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Updated: Jul 16, 2026

Modifying Levels of Maternal Dietary Folic Acid or Choline to Study the Impact of Deficiencies on Offspring Health Outcomes
Published on: June 28, 2024
[Hyperhomocysteinemia in pediatric age and nutritional aspects of folates: an early cardiovascular risk factor]
Giuseppe Caramia1, Romualdo Belardinelli
1Azienda Ospedaliera Materno-Infantile "G. Salesi", Ancona.
Insights
Elevated homocysteine levels increase cardiovascular and atherosclerosis risk. Further research is needed to confirm if lowering homocysteine with supplements reduces cardiovascular events, especially in high-risk patients.
Area of Science:
- Cardiovascular Science
- Biochemistry
- Medical Research
Context:
- Growing evidence links elevated plasma homocysteine to increased risk of atherosclerosis and cardiovascular ischemic events.
- The precise mechanisms of homocysteine's pro-atherogenic effects and the impact of its reduction on cardiovascular risk remain under investigation.
- Experimental studies suggest multiple mechanisms contribute to homocysteine's pro-atherogenic effects, including endothelial dysfunction.
Purpose:
- To review the current understanding of homocysteine's role in cardiovascular disease.
- To explore the mechanisms by which homocysteine may exert its pro-atherogenic effects.
- To assess the potential impact of homocysteine reduction on cardiovascular risk.
Summary:
- Elevated homocysteine is associated with atherosclerosis and ischemic events, with endothelial dysfunction being a key implicated mechanism.
- Exercise training can lower homocysteine and improve endothelial function, but clinical outcome benefits are not yet proven.
- Larger studies are required to establish whether reducing homocysteine levels with folate and B vitamin supplementation decreases ischemic event incidence, particularly in patients with existing coronary artery disease or ischemic encephalopathy.
Impact:
- Highlights the need for further clinical trials to validate homocysteine-lowering therapies for cardiovascular risk reduction.
- Emphasizes the importance of understanding the mechanistic links between homocysteine, endothelial function, and atherogenesis.
- Provides a concise overview for researchers and clinicians regarding the current state of knowledge on homocysteine and cardiovascular health.
Abstract:
During the last decade, scientific evidence is mounting that elevated plasma levels of homocysteine are associated with an increased risk of atherosclerosis and cardiovascular ischemic events. Despite this evidence, however, there are still concerns about the mechanisms(s) by which homocysteine exerts its pro-atherogenic effect, and it is unclear whether the decreased plasma levels of homocysteine through diet or drugs may be paralleled by a reduction in cardiovascular risk. Experimental studies have shown that many possible mechanisms are implicated in the pro-atherogenic effect of homocysteine. Endothelial function is altered in subjects with hyperhomocysteinemia, and endothelial dysfunction is correlated with plasma levels of homocysteine. Exercise training reduces plasma levels of homocysteine and improves endothelial function, however without evidence of a better outcome. Larger studies are needed in order to demonstrate that the reduction of plasma levels of homocysteine by oral supplementation with folates and vitamins B6 and B12 translates into a decreased incidence of ischemic events, in particular in patients with documented coronary artery disease and ischemic encephalopathy.
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