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Letters to the Editor |
Albion Laboratories, Inc 101 North Main Street Clearfield, UT 84015 E-mail: albionlabs{at}aol.com
Dear Sir:
The title and conclusions of the article, "Bioavailability of iron glycine as a fortificant in infant foods," by Fox et al (1) are not supported by the data presented. Their data show that the absorption of iron from a glycine chelate is as well regulated by the body as is iron absorption from FeSO4. Their data do not address bioavailability because regulation of iron absorption when there are sufficient iron stores in the body is the predominant feature of the research.
The first paragraph of the Results section states that the initial mean hemoglobin concentration of the subjects in study 1 was 114.0 ± 1.4 g/L and in study 2 was 118.0 ± 1.9 g/L. Rather than being iron deficient, the children involved in this test were iron sufficient from the beginning. Data from a 7-mo study involving 185 children with a broad range of iron status indicated that no significant change in hemoglobin status can be expected when initial hemoglobin concentrations are >110 g/L (2).
The claim of degradation of the chelate in the presence of phytates is hypothetical because no attempts were made to determine the molecular natures of the compounds being absorbed. The findings of other experiments indicate different conclusions. Isotope data of Bovell-Benjamin et al (unpublished observations, 1998) confirmed that iron glycinate does not mix with the inorganic iron pool, indicating that the iron glycinate must be absorbed differently than is FeSO4. If the iron glycinate were being broken apart during digestion, there would be no differentiation of the iron pool.
In their discussion, Fox et al cited other investigations in support of their hypotheses. These citations are brief and do not represent all of the conclusions of the authors being cited. The researchers cited by Fox et al (3) actually stated that in their study of weanling rats, mean hemoglobin concentrations increased significantly (P < 0.001) with iron glycinate but not with FeSO4. Liver concentrations were also higher with iron glycinate, but the increase was not significant because the animals were growing rapidly. The authors concluded, "Ferrous sulfate is often used as a standard with which to compare the bioavailability of different dietary sources of Fe, and it is unusual to find a compound that has Fe of higher bioavailability, but clearly, the Fe glycine complex was more readily utilized than ferrous sulfate" (3).
The fact that Fox et al included large amounts of ascorbic acid (0.83 mg ascorbic acid/mg Fe) with the FeSO4 doses, but not with the iron glycinate chelate, suggests that they were actually intending to compare the absorption of ferrous ascorbate (and not FeSO4) with that of iron glycinate. Fox et al cited the results of Olivares et al (4) as further proof of the lower bioavailability of the chelate than of FeSO4. Olivares et al also claimed that the absorption of iron glycinate is no different from that of ferrous ascorbate. Olivares et al reported that FeSO4 absorption in milk is only 4–5% compared with 15.4% (when normalized) for iron glycinate. They also reported that FeSO4 absorption can double when ascorbic acid is added. Olivares et al concluded, "Iron bis-glycine has a bioavailability comparable to that of FeSO4, plus ascorbic acid in milk." When ascorbic acid was not present with FeSO4, they found that iron glycinate had a bioavailability 2–2.5-fold higher than that of FeSO4.
Finally, Fox et al conjecture that if their hypothesis that iron glycinate disassociates in a manner similar to that of FeSO4 is correct, then iron glycinate will have the same poor organoleptic properties as FeSO4. On the contrary, Olivares et al (4) state that iron glycinate (as the amino acid chelate) has low prooxidant properties and is stable when exposed to ambient air and temperatures. They further state that iron glycinate has a shelf life of >6 mo when mixed with milk and stored at room temperature.
In conclusion, it can be deduced from the data presented by Fox et al that absorption of iron from chelated iron glycinate is as well regulated by the body as is iron from FeSO4 (or ferrous ascorbate) in situations in which there is not a great metabolic need for iron uptake, as indicated by a hemoglobin concentration >110 g/L. No data from a comparison of the bioavailability of iron glycinate and FeSO4 (or ferrous ascorbate) are presented by Fox et al because sufficient iron stores existed at the onset of the study, ensuring that iron uptake from all sources would be tightly regulated by normal physiology to prevent the overabsorption of iron and its subsequent toxicity.
REFERENCES
Institute of Food Research Norwich Research Park Colney, Norwich NR4 7UA United Kingdom E-mail: tom.fox{at}bbsrc.ac.uk
Dear Sir:
The results of our study entirely support Ashmead's proposal that absorption from iron glycine chelate is regulated to the same extent as that from FeSO4 (or ferrous ascorbate). However, we disagree with his statement that we were not measuring bioavailability.
The conclusions drawn from our study are based on the measurement of hemoglobin incorporation of an oral dose of stable isotope–labeled FeSO4 and stable isotope–labeled iron glycine chelate. This technique assumes that 90% of the absorbed iron is used for hemoglobin (1) and is a valid method for comparing the absorption and bioavailability of 2 different chemical forms of iron within the same individual (when 2 different stable isotopes are used to label the compounds). The use of subjects who are iron deficient would increase the sensitivity of iron absorption measurements. Although the infants in our study had hemoglobin concentrations >110 g/L, their neonatal iron stores would have been depleted by 9 mo of age and thus they would have had a high iron requirement due to rapid growth and, hence, a high efficiency of iron absorption. However, even in the absence of iron deficiency, the method used in our study would still be a valid technique to compare the bioavailability of different chemical forms of iron. As for Ashmead's comments on our earlier work, it is difficult to extrapolate iron absorption data from animal studies to humans because rats are known to have a higher fractional absorption of iron and are less sensitive to differences in iron bioavailability than are humans.
Many studies investigating the bioavailability or absorption of iron use a reference dose to normalize results between individuals. FeSO4 in combination with ascorbic acid is the most commonly used reference dose and many researchers have used molar ratios of ascorbate to iron >1:1 [Cook et al (2), 2:1; Bezwoda et al (3), 10:1; and Hallberg et al (4), 10:1]. We used a molar ratio of 1:1 [iron as Fe2(SO4)3] and most of the ascorbate involved in the reduction of ferric iron to ferrous iron would have been oxidized to dehydroascorbic acid or dioxogulonic acid. The resulting solution would therefore be mainly FeSO4 and not ferrous ascorbate.
Our findings confirm that the iron glycine chelate is indeed a highly bioavailable form of iron because hemoglobin incorporation was comparable with that of freshly prepared FeSO4 in the presence of ascorbic acid. Ashmead's comment that our reference to the work of Olivares et al (5) was further proof of the iron glycine chelate having a lower bioavailability is incorrect; we cited this reference in support of our observation that the absorption of iron glycine chelate and FeSO4 are similarly affected by dietary modifiers. There was no mention made in our paper that the iron glycine chelate had a lower bioavailability than FeSO4 or ferrous ascorbate. The absorption of iron from the glycine chelate was reduced by the presence of a known inhibitor of iron absorption, phytic acid. From this observation we concluded that some or all of the iron from the chelate had dissociated at some point and mixed with the intraluminal pool of ingested nonheme iron, where some of it was rendered unavailable through ligand formation with phytic acid.
Olivares et al (5), who used the same chelate we did (prepared by Albion Laboratories), also found that the absorption of iron glycine chelate was reduced by inhibitors found in milk and that a known enhancer (ascorbic acid) increased iron absorption from the chelate. These observations further substantiate our conclusion that iron is dissociated from the chelate in the gastrointestinal tract, where it can participate in chemical reactions with other dietary constituents. Exactly where, when, and how much of this dissociation takes place is open to further investigation. What can be postulated is that if the poor organoleptic properties associated with FeSO4 under certain food conditions are not observed with the chelate, then dissociation of the iron glycine complex must be occurring within the gastrointestinal tract after ingestion. Ashmead cites unpublished work that apparently refutes our findings. Clearly, we cannot comment on this at present.
If absorption of the iron glycine chelate is being regulated by the body, as proposed by Ashmead in his letter, we must ask by what mechanism? If the iron chelate is absorbed intact by an amino acid transport mechanism, regulation would be governed by the presence of glycine and not iron. Thus, there would be no regulation of iron absorption per se. The other possibility is that the chelate dissociates and iron enters the common nonheme pool, the absorption of which is controlled by host-related factors such as iron stores, which is the mechanism indicated by our data and that of Olivares et al (5).
REFERENCES
This article has been cited by other articles:
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  D. I. Mazariegos, F. Pizarro, M. Olivares, M. T. Nunez, and M. Arredondo The Mechanisms for Regulating Absorption of Fe Bis-Glycine Chelate and Fe-Ascorbate in Caco-2 Cells Are Similar J. Nutr., February 1, 2004; 134(2): 395 - 398. [Abstract] [Full Text] [PDF]
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