The major liabilities of Fe lack include defects in psychomotor development
in infants, impaired educational performance in schoolchildren, increased
perinatal morbidity, and impaired work capacity. Few if any of the relevant
investigations have demonstrated these abnormalities in the absence of ana
emia. Consequently, adequate Fe nutrition can be defined as a normal haemog
lobin concentration. On the other hand, optimal Fe nutrition should be rega
rded as sufficient body Fe to avoid any limitation in tissue Fe supply, ter
med Fe-deficient erythropoiesis. A variety of laboratory measurements have
been used to identify this milder form of Fe deficiency, including serum fe
rritin, transferrin saturation, erythrocyte protoporphyrin, mean corpuscula
r volume, and more recently the concentration of the soluble fragment of tr
ansferrin receptor in serum. Recent studies indicate that the serum transfe
rrin receptor is the preferred measurement, because enhanced synthesis of t
he transferrin receptor represent the initial cellular response to a declin
ing Fe supply. Moreover, unlike other methods, it is not affected by chroni
c inflammation or infection which are often confused with Fe deficiency. In
an otherwise normal healthy population the transferrin receptor:ferritin v
alue provides a useful quantitative index of body Fe over a wide spectrum o
f Fe status, ranging from Fe repletion to Fe-deficiency anaemia. It is conc
luded that optimal Fe nutrition is best defined as a normal haemoglobin, se
rum ferritin and transferrin receptor concentration.