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Published on: September 15, 2017
The effect of homocysteine reduction by B-vitamin supplementation on inflammatory markers
Anita C T M Peeters1, Benien E van Aken, Henk J Blom
1Department of Endocrinology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.
Insights
High homocysteine levels are linked to vascular disease, but this study found no evidence of increased inflammation markers. Vitamin supplementation reduced homocysteine but did not affect inflammatory markers, suggesting vascular inflammation is not the primary mechanism.
Area of Science:
- Biochemistry
- Cardiovascular Medicine
- Inflammation Research
Background:
- Hyperhomocysteinemia is epidemiologically linked to vascular disease.
- The underlying pathophysiology remains unclear, with a hypothesis suggesting homocysteine induces endothelial inflammation via cytokines.
- This study investigated the relationship between homocysteine and specific inflammatory markers.
Purpose of the Study:
- To determine if plasma concentrations of interleukin-6 (IL-6), interleukin-8 (IL-8), C-reactive protein (CRP), and monocyte chemoattractant protein-1 (MCP-1) are elevated with higher homocysteine levels.
- To assess if reducing homocysteine through vitamin supplementation impacts these inflammatory markers.
Main Methods:
- Measured plasma homocysteine, IL-6, IL-8, CRP, and MCP-1 in 230 volunteers.
- Administered multivitamin supplementation (folic acid, B6, B12) for 8 weeks.
- Analyzed changes in these markers before and after supplementation.
Main Results:
- Baseline homocysteine showed a weak association with IL-8 only, not IL-6, CRP, or MCP-1.
- Vitamin supplementation significantly decreased homocysteine levels.
- No significant changes were observed in IL-6, IL-8, CRP, or MCP-1 levels post-supplementation.
Conclusions:
- Homocysteine levels were only weakly correlated with IL-8 at baseline.
- Vitamin supplementation effectively lowered homocysteine but did not alter measured inflammatory markers.
- The study does not support the hypothesis that hyperhomocysteinemia increases arteriosclerotic or thrombotic risk via vascular inflammation.
Background:
Hyperhomocysteinemia has been associated with vascular disease in many epidemiological studies. However, the pathophysiology is unclear. It is postulated that increased levels of homocysteine induce an inflammatory response in endothelial cells, mediated by pro-inflammatory cytokines and chemokines. The aim of this study was to investigate whether plasma concentrations of interleukin-6, interleukin-8, C-reactive protein, and monocyte chemoattractant protein-1 are increased with higher plasma homocysteine concentrations and whether decreasing homocysteine by vitamin supplementation decreases the concentration of these markers.
Methods:
Plasma homocysteine, interleukin-6, interleukin-8, C-reactive protein, and monocyte chemoattractant protein-1 concentrations were measured in 230 volunteers before and after 8 weeks of multivitamin supplementation (folic acid, B(6), and B(12)).
Results:
At baseline, plasma homocysteine concentration was weakly associated with interleukin-8, but not with interleukin-6, C-reactive protein or monocyte chemoattractant protein-1. Vitamin supplementation resulted in a significant decrease in homocysteine concentration, but no effect on interleukin-6, interleukin-8, C-reactive protein or monocyte chemoattractant protein-1 was observed.
Conclusions:
At baseline homocysteine was only weakly correlated with interleukin-8, but not with interleukin-6, C-reactive protein or monocyte chemoattractant protein-1. Vitamin supplementation affected homocysteine concentration, but not cytokine levels. The hypothesis that hyperhomocysteinemia increases arteriosclerotic or thrombotic risk through vascular inflammation was not supported by this study.
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