a

 ภาวะโลหิตจางเกิดได้จากหลายสาเหตโดยที่พบบ่อยที่สุดคือโลหิตจางจากการขาดธาตุเหล็ก เหล็กที่เราพูดถึงกันนี้ไม่ใช่เหล็กเป็นแท่งๆ แต่จะหมายถึงธาตุเหล็กที่อยู่ในรูปแร่ธาตุซึ่งเป็นส่วนประกอบในเซลล์ต่างๆของร่างกาย เราจะได้รับธาตุเหล็กจากอาหารเป็นหลัก  โดยอาหารที่พบธาตุเหล็กมาก ได้แก่ เนื้อสัตว์เนื้อแดง เครื่องในสัตว์ เช่น ตับ นอกจากนี้ ยังพบธาตุเหล็กได้ในผักใบเขียวและธัญพืช  แต่ธาตุเหล็กในอาหารประเภทหลังนี้จะถูกดูดซึมได้ไม่ดีเท่าธาตุเหล็กจากอาหารพวกเนื้อสัตว์และอาจมีสารยับยั้งการดูดซึมธาตุเหล็กได้ด้วย  อาหารและเครื่องดื่มบางประเภทอาจมีผลยับยั้งการดูดซึมธาตุเหล็กได้ เช่น ชา กาแฟ  ผู้ที่รับประทานยาเสริมแคลเซียมก็อาจไปรบกวนการดูดซึมธาตุเหล็กหากรับประทานพร้อมกัน  ส่วนอาหารที่วิตามินซีสูง เช่น ผลไม้รสเปรี้ยว พบว่าช่วยการดูดซึมธาตุเหล็กให้ดีขึ้นได้บ้าง

เมื่อรับประทานอาหารที่มีธาตุเหล็กแล้ว จะเกิดการดูดซึมธาตุเหล็กต่อ โดยอาศัยความเป็นกรดในกระเพาะอาหารช่วย  การดูดซึมจะเกิดที่ลำไส้เล็กส่วนต้น  หลังจากนั้นจะมีโปรตีนส่งธาตุเหล็กไปตามเซลล์ต่างๆและไปเป็นส่วนประกอบของเอนไซม์  โดยกว่าสองในสามของธาตุเหล็กในร่างกายจะอยู่ในเม็ดเลือดแดงในส่วนที่เรียกว่า “ฮีม” ซึ่งจะเป็นส่วนที่ช่วยในการจับกับออกซิเจนและส่งไปให้ส่วนต่างๆของร่างกายนั่นเอง  ส่วนที่เหลือของธาตุเหล็กจะถูกเก็บสะสมไว้ในตับ ม้าม และไขกระดูก

เราขาดธาตุเหล็กเพราะอะไร

สาเหตุของการขาดธาตุเหล็กพบได้หลากหลาย  ที่พบบ่อย เช่น

1. รับประทานอาหารที่มีธาตุเหล็กน้อย  พบได้บ่อยในเด็กทารกที่รับประทานแต่นมเพียงอย่างเดียว เนื่องจากในนมมีปริมาณธาตุเหล็กเพียงเล็กน้อย  ในผู้ใหญ่ การขาดธาตุเหล็กจากการรับประทานน้อยเจอได้ไม่บ่อย

2. การดูดซึมธาตุเหล็กผิดปกติ  เป็นสาเหตุที่พบได้ไม่บ่อย  อาจเกิดจากการมีกรดในกระเพาะอาหารลดลง เช่น ผู้ที่รับประทานยาลดกรดในกระเพาะอาหารนานๆหรือผู้สูงอายุ  ผู้ที่เคยได้รับการผ่าตัดเอากระเพาะอาหารออก  ผู้ที่ได้รับการผ่าตัดเอาลำไส้เล็กส่วนต้นออก  ผู้ที่มีการอักเสบของลำไส้เล็กส่วนต้นเรื้อรัง เป็นต้น
3. ความต้องการธาตุเหล็กเพิ่มมากขึ้น  พบได้บ่อยในผู้ที่ตั้งครรภ์อยู่ หรือมีการให้นมบุตร  โดยความต้องการธาตุเหล็กของคนกลุ่มนี้จะมากกว่าคนทั่วไปถึงสามเท่า  ในเด็กเล็กที่กำลังเจริญเติบโตก็มีความต้องการธาตุเหล็กเพิ่มขึ้นด้วยเช่นกัน

     4. สูญเสียธาตุเหล็กมากกว่าปกติ  มักเกิดจากการเสียเลือดเรื้อรัง  สาเหตุที่พบบ่อย ได้แก่ เลือดประจำเดือนออกมากและนานกว่าปกติในผู้หญิงวัยเจริญพันธุ์  เลือดออกในทางเดินอาหารจากสาเหตุต่างๆ เช่น แผลในกระเพาะอาหารเรื้อรัง เลือดออกในหลอดอาหาร ริดสีดวงทวารหนัก หรือแม้แต่มะเร็งลำไส้ใหญ่ก็อาจจะมีอาการนำให้ทราบได้จากภาวะขาดธาตุเหล็ก การเสียเลือดจากสาเหตุอื่นๆที่พบไม่บ่อย เช่น จากเม็ดเลือดแดงแตกและเสียเลือดในทางเดินปัสสาวะ เสียเลือดจากระบบทางเดินหายใจ  การบริจาคเลือดบ่อยครั้งกว่าที่กำหนดและไม่รับประทานยาเสริมธาตุเหล็กทดแทน เป็นต้น


จะเกิดอาการอย่างไรเมื่อขาดธาตุเหล็ก

ผู้ที่ขาดธาตุเหล็กในระยะแรกอาจยังไม่มีอาการใดๆ เนื่องจากมีธาตุเหล็กที่เก็บสะสมสำรองอยู่  ต่อเมื่อการขาดธาตุเหล็กนั้นเป็นมากขึ้นจึงค่อยๆเริ่มเกิดอาการ  อาการอาจเป็นแบบไม่จำเพาะ เช่น รู้สึกหงุดหงิด ความคิดความอ่านไม่แจ่มใส นอนไม่หลับ  อาการที่เกิดได้บ่อยและทำให้แพทย์วินิจฉัยภาวะขาดธาตุเหล็กได้นั้นมักเกิดจากอาการทางระบบเลือด ได้แก่การเกิดภาวะโลหิตจางนั่นเอง  อาการของภาวะโลหิตจาง ได้แก่ อ่อนเพลีย เหนื่อยง่ายมากขึ้นเวลาออกแรง หรือหากเป็นมากอาจมีอาการเหนื่อยเวลาอยู่เฉยๆ มีอาการเวียนศีรษะ หมดสติ ใจสั่น หัวใจล้มเหลว  ผู้ป่วยบางรายอาจมีคนทักว่าดูซีดลง กินอาหารรสเผ็ดแล้วแสบลิ้นเนื่องจากมีลิ้นเลี่ยน  ในรายที่เป็นมานานๆอาจมีเล็บผิดรูปโดยงอเป็นรูปช้อน

จะวินิจฉัยภาวะโลหิตจางจากการขาดธาตุเหล็กได้อย่างไร

โดยทั่วไปแพทย์จะวินิจฉัยภาวะนี้จะการซักถามประวัติและตรวจร่างกายอย่างละเอียดก่อน  จากนั้นจึงส่งตรวจเลือดเพื่อดูเม็ดเลือดสมบูรณ์, ปริมาณธาตุเหล็กในร่างกาย, และปริมาณธาตุเหล็กสะสม  ในสถานที่ที่การตรวจทำได้ไม่สมบูรณ์ อาจใช้การให้การรักษาด้วยยาธาตุเหล็กและตรวจติดตามว่าตอบสนองดีหรือไม่  หากตอบสนองดีก็น่าจะเป็นโลหิตจางจากการขาดธาตุเหล็กจริง  แต่หากไม่ดีขึ้นก็ควรนึกถึงภาวะโลหิตจางจากสาเหตุอื่น

การรักษาภาวะโลหิตจางจากการขาดธาตุเหล็ก

การรักษาขึ้นกับความเร่งด่วนของอาการ  หากมีภาวะโลหิตจางรุนแรงมากหรือเป็นในผู้สูงอายุก็ควรได้รับการรักษาตัวในโรงพยาบาล ให้ออกซิเจน ให้เลือดแดงทดแทน  จากนั้นจึงให้ธาตุเหล็กทดแทนร่วมไปด้วย โดยที่มีใช้จะอยู่ในรูปของยารับประทานและยาฉีดเข้าเส้นเลือด  ยาธาตุเหล็กในรูปรับประทานมักจะถูกใช้ก่อนเป็นอันดับแรก เนื่องจากใช้ง่าย ให้ผลการรักษาดีและราคาไม่แพง  ยาจะมีหลายรูปแบบซึ่งจะแตกต่างกันขึ้นอยู่กับปริมาณธาตุเหล็กที่เป็นส่วนประกอบ ส่วนใหญ่จะให้ผลการรักษาไม่ต่างกัน  เมื่อรับประทานยาธาตุเหล็กแล้วจะมีอุจจาระสีดำ ซึ่งเป็นสิ่งปกติที่เกิดขึ้นกับทุกคนที่กินยา  ผลข้างเคียงที่พบบ่อย คือ อาการมวนท้อง คลื่นไส้ ท้องอืด ซึ่งมักไม่ใช่ภาวะแทรกซ้อนที่รุนแรง แต่ในบางคนอาจทนภาวะนี้ไม่ไหว จำเป็นต้องให้ในรูปยาฉีดแทน ซึ่งจะยุ่งยากมากกว่า ราคาแพงและอาจมีภาวะแทรกซ้อนรุนแรงได้  การรักษามักต้องใช้เวลานานอย่างน้อย 3 – 6 เดือนเพื่อให้ธาตุเหล็กเก็บสะสมในร่างกายเต็มที่  ที่สำคัญระหว่างการรักษาโดยให้ธาตุเหล็กทดแทน จะต้องมีการหาสาเหตุที่ขาดธาตุเหล็กและรักษาไปด้วยเสมอเพื่อเป็นการรักษาที่ต้นเหตุ  ในผู้ที่มีความเสี่ยงของการขาดธาตุเหล็ก เช่น หญิงตั้งครรภ์ หญิงให้นมบุตร เด็กที่กำลังเจริญเติบโต ผู้ที่บริจาคโลหิตเป็นประจำ ถึงแม้ยังไม่เป็นโรคโลหิตจางจากการขาดธาตุเหล็ก ก็ควรพิจารณารับประทานอาหารที่มีธาตุเหล็กสูงอย่างเป็นประจำ

 

Iron Deficiency

Isolated iron deficiency is uncommon in the United States. Because iron deficiency is associated with poor diet, malabsorptive disorders, and blood loss, people with iron deficiency usually have other nutrient deficiencies [2]. The World Health Organization (WHO) estimates that approximately half of the 1.62 billion cases of anemia worldwide are due to iron deficiency [32]. In developing countries, iron deficiency often results from enteropathies and blood loss associated with gastrointestinal parasites [2].

Iron depletion and deficiency progresses through several stages [8]:

  1. Mild deficiency or storage iron depletion: Serum ferritin concentrations and levels of iron in bone marrow decrease.
  2. Marginal deficiency, mild functional deficiency, or iron-deficient erythropoiesis (erythrocyte production): Iron stores are depleted, iron supply to erythropoietic cells and transferrin saturation decline, but hemoglobin levels are usually within the normal range. In addition, plasma iron levels decline and plasma transferrin concentrations (measured by plasma total iron-binding capacity) rise, resulting in decreased transferrin saturation. Serum transferrin receptor concentrations also increase.
  3. IDA: Iron stores are exhausted; hematocrit and levels of hemoglobin decline; and the resulting microcytic, hypochromic anemia is characterized by small red blood cells with low hemoglobin concentrations.

IDA is defined as a hemoglobin level that is lower than two standard deviations from the mean distribution in a healthy population of the same gender and age living at the same altitude [33]. At sea level, hemoglobin concentrations lower than 11 to 12 g/dL in children younger than 12, 12 g/dL in adolescents and women, and 13 g/dL in men indicate the presence of IDA [2]. In 2002, the WHO characterized IDA as one of the 10 leading risk factors for disease around the world [34]. Although iron deficiency is the most common cause of anemia, deficiencies of other micronutrients (such as folate and vitamin B12) and other factors (such as chronic infection and inflammation) can cause different forms of anemia or contribute to their severity.

The functional deficits associated with anemia include gastrointestinal disturbances and impaired cognitive function, immune function, exercise or work performance, and body temperature regulation [35]. In infants and children, IDA can result in psychomotor and cognitive abnormalities that, without treatment, can lead to learning difficulties [2,35]. Some evidence indicates that the effects of deficiencies early in life persist through adulthood [2]. Because iron deficiency is often accompanied by deficiencies of other nutrients, the signs and symptoms of iron deficiency can be difficult to isolate [2].

Groups at Risk of Iron Inadequacy

The following groups are among those most likely to have inadequate intakes of iron.

Pregnant women
During pregnancy, plasma volume and red cell mass expand due to dramatic increases in maternal red blood cell production [2]. As a result of this expansion and to meet the needs of the fetus and placenta, the amount of iron that women need increases during pregnancy. Iron deficiency during pregnancy increases the risk of maternal and infant mortality, premature birth, and low birthweight [33].

Infants and young children
Infants—especially those born preterm or with low birthweight or whose mothers have iron deficiency—are at risk of iron deficiency because of their high iron requirements due to their rapid growth [25,36]. Full-term infants usually have sufficient iron stores and need little if any iron from external sources until they are 4 to 6 months old [2]. However, full-term infants have a risk of becoming iron deficient at 6 to 9 months unless they obtain adequate amounts of solid foods that are rich in bioavailable iron or iron-fortified formula.

Women with heavy menstrual bleeding
Women of reproductive age who have menorrhagia, or abnormally heavy bleeding during menstruation, are at increased risk of iron deficiency. At least 10% of menstruating women are believed to have menorrhagia, but the percentage varies widely depending on the diagnostic criteria used [37-39]. Women with menorrhagia lose significantly more iron per menstrual cycle on average than women with normal menstrual bleeding [40]. Limited evidence suggests that menorrhagia might be responsible for about 33% to 41% of cases of IDA in women of reproductive age [41,42].

Frequent blood donors
Frequent blood donors have an increased risk of iron deficiency [5]. In the United States, adults may donate blood as often as every 8 weeks, which can deplete iron stores. About 25%–35% of regular blood donors develop iron deficiency [43]. In a study of 2,425 blood donors, men who had given at least three and women who had given at least two whole-blood donations in the previous year were more than five times as likely to have depleted iron stores as first-time donors [44]. A clinical trial of iron supplementation found that of 215 adults who had donated a unit of blood within the past 3–8 days, those randomized to take an iron supplement (37.5 mg/day elemental iron from ferrous gluconate) for 24 weeks recovered their lost hemoglobin and iron in less than half the time of those not given the supplement [43]. Without iron supplementation, two-thirds of the donors had not recovered the iron they lost, even after 24 weeks.

People with cancer
Up to 60% of patients with colon cancer have iron deficiency at diagnosis, probably due to chronic blood loss [45]. The prevalence of iron deficiency in patients with other types of cancer ranges from 29% to 46%. The main causes of iron deficiency in people with cancer are anemia of chronic disease (discussed in the Iron and Health section below) and chemotherapy-induced anemia. However, chronic blood loss and deficiencies of other nutrients (due, for example, to cancer-induced anorexia) can exacerbate iron deficiency in this population.

People who have gastrointestinal disorders or have had gastrointestinal surgery
People with certain gastrointestinal disorders (such as celiac disease, ulcerative colitis, and Crohn’s disease) or who have undergone certain gastrointestinal surgical procedures (such as gastrectomy or intestinal resection) have an increased risk of iron deficiency because their disorder or surgery requires dietary restrictions or results in iron malabsorption or blood loss in the gastrointestinal tract [46-48]. The combination of low iron intake and high iron loss can lead to a negative iron balance; reduced production of hemoglobin; or microcytic, hypochromic anemia [49].

People with heart failure
Approximately 60% of patients with chronic heart failure have iron deficiency and 17% have IDA, which might be associated with a higher risk of death in this population [50,51]. Potential causes of iron deficiency in people with heart failure include poor nutrition, malabsorption, defective mobilization of iron stores, cardiac cachexia, and use of aspirin and oral anticoagulants, which might result in the loss of some blood in the gastrointestinal tract [52].

Iron and Health

This section focuses on the role of iron in IDA in pregnant women, infants, and toddlers, as well as in anemia of chronic disease.

IDA in pregnant women
Insufficient iron intakes during pregnancy increase a woman’s risk of IDA [53-56]. Low intakes also increase her infant’s risk of low birthweight, premature birth, low iron stores, and impaired cognitive and behavioral development.

An analysis of 1999–2006 data from the National Health and Nutrition Examination Survey (NHANES) found that 18% of pregnant women in the United States had iron deficiency [29]. Rates of deficiency were 6.9% among women in the first trimester,14.3% in the second trimester, and 29.7% in the third trimester.

Randomized controlled trials have shown that iron supplementation can prevent IDA in pregnant women and related adverse consequences in their infants [57,58]. A Cochrane review showed that daily supplementation with 9–90 mg iron reduced the risk of anemia in pregnant women at term by 70% and of iron deficiency at term by 57% [55]. In the same review, use of daily iron supplements was associated with an 8.4% risk of having a low-birthweight newborn compared to 10.2% with no supplementation. In addition, mean birthweight was 31 g higher for infants whose mothers took daily iron supplements during pregnancy compared with the infants of mothers who did not take iron.

Guidelines on iron supplementation during pregnancy vary, but many recommend some form of iron supplementation to prevent IDA:

The IOM notes that because the median intake of dietary iron by pregnant women is well below the EAR, pregnant women need iron supplementation [5]. The Dietary Guidelines for Americans advises that women who are pregnant take an iron supplement when recommended by an obstetrician or other health-care provider [11]. It adds that low intakes of iron are a public health concern for pregnant women.

IDA in infants and toddlers
Approximately 12% of infants aged 6 to 11 months in the United States have inadequate iron intakes, and 8% of toddlers have iron deficiency [27,61]. The prevalence of IDA in U.S. toddlers aged 12 to 35 months ranges from 0.9% to 4.4% depending on race or ethnicity and socioeconomic status [12]. Full-term infants typically have adequate iron stores for approximately the first 4 to 6 months, but the risk of iron deficiency in low-birthweight and preterm infants begins at birth because of their low iron stores.

IDA in infancy can lead to adverse cognitive and psychological effects, including delayed attention and social withdrawal; some of these effects might be irreversible [2,12]. In addition, IDA is associated with higher lead concentrations in the blood (although the cause of this is not fully understood), which can increase the risk of neurotoxicity [12].

A Cochrane review of 26 studies in 2,726 preterm and low-birthweight infants found that enteral iron supplementation (at least 1 mg/kg/day) reduces the risk of iron deficiency, but the long-term effects of supplementation on neurodevelopmental outcomes and growth is not clear [62]. Another Cochrane review of 8 trials in 3,748 children younger than 2 in low-income countries showed that home fortification of semi-solid foods with micronutrient powders containing 12.5 mg to 30 mg elemental iron as ferrous fumarate and 4 to 14 other micronutrients for 2 to 12 months reduced rates of anemia by 31% and of iron deficiency by 51% compared with no intervention or placebo but had no effect on any growth measurements [63].

Guidelines vary on dietary iron intakes and possible supplementation to ensure adequate iron status and to prevent or treat IDA in infants and young children:

Some studies have suggested that iron supplementation in young children living in areas where malaria is endemic could increase their risk of malaria [66,67]. However, a Cochrane review of 33 trials in 13,114 children showed that intermittent supplementation does not appear to have this effect [68]. The WHO therefore recommends 6-month supplementation cycles as follows: children aged 24 to 59 months should receive 25 mg iron and those aged 5 to 12 years should receive 45 mg every week for 3 months, followed by 3 months of no supplementation [66]. The WHO recommends providing these supplements in malaria-endemic areas in conjunction with measures to prevent, diagnose, and treat malaria.

Anemia of chronic disease
Certain inflammatory, infectious, and neoplastic diseases (such as rheumatoid arthritis, inflammatory bowel disease, and hematologic malignancies) can cause anemia of chronic disease, also known as anemia of inflammation [2,69]. Anemia of chronic disease is the second most common type of anemia after IDA [70]. In people with anemia of chronic disease, inflammatory cytokines upregulate the hormone hepcidin. As a result, iron homeostasis is disrupted and iron is diverted from the circulation to storage sites, limiting the amount of iron available for erythropoiesis.

Anemia of chronic disease is usually mild to moderate (hemoglobin levels 8 to 9.5 g/dL) and is associated with low counts of erythrocytes and decreased erythropoiesis [69]. The condition can be difficult to diagnose because, although low serum ferritin levels indicate iron deficiency, these levels tend to be higher in patients with infection or inflammation [71].

The clinical implications of iron deficiency in people with chronic diseases are not clear. Even mild anemia of chronic disease is associated with an increased risk of hospitalization and mortality in elderly people [72]. Two prospective observational studies found that iron deficiency in patients with objectively measured heart failure was associated with an increased risk of heart transplantation and death, and this association was independent of other well-established prognostic factors for poor outcomes, including anemia [73,74]. However, an analysis of NHANES data on 574 adults with self-reported heart failure found no association between iron deficiency and all-cause or cardiovascular mortality [51].

The main therapy for anemia of chronic disease is treatment of the underlying disease [70]. But when such treatment is not possible, iron supplementation and/or erythropoiesis-stimulating agents (ESAs) are sometimes used. The use of iron supplements—whether oral, intravenous, or parenteral—in this setting is controversial because they might increase the risk of infection and cardiovascular events and could cause tissue damage [70].

Only a few small studies have evaluated the benefits of oral iron supplementation alone or in combination with ESAs to treat anemia of chronic disease. For example, a prospective observational study in 132 patients with anemia and chronic kidney disease who were not on dialysis or ESAs found that oral supplements (130 mg/day elemental iron from ferrous sulfate twice daily) for 1 year resulted in a decline in hemoglobin of only 0.13 g/dL compared with 0.46 g/dL in the placebo group [75]. A randomized trial of oral iron supplements (equivalent to 200 mg/day elemental iron, form of iron not specified) taken with an ESA once weekly in 100 patients with cancer-related anemia resulted in a mean increase of 2.4 g/dL hemoglobin after 24 weeks compared with oral supplements only [76]. Iron administered parentally increases hemoglobin levels to a greater extent and is associated with fewer side effects than oral iron supplementation in patients with anemia of chronic disease [77].

Health Risks from Excessive Iron

Adults with normal intestinal function have very little risk of iron overload from dietary sources of iron [2]. However, acute intakes of more than 20 mg/kg iron from supplements or medicines can lead to gastric upset, constipation, nausea, abdominal pain, vomiting, and faintness, especially if food is not taken at the same time [2,5]. Taking supplements containing 25 mg elemental iron or more can also reduce zinc absorption and plasma zinc concentrations [3,78,79]. In severe cases (e.g., one-time ingestions of 60 mg/kg), overdoses of iron can lead to multisystem organ failure, coma, convulsions, and even death [18,80].

Between 1983 and 2000, at least 43 U.S. children died from ingesting supplements containing high doses of iron (36–443 mg iron/kg body weight) [18]. Accidental ingestion of iron supplements caused about a third of poisoning deaths among children reported in the United States between 1983 and 1991.

In 1997, the FDA began requiring oral supplements containing more than 30 mg elemental iron per dose to be sold in single-dose packaging with strong warning labels. At the same time, many manufacturers voluntarily replaced the sugar coating on iron tablets with film coatings. Between 1998 and 2002, only one child death due to ingesting an iron-containing tablet was reported [18]. As a result of a court decision, the FDA removed its single-dose packaging requirement for iron supplements in 2003 [81]. FDA currently requires that iron-containing dietary supplements sold in solid form (e.g., tablets or capsules but not powders) carry the following label statement: "WARNING: Accidental overdose of iron-containing products is a leading cause of fatal poisoning in children under 6. Keep this product out of reach of children. In case of accidental overdose, call a doctor or poison control center immediately" [82]. In addition, since 1978, the Consumer Product Safety Commission has required manufacturers to package dietary supplements containing 250 mg or more elemental iron per container in child-resistant bottles or packaging to prevent accidental poisoning [83,84].

Hemochromatosis, a disease caused by a mutation in the hemochromatosis (HFE) gene, is associated with an excessive buildup of iron in the body [3,30,85]. About 1 in 10 whites carry the most common HFE mutation (C282Y), but only 4.4 whites per 1,000 are homozygous for the mutation and have hemochromatosis [86]. The condition is much less common in other ethnic groups. Without treatment by periodic chelation or phlebotomy, people with hereditary hemochromatosis typically develop signs of iron toxicity by their 30s [3]. These effects can include liver cirrhosis, hepatocellular carcinoma, heart disease, and impaired pancreatic function. The American Association for the Study of Liver Diseases recommends that treatment of hemochromatosis include the avoidance of iron and vitamin C supplements [30].

The FNB has established ULs for iron from food and supplements based on the amounts of iron that are associated with gastrointestinal effects following supplemental intakes of iron salts (see Table 3). The ULs apply to healthy infants, children, and adults. Physicians sometimes prescribe intakes higher than the UL, such as when people with IDA need higher doses to replenish their iron stores [5].

Table 3: Tolerable Upper Intake Levels (ULs) for Iron [5]*
Age Male Female Pregnancy Lactation
Birth to 6 months 40 mg 40 mg    
7–12 months 40 mg 40 mg    
1–3 years 40 mg 40 mg    
4–8 years 40 mg 40 mg    
9–13 years 40 mg 40 mg    
14–18 years 45 mg 45 mg 45 mg 45 mg
19+ years 45 mg 45 mg 45 mg 45 mg

* Breast milk, formula, and food should be the only sources of iron for infants.

Interactions with Medications

Iron can interact with certain medications, and some medications can have an adverse effect on iron levels. A few examples are provided below. Individuals taking these and other medications on a regular basis should discuss their iron status with their health care providers.

Levodopa
Some evidence indicates that in healthy people, iron supplements reduce the absorption of levodopa (found in Sinemet® and Stalevo®), used to treat Parkinson’s disease and restless leg syndrome, possibly through chelation [87-89]. In the United States, the labels for levodopa warn that iron-containing dietary supplements might reduce the amount of levodopa available to the body and, thus, diminish its clinical effectiveness [90,91].

Levothyroxine
Levothyroxine (Levothroid®, Levoxyl®, Synthroid®, Tirosint®, and Unithroid®) is used to treat hypothyroidism, goiter, and thyroid cancer. The simultaneous ingestion of iron and levothyroxine can result in clinically significant reductions in levothyroxine efficacy in some patients [92]. The labels for some of these products [93,94] warn that iron supplements can reduce the absorption of levothyroxine tablets and advise against administering levothyroxine within 4 hours of iron supplements.

Proton pump inhibitors
Gastric acid plays an important role in the absorption of nonheme iron from the diet. Because proton pump inhibitors, such as lansoprazole (Prevacid®) and omeprazole (Prilosec®), reduce the acidity of stomach contents, they can reduce iron absorption [3]. Treatment with proton pump inhibitors for up to 10 years is not associated with iron depletion or anemia in people with normal iron stores [95]. But patients with iron deficiency taking proton pump inhibitors can have suboptimal responses to iron supplementation [96].

Iron and Healthful Diets

The federal government's 2015-2020 Dietary Guidelines for Americans notes that "Nutritional needs should be met primarily from foods. ... Foods in nutrient-dense forms contain essential vitamins and minerals and also dietary fiber and other naturally occurring substances that may have positive health effects. In some cases, fortified foods and dietary supplements may be useful in providing one or more nutrients that otherwise may be consumed in less-than-recommended amounts."

For more information about building a healthy diet, refer to theDietary Guidelines for Americansexternal link disclaimer and the U.S. Department of Agriculture's MyPlateexternal link disclaimer.

The Dietary Guidelines for Americans describes a healthy eating pattern as one that:

What are the symptoms of anemia?

There are several symptoms that may occur in all types of anemia. They are:

Who is most likely to develop iron-deficiency anemia?

Anyone can develop iron-deficiency anemia, although the following groups have a higher risk:

How is anemia diagnosed?

Your health care provider can perform blood tests to tell if you have anemia. The type and number of blood tests will depend on what type of anemia your doctor thinks you might have.

The blood tests will measure your hemoglobin and how much iron is in your body. If these levels are low, the doctor can make a diagnosis of anemia.

How is anemia treated?

Your health care provider will decide on the proper treatment, depending on the type of anemia and what is causing it.

Your doctor must first find out if the anemia is being caused by a poor diet or a more serious health problem. You can then be treated for both the anemia and its cause.

Iron-deficiency anemia is treated by eating foods that are high in iron, or with oral (taken by mouth) iron supplements.

How Do You Know If You're Iron Deficient?

"People often don't know they have anemia until they have signs or symptoms -- they appear pale or 'sallow,' are fatigued, or have difficulty exercising," Chottiner says.

If you're low in iron, you may also:

If you're tired and dragging, see your doctor. "It's fairly easy to detect and diagnose the different stages of iron deficiency with a simple blood test," Thomas says. Women who are pregnant and people with a gastrointestinal disorder such as Crohn's,ulcerative colitis, or celiac disease should have their iron tested on a regular basis.