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Research investigating how control over stressors affects behavior often utilizes freezing and shuttle escape learning as the behavioral endpoints. These endpoints have been argued to reflect anxious or depressed states, but these descriptions are problematic. The present study sought to determine the impact of stressor controllability and the dorsal raphé nucleus (DRN) on sucrose preference and juvenile social exploration, putative measures of anhedonia and anxiety that are commonly used in studies of stress per se. In Experiment 1 rats were exposed to escapable stress (ES) or yoked-inescapable stress (IS) tailshocks. In Experiment 2 ES or IS was given 7 days before all rats received IS. In Experiment 3 the DRN was inactivated during IS by microinjection of 8-OH-DPAT. Sucrose preference and social exploration were tested for several days after stress. A fourth experiment confirmed that juvenile social exploration is sensitive to traditional beta-carboline and benzodiazepine manipulations. Both ES and IS reduced sucrose preference, but only IS reduced social exploration. Prior treatment with ES prevented the effect of IS on social exploration but did not prevent the effect of IS on sucrose preference and inactivation of the DRN prevented the effect of IS on social exploration but did not change sucrose preference. The present results indicate that social exploration but not sucrose preference is sensitive to prior stressor controllability, and that DRN activation mediates the effect of IS on social exploration. We argue that DRN-5-HT activation mediates a state of generalized anxiety produced by uncontrollable stress and that juvenile social exploration is a useful behavioral endpoint in stressor controllability studies.

One goal of genetic counseling is to facilitate client adaptation to a genetic condition or risk. Adaptation refers to both the process of coming to terms with the implications of the condition or risk and the observable outcomes of that process. This review summarizes existing studies on how well clients adapt to living with a common chronic disease, and more specifically, a genetic condition. Overall, it appears that about one-third of clients do not adjust well to the stress of living with a genetic condition or at risk. However, the data are limited by inconsistencies in the conceptualization of adaptation, a paucity of theoretical models, poor study design and inadequate outcome measures. Well-designed studies based upon multidimensional models are needed that focus on familial as well as individual adaptation. We conclude with a summary of studies that have explored the use of interventions to enhance adaptation and suggest improved client outcomes. Further research should result in evidence-based interventions to facilitate client adaptation that can be used effectively by genetic providers within the confines of their clinical work.

The objective of this study was to evaluate the perceived stress index, quality of life, and hypothalamus-pituitary-adrenal axis activity in women with endometriosis and chronic pelvic pain. For the study, 93 women with endometriosis and 82 healthy women volunteered. The visual analogue scale (VAS) (0=no pain; 10=severe pain) was used to determine pain intensity; the perceived stress questionnaire (PSQ) defined stress index, and the health-related quality-of-life (HRQOL)-SF-36 questionnaire was used to evaluate quality of life. Salivary cortisol was measured at 0800, 1600, and 2000 h and the awakening cortisol response was assessed to evaluate the hypothalamus-pituitary-adrenal axis activity. The results show that women with endometriosis and chronic pelvic pain of moderate intensity (4.1+/-0.58, mean+/-SEM) have higher levels of perceived stress (0.55+/-0.01 versus 0.42+/-0.01, p<0.05), a poorer quality of life expressed as lower scores for all items of the inventory and hypocortisolism. Lower levels of salivary cortisol were observed in all three samples collected, as well as in the awakening cortisol response, for women with endometriosis (0.19+/-0.09 microg/dl) when compared with controls (0.78+/-0.08 microg/dl, p<0.05 l), and it was independent of pain intensity and Mental health (MH) scores in SF-36. We concluded that women with endometriosis and chronic pelvic pain show low concentrations of salivary cortisol and a high level of perceived stress, associated with a poor quality of life. Whether the hypocortisolism was an adaptive response to the aversive symptoms of the disorder or a feature related to the etiology of endometriosis remains to be elucidated.

Parental responses play a central role in the development and maintenance of children's pain behavior. Previous studies examining the impact of parental responses on children's pain have focused mainly on protective or solicitous responses. This study examined the impact of parental responses, including protectiveness, minimization of pain, and encouraging and monitoring responses, on children's functional disability and somatic symptoms. Participants included 327 patients with chronic pain, ages 8-17, who completed measures of pain, disability, somatic symptoms, depression, and anxiety. Patients' parents completed a measure assessing parental responses to their children's pain. Results show that for children with higher levels of emotional distress, maladaptive parental responses to pain (e.g., criticism, discounting of pain, increased attention to pain, and granting of special privileges) were associated with increased disability and somatic symptoms. Results of this study demonstrate the important ways in which parents can influence how their children cope with and manage chronic pain. Children whose parents are overly protective or critical of their pain may experience more impairment or somatic symptoms, particularly those children who are already at risk for difficulties due to higher levels of emotional distress.

Consolation, i.e., postconflict affiliative interaction directed from a third party to the recipient of aggression, is assumed to have a stress-alleviating function. This function, however, has never been demonstrated. This study shows that consolation in chimpanzees reduces behavioral measures of stress in recipients of aggression. Furthermore, consolation was more likely to occur in the absence of reconciliation, i.e., postconflict affiliative interaction between former opponents. Consolation therefore may act as an alternative to reconciliation when the latter does not occur. In the debate about empathy in great apes, evidence for the stress-alleviating function of consolation in chimpanzees provides support for the argument that consolation could be critical behavior. Consistent with the argument that relationship quality affects their empathic responses, we found that consolation was more likely between individuals with more valuable relationships. Chimpanzees may thus respond to distressed valuable partners by consoling them, thereby reducing their stress levels, especially in the absence of reconciliation.

This study examined stability and change in maternal anxiety, stress and depression both during the second half of pregnancy and from pregnancy to six weeks and two years postpartum. Self-report measures included those designed to measure mood and state as well as more persistent attributes. Longitudinal data were collected from 137 women during pregnancy, 120 at six weeks, and 97 at two years. There was significant individual stability in scores on specific measures during pregnancy (range in Pearson rs=0.30-0.86) and from pregnancy through two years postpartum (rs=0.30-0.74). Comparable levels of convergence among measures of different constructs both within pregnancy and over time were also demonstrated, suggesting lack of precision in measurement instruments designed for specific constructs. Despite intra-individual stability, changes in mean levels were also observed over time with somewhat different patters for each variable. However, maternal parity was an important contributor to both level and trajectory. A summary composite score showed an elevated level of psychological distress during pregnancy in multiparous women, followed by a decline through two years postpartum; primiparous women displayed a gradual increase in distress [main effect F (1,87)=3.97, p < 0.05; time interaction F (2,174)= 7.15, p < 0.001] to multiparous levels by two years. Results are discussed in terms of a "motherhood" effect on psychological distress.

This study assessed whether the Recovery-Stress Questionnaire for Athletes (RESTQ-Sport) could be used to monitor changes in perceived stress and recovery during intensified training of rugby league players. 20 semiprofessional rugby league players were divided into two equal groups randomly assigned to complete 6 wk. of Normal Training or Intensified Training, each followed with a 7-day taper. Multistage Fitness Test performance and RESTQ-Sport measures were taken at the beginning, at 2-wk. intervals, and at the end of the training period. Endurance significantly decreased with Intensified Training and returned to baseline levels following the taper, while remaining unchanged in the Normal Training group. The RESTQ-Sport scores with training were positively related to stress subscale scores (Fatigue, Disturbed Breaks, and General Stress) and recovery subscale measures (Success, Physical Recovery, Being in Shape, Self-efficacy, Social Relaxation, General Well-being, and Sleep Quality) decreasing in the Intensified Training group and then normalising following the taper (Stress subscales: Fatigue and General Stress, and Recovery subscales: Physical Recovery and General Well-being). The RESTQ-Sport is a practical psychometric tool for monitoring responses to training in team-sport athletes.

Unlike responses to acute stressful events that are protective and adaptive in nature, chronic stress elicits neurochemical, neuroanatomical and cellular changes that may have deleterious consequences upon higher brain functioning. For example, while exposure to acute stress facilitates memory formation and consolidation, chronic stress or chronic exposure to stress levels of glucocorticoids impairs cognitive performance. Chronic stress or glucocorticoid exposure, as well as impairments in hypothalamic-pituitary-adrenal (HPA) axis function are proposed to participate in the etiology and progression of neurological disorders such as depressive illness, anxiety disorders and post-traumatic stress disorder (PTSD). HPA axis dysfunction, impaired stress responses and elevated basal levels of glucocorticoids are also hallmark features of experimental models of type 1 and type 2 diabetes, as well as diabetic subjects in poor glycemic control. Such results suggest that stress and glucocorticoids contribute to the neurological complications observed in diabetes patients. Interestingly, many of the hyperglycemia mediated changes in the brain are similar to those observed in depressive illness patients and in experimental models of chronic stress. Such results suggest that common mechanisms may be involved in the development of the neurological complications associated with Anxiety, Depressive illness and Diabetes: the As and Ds of stress. The aim of the current review will be to discuss the mechanisms through which limbic structures such as the hippocampus and amygdala respond and adapt to the deleterious consequences of chronic stress and hyperglycemia.

Background: A relationship between smoking and development of pain syndromes has been suggested in the literature. The present study examined associations between smoke exposure and other related variables, and pain response to suprathreshold electrical stimulation., Methods: Subjects were prospectively recruited from a population referred to an electrodiagnostic clinic. Information about age, smoke exposure, caffeine and alcohol consumption was obtained, as well as documented objective signs of stress through physical assessment. One investigator applied two standardized 0.1 ms electrical stimulations (50 mA followed by 100 mA) to asymptomatic extremities at the beginning of each electrodiagnostic session, using consistent technique. Subjects used a visual analogue scale to indicate the level of pain felt after each stimulation., Results: Two hundred fifteen women were included. Current smokers and those currently exposed to second-hand smoke had significantly higher pain ratings (P=0.003 for 50 mA, P=0.005 for 100 mA) than those not currently exposed to smoke. Time since exposure was negatively associated with pain ratings. Those with objective signs of stress reported higher levels of pain, which was significant for the 100 mA stimulation (P=0.046). Linear regression modelling indicated that current smoke exposure and alcohol use were associated with higher pain ratings at both 50 mA and 100 mA, while stress was associated with higher pain ratings and older age was associated with lower pain ratings at 100 mA only., Interpretation: Exposure to cigarette smoke is significantly related to higher reported levels of pain experienced in response to electrical stimulation in this study population. Exposure to smoke can add 10 points to the 100-point visual analogue scale compared with subjects without exposure, with alcohol use adding another eight points. Reported pain decreases as length of time since previous exposure to smoke increases.

Background: This study examined the interaction between restraint stress and ethanol drinking in mice that consume low and high amounts of ethanol., Methods: Two strains of mice (129SVEV and C57BL/6J) underwent 1 hour of restraint stress twice per day for 4 days in the presence of a CRF-1 receptor antagonist, a glucocorticoid receptor antagonist or vehicle. Ethanol preference and consumption were assessed using a two bottle choice design. In another study, mice were implanted with pellets containing corticosterone; ethanol preference and consumption were assessed using a two bottle choice design., Results: Restraint stress significantly increased ethanol preference and consumption in 129SVEV mice but not in C57BL/6J mice. Then 129SVEV mice underwent the identical stress procedure; however, mice received either the CRF-1 receptor antagonist, R121919 (15 or 20 mg/kg, ip) or vehicle 30 minutes prior to stress. R121919 did not block the stress-induced change in ethanol preference despite causing a significant blunting in the HPA axis. Negative results were also obtained using the CRF-1 receptor antagonist, Antalarmin (20 mg/kg, ip). In another study, 129SVEV mice were administered either the glucocorticoid receptor antagonist Mifepristone (25, 50 or 100 mug/kg, ip) or vehicle under the same procedure. Mifepristone did not alter ethanol preference. Moreover, the three receptor antagonist did not alter nonstress ethanol consumption either. In the last study, both mouse strains underwent active or sham adrenalectomy, then pellets containing corticosterone or placebo were implanted and preference for ethanol versus water was tested. Corticosterone administration decreased ethanol consumption in a strain-dependent manner., Conclusion: These data show the restraint model for stress can modestly increase ethanol consumption in 129SVEV mice but not in C57BL/6J mice. Pharmacologic manipulation of CRF and corticosterone did not blunt baseline or stress-induced change in ethanol preference nor did administration of corticosterone mimic the effects of restraint stress on ethanol consumption. These findings suggest the mechanism responsible for increasing ethanol consumption in this model is independent of the HPA axis and extra-hypothalamic CRF.

Understanding inter-individual differences in stress response requires the explanation of genetic influences at multiple phenotypic levels, including complex behaviours and the metabolic responses of brain regions to emotional stimuli. Neuropeptide Y (NPY) is anxiolytic and its release is induced by stress. NPY is abundantly expressed in regions of the limbic system that are implicated in arousal and in the assignment of emotional valences to stimuli and memories. Here we show that haplotype-driven NPY expression predicts brain responses to emotional and stress challenges and also inversely correlates with trait anxiety. NPY haplotypes predicted levels of NPY messenger RNA in post-mortem brain and lymphoblasts, and levels of plasma NPY. Lower haplotype-driven NPY expression predicted higher emotion-induced activation of the amygdala, as well as diminished resiliency as assessed by pain/stress-induced activations of endogenous opioid neurotransmission in various brain regions. A single nucleotide polymorphism (SNP rs16147) located in the promoter region alters NPY expression in vitro and seems to account for more than half of the variation in expression in vivo. These convergent findings are consistent with the function of NPY as an anxiolytic peptide and help to explain inter-individual variation in resiliency to stress, a risk factor for many diseases.

Depression is strongly related to social behavior. We have previously shown that social behavior of rats is individually stable. The purpose of the present study was to compare the sensitivity of animals with different sociability to chronic variable stress (CVS). Four social interaction tests were performed with 60 single-housed male Sprague-Dawley rats. Twenty rats with the lowest and 20 with the highest average social activity time were selected as low sociability (LS) and high sociability (HS) rats, respectively. Both groups were further divided into control and stress groups with equal average body weight. The CVS procedure lasted for 3 weeks. The stressors applied were cold water and wet bedding, imitation of injection, stroboscopic light, movement restriction in a small cage, tail pinch with a clothespin, and strong illumination during the predicted dark phase. In HS-rats, but not in LS-rats, CVS reduced sucrose intake compared with baseline after 3 weeks, suggesting that HS-rats are more vulnerable to anhedonia elicited by CVS. LS-animals were more anxious in the social interaction and open field tests, but stress eliminated differences with HS-animals in the social interaction test and increased their activity in the forced swimming test. In LS-rats stress increased ex vivo dopamine levels and reduced 5-HT levels in the frontal cortex, suggesting that the increased behavioral activity after stress may be related to increased impulsivity. This study thus revealed that animals with high sociability trait are more vulnerable to anhedonia elicited by chronic stress in conditions of single housing.

Risk of developing certain diseases correlates with human personality. Cardiologists have defined Type "A" personalities as coronary-prone. Associated psychological peculiarities are easily angered, competitive, impatient and hard-driving. Psychologically-opposite people who are prone to suppress emotions and avoid conflicts (Type "C"), have a high risk of infectious diseases and certain forms of cancer. The development of contemporary biology and medicine determined an important role of the neuroendocrine and immune systems in these correlations. The peculiarity of human personality, as much as of animal behavioral patterns, is strongly expressed under stress conditions. The strategies of stress coping display a normal distribution in the human and wild animal populations, with truly passive and active coping styles located at the outermost regions of the curve. However, there are a number of strategies to breed experimental animals with extreme coping styles; animals selected for a passive coping style to acute stress show marked activation of the hypothalamic-pituitary-adrenal (HPA) axis and low stimulation of the sympathetic-adrenal system; both are associated with immunosuppression. An opposite reaction of the neuroendocrine system has been shown in animals with an active coping style to stress; this was associated with the signs of immunostimulation. Similarly, people with passive coping style (type "C") might be at higher risk of infectious diseases and cancer, while people with active coping style (type "A") might be predisposed to coronary, allergic, and autoimmune diseases. Furthermore, pain, decreased productivity, and anxiety, all common in patients with different diseases, are additional stressful entities. Thus, an adequate coping with a disease is an important approach to improve life quality and disease prognosis. Therefore, psychological and psychopharmacotherapeutic interventions that enhance effective coping should have beneficial effects in patients with immune-mediated diseases.

Clinical literature has established a link between early childhood incidents of neglect and trauma and adult problems with substance abuse. In rats, such early life stress has been modeled using a maternal separation (MS) paradigm in which rat pups were removed from their mothers for a few hours daily during the first two postnatal weeks. In this study, we used the MS model to investigate the effects of early postnatal stress on place conditioning to both mu- and kappa-opioid agonists in male and female Long-Evans rats. Offspring of both rearing conditions [MS or nonhandled (NH)] were conditioned using a biased procedure to saline, the mu-opioid agonist morphine (3.0, 5.6, and 10 mg/kg s.c.), or the kappa-opioid agonist spiradoline (0.3, 1.0, and 3.0 mg/kg) for 3 days, followed by a drug-free place-conditioning test 24 h later. Saline was administered in the morning, 30 min before confinement in one compartment, whereas morphine or spiradoline was administered in a similar manner 6 h later in the opposite compartment. MS offspring spent significantly more time in the morphine-paired compartment than NH offspring, indicating a greater place preference for the mu-opioid agonist. In the case of spiradoline, NH offspring spent significantly less time in the spiradoline-paired compartment, indicating a greater aversion to the kappa-opioid agonist in these animals than in MS offspring. These findings indicate that early postnatal stress can significantly alter the rewarding or aversive value of mu- and kappa-opioid agonists when measured using place conditioning.

Having reported that traumatic brain injury (TBI), produced by moderate lateral controlled cortical impact (CCI), causes long-term dysregulation of the neuroendocrine stress response, the aim of this study was to assess short- and long-term effects of both moderate and mild CCI on stress-induced hypothalamic-pituitary-adrenal (HPA) function. TBI was induced to the left parietal cortex in adult male rats with a pneumatic piston, at two different impact velocities and compression depths to produce either a moderate or mild CCI. Controls underwent sham surgery without injury. Commencing at one week after recovery from surgery, rats were exposed to stressors: 30-min restraint (days 7, 34, and 70) or 15-min forced swim (days 21 and 54). Tail vein blood was analyzed for corticosterone (CORT) content by radioimmunoassay. On days 7 and 21, the stress-induced HPA responses were significantly attenuated by both mild and moderate CCI. Significant attenuation of the CORT response to stress persisted through day 70 after moderate CCI. In contrast, stress-induced CORT levels on days 34, 54, and 70 were significantly enhanced after mild CCI. Differential effects of injury severity were also observed on motor function in a forelimb test on post-injury day 12 and on cortical lesion volume and hippocampal cell loss at day 70, but not on working memory in a radial maze on day 15. The differing short- and long-term stress-induced HPA responses may be mediated by differential effects of moderate and mild CCI on the efficiency of glucocorticoid negative feedback or signaling among hypothalamic and extrahypothalamic components of the neuroendocrine stress-response system.

Chronic stress is a powerful modulator of emotional behaviour. Previous studies have shown that distinct neuronal pathways modulate different emotional behaviours: while the amygdala plays a key role in fear-conditioned-to-cue stimuli, the bed nucleus of stria terminalis (BNST) is implicated in anxiety behaviour and responses to contextual stimuli. In addition, the BNST is directly involved in the regulation of the hypothalamus-pituitary-adrenal (HPA) axis. In the present study, we assessed anxiety (measured in the elevated-plus maze and acoustic startle apparatus) and fear-conditioned responses to light stimuli in rats that had been exposed to either chronic unpredictable stress or corticosterone for 28 days; thereafter, stereological estimates of the BNST and amygdaloid complex were performed, followed by three-dimensional morphometric dendritic analysis. Results show that chronic stress induces hyperanxiety without influencing fear conditioning or locomotion and exploratory activity. Stress-induced hyperanxiety was correlated with increased volumes of the BNST but not of the amygdala. Dendritic remodelling was found to make a significant contribution to the stress-induced increase in BNST volume, primarily due to changes in the anteromedial area of the BNST, an area strongly implicated in emotional behaviour and in the neuroendocrine control of the stress response. Importantly, all of the effects of stress were recapitulated by exogenous corticosterone. In conclusion, this study shows that chronic stress impacts on BNST structure and function; its findings pertain to the modulation of emotional behaviour and the maladaptive response to stress.

The aim of the present experiment was to extend the literature on hostility and a cerebral systems based model of sympathetic arousal to a vestibular-based stress. Several authors have concluded that autonomic stress reactivity in high hostile individuals must be interpersonally based, whereas healthy vestibular system functioning does not depend on interpersonal features. Utilizing a vestibular activation paradigm, skin conductance levels of 15 high hostile and 15 low hostile men were recorded after brief passive rotation about the vertical neuroaxis. It was expected that hostile individuals would exhibit higher skin conductance levels after rotation compared with low hostile individuals. The results confirmed expectations of heightened sympathetic tone among high hostiles subsequent to vestibular stress. Overall, the findings are interpreted to support a cerebral model of frontal region capacity limitation for regulation of vestibular stress that is independent of psychosocial mechanisms.

Repeated administration of addictive drugs and prolonged exposure to stressful stimuli induce sensitization to their behavioural stimulant properties. In this study, male Sprague-Dawley rats were repeatedly exposed to morphine [twice a day for 3 days at increasing doses, 10, 20, 40 mg/kg subcutaneously (s.c)], amphetamine (1 mg/kg s.c., once a day for 10 days), nicotine (0.4 mg/kg s.c., once a day for 5 days) and stress (food restriction for 7 days). After an interval of 3-30 days, depending on the pretreatment, rats were challenged with vehicle, with the same drug received as pretreatment (5 mg/kg of morphine, 0.5 mg/kg of amphetamine or 0.4 mg/kg of nicotine, respectively) or, in the case of food-restricted rats, with 0.5 mg/kg of amphetamine. Thereafter, changes in the expression of glutamic acid decarboxylase (GAD)67 mRNA were estimated by in situ hybridization in the central nucleus of the amygdala (CeA), basolateral amygdala (BLA), dorsolateral striatum (dLStr), nucleus accumbens shell (AcS) and core (AcC). All sensitizing pretreatments increased GAD67 mRNA in the CeA. Drug challenge did not further affect GAD67 mRNA in the CeA of saline, drug and stress pre-exposed rats. As to the other areas, no differences were observed in drug pre-exposed compared with saline pre-exposed and fed ad libitum rats, except for amphetamine. Amphetamine pre-exposure decreased GAD67 mRNA levels in the dLStr and the AcC and AcS, and this effect was reversed by amphetamine challenge. The results show that different drugs and stress models of behavioural sensitization have in common an increase of GA67 in the CeA but not in the BLA, and suggest the changes of GAD67 in the CeA are a substrate of the sensitized response to drug challenge.

Hypoxia is an environmental stressor that is known to elicit alterations in both the autonomic nervous system and endocrine functions. The free radical or oxidative stress theory holds that oxidative reactions are mainly underlying neurodegenerative disorders. In fact among complex metabolic reactions occurring during hypoxia, many could be related to the formation of oxygen derived free radicals, causing a wide spectrum of cell damage. In present study, we investigated possible involvement of GABAergic mechanism in the protective effect of zolpidem against acute hypoxia-induced behavioral modification and biochemical alterations in mice. Mice were subjected to acute hypoxic stress for a period of 2 h. Acute hypoxic stress for 2 h caused significant impairment in locomotor activity, anxiety-like behavior, and antinocioceptive effect in mice. Biochemical analysis revealed a significant increased malondialdehyde, nitrite concentrations and depleted reduced glutathione and catalase levels. Pretreatment with zolpidem (5 and 10 mg/kg, i.p.) significantly improved locomotor activity, anti-anxiety effect, reduced tail flick latency and attenuated oxidative damage (reduced malondialdehyde, nitrite concentration, and restoration of reduced glutathione and catalase levels) as compared to stressed control (hypoxia) (P < 0.05). Besides, protective effect of zolpidem (5 mg/kg) was blocked significantly by picrotoxin (1.0 mg/kg) or flumazenil (2 mg/kg) and potentiated by muscimol (0.05 mg/kg) in hypoxic animals (P < 0.05). These effects were significant as compared to zolpidem (5 mg/kg) per se (P < 0.05). Present study suggest that the possible involvement of GABAergic modulation in the protective effect of zolpidem against hypoxic stress.

Background: Lithium has been shown to relieve mania and induce antinociception. In the present study, swim stress at 8C induced antinociception in both phases of the formalin test. Intraperitoneal administration of lithium chloride (LiCl) (0.05, 0.25, and 0.5 mg/kg) also induced antinociception in both phases of the formalin test., Methods: Antinociception was assessed by the formalin test method. Swim stress was achieved in the 8C water in a container 5 cm in diameter and 20 cm tall filled with water do a depth of 11 cm., Results: The drug (0.5 and 5 mg/kg) potentiated swim stress-induced antinociception in the second phase of the test. Repeated exposure to water swimming stress with a period of 40 sec, once daily for three days, in combination with lithium chloride did not alter stress-induced antinociception in either phases of the formalin test, when swim stress-induced antinociception was tested on the fourth day. Subchronic treatment with morphine (25 mg/kg), once daily for three days, in the presence or absence of lithium chloride (5 mg/kg) did not alter swim stress-induced antinociception, either, when swim stress-induced antinociception was tested on the fourth day., Conclusion: It may be concluded that lithium chloride potentiates swim stress-induced antinociception, but the drug has no influence on the response of subchronic administration swim stress or morphine.

Goals: In this theoretical paper, we present the Edmonton Fatigue Framework (EFF), a new framework for the study of tiredness, fatigue, and exhaustion in advanced cancer., Materials and Methods: The Fatigue Adaptation Model (FAM), the starting point for the EFF, was drawn from a literature review pertaining to fatigue in depression, chronic fatigue syndrome, cancer, shift workers, and athletes published in the Cumulative Index to Nursing and Allied Health Literature (CINAHL), Medical Literature Analysis and Retrieval System Online (MEDLINE), PubMed, PsychINFO, SPORTdiscus, and CancerLit between 1995 and 2004, and from seven qualitative studies conducted by our group. The EFF, an elaboration of the FAM, was constructed after an expansion of our literature review to 2006 and team discussion. The EFF provides new insights into possible links between behavioral and physiological indices of tiredness, fatigue, and exhaustion as they occur in both ill and non-ill states. In this paper, however, we consider only possible links in advanced cancer., Conclusions: We propose that stressors associated with advanced cancer and its supportive treatment trigger declines in four systems -- cognitive function, sleep quality, nutrition, and muscle endurance -- and that these declines reduce one's ability to adapt. While these systems each likely has its own effect on adaptation, we propose that the most important and serious effects arise from interactions among declines in cognitive function, sleep quality, nutrition, and muscle endurance., Conclusions: Interventions for fatigue have been limited by a lack of understanding about its etiology. Hypotheses arising from the EFF; suggest a new direction for further study that focuses on interactions among cognitive function, sleep quality, nutrition, and muscle endurance.

With this work we examine common pathways and autoregulatory similarities between different physiological phenomena, particularly with regard to stress, relaxation and love responses, against the background of recent research findings. Various stress reducing practices that incorporate an initial and short-lived stress pathway activation, e.g., love, relaxation and placebo responses, exhibit anticipatory stress response (ASR) physiology. The initial activation of this stress component of the total response, i.e., love, relaxation, and mental or physical stress responses, is significant and, as we speculate, may represent a common protective mechanism, since activation (i.e., stress response) is started first and, if the situation appears to be 'safe', may be followed by relaxation, if appropriate. Also, the emergence of love became evolutionarily important in organisms exhibiting cognition, because it deployed the validation for emotionality-controlling logical behavior. Therefore, love and relaxation responses may be considered as intrinsic health promoting physiological capabilities.

Problem: Maternal stress perception is frequently alleged as a cause of infertility, miscarriages, late pregnancy complications or impaired fetal development. The purpose of the present review is to critically assess the biological and epidemiological evidence that considers the plausibility of a stress link to human reproductive failure., Methods: All epidemiological studies published between 1980 and 2007 that tested the link between stress exposure and impaired reproductive success in humans were identified. Study outcomes were evaluated on the basis of how associations were predicted, tested and integrated with theories of etiology arising from recent scientific developments in the basic sciences. Further, published evidence arising from basic science research has been assessed in order to provide a mechanistic concept and biological evidence for the link between stress perception and reproductive success., Results: Biological evidence points to an immune-endocrine disequilibrium in response to stress and describes a hierarchy of biological mediators involved in a stress trigger to reproductive failure. Epidemiological evidence presents positive correlations between various pregnancy failure outcomes with pre-conception negative life events and elevated daily urinary cortisol. Strikingly, a relatively new conceptual approach integrating the two strands of evidence suggests the programming of stress susceptibility in mother and fetus via a so-called pregnancy stress syndrome., Conclusions: An increasing specificity of knowledge is available about the types and impact of biological and social pathways involved in maternal stress responses. The present evidence is sufficient to warrant a reconsideration of conventional views on the etiology of reproductive failure. Physicians and patients will benefit from the adaptation of this integrated evidence to daily clinical practice.

This paper studies the contribution of anxiety in origin of functional behavioural disorders of children. The intense sensing of anxiety attributes to the shaping of one's personality. Adaptation and adjustment, accommodation and assimilation to stressful conditions producing anxiety are analyzed. There are diagnosed reactions of organism to the circumstances of the CAN syndrome and trauma. In these circumstances, a primary perception of reality is at stake that consequently leads to sociopathological features. This paper also provides the authors' opinions of psychoanalytical and behavioural schools on origin of personal decompensation and neurotic disorders. Causes of panic disorder and other diseases, in which a stress trauma plays a role, are considered. For these reasons the authors suggest classifying the CAN syndrome as a separate nosologic unit in the future ICD-11.

A prior experience of behavioral control over a stressor interferes with subsequent Pavlovian fear conditioning, and this effect is dependent on the activation of the ventral medial prefrontal cortex (mPFCv) at the time of the initial experience with control. It is unknown whether mPFCv activity is necessary during fear learning and/or testing for this interference to occur. One week following controllable stress, the infralimbic cortex (IL) was temporarily inactivated either before fear learning or later testing. Inactivation of the IL before the test for conditioned fear, but not before conditioning, blocked the fear reducing effects of prior controllable stress. This suggests that the experience with control interferes with the expression of fear behavior and not the learning of the association, and that the mPFCv is needed to regulate conditioned fear behavior.

This paper's primary objective is to analyse the physiological (cortisol) and behavioral responses of military working dogs (MWD). Dogs (N=27) were submitted twice to environmental challenges (challenge 1 and 2, 20 days in-between) composed of social (training), visual (mobile toy car) and auditory (air blast) stimuli. Cortisol levels decreased back to the baseline after the second challenge. The behavioral observations showed that these MWD were more active, and presented less stereotypic behaviors (pacing, manipulation of the environment) during both visual challenges, whereas half low posture was observed during the first but not during the second visual challenge. The present study shows that this group of MWD still has an adaptation capacity to an environmental challenge (return to baseline of the cortisol levels, a higher posture during the second than at the first challenge). These results are encouraging and indicate that the dogs might have a diminished welfare (i.e. stereotypic behaviors), but are not chronically stressed.

Gene-environment interactions involving the catechol-O-methyltransferase Val(158)Met polymorphism (COMT(Val158Met)) have been implicated in the causation of psychosis. Evidence from general population studies suggests that Met/Met subjects are sensitive to stress, a trait associated with psychosis. We hypothesized that the Met allele would moderate the effects of stress on negative affect (NA) in controls, and on NA and psychosis in patients with a psychotic disorder. Thirty-one patients with a psychotic disorder and comorbid cannabis misuse and 25 healthy cannabis users were studied with the experience sampling method (ESM), a structured diary technique assessing current context and emotional and psychotic experiences in daily life. A significant interaction between COMT(Val158Met) genotype and ESM stress in the model of NA was found for patients (interaction chi(2) = 7.4, P = 0.02), but not for controls (interaction chi(2) = 3.8, P = 0.15). In the model of ESM psychosis, a significant interaction between COMT(Val158Met) genotype and ESM stress was also apparent (interaction chi(2) = 11.6, P < 0.01), with Met/Met patients showing the largest increase in psychotic experiences as well as NA in reaction to ESM stress. The findings suggest that the COMT(Val158Met) polymorphism moderates affective and psychotic responses to stress in patients with psychosis, providing evidence for gene-environment interaction mechanisms in the formation of psychotic symptoms., ((c) 2007 Wiley-Liss, Inc.)

Corticosterone (CORT) is seasonally modulated in many passerines, with plasma CORT concentrations lowest during the prebasic molt, when all feathers are replaced. Recent evidence indicating that CORT implants slow the rate of feather regrowth in molting birds suggests that plasma CORT concentrations are downregulated during molt in order to avoid the inhibition of feather growth caused by the protein catabolic activity of CORT. To further test this hypothesis, we examined whether endogenous CORT release, stimulated by exposure to either psychological stress or physical stress (food restriction), could inhibit feather regrowth rates or decrease feather quality in birds undergoing an induced molt (feather replacement after plucking). European starlings (Sturnus vulgaris) were exposed to chronic psychological stress or food restriction for three weeks of the feather regrowth period. Throughout this time, the length of growing primary, secondary, and tail feathers was measured and blood samples were collected to measure baseline and stress-induced CORT concentrations. Upon completion of growth, feather quality was analyzed via measurements of mass, rachis length, feather area, and presence of fault bars. Both psychological and physical stress protocols elevated circulating plasma CORT but significantly less than implants from an earlier study did. Psychological stress had no effect on feather regrowth rates or feather quality. Food restriction had no effect on feather growth rate but caused asynchronous feather replacement. When combined with psychological stress, physical stress also resulted in smaller feather area. Results indicate that CORT implants may not accurately represent chronic stress physiology. Additionally, the purpose for downregulating CORT concentrations during molt appears to be more complicated than simply protecting feather production from CORT's catabolic effects.

Numerous studies have established that adolescence is marked by substantial changes in stress reactivity and hippocampal function. Glucocorticoid receptors (GRs) in the hippocampus are imperative in corticosterone-dependent gene transcription when glucocorticoid levels are relatively high, such as during periods of stress. As reported previously, in reaction to acute stress, prepubertal animals show a significantly more protracted corticosterone response compared to adults. Chronic stress, however, results in a higher peak response, but a faster return to baseline in prepubertal compared to adult animals. Thus, depending on the developmental stage and experience of the animal, the hippocampus is exposed to different concentrations and durations of corticosterone. The present set of experiments assessed the effects of acute or repeated stress on GR mRNA expression in the dorsal and ventral hippocampal formation either before or after pubertal maturation in male rats. We found that acute stress results in a significant decrease in GR mRNA in the CA1 pyramidal cell layer and dentate gyrus in the dorsal and ventral hippocampal formation of both prepubertal and adult males. In response to repeated stress, we found no differences in GR expression in either the dorsal or ventral hippocampus. Thus, despite the dramatic differences in corticosterone concentration following stress at these two developmental stages, the stress-induced changes in GR expression in the hippocampus before and after pubertal maturation were more similar than different. These data point to a dissociation between differential stress-induced corticosterone responses and regulation of hippocampal GR levels in prepubertal and adult animals., ((c) 2007 S. Karger AG, Basel)

Background: In the very first years of life, parenting is considered to be important for the regulation of the infant's emotional and physiological states. In the present study, three-month-old infants' cortisol responses (reactivity and recovery) to a mild everyday stressor, namely being taken out of the bath, were examined in relation to the quality of maternal behavior. It was hypothesized that a higher quality of maternal behavior towards the infant predicted lower cortisol reactivity as well as a better recovery from the reaction., Method: The participants were 64 infants (34 boys and 30 girls) and their mothers. Maternal behavior (sensitivity and cooperation) towards the infant during the bathing routine was rated from videotapes. Salivary cortisol was obtained from the infants three times: before the bathing routine (T1), and 25 minutes (T2) and 40 minutes (T3) after the infants were taken out of the bath., Results: The infants reacted with a significant increase in cortisol to the stressor (from 6.8 nmol/l to 9.9 nmol/l), and regression analysis showed that the higher the quality of maternal behavior the better the cortisol recovery from the stressor., Conclusion: Our findings indicate the potential importance of social processes for physiological recovery from everyday stressful situations in infants.

Objective: To investigate individual differences in the effects of stress on BMI., Research Methods and Procedures: Participants were 71 healthy women volunteers enrolled in a university-based nurse practitioner program. Predictors of change in BMI were hypothesized to be cortisol secretion, dietary restraint, binging, mastery, mood, and eating attitudes. Measures were made at the beginning of the academic semester and 12 weeks later during the participants' examination period., Results: The women were of normal weight (BMI 25.2 +/- 4.3) for their age [43; standard deviation (SD), 7]. By the examination period, 40 had gained weight (mean, 5.5 pounds; SD, 2.2), 19 lost weight (mean, 2.5 pounds; SD, 1.5), and 12 had stable weight. BMI, salivary cortisol secretion, binging behavior, depression, and anxiety increased significantly, whereas scores on dietary restraint, weight, shape, and eating concerns, and mastery decreased significantly. Regression analysis showed that change in daily cortisol secretion significantly predicted change in BMI and that mastery significantly moderated this relationship. However, a reduction in dietary restraint was a perfect mediator of this relationship. Change in cortisol secretion also significantly predicted change in dietary restraint, and this was moderated by dietary restraint at the beginning of the academic semester. Reduction in dietary restraint was also predicted by a reduction in mastery and weight concern., Discussion: We identified individual differences that confer vulnerability to weight gain during stressful life events (dietary restraint and mastery). Given that women are exposed to daily stressors and use cognitive strategies to restrain their dietary intake, increasing awareness of the role of stress on eating behavior and weight is an important goal.

Objective: To evaluate the stress presence and its influence in the quality of life of patients with chronic daily headache (CDH)., Method: A hundred patients with at least 18 years old, with primary headache with duration greater than 4 hours a day, and frequency of 15 or more days monthly for at least three months were studied. Lipp's Inventory of Stress Symptoms and the Medical Outcomes Study Short Form (SF-36) were used., Results: Stress was observed in 90% of the patients; nearly half of them was in the phase almost exhaustion. Patients with stress when compared with the ones with no stress presented significantly lower scores in all the domains of SF-36; except in physical functioning. The resistance phase presented scores significantly higher than almost exhaustion; except for bodily pain., Conclusion: The majority of the patients presented stress with significant reduction in their quality of life. Consequently, the stress could be related with both the development and the maintenance of CDH.

Stress is an association of physiological and psychological reactions of a person confronted to a change of situation he cannot face. The relationship between stress and any disease is explained by hormonal modifications and behavioural changes induced by the stress. The evidence of such an association between stress and periodontal disease will be evaluated. The purpose of the present review article is to differentiate between old feelings and knowledge, and present findings which show that a lot of prospective studies are still needed for a more defined role of stress and periodontal disease.

Objectives: Small size at birth is linked with metabolic and cardiovascular disease. There is increasing evidence that it is also linked with physiologic stress responses and abnormal behavior, in particular, symptoms of hyperactivity. Therefore, we investigated associations between size at birth and motor activity during psychosocial stress., Methods: In 123 children aged 7 to 9 years, we examined the relations of birth weight, head circumference, length, and ponderal index at birth with motor activity on exposure to both stress and nonstress situations. Videos were recorded while the children performed a story and a math task in front of an audience (stress) and watched a movie (nonstress); motor activity was defined as lifting or tilting of a foot., Results: Children who had had a smaller head circumference at birth demonstrated greater motor activity during the stress test. There were marked gender differences in the results. In boys, lower birth weight, head circumference, and ponderal index were associated with greater motor activity during the stress test but not associated with motor activity during the nonstress situation. The findings remained significant when potential confounding variables were controlled for. There were no associations in girls., Conclusions: The findings suggest long-term effects of an adverse fetal environment on the behavioral stress response in boys and parallel similar gender-specific effects on different stress response systems in humans and animals. The results could reflect permanent alterations of dopaminergic neurotransmission and have implications for the etiology of clinical hyperactivity.

There is still much debate as to the pathways through which some children develop asthma and others do not. One possible mechanism outlined here concerns the way in which stress may influence the neuroendocrine system and thence the immune system. Supporting evidence from animal experiments suggests that maternal prenatal stress may be of importance, resulting in programming of the infant's HPA axis. In addition, social stressors during the early part of a child's life may also affect the HPA axis and thence dysregulation of immune system functioning with implications for the development of asthma.

Preferential preattentive processing towards threat has been proposed to play a casual role in the development of anxiety, mainly because it reliably predicts emotional responding to stressful events. However, in the investigation of the predictive value of preferential preattentive processing towards threat, the emotional Stroop task has exclusively being used. This study was designed to prospectively investigate the predictive value of skin conductance reactivity in response to masked (i.e., preattentively perceived) threatening pictures on emotional responding following stressful life events. To collect skin conductance data, the picture perception task was administered to 136 police recruits due to enroll into active duty within 2-4 months. To assess psychological distress following emotionally stressful life events, the impact of event scale were administered approximately 24 months later. Controlling for trait anxiety, analyses indicated that enhanced skin conductance reactivity in response to masked threatening pictures (relative to neutrals) was a strong predictor of emotional responding to stressful life events. This finding support preferential preattentive processing towards threat as a relatively independent factor predictive of emotional responding.

Puberty is a plastic period of neurological development when critical maturation of stress pathways occurs. Abnormal maturation may be predictive of future stress sensitivity and affective disorder risk. To identify potential early markers of stress-related disease predisposition, we examined physiological and behavioral stress responses in male pubertal mice compared with adults, using a genetic model of elevated stress sensitivity, CRF receptor-2 (CRFR2)-deficient mice. Juvenile mice of both genotypes exhibited greater basal and stress-induced corticosterone levels than adult mice, indicating that overall hypothalamic-pituitary-adrenal axis sensitivity diminishes in adulthood. However, juvenile CRFR2-deficient mice displayed a delayed stress recovery typical of adults of this genotype, suggesting an early marker of stress sensitivity. The adult phenotype of reduced hippocampal glucocorticoid receptor expression in these sensitive mice was also detected during puberty. This reduction may account for an impaired hypothalamic-pituitary-adrenal axis negative feedback and as such be an early indicator of a stress-sensitive phenotype. Examination of behavioral responses to stress revealed that CRFR2-deficient mice show exaggerated postpubertal maturation. Although wild-type mice did not alter their burying response to stress-provoking marbles after puberty, CRFR2-deficient mice showed a dramatic increase in burying behavior. We conclude that identification of abnormal pubertal stress pathway maturation may be predictive of adult heightened stress sensitivity and future susceptibility to stress-related affective disorders.

People with medically unexplained symptoms (MUS) often have a comorbid history of stress and negative affect. Although the verbal-cognitive and (peripheral) physiological stress systems have shown a great degree of independence, at the same time it is claimed that chronic stress and negative affect can result in a disregulated physiological stress system, which may lead to MUS. Previous studies could not demonstrate a straightforward between subject relationship between MUS and stress physiology, supporting the view of independence. The aim of the current study was to further explore this relationship using an improved methodology based on ecologically valid 24-h real-life ambulatory recordings. Seventy-four participants (19 male; 55 female) with heterogeneous MUS were compared with 71 healthy controls (26 male; 45 females). Momentary experienced somatic complaints and mood, heart rate, cardiac autonomic activity, respiration and saliva cortisol were monitored using electronic diary and ambulatory registration devices. Participants with MUS reported much more momentary complaints and negative affect as compared to controls. Although MUS seemed to be associated with elevated heart rate and reduced low and very-low frequency heart period variability, these effects disappeared after controlling for differences in sports behaviour. No group differences were found for cardiac autonomic activity, respiration, end-tidal CO(2) and saliva cortisol. Our 24-h real-life ambulatory study did not support the existence of a connection between MUS and disregulated peripheral stress physiology. Future studies may instead focus on central measures to reveal potential abnormalities such as deviant central processing of visceral signals in MUS patients.

Objective: To evaluate the efficacy of a program of lifestyle change through psychological intervention, combined with pharmacological therapy, for coronary risk reduction in uncontrolled hypertensive patients with overweight and dyslipidemia over 11 months of follow-up., Methods: A randomized controlled trial with 74 patients assigned to three different treatment programs. One group (CT) only received conventional pharmacological treatment. Another group (OG) received pharmacological treatment and participated in a guidance program to control cardiovascular risk factors. A third group (LSPI) received pharmacological treatment and participated in a brief psychological intervention program for reduction of estresse levels and changing of eating behavior. The main measure was the Framingham risk index., Results: CT patients presented an average reduction of 18% (p = 0.001) in coronary risk; OG patients elevated the risk by 0.8% (NS) and the LSPI group showed an average reduction of 27% on the Framingham risk index (p = 0.001)., Conclusion: Pharmacological treatment combined with psychological intervention for reduction of estresse level and changing of eating behavior resulted in additional benefits in coronary risk reduction.

Objectives: Inflammation is assumed to play a major role in the progress of atherosclerotic disease. We hypothesized that an altered hypothalamic-pituitary adrenal (HPA) axis activity was linked to a disinhibited inflammatory activity in patients with coronary artery disease (CAD)., Methods: Thirty CAD patients were assessed 12-14 weeks after a first-time acute coronary syndrome. Serum samples were assayed for C-reactive protein (CRP) and interleukin-6. Free cortisol was measured in a 24-h urine sample and in repeated saliva samples 30 min after awakening and at bedtime. The levels of inflammatory markers and cortisol were also determined before and after standardized physical and psychological stress tests., Results: The CAD patients had a higher 24-h cortisol secretion and a flattened diurnal slope, resulting from significantly higher cortisol levels at bedtime, compared to clinically healthy controls. The levels of evening cortisol were strongly related to inflammatory markers in serum. When exposed to acute physical and psychological stressors, the CAD patients showed a significantly blunted cortisol response compared to controls. In addition, a stress-induced increase in CRP was only observed in the patient group., Conclusions: Patients with CAD exhibited a cortisol pattern that markedly differed from controls. The data indicate that a dysfunctional HPA axis response involves a failure to contain inflammatory activity in CAD patients, thus providing a possible link between stress and inflammation in disease.

An increasing number of studies consider the specific processes by which distressing sensations, thoughts, and emotional experiences exert their influence on the daily functioning of those who suffer with chronic pain. Clinical methods of mindfulness and the processes that underlie them appear to have clear implications in this area, but have not been systematically investigated to this point in time. The purpose of the present study was to examine mindfulness in relation to the pain, emotional, physical, and social functioning of individuals with chronic pain. The present study included 105 consecutive patients attending a clinical assessment for treatment of chronic pain. Each completed a standardized battery of questionnaires, including a measure of mindfulness, the Mindful Attention Awareness Scale [Brown KW, Ryan RM. The benefits of being present: mindfulness and its role in psychological well-being. J Pers Soc Psychol 2003;84:822-48]. Correlation analyses indicated that mindfulness was unrelated to age, gender, education, or chronicity of pain, but was significantly related to multiple measures of patient functioning. In multiple regression analyses, after controlling for patient background variables, pain intensity, and pain-related acceptance, mindfulness accounted for significant variance in measures of depression, pain-related anxiety; physical, psychosocial, and "other" disability. In each instance greater mindfulness was associated with better functioning. The combined increments of variance explained from acceptance of pain and mindfulness were at least moderate and, in some cases, appeared potentially meaningful. The behavioral processes of mindfulness and their accessibility to scientific study are considered.

Little is known about how patient functioning changes after completion of multidisciplinary pain programs, and what factors are associated with such changes when they occur; for example, whether improvement or deterioration in functioning corresponds to changes in patient beliefs and coping during this period. The objective of this study was to examine the extent to which changes in patient pain and functioning were associated with changes in beliefs and coping after multidisciplinary pain treatment. Patients with chronic pain (N=141) completed outcome (pain, functioning) and process (beliefs, catastrophizing, coping) measures at the end of multidisciplinary pain treatment and 12 months posttreatment. On average, patients reported similar levels of pain at both times, but showed a small worsening in disability and depression outcomes between posttreatment and follow-up, which were associated significantly with concurrent changes in the process measures. In particular, increased belief in oneself as disabled by pain, catastrophizing, and increased use of resting, guarding and asking for assistance in response to pain were linked with increased disability and depression. Decreased perceived control over pain was also consistently associated with worsening of these outcomes. The results highlight the potential importance of specific pain-related beliefs and coping responses in long-term patient pain and adjustment. Research is needed to determine whether booster interventions after the end of intensive multidisciplinary treatment that target these beliefs and coping responses improve long-term outcomes.

Purpose: Discomfort and reduced visual performance due to glaring light conditions are common complaints for most individuals. Past studies have shown that macular pigment (MP) reduces discomfort due to glare. In this study, we evaluated whether MP was related to visual performance under glare conditions., Methods: Thirty-six healthy subjects participated (age range, 18 to 41). Spatial profiles of MP optical density were measured using heterochromatic flicker photometry with a Newtonian-view macular densitometer. Photostress recovery and grating visibility under veiling conditions were assessed in a Maxwellian-view optical system. Both experiments used six monochromatic lights (from 440 to 620 nm) and a broadband xenon white. For the veiling glare experiment, subjects fixated a 1 degrees diameter disk containing a black and white 100% contrast grating stimulus. The intensity of an annulus (the glare source) with an 11 degrees inner and 12 degrees outer diameter was adjusted by the subject until the grating stimulus was no longer seen. For the photostress recovery experiment, the time required to detect a 1 degrees -diameter grating stimulus (detailed above) after a 5-s exposure to a 2.5 microW/cm2, 5 degrees -diameter disk was recorded. Both central and eccentric (10 degrees temporal retina) viewing conditions were assessed., Results: MP at 30' eccentricity ranged from 0.08 to 1.04 OD, and was found to dramatically reduce the deleterious effects of glare. Visual thresholds under glare conditions were strongly related to MP density (e.g., r = 0.76, p = 0.0001 when using white light). Photostress recovery time, after exposure to xenon-white light, was significantly shorter for subjects with higher MP levels (r = -0.79, p = 0.0001). Both photostress recovery and veiling glare functions were well-described by the photopic spectral sensitivity function (Vlambda)., Conclusions: MP is strongly related to improvements in glare disability and photostress recovery in a manner consistent with its spectral absorption and spatial profile.