Chronic Life Stress Alters Sympathetic, Neuroendocrine, and Immune Responsivity to an Acute Psychological Stressor in Humans

Pike, Jennifer; Smith, Tom L.; Hauger, Richard L.; Nicassio, Perry M.; Patterson, Thomas L.; McClintick, J; Costlow, Carolyn; Irwin, Michael R.

doi:10.1097/00006842-199707000-00015

Cited by 216 publications

(128 citation statements)

References 33 publications

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“…Moreover, both the duration and the frequency of experienced stress are important determinants of its impact on health and illness. Variable response to acute challenges (e.g., high frequency of exposure to violence) superimposed on chronic stressors (e.g., other components of neighborhood disadvantage) may have different implications on disease expression (22). Events that last a very short time can also have more long-term stress effects through lasting physiologic responses thought to be maintained by recurrent unwanted or "intrusive" thoughts about past events (23).…”

Section: Discussionmentioning

confidence: 99%

“…Controlled animal studies consistently demonstrate higher lead levels in iron-deficient animals than in iron-replete controls (18)(19)(20)(21)(22)(23). The mechanism for enhanced absorption is likely to be substitution of Fe +2 with Pb +2 and increased active transport into the body (19,22,24,25). Similarly, it is possible that Pb +2 may occupy vacant Fe +2 sites in the hematopoeitic system, thereby reducing lead excretion.…”

mentioning

confidence: 99%

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Iron Deficiency Associated with Higher Blood Lead in Children Living in Contaminated Environments

Bradman¹,

Eskenazi²,

Sutton³

et al. 2001

Environmental Health Perspectives

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Iron Deficiency Associated with Higher Blood Lead in Children Living in Contaminated Environments

Bradman¹,

Eskenazi²,

Sutton³

et al. 2001

Environmental Health Perspectives

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“…29 However, the shift in cytokine profile (increase in IL1 and TNF␣, reduction in IL2), as with long-term challenges, suggests a prolonged activity of the stressor on humoral homeostasis. 22,30 Our data, however, did not address any of the possible molecular mechanisms that might be involved in this rearrangement, although it is well recognized that elevated glucocorticoid levels might interfere, eg, with transcription proteins, such as nuclear transcription factor B (NF-B). 31…”

Section: Real Life Stressmentioning

confidence: 93%

Hemodynamic and Autonomic Adjustments to Real Life Stress Conditions in Humans

et al. 2002

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Abstract-Psychological stress represents a risk factor for hypertension, but mechanisms are not known in detail. In this investigation we tested the hypothesis that real-life stress conditions produce changes in autonomic cardiac and vascular regulation that might differ in magnitude. University students, a well-established model of mild real-life stress, were examined shortly before a university examination, and a second time 3 months afterward, during holiday. Autonomic cardiovascular regulation was assessed by a noninvasive approach, based on autoregressive analysis of RR interval variability (V) and of systolic arterial pressure (SAP) V. The overall level of stress in the two sessions was gauged from the elevated salivary cortisol (5.6Ϯ0.5 versus 2.4Ϯ0.2 ng/mL, PϽ0.05) and altered cytokine profile (PϽ0.05). During the stress day, the RR interval was reduced and arterial pressure increased significantly; simultaneously, the normalized low frequency component of RRV (a marker of sympathetic modulation of the sinoatrial node) was increased and the index ␣ (a measure of baroreflex gain) reduced. Concomitantly, the autonomic response to the sympathetic excitation produced by standing was altered: cardiac response was impaired and vascular responsiveness increased. Markers of autonomic regulation of the sinoatrial node correlated significantly with cortisol levels, both at rest and also considering standing induced changes, suggesting a gradual range of effects. The data support the concept that mild real-life stress increases arterial pressure and impairs cardiovascular homeostasis. These changes, assessable with spectral analysis of cardiovascular variability, might contribute, in susceptible individuals, to the link between psychological stress and increased cardiovascular risk of hypertension. Key Words: autonomic nervous system Ⅲ baroreceptors Ⅲ stress hormones Ⅲ risk factors T he importance and nature of the complex, multifarious mechanisms linking psychological stress to arterial hypertension 1,2 have been extensively explored in simulated conditions. In laboratory models, mental stress leads to a rise in arterial pressure and heart rate, by way of altered neural cardiovascular regulation, typically consisting of increased sympathetic activity 3-5 and reduced baroreflex gain, 6,7 coupled to a prolonged endothelial dysfunction. 8,9 Sympathetic activation is noninvasively recognized by spectral analysis of RR variability, 10,11 indicating a predominant low frequency (LF) component of RR variability, in conditions of acute laboratory stress. 7 Data from laboratory experiments, however, are limited by their intrinsic artificiality and by the fact that some of the more efficacious models, such as public speaking and mental arithmetic, might involve changes in respiration that could obscure the interpretation of results, particularly when autonomic regulation is inferred solely by spectral analysis of RR variability. 12 Conversely, the effects of real-life psychological stressors on cardiovascular regulations, al...

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“…3,4 A considerable body of research has linked depression and chronic stress to elevated stress hormones, mainly cortisol and catecholamines, 3,[15][16][17] though not in all cases. [18][19][20] While around 40% of depression is characterized by high cortisol levels, both depression and chronic stress have also been linked to hypocortisolemia or low Corticotropin-Releasing Hormone (CRH). 21,22 In particular, atypical depression, states of chronic fatigue, and post-traumatic stress syndrome are linked to profiles of low cortisol and/or enhanced HPA axis negative feedback.…”

Section: B2 the Anabolic/catabolic Hormonal Balancementioning

confidence: 99%

Psychological and metabolic stress: A recipe for accelerated cellular aging?

Epel

2009

373

329

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Chronic stress can affect human health through a myriad of behavioral and biochemical pathways. Τhis review focuses on some key hormonal and metabolic pathways that appear important today. In modern society, we are faced with excessive psychological stress, as well as an epidemic of overeating, and the two together appear to have synergistic effects. Chronic stress can lead to overeating, co-elevation of cortisol and insulin, and suppression of certain anabolic hormones. This state of metabolic stress in turn promotes abdominal adiposity. Both the direct stress response and the accumulation of visceral fat can promote a milieu of systemic inflammation and oxidative stress. This biochemical environment appears to be conducive to several cell aging mechanisms, mainly dampening telomerase and leading to telomere length (TL) shortening and cell senescence. Immune cell telomere shortness is linked with many chronic disease states and earlier mortality. In this way, chronic stress may influence a variety of diseases through a biochemical cascade leading to immune cell senescence. Certain psychological temperaments at high risk of this stress cascade (mainly anxiety prone), gene-environment interactions, and potential interventions for interrupting the stress-aging cascade are discussed.

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Chronic Life Stress Alters Sympathetic, Neuroendocrine, and Immune Responsivity to an Acute Psychological Stressor in Humans

Cited by 216 publications

References 33 publications

Iron Deficiency Associated with Higher Blood Lead in Children Living in Contaminated Environments

Iron Deficiency Associated with Higher Blood Lead in Children Living in Contaminated Environments

Hemodynamic and Autonomic Adjustments to Real Life Stress Conditions in Humans

Psychological and metabolic stress: A recipe for accelerated cellular aging?

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