The DOI matches its Crossref record; 41 of the 42 references it cites were found in a registry or an index; 17 of the 33 sources its claims cite were checked for support.
Clustering of Depression and Inflammation in Adolescents Previously Exposed to Childhood Adversity
Open accessAbstract
Background There is mounting interest in the hypothesis that inflammation contributes to the pathogenesis of depression, and underlies depressed patients’ vulnerability to comorbid medical conditions. However, research on depression and inflammation has yielded conflicting findings, fostering speculation that these conditions associate only in certain subgroups, like patients exposed to childhood adversity. Methods We studied 147 adolescent females. All were in good health at baseline, but at high risk for depression by virtue of family history and/or cognitive vulnerability. Subjects were assessed every six months for 2.5 years, undergoing diagnostic interviews and venipuncture for measurement of two inflammatory biomarkers, C-reactive protein (CRP) and interleukin-6 (IL-6). Childhood adversity was indexed by parental separation, low socioeconomic status, and familial psychopathology. Results Multilevel models indicated that childhood adversity promotes clustering of depression and inflammation. Among subjects exposed to high childhood adversity, the transition to depression was accompanied by increases in both CRP and IL-6. The higher CRP remained evident six months later, even after depressive symptoms had abated. These lingering effects were bi-directional, such that among subjects with childhood adversity, high IL-6 forecasted depression six months later, even after concurrent inflammation was considered. This coupling of depression and inflammation was not apparent in subjects without childhood adversity. Conclusions These findings suggest that childhood adversity promotes the formation of a neuroimmune pipeline, wherein inflammatory signaling between the brain and periphery is amplified. Once established, this pipeline leads to a coupling of depression and inflammation, which may contribute to later affective difficulties and biomedical complications.
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Claims the paper makes
17 of 33 cited sources checked · 10 supported · 0 flagged · accuracy not yet measured
Every source the paper cites for this claim was checked and supports it.
In the paper
“However, depressed subjects who were negative for maltreatment were statistically indistinguishable from controls.”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > Abstract > Conclusions
What the sources say
- Supportedcites [14] Danese, 2008, Elevated inflammation levels in depressed adults with a history of childhood maltreatment, Arch Gen Psychiatry source
The Results section (‘Which depressed individuals show increased inflammation?’) says that depressed-only individuals had a non-significant elevation in inflammatory markers relative to controls. The Conclusions likewise report a non-significant increase in their risk for high hsCRP. This supports the claim of no statistically significant difference, though it does not establish that the groups were equivalent. (LLM, conf=0.91)
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Rests on an assumption: The childhood adversity index formed from parental age, familial disruption, parental affective illness, low household education, and limited economic resources validly captures the childhood adversity relevant to depression-inflammation clustering.
- Rests on an assumption: CRP and IL-6 measurements validly index the inflammatory processes relevant to depression.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Greater inflammation was also seen among subjects exposed to maltreatment alone.”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > Abstract > Conclusions
What the sources say
- Supportedcites [14] Danese, 2008, Elevated inflammation levels in depressed adults with a history of childhood maltreatment, Arch Gen Psychiatry source
The Results section, “Which depressed individuals show increased inflammation?” (page not provided), states that the maltreated-only group had higher inflammation markers than controls, though to a lesser extent than the depressed-and-maltreated group. (LLM, conf=0.94)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Rests on an assumption: The childhood adversity index formed from parental age, familial disruption, parental affective illness, low household education, and limited economic resources validly captures the childhood adversity relevant to depression-inflammation clustering.
- Rests on an assumption: CRP and IL-6 measurements validly index the inflammatory processes relevant to depression.
- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Consistent with this possibility, recent studies have found that depression and inflammation cluster in persons who experienced childhood adversity.”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > Abstract > Conclusions
What the sources say
- Supportedcites [14] Danese, 2008, Elevated inflammation levels in depressed adults with a history of childhood maltreatment, Arch Gen Psychiatry source
The Abstract Conclusions state that childhood maltreatment contributes to the co-occurrence of depression and inflammation. The Results also report elevated inflammation markers in maltreated individuals and examine their co-occurrence with depression, supporting the citing sentence’s paraphrase. (LLM, conf=0.93)
- Not checked — no full text of the sourcecites [17] Pace, 2006, Increased stress-induced inflammatory responses in male patients with major depression and increased early life stress, Am J Psychiatry source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Rests on an assumption: The childhood adversity index formed from parental age, familial disruption, parental affective illness, low household education, and limited economic resources validly captures the childhood adversity relevant to depression-inflammation clustering.
- Rests on an assumption: CRP and IL-6 measurements validly index the inflammatory processes relevant to depression.
- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“More broadly, the findings contribute to an emerging consensus that childhood social conditions are important in establishing lifecourse trajectories that eventuate in differential vulnerability to disease and disability (15, 36).”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > Discussion
What the sources say
- Supportedcites [15] Miller, 2011, Psychological stress in childhood and susceptibility to the chronic diseases of aging: Moving toward a model of behavioral and biological mechanisms, Psychol Bull source
The Background section reports that low childhood socioeconomic status is associated with lasting excess disease risk. In “Insights from Other Models,” the paper describes trajectories set by childhood experience and accumulating disadvantage that can increase later illness risk. The cited paper therefore supports the broader point; the citing authors’ statement about what their own findings contribute is not attributed to it. Page numbers were not supplied. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites [36] Hertzman, 2010, How experience gets under the skin to create gradients in developmental health, Annu Rev Public Health source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- The authors state this as an assumption: The outcome (depression status) follows an underlying Bernoulli distribution.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Composite scores were higher among subjects with a maltreatment history and recent depression, relative to controls with neither.”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > Abstract > Conclusions
What the sources say
- Supportedcites [14] Danese, 2008, Elevated inflammation levels in depressed adults with a history of childhood maltreatment, Arch Gen Psychiatry source
The Results section (‘Which depressed individuals show increased inflammation?’) reports higher mean levels of the inflammation factor in the depressed-and-maltreated group than in controls. The Methods define controls as having neither current depression nor a maltreatment history, and the cohort description identifies the Dunedin study. Page numbers were not provided in our copy. (LLM, conf=0.92)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Rests on an assumption: The childhood adversity index formed from parental age, familial disruption, parental affective illness, low household education, and limited economic resources validly captures the childhood adversity relevant to depression-inflammation clustering.
- Rests on an assumption: CRP and IL-6 measurements validly index the inflammatory processes relevant to depression.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“As a consequence of these lingering effects, childhood adversity may predispose individuals to complicated depressions, characterized by treatment non-response, residual mood symptoms, or frequent relapse (3, 35).”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > Discussion
What the sources say
- Partly supportedcites [3] Miller, 2009, Inflammation and its discontents: The role of cytokines in the pathophysiology of major depression, Biol Psychiatry sourceExperimental — accuracy not yet measured
In “Cytokines, Stress, and Depression” (page unavailable), the paper associates childhood maltreatment with elevated inflammatory markers. In “Translational Implications” (page unavailable), it links inflammation to poorer antidepressant response. It does not directly say that childhood adversity predisposes people to treatment non-response, residual mood symptoms, or frequent relapse. (LLM, conf=0.78)
- Not checked — no full text of the sourcecites [35] Nanni, 2011, Childhood maltreatment predicts unfavorable course of illness and treatment outcome in depression: A meta-analysis, Am J Psychiatry source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- The authors state this as an assumption: The outcome (depression status) follows an underlying Bernoulli distribution.
- 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
“These lingering effects were bi-directional, such that among subjects with childhood adversity, high IL-6 forecasted depression six months later, even after concurrent inflammation was considered.”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > Abstract > Results
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Rests on an assumption: The childhood adversity index formed from parental age, familial disruption, parental affective illness, low household education, and limited economic resources validly captures the childhood adversity relevant to depression-inflammation clustering.
- Rests on an assumption: CRP and IL-6 measurements validly index the inflammatory processes relevant to depression.
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
“This coupling of depression and inflammation was not apparent in subjects without childhood adversity.”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > Abstract > Results
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Rests on an assumption: The childhood adversity index formed from parental age, familial disruption, parental affective illness, low household education, and limited economic resources validly captures the childhood adversity relevant to depression-inflammation clustering.
- Rests on an assumption: CRP and IL-6 measurements validly index the inflammatory processes relevant to depression.
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
“Among subjects exposed to high childhood adversity, the transition to depression was accompanied by increases in both CRP and IL-6.”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > Abstract > Results
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Rests on an assumption: The childhood adversity index formed from parental age, familial disruption, parental affective illness, low household education, and limited economic resources validly captures the childhood adversity relevant to depression-inflammation clustering.
- Rests on an assumption: CRP and IL-6 measurements validly index the inflammatory processes relevant to depression.
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 higher CRP remained evident six months later, even after depressive symptoms had abated.”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > Abstract > Results
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Rests on an assumption: The childhood adversity index formed from parental age, familial disruption, parental affective illness, low household education, and limited economic resources validly captures the childhood adversity relevant to depression-inflammation clustering.
- Rests on an assumption: CRP and IL-6 measurements validly index the inflammatory processes relevant to depression.
- Probably not a substantial claim. 25
- It may state two separate claims as one. 23
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Previous research in this area has focused on maltreatment, but other kinds of childhood adversity, such as low socioeconomic status (SES), have been linked to low-grade inflammation in adulthood (18–20), as well as mental and physical health problems across the lifespan (21).”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > Abstract > Conclusions
What the sources say
- Supportedcites [18] Miller, 2009, Low early-life social class leaves a biological residue manifest by decreased glucocorticoid and increased pro-inflammatory signaling, Proc Natl Acad Sci U S A source
The Abstract reports that healthy adults with low early-life SES had heightened expression of proinflammatory transcripts and greater stimulated production of IL-6. The Discussion likewise describes increased inflammatory gene expression in adults aged 25–40. This supports the cited link to adult inflammation; the sentence cites a different source for mental and physical health problems. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites [19] Taylor, 2006, Relationship of early life stress and psychological functioning to adult C-reactive protein in the coronary artery risk development in young adults study, Biol Psychiatry source
- Not checked — no full text of the sourcecites [20] Tabassum, 2008, Effects of socioeconomic position on inflammatory and hemostatic markers: A life-course analysis in the 1958 British birth cohort, Am J Epidemiol source
- Not checked — no full text of the sourcecites [21] Shonkoff, 2009, Neuroscience, molecular biology, and the childhood roots of health disparities: building a new framework for health promotion and disease prevention, JAMA source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Rests on an assumption: The childhood adversity index formed from parental age, familial disruption, parental affective illness, low household education, and limited economic resources validly captures the childhood adversity relevant to depression-inflammation clustering.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“We examined alternative explanations by statistically controlling for plausible demographic and biobehavioral confounders (29).”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > METHODS > Procedures
What the sources say
- Supportedcites [29] O'Connor, 2009, To assess, to control, to exclude: Effects of biobehavioral factors on circulating inflammatory markers, Brain Behav Immun source
The citing authors describe their own statistical controls; the citation supports the choice of demographic and biobehavioral factors as potential confounders. The source’s Summary says these factors may confound associations, and its Results section on ethnic and racial differences explicitly recommends statistical control. The source does not purport to have performed the citing study’s analysis. (LLM, conf=0.89)
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“This hypothesis grows out of mounting evidence that severe childhood stressors promote the formation of a neural-immune pipeline (15), wherein inflammatory cytokine signaling between the brain and the periphery is markedly amplified (16).”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > Abstract > Conclusions
What the sources say
- Partly supportedcites [15] Miller, 2011, Psychological stress in childhood and susceptibility to the chronic diseases of aging: Moving toward a model of behavioral and biological mechanisms, Psychol Bull sourceExperimental — accuracy not yet measured
In “Mechanisms of Embedding” (page unavailable), the paper proposes that childhood stress could alter connections between the nervous and immune systems and reports evidence that stress can change those connections. It presents the childhood-stress mechanism as a possibility, rather than establishing that severe childhood stressors form a neural-immune pipeline. The amplified cytokine-signaling clause is attached to a different citation and is not judged here. (LLM, conf=0.84)
- Partly supportedcites [16] Irwin, 2011, Reciprocal regulation of the neural and innate immune systems, Nat Rev Immunol sourceExperimental — accuracy not yet measured
The Abstract and ‘Neural influences on disease’ section describe reciprocal brain–immune signaling and report that acute stress can increase circulating pro-inflammatory cytokines. They do not establish that cytokine signaling between the brain and periphery is markedly amplified; the childhood-stressor premise is attached to a different citation. (LLM, conf=0.84)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may state two separate claims as one.
- Rests on an assumption: The childhood adversity index formed from parental age, familial disruption, parental affective illness, low household education, and limited economic resources validly captures the childhood adversity relevant to depression-inflammation clustering.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“These findings converge with and extend studies of remitted depressed patients, in some of whom CRP remains elevated after symptom remission (34).”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > Discussion
What the sources say
- Supportedcites [34] Kling, 2007, Sustained low-grade pro-inflammatory state in unmedicated, remitted women with major depressive disorder as evidenced by elevated serum levels of the acute phase proteins C-reactive protein and serum amyloid A, Biol Psychiatry source
The Discussion reports significantly elevated CRP in remitted, unmedicated women with MDD compared with BMI-matched controls. It states that CRP elevation is not confined to the depressive state, supporting the claim that CRP can remain elevated after symptom remission. (LLM, conf=0.92)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“These symptoms are thought to further exacerbate inflammation and, in doing so, contribute to the pathogenesis of various diseases of aging (6–8), many of which involve excessive cytokine activity (9, 10).”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > Abstract > Conclusions
What the sources say
- Not checked — no full text of the sourcecites [6] Miller, 2006, Turning up the heat: Inflammation as a mechanism linking chronic stress, depression, and heart disease, Curr Dir Psychol Sci source
- Partly supportedcites [7] Antoni, 2006, The influence of bio-behavioural factors on tumour biology: Pathways and mechanisms, Nat Rev Cancer sourceExperimental — accuracy not yet measured
The passage indexed as Abstract (page unavailable) says pro-inflammatory cytokines might promote tumorigenesis, supporting the cytokine-related point for cancer. It does not establish that many diseases of aging involve excessive cytokine activity. In the citing sentence, the claim that symptoms exacerbate inflammation has separate citations (6–8), so it is not assessed against this source. (LLM, conf=0.83)
- Not checked — no full text of the sourcecites [8] Irwin, 2002, Psychoneuroimmunology of depression: Clinical implications, Brain Behav Immun source
- Not checked — no full text of the sourcecites [9] Nathan, 2010, Nonresolving inflammation, Cell source
- Not checked — no full text of the sourcecites [10] Libby, 2011, Progress and challenges in translating the biology of atherosclerosis, Nature source
Strength:hedged· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Thus, we followed published guidelines that recommend excluding such observations from analyses (30).”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > METHODS > Statistical Approach
What the sources say
- Partly supportedcites [30] Yeh, 2003, Coming of age of C-reactive protein: Using inflammation markers in cardiology, Circulation sourceExperimental — accuracy not yet measured
The opening section and “CRP as a Clinical Test in Cardiovascular Practices” recommend repeating CRP tests above the stated threshold to rule out infection or other inflammatory processes. They do not recommend excluding those observations from analyses, so the cited paper supports the threshold-related caution but not the claimed analytical exclusion. (LLM, conf=0.86)
Strength:plain· not yet calibratedn = 6Tests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Rests on an assumption: CRP and IL-6 measurements validly index the inflammatory processes relevant to depression.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Most center around the notion that stress triggers the release of pro-inflammatory cytokines, which access the central nervous system, eliciting neurobehavioral adjustments that manifest as depressive symptoms (3–5).”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > Abstract > Conclusions
What the sources say
- Supportedcites [3] Miller, 2009, Inflammation and its discontents: The role of cytokines in the pathophysiology of major depression, Biol Psychiatry source
The “Cytokines, Stress, and Depression” section says psychosocial stress activates inflammatory responses in the periphery and brain. “Mechanisms and Mediators of Cytokine-Induced Behavioral Change” describes how peripheral cytokine signals reach the brain, while “Evidence for a Cytokine Basis for Major Depression” reports that cytokines can produce behavioral symptoms overlapping with depression. Together, these passages support the proposed pathway; page numbers are unavailable in our copy. (LLM, conf=0.90)
- Partly supportedcites [4] Dantzer, 2008, From inflammation to sickness and depression: When the immune system subjugates the brain, Nat Rev Neurosci sourceExperimental — accuracy not yet measured
The review’s ‘Immune signals from periphery to brain’ passage describes how peripheral cytokine signals reach the brain, and its discussion of cytokine-induced depression links those signals to depressive symptoms. It does not establish the claim’s initiating step—that stress triggers the release of pro-inflammatory cytokines; the pathways described here concern peripheral immune responses, including infection. (LLM, conf=0.86)
- Supportedcites [5] Slavich, 2010, Black sheep get the blues: A psychobiological model of social rejection and depression, Neurosci Biobehav Rev source
Section 3.2 reports that social-evaluative stress increases pro-inflammatory cytokines and that these cytokines signal the central nervous system, eliciting sickness behaviors that include depressotypic symptoms. Section 3.3 further describes evidence linking inflammatory activity to depressed mood. The paper presents this as a model of rejection-related stress, not as an inevitable response to every stressor. (LLM, conf=0.88)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“We view this scenario as somewhat unlikely, given prospective data showing that both impoverished and maltreated children go on to have more adult inflammation, and these effects are statistically independent (45).”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > Discussion
What the sources say
- Partly supportedcites [45] Danese, 2009, Adverse childhood experiences and adult risk factors for age-related disease: Depression, inflammation, and clustering of metabolic risk markers, Arch Pediatr Adolesc Med sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Load-bearingStrength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- 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
“All that said, these findings emerged in only a small group of subjects, and were not paralleled by effects for IL-6 or continuous CRP (see Table 3; p’s = .14 and .22, respectively.)”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > RESULTS > Lagged Analyses
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
“Preliminary analyses revealed that alcohol and contraceptive use were stable over follow-up (intra-class correlations = .72, 65).”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > METHODS > Procedures
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
“At study entry, CRP and IL-6 values were well within normal limits, except 8 subjects with CRP > 3 mg/L.”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > RESULTS > Preliminary Analyses
Strength:plain· not yet calibratedn = 8Tests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Rests on an assumption: CRP and IL-6 measurements validly index the inflammatory processes relevant to depression.
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 Table 2 indicates, significant cross-level interactions were observed for CRP, both as a continuous and categorical outcome, and for IL-6 (p’s from .001–.05).”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > RESULTS > Concurrent Analyses
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The childhood adversity index formed from parental age, familial disruption, parental affective illness, low household education, and limited economic resources validly captures the childhood adversity relevant to depression-inflammation clustering.
- Rests on an assumption: CRP and IL-6 measurements validly index the inflammatory processes relevant to depression.
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
“Childhood adversity was not directly related to the inflammatory biomarkers, either at baseline (p’s > .84) or over follow-up (p’s > .15).”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > RESULTS > Preliminary Analyses
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The childhood adversity index formed from parental age, familial disruption, parental affective illness, low household education, and limited economic resources validly captures the childhood adversity relevant to depression-inflammation clustering.
- Rests on an assumption: CRP and IL-6 measurements validly index the inflammatory processes relevant to depression.
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
“Few subjects received anti-depressant medication for their symptoms (12.5%), and childhood adversity was unrelated to the likelihood of doing so (p = .70).”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > RESULTS > Preliminary Analyses
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Rests on an assumption: The childhood adversity index formed from parental age, familial disruption, parental affective illness, low household education, and limited economic resources validly captures the childhood adversity relevant to depression-inflammation clustering.
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
“Among subjects exposed to higher levels of childhood adversity, the transition to depression was accompanied by a relative increase in CRP (middle panel), and a greater likelihood of having CRP ≥ 3 mg/L (lower panel), placing them in the elevated risk category by AHA/CDC guidelines.”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > RESULTS > Concurrent Analyses
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The childhood adversity index formed from parental age, familial disruption, parental affective illness, low household education, and limited economic resources validly captures the childhood adversity relevant to depression-inflammation clustering.
- Rests on an assumption: CRP and IL-6 measurements validly index the inflammatory processes relevant to depression.
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
“Of the 53 total episodes catalogued, 25 met criteria for Major Depression and 28 for Minor Depression.”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > RESULTS > Preliminary Analyses
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. 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 study involved 147 adolescent females who mirrored the broader Vancouver population in terms of racial/ethnic background (Table 1).”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > RESULTS > Preliminary Analyses
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
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
“On six occasions subjects had CRP > 10 mg/L.”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > METHODS > Statistical Approach
Strength:plain· not yet calibratedn = 6Tests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Rests on an assumption: CRP and IL-6 measurements validly index the inflammatory processes relevant to depression.
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 fact, 10.7% of the depressed subjects in the high childhood adversity category showed this pattern, whereas none of the other subjects did.”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > RESULTS > Lagged Analyses
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
“By contrast, analyses showed that WHR increased over time (B = .024, SE = .013, p = .06), so we modeled it as a time-varying covariate.”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > METHODS > Procedures
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
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
“We observed a relatively small number of depressive episodes, and they were generally of brief duration and mild severity.”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > Discussion
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
“After the outliers were removed, both CRP and IL-6 showed roughly normal distributions.”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > METHODS > Statistical Approach
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: CRP and IL-6 measurements validly index the inflammatory processes relevant to depression.
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
“Neither the duration (p = .65) nor severity of episodes (p = .49) varied by childhood adversity.”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > RESULTS > Preliminary Analyses
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The childhood adversity index formed from parental age, familial disruption, parental affective illness, low household education, and limited economic resources validly captures the childhood adversity relevant to depression-inflammation clustering.
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
“However, only 3 subjects were regular smokers at any point in the study, so there was too little variance to justify modeling its effects.”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > METHODS > Procedures
Strength:plain· not yet calibratedn = 3Tests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“Additionally, depression heightens risks for morbidity and mortality from chronic diseases associated with aging, including autoimmune, metabolic, and cardiovascular conditions (2).”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > Abstract > Conclusions
What the sources say
- Not checked — no full text of the sourcecites [2] Evans, 2005, Mood disorders in the medically ill: Scientific review and recommendations, Biol Psychiatry source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
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
“Once established, this pipeline leads to a coupling of depression and inflammation, which may contribute to later affective difficulties and biomedical complications.”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > Abstract > Conclusions
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The childhood adversity index formed from parental age, familial disruption, parental affective illness, low household education, and limited economic resources validly captures the childhood adversity relevant to depression-inflammation clustering.
- Rests on an assumption: CRP and IL-6 measurements validly index the inflammatory processes relevant to depression.
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
“Our findings suggest that such treatments would be ineffective for patients without childhood adversity, as depression and inflammation tend to dissociate in them.”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > Discussion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- The authors state this as an assumption: The outcome (depression status) follows an underlying Bernoulli distribution.
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
“From observational data like these, inferences about causality cannot be made.”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > Discussion
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably 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
“Whenever an interview suggested a possible disorder, the entire team reviewed the SCID by audiotape, and derived a consensus diagnosis.”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > METHODS > Procedures
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
In the paper
“In this work, adults who were currently depressed, and had been maltreated in childhood, exhibited showed larger stress-related increases in plasma IL-6 than healthy controls, as well as enhanced DNA binding of the pro-inflammatory transcription factor nuclear factor-kappa B.”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > Abstract > Conclusions
What the sources say
- Not checked — no full text of the sourcecites [17] Pace, 2006, Increased stress-induced inflammatory responses in male patients with major depression and increased early life stress, Am J Psychiatry source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The childhood adversity index formed from parental age, familial disruption, parental affective illness, low household education, and limited economic resources validly captures the childhood adversity relevant to depression-inflammation clustering.
- Rests on an assumption: CRP and IL-6 measurements validly index the inflammatory processes relevant to depression.
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
“For similar reasons we excluded five IL-6 values > 10 pg/ml.”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > METHODS > Statistical Approach
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Rests on an assumption: CRP and IL-6 measurements validly index the inflammatory processes relevant to depression.
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
“The increased exposure to inflammatory mediators may also heighten these patients’ vulnerability to comorbid medical conditions, like diabetes, autoimmune disorders, and cardiovascular disease.”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > Discussion
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
- The authors state this as an assumption: The outcome (depression status) follows an underlying Bernoulli distribution.
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
“This clustering has implications for our understanding of depression’s pathogenesis, the mechanisms by which it confers susceptibility to comorbidities, and possibly for targeted application of anti-inflammatory therapy.”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > Discussion
Tests✓ Asserted: passes✗ Checkable: fails✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may be too vague to check against evidence. It may state two separate claims as one.
- The authors state this as an assumption: The outcome (depression status) follows an underlying Bernoulli distribution.
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
“Re-analysis of the data including outliers yielded identical findings.”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > METHODS > Statistical Approach
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Rests on an assumption: CRP and IL-6 measurements validly index the inflammatory processes relevant to depression.
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 median weighted kappa was .69.”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > METHODS > Procedures
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably 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
“In the absence of such data, it remains uncertain whether the observed clustering arises from the “mundane” adversity captured by our index, versus unmeasured but co-occuring experiences with maltreatment.”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > Discussion
Strength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably 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 intra-class correlation for HRSD ratings was .64.”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > METHODS > Procedures
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Research has documented associations between syndromal depression and inflammatory biomarkers, as well as a graded, linear relation of the latter with dysphoric symptoms (11).”
§ CLUSTERING OF DEPRESSION AND INFLAMMATION IN ADOLESCENTS PREVIOUSLY EXPOSED TO CHILDHOOD ADVERSITY > Abstract > Conclusions
What the sources say
- Not checked — no full text of the sourcecites [11] Raison, 2006, Cytokines sing the blues: Inflammation and the pathogenesis of depression, Trends Immunol source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may state two separate claims as one.
The paper relies on this without support.
The childhood adversity index formed from parental age, familial disruption, parental affective illness, low household education, and limited economic resources validly captures the childhood adversity relevant to depression-inflammation clustering.
“Using data from baseline interviews, we formed a childhood adversity index. One point was assigned for each of the following risks: (a) birth to a teenage mother, who was < 20 years old at delivery, (b) familial disruption before age 15, caused by the death of a parent or divorce; or separation from a parent that lasted more than one year; (c) a history of affective illness in parents/guardians; (”
The paper relies on this without support.
CRP and IL-6 measurements validly index the inflammatory processes relevant to depression.
“CRP was measured by high-sensitivity chemiluminescence on an Immulite 2000 (Diagnostic Products Corporation, Los Angeles, CA).”
“IL-6 was measured in duplicate by commercially available high-sensitivity ELISA (R&D Systems; Minneapolis, MN).”
The authors state this as an assumption.
The outcome (depression status) follows an underlying Bernoulli distribution.
“Using multilevel models that assumed an underlying Bernoulli distribution of the outcome”
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 cited source doesn’t support the claim as written.
In the citing paper
“whereas adolescents in this study who did not have a history of early life stress exhibited reductions in CRP as their depressive symptoms abated, those with a history of early life stress showed no such association, instead exhibiting elevations in CRP that persisted in the absence of depression”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as G. E. Miller & Cole, 2012
Checked by a reasoning model — may be wrong.
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
“Most findings, but not all, suggest a robust correlation between ELS/CT and adult CRP levels (165, 166, 170, 199–202).”
From Developmental Trajectories of Early Life Stress and Trauma: A Narrative Review on Neurobiological Aspects Beyond Stress System Dysregulation (2019) · cites this paper as [202]
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
“engagement of these pathways may become selfpromoting as a result of neuro-inflammatory sensitization and thus drive heightened levels of inflammation and exaggerated perceptions of social threat for months or years after the original social-environmental impetus has passed”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as G. E. Miller & Cole, 2012
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
“Finally, after years of sustained engagement, these dynamics may confer increased risk for inflammation-related disorders, infection, accelerated biological aging, and early mortality”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as G. E. Miller & Cole, 2012
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“adolescents with a history of more common forms of early life stress, such as low socioeconomic status or parental separation, had greater increases in both IL-6 and CRP when becoming depressed than their counterparts without a history of these early life stressors”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as G. E. Miller & Cole, 2012
In the citing paper
“There is also an emerging body of evidence that more chronic childhood stressors such as parent psychopathology (e.g., MDD), low SES, and parent separation are prospectively associated with elevated inflammation when adolescent girls become depressed, and that inflammatory markers remain elevated even after symptoms recover (Miller and Cole, 2012).”
From Developmental psychoneuroendocrine and psychoneuroimmune pathways from childhood adversity to disease (2017) · cites this paper as Miller and Cole, 2012
In the citing paper
“Furthermore, high circulating IL-6 predicted depressive episodes 6 months later (Miller and Cole, 2012).”
From Repeated Social Defeat, Neuroinflammation, and Behavior: Monocytes Carry the Signal (2017) · cites this paper as Miller and Cole, 2012
In the citing paper
“Childhood adversity promoted clustering of depressive episodes along with elevated circulating IL-6 and CRP.”
From Repeated Social Defeat, Neuroinflammation, and Behavior: Monocytes Carry the Signal (2017) · cites this paper as Miller and Cole, 2012
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.
Lagged IL-6 finding claims an unreported inflammation adjustment
MinorThe abstract says IL-6 predicted depression after concurrent inflammation was considered. The described lagged model instead adjusts for prior depression status and other covariates; it does not list concurrent inflammation as an adjustment.
“high IL-6 forecasted depression six months later, even after concurrent inflammation was considered.”
“Also in the models were time, depression status at Visit ‘N-1’, childhood adversity, and demographic and biobehavioral covariates.”
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Sorted by citations
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“…sensitization and thus drive heightened levels of inflammation and exaggerated perceptions of social threat for months or years after the original social-environmental impetus has passed (see Figure 3; G. E. Miller, Chen, & Parker, 2011; G. E. Miller & Cole, 2012; Slavich & Cole, 2013).”
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Metadata
- Authors
- Miller, G. E., & Cole, S. W.
- Affiliations
- University of British Columbia (CA)
- University of California, Los Angeles (US)
- Corresponding author
- Miller, Gregory E.
- Venue
- Biological Psychiatry
- Publisher
- Elsevier BV
- Published
- 2012-07
- Volume
- 72
- Issue
- 1
- Pages
- 34-40
- ISSN
- 0006-3223 (ISSN-L)
- PMC
- PMC3493164
- OpenAlex
- W2037158815
- Semantic Scholar
- 40b98ebc414e522ac6f151029266ea66acadc3e5
- Cited by
- 331
- References
- 42
- Citations by year
- 2026: 6 · 2025: 23 · 2024: 20 · 2023: 22 · 2022: 20 · 2021: 28 · 2020: 32 · 2019: 30 · 2018: 29 · 2017: 20 · 2016: 36 · 2015: 34 · 2014: 11 · 2013: 16 · 2012: 4
- FWCI
- 6.46
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Biological Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Canadian Institutes of Health Research (67191)
- National Alliance for Research on Schizophrenia and Depression Brain and Behavior Research Fund
- Heart and Stroke Foundation of Canada
- National Institute of Child Health and Human Development (R01 HD058502)
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Social Sciences › Psychology › Clinical Psychology › Child Abuse and Trauma
- Keywords
- childhood adversity, depression, inflammation, C-reactive protein, interleukin-6, adolescents, adolescent girls, parental separation, low socioeconomic status, inflammatory markers, comorbidities
- MeSH terms
- Adolescent, Adult, C-Reactive Protein, Canada, Depressive Disorder, Female, Follow-Up Studies, Humans, Inflammation, Interview, Psychological, Life Change Events, Psychiatric Status Rating Scales, Risk Factors, Biomarkers, Interleukin-6, Cluster Analysis, Young Adult
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