We agree with Mascitelli and colleagues that an interaction between polyphenols from olive oil and iron metabolism could, at least in part, explain the reduction in oxidative lipid damage observed in the Effect of Olive Oil on Oxidative Damage in European Populations (EUROLIVE) study. However, a reduction of iron absorption by polyphenols seems currently to be the most probable mechanism for the interaction. In vivo changes in the iron–ascorbate–oxygen–radical generating system are not yet well defined (1), whereas the inhibition of nonheme iron absorption by dietary polyphenols (that is, from tea) is well known (2). The potential effect of low iron status, such as that induced by blood donation, on LDL oxidation markers is still under debate (3). Although iron depletion by blood donations increases HDL cholesterol levels in humans (4), an experimental study in hypercholesterolemic rats showed that the excess of iron, not its depletion, increased HDL cholesterol levels (5). Mascitelli and colleagues suggest that lowering the availability of reactive iron in vivo either by decreasing stored iron level or by acute iron chelation may improve antioxidant activity and increase HDL cholesterol levels by closely related mechanisms. However, this can neither be supported nor dismissed on the basis of our presented findings. The interaction among polyphenols from olive oil, iron absorption, and oxidative stress merits further investigation.

Regarding the question from Mr. Roufs, the polyphenolic content of the olive oils described is correct, as well as the estimated (0, 4, and 9 mg/d) intake from 25 mL/d of olive oils. The antioxidant activity of hydroxytyrosol, the major olive oil phenolic compound, has been reported to be 5 times greater than that of vitamin E (6). The recommended dietary allowance for vitamin E is 15 mg/d (7). Thus, 9 mg/d of olive oil phenolic compounds does not seem to be a very low dosage to achieve protective effects.