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Homocyst(e)ine and stroke

Karen L Furie1, Peter J Kelly

  • 1Stroke Service, Massachusetts General Hospital, Harvard Medical School, Boston, 02114, USA.

Seminars in Neurology
|February 16, 2006
PubMed

Insights

Elevated homocysteine levels significantly increase ischemic stroke risk. While genetic factors and vitamin deficiencies play a role, current research is exploring the benefits of vitamin supplementation for stroke prevention.

Area of Science:

  • Neurology
  • Cardiovascular Medicine
  • Nutritional Science

Background:

  • Elevated homocysteine (hyperhomocysteinemia) is a significant risk factor for ischemic stroke, increasing risk by two- to threefold.
  • Homocysteine levels are influenced by genetic factors regulating metabolic enzymes and by essential vitamin cofactors: folate, vitamin B6, and vitamin B12.
  • Genetic variations in key enzymes like methylenetetrahydrofolate reductase (MTHFR) and cystathionine beta-synthase (CBS) are linked to increased ischemic stroke risk.

Purpose of the Study:

  • To review the association between homocysteine levels and ischemic stroke risk.
  • To discuss the role of genetic and nutritional factors in hyperhomocysteinemia.
  • To evaluate the impact of interventions like folate fortification and vitamin supplementation on stroke risk.

Main Methods:

  • Literature review of studies investigating homocysteine metabolism, genetic associations, and vitamin supplementation trials related to stroke.
  • Analysis of the impact of public health initiatives such as folate fortification on population homocysteine levels.
  • Examination of clinical trial data, including the Vitamin Intervention in Stroke Prevention (VIST) study.

Main Results:

  • Homocysteine elevation is a confirmed risk factor for ischemic stroke through various mechanisms beyond large-artery atherosclerosis.
  • Genetic variations in homocysteine metabolism pathways contribute to stroke risk.
  • Folate fortification has demonstrably lowered homocysteine levels in the U.S. population.
  • The VIST study did not show a significant reduction in recurrent stroke or myocardial infarction with high-dose vitamin supplementation over 2 years.

Conclusions:

  • Hyperhomocysteinemia remains a critical factor in ischemic stroke etiology.
  • Screening for vitamin B12 deficiency is crucial, and awareness of potential vitamin B6 deficiency in specific populations is necessary.
  • While initial supplementation trials were inconclusive, ongoing research continues to explore the therapeutic potential of vitamin supplementation in stroke prevention.

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