TABLE 7-1 Relevant Data Identified for Vitamin E (alpha-tocopherol, alpha-tocotrienol)


Type of Injury/Insult

Type of Study and Subjects



Tier 1: Clinical trials

Razmkon et al., 2010

TBI (Glasgow Coma Scale scores of 8 or less and radiologic diagnoses of diffuse axonal injury)

Multi-center, randomized, double-blind, placebo-controlled trial,

Postinjury, vitamin E (intravenous at 400 IU/day for 7 days)

The vitamin E group had significantly better Glasgow Outcome Scale scores at discharge and at 2 and 6 months of follow up (p=0.04).

Vitamin E significantly decreased in-hospital mortality following TBI by 8% (p=0.01).

Postinjury, vitamin C (500 mg/day for seven days or 10 g on the day of admission and 4 days later), or placebo

na=100 (83 male)

No adverse effects were observed.

Schürks et al., 2010


Metaanalysis of 9 randomized, controlled trials

Vitamin E supplementation

Vitamin E supplementation did not reduce the risk for total stroke, but it was associated with increased risk for hemorrhagic stroke (pooled RRb=1.22; 95% CIc: 1.00, 1.48, p=0.045). And vitamin E was associated with decreased risk for ischemic stroke (pooled RR=0.90; 95% CI: 0.82, 0.99, p < 0.02).

There was no evidence of heterogeneity (I2d=0.0%) or small study effect for either variable.

Data on adverse bleeding from vitamin E treatment is unclear: fatal bleeding among two individuals in the treatment group was reported in one trial, while another trial reported non-fatal bleedings among both the treatment and placebo groups. A third trial found no overall increased rate of bleeding, but observed a small significantly increased risk for epistaxis among the treatment group.

Milman et al., 2008

Cardiovascular events (i.e, myocardial infarction [MI], stroke, or cardiovascular death) in patients with type 2 diabetes mellitus (DM)

Randomized, prospective, double-blind trial

Vitamin E (400 IU/day) or placebo

Analysis of composite cardiovascular disease events (CVD death, non-fatal MI, and stroke) show that subjects in vitamin E group had significantly fewer events than control group (2.2% in vitamin E vs. 4.7% in placebo; HRe=0.47, 95% CI: 0.27–0.82; p=0.01 by Log-Rank). This significance can largely be attributed to vitamin E treatment effect on MI (1.0% in vitamin E vs. 2.4% in placebo; p=0.04).

n=1,434 DM individuals aged 55 years or older with Hp 2-2 genotype

Perceived side effects caused 11 individuals (5 in vitamin E group and 6 in placebo group) to discontinue their participation in the study.

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