<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="6.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Brunner, E J</style></author><author><style face="normal" font="default" size="100%">Hemingway, H</style></author><author><style face="normal" font="default" size="100%">Walker, B R</style></author><author><style face="normal" font="default" size="100%">Page, M</style></author><author><style face="normal" font="default" size="100%">Clarke, P</style></author><author><style face="normal" font="default" size="100%">Juneja, M</style></author><author><style face="normal" font="default" size="100%">Shipley, M J</style></author><author><style face="normal" font="default" size="100%">Kumari, M</style></author><author><style face="normal" font="default" size="100%">Andrew, R</style></author><author><style face="normal" font="default" size="100%">Seckl, J R</style></author><author><style face="normal" font="default" size="100%">Papadopoulos, A</style></author><author><style face="normal" font="default" size="100%">Checkley, S</style></author><author><style face="normal" font="default" size="100%">Rumley, A</style></author><author><style face="normal" font="default" size="100%">Lowe, G D O</style></author><author><style face="normal" font="default" size="100%">Stansfeld, S A</style></author><author><style face="normal" font="default" size="100%">Marmot, M G</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Adrenocortical, autonomic, and inflammatory causes of the metabolic syndrome: nested case-control study.</style></title><secondary-title><style face="normal" font="default" size="100%">Circulation</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2002</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2002 Nov 19</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">106</style></volume><pages><style face="normal" font="default" size="100%">2659-65</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">{BACKGROUND: The causes of metabolic syndrome (MS), which may be a precursor of coronary disease, are uncertain. We hypothesize that disturbances in neuroendocrine and cardiac autonomic activity (CAA) contribute to development of MS. We examine reversibility and the power of psychosocial and behavioral factors to explain the neuroendocrine adaptations that accompany MS. METHODS AND RESULTS: This was a double-blind case-control study of working men aged 45 to 63 years drawn from the Whitehall II cohort. MS cases (n=30) were compared with healthy controls (n=153). Cortisol secretion, sensitivity, and 24-hour cortisol metabolite and catecholamine output were measured over 2 days. CAA was obtained from power spectral analysis of heart rate variability (HRV) recordings. Twenty-four-hour cortisol metabolite and normetanephrine (3-methoxynorepinephrine) outputs were higher among cases than controls (+ 0.49, +0.45 SD, respectively). HRV and total power were lower among cases (both -0.72 SD). Serum interleukin-6, plasma C-reactive protein, and viscosity were higher among cases (+0.89, +0.51, and +0.72 SD). Lower HRV was associated with higher normetanephrine output (r=-0.19; P=0.03). Among former cases (MS 5 years previously</style></abstract></record></records></xml>