A pro-inflammatory diet is associated with increased odds of frailty after 12-year follow-up in a cohort of adults

Author(s):  
Courtney L Millar ◽  
Alyssa B Dufour ◽  
Nitin Shivappa ◽  
Daniel Habtemariam ◽  
Joanne M Murabito ◽  
...  

Abstract Background Frailty occurs in 10-15% of community-living older adults and inflammation is a key determinant of frailty. Though diet is a modulator of inflammation, there are few prospective studies elucidating the role of diet-associated inflammation on frailty. Objective To determine whether a pro-inflammatory diet was associated with increased odds of frailty in adults from the Framingham Heart Study (FHS). Design and Methods This study is nested in a prospective cohort that included individuals without frailty. Diet was assessed in 1998-2001 using a valid food frequency questionnaire (FFQ) and frailty was measured in 2011-2014. FFQ-derived energy-adjusted dietary inflammatory index (E-DII®) scores were computed, with higher E-DII scores indicating a more pro-inflammatory diet. Frailty was defined as fulfilling ≥3 of 5 Fried Phenotype criteria. Information on potential mediators, serum interleukin-6 and C-reactive protein was obtained in 1998-2001. Logistic regression estimated odds ratios (OR) and 95% confidence intervals (95% CI) for E-DII (as continuous and in quartiles) and frailty onset adjusting for relevant confounders. Results Of 1,701 individuals without frailty at baseline (mean age = 58 years, SD = 8, range: 33–81; 55% female), 224 developed frailty (13% incidence) over ∼12 years. Mean E-DII score was -1.95 (SD = 2.20; range: -6.71 to +5.40). After adjusting for relevant confounders, a one-unit higher E-DII score was associated with 16% increased odds of developing frailty (95% CI = 1.07, 1.25). In categorical analyses, participants in the highest (pro-inflammatory) vs. lowest quartile of E-DII had >2-fold increased odds of frailty (ORquartile4vs.1 = 2.22, 95% CI = 1.37, 3.60, Ptrend<0.01). Interleukin-6 and C-reactive protein were not major contributors in the pathway. Conclusions In this cohort of middle-aged and older adults, a pro-inflammatory diet was associated with increased odds of frailty over ∼12 years of follow-up. Trials designed to increase consumption of anti-inflammatory foods for frailty prevention are warranted. Clinical registry number and website: Not applicable

2016 ◽  
Vol 4 (6) ◽  
pp. 1125-1134 ◽  
Author(s):  
Tasnime N. Akbaraly ◽  
Clarisse Kerleau ◽  
Marilyn Wyart ◽  
Nathalie Chevallier ◽  
Louise Ndiaye ◽  
...  

There is a growing interest in understanding the role of inflammation in the diet–depression relationship. The present study examined whether the Dietary Inflammatory Index (DII; a measure of the inflammatory potential of individuals’ diets) is associated with recurrent depressive symptoms (DepS) (Center for Epidemiologic Studies Depression Scale score > 16 or taking antidepressants both at baseline and follow-up) assessed over 5 years in middle-aged men ( n = 3,178) and women ( n = 1,068) from the Whitehall II Study. For each increment of 1 SD of DII score, odds of recurrent DepS increased by 66% (95% confidence interval [CI] = [1.30, 2.12]) in women, whereas no significant association between DII and recurrent DepS was observed in men (odds ratio [OR] = 1.12; 95% CI = [0.92, 1.36]). This association was little attenuated after adjustment for confounders and after taking into account levels of interleukin-6 and C-reactive protein. In conclusion, there is an association between proinflammatory diet and recurrent DepS in women that seems to not be driven by circulating inflammatory markers.


Angiology ◽  
2010 ◽  
Vol 62 (4) ◽  
pp. 310-316 ◽  
Author(s):  
Stavroula N. Psychari ◽  
Dionyssios Chatzopoulos ◽  
Efstathios K. Iliodromitis ◽  
Thomas S. Apostolou ◽  
Dimitrios T. Kremastinos

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Lise Lund Håheim ◽  
Kjersti S. Rønningen ◽  
Morten Enersen ◽  
Ingar Olsen

The predictive role of high-sensitivity C-reactive protein (hs-CRP), number of tooth extractions, and oral infections for mortality in people with and without diabetes is unclear. This prospective cohort study is a 12 1/2-year follow-up of the Oslo II study, a health survey in 2000. In all, 12,764 men were invited. Health information was retrieved from 6434 elderly men through questionnaire information, serum measurements, and anthropometric and blood pressure measurements. Diabetes was reported by 425 men. Distinct differences were observed in baseline characteristics in individuals with and without diabetes. In the diabetes group, age and hs-CRP were statistically significant whereas in the nondiabetes group, age, hs-CRP, number of tooth extractions, tooth extractions for infections and oral infections combined, nonfasting glucose, systolic blood pressure, total cholesterol, regular alcohol drinking, daily smoking, and level of education were independent risk factors. The number of tooth extractions <5 was inversely related whereas more extractions increased the risk. Multivariate analyses showed that hs-CRP was a significant predictor in persons with diabetes and tooth extractions and oral infections combined; the number of teeth extracted and hs-CRP were for persons without diabetes. Infection and inflammation were associated with mortality in individuals both with and without diabetes.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
W Magon ◽  
J Stepniewski ◽  
K Jonas ◽  
M Waligora ◽  
P Podolec ◽  
...  

Abstract Introduction Pulmonary endarterectomy leads to a decrease in systemic inflammation and improvement in endothelial function in patients with chronic thromboembolic pulmonary hypertension (CTEPH). Balloon pulmonary angioplasty (BPA) improves pulmonary hemodynamics in patients with inoperable CTEPH. Aim To assess changes in systemic inflammation and endothelial dysfunction after a single BPA session and after completion of the treatment. Methods We enrolled consecutive, inoperable CTEPH patients who underwent BPA. Interleukin 6, 10 (IL-6, IL-10), and C-reactive protein (hsCRP) constituted markers of systemic inflammation. Endothelin-1 (ET-1) served as a marker of endothelial dysfunction. Serum concentration of selected markers was assessed in every patient before, 24 hours after the first BPA session and 6 months after completion of the BPA treatment. Age- and sex-matched healthy subjects served as a control group. Results We recruited 20 patients with inoperable CTEPH (6 males [30%]), aged 67 [61–74] years in New York Heart Association class III (n=19 [95%]) and II (n=1 [5%]). BPA treatment was completed with a median of 5 [2–8] BPA sessions per patient. Before starting the treatment CTEPH patients, as compared to controls (n=10), had raised serum level of IL-6 (3.82 [2.75 - 6.03] vs. 2.64 [0.88 - 4.75] pg/ml; p=0.04), hsCRP (2.47 [0.93 - 4.27] vs. 1.23 [0.48–3.21] ng/ml; p=0.02) and ET-1 (2.68 [2.24 - 3.64] vs. 1.47 [1.4 - 1.82] pg/ml; p=0.004). There was no difference in IL-10 level. 24 hours after a BPA session we observed an increased level of IL-6, IL-10 and hsCRP. (Tab.) 6 months after completion of the BPA treatment there was a reduced level of IL-6, hsCRP and ET-1 (Tab.) Table 1. Changes (Δ) in serum concentration of analyzed markers 24 hours after a single BPA session and at 6-months assessment after completion of the BPA treatment (n=20) Initial Δ at 24 hours after single BPA p Δ at 6-months follow-up p ET-1 [pg/ml] 2.68 [2.24; 3.64] −0.2 [−0.5; 0.23] 0.21 −0.47 [−0.96; 0.05] 0.004 IL-6 [pg/ml] 3.82 [2.75; 6.03] 3.67 [1.41; 7.16] 0.008 −0.82 [−3.11; 0.54] 0.04 IL-10 [pg/ml] 0.53 [0.44; 0.58] 0.32 [0.21; 0.87] 0.006 −0.11 [−0.33; 0.14] 0.94 hsCRP [ng/ml] 2.47 [0.93; 4.27] 5.4 [3.96; 10.59] 0.008 −0.36 [−0.94; 0.16] 0.02 ET-1, endothelin 1; hsCRP, C-reactive protein; IL-6, interleukin 6; IL-10, interleukin 10. Conclusions Patients with inoperable CTEPH, as compared to healthy controls, exhibit an increased systemic inflammation and endothelial dysfunction, which both improve after completion of the BPA treatment. At short-term follow-up after single BPA session there is an increase in systemic inflammatory response.


2018 ◽  
Vol 10 ◽  
pp. 204062231880684 ◽  
Author(s):  
Elliot M. Friedman ◽  
Daniel K. Mroczek ◽  
Sharon L. Christ

Background: Using longitudinal data from the Survey of Mid-Life Development in the United States, this study examined the role of systemic inflammation in mediating the link between multimorbidity and increases in and onset of functional limitations over a 17–19 year follow-up period. Methods: Participants completed questionnaire assessments of chronic conditions and functional limitations. Interleukin-6, C-reactive protein, and fibrinogen were assayed in serum. Structural equation models were used to predict increases in and onset of functional limitations associated with baseline multimorbidity status; mediation by inflammation was also determined. Results: Multimorbidity ( versus 0–1 conditions) predicted more functional limitations and greater odds of onset of limitations over time. Significant indirect effects showed that inflammation partially mediated the link between multimorbidity and changes in, but not onset of, limitations. Discussion: These results show that inflammation, a nonspecific marker of multiple disease conditions, explains in part the degree to which multimorbidity is disabling.


2013 ◽  
Vol 14 (1) ◽  
pp. 24 ◽  
Author(s):  
Renata Ferrari ◽  
Suzana E Tanni ◽  
Laura MO Caram ◽  
Corina Corrêa ◽  
Camila R Corrêa ◽  
...  

1995 ◽  
Vol 310 (1) ◽  
pp. 143-148 ◽  
Author(s):  
D Zhang ◽  
S L Jiang ◽  
D Rzewnicki ◽  
D Samols ◽  
I Kushner

The combination of interleukin 6 (IL-6) and interleukin 1 (IL-1) synergistically induces the human acute-phase reactant, C-reactive protein (CRP) in Hep3B cells. While previous studies have indicated that IL-6 induces transcription of CRP, the mode of action of IL-1 has not been clearly defined. It has been suggested that the effect of IL-1 might be post-transcriptional, exerted through the 5′-untranslated region (5′-UTR). To evaluate the role of IL-1 in CRP gene expression, we studied the effects of interleukin-6 (IL-6) and interleukin-1 beta (IL-1 beta) on both the endogenous CRP gene and on transfected CRP-CAT constructs in Hep3B cells. In kinetic studies of the endogenous CRP gene, IL-1 beta alone had no effect on CRP mRNA levels, but when added to IL-6, synergistically enhanced both CRP mRNA levels and transcription, as determined by Northern-blot analyses and nuclear run-on studies. IL-6 alone and the combination of [IL-1 beta + IL-6] each induced increases in mRNA levels roughly comparable with observed increases in transcription. These findings indicate that the effect of IL-1 beta on CRP expression is exerted largely at the transcriptional level in this system. This conclusion was confirmed by studies in Hep3B cells transiently transfected with CRP-CAT constructs, each containing 157 bp of the CRP 5′-flanking region but differing in the length of the 5′-UTR from 104 bp to 3 bp. All constructs responded in the same way; IL-6, but not IL-1 beta, induced significant chloramphenicol acetyltransferase (CAT) expression which was synergistically enhanced 2- to 3-fold by IL-1 beta. These results indicate that IL-1 beta stimulates transcriptional events in the presence of IL-6 and that the upstream 157 bases of the CRP promoter contain elements capable of both IL-6 induction and the synergistic effect of IL-1 beta on transcription.


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