scholarly journals Duration of Family Caregiving and Its Effects on Inflammation in the Caregiving Transitions Study

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 322-323
Author(s):  
David Roth

Abstract Sustained caregiving for older adult family members with disabilities can be a chronically stressful experience that may adversely affect the health of caregivers. Systemic inflammation is thought to be one mechanism by which caregiving stress might impact health, but previous studies of inflammation in caregivers have generally found inconsistent or very small effects with questionable clinical significance when comparing caregiving and non-caregiving control samples. The Caregiving Transitions Study (CTS) enrolled 283 family caregivers and 283 carefully-matched controls from an ongoing national epidemiologic study. This population-based sample of caregivers included an unusual subsample of 32 long-term caregivers who had been providing care to the same care recipients for over 9 consecutive years. Analyses of covariance indicated that these 32 long-term caregivers had statistically significant (p < 0.05) elevations on three circulating biomarkers of inflammation – C-reactive protein, Interleukin-6, and D-dimer – compared 1) to their 32 individually-matched non-caregiving controls, and 2) to the 248 caregivers who had been providing care for less than 9 years. Covariates in the analytic models included age, sex, race, and body mass index. Similar effects were observed for caregivers of persons with or without dementia. Polynomial regression models across all caregivers revealed significant curvilinear associations of inflammation with caregiving duration. Inflammation was not markedly elevated throughout the first several years of caregiving but then begin to increase more dramatically at around 10 years of caregiving. These findings suggest that long-term caregiving, in particular, may be associated with specific physical health risks through chronically elevated systemic inflammation.

VASA ◽  
2017 ◽  
Vol 46 (4) ◽  
pp. 291-295 ◽  
Author(s):  
Soumia Taimour ◽  
Moncef Zarrouk ◽  
Jan Holst ◽  
Olle Melander ◽  
Gunar Engström ◽  
...  

Abstract. Background: Biomarkers reflecting diverse pathophysiological pathways may play an important role in the pathogenesis of abdominal aortic aneurysm (aortic diameter ≥30 mm, AAA), levels of many biomarkers are elevated and correlated to aortic diameter among 65-year-old men undergoing ultrasound (US) screening for AAA. Probands and methods: To evaluate potential relationships between biomarkers and aortic dilatation after long-term follow-up, levels of C-reactive protein (CRP), proneurotensin (PNT), copeptin (CPT), lipoprotein-associated phospholipase 2 (Lp-PLA2), cystatin C (Cyst C), midregional proatrial natriuretic peptide (MR-proANP), and midregional proadrenomedullin (MR-proADM) were measured in 117 subjects (114 [97 %] men) aged 47–49 in a prospective population-based cohort study, and related to aortic diameter at US examination of the aorta after 14–19 years of follow-up. Results: Biomarker levels at baseline did not correlate with aortic diameter after 14–19 years of follow up (CRP [r = 0.153], PNT [r = 0.070], CPT [r = –.156], Lp-PLA2 [r = .024], Cyst C [r = –.015], MR-proANP [r = 0.014], MR-proADM [r = –.117]). Adjusting for age and smoking at baseline in a linear regression model did not reveal any significant correlations. Conclusions: Tested biomarker levels at age 47–49 were not associated with aortic diameter at ultrasound examination after 14–19 years of follow-up. If there are relationships between these biomarkers and aortic dilatation, they are not relevant until closer to AAA diagnosis.


Author(s):  
Mona Elbarbary ◽  
Artem Oganesyan ◽  
Trenton Honda ◽  
Geoffrey Morgan ◽  
Yuming Guo ◽  
...  

There is an established association between air pollution and cardiovascular disease (CVD), which is likely to be mediated by systemic inflammation. The present study evaluated links between long-term exposure to ambient air pollution and high-sensitivity C reactive protein (hs-CRP) in an older Chinese adult cohort (n = 7915) enrolled in the World Health Organization (WHO) study on global aging and adult health (SAGE) China Wave 1 in 2008–2010. Multilevel linear and logistic regression models were used to assess the associations of particulate matter (PM) and nitrogen dioxide (NO2) on log-transformed hs-CRP levels and odds ratios of CVD risk derived from CRP levels adjusted for confounders. A satellite-based spatial statistical model was applied to estimate the average community exposure to outdoor air pollutants (PM with an aerodynamic diameter of 10 μm or less (PM10), 2.5 μm or less (PM2.5), and 1 μm or less (PM1) and NO2) for each participant of the study. hs-CRP levels were drawn from dried blood spots of each participant. Each 10 μg/m3 increment in PM10, PM2.5, PM1, and NO2 was associated with 12.8% (95% confidence interval; (CI): 9.1, 16.6), 15.7% (95% CI: 10.9, 20.8), 10.2% (95% CI: 7.3, 13.2), and 11.8% (95% CI: 7.9, 15.8) higher serum levels of hs-CRP, respectively. Our findings suggest that air pollution may be an important factor in increasing systemic inflammation in older Chinese adults.


Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Jun Dai ◽  
Anthony J Acton ◽  
Robert V Considine ◽  
Ruth E Krasnow ◽  
Terry Reed

Introduction: Whole diet evaluated using dietary pattern is associated with systemic inflammation and coronary heart disease (CHD). Systemic inflammation also contributes to CHD risk. Genetic factors explain variations in whole diet, systemic inflammation, and CHD. However, it is unknown whether systemic inflammation is a mechanism linking whole diet to the long-term mortality risk from coronary heart disease independent of genes. Hypothesis: Systemic inflammation measured as plasma interleukin-6 levels medicates the association between whole diet and long-term mortality risk from coronary heart disease independent of genes. Methods: From the National Heart, Lung, and Blood Institute Twin Study, we included 554 white, middle-aged, veteran male twins (105 monozygotic and 109 dizygotic twin pairs; 65 monozygotic and 61 dizygotic unpaired twins). The twins were not on antihypertensive medication and had diastolic blood pressure below 105 mmHg at baseline (1969-1973) and did not have suspected acute inflammation [plasma levels of interleukin-6 (IL-6) above 10 pg/mL or C-reactive protein above 30 mg/L)]. Usual dietary data at baseline were collected through nutritionist-administered dietary history interview. Your-Choice American Heart Diet (YCARD) score was devised to quantitatively evaluate whole diet. Plasma interleukin-6 and C-reactive protein levels were measured with ELISA. Data on vital status and death causes were collected through death certificates until Dec 31, 2010. A frailty survival model was used to estimate various associations: overall (equivalent to the association in the general population), within-pair (independent of genes and environment common to co-twins), and between-pair (indicating influence of the common factors). We controlled for total caloric intake and known CHD risk factors including body mass index and modified Framingham Risk Score. Results: There were 75 CHD deaths during a 41-year follow-up (median follow-up of 34 years). The adjusted overall association between YCARD score and the CHD mortality risk was negative [partial coefficient for a 10-unit increment in the YCARD score: βo (95% confidence interval (CI)): -0.13 (-0.24, -0.02); hazard ratio (95% CI): 0.88 (0.78, 0.98)]. The partial regression coefficient was -0.02 [95% CI (-0.23, 0.19)] for the within-pair effect of YCARD (βw) and -0.12 [95% CI (-0.26, 0)] for the between-pair effect of YCARD (βb) in relation to CHD mortality risk. Additional adjustment for IL-6 led to a 15.4% reduction in the βo, a 100% increment in the βw, and a 16.7% reduction in the βb. Conclusions: Systemic inflammation measured as interleukin-6 mediates the association between whole diet and long-term coronary heart mortality risk, which is largely through genetic and environmental factors shared between co-twins.


2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Wenjie Ma ◽  
Long H. Nguyen ◽  
Mingyang Song ◽  
Dong D. Wang ◽  
Eric A. Franzosa ◽  
...  

Abstract Background A higher intake of dietary fiber is associated with a decreased risk of chronic inflammatory diseases such as cardiovascular disease and inflammatory bowel disease. This may function in part due to abrogation of chronic systemic inflammation induced by factors such as dysbiotic gut communities. Data regarding the detailed influences of long-term and recent intake of differing dietary fiber sources on the human gut microbiome are lacking. Methods In a cohort of 307 generally healthy men, we examined gut microbiomes, profiled by shotgun metagenomic and metatranscriptomic sequencing, and long-term and recent dietary fiber intake in relation to plasma levels of C-reactive protein (CRP), an established biomarker for chronic inflammation. Data were analyzed using multivariate linear mixed models. Results We found that inflammation-associated gut microbial configurations corresponded with higher CRP levels. A greater intake of dietary fiber was associated with shifts in gut microbiome composition, particularly Clostridiales, and their potential for carbohydrate utilization via polysaccharide degradation. This was particularly true for fruit fiber sources (i.e., pectin). Most striking, fiber intake was associated with significantly greater CRP reduction in individuals without substantial Prevotella copri carriage in the gut, whereas those with P. copri carriage maintained stable CRP levels regardless of fiber intake. Conclusions Our findings offer human evidence supporting a fiber-gut microbiota interaction, as well as a potential specific mechanism by which gut-mediated systemic inflammation may be mitigated.


2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 680-681
Author(s):  
Jacqueline Chattopadhyay

Abstract Most Americans prefer to “age-in-place” as long as possible, but to do so often need overlapping resources—one of which is help from “formal” or “informal” caregivers (family and friends). Family and friends often want to provide care for as long as safely possible. However, informal caregiving can pose financial and physical risks to the caregiver that—as many scholars have noted—public policy in the U.S. does relatively little to mitigate. This policy shortfall also hurts care recipients since the risks that informal caregivers face can prematurely curtail their ability to provide care. Why does policy in the U.S. not better support informal caregivers? By synthesizing family caregiving research and political science research that has addressed long-term care, this paper surveys nine factors in the political system that may help answer this question. Four emanate from policy history. Three concern the mass public. Two vary at the policy level.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 269-269
Author(s):  
Eric Jutkowitz ◽  
Joseph Gaugler ◽  
Zachary Baker

Abstract Due to multiple long-term sociodemographic and health trends contributing to the impending family care gap, there likely is no single policy or intervention that could increase the number of family caregivers in the U.S. to the levels required to fill such a gap. However, the amount of time that a family caregiver spends providing assistance is potentially mutable. Given the pressing concerns of the family care gap, identifying interventions or approaches that could reduce existing caregiving time is of considerable importance. This presentation provides the results of a systematic review of published research to identify the effects of interventions on the amount of time family caregivers spend on their caregiving tasks. Pharmaceutical approaches directed to care recipients, technology interventions, case management, multicomponent interventions, and care settings all appeared to reduce caregiving time. Improved operationalization, study design, and similar factors will help guide future intervention research to reduce caregiving time.


2014 ◽  
Vol 62 (9) ◽  
pp. 1683-1691 ◽  
Author(s):  
Margarete A. Wichmann ◽  
Karen J. Cruickshanks ◽  
Cynthia M. Carlsson ◽  
Rick Chappell ◽  
Mary E. Fischer ◽  
...  

Author(s):  
Eline Aas ◽  
Emily Burger ◽  
Kine Pedersen

The objective of medical screening is to prevent future disease (secondary prevention) or to improve prognosis by detecting the disease at an earlier stage (early detection). This involves examination of individuals with no symptoms of disease. Introducing a screening program is resource demanding, therefore stakeholders emphasize the need for comprehensive evaluation, where costs and health outcomes are reasonably balanced, prior to population-based implementation. Economic evaluation of population-based screening programs involves quantifying health benefits (e.g., life-years gained) and monetary costs of all relevant screening strategies. The alternative strategies can vary by starting- and stopping-age, frequency of the screening and follow-up regimens after a positive test result. Following evaluation of all strategies, the efficiency frontier displays the efficient strategies and the country-specific cost-effectiveness threshold is used to determine the optimal, i.e., most cost-effective, screening strategy. Similar to other preventive interventions, the costs of screening are immediate, while the health benefits accumulate after several years. Hence, the effect of discounting can be substantial when estimating the net present value (NPV) of each strategy. Reporting both discounting and undiscounted results is recommended. In addition, intermediate outcome measures, such as number of positive tests, cases detected, and events prevented, can be valuable supplemental outcomes to report. Estimating the cost-effectiveness of alternative screening strategies is often based on decision-analytic models, synthesizing evidence from clinical trials, literature, guidelines, and registries. Decision-analytic modeling can include evidence from trials with intermediate or surrogate endpoints and extrapolate to long-term endpoints, such as incidence and mortality, by means of sophisticated calibration methods. Furthermore, decision-analytic models are unique, as a large number of screening alternatives can be evaluated simultaneously, which is not feasible in a randomized controlled trial (RCT). Still, evaluation of screening based on RCT data are valuable as both costs and health benefits are measured for the same individual, enabling more advanced analysis of the interaction of costs and health benefits. Evaluation of screening involves multiple stakeholders and other considerations besides cost-effectiveness, such as distributional concerns, severity of the disease, and capacity influence decision-making. Analysis of harm-benefit trade-offs is a useful tool to supplement cost-effectiveness analyses. Decision-analytic models are often based on 100% participation, which is rarely the case in practice. If those participating are different from those not choosing to participate, with regard to, for instance, risk of the disease or condition, this would result in selection bias, and the result in practice could deviate from the results based on 100% participation. The development of new diagnostics or preventive interventions requires re-evaluation of the cost-effectiveness of screening. For example, if treatment of a disease becomes more efficient, screening becomes less cost-effective. Similarly, the introduction of vaccines (e.g., HPV-vaccination for cervical cancer) may influence the cost-effectiveness of screening. With access to individual level data from registries, there is an opportunity to better represent heterogeneity and long-term consequences of screening on health behavior in the analysis.


Helicobacter ◽  
2009 ◽  
Vol 14 (5) ◽  
pp. 460-465 ◽  
Author(s):  
Louisa Jackson ◽  
John Britton ◽  
Sarah A. Lewis ◽  
Tricia M. McKeever ◽  
John Atherton ◽  
...  

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