=0.55), HRA (p=0.83), low-frequency power (p=0.99) and high-frequency power (p=0.97) prior to or during an attack. Post hoc analysis of the subgroup of nine stress-sensitive patients who felt that >2/3 of their migraine attacks were triggered by psychosocial stress, revealed an increase for perceived stress (p=0.04) but no changes in objective stress response measures. At baseline, this group also showed higher scores on the Penn State Worry Questionnaire (p=0.003) and the Cohen Perceived Stress Scale (p=0.001) compared to non-stress-sensitive patients.
Conclusions
Although stress-sensitive patients, in contrast to non-stress-sensitive patients, may perceive more stress in the days before an impending migraine attack, we failed to detect any objective evidence for a biological stress response before or during migraine attacks.