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Editorial |
1 From The Department of Nutrition and the Graduate Program in Nutritional Sciences, The Pennsylvania State University, University Park.
2 Address correspondence to J Beard, Department of Nutrition, 125 Henderson Building, The Penn State University, University Park, PA 16802. E-mail: its{at}psu.edu.
See corresponding article on page638.
The question of iron accumulation during aging has interested nutritionists for many years. Some have argued that the iron needs of the elderly are lower than those of younger people (1). Both a smaller lean body mass and a decreased loss of iron through menstruation contribute to a lower iron requirement. In 1959, Finch (2) found that urinary losses of iron in 57–84-y-old men and 59–77-y-old women were significantly lower than those in a younger cohort of subjects. Similar values were reported more than a decade later in another study of iron metabolism in the elderly (3). In contrast, there are clear variations in the intake of factors that affect iron absorption in the elderly. These include the amount and forms of dietary iron and the amounts of inhibitors and enhancers of iron absorption (4). The assessment of iron status in an aging population is a challenge because chronic diseases are observed frequently in this group (5). Chronic inflammatory or neoplastic disease interferes with the ability of diagnosticians to easily interpret plasma iron, transferrin saturation, and ferritin as indexes of iron status (6). The anemia of chronic disease is characterized by lower plasma iron and elevated plasma ferritin. A significant challenge to nutritional gerontologists who are interested in iron metabolism has been to separate the effect of disease from the effect of aging on iron-status indicators. This question has risen to a new level of importance in the past decade with the emergence of the concept that iron accumulation is a risk factor for several disease processes.
The study by Fleming et al (7) used one approach to tackle these questions. These investigators used the Framingham Heart Study population to evaluate the effect of chronic disease on iron-status indexes and, secondarily, to determine whether chronic disease was associated with elevated iron stores. The data set used for these analyses is not a nationally representative sample. Rather, it was derived from the cycle 20 cohort collected some 50 y after the original enrollment of participants in 1948–1950. Although the authors' approach regarding the effect of disease on iron-status measurements is not unique, it is powerful and useful. These researchers created disease category criteria that allowed them to examine clusters of individuals who were likely to have or not have inflammatory or disease processes that would lead to alterations in iron-status indexes. The normal battery of iron-status indicators and commonly accepted cutoff points were used to estimate the prevalence of low, normal, and elevated iron status. In this cohort of 
1000 subjects, the prevalence of iron deficiency was only 1%, whereas 12–28% of the sample was identified as having elevated iron stores. The effect of a disease process on iron status was apparent. There was a significantly greater risk of anemia and high iron stores in this group than in the nondiseased group. This observation adds to the already substantial literature reporting that chronic diseases, especially those with an inflammatory component, negatively affect iron metabolism. The authors ask the key question, "to what extent are population prevalence estimates of iron status affected by chronic disease in the elderly?" In this somewhat selective study population, the conclusion is: hardly at all. It remains to be seen whether one could reach the same conclusion from an analysis of data from the third National Health and Nutrition Examination Survey.
The prevalence of high iron stores (ferritin > 300 µg/L) was nearly 14% in men and 6% in women, in agreement with other reports cited by Fleming et al (8). The estimates nearly doubled, however, when a cutoff of 200 µg ferritin/L was used instead of 300 µg/L. Is there reason to be concerned that more than one-quarter of elderly men have elevated iron concentrations? How long have these men had these elevated concentrations of storage iron? What caused the elevations? This research group addressed the last question in a previous study (4) in which they noted that >15% of this elderly cohort took iron supplements and that their dietary factors likely contributed to the accumulation of iron stores. Tight regulation of iron absorption via body iron stores is believed to prevent the excess accumulation of dietary iron (9). Failure to correlate higher iron intakes with higher iron stores suggests causes other than dietary factors of elevated iron stores in an aging population.
Hereditary hemochromatosis results in iron overload–associated pathology when plasma ferritin is much higher than the cutoff values used to define abnormal in the current study (10). Are people with the higher iron concentrations at greater risk of heart attacks, neoplastic diseases, or neuropathologies? Although Salonen et al (11) noted a significantly higher risk of myocardial infarction in individuals with concentrations higher than this cutoff, several other studies did not find an association between cardiovascular disease and this ferritin concentration (12). The fact that a consistent relation between pathology and elevated ferritin was not found does not mean that such a relation does not exist in some populations and in some age groups. Genetic mutations leading to an accumulation of iron do lead to an increased risk of pathology (10). The current report by Fleming et al does not address the relation of increased risk of illness if the individuals are classified as having elevated iron stores. The recommendations regarding continued use of iron-containing supplements and iron-rich foods by the elderly depend on the strength of this relation.
In conclusion, the accurate assessment of iron status in free-living populations with chronic diseases is difficult. The ability of investigators to use markers of disease processes, gene markers for hereditary hemochromatosis, and multiple indexes of iron status will make it possible to assess iron status in elderly populations with confidence.
REFERENCES
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