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Published on: August 18, 2015
Is plasma homocysteine a modifiable risk factor for stroke?
1Stroke Unit, Department of Neurology, Royal Perth Hospital, Perth, WA, Australia. gjhankey@cyllene.uwa.edu.au
Insights
High homocysteine levels are linked to stroke risk, but B-vitamin therapy did not significantly reduce stroke in a major trial. More research is needed to confirm if lowering homocysteine prevents stroke.
Area of Science:
- Neurology
- Cardiovascular Medicine
- Nutritional Science
Background:
- Elevated plasma total homocysteine (tHcy) is associated with increased risk of atherothrombotic vascular disease, including ischemic stroke.
- This association is independent of other vascular risk factors and is biologically plausible.
- However, randomized controlled trials have not yet confirmed a causal relationship.
Purpose of the Study:
- To investigate whether lowering plasma total homocysteine (tHcy) levels with B-vitamin therapy reduces the risk of stroke.
- To evaluate the efficacy of B-vitamin supplementation in preventing recurrent ischemic stroke.
Main Methods:
- The Vitamins In Stroke Prevention (VISP) trial involved 3,680 patients with recent ischemic stroke.
- Participants received either B-vitamin therapy or a placebo.
- Plasma tHcy levels were monitored, and stroke events were recorded.
Main Results:
- B-vitamin therapy did not result in a statistically significant reduction in the relative risk of stroke.
- The trial could not reliably exclude a modest but potentially important risk reduction of up to 20% in stroke.
- No significant effect on stroke prevention was observed with homocysteine lowering therapy.
Conclusions:
- There is currently insufficient evidence to establish homocysteine as a modifiable causal risk factor for stroke.
- Routine screening for, or treatment of, elevated tHcy concentrations with folic acid and other vitamins is not recommended for stroke prevention based on current data.
Abstract:
Increased levels of plasma total homocysteine (tHcy) can be caused by genetic mutations, vitamin deficiencies, renal and other diseases, and numerous drugs. Raised tHcy also correlate with increasing age, and are associated with laboratory evidence of atherogenesis (e.g. endothelial dysfunction) and thrombosis, and with epidemiological evidence of an increased risk of atherothrombotic vascular disease, including ischemic stroke. The association between raised tHcy and increased risk of ischemic stroke is independent of other known vascular risk factors and is biologically plausible; however, randomized controlled trials have not revealed a causal relationship. The recently published Vitamins In Stroke Prevention (VISP) trial identified no significant reduction in the relative risk of stroke by lowering tHcy with B-vitamin therapy among 3,680 patients with recent ischemic stroke. It did not, however, reliably exclude a modest but important reduction of up to 20% in relative risk of stroke. Currently, there is insufficient evidence to confirm that homocysteine is a modifiable causal risk factor for stroke, or to recommend routine screening for, or treatment of, raised tHcy concentrations with folic acid and other vitamins, to prevent ischemic stroke.
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