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The present study furthers understanding of how childhood adversity connects to inflammation and, in turn, poor health. Using the publicly available Midlife in the United States II (MIDUS II) dataset, we test a recent theoretical model that suggests emotion regulation is a potential mechanism of associations between adversity and inflammation. We examined the indirect effects of various types of adversity (e.g., stressful events, maltreatment, threat, and deprivation) on inflammation via two emotion regulation strategies (i.e., expressive suppression and reappraisal). Participants included 1096 adults without a history of cancer or HIV/AIDS who had completed the initial MIDUS II follow up and a sub-study examining biomarkers. Participants completed self-report measures inquiring about psychosocial factors including stressful life events, childhood trauma, and emotion regulation as well as provided blood samples. Bivariate correlation indicated that multiple forms of childhood adversity were associated with both C-reactive protein and fibrinogen. Deprivation, as measured by a stressful life events scale, was positively associated with both reappraisal and suppression. Tests of indirect effects indicated that deprivation was positively associated with fibrinogen through both emotion regulation strategies, particularly for female participants. Our findings partially support recent theory positing emotion regulation as a pathway through which childhood adversity may impact inflammation in adulthood. Further, deprivation may be particularly critical in understanding how adversity is connected to maladaptive emotion regulation and inflammation. Emotion regulation may be an important treatment target to mitigate the negative impact of childhood adversity on health and well-being. Supplementary Information: The online version contains supplementary material available at 10.1007/s40653-023-00594-2.
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War veterans, in particular, are more prone to mental illness as they are more likely to have encountered multiple traumatic brain injuries (TBIs) whilst serving on active duty in war zone areas. A TBI is known to cause mortality or serious neurological disabilities among survivors and elicits a number of pathological processes, including neuroinflammation and blood brain barrier (BBB) disruption, leading to secondary brain damage and subsequent impairment of the neurovascular unit. Although several drugs exhibit promising effects for TBI, the repertoire of currently available therapeutic strategies remains limited. Thymosin 4 (Tß4) is a 43-amino acid G-acting sequestering peptide that confers neuroprotective potential in TBI models. However, its role in BBB function remains unclear. Further research into the mechanism of BBB disruption induced by TBI and its specific role in neurovascular pathophysiology is necessary. In the present study, the protective effects of Tß4 in lipopolysaccharide (LPS)-stimulated gene expression of several tight junction proteins, inflammatory genes, apoptotic genes, and adhesion genes in human brain microvascular endothelial cells (hBMVECs), one of the pivotal cell types in the BBB, were reported. The results suggested that pretreatment with Tß4 reversed the LPS-induced damage of BBB components in hBMVECs. Furthermore, these results identified neuregulin 1 as a possible target for Tß4. Therefore, it is proposed that Tß4-mediated cellular signaling in hBMVEC may be vital for understanding the association between the BBB and TBI pathophysiology, which warrants further investigation.
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Objective: Alcohol use and alcohol use disorders (AUDs) are an increasing concern among veterans, particularly those from recent conflicts in Iraq and Afghanistan. The study of biomarkers in alcohol use and AUD has moved to enhancing the understanding of the development and maintenance of AUDs, as well as investigating its association with clinical severity and potential predictors of treatment response. Cortisol, a glucocorticoid known as a stress hormone, has been linked with both stress and trauma, as well as increased alcohol suppression effects. Method/Results: The present review summarizes existing literature and presents suggestions for future research to evaluate whether cortisol may be a possible biomarker of alcohol use disorder risk in combat veterans. Specifically, aspects of combat deployments and high levels of PTSD, coupled with the stress of reintegration may dysregulate cortisol and increase risk to AUD. There may also be bidirectional impacts, such that alcohol is used as a coping mechanism and can dysregulate hypothalamic pituitary adrenal (HPA) axis functioning and cortisol. Conclusions: In the context of this framework, cortisol may serve as a biomarker for the development of AUD, as well as a biomarker of risk or relapse. This review ends with both theoretical and clinical implications, as well as directions for future research.
