Disentangling the Links Between Psychosocial Stress and Cardiovascular Disease.
Ontology highlight
ABSTRACT:
SUBMITTER: Osborne MT
PROVIDER: S-EPMC7430065 | biostudies-literature | 2020 Aug
REPOSITORIES: biostudies-literature
Publications
Disentangling the Links Between Psychosocial Stress and Cardiovascular Disease.
Osborne Michael T MT Shin Lisa M LM Mehta Nehal N NN Pitman Roger K RK Fayad Zahi A ZA Tawakol Ahmed A
Circulation. Cardiovascular imaging 20200814 8
Stress is a pervasive component of the human experience. While often considered an adversity to be ignored, chronic stress has important pathological consequences, including cardiovascular disease (CVD). Stress also increases the prevalence and severity of several CVD risk factors, including hypertension, diabetes mellitus, and obesity. Yet even after adjustment, stress' attributable CVD risk is similar to those risk factors, suggesting it is a particularly potent contributor. Nevertheless, ther ...[more]
Similar Datasets
Project description:The root cause of non-inherited Alzheimer's disease (AD) remains unknown despite hundreds of research studies performed to attempt to solve this problem. Since proper prophylaxis remains the best strategy, many scientists have studied the risk factors that may affect AD development. There is robust evidence supporting the hypothesis that cardiovascular diseases (CVD) may contribute to AD progression, as the diseases often coexist. Therefore, a lack of well-defined diagnostic criteria makes studying the relationship between AD and CVD complicated. Additionally, inflammation accompanies the pathogenesis of AD and CVD, and is not only a consequence but also implicated as a significant contributor to the course of the diseases. Of note, АроЕε4 is found to be one of the major risk factors affecting both the cardiovascular and nervous systems. According to genome wide association and epidemiological studies, numerous common risk factors have been associated with the development of AD-related pathology. Furthermore, the risk of developing AD and CVDs appears to be increased by a wide range of conditions and lifestyle factors: hypertension, dyslipidemia, hypercholesterolemia, hyperhomocysteinemia, gut/oral microbiota, physical activity, and diet. This review summarizes the literature and provides possible mechanistic links between CVDs and AD.
| S-EPMC8033981 | biostudies-literature
Project description:Psychosocial stress is a critical inducing factor of inflammatory bowel diseases (IBD), while autophagy is a novel central issue of IBD development. The present study investigated the potential role of autophagy in stress-related IBD in patients and animal model. The correlation between psychosocial stress and intestinal autophagy was determined in 23 patients with IBD. Corticotropin-releasing hormone (CRH), a well-established inducer of psychosocial stress, was administrated in dextran sulfate sodium (DSS)-induced IBD mice and lipopolysaccharide (LPS)-stimulated bone marrow-derived macrophages (BMDM). In IBD patients, the autophagy markers beclin-1, LC3-II/I ratio, Atg16L1, and Atg4B were significantly enhanced. The psychosocial stress score was positively associated with the levels of beclin-1 and the LC3II/I ratio in intestinal biopsy specimens. In IBD mouse model, CRH significantly aggravated intestinal inflammation, increased Paneth cell metaplasia, and enhanced intestinal autophagy (beclin-1, Atg16L1, PIK3R4, and Atg4B upregulation; GAA, CTSD, and PPKAA1 downregulation). Additionally, the CRH-induced gut microbial dysbiosis was evidenced by a marked increase in the number of detrimental bacteria. In LPS-stimulated BMDM, CRH substantially increased M1/M2 polarization and thus promoted inflammation. In both IBD mice and LPS-treated BMDM, blockade of autophagy by chloroquine abrogated the unbeneficial effects of CRH, whereas autophagy inducer rapamycin resulted in a pronounced protective effect against IBD lesion. Our data demonstrate that psychosocial stress may link the enhanced intestinal autophagy by modulating gut microbiota and inflammation to aggravate IBD. These data indicate autophagy as a promising therapeutic target for psychosocial stress-related IBD.
| S-EPMC6766473 | biostudies-literature
Project description:Habitat complexity is one of the most important factors modulating species diversity. This feature comprises several interrelated attributes, such as number, size, and spatial arrangement of complexity-forming elements. However, the separate and joint effects of these attributes on diversity and community structure are still not well understood. Here, we assess the relationships between several structural-complexity attributes of the subantarctic kelp Lessonia flavicans and species richness, total abundance, and structure of kelp-associated macrobenthic communities. We predicted that longer thalli and larger holdfasts favor greater species richness and total abundance of invertebrate organisms. To test the prediction, an observational sampling program was established in two sites of the Strait of Magellan. Uni- and multivariate analyses revealed both positive and negative effects of kelp structural-complexity attributes on diversity. Holdfast diameter and maximum frond length, followed by thallus wet weight, had the strongest positive fits to species richness and total abundance; the number of stipes, on the other hand, was negatively associated with both response variables. Longer fronds were associated with greater abundances of spirorbid polychaetes. Larger holdfasts supported larger abundances of Nereididae and Terebelidae polychaetes and the limpet Nacella mytilina. Contrarily, kelps with longer fronds and more stipes supported fewer amphipods. In this way, we demonstrate that different dimensions of habitat complexity can have contrasting effects on diversity and community structure, highlighting the fundamental role of multiple dimensions of kelp habitat complexity for local biodiversity.
| S-EPMC7863391 | biostudies-literature
Project description:BackgroundResearch implicates acute and chronic stressors in racial/ethnic health disparities, but the joint impact of multiple stressors on racial/ethnic disparities in cardiovascular health is unknown.MethodsIn 25 062 women (24 053 white; 256 Hispanic; 440 black; 313 Asian) articipating in the Women's Health Study follow-up cohort, we examined the relationship between cumulative psychosocial stress (CPS) and ideal cardiovascular health (ICH), as defined by the American Heart Association's 2020 strategic Impact Goals. This health metric includes smoking, body mass index, physical activity, diet, blood pressure, total cholesterol, and glucose, with higher levels indicating more ICH and less cardiovascular risk (score range, 0-7). We created a CPS score that summarized acute stressors (eg, negative life events) and chronic stressors (eg, work, work-family spillover, financial, discrimination, relationship, and neighborhood) and traumatic life event stress reported on a stress questionnaire administered in 2012 to 2013 (score range, 16-385, with higher scores indicating higher levels of stress).ResultsWhite women had the lowest mean CPS scores (white: 161.7±50.4; Hispanic: 171.2±51.7; black: 172.5±54.9; Asian: 170.8±50.6; Poverall<0.01). Mean CPS scores remained higher in Hispanic, black, and Asian women than in white women after adjustment for age, socioeconomic status (income and education), and psychological status (depression and anxiety) ( P<0.01 for each). Mean ICH scores varied by race/ethnicity ( P<0.01) and were significantly lower in black women and higher in Asian women compared with white women (β-coefficient [95% CI]: Hispanics, -0.02 [-0.13 to -0.09]; blacks, -0.34 [-0.43 to -0.25]; Asians, 0.34 [0.24 to 0.45]); control for socioeconomic status and CPS did not change these results. Interactions between CPS and race/ethnicity in ICH models were not significant.ConclusionsBoth CPS and ICH varied by race/ethnicity. ICH remained worse in blacks and better in Asians compared with whites, despite taking into account socioeconomic factors and CPS.
| S-EPMC6478505 | biostudies-literature
Project description:BackgroundNon-alcoholic fatty liver disease (NAFLD) is rapidly becoming a global health problem. Cardiovascular diseases (CVD) are the most common cause of mortality in NAFLD patients. NAFLD and CVD share several common risk factors including obesity, insulin resistance, and type 2 diabetes (T2D). Atherogenic dyslipidemia, characterized by plasma hypertriglyceridemia, increased small dense low-density lipoprotein (LDL) particles, and decreased high-density lipoprotein cholesterol (HDL-C) levels, is often observed in NAFLD patients.Scope of reviewIn this review, we highlight recent epidemiological studies evaluating the link between NAFLD and CVD risk. We further focus on recent mechanistic insights into the links between NAFLD and altered lipoprotein metabolism. We also discuss current therapeutic strategies for NAFLD and their potential impact on NAFLD-associated CVD risk.Major conclusionsAlterations in hepatic lipid and lipoprotein metabolism are major contributing factors to the increased CVD risk in NAFLD patients, and many promising NASH therapies in development also improve dyslipidemia in clinical trials.
| S-EPMC7600388 | biostudies-literature
Project description:Epidemiological studies indicate that elevated alkaline phosphatase activity is associated with increased cardiovascular disease risk. Other epidemiological data demonstrate that mothers giving multiple childbirths (multipara) are also at increased risk of developing late-onset cardiovascular disease. We hypothesized that these two associations stem from a common cause, the insufficient plasma level of the ectopic mineralization inhibitor inorganic pyrophosphate, which is a substrate of alkaline phosphatase. As alkaline phosphatase activity is elevated in pregnancy, we hypothesized that pyrophosphate concentrations decrease gestationally, potentially leading to increased maternal vascular calcification and cardiovascular disease risk in multipara. We investigated plasma pyrophosphate kinetics pre- and postpartum in sheep and at term in humans and demonstrated its shortage in pregnancy, mirroring alkaline phosphatase activity. Next, we tested whether multiparity is associated with increased vascular calcification in pseudoxanthoma elasticum patients, characterized by low intrinsic plasma pyrophosphate levels. We demonstrated that these patients had increased vascular calcification when they give birth multiple times. We propose that transient shortages of pyrophosphate during repeated pregnancies might contribute to vascular calcification and multiparity-associated cardiovascular disease risk threatening hundreds of millions of healthy women worldwide. Future trials are needed to assess if gestational pyrophosphate supplementation might be a suitable prophylactic treatment to mitigate maternal cardiovascular disease risk in multiparous women.
| S-EPMC7755719 | biostudies-literature
Project description:Internalizing mental health issues are a significant developmental and clinical concern during adolescence, but rarely identified as a problem among school staff. Using data from the National Longitudinal Study of Adolescent Health, this study examined the associations between adolescent emotional distress, school connectedness, and educational achievement by exploring potential mechanistic and interactive roles of perceived school connectedness on the emotion-education association. Emotional distress was negatively associated with adolescents' perceptions of belonging to school, which, in turn, may negatively influence educational achievement. School connectedness also had both additive and multiplicative interaction effects on the emotion-education relationship. Results support previous evidence of school connectedness as a protective factor for adolescents with internalizing mental health concerns, although much of the work to date has focused on externalizing problems. This study informs our understanding of how, why, and for whom emotional problems influence educational outcomes in light of social support in the school context.
| S-EPMC5609502 | biostudies-literature
Project description:Lafora disease is a rare, fatal form of progressive myoclonus epilepsy characterized by continuous neurodegeneration with epileptic seizures, characterized by the intracellular accumulation of aberrant polyglucosan granules called Lafora bodies. Several works have provided numerous evidence of molecular and cellular alterations in neural tissue from experimental mouse models deficient in either laforin or malin, two proteins related to the disease. Oxidative stress, alterations in proteostasis, and deregulation of inflammatory signals are some of the molecular alterations underlying this condition in both KO animal models. Lafora bodies appear early in the animal's life, but many of the aforementioned molecular aberrant processes and the consequent neurological symptoms ensue only as animals age. Here, using small RNA-seq and quantitative PCR on brain extracts from laforin and malin KO male mice of different ages, we show that two different microRNA species, miR-155 and miR-146a, are overexpressed in an age-dependent manner. We also observed altered expression of putative target genes for each of the microRNAs studied in brain extracts. These results open the path for a detailed dissection of the molecular consequences of laforin and malin deficiency in brain tissue, as well as the potential role of miR-155 and miR-146a as specific biomarkers of disease progression in LD.
| S-EPMC9865572 | biostudies-literature
Project description:The income-achievement gap is a significant and stubborn problem in the United States, which has been exacerbated by the Covid-19 pandemic. In this article, we link two emerging literatures that have historically been disparate: the neurobiology of poverty as a form of early life stress, and research on educational policies with the potential to reduce SES-based disparities in academic achievement. In doing so, we (1) integrate the literature on poverty-related mechanisms that contribute to early life stress, alter neurobiology, and lead to educational inequities, and (2) based on this research, highlight policies and practices at the school/classroom level and broader structural level that have the potential to address the problem of inequity in our educational systems. We emphasize that educational inequity is a systemic issue, and its resolution will require coordination of local, state, and national policies.
| S-EPMC10662171 | biostudies-literature
Project description:BackgroundPeriodontitis (PD) and cardiovascular diseases (CVD) rank among the most prevalent pathologies worldwide, and their correlation has been a subject of prolonged investigation. Numerous studies suggest shared etiological factors; however, a definitive causal connection remains unestablished. The objective of this study was to employ bibliometric and visual analyses in order to comprehensively examine the overarching characteristics, focal areas of research, and prospective trends pertaining to the PD-CVD relationship.MethodsWe sourced articles, reviews, and online publications on PD- and CVD- research from the Web of Science Core Collection (WoSCC) spanning from January 1, 1993, to May 15, 2023. A triad of analytical tools (R-Bibliometrix, VOSviewer 1.6.19, and CiteSpace 6.2.R3) were utilized to facilitate collaboration network analysis, co-citation analysis, co-occurrence analysis, and citation burst detection.ResultsOut of the 1,116 publications that fulfilled the eligibility criteria in the WoSCC database, the comprehensive characteristics analysis divulged a sustained growth trend in publication frequency. In the cluster analysis of reference co-citation and keyword co-occurrence, prominent themes such as "periodontitis", "cardiovascular diseases", "inflammation", "Porphyromonas gingivalis", and "atherosclerosis" consistently emerged. Contemporary topics such as "peri-implantitis," "COVID-19", "cardiovascular risk factors," and "endocarditis" were pinpointed as burgeoning research hotspots.ConclusionBased on this bibliometric study, in the field of association studies between PD and CVD, the etiologic mechanisms of both diseases have been intensively studied in the last three decades. Periodontal pathogens might serve as potential initiating factors linking PD and CVD. Inflammation may constitute a significant etiological factor shared by both diseases. Several emerging topics, such as COVID-19 and peri-implantitis, exhibit promising potential. This exhaustive overview casts light on pivotal research arenas, augmenting the field's understanding and stimulating further scholarly investigations.
| S-EPMC10512184 | biostudies-literature