Two-hundred and seven obese and 178 nonobese adults were enrolled (). Data from 10 subjects were excluded for reporting implausible energy intake of <600 calories or >3,500 calories per day for women and <800 calories or >4,200 calories per day for men (12
), or for incomplete dietary records. Obese and nonobese subjects did not differ substantially in their demographic characteristics, other than BMI.
Clinical characteristics of obese and nonobese adults with completed 7-day food records and fasting laboratory values (n=384)
Hypoferremia was significantly more prevalent in obese compared to nonobese adults (25.1% [95% confidence interval: 10.1% to 20.6%] vs 14.6% [95% confidence interval: 19.7% to 31.5%]; P
<0.05), and mean serum iron was lower among obese subjects (72.0±61.7 vs 85.3±58.1 µg/dL [12.888±11.0443 vs 15.2687±10.3999 µmol/L]; P
<0.001). Results are in accord with most previous studies (1
). Further, transferrin saturation (20.7%±17.6% vs 23.3%±16.6%; P
=0.012) was lower among obese compared with nonobese subjects (). There was no difference in hemoglobin or ferritin concentrations between obese and nonobese groups.
Mean total daily dietary iron intake, including supplements containing iron, was not significantly different between obese and nonobese subjects (P=0.10). The obese cohort, though, consumed more heme iron (3.6±2.8 vs 2.7±2.6 mg/day; P<0.001) than the nonobese cohort ().
Obese subjects reported consuming less vitamin C (77.2±94.9 vs 91.8±89.5 mg/day; P=0.01) and calcium (766.2±665.0 vs 848.9±627.2 mg/day; P=0.04) than nonobese subjects (), and more animal protein (63.5±34.5 vs 55.7±32.6 g/day; P<0.001) than nonobese subjects. Groups did not differ, however, in mean daily intake of copper, vegetable protein, phytic acid, oxalic acid, zinc, eggs, tea, or coffee ().
Total dietary intake among obese and nonobese adults of factors known to enhance and inhibit heme and nonheme iron absorption.
After accounting for demographic covariates, a multiple linear regression analysis, which included variables known to affect iron absorption, showed that fat mass (β=−.330; P<0.05) remained a significant negative predictor of serum iron concentration. Other than percentage of calories from vegetable protein, which was a negative predictor for serum iron (P=0.004), none of the remaining factors known to affect dietary iron absorption were significant predictors of serum iron in this model.
Although there were small but significant differences between obese and nonobese study participants in consumption of dietary heme iron, vitamin C, and calcium, these differences were not associated with the inverse relationship observed between adiposity and serum iron. In addition, obese subjects reported consuming less vitamin C than nonobese subjects. The enhancing effect of vitamin C on iron absorption is due to both its reducing and chelating properties (15
). An acidic environment in the stomach can solubilize dietary iron and has been shown to be an efficient enhancer of nonheme iron absorption in humans (15
). Vitamin C intake, however, did not predict serum iron in the multiple regression model. Consistent with a lack of clinical impact on serum iron from dietary vitamin C, is a prior study that found addition of 2,000 mg/day of vitamin C to the diet for 2 years did not significantly alter iron stores (16
). Dietary intake of calcium was also lower in obese compared with nonobese subjects. Calcium has been shown to diminish iron absorption, by inhibiting the transfer of heme and nonheme iron into mucosal cells, and by interfering with degradation of phytic acid (8
). Because calcium intake was lower in the obese group, dietary calcium intake could not, however, help explain the hypoferremia of obesity.
One previously proposed cause of hypoferremia among the obese is a deficient iron store due to a greater iron requirement in obese adults because of their larger blood volume. Because obesity is considered a chronic inflammatory state, inflammatory-mediated sequestration of iron in the reticuloendothelial system, with resultant hypoferremia, despite adequate or even increased iron stores could also play a role in the hypoferremia of obesity (17
The health consequences of hypoferremia may have important clinical implications in adults. In one study, presence of hypoferremia was found to impair aerobic adaptation among untrained women (18
). No longitudinal studies have been performed, however, to determine whether hypoferremia precedes development of obesity or is the result of the obese state.
Limitations to this study include the fact that 7-day food records were self-recorded and may not necessarily reflect habitual iron intake. Obese subjects are known to underreport dietary intake to a greater extent compared to lean subjects (19
), which may have affected results. However, if obese subjects underreported iron intake, this would bias the results toward underestimating the available dietary iron and make dietary factors less likely to be an explanation for obesity-related hypoferremia. In addition, other factors that can affect iron absorption, including heat treatment of foods, which denatures the cysteine groups in heme iron, decreasing iron absorption (22
), and use of nonprescription antacids were not accounted for. Finally, menstrual blood flow, which contributes to serum iron concentrations, was not included as a covariate.