File - Courtney Leinen

Iron Lab Report
Courtney Leinen
FSCN 4613
Iron deficiency anemia is the most common nutritional deficiency around the
world1, with 65-80% of the population possibly suffering from iron deficit2. Pregnant
women, women who are lactating, infants, and children are at a higher risk for iron
deficiency. Women are also more likely to be deficient during their menstrual cycle.
Populations who are starving are more likely to be deficient in iron as well, as an
inadequate dietary intake can increase the possibility of iron deficiency.
Iron deficiency anemia (IDA) can present with varying symptoms. The most
common symptom is weakness or chronic fatigue2, while the most serious is mycrocytic,
hypochromic anemia, and also includes numbness and tingling in the body, atrophy of
epithelium of tongue, pica (the appetite for substances not considered food, like clay, dirt,
or paper), and in rare cases, spoon-shaped nails (called koilonychia2). In infants, this can
present as premature birth, low birth weight, and an increased rate of infections, all of
which can cause unfavorable affects on cognitive performance, which are often
There are many causes of iron deficiency anemia; some are related to diet and
some are not. A lack of heme iron in the diet can lead to IDA. The heme iron (or iron
more commonly found in meat, particularly red meats) is absorbed by the body better,
and is broken down in the intestine, resulting in free iron. Non-heme iron, commonly
found in cereal, beans, vegetables, and whole grain carbohydrates, are more highly
regulated, and focus more on maintaining iron levels2. Essentially, the body finds it easier
to digest and use heme iron instead of non-heme iron. People who refrain from eating
meats can find themselves anemic because their body isn’t taking up enough iron from
their non-heme sources. The major influences in the uptake of non-heme iron are the
brush border proteins, which paired along with DMT 1 that also resides on the brush
border, control the non-heme iron absorption process of transferring into mucosal cells.
Non-dietary factors are usually related to illnesses or other medical issues.
Chronic inflammation and certain mediations can lead to IDA, and more commonly
blood loss and gastrointestinal conditions. Blood loss can be defined as a menstrual cycle,
or any other bodily loss of blood, including ulcers, parasite (leeching blood from the
body), blood donations, or excessive surgical blood loss.
The metabolism of iron in the body is a complex process that is still being
researched today. The current model relies on intestinal iron absorption, were a majority
of absorption taking place in the intestines through enterocytes and the brush border. Iron
is absorbed through three different methods: divalent metal transporter 1 (DMT 1),
duodenal cytochrome b (Dcytb), and heme carrier protein 1 (HCP1) 2. Iron then goes into
an intracellular iron pool. Ferritin is then absorbed into the blood stream. Iron is
transported with transferrin (Tf), a glycoprotein with one binding site and binds virtually
all plasma iron. Transferrin receptors (TfR) are transmembrane glycoproteins with a high
affinity for diferrin Tf, and the number of receptors are regulated by intracellular
available iron, allowing the TfR to mediate iron uptake into cells2. The intracellular iron
has two fates; either incorporation into proteins that are dependent on iron or stored in
ferritin2. 75% of the transported iron goes to hemoglobin or erythropoiesis, and 10-20%
to storage in ferritin. Ferritin tissue, where iron is stored, is a large protein with pores that
allow the entry and exit of iron2. Iron is stored primarily in liver, but a small amount of
ferritin does leak into the plasma, which is proportional to the iron stored in the liver.
This means plasma ferritin can be a direct reflection of iron stores.
The ways to measure iron status include hematocrit, whole blood hemoglobin,
serum iron, serum ferritin, total iron binding capacity (TIBC), and a calculated
unsaturated iron binding capacity. When a person is iron depleted it can show in varying
degrees before reaching full IDA. With low level depletion comes increased TIBC and
iron absorption, as well as decreased plasma ferritin. Iron deficient erythropoiesis is a
continuation of the previous changes, plus decreases in plasma iron and transferrin
saturation. When the person develops full IDA all the above changes are exacerbated and
the erythrocytes develop microcytic/hypochromic anemia2.
The objectives of the labs performed were to determine our personal iron status’
through basic blood iron markers and to determine the bioavailability of iron in different
μg/100 mL
Serum Iron
Total Iron Binding
Capacity (TIBC)
Relation to
Reference Values
Low Risk
Iron Deficient Value
Other Measures
Hematocrit %
% Transferrin Saturation
Serum Ferritin
Serum Transferrin Receptor
TfR-F Index
Total Body Iron
11.4 g/dL
9.7 ng/mL
40.8 mg/L
Relation to Reference Value
Medium Risk
Medium Risk
Low Risk
Iron Deficient
Iron Deficient
Not Iron Deficient
Not Iron Deficient
Personal Iron Status
My personal values were mixed. The serum iron and percent transferrin saturation
show that I have a low risk of IDA, along with my TfR-F Index and Total Body Iron. The
total body iron and TfR-F Index, however, are most likely skewed because they are
reliant on serum transferrin receptor. A TA reported this data point as 40.8 mg/L, and
seeing as an average number is around 1-3 mg/L according to Professor Gallaher, this
number is obviously flawed. The percent hematocrit and hemoglobin levels show I have a
medium risk of iron deficiency, while my serum ferritin and TIBC show I am iron
deficient. Overall, based on the reference values, it would be safest to assume I am at an
elevated risk of iron deficiency anemia, and should take precautionary steps to prevent it.
Based on my diet and lifestyle I would believe that I am iron deficient, which is
supported by most of the values found in this lab. I refrain from eating most red meats,
suffer from heavy blood loss during my menstrual cycle, and often have an overall
inadequate dietary intake stemming from persistent GI discomfort, which presents as
bloating with distention and an almost constant feeling of fullness. In order to increase
my iron levels, I began supplementing with iron about a year ago, when I was diagnosed
with chronic anemia. I have a strict schedule of strength training that helps me keep my
body from feeling as much weakness, however it can be counter productive if my diet
doesn’t include some red meat prior, and leads my body to fatigue faster.
Iron Bioavailability Study
In the study testing iron bioavailability there were various measurements
determined that shed light on how the different diets affected the subjects. The
observations showed a fairly consistent body weight gain for all participating rats, a
higher average hematocrit for diets containing ferrous sulfate as well as significantly
higher hemoglobin for aforementioned diet. The higher calcium diets showed higher
plasma iron concentration and higher bone iron concentration, while low calcium diets
had higher liver iron concentration and higher kidney iron concentration4.
From the data provided it can be noted that there appeared to be a higher
bioavailability with the ferrous sulfate than the Total cereal, based on higher average
hematocrit percentages and a higher hemoglobin regeneration efficiency. The difference
between calcium levels also influenced the iron bioavailability. Higher calcium led to
higher plasma iron and bone iron concentrations, while low calcium diets led to higher
liver iron and kidney iron concentration. Higher concentrations in the kidney and liver are
indicative of iron storage, meaning the iron wasn’t necessarily as available to the body
because it was being stored instead of utilized. This indicates that higher calcium can lead
to better bioavailability.
The bone calcium concentration values only showed a slight difference between
low and high calcium diets. Low calcium diets in both categories had higher outliers,
however high calcium diets had an overall average greater than low calcium diets. This
data would need to be further researched in a more controlled environment to properly
show significant data.
1. Clark, Susan. (2009). Iron deficiency anemia: diagnosis and management.
Current Opinion in Gastroenterology. 25: 122-128.
2. Gallaher, Daniel. (2014). Iron Metabolism. FScN 4613. Spring 2014.
3. Gallaher, Daniel. (2014). Laboratory Exercise 11. FScN 4613. Spring 2014.
4. Gallaher, Daniel. (2014). Results from the Iron Bioavailability Rat Feeding Trial.
FScN 4613. Spring 2014.