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Department of Nutrition, University of North Carolina Schools of Public Health and Medicine, Chapel Hill, NC and the * Maternal and Child Nutrition Branch, Division of Nutrition and Physical Activity, Centers for Disease Control and Prevention, Atlanta, GA
1To whom correspondence should be addressed. E-mail: mec0{at}cdc.gov.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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2 of 3 iron status measures (serum ferritin, free erythrocyte protoporphyrin, transferrin saturation). Iron deficiency prevalences for women 0–6, 7–12 and 13–24 mo postpartum were 12.7, 12.4 and 7.8%, respectively, and 6.5% among never-pregnant women. After adjustment for confounding, the risk of iron deficiency among women with a poverty index ratio 
130% who were 0–6, 7–12 and 13–24 mo postpartum was 4.1 (95% confidence interval 2.0, 7.2), 3.1 (1.3, 6.5) and 2.0 (0.8, 4.1) times as great, respectively, as never-pregnant women with a poverty index ratio > 130%, but risk was not elevated for never-pregnant women with a poverty index ratio 130%. Compared with the same referent, the risk of iron deficiency was not meaningfully different for women with a poverty index ratio > 130% who were 0–6, 7–12 or 13–24 mo postpartum. Given that low income postpartum women bear a substantially greater iron deficiency risk than never-pregnant women, more attention should be given to preventing iron deficiency among low income women during and after pregnancy.
KEY WORDS: • iron deficiency • postpartum • women • low income • iron
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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,2
) and impairments in cognitive function (3
,4
). In addition, iron deficiency can progress to iron deficiency anemia, which causes impaired aerobic capacity (1
,5
) and is associated with decreased voluntary activity and lower economic productivity (6
,7
). Among healthy people, pregnant women and infants comprise the populations most vulnerable to iron deficiency because the iron requirements of both groups are so great (8
). Pregnant women require 
1000 mg of total body iron, primarily for supplying oxygen to the fetus and increasing maternal red cell mass (9
). Because these requirements are difficult to meet through an ordinary diet, pregnant women carry a considerable risk of developing iron deficiency, if not supplemented during pregnancy (9
).
In contrast to their experience in pregnancy, during the postpartum period, women are thought to be at lowest risk of iron deficiency (9
). Iron stores are expected to be enhanced after delivery because a large proportion of the 450 mg of iron required for red cell production during pregnancy returns to maternal stores when the red cell mass contracts (9
). In addition, delayed return to menses in the postpartum period significantly reduces iron losses; at the same time, there is a relatively small amount of iron lost through human milk during lactation (9
).
The conventional wisdom notwithstanding, several small studies have shown that iron stores, as measured by serum ferritin, remain at deficient levels through 6 mo postpartum among women not supplemented with iron during pregnancy (10
–12
). Additionally, recent research suggests that postpartum anemia is common among low income women (13
,14
). Consequently, postpartum women may be at high risk of iron deficiency and iron deficiency anemia.
We estimated the prevalence of postpartum iron deficiency, iron deficiency anemia, and anemia in the United States and compared the prevalence of iron deficiency among postpartum women with that of women of childbearing age who have never been pregnant.
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SUBJECTS AND METHODS |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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). Data were collected via household interviews and physical examinations in mobile examination centers. Ethical approval was obtained and written consent was received from all participants (16
). Detailed procedures for data collection and analysis are described elsewhere (15
–17
). For this analysis, we defined the postpartum period by the number of months after the last pregnancy. Although the clinical definition of postpartum is based upon completion of childbirth, NHANES III did not collect data on the length or outcome of the last pregnancy. Thus, our postpartum sample included some women whose pregnancies were terminated early, leading to conservative estimates of the iron deficiency prevalence in the postpartum period. We restricted this analysis to nonpregnant women aged 20–40 y who were 0–24 mo postpartum (n = 811) or who had never been pregnant (n = 693). We excluded 29 women from our sample because they had missing data on 1 of the 4 indicators of iron status, i.e., hemoglobin (Hb), serum ferritin (SF), free erythrocyte protoporphyrin (FEP) and transferrin saturation (TS). We also excluded 208 women who had missing data for ethnicity/race, marital status, poverty index ratio, use of iron and/or vitamin C supplements, or serum vitamin A concentration. Excluded women were more likely to be non-Hispanic African-American (% ± SEM, 15.9 ± 2.2 vs. 9.9 ± 0.9) than were women in the final sample. The prevalence of iron deficiency was slightly higher for excluded women than for those women included (% ± SEM, 8.7 ± 1.1 vs. 6.9 ± 2.2). The final sample consisted of 1267 women; 680 were postpartum and 587 had never been pregnant.
All iron assays were conducted at the NHANES laboratory, National Center for Environmental Health (NCEH), Centers for Disease Control and Prevention (CDC). SF was measured using a Quantimmune Ferritin IRMA kit (Bio-Rad Laboratories, Hercules, CA) (15
). TS was determined by dividing the concentration of serum iron (mmol/L) by total iron binding capacity (mmol/L) as assessed by a modification of the automated AAII-25 colorimetric method (15
). FEP was measured by a modification of the method of Sassa et al. (17
) as follows: protoporphyrin was extracted from EDTA-whole blood and measured fluorometrically using a corrected millimolar absorptivity of 297 L/(mmol · cm). Hb was measured using the Coulter Counter Model S-Plus JR electronic counter (Coulter Electronics, Hialeah, FL) (15
).
Iron deficiency was defined as abnormal results for 2 of 3 tests, i.e., SF <27 pmol/L (<12 µg/L), FEP >1.24 mmol/L and TS <15% for women 20–40 y (18
). We defined iron deficiency anemia as iron deficiency plus anemia with the latter defined as Hb <120 g/L, the cut-off value for 20- to 40-y-old nonpregnant women after adjusting Hb for smoking (19
).
We categorized postpartum women into 3 groups by their months postpartum, i.e., 0 to 6 (n = 220), 7 to 12 (n = 198) and 13 to 24 (n = 262). Gravidity was defined as the number of previous pregnancies. The poverty index ratio was defined as the total household income divided by the poverty threshold in the interview year (20
). We defined low income as a poverty index ratio of 0–130%, the range allowed for participation in the Food Stamp program. All participants were classified as married or unmarried. Daily intakes of iron and vitamin C supplements were based on the average daily dose of supplements reported for the previous month and were categorized on the basis of the recommended dietary allowances for nonpregnant women (21
,22
). Current breast-feeding status was self-reported. Menstruating was based on a self-report of a menstrual period in the past 2 mo.
Serum vitamin A assays were conducted in the NHANES laboratory at the NCEH by isocratic HPLC with detection at three different wavelengths (15
). Because there was a linear relationship between serum vitamin A concentration and log odds of iron deficiency, we treated serum vitamin A as a continuous variable in the modeling.
Statistical analysis.
We weighted all statistical analyses and used SUDAAN (version 7.5, Research Triangle Institute, Research Triangle Park, NC) to account for the complex sample design and to make our estimates representative of the population of interest. We tested for significant differences in prevalence of iron deficiency, anemia and iron deficiency anemia using the 
2 test for homogeneity. We used one-way ANOVA to test for differences in mean values of iron status indicators. Because the distribution of SF was not normal, we calculated geometric means. P < 0.05 was used to indicate statistical significance. We used multiple logistic regression to determine the independent association between postpartum status and iron deficiency. We tested numerous covariates as confounders in this model if they were associated with iron deficiency and postpartum status. Confounding was defined as a change of >10% in a comparison of crude and adjusted beta coefficients for the association between postpartum status and iron deficiency. Ethnicity/race, poverty index ratio, marital status, iron supplement use, vitamin C supplement use and serum vitamin A concentration met our definition of confounding. Even so, because age is an accepted confounder of this relationship, we included it with the other confounders in the logistic model. Effect modification by income status and age was assessed independently by comparing log-likelihood ratios of models with and without interaction terms included (P < 0.10).
Because iron deficiency is common in the population of interest, the adjusted odds ratio (AOR) overestimates the prevalence ratio (PR) if the AOR is > 2.5. Thus, to estimate the risk of iron deficiency more accurately among postpartum groups, we corrected AOR in the final model as recommended by Zhang and Yu (23
) using the equation 
, where PR and AOR are defined as above and P0 is the prevalence of the outcome in the unexposed.
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RESULTS |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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130% and married (data not shown). Nearly three fourths of all postpartum women were multigravid. Women 0–6 mo postpartum were most likely to be using iron supplements (% ± SEM, 42.0 ± 5.8) or vitamin C supplements (48.3 ± 6.6). The proportion of women breast-feeding declined from 27 ± 6.2% at 0–6 mo postpartum to 7 ± 1.3% at 7–12 mo. Nearly one fourth of women 0–6 mo postpartum were not menstruating (24.2 ± 5.2%) whereas this proportion was < 5% for all other groups. A majority of nonmenstruating women 0–6 mo postpartum were currently breast-feeding (77.8 ± 11.9%).
The prevalence of iron deficiency for women 0–6, 7–12, and 13–24 mo postpartum was 12.7, 12.4 and 7.8%, respectively (Table 1
). Overall, neither the prevalences of iron deficiency, anemia or iron deficiency anemia, nor the mean Hb or TS values differed by reproductive status. SF was lowest among women 7–12 mo postpartum, and FEP was highest in women 0–6 mo postpartum.
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130% was substantially higher than those with a poverty index ratio > 130% (Table 2
). Furthermore, compared with women 0–6 mo postpartum who had a poverty index ratio > 130%, their lower income counterparts were 3 times as likely to have anemia (% ± SEM: 22.2 ± 5.9 vs. 6.3 ± 2.1) and iron deficiency anemia (% ± SEM: 10.3 ± 3.3 vs. 2.1 ± 1.3). The prevalence of iron deficiency anemia for low income and higher income women 7–12 mo postpartum was 5.5 ± 3.2 and 3.9 ± 2.5%, respectively.
|
. Compared with women with a poverty index ratio > 130% who had never been pregnant, the risk of iron deficiency was 4 times as great for low-income women who were 0–6 mo postpartum, and 3 times as great for low income women 7–12 mo postpartum after adjusting for confounders. The risk of iron deficiency was elevated, but less so, for low income women 13–24 mo postpartum compared with the same referent. PR for iron deficiency were only slightly elevated for women 0–6 mo and 7–12 mo postpartum with a poverty index ratio > 130% compared with never-pregnant women with the same income status, but wide confidence intervals did not allow for precise estimation. Age did not further modify this relationship. The results did not change when we eliminated breast-feeding women, multigravidae, or nonmenstruating women from the analysis (data not shown). |
DISCUSSION |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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1 in 12 women is iron deficient (8%). Using the same definition of iron deficiency as the present study, Preziosi and colleagues (10
) found a 15 and 18% prevalence of iron deficiency at 3 and 6 mo postpartum, respectively, among a sample of Nigerian women randomly assigned to receive iron during pregnancy. To compare our results with others who defined iron deficiency on the basis of SF alone, we calculated a 16% prevalence of low iron stores (SF < 15 µg/L) among women 0–6 mo postpartum. Without prenatal iron supplementation, the prevalence of low iron stores has been shown to be >50% (11
,24
). We had no data on prenatal supplementation. In contrast, one study reported a prevalence of low iron stores between 4 and 8% among women treated with prenatal iron (11
).
Previous studies have not estimated the prevalence of iron deficiency or low iron stores beyond 6 mo postpartum. Thus, it is not known whether postpartum iron deficiency resolves over time. In previous studies, the prevalence of iron deficiency or low iron stores had resolved to 1st trimester levels before 6 mo postpartum among women randomly assigned to receive prenatal iron supplements but not among those receiving a placebo (10
–12
). These investigations, however, sampled mainly low risk, Caucasian women who were not representative of the general population. Our data were cross-sectional and could provide only a "snapshot in time." Longitudinal studies that follow women beyond 6 mo postpartum are warranted to provide a definitive answer to this question.
Our results showed that 10% of U.S. women 0–6 mo postpartum are anemic. This estimate reaches 22% for low income women, however. These results are consistent with recent reports of high prevalences of postpartum anemia up to 6 mo postpartum among low-income women in the United States (13
,14
).
Although the postpartum period is considered a woman’s time of lowest iron deficiency risk (9
), we found that low income women 0–6 mo postpartum have four times the risk of higher income women of reproductive age who have never been pregnant. Risk of iron deficiency for low income women 7–12 and 13–24 mo postpartum was three and two times as great, respectively, compared with the same referent. Several factors common to low income women could account for this elevated risk.
Women of low socioeconomic status (SES) use multivitamin/mineral supplements less often during pregnancy than women of higher SES (25
). This difference is important because red cell mass expansion among women who do not use prenatal iron supplements is half that of women who are supplemented (26
). A large proportion of the iron in the expanded red cell mass is thought to help rebuild iron stores early in the postpartum period when red cell mass contracts after delivery (12
). It is not surprising, then, that several small studies have shown that iron stores, as measured by SF, remain at low levels up to 6 mo postpartum among women not supplemented with iron during pregnancy (10
–12
). Inadequate dietary iron intake may also contribute to this elevated risk. Among all U.S. women 20–39 y old, low income women on average consume less iron than higher income women (27
).
Compared with higher income women, low income women are not only less likely to initiate breast-feeding, but also have shorter durations of breast-feeding (28
). Breast-feeding may be protective against the development of iron deficiency because it lengthens amenorrhea (29
), thereby reducing bodily iron losses. Our previous study showed breast-feeding to be an important predictor of postpartum anemia risk (13
), but it is not known at this time whether the protective effect is because of amenorrhea or other healthy behaviors that are associated with breast-feeding. In this study, the prevalence of iron deficiency did not differ by breast-feeding status, but the value of these findings is limited because we could not assess frequency and duration of breast-feeding and were working with small sample sizes.
Obesity is common among all U.S. women of childbearing age, but far more so for low income women than other groups (30
,31
). High pregravid body mass index has been shown to be an important risk marker of postpartum anemia (13
) and may be related to iron deficiency as well. The mechanism underlying the relationship between obesity and postpartum iron deficiency and/or anemia has not yet been studied, but there are several hypotheses that could account for this relationship. Compared with nonobese women, obese women have a greater risk of postpartum hemorrhage (32
) and cesarean delivery (33
). These complications can result in blood losses exceeding 1000 mL (34
), the equivalent of 400 mg of iron (8
). Obese women also have a high risk of delivering a macrosomic infant (birthweight > 4000 g) (35
), which causes higher delivery blood loss (36
) and lengthens duration of lochia (37
), the vaginal discharge of blood after childbirth. We could not assess the interrelationships among prepregnancy obesity, delivery complications and iron deficiency because NHANES III did not collect such data.
Women of low SES frequently receive inadequate or no prenatal or postpartum care (38
), which may prevent them from receiving risk assessment, education or treatment for medical conditions. Additionally, interpregnancy interval has been shown to be shorter for women of low SES (39
). This inadequate birth spacing may result in a cycle in which iron status never completely recovers.
The present study had several limitations. First, NHANES III did not obtain data on prenatal and delivery risk factors for postpartum iron deficiency, such as prenatal iron supplement use, multiple births and blood loss at delivery. Thus, we were unable to determine whether any of these factors modified the observed association between postpartum status and iron deficiency. Additionally, we were not able to eliminate women <1 mo postpartum from this analysis because the first postpartum category in NHANES III was 0–3 mo. The prevalence of iron deficiency is likely to be higher among women <1 mo postpartum than those 1–6 mo postpartum because the expanded red cell mass of pregnancy may not have contracted yet, and iron may not have returned to maternal stores. We can report that the prevalence (±SEM) of iron deficiency was 13.0 ± 2.2% among women 0–3 mo postpartum and 12.4 ± 5.4% among women 4–6 mo postpartum. Finally, NHANES III collected data on a relatively small number of postpartum women, and thus some of our estimates are imprecise.
One of the main goals of Healthy People 2010 is to eliminate health disparities among segments of the population, including differences that occur among income groups (30
). This study provides evidence that disparities in the burden of iron deficiency exist by income status in the postpartum period. Future research should determine which prevention efforts are most effective in reducing the burden among low income women so as to reduce iron-deficiency related functional consequences in the postpartum period.
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FOOTNOTES |
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Manuscript received 26 March 2002. Initial review completed 18 April 2002. Revision accepted 27 April 2002.
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LITERATURE CITED |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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