scholarly journals Daytime napping, sleep duration and serum C reactive protein: a population-based cohort study

BMJ Open ◽  
2014 ◽  
Vol 4 (11) ◽  
pp. e006071 ◽  
Author(s):  
Yue Leng ◽  
Sara Ahmadi-Abhari ◽  
Nick W J Wainwright ◽  
Francesco P Cappuccio ◽  
Paul G Surtees ◽  
...  
2011 ◽  
Vol 17 (4) ◽  
pp. 627-632 ◽  
Author(s):  
K.O. Gradel ◽  
R.W. Thomsen ◽  
S. Lundbye-Christensen ◽  
H. Nielsen ◽  
H.C. SchØnheyder

2005 ◽  
Vol 26 (17) ◽  
pp. 1783-1789 ◽  
Author(s):  
David E. Laaksonen ◽  
Leo Niskanen ◽  
Kristiina Nyyssönen ◽  
Kari Punnonen ◽  
Tomi-Pekka Tuomainen ◽  
...  

2015 ◽  
Vol 51 (11) ◽  
pp. 1365-1370 ◽  
Author(s):  
Perfenia Paul Pletnikoff ◽  
Jari A. Laukkanen ◽  
Tomi-Pekka Tuomainen ◽  
Jussi Kauhanen ◽  
Rainer Rauramaa ◽  
...  

2009 ◽  
Vol 17 (2) ◽  
pp. 168-173 ◽  
Author(s):  
G. Engström ◽  
M. Gerhardsson de Verdier ◽  
J. Rollof ◽  
P.M. Nilsson ◽  
L.S. Lohmander

2017 ◽  
Vol 32 (6) ◽  
pp. e2632 ◽  
Author(s):  
Henriette Thisted Horsdal ◽  
Theresa Wimberley ◽  
Michael Eriksen Benros ◽  
Christiane Gasse

2019 ◽  
Vol 32 (7-8) ◽  
pp. 892-903 ◽  
Author(s):  
Aniruddha Das

Objectives: Literature suggests C-reactive protein (CRP)—as a marker of low-grade systemic inflammation—may mediate the linkage between chronic stressors and cardiometabolic conditions. Previous population-based reports are based on weak methodologies and may have yielded incorrect inferences. The current study examined linkages of within-person CRP variation with corresponding variation in stressor burdens. Method: Data were from the 2006, 2010, and 2014 waves of the U.S. Health and Retirement Study. Analysis was through unit fixed effects and first-difference estimators. Both gender-combined and gender-specific models were run. Results: In none of the analyses was CRP positively associated with chronic stressors. This was true among both genders, and in models of linear as well as nonlinear change. Results held in a series of separate robustness checks. Discussion: CRP may not mediate the social etiology of degenerative diseases. Population representative evidence of inflammation’s role in these processes remains absent.


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