Current Data on Dietary Sodium, Arterial Structure and Function in Humans: A Systematic Review.
arterial function
arterial hypertrophy
arterial plaques
arterial remodeling
arterial stiffness
arterial structure
arteriosclerosis
atheromatosis
dietary sodium
Journal
Nutrients
ISSN: 2072-6643
Titre abrégé: Nutrients
Pays: Switzerland
ID NLM: 101521595
Informations de publication
Date de publication:
18 Dec 2019
18 Dec 2019
Historique:
received:
23
10
2019
revised:
03
12
2019
accepted:
09
12
2019
entrez:
22
12
2019
pubmed:
22
12
2019
medline:
28
8
2020
Statut:
epublish
Résumé
Subclinical arterial damage (SAD) (arteriosclerosis, arterial remodeling and atheromatosis) pre-exists decades before cardiovascular disease (CVD) onset. Worldwide, sodium (Na) intake is almost double international recommendations and has been linked with CVD and death, although in a J-shape manner. Studies regarding dietary Na and major types of SAD may provide pathophysiological insight into the association between Na and CVD. Systematic review of data derived from observational and interventional studies in humans, investigating the association between dietary Na with (i) atheromatosis (arterial plaques); (ii) arteriosclerosis (various biomarkers of arterial stiffness); (iii) arterial remodeling (intima-media thickening and arterial lumen diameters). Applying the PRISMA criteria, the PubMed and Scopus databases were used. 36 studies were included: 27 examining arteriosclerosis, four arteriosclerosis and arterial remodeling, three arterial remodeling, and two arterial remodeling and atheromatosis. (i) Although several studies exist, the evidence does not clearly support a clinically meaningful and direct (independent from blood pressure) effect of Na on arterial wall stiffening; (ii) data regarding the association of dietary Na with arterial remodeling are limited, mostly suggesting a positive trend between dietary Na and arterial hypertrophy but still inconclusive; (iii) as regards to atheromatosis, data are scarce and the available studies present high heterogeneity. Further state-of-the-art interventional studies must address the remaining controversies.
Sections du résumé
BACKGROUND
BACKGROUND
Subclinical arterial damage (SAD) (arteriosclerosis, arterial remodeling and atheromatosis) pre-exists decades before cardiovascular disease (CVD) onset. Worldwide, sodium (Na) intake is almost double international recommendations and has been linked with CVD and death, although in a J-shape manner. Studies regarding dietary Na and major types of SAD may provide pathophysiological insight into the association between Na and CVD.
OBJECTIVES
OBJECTIVE
Systematic review of data derived from observational and interventional studies in humans, investigating the association between dietary Na with (i) atheromatosis (arterial plaques); (ii) arteriosclerosis (various biomarkers of arterial stiffness); (iii) arterial remodeling (intima-media thickening and arterial lumen diameters).
DATA SOURCES
METHODS
Applying the PRISMA criteria, the PubMed and Scopus databases were used.
RESULTS
RESULTS
36 studies were included: 27 examining arteriosclerosis, four arteriosclerosis and arterial remodeling, three arterial remodeling, and two arterial remodeling and atheromatosis.
CONCLUSIONS
CONCLUSIONS
(i) Although several studies exist, the evidence does not clearly support a clinically meaningful and direct (independent from blood pressure) effect of Na on arterial wall stiffening; (ii) data regarding the association of dietary Na with arterial remodeling are limited, mostly suggesting a positive trend between dietary Na and arterial hypertrophy but still inconclusive; (iii) as regards to atheromatosis, data are scarce and the available studies present high heterogeneity. Further state-of-the-art interventional studies must address the remaining controversies.
Identifiants
pubmed: 31861381
pii: nu12010005
doi: 10.3390/nu12010005
pmc: PMC7019233
pii:
doi:
Substances chimiques
Sodium, Dietary
0
Types de publication
Journal Article
Systematic Review
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Hellenic Foundation for Research and Innovation
ID : 186619/Ι2
Déclaration de conflit d'intérêts
The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results.
Références
Am J Clin Nutr. 2009 Feb;89(2):485-90
pubmed: 19106240
BMJ. 2009 Nov 24;339:b4567
pubmed: 19934192
J Hypertens. 2018 Apr;36(4):734-743
pubmed: 29084085
Eur J Nutr. 2019 Jun;58(4):1659-1671
pubmed: 29761317
Am J Hypertens. 2014 Sep;27(9):1129-37
pubmed: 24651634
Atherosclerosis. 2012 Dec;225(2):497-503
pubmed: 23084712
Hypertension. 1991 Jun;17(6 Pt 2):989-96
pubmed: 2045181
J Am Soc Hypertens. 2017 Oct;11(10):627-634
pubmed: 28830669
J Am Coll Cardiol. 2001 Aug;38(2):506-13
pubmed: 11499745
Eur J Nutr. 2018 Oct;57(7):2649-2656
pubmed: 30032457
Am J Hypertens. 2003 Dec;16(12):1074-8
pubmed: 14643585
Hypertension. 2016 Sep;68(3):e7-e46
pubmed: 27443572
Lancet. 2016 Jul 30;388(10043):465-75
pubmed: 27216139
Eur Heart J. 2012 Jan;33(2):183-90
pubmed: 21666250
J Hum Hypertens. 2015 Oct;29(10):592-8
pubmed: 25673113
Exp Gerontol. 2018 Jul 15;108:256-261
pubmed: 29747013
Nutr Res Pract. 2016 Jun;10(3):288-93
pubmed: 27247725
Blood Press Monit. 2016 Oct;21(5):301-6
pubmed: 27495189
Curr Opin Nephrol Hypertens. 2015 Jan;24(1):8-13
pubmed: 25415615
Am J Physiol Heart Circ Physiol. 2016 Jun 1;310(11):H1827-33
pubmed: 27059075
Rev Port Cardiol. 2006 Sep;25(9):801-17
pubmed: 17100171
Am J Hypertens. 2011 Jan;24(1):70-6
pubmed: 20508622
Circulation. 2007 Jan 30;115(4):459-67
pubmed: 17242284
Curr Opin Nephrol Hypertens. 2013 Jan;22(1):65-76
pubmed: 23197156
J Am Soc Nephrol. 2013 Dec;24(12):2096-103
pubmed: 24204003
J Hum Hypertens. 2012 Dec;26(12):701-5
pubmed: 22089729
Hypertension. 2009 Sep;54(3):475-81
pubmed: 19620517
BMJ Open. 2013 Dec 23;3(12):e003733
pubmed: 24366578
Nephrology (Carlton). 2012 Mar;17(3):249-56
pubmed: 22171802
Hypertension. 2004 Jul;44(1):35-41
pubmed: 15173128
Atherosclerosis. 2015 Aug;241(2):507-32
pubmed: 26117398
Am J Clin Nutr. 2010 Mar;91(3):557-64
pubmed: 20107199
Hypertension. 2009 Sep;54(3):482-8
pubmed: 19620514
BMJ. 2009 Jul 21;339:b2535
pubmed: 19622551
Ren Fail. 2015;37(8):1285-92
pubmed: 26333718
Am J Hypertens. 2015 Aug;28(8):1010-6
pubmed: 25534867
Arteriosclerosis. 1986 Mar-Apr;6(2):166-9
pubmed: 3954670
Int J Hypertens. 2018 Dec 16;2018:7620563
pubmed: 30643643
J Renin Angiotensin Aldosterone Syst. 2014 Dec;15(4):498-504
pubmed: 24833624
N Engl J Med. 2014 Nov 27;371(22):2138-9
pubmed: 25436267
N Engl J Med. 2014 Aug 14;371(7):612-23
pubmed: 25119607
Hypertension. 2016 Jun;67(6):1189-95
pubmed: 27160199
J Clin Hypertens (Greenwich). 2018 Nov;20(11):1587-1594
pubmed: 30295011
Hypertens Res. 2017 Aug;40(8):746-751
pubmed: 28250414
Atherosclerosis. 2014 Mar;233(1):32-8
pubmed: 24529119
Braz J Med Biol Res. 2015 Jan;48(1):83-90
pubmed: 25493387
J Nutr. 2011 May;141(5):877-82
pubmed: 21430243
BMJ. 2013 Apr 03;346:f1326
pubmed: 23558163
N Engl J Med. 2014 Nov 27;371(22):2135-6
pubmed: 25427120
Br J Nutr. 2015 Sep 28;114(6):936-42
pubmed: 26243465
J Hypertens. 1992 Apr;10(4):355-60
pubmed: 1316401
JAMA. 2011 Nov 23;306(20):2229-38
pubmed: 22110105
Am J Hypertens. 2012 Jul;25(7):727-34
pubmed: 22627176
Nutrients. 2016 Oct 01;8(10):
pubmed: 27706075