The DOI matches its Crossref record; 37 of the 37 references it cites were found in a registry or an index; 9 of the 33 sources its claims cite were checked for support.
Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk
Open accessAbstract
We propose a model wherein chronic stress results in glucocorticoid receptor resistance (GCR) that, in turn, results in failure to down-regulate inflammatory response. Here we test the model in two viral-challenge studies. In study 1, we assessed stressful life events, GCR, and control variables including baseline antibody to the challenge virus, age, body mass index (BMI), season, race, sex, education, and virus type in 276 healthy adult volunteers. The volunteers were subsequently quarantined, exposed to one of two rhinoviruses, and followed for 5 d with nasal washes for viral isolation and assessment of signs/symptoms of a common cold. In study 2, we assessed the same control variables and GCR in 79 subjects who were subsequently exposed to a rhinovirus and monitored at baseline and for 5 d after viral challenge for the production of local (in nasal secretions) proinflammatory cytokines (IL-1β, TNF-α, and IL-6). Study 1: After covarying the control variables, those with recent exposure to a long-term threatening stressful experience demonstrated GCR; and those with GCR were at higher risk of subsequently developing a cold. Study 2: With the same controls used in study 1, greater GCR predicted the production of more local proinflammatory cytokines among infected subjects. These data provide support for a model suggesting that prolonged stressors result in GCR, which, in turn, interferes with appropriate regulation of inflammation. Because inflammation plays an important role in the onset and progression of a wide range of diseases, this model may have broad implications for understanding the role of stress in health.
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Claims the paper makes
18 Own result · 13 No full text of the sources · 9 Own interpretation · 8 Own method · 4 Partly supported · 2 Couldn’t confirm · 2 Sources not found · 2 No basis given · 1 Supported · accuracy not yet measured
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The simple notion that chronic stress acts through the direct effects of elevated circulating cortisol is becoming less likely (5,6).”
What the sources say
- Partly supportedcites [5] 5. Cole SW (2008) Social regulation of leukocyte homeostasis: The role of glucocorticoid sensitivity. Brain Behav Immun 22:1049-1055. sourceExperimental — accuracy not yet measured
The Introduction reports glucocorticoid resistance in chronically stressed people, and the Discussion reports reduced leukocyte sensitivity to cortisol among lonely older adults. These findings challenge an explanation based solely on cortisol’s direct effects, but the paper does not establish that elevated circulating cortisol is an increasingly unlikely explanation for chronic stress generally. (LLM, conf=0.82)
- Not checked — no full text of the sourcecites [6] 6. Meagher MW, Johnson RR, Good E, Welsh TH (2006) Psychoneuroimmunology, eds Ader R, Felton D, Cohen N (Academic, New York), 4th Ed, Vol II, pp 1107-1124. source
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
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- Based: passes — The paper gives a reason why it holds.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“and that the indirect assessment used here correlates with blunting of lymphocyte redistribution in response to dexamethasone injection (24).”
§ Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk > Discussion
What the sources say
- Supportedcites [24] 24. Cole SW, Mendoza SP, Capitanio JP (2009) Social stress desensitizes lymphocytes to regulation by endogenous glucocorticoids: Insights from in vivo cell trafficking dy- namics in rhesus macaques. Psychosom Med 71:591-597. source
The Results section (“Relationship to HPA axis glucocorticoid response”) reports a significant sample-wide correlation between lymphocyte sensitivity to endogenous cortisol variation—the indirect hematological assessment—and lymphocyte redistribution after dexamethasone (p = .006). The Discussion explicitly describes desensitization of that probe as correlated with blunted lymphocyte redistribution in response to dexamethasone. (LLM, conf=0.94)
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The logic of the measure is that there is a strong physiologic correlation between cortisol levels and the number of circulating leukocytes only if leukocyte glucocorticoid receptors are sensitive (i.e., signaling cells to redistribute).”
§ Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk > Results
What the sources say
- Partly supportedcites [5] 5. Cole SW (2008) Social regulation of leukocyte homeostasis: The role of glucocorticoid sensitivity. Brain Behav Immun 22:1049-1055. sourceExperimental — accuracy not yet measured
The Introduction (page not provided) says cortisol correlates with neutrophil-to-lymphocyte and neutrophil-to-monocyte ratios when leukocyte glucocorticoid receptors are sensitive, and that desensitization attenuates those correlations. But the claim broadens this to the number of circulating leukocytes: Table 2 (Results; page not provided) finds no significant association with total white-blood-cell count. The Discussion also says the observed correlations with hematologic measures rarely exceeded r = .20, so calling them strong overstates the findings. (LLM, conf=0.88)
- Partly supportedcites [24] 24. Cole SW, Mendoza SP, Capitanio JP (2009) Social stress desensitizes lymphocytes to regulation by endogenous glucocorticoids: Insights from in vivo cell trafficking dy- namics in rhesus macaques. Psychosom Med 71:591-597. sourceExperimental — accuracy not yet measured
The Introduction says glucocorticoid-receptor signaling mediates leukocyte redistribution and that the strength of its association with cortisol is a measure of sensitivity. But the Results report only a weak correlation for lymphocyte counts (rS = −.20), with no significant association for monocytes or neutrophils. Thus the claim overstates the strength and breadth of the correlation. Page numbers were not available in our copy. (LLM, conf=0.86)
boostedcorrelationaln = 83- Asserted: passes — The authors put it forward as true.
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- Partly supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“However, cortisol levels based on 24-h urine (15) and waking diurnal assessments in saliva (19,20) do not play a part in this process.”
What the sources say
- Not checked — no full text of the sourcecites [15] 15. Cohen S, et al. (1998) Types of stressors that increase susceptibility to the common cold in healthy adults. Health Psychol 17:214-223. source
- Could not verifycites [19] 19. Cohen S, et al. (2008) Objective and subjective socioeconomic status and susceptibility to the common cold. Health Psychol 27:268-274. sourceExperimental — accuracy not yet measured
The Potential Mediating Variables section lists the measures assessed as pathways to colds but does not include cortisol. The Discussion addresses sleep and psychological variables, not whether cortisol measured in 24-hour urine or waking saliva plays a role. Searches for those cortisol measures and for cortisol as a mediator found no passage establishing the claim. (LLM, conf=0.77)
- Not checked — no full text of the sourcecites [20] 20. Edwards S, Hucklebridge F, Clow A, Evans P (2003) Components of the diurnal cortisol cycle in relation to upper respiratory symptoms and perceived stress. Psychosom Med 65:320-327. source
plain- Asserted: passes — The authors put it forward as true.
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The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Chronic stress does not appear to affect expression of GRα, the active isoform of the receptor (11).”
§ Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk > Discussion
What the sources say
- Partly supportedcites [11] 11. Miller GE, et al. (2008) A functional genomic fingerprint of chronic stress in humans: Blunted glucocorticoid and increased NF-kappaB signaling. Biol Psychiatry 64:266-272. sourceExperimental — accuracy not yet measured
The Results (page not provided) report similar GR mRNA levels in monocytes from chronically stressed caregivers and controls, and the Discussion (page not provided) draws the same conclusion. The paper does not identify the measured mRNA as GRα or establish that expression of that specific isoform was unaffected. (LLM, conf=0.86)
hedged- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In contrast, consistent with the hypothesis that stress results in GCR, there were no associations between cortisol and leukocytes among those who did experience a stressor (n = 193).”
§ Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk > Results
plainn = 193- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Similarly we find the expected associations between cortisol and leukocyte counts for persons who did not develop a cold following viral challenge (n = 167).”
§ Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk > GCR and colds.
plaincorrelationaln = 167- Asserted: passes — The authors put it forward as true.
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- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“As expected, plasma cortisol levels did not predict who developed a cold (OR = 1.27,CI = 0.20, 7.94).”
§ Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk > GCR and colds.
plain- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Greater IL-1β GCR was also associated with greater local IL-6 production.”
§ Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk > Consideration of alternative explanations.
plaincorrelational- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In contrast, and consistent with GCR putting people at greater risk for illness, there were no associations between cortisol and leukocyte counts among those who did develop a cold (n = 109).”
§ Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk > GCR and colds.
plainn = 109- Asserted: passes — The authors put it forward as true.
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- It may state two separate claims as one. 20
- Probably not a substantial claim. 9
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Evidence for GCR in response to chronic stress has been found in parents of children with cancer (10), spouses of brain-cancer patients (11) and in persons reporting high levels of loneliness (5).”
What the sources say
- Not checked — no full text of the sourcecites [10] 10. Miller GE, Cohen S, Ritchey AK (2002) Chronic psychological stress and the regulation of pro-inflammatory cytokines: A glucocorticoid-resistance model. Health Psychol 21: 531-541. source
- Partly supportedcites [11] 11. Miller GE, et al. (2008) A functional genomic fingerprint of chronic stress in humans: Blunted glucocorticoid and increased NF-kappaB signaling. Biol Psychiatry 64:266-272. sourceExperimental — accuracy not yet measured
The Methods and Results (page numbers unavailable) identify the participants as familial caregivers of brain-cancer patients and report diminished glucocorticoid-related transcription in caregivers versus controls. The copy does not establish that the caregivers were spouses, so it supports the finding but not that specific relationship. (LLM, conf=0.86)
- Supportedcites [5] 5. Cole SW (2008) Social regulation of leukocyte homeostasis: The role of glucocorticoid sensitivity. Brain Behav Immun 22:1049-1055. source
Citation (5) is attached to the claim about people reporting high levels of loneliness, not the two cancer-related groups. The Results report reduced leukocyte sensitivity to cortisol in lonely individuals, and the Discussion reports reduced sensitivity in those experiencing frequent loneliness. (LLM, conf=0.92)
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“We found no effects of cortisol levels on disease risk (e.g., refs.19, 20), GCR, or inflammation.”
§ Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk > Discussion
What the sources say
- Could not verifycites [19] 19. Cohen S, et al. (2008) Objective and subjective socioeconomic status and susceptibility to the common cold. Health Psychol 27:268-274. sourceExperimental — accuracy not yet measured
The citation is attached to the disease-risk portion of the sentence, not the claims about GCR or inflammation. The Data Analysis section reports predictors of clinical colds but does not report an analysis of cortisol levels and disease risk. A mention of cortisol in the introductory material describes another study, not a result of this paper. (LLM, conf=0.73)
- Not checked — no full text of the sourcecites [20] 20. Edwards S, Hucklebridge F, Clow A, Evans P (2003) Components of the diurnal cortisol cycle in relation to upper respiratory symptoms and perceived stress. Psychosom Med 65:320-327. source
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
- Could not verify
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“That the slopes of the stressed and nonstressed subjects were different from each other is supported by stress-by-cortisol level interactions found in linear regressions predicting lymphocytes (P = 0.03), neutrophils (P = 0.03) and the N/L ratio (P = 0.03).”
§ Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk > Results
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Cortisol levels as assessed by multiple samples of saliva collected across the day before viral challenge were unrelated to any of the three GCR measures (all P > 0.20) or to proinflammatory cytokine levels (all P > 0.40).”
§ Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk > Consideration of alternative explanations.
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The correlation of IL-1β GCR with local IL-1β release was in the expected direction, but was not significant.”
§ Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk > Consideration of alternative explanations.
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Here linear regressions indicate stress-by-cortisol interactions for lymphocytes (P = 0.02), neutrophils (marginal at P = 0.08), and N/L ratio (P = 0.02).”
§ Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk > GCR and colds.
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“For all three analyses, simple slopes among those who did not develop a cold were significantly different from 0, whereas slopes for those who did develop a cold were not (Table 2).”
§ Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk > GCR and colds.
plainn = 167 ·- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“For all three analyses, simple slopes for those without stress were significantly different from 0, whereas slopes for those with stress were not (Table 1).”
§ Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk > Results
plain- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“We also found consistent evidence across studies 1 and 2, even though study 2 used a standard direct assessment of GCR.”
§ Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk > Discussion
plain- Asserted: passes — The authors put it forward as true.
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What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The use of multiple control variables also eliminates many potential spurious explanations.”
§ Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk > Discussion
plaindirect- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Because the analyses in both studies were prospective, we can eliminate reverse causation (colds did not cause stress, colds did not cause GCR, and cytokine release did not cause GCR) as an alternative explanation.”
§ Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk > Discussion
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Without sufficient glucocorticoid regulation, the duration and/or intensity of the inflammatory response increases, heightening risk for acute exacerbations such as occur in asthma and autoimmune diseases, as well as for the onset and progression of chronic inflammatory diseases such as CVD, and type II diabetes (12).”
What the sources say
- Not checked — no full text of the sourcecites [12] 12. Nathan C (2002) Points of control in inflammation. Nature 420:846-852. source
plaindirect- Asserted: passes — The authors put it forward as true.
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What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Health is not an issue here, because subjects are carefully screened for excellent health.”
§ Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk > Discussion
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Because inflammation plays a role in progression of multiple diseases, this model not only provides an explanation for the increased risk for URI under stress, but might provide a more general explanation for why prolonged stress would play a role in other inflammatory diseases as well.”
§ Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk > Discussion
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Rests on an assumption: Inflammation plays an important role in the onset and progression of a wide range of diseases.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Greater levels of glucocorticoid are associated with higher numbers of circulating neutrophils, lower numbers of circulating lymphocytes, and a lower neutrophil-to-lymphocyte (N/L) ratio-an overall marker of the trafficking of these cells (e.g., refs.22,23).”
§ Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk > Results
What the sources say
- Not checked — no full text of the sourcecites [22] 22. Fauci AS, Dale DC, Balow JE (1976) Glucocorticosteroid therapy: Mechanisms of action and clinical considerations. Ann Intern Med 84:304-315. source
- Not checked — no full text of the sourcecites [23] 23. Dhabhar FS, Miller AH, McEwen BS, Spencer RL (1996) Stress-induced changes in blood leukocyte distribution. Role of adrenal steroid hormones. J Immunol 157:1638-1644. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The viral-challenge paradigm provides an ideal context to study the general model of stress leading to disease via effects on the HPA and inflammatory regulation.”
plaindirect- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. It may be too vague to check against evidence. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These data are consistent with a model wherein stress leads to GCR, which in turn results in greater risk for developing a cold.”
§ Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk > Discussion
hedgeddirect- Asserted: passes — The authors put it forward as true.
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- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Together, results from these prospective analyses support the hypothesis that GCR predicts an increased risk for colds following viral exposure, whereas levels of circulating cortisol do not.”
- Also stated in: § Discussion · plain
“In turn, GCR was prospectively associated with increased risk of developing a common cold following experimental inoculation with a cold virus.”
§ Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk > GCR and colds.
plaincorrelationaln = 109- Asserted: passes — The authors put it forward as true.
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- Also stated in: § Discussion · plain
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Ratings of events were performed in an independent laboratory by consensus groups consisting of at least four trained interviewers.”
- Also stated in: § Methods · plain
“The interview staff was blind to other study measures.”
- Also stated in: § Methods · plain
“Raters were also blind to individuals' subjective responses to the stressful events”
§ Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk > Methods
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Also stated in: § Methods · plain
In the paper
“This could prove important because GRβ is a dominant negative receptor for cortisol, which can suppress GRα activity and thereby contribute to GCR (28).”
§ Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk > Discussion
What the sources say
- Not checked — no full text of the sourcecites [28] 28. Derijk RH, et al. (2001) A human glucocorticoid receptor gene variant that increases the stability of the glucocorticoid receptor beta-isoform mRNA is associated with rheumatoid arthritis. J Rheumatol 28:2383-2388.
hedgedconditional- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
In the paper
“Life events were assessed by a standardized semistructured interview, the Bedford College Life Events and Difficulties Schedule (LEDS) (29), and conducted by trained interviewers.”
§ Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk > Methods
What the sources say
- Not matchedcites [29] 29. Brown GW, Harris TO (1989) Life Events and Illness (Guilford, New York).
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim.
- Not matched
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“All investigators were blinded to subjects' status on all baseline assessments.”
§ Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk > Methods
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Three subjects were excluded due to incomplete nasal cytokine data.”
§ Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk > Methods
plainn = 3- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The investigators were blinded to all baseline measures.”
§ Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk > Methods
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Correlations between cell counts from the two blood draws ranged from 0.61 to 0.76, P < 0.001.”
- Also stated in: § Methods · plain
“The correlation between cortisol in the two samples was 0.70, P < 0.001.”
§ Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk > Methods
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Also stated in: § Methods · plain
In the paper
“We used a standard in vitro assay to measure GCR that assessed the ability of dexamethasone (0, 10, 50, and 250 nM) to suppress lipopolysaccharide (30 ng/mL) stimulated lymphocyte production of IL-1β, IL-6, and TNFα.”
§ Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk > Methods
What the sources say
- Not checked — no full text of the sourcecites [6] 6. Meagher MW, Johnson RR, Good E, Welsh TH (2006) Psychoneuroimmunology, eds Ader R, Felton D, Cohen N (Academic, New York), 4th Ed, Vol II, pp 1107-1124. source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
In the paper
“Parodoxically, proinflammatory cytokines are thought to both up-regulate immunity to the virus and produce cold symptoms (13).”
§ Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk > Discussion
What the sources say
- Not checked — no full text of the sourcecites [13] 13. Hendley JO (1998) The host response, not the virus, causes the symptoms of the common cold. Clin Infect Dis 26:847-848. source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The paper relies on this without support.
Inflammation plays an important role in the onset and progression of a wide range of diseases.
“Because inflammation plays an important role in the onset and progression of a wide range of diseases, this model may have broad implications for understanding the role of stress in health.”
The paper relies on this without support.
Few human studies include assessments of stressful events, HPA response, and a disease outcome in the same subjects.
“few human studies include assessments of stressful events, HPA response, and a disease outcome in the same subjects.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“However, exposure to chronic stress promotes sustained, non-resolving inflammation within the CNS through the gradual development of glucocorticoid resistance, which further drives inflammation.”
From The Role of Cortisol in Chronic Stress, Neurodegenerative Diseases, and Psychological Disorders (2023) · cites this paper as [22]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Once GC resistance develops, the “fight or flight” response to social threats is altered and results in exaggerated inflammation, consequently perpetuating the proinflammatory state [22].”
From The Role of Cortisol in Chronic Stress, Neurodegenerative Diseases, and Psychological Disorders (2023) · cites this paper as [22]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“ELS/CT together with higher cortisol during this SHRP could possibly lead to GR insensitivity through greater exposure to GC over time, thus altering the physiological of HPA axis development (101, 112).”
From Developmental Trajectories of Early Life Stress and Trauma: A Narrative Review on Neurobiological Aspects Beyond Stress System Dysregulation (2019) · cites this paper as [112]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Thus, the presence of these FKPB5 alleles can result in low levels of circulating cortisol and/or GR resistance in PTSD can lead to a pro-inflammatory state via decreases in antiinflammatory GR signaling (Cohen et al, 2012).”
From Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond (2017) · cites this paper as Cohen et al, 2012
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“In the case of GC resistance due to chronic stress, immune cells demonstrate decreased sensitivity to glucocorticoids. Therefore, in this case, cortisol release does not result in significant anti-inflammatory effects, as one would otherwise expect.”
From The Role of Cortisol in Chronic Stress, Neurodegenerative Diseases, and Psychological Disorders (2023) · cites this paper as [22]
The cited source says what the claim attributes to it.
In the citing paper
“experiencing even one recent major life event (as rated by the LEDS) predicts greater glucocorticoid resistance”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Cohen et al., 2012
In the citing paper
“Similarly, prolonged or chronic stress in humans can lead to GR insensitivity, meaning that GRs in immune cells are not able to “hear” the inhibitory signals of glucocorticoids (Cohen et al., 2012; Miller et al., 2002).”
From Developmental psychoneuroendocrine and psychoneuroimmune pathways from childhood adversity to disease (2017) · cites this paper as Cohen et al., 2012
In the citing paper
“For instance, continued exposure to high cortisol may eventually lead to glucocorticoid insensitivity (Cohen et al., 2012; Miller et al., 2002)”
From Developmental psychoneuroendocrine and psychoneuroimmune pathways from childhood adversity to disease (2017) · cites this paper as Cohen et al., 2012
In the citing paper
“psychological stressors that are persistently present in some contemporary work environments, such as those characterized by high job demand and low control, can cause physiologic changes155 that disrupt the ability for glucocorticoids to effectively down-regulate inflammatory activity due to decreased sensitivity caused by chronic elevation in cortisol, leading in turn to SCI and poor health156”
From Chronic inflammation in the etiology of disease across the life span (2019) · cites this paper as [156]
In the citing paper
“Previous literature has shown that chronic stress (associated with depression) is also linked to glucocorticoid receptor resistance, as well as problems with the regulation of the inflammatory response [484].”
From Biological, Psychological, and Social Determinants of Depression: A Review of Recent Literature (2021) · cites this paper as [484]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk > Methods
“The second set included standard covariates, dichotomous variables for life stress, and cold status (1 = cold, 0 = no cold) and the interaction of life stress and cold status.We again predicted an interaction with cortisol associated with leukocyte counts among those without colds but not among those with colds.”
§ Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk > GCR and colds.
“Here linear regressions indicate stress-by-cortisol interactions for lymphocytes (P = 0.02), neutrophils (marginal at P = 0.08), and N/L ratio (P = 0.02).”
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“Over time, however, this response can cause increased epinephrine and norepinephrine sensitivity, and reduced glucocorticoid sensitivity (Cohen et al., 2012; Silverman & Sternberg, 2012), which promotes chronic, low-grade inflammation that leads to oxidative stress and increased risk for…”
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Metadata
- Authors
- Cohen, S., Janicki-Deverts, D., Doyle, W. J., Miller, G. E., Frank, E., Rabin, B. S., & Turner, R. B.
- Affiliations
- Carnegie Mellon University (US)
- Department of Psychology, Carnegie Mellon University, Pittsburgh, PA 15213;
- Children's Hospital of Pittsburgh (US)
- University of British Columbia (CA)
- University of Pittsburgh (US)
- University of Virginia (US)
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2012-04-02
- Volume
- 109
- Issue
- 16
- Pages
- 5995-5999
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC3341031
- OpenAlex
- W2125978064
- Cited by
- 1,419
- References
- 36
- Citations by year
- 2026: 114 · 2025: 112 · 2024: 101 · 2023: 156 · 2022: 114 · 2021: 136 · 2020: 123 · 2019: 103 · 2018: 97 · 2017: 107 · 2016: 67 · 2015: 73 · 2014: 70 · 2013: 31 · 2012: 14
- FWCI
- 25.06
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- KiltHub Repository (submittedVersion)
- Figshare (submittedVersion, cc-by)
- KiltHub Repository
- Funders
- John D. and Catherine T. MacArthur Foundation
- National Institutes of Health (5r01mh047234-03, 5r01mh050430-04)
- National Heart, Lung, and Blood Institute (HL65111, HL65112, P50HL065112, P50HL065111)
- National Institute of Mental Health (MH-47234, MH 50430)
- National Center for Complementary and Alternative Medicine (AT006694)
- National Center for Complementary and Integrative Health (R01AT006694, AT006694)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Stress, Anesthesia, and Immune Response
- Keywords
- chronic stress, inflammation, rhinovirus infection, common cold, inflammatory cytokines, IL-1β, TNF-α, interleukin-6, life events, disease risk, stress and health
- MeSH terms
- Adult, Chronic Disease, Common Cold, Disease Susceptibility, Female, Humans, Hydrocortisone, Inflammation, Leukocyte Count, Male, Middle Aged, Models, Psychological, Quarantine, Receptors, Glucocorticoid, Rhinovirus, Risk Factors, Stress, Psychological, Cytokines, Nasal Lavage Fluid, Young Adult
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-09, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-09 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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