Document Detail

Metabolic syndrome and salt sensitivity of blood pressure in non-diabetic people in China: a dietary intervention study.
MedLine Citation:
PMID:  19223069     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: Since insulin resistance is thought to be the underlying mechanism for metabolic syndrome, affected individuals might be sensitive to a dietary sodium intervention. We aimed to examine the association between metabolic syndrome and salt sensitivity of blood pressure.
METHODS: 1906 Chinese participants without diabetes, aged 16 years or more, were selected to receive a low-sodium diet (51.3 mmol per day) for 7 days followed by a high-sodium diet (307.8 mmol per day) for an additional 7 days. Participants were excluded from the analysis if metabolic risk factor information was missing or if they did not complete their dietary interventions. Blood pressure was measured at baseline and on days 2, 5, 6, and 7 of each intervention. Metabolic syndrome was defined as the presence of three or more of: abdominal obesity, raised blood pressure, high triglyceride concentration, low HDL cholesterol, or high glucose. High salt sensitivity was defined as a decrease in mean arterial blood pressure of more than 5 mm Hg during low-sodium or an increase of more than 5 mm Hg during high-sodium intervention. This study is registered with, number NCT00721721.
FINDINGS: Of the 1881 participants with information regarding metabolic syndrome, 283 had metabolic syndrome. 1853 participants completed the low-sodium diet and 1845 completed the high-sodium diet. Multivariable-adjusted mean changes in blood pressure were significantly greater in participants with metabolic syndrome than in those without on both low-sodium and high-sodium diets (p<0.0001 for all comparisons). Additionally, risk of salt sensitivity rose with increasing numbers of risk factors for metabolic syndrome. Compared with those with no risk factors, participants with four or five had a 3.54-fold increased odds (95% CI 2.05-6.11) of high salt-sensitivity during the low-sodium and a 3.13-fold increased odds (1.80-5.43) of high salt-sensitivity during the high-sodium intervention.
INTERPRETATION: These results suggest that metabolic syndrome enhances blood pressure response to sodium intake. Reduction in sodium intake could be an especially important component in reducing blood pressure in patients with multiple risk factors for metabolic syndrome.
Jing Chen; Dongfeng Gu; Jianfeng Huang; Dabeeru C Rao; Cashell E Jaquish; James E Hixson; Chung-Shiuan Chen; Jichun Chen; Fanghong Lu; Dongsheng Hu; Treva Rice; Tanika N Kelly; L Lee Hamm; Paul K Whelton; Jiang He;
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Publication Detail:
Type:  Clinical Trial; Journal Article; Research Support, N.I.H., Extramural     Date:  2009-02-14
Journal Detail:
Title:  Lancet     Volume:  373     ISSN:  1474-547X     ISO Abbreviation:  Lancet     Publication Date:  2009 Mar 
Date Detail:
Created Date:  2009-03-09     Completed Date:  2009-03-13     Revised Date:  2014-09-24    
Medline Journal Info:
Nlm Unique ID:  2985213R     Medline TA:  Lancet     Country:  England    
Other Details:
Languages:  eng     Pagination:  829-35     Citation Subset:  AIM; IM    
Data Bank Information
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MeSH Terms
Blood Pressure / drug effects*
China / epidemiology
Hypertension / chemically induced,  complications*,  diet therapy
Linear Models
Metabolic Syndrome X / diet therapy,  epidemiology,  etiology*
Middle Aged
Risk Factors
Rural Population
Sodium Chloride, Dietary / administration & dosage,  adverse effects*,  pharmacology
Young Adult
Grant Support
U01 HL072507/HL/NHLBI NIH HHS; U01 HL072507-01/HL/NHLBI NIH HHS; U01 HL072507-02/HL/NHLBI NIH HHS; U01 HL072507-03/HL/NHLBI NIH HHS; U01 HL072507-03S1/HL/NHLBI NIH HHS; U01 HL072507-04/HL/NHLBI NIH HHS; U01 HL072507-04S1/HL/NHLBI NIH HHS; U01 HL072507-05/HL/NHLBI NIH HHS; U01 HL072507-06/HL/NHLBI NIH HHS; U01HL072507/HL/NHLBI NIH HHS
Reg. No./Substance:
0/Sodium Chloride, Dietary
Lydia A Bazzano / ; Mei Hao / ; Paul Muntner / ; Kristi Reynolds / ; Wenjie Yang / ; Qi Zhao / ; Matthew Brown / ; Charles Gu / ; Hongyan Huang / ; Treva Rice / ; Karen Schwander / ; Shiping Wang / ; Lawrence C Hixson / ; Cashell E Jaquish / ; Jie Cao / ; Jingping Chen / ; Zhenhan Du / ; Hongwen Jiang / ; Jianxin Li / ; Xiaohua Liang / ; Depei Liu / ; Xiangfeng Lu / ; Donghua Liu / ; Qunxia Mao / ; Dongling Sun / ; Hongwei Wang / ; Qianqian Wang / ; Xigui Wu / ; Ying Yang / ; Dahai Yu / ; Fanghong Lu / ; Zhendong Liu / ; Shikuan Jin / ; Yingxin Zhao / ; Shangwen Sun / ; Shujian Wang / ; Qengjie Meng / ; Baojin Liu / ; Zhaodong Yang / ; Chuanrui Wei / ; Jixiang Ma / ; Jiyu Zhang / ; Junli Tang / ; Dongsheng Hu / ; Hongwei Wen / ; Chongjian Wang / ; Minghui Shen / ; Jingjing Pan / ; Liming Yang / ; Xu Ji / ; Rongyan Li / ; Haijun Zu / ; Junwei Song / ; Guanji Wu / ; Zhi-Jian Yao / ; Shufeng Chen / ; Dongfeng Gu / ; Hongfan Li / ; Laiyuan Wang / ; Penghua Zhang /
Comment In:
Lancet. 2009 Mar 7;373(9666):792-4   [PMID:  19223068 ]
Lancet. 2009 Jun 6;373(9679):1946; author reply 1946-7   [PMID:  19501741 ]

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