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Nutr Metab Cardiovasc Dis. 2014 Jul;24(7):760-6. doi: 10.1016/j.numecd.2014.01.008. Epub 2014 Jan 31.

B-vitamin levels and genetics of hyperhomocysteinemia are not associated with arterial stiffness.

Author information

1
Erasmus Medical Center, Department of Internal Medicine, Section of Geriatrics, P.O. Box 2040, 3000 CA Rotterdam, the Netherlands. Electronic address: s.c.vandijk@erasmusmc.nl.
2
Erasmus Medical Center, Department of Internal Medicine, Section of Geriatrics, P.O. Box 2040, 3000 CA Rotterdam, the Netherlands.
3
VU University Medical Center, EMGO Institute for Health and Care Research, Department of Epidemiology and Biostatistics, Amsterdam, the Netherlands.
4
Wageningen University, Division of Human Nutrition, Wageningen, the Netherlands.
5
Erasmus Medical Center, Department of Internal Medicine, Section of Geriatrics, P.O. Box 2040, 3000 CA Rotterdam, the Netherlands; Netherlands Consortium of Healthy Ageing, Rotterdam, the Netherlands; Netherlands Consortium of Healthy Ageing, Leiden, the Netherlands.
6
VU University Medical Center, Department of Clinical Chemistry, Metabolic Unit, Amsterdam, the Netherlands.
7
VU University Medical Center, Department of Internal Medicine, Amsterdam, the Netherlands.
8
VU University Medical Center, Department of Internal Medicine, Amsterdam, the Netherlands; Institute for Cardiovascular Research ICaR-VU, Amsterdam, the Netherlands.
9
Erasmus Medical Center, Department of Internal Medicine, Section of Geriatrics, P.O. Box 2040, 3000 CA Rotterdam, the Netherlands; Academic Medical Center, Department of Internal Medicine, Section of Geriatrics, Amsterdam, the Netherlands.

Abstract

BACKGROUND AND AIMS:

Hyperhomocysteinemia is associated with arterial stiffness, but underlying pathophysiological mechanisms explaining this association are to be revealed. This study was aimed to explore two potential pathways concerning the one-carbon metabolism. A potential causal effect of homocysteine was explored using a genetic risk score reflecting an individual's risk of having a long-term elevated plasma homocysteine level and also associations with B-vitamin levels were investigated.

METHODS AND RESULTS:

Baseline cross-sectional data of the B-PROOF study were used. In the cardiovascular subgroup (n = 567, 56% male, age 72.6 ± 5.6 yrs) pulse wave velocity (PWV) was determined using applanation tonometry. Plasma concentrations of vitamin B12, folate, methylmalonic acid (MMA) and holo transcobalamin (holoTC) were assessed and the genetic risk score was based on 13 SNPs being associated with elevated plasma homocysteine. Associations were examined using multivariable linear regression analysis. B-vitamin levels were not associated with PWV. The genetic risk score was also not associated with PWV. However, the homocysteine-gene interaction was significant (p < 0.001) in the association of the genetic risk score and PWV. Participants with the lowest genetic risk of having long-term elevated homocysteine levels, but with higher measured homocysteine levels, had the highest PWV levels.

CONCLUSION:

Homocysteine is unlikely to be causally related to arterial stiffness, because there was no association with genetic variants causing hyperhomocysteinemia, whereas non-genetically determined hyperhomocysteinemia was associated with arterial stiffness. Moreover, the association between homocysteine and arterial stiffness was not mediated by B-vitamins. Possibly, high plasma homocysteine levels reflect an unidentified factor, that causes increased arterial stiffness.

KEYWORDS:

Arterial stiffness; B-vitamin status; Genetics; Homocysteine; Pathophysiology

PMID:
24656138
DOI:
10.1016/j.numecd.2014.01.008
[Indexed for MEDLINE]

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