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PubMed1991

Early developmental and temporal characteristics of stress-induced secretion of pituitary-adrenal hormones in prenatally stressed rat pups.

Previous experiments revealed that 14-day-old prenatally stressed rats have significantly elevated concentrations of plasma adrenocorticotrophic hormone (ACTH) and corticosterone suggesting these animals have an overactive hypothalamic-pituitary-adrenal (HPA) system. In these studies, however, stress-induced hormone levels were determined only immediately after exposure to an acute stressor. Therefore, in the current study, we examined in postnatal days 7, 14 and 21 prenatally stressed rats the stress-induced time course of this pituitary-adrenal hormone elevation. Plasma ACTH and corticosterone were measured in the basal state and at 0.0, 0.5, 1.0, 2.0 and 4.0 h after a 10-min exposure period to foot shocks administered in the context of social isolation. Results indicated that at all 3 ages, plasma ACTH in prenatally stressed rats was significantly elevated. Corticosterone concentrations were also significantly higher in prenatally stressed than in control rats, especially in day 14 rats. Analysis of stress-induced hormone fluctuations over time indicated that by 14 days of age, both prenatally stressed than in control and control rats had significant increases in plasma ACTH and corticosterone after exposure to stress. Furthermore, although prenatally stressed rats had significantly higher pituitary-adrenal hormone concentrations than control animals, the post-stress temporal patterns of decline in ACTH and corticosterone levels were similar between groups. Results suggest that throughout the preweaning period, prenatal stress produces an HPA system that functions in a manner similar to that of controls but at an increased level.

Adrenal Cortex Hormones↗
PubMed1989

Alterations in stress-induced prolactin release in adult female and male rats exposed to stress, in utero.

Prenatal stress alters the endocrine as well as the behavioral responses of rodents. Because of the reductions in both estradiol-induced and ether-induced prolactin (Prl) release reported in prenatally-stressed (P-S) rats, we were interested in whether prenatal stress might also modify the prolactin response of male and female rats to a moderate stressor in adulthood, viz., restraint stress. Timed-mated Sprague-Dawley females were exposed to a daily regimen of heat and restraint stress from days 15-22 of gestation. Control animals remained undisturbed throughout pregnancy. In adulthood, half of the male and female P-S and Control offspring were stressed by placing them in a Plexiglas restraint tube for 60 min (restraint stressed; S; referred to as P-SS and CS, respectively). The remaining half of the P-S and Control animals were left undisturbed (these were nonrestrained; NR; referred to as P-SNR and CNR, respectively). Blood samples (decapitation) were then collected from all animals and plasma was assayed for Prl content. P-SNR and CNR males did not differ in baseline Prl levels, nor did P-SNR and CNR females. Following the restraint stress in adulthood, P-SS males as well as PSS females exhibited significantly less of an increase in Prl relative to CS males and CS females, respectively. In addition, baseline Prl levels differed between the sexes, with females--regardless of prenatal condition--having higher plasma Prl levels than males. These sex differences were no longer evident following restraint stress. These data, in combination with other work in P-S animals in the areas of Prl release and stress responses, demonstrate that prenatal stress renders the rat less hormonally (Prl) responsive to stress, with the effect being more pronounced in the female.

Animals↗
PubMed1992

Effects of controllable vs. uncontrollable chronic stress on stress-responsive plasma hormones.

We have previously reported effects of chronic stress on circadian rhythms of temperature, eating, and locomotor activity. These studies were conducted using an around-the-clock signalled intermittent footshock paradigm in which some rats have control over shock termination while other rats are yoked to the rats with control. Although this paradigm is stressful, as suggested by decreases in food intake and disrupted circadian rhythms, rats tolerate the paradigm well, continuing to eat, drink, gain weight, and groom. In the present studies, rats were sacrificed following 3 or 14 days of stress, and plasma was collected for hormonal assays. After 3 days of stress, plasma corticosterone and prolactin levels were elevated in both stress groups compared to controls; yoked rats had higher levels of corticosterone than rats in the group with control over shock termination, while prolactin levels in both stressed groups were similar. ACTH levels were similar in stressed and control rats. After 14 days of stress, ACTH and corticosterone levels in both stress groups were similar to control levels. Prolactin levels were elevated in the yoked experimental group compared to levels in control or controllable stress groups. These data support previous studies suggesting that control over stressors attenuates the effects of stress on physiology and demonstrate that two hormones with diverse biological effects are elevated by chronic stress.

Adrenocorticotropic Hormone↗
PubMed1988

Naloxone, given before but not after stress exposure, enhances stress-induced increases in regional brain noradrenaline release.

Male Wistar rats were injected with either saline or naloxone at a dose of 5 mg/kg either 10 min before exposure to a 1-hour period of immobilization stress or after exposure to the same stress for 2 hours which was then followed by a further 1-hour stress exposure (a total of 3 hours of immobilization stress). Levels of noradrenaline (NA) and its major metabolite, 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MHPG-SO4) in six discrete brain regions were determined fluorometrically. Both one hour and three hours of immobilization stress significantly increased MHPG-SO4 levels in all brain regions examined. This effect was accompanied by significant reductions of NA levels excluding the cerebral cortex after 1 hour of stress. Naloxone, injected prior to stress exposure, significantly enhanced MHPG-SO4 increases in the hypothalamus, amygdala and thalamus, but did not do so when injected 2 hours after stress exposure. Naloxone administration at either time did not affect stress-induced increases in MHPG-SO4 levels in the hippocampus, cerebral cortex or pons plus medulla oblongata. These results suggest that naloxone enhances stress-induced increases in NA release in the hypothalamus, amygdala and thalamus only during the early period of immobilization stress. Furthermore, these findings suggest that endogenous opioid peptides might be preferentially released during the initial exposure to stress.

Animals↗
PubMed1989

Met-enkephalin, injected during the early phase of stress, attenuates stress-induced increases in noradrenaline release in rat brain regions.

By measuring levels of 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MHPG-SO4), the major metabolite of noradrenaline (NA), we investigated the effects of Met-enkephalin (Met-ENK) ICV injected at three different stages of stress, i.e., 0 min, 5 min, or 10 min after exposure to immobilization stress. Immobilization stress caused significant increases in MHPG-SO4 levels in all brain regions examined, i.e., the hypothalamus, amygdala, thalamus, midbrain, hippocampus and locus coeruleus (LC), which suggests that stress increases NA release in these regions. Met-ENK at a dose of 50 micrograms, injected ICV immediately before stress exposure significantly attenuated stress-induced increases in MHPG-SO4 in the amygdala, thalamus and LC, but did not have such an effect when injected either 5 min or 10 min or 10 min after exposure to stress. Similarly, Met-ENK at 150 micrograms at 0 min significantly attenuated these increases in all brain regions examined, however, it did not do so when given at 5 min or 10 min after stress initiation. The amount of defecation and the weight loss caused by stress were also significantly attenuated by Met-ENK injected but only at 0 min. These results suggest that the attenuating effect of Met-ENK on stress-induced increases in NA release is greatly affected by the time of the peptide administration and that Met-ENK might inhibit stress-induced increases in NA release in these regions by affecting the initial changes induced by stress.

Animals↗
PubMed2006

Juvenile stress induces a predisposition to either anxiety or depressive-like symptoms following stress in adulthood.

Epidemiological studies indicate that childhood trauma is predominantly associated with later emergence of several stress-related psychopathologies. While most 'early-stress' animal models focus on pre-weaning exposure, we examined the consequences of exposure to stress during the early pre-pubertal period, "juvenile stress", on adulthood stress responses. Following two different juvenile stress protocols, predator scent or short-term variable stress, we examined adulthood stress responses using the elevated plus-maze and startle response or exploration and avoidance learning. Employing Cut-off Behavioral Criteria analyses of clustering symptoms on the rats' altered stress responses discriminated between different patterns of maladaptive behaviors. Exposure to either juvenile stress protocols resulted in lasting alteration of stress responses with the majority of rats exhibiting anxiety-like behaviors, while the remaining third displayed depressive-like behaviors. The results suggest that the presented "Juvenile stress" model may be relevant to the reported predisposition to develop both anxiety and depression following childhood trauma.

Acoustic Stimulation↗
PubMed2005

Chronically increased oxidative stress in fibroblasts from Alzheimer's disease patients causes early senescence and renders resistance to apoptosis by oxidative stress.

It is well established that oxidative stress is involved in several neurodegenerative disorders, including Alzheimer's disease (AD). Study of the induction and consequences of oxidative stress in the peripheral tissues of the familial AD patients can help to elucidate the inherent abnormalities and the mechanism of pathogenesis of this disease. AD fibroblasts have been used as a model to investigate the underlying mechanisms of oxidative stress. In our study, we used AD fibroblasts from six different donors who are either at high risk of developing AD or have already been diagnosed with AD to study the effect of oxidative stress in comparison with the effect on non-AD normal human fibroblast. Oxidative stress was induced by a brief exposure of the cells to 250microM H(2)O(2) followed by incubation in normal conditions. Neuronal loss due to oxidative stress is a characteristic of Alzheimer's patients; however, our results showed that AD fibroblasts were more resistant to oxidative stress compared to non-AD fibroblasts. Measurement of reactive oxygen species (ROS) indicated that AD fibroblasts produced more ROS than did non-AD NHF cells either in basal conditions or after induction of oxidative stress. Furthermore, we found that expression of p21 was significantly higher in AD cells than in non-AD cells and expression of Bax, a pro-apoptotic protein was downregulated/absent in AD cells during normal or under conditions of external oxidative stress. Further experiments revealed that mitochondria in AD cells moved to the peri-nuclear region following induction of oxidative stress. Thus, these results suggest that AD fibroblasts are chronically exposed to oxidative stress that may trigger senescent phenotype, making AD cell resistant to apoptosis by external oxidative stress.

Alzheimer Disease↗
PubMed2002

Maternal stress beginning in infancy may sensitize children to later stress exposure: effects on cortisol and behavior.

BACKGROUND: Preclinical studies demonstrate that the neonatal environment can permanently alter an individual's responses to stress. To demonstrate a similar phenomenon in humans, we prospectively examined the relationships of maternal stress beginning in infancy and concurrent stress on preschoolers' hypothalamic-pituitary-adrenal activity and later mental health symptoms. METHODS: Salivary cortisol levels were assessed in 282 4.5-year-old children and 154 of their siblings. Maternal reports of stress were obtained when the children were ages 1, 4, and 12 months, and again at 4.5 years. Children's mental health symptoms were assessed in first grade. RESULTS: A cross-sectional analysis revealed that preschoolers exposed to high levels of concurrent maternal stress had elevated cortisol levels; however, a longitudinal analysis revealed that concurrently stressed children with elevated cortisol also had a history of high maternal stress exposure in infancy. Importantly, children exposed only to high levels of concurrent or early stress had cortisol levels that did not significantly differ from those never exposed to stress. Further analysis of the components of stress indicated that maternal depression beginning in infancy was the most potent predictor of children's cortisol. We also found that preschoolers with high cortisol levels exhibited greater mental health symptoms in first grade. CONCLUSIONS: These results link the findings of preclinical studies to humans by showing that exposure to early maternal stress may sensitize children's pituitary-adrenal responses to subsequent stress exposure.

Adult↗
PubMed2002

Behavioral reactivity to stress: amplification of stress-induced noradrenergic activation elicits a galanin-mediated anxiolytic effect in central amygdala.

Brain norepinephrine (NE) modulates many aspects of the stress response. The interaction between NE and neuropeptides such as galanin, with which it is closely associated and which may be released from noradrenergic terminals under conditions of high activity, has not been well studied. We therefore investigated the modulatory effects of galanin in the central nucleus of the amygdala (CeA) on behavioral responsivity to stress when activation of the noradrenergic system was amplified using the adrenergic autoreceptor antagonist yohimbine (2.5 mg/kg ip). Either immobilization stress or yohimbine alone had anxiogenic effects on rat behavior in the elevated plus maze. However, yohimbine pretreatment before stress produced a paradoxical anxiolytic response, which we hypothesized was attributable to galanin release in CeA. Microdialysis verified that yohimbine amplified NE release in CeA during immobilization stress, and also showed that whereas there was no detectable change in galanin release in CeA during stress alone, there was an increase during immobilization stress after yohimbine pretreatment. Bilateral administration of the galanin antagonist M40 into CeA before stress blocked the anxiolytic influence of yohimbine pretreatment. Exogenous galanin mimicked the anxiolytic effect of yohimbine pretreatment, and this too was blocked by M40. These results suggest that amplifying the noradrenergic response to stress can recruit galanin release in CeA, which buffers the anxiety-like behavioral response to acute stress. The balance between noradrenergic and peptidergic neurotransmission may be modified by prior stress, drug treatment or genetic variability, and may represent a novel target for treatment of stress-related neuropsychiatric disorders.

Adrenergic alpha-Antagonists↗
PubMed2002

Stress-induced augmentation of immune function--the role of stress hormones, leukocyte trafficking, and cytokines.

Delayed-type hypersensitivity (DTH) reactions represent cell-mediated immune responses that exert important immunoprotective (resistance to viruses, bacteria, and fungi) or immunopathological (allergic or autoimmune hypersensitivity) effects. We initially utilized the skin DTH response as an experimental in vivo model to study neuro-endocrine-immune interactions in rodents. We hypothesized that just as an acute stress response prepares the cardiovascular and musculoskeletal systems for fight or flight, it may also prepare the immune system for challenges which may be imposed by a stressor. The skin DTH model allowed us to examine the effects of stress at the time of primary and secondary exposure to antigen. Studies showed that acute (2h) stress experienced before primary or secondary antigen exposure induces a significant enhancement of skin DTH. Importantly, this enhancement involved innate as well as adaptive immune mechanisms. Adrenalectomy eliminated the stress-induced enhancement of DTH. Acute administration of physiological (stress) concentrations of corticosterone and/or epinephrine to adrenalectomized animals enhanced skin DTH. Compared with controls, DTH sites from acutely stressed or hormone-injected animals showed significantly greater erythema and induration, numbers of infiltrating leukocytes, and levels of cytokine gene expression. In contrast to acute stress, chronic stress was immunosuppressive. Chronic exposure to corticosterone, or acute exposure to dexamethasone significantly suppressed skin DTH. These results suggest that during acute stress, endogenous stress hormones enhance skin immunity by increasing leukocyte trafficking and cytokine gene expression at the site of antigen entry. While these results are discussed from a mechanistic and clinical relevance perspective, it is acknowledged that much work remains to be done to elucidate the precise mechanisms mediating these bi-directional effects of stress and stress hormones and their clinical ramifications.

Animals↗
PubMed2002

Platelet alpha2-adrenoceptor density in humans: relationships to stress-induced anxiety, psychasthenic constitution, gender and stress-induced changes in the inflammatory response system.

BACKGROUND: This study examined the effects of psychological stress on platelet alpha2-adrenergic receptor (alpha2-AR) binding sites in relation to stress-induced anxiety and changes in the inflammatory response system (IRS). METHODS: The maximum number of binding sites (Bmax) and their affinity (Kd) for [3H]rauwolscine, a selective alpha2-AR antagonist, and the stimulated production of tumor necrosis factor-alpha (TNFalpha), the Th1-like cytokine, interferon-gamma (IFNgamma), and the Th2-like cytokines, interleukin-10 (IL-10) and IL-5, were measured in 35 university students a few weeks before (baseline) as well as on the day before a difficult, oral examination (stress condition). The State-Trait-Anxiety Inventory (STAI) was recorded during both conditions. The Minnesota Multiphase Personality Inventory (MMPI-2) was used to assess psychasthenia (Scale 7). RESULTS: Academic examination stress induced a significant increase in alpha2-AR density in students whose STAI scores increased in the stress period, in female students and in students who scored higher on psychasthenia. There were significant and positive correlations between stress-induced anxiety and changes in alpha2-AR density. Stress-induced anxiety was accompanied by a pro-inflammatory and Th1-like response, i.e. increased IFNgamma and TNFalpha production. The stress-induced changes in platelet alpha2-AR density were significantly and positively related to the production of TNFalpha, IL-10 and IL-5 and negatively to that of IFNgamma. CONCLUSIONS: Subchronic psychological stress in humans induces increased alpha2-AR density, which is related to stress-induced anxiety, an anxiety-prone constitution and female sex. Increased alpha2-AR density is accompanied by a Th2-like response and increased TNFalpha production. The results suggest that: (i) alpha2-AR density is sensitive to graded differences in stress-induced anxiety; and (ii) psychological stress is accompanied by intertwined responses in the catecholaminergic system, such as alpha2-ARs, and the IRS, such as Th1/Th2-like functions and the production of TNFalpha.

Adult↗
PubMed2001

Stress proteins in oligodendrocytes: differential effects of heat shock and oxidative stress.

Heat shock proteins (HSP) or stress proteins serve as biomarkers to identify the contribution of stress situations underlying the pathogenesis of degenerative diseases of the CNS. We have analyzed by immunoblot technique the constitutive and inducible occurrence of stress proteins in cultured rat brain oligodendrocytes subjected to heat shock or oxidative stress exerted by hydrogen peroxide, or a combination of both. The data demonstrate that oligodendrocytes constitutively express HSP32, HSP60 and the cognate form of the HSP70 family of proteins, HSC70. After heat shock, HSP25, alpha B-crystallin and HSP70 were up-regulated, while after oxidative stress the specific induction of HSP32 and alpha B-crystallin was observed. HSP32 represents heme oxygenase 1 (HO-1), a small stress protein with enzymatic activity involved in the oxidative degradation of heme which participates in iron metabolism. The presence of the iron chelators phenanthroline or deferoxamine (DFO), which previously has been shown to protect oligodendrocytes from oxidative stress-induced onset of apoptosis, caused a marked stimulation of HSP32 without affecting HSP70. This indicates that DFO possibly exerts its protective role by directly influencing the antioxidant capacity of HO-1. In summary, HSP in oligodendrocytes are differentially stimulated by heat stress and oxidative stress. Heme oxygenase-1 has been linked to inflammatory processes and oxidative stress, its specific up-regulation after oxidative stress in oligodendrocytes suggests that it is an ideal candidate to investigate the involvement of oxidative stress in demyelinating diseases.

Animals↗
PubMed2002

Plasminogen activator inhibitor-1 is a major stress-regulated gene: implications for stress-induced thrombosis in aged individuals.

Plasminogen activator inhibitor-1 (PAI-1) is one of the primary inhibitors of the fibrinolytic system and has been implicated in a variety of thrombotic disorders. In this report, stress-induced changes in murine PAI-1 gene expression were investigated to study the role of this inhibitor in the development of stress-induced hypercoagulability. Restraint stress led to a dramatic induction of plasma PAI-1 antigen and of tissue PAI-1 mRNA with maximum induction in adipose tissues. In situ hybridization analysis of the stressed mice revealed that strong signals for PAI-1 mRNA were localized to hepatocytes, renal tubular epithelial cells, adrenomedullar chromaffin cells, neural cells in the paraaortic sympathetic ganglion, vascular smooth muscle cells, and adipocytes, but not to endothelial cells. These observations indicate that the stress induces the PAI-1 gene expression in a tissue-specific and cell type-specific manner. The induction of PAI-1 mRNA by restraint stress was greater than that observed for heat shock protein, a typical stress protein, suggesting that PAI-1 is one of the most highly induced stress proteins. Importantly, the magnitude of induction of PAI-1 mRNA by stress increased markedly with age, and this increase in PAI-1 correlated with tissue thrombosis in the older stressed mice. Moreover, much less tissue thrombosis was induced by restraint stress in young and aged PAI-1-deficient mice compared with age-matched wild-type mice. These results suggest that the large induction of PAI-1 by stress increases the risk for thrombosis in the older populations, and that the adipose tissue may be involved.

Aging↗
PubMed1998

Metallothionein induction in response to restraint stress. Transcriptional control, adaptation to stress, and role of glucocorticoid.

Metallothioneins (MT) have been implicated in the protection of cells from oxidative stress. We studied the molecular mechanism of induction of MT-I and MT-II in response to restraint stress using a mouse model system in which the animals were restrained in well ventilated polypropylene tubes for 12 h each day (one cycle). Here, we show that MT-I and MT-II mRNA levels were elevated as much as 10-20-fold after just one cycle of this simple stress. Stress-mediated MT induction occurred at the transcriptional level. The level of MT mRNA correlated with the stress-induced increase, and not with the diurnal variation, in the level of serum glucocorticoid. Treatment of the mice with RU 486, a glucocorticoid receptor antagonist, prior to restraint stress inhibited MT induction by at least 50%. Furthermore, the glucocorticoid responsive element-binding activity in the liver nuclear extracts from the stressed mice was significantly higher than that in the control mice. The complex formations between the transcription factor Sp1, MTF1, or MLTF/ARE and the respective specific oligonucleotides were not altered in the liver from the stressed mouse. The MT mRNA levels returned to the basal level at the end of nine cycles of stress, indicating habituation of the animals to restraint stress. At this stage, exposure of the animals to another type of stress, treatment with heavy metals, resulted in further induction of MT. These data indicate that glucocorticoid is the primary physiological factor responsible for MT induction following restraint stress, and the glucocorticoid receptor is the major transcription factor involved in this process.

Adaptation, Biological↗
PubMed2006

Examination stress as an ecological inducer of cortisol and psychological responses to stress in undergraduate students.

The purpose of the present study was to investigate basic methodological issues related to the usage of an examination stress protocol in studies of psychoneuroendocrinology. In the present study, 57 undergraduate students served as participants. All subjects provided salivary samples and completed psychological inventories during a low examination stress period and again during a high examination stress period. Salivary samples were analyzed for cortisol. Three major findings were observed. First, the examination stress protocol proved to be an effective trigger of elevations in both psychological measures of stress and in cortisol levels. Second, sex differences were observed in cortisol levels, such that males showed an elevation in cortisol during the high examination stress session whereas females did not. Finally, no significant correlations were observed between elevations in psychological measures of stress and elevations in cortisol levels. These findings suggest that the examination stress protocol used in the present study effectively elevated both psychological stress and cortisol levels. Furthermore, these findings suggest that there are biological differences in how males and females respond to stress. Finally, no evidence was found to suggest a relationship between psychological and hormonal levels of stress. Together, these findings suggest the need to better define and consider the implications of both the specific measures of stress being used and individual differences in the subject samples in psychoendocrine studies.

Adolescent↗
PubMed1997

Adaptation to prolonged or repeated stress--comparison between rat strains showing intrinsic differences in reactivity to acute stress.

Sprague-Dawley (SD), Fischer 344 (F344) and Lewis (LEW) rats are used in a wide variety of laboratory studies. Compared to SD and LEW rats, F344 rats show significantly greater activation of the hypothalamic-pituitary-adrenal (HPA) axis in response to acute stress, or to immunologic challenge. These differences in HPA axis responsivity have been the basis for numerous studies investigating strain differences in immunological and behavioral parameters. However, strain differences in the adaptation of the HPA axis response to prolonged stress, or to repeated stress, have not been investigated. This series of studies demonstrates that F344 rats maintain significantly higher ACTH and corticosterone levels than SD and LEW rats during a single prolonged stress session. Furthermore, F344 rats show virtually no habituation or adaptation of the corticosterone stress response during a single prolonged (4 h) stress session, or during stress sessions repeated over a period of 10 days. In contrast, SD and LEW rats show habituation both within and across stress sessions. Strain differences in HPA axis responsivity are also reflected in the significant adrenal hypertrophy observed in F344 rats (but not in SD or LEW rats) following repeated stress. These results show that strain differences in HPA axis responsivity, which are observed under conditions of acute stress, are further amplified during prolonged or repeated stress. These differences under prolonged or repeated stress conditions may consequently magnify the behavioral and immunological differences observed between strains under basal as well as challenged conditions.

Adaptation, Physiological↗
PubMed2006

Increased stress-induced inflammatory responses in male patients with major depression and increased early life stress.

OBJECTIVE: The authors sought to determine innate immune system activation following psychosocial stress in patients with major depression and increased early life stress. METHOD: Plasma interleukin (IL)-6, lymphocyte subsets, and DNA binding of nuclear factor (NF)-kB in peripheral blood mononuclear cells were compared in medically healthy male subjects with current major depression and increased early life stress (N=14) versus nondepressed male comparison subjects (N=14) before and after completion of the Trier Social Stress Test. RESULTS: Trier Social Stress Test-induced increases in IL-6 and NF-kappaB DNA-binding were greater in major depression patients with increased early life stress and independently correlated with depression severity, but not early life stress. Natural killer (NK) cell percentages also increased following stress. However, there were no differences between groups and no correlation between NK cell percentage and stress-induced NF-kappaB DNA-binding or IL-6. CONCLUSIONS: Male major depression patients with increased early life stress exhibit enhanced inflammatory responsiveness to psychosocial stress, providing preliminary indication of a link between major depression, early life stress and adverse health outcomes in diseases associated with inflammation.

Adult↗
PubMed2004

[Job stress among Japan Overseas Cooperation volunteers--using the Brief Job Stress Questionnaire].

Mental health problems have recently increased among Japan Overseas Cooperation volunteers since 1965, when the Ministry of Foreign Affairs (Japan International Cooperation Agency) launched this volunteer work project for improving hygiene and socioeconomic conditions in developing countries. There was little research on job stress among them dispatched despite previous surveys indicating job as an important stressor. To investigate stress and job-related stressors among them, we conducted a cross-sectional epidemiological study from October to December in 2003. The subjects were all 1,084 Japan Overseas Cooperation volunteers aged 20-40, who worked in 67 countries worldwide at the time of this study (485 and 599 males and females, 316, 332 and 436 for those staying overseas for 11, 7 and 4 months, respectively). Approximately 80% were involved in their dispatching occupational organizations as professionals in information technology, health & welfare, education, and research. Our main outcome measure used was the Brief Job Stress Questionnaire, which was developed to assess stress and job-related stressors or buffers for Japanese workers. Demographic and personality (Egogram) characteristics as well as other health information were obtained. The response rate was 86.9%. For psychological stress, prevalence was 5.5% (n = 49). Means (+/- SD) were 4.22 (+/- 3.98), and 4.89 (+/- 4.40) for males and females (p < 0.05), and 5.15 (+/- 4.17), 5.05 (+/- 4.45), 3.93 (+/- 4.40) for those staying overseas for 11, 7 and 4 months (p < 0.01), respectively. For physical stress, prevalence was 2.9% (n = 26). Means (+/- SD) were 1.10 (+/- 1.68), and 1.41 (+/- 1.74) for males and females (p < 0.01), and 1.47 (+/- 1.77), 1.35 (+/- 1.89), 1.11 (+/- 1.55) for those staying overseas for 11, 7 and 4 months (p < 0.05), respectively. The factors significantly associated with psychological stress were high job demand, poor human relationships at work, low job suitability, low social support from supervisors and colleagues, and being dissatisfied with their life, according to multiple logistic regression analysis. The present study suggested that psychological stress was more prevalent than physical. It also implied a significant relationship between psychological stress and job-related stressors among the subjects of this study as in employees in Japan. Mental health check-ups and counseling in the early stage of psychological stress is important from the viewpoint of prevention of developing stress-related mental health disorders. Education on stress-coping skills should be considered in a training program before they are sent overseas.

Adaptation, Psychological↗