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Department of Human Nutrition University of Otago PO Box 56 Dunedin New Zealand
Dear Sir:
We read with great interest the article by Patterson et al (1) published recently in the Journal. In the conclusion of their abstract, the authors purport to have shown that "in iron-deficient women of childbearing age, a high-iron diet produced smaller increases in SF [serum ferritin] than did iron supplementation but resulted in continued improvements in iron status during a 6-mo follow-up."
Certainly, the iron-deficient women in the diet group were advised to consume a diet high in absorbable iron for the first 12 wk of the study. However, they did not do this. Throughout the 12-wk intervention, there was no significant increase in either heme or nonheme iron intake; nor were there any significant changes in the intakes of vitamin C, meat, alcohol, phytate, calcium, or tea. Furthermore, 6 mo after the end of the formal intervention, bioavailable iron intake was, if anything, lower than at baseline; yet, the diet group’s serum ferritin concentration was slightly (2.1 µg/L) higher at the end of the 12-wk intervention and moderately higher (4.2 µg/L) 6 mo after the intervention. Given that any change in the intake of dietary iron or its absorption modifiers throughout the 9-mo study was negligible, what could account for the increase in serum ferritin concentration?
It is possible that at the end of the 12-wk intervention, women in the diet group chose to take or were prescribed an iron supplement because they knew that they were iron deficient and had not received an iron supplement during the study. It is also possible that because serum ferritin is an acute-phase reactant, the small increase in mean serum ferritin concentration at follow-up resulted from the inclusion of one or more individuals with a serum ferritin concentration that was elevated because of infection.
The absence of a true control group makes it particularly difficult to conclude that the changes in serum ferritin concentration were the result of an improvement in diet. The cornerstone of scientific research into the effects of diet on nutritional status is the randomized controlled trial in which participants are randomly assigned to treatment or control groups. Without an iron-deficient control group, it is difficult to quantify the effects on iron status of factors beyond the investigators’ control. For instance, it is well known that if a group of individuals is identified on the basis of a low biochemical index measured on one occasion, a subsequent measurement is likely, by chance, to be higher (ie, closer to the mean) even in the absence of any intervention effect. The only way to determine whether the increase in serum ferritin concentration in the iron-deficient diet group in this study was real, and not merely the result of a phenomenon such as regression to the mean, would be to compare it to changes in serum ferritin concentration in an iron-deficient control group. Concern about the ethics of not treating women with iron deficiency could have been minimized by recruiting women with low serum ferritin concentrations but normal hemoglobin concentrations.
In conclusion, the article does not show that dietary change is an effective treatment for iron deficiency. Rather, it strongly shows the difficulties that even motivated volunteers experience in attempting to modify their diets to increase iron absorption and suggests that iron supplementation is the most effective treatment for iron deficiency.
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