Childhood maltreatment and inflammatory markers: a systematic review

Coelho, Roberta Paula Schell; Viola, Thiago Wendt; Walss‐Bass, Consuelo; Brietzke, Elisa; Grassi‐Oliveira, Rodrigo

doi:10.1111/acps.12217

Cited by 361 publications

(282 citation statements)

References 73 publications

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“…The association was not explained by key potential confounders, such as low birth weight, disadvantaged socio-economic conditions of the family, and low IQ, or by potential mediators, such as adult stressors, poor adult health, unhealthy behaviors, or acute infections at the time of inflammation assessment. Two dozen independent studies have since tested this association, and qualitative and quantitative reviews found reliable evidence of small elevations in inflammation biomarkers in maltreated individuals (Baumeister et al, 2015;Coelho et al, 2014). Of note, elevated inflammation levels are observed not only after maltreatment by adults, but also after other common and severe childhood stressors, such as bullying by peers (Takizawa et al, 2015).…”

Section: Brain Developmentmentioning

confidence: 98%

Psychoneuroimmunology of Early-Life Stress: The Hidden Wounds of Childhood Trauma?

Danese

Lewis

2016

Neuropsychopharmacol

294

191

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The brain and the immune system are not fully formed at birth, but rather continue to mature in response to the postnatal environment. The two-way interaction between the brain and the immune system makes it possible for childhood psychosocial stressors to affect immune system development, which in turn can affect brain development and its long-term functioning. Drawing from experimental animal models and observational human studies, we propose that the psychoneuroimmunology of early-life stress can offer an innovative framework to understand and treat psychopathology linked to childhood trauma. Earlylife stress predicts later inflammation, and there are striking analogies between the neurobiological correlates of early-life stress and of inflammation. Furthermore, there are overlapping trans-diagnostic patterns of association of childhood trauma and inflammation with clinical outcomes. These findings suggest new strategies to remediate the effect of childhood trauma before the onset of clinical symptoms, such as anti-inflammatory interventions and potentiation of adaptive immunity. Similar strategies might be used to ameliorate the unfavorable treatment response described in psychiatric patients with a history of childhood trauma.

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Section: Brain Developmentmentioning

confidence: 98%

Psychoneuroimmunology of Early-Life Stress: The Hidden Wounds of Childhood Trauma?

Danese

Lewis

2016

Neuropsychopharmacol

294

191

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“…Maladaptive habits, including unhealthy diet and smoking, as well as environmental factors, including childhood abuse, have been consistently associated with pro-inflammatory activation 59 . For instance, individuals with a history of childhood abuse exhibit higher plasma CRP, IL-6 and TNF-α levels during adulthood in comparison to healthy controls 60 and are exposed to greater risk of chronic diseases in adulthood including cancer, depression, cardiovascular disease and metabolic syndrome 61 .…”

Section: Inflammatory Aberrations Associated With Depressionmentioning

confidence: 99%

Depression in cancer: The many biobehavioral pathways driving tumor progression

Bortolato

Hyphantis

Valpione

et al. 2017

Cancer Treatment Reviews

248

179

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Major Depressive Disorder (MDD) is common among cancer patients, with prevalence rates up to four-times higher than the general population. Depression confers worse outcomes, including non-adherence to treatment and increased mortality in the oncology setting. Advances in the understanding of neurobiological underpinnings of depression have revealed shared biobehavioral mechanisms may contribute to cancer progression. Moreover, psychosocial stressors in cancer promote:(1) inflammation and oxidative/nitrosative stress; (2) a decreased immunosurveillance; and (3) a dysfunctional activation of the autonomic nervous system and of the hypothalamic-pituitary-adrenal axis. Consequently, the prompt recognition of depression among patients with cancer who may benefit of treatment strategies targeting depressive symptoms, cognitive dysfunction, fatigue and sleep disturbances, is a public health priority. Moreover, behavioral strategies aiming at reducing psychological distress and depressive symptoms, including addressing unhealthy diet and life-style choices, as well as physical inactivity and sleep dysfunction, may represent important strategies not only to treat depression, but also to improve wider cancer-related outcomes. Herein, we provide a comprehensive review of the intertwined biobehavioural pathways linking depression to cancer progression. In addition, the clinical implications of these findings are critically reviewed.

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“…In terms of mechanisms, it is noteworthy that early-life psychosocial stressors, notably emotional and sexual abuses are associated to early AAO [8,9]. Such stressful events are also known to induce acute and chronic immune/inflammatory alterations [10][11][12][13] possibly leading to an increased vulnerability to diabetes, obesity, cardiovascular disorders, autoimmunity, cancer and neurodegeneration commonly observed in adults with history of childhood maltreatment [14][15][16][17][18]. Of interest is that elevated C-reactive-protein (CRP), as well as high prevalence of cardiovascular disorders, type 2 diabetes mellitus, hypertension and obesity, are observed in early onset BD [19,20] and that some of these conditions even precede the diagnosis of BD in pediatric patients [20].…”

Section: Introductionmentioning

confidence: 99%

Combined Effect of TLR2 Gene Polymorphism and Early Life Stress On the Age at Onset of Bipolar Disorders

Oliveira

Étain

Lajnef

et al. 2015

European Psychiatry

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Gene-environment interactions may play an important role in modulating the impact of earlylife stressful events on the clinical course of bipolar disorder (BD), particularly associated to early age at onset. Immune dysfunction is thought to be an important mechanism linking childhood trauma with early-onset BD, thus the genetic diversity of immune-related loci may account for an important part of the interindividual susceptibility to this severe subform. Here we investigated the potential interaction between genetic variants of Toll-like receptors 2 (TLR2) and 4 (TLR4), major innate immune response molecules to pathogens, and the childhood trauma questionnaire (CTQ) in age at onset of BD. We recruited 531 BD patients (type I and II or not otherwise specified), genotyped for the TLR2 rs4696480 and rs3804099 and TLR4 rs1927914 and rs11536891 single-nucleotide polymorphisms and recorded for history of childhood trauma using the CTQ. TLR2 and TLR4 risk genotype carrier state and history of childhood emotional, physical and sexual abuses were evaluated in relation to age at onset as defined by the age at first manic or depressive episode. We observed a combined effect of TLR2 rs3804099 TT genotype and reported sexual abuse on determining an earlier age at onset of BD by means of a Kaplan-Meier survival curve (p = 0.002; corrected p = 0.02). Regression analysis, however, was non-significant for the TLR2-CTQ sexual abuse interaction term. The negative effects of childhood sexual abuse on age at onset of BD may be amplified in TLR2 rs3804099 risk genotype carriers through immune-mediated pathways. Clinical characteristics of illness severity, immune phenotypes and history of early life infectious insults should be included in future studies involving large patient cohorts.

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Childhood maltreatment and inflammatory markers: a systematic review

Cited by 361 publications

References 73 publications

Psychoneuroimmunology of Early-Life Stress: The Hidden Wounds of Childhood Trauma?

Psychoneuroimmunology of Early-Life Stress: The Hidden Wounds of Childhood Trauma?

Depression in cancer: The many biobehavioral pathways driving tumor progression

Combined Effect of TLR2 Gene Polymorphism and Early Life Stress On the Age at Onset of Bipolar Disorders

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