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Homocysteine as a risk factor for cardiovascular disease: should we (still) worry about?
David Faeh1, Arnaud Chiolero, Fred Paccaud
1University Institute for Social and Preventive Medicine, Lausanne, Switzerland. David.Faeh@unil.ch
Insights
Elevated homocysteine levels are not proven to increase cardiovascular disease (CVD) risk. Current evidence does not support screening or treating hyperhomocysteinaemia to reduce CVD incidence.
Area of Science:
- Cardiology
- Biochemistry
- Public Health
Background:
- Cardiovascular disease (CVD) is a primary global cause of mortality.
- Classical risk factors for CVD include hypertension, dyslipidemia, hyperglycemia, and smoking.
- Elevated plasma homocysteine is a potential, though debated, CVD risk factor.
Purpose of the Study:
- To evaluate the association between elevated homocysteine levels and cardiovascular disease risk.
- To assess the efficacy of lowering homocysteine concentrations in preventing CVD events.
Main Methods:
- Review of population-based studies examining homocysteine and CVD risk.
- Analysis of randomized clinical trials assessing homocysteine-lowering interventions.
Main Results:
- Population studies show limited association between moderate hyperhomocysteinaemia and CVD risk.
- Randomized trials have not conclusively demonstrated that lowering homocysteine reduces CVD incidence.
Conclusions:
- Screening and treating asymptomatic hyperhomocysteinaemia is currently not recommended.
- Focusing on established CVD risk factors remains the priority for cardiovascular health.
Abstract:
Cardiovascular disease (CVD) is the leading cause of death worldwide. CVD is causally related to "classical" risk factors such as elevated blood pressure, cholesterol, or glucose level and smoking. A causal role in the development of CVD is also suggested for numerous other factors, including an elevated plasma homocysteine concentration. Variation of homocysteinaemia is mainly due to genetic mutations and/or vitamin deficiency. The homocysteine concentration can be lowered with folate. Vitamin supplementation has thus been proposed in individuals with hyperhomocysteinaemia in order to reduce their CVD risk. On the other hand, population-based studies show little or no association between moderate hyperhomocysteinaemia and CVD risk. Nor has any randomised clinical trial clearly proven the efficacy of lowering the homocysteine concentration as a means of lowering the incidence of CVD. Hence at present it is inappropriate to recommend screening and treatment of hyperhomocysteinaemia in asymptomatic persons with or without other CVD risk. Until new evidence is available, clinicians should focus on better control of the "classical" risk factors for CVD.
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