Research Papers: Gerotarget (Focus on Aging):

Age-independent rise of inflammatory scores may contribute to accelerated aging in multi-morbidity

Maria Stepanova _, Edgar Rodriguez, Aybike Birerdinc and Ancha Baranova

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Oncotarget. 2015; 6:1414-1421. https://doi.org/10.18632/oncotarget.2725

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Maria Stepanova1,2, Edgar Rodriguez1, Aybike Birerdinc1,2, Ancha Baranova1,2,3,4

1Center for the Study of Chronic Metabolic Diseases, School of System Biology, George Mason University, Fairfax, VA, USA

2Betty and Guy Beatty Center for Integrated Research, Inova Health Systems, Falls Church, VA, USA

3Research Center for Medical Genetics RAMS, Moscow, Russian Federation

4Atlas Biomed Group, Moscow, Russia

Correspondence to:

Ancha Baranova, e-mail: [email protected]

Keywords: multi-morbidity, C-reactive protein, systemic inflammation, Glasgow Prognostic Score, aging

Received: October 21, 2014     Accepted: November 10, 2014     Published: February 10, 2015


Aging is associated with an increase in a chronic, low-grade inflammation. This phenomenon, termed “inflammaging” is also a risk factor for both morbidity and mortality in the elderly. Frequent co-occurrence of chronic diseases, known as multi-morbidity, may be explained by interconnected pathophysiology of these conditions, most of which depend on its inflammatory component. Here we present an analysis of the U.S. National Health and Nutrition Examination Survey data collected between 1999 and 2008, for the presence, and the number, of chronic diseases along with HDL-cholesterol, C-reactive protein, white blood cell count, lymphocyte percent, monocyte percent, segmented neutrophils percent, eosinophils percent, basophils percent, and glycohemoglobin levels. Importantly, even after adjustment for age and BMI, many inflammatory markers continued to be associated to multi-morbidity. C-reactive protein (CRP) levels and Glasgow Prognostic Score (GPS) were most dramatically increased in parallel with an accumulation of chronic diseases, and may be utilized as multi-morbidity predictors. These observations point at background inflammation as direct, age-independent contributor to an accumulation of the disease burden. Our findings also suggest a possibility that systemic inflammation associated with chronic diseases may explain accelerated aging phenomenon previously observed among the patients with heavy disease burden.

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