Benfotiamine counteracts smoking-induced vascular dysfunction in healthy smokers.
Study Goal
The researchers aimed to determine whether benfotiamine could mitigate smoking-induced endothelial dysfunction in healthy human volunteers, as it had shown protective effects in rats.
Results Summary
Benfotiamine significantly reduced smoking-induced decreases in flow-mediated vasodilation (FMD) by 50% to 25% and prevented increases in sVCAM-1, demonstrating protective vascular effects. The endothelium-independent vasodilation remained unchanged.
Population
20 healthy volunteers (mean age 38 years)
Effective Dosage
1050 mg/day
Duration
3 days
Interactions
None mentioned
| Intervention | Direction | Endpoint | Population | Dosage | Impact | Claim # |
|---|---|---|---|---|---|---|
smoking | decrease | flow-mediated vasodilatation (FMD) of the brachial artery | healthy volunteers | by 50% | acutely induced a decrease | #1 |
benfotiamine treatment | decrease | smoking-induced decrease in flow-mediated vasodilatation (FMD) | healthy volunteers | to 25% | significantly reduced | #2 |
smoking | increase | soluble vascular cell adhesion molecule (sVCAM)-1 | healthy volunteers | - | induced elevation | #3 |
benfotiamine | no change | smoking-induced elevation in soluble vascular cell adhesion molecule (sVCAM)-1 | healthy volunteers | - | prevented | #4 |
smoking | decrease | vascular function | healthy volunteers | - | blunts | #5 |
short-term treatment with benfotiamine | decrease | smoking-induced effects on vascular function | healthy volunteers | - | significantly reduces | #6 |
Background. Smoking induces endothelial dysfunction (ED) mainly by exacerbating oxidative stress (OS) and inflammation. Benfotiamine, a thiamine prodrug with high bioavailability, prevents nicotine-induced vascular dysfunction in rats. It remained unknown whether this effect also occurs in humans. Methods. Therefore, 20 healthy volunteers (mean age: 38 years) were investigated twice, 7-10 days apart in a randomized, cross-over, and investigator-blinded design. Vascular function was assessed by flow-mediated vasodilatation (FMD) of the brachial artery and by measurements of the soluble vascular cell adhesion molecule (sVCAM)-1. Investigations were performed after an overnight fast as well as 20 minutes after one cigarette smoking. On another day, the same procedure was applied following a 3-day oral therapy with benfotiamine (1050 mg/day). Ten patients were randomized to start with smoking alone, and ten started with benfotiamine. Results. Results are expressed as (mean ± SEM). Smoking acutely induced a decrease in FMD by 50% ((∗∗)P < 0.001 versus baseline) an effect significantly reduced by benfotiamine treatment to 25%(∗§) ((∗)P < 0.05 versus baseline, (§)P < 0.05 versus smoking alone). Smoking-induced elevation in sVCAM-1 was also prevented by benfotiamine. The endothelium-independent vasodilatation remained unaltered between days. Conclusion. In healthy volunteers, smoking blunts vascular function mirrored by a decrease in FMD and an increase in sVCAM-1. Short-term treatment with benfotiamine significantly reduces these effects, showing protective vascular properties.