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The fortification of processed
foods helps to prevent iron deficiency, but may cause an iron imbalance
(either iron overload or iron deficiency)
in certain people.1-4 In developed countries, iron fortification
of white flour began in the 1930s. All cereals (including white rice
and
cornmeal), pasta, and bread have been "enriched" with added
iron. The standards for iron fortification differ among countries
and have changed over time. For example, enrichment of these foods
is mandatory
at the state level for almost two-thirds of the United States, and
yet fortification has been abolished in Finland and Denmark because
of fears of iron overload.1
Are these fears justified? Recently, when twenty-nine breakfast cereals
were analyzed for iron content in the US, the levels of iron per serving
were found to be substantially higher than the declared labeled values.
The amount of cereal consumed in a serving by seventy-two adults was
about twice the labeled serving size. Therefore, in a single serving
of ready-to-eat cereal, adults are often consuming more than double
the recommended Reference Daily Intake (or Daily Value) for iron, which
is 18 mg.2 All these fortified products can cause iron overload in
people with a high iron intake and a sufficiently acid stomach.3,4
Symptoms of excess iron can occur with a daily intake of over 75 mg
of added iron, as long as there is a healthy production of stomach
acid.4,5 Researchers have found that the stomach's pH must be
less than 2.0 to extract iron from a fortified product and dissolve
it.4
On the other hand, people with even a slightly lower production of
stomach acid could become iron-deficient on a diet that is heavy
in these "enriched" products
or in grains, legumes, seeds, and vegetables, because non-heme iron is much
more difficult to absorb than the heme iron in rneat.4 A diet that contains
mainly vegetarian foods could also result in iron deficiency if that diet was
rich in fiber and therefore rich in phytates and phosphates. These nutrients
reduce the absorption of iron.3 Eggs are often listed among the foods that
are good sources of iron. However, the content of a nutrient in a food is not
as important as the nutrient's digestibility. Egg yolks inhibit iron
absorption, and egg whites contain the iron-binding compound ovotransferrin.6,7
Aside from low stomach acid and a highly fibrous diet, or a diet consisting
mainly of eggs, common causes of iron deficiency include the following:
- Blood loss, e.g., from menstruation,
chronic inflammation, surgery, aspirin or anti-inflammatory drug
usage, hemorrhoids, an ulcer or tumor,
diverticulosis, infestation by specific parasites or fungi, ulcerative
colitis, Crohn's disease, or from regularly donating blood.3,6
- Malabsorption, e.g., caused by a copper deficiency; a gastrointestinal
infection or damage; a consumption of laxatives, antacids, or
acid stoppers; food allergies; celiac disease; liver/gallbladder
disease;
digitalis treatment; or radiation therapy.3,8
- Poor dietary intake
of iron, which often applies to infants but also affects the elderly.
A diet of tea and toast or milk
and crackers is
likely to cause iron deficiency.3 Polyphenols in tea inhibit
iron absorption. Bovine milk contains a negligible amount of
iron.9 Furthermore, the
absorption of iron is reduced by calcium-rich foods.10 Meat,
citrus fruits, and vitamin C (found with iron in, for example,
dark-green
leafy vegetables) improve the absorption of iron.1,11
- Physical
or emotional duress, strenuous exercise, and heavy perspiration.
Chronic physical and emotional stress have been
shown to cause a greater
loss of iron (44%) than of any other trace mineral tested.12
- Pregnancy, lactation, and
periods of rapid growth in infancy and adolescence.3,10 An adequate
supply of iron is essential for the regulation of cell growth. However,
infections and tumors also require iron to grow.3,
13 Therefore,
if you feel that you are deficient in iron, before increasing your
intake, you would be well advised to have a nutritionally oriented
doctor's assessment of your digestion, your need for iron,
and the cause of the deficiency.3,4 Adult men and women past menopause
rarely need extra iron.14 Excess amounts of iron can lead to toxicity
and even death.10
The following are some common causes of iron overload:
- Increased iron uptake accompanied
by increased iron absorption, as seen in heavy drinkers of alcohol
or red wine, or found in patients after a prolonged intake of foods
fortified with iron, iron supplements, iron tonics,
or acidic foods cooked in iron cookware.3 The consumption of traditional
beers that have been brewed and fermented in iron-clad pots has
been linked with high serum ferritin iron concentrations in sub-Saharan
populations.15 However, only some of the consumers of this beer
(which
contains as much as 82.0 mg/I) develop iron overload.15,16 Scientists
have discovered that a variable mutation in the gene ferroportin
(hemochromatosis type 4) is the actual reason for the absorption
of excess iron in certain
people of African descent.16 Liver disease can also cause increased
storage of iron.3
- Hereditary hemochroinatosis is a common genetic
iron overload disorder.3 Iron accumulates initially in the organs,
then throughout the body.3,17
At least two white American males in every 500 suffer from it.10
More men than women are afflicted.3 Genetic studies point to the disorder's
Celtic origin during a time of dietary iron deficiency about
2000 years ago when this mutant gene was actually an advantage.16 The
large majority
of cases have various mutations in the HFE gene; several other
mutations that cause the disease have also been identified.16,18
- Focal
hemosiderosis occurs mainly in the lungs and kidneys and is secondary to
another disease process that causes episodes of pulmonary hemorrhage
(as in pulmonary aspergillosis) or extensive intravascular
hemolysis (as in
autoimmune diseases such as rheumatoid arthritis).3,18,19
- Sideroblastic
anemias can be inherited or acquired. Iron accumulates first in
the bone marrow. Hereditary sideroblastic
anemia, affecting
mostly men, may respond to vitamin B6 therapy. Patients requiring
either regular blood transfusions or chloramphenicol treatment
or taking anti-tubercular,
antimicrobial, or anti-Parkinsonian drugs that inhibit B6
metabolism develop iron overload, as do patients with chronic infections
or malignancies.3
- Porphyria (a sideroblastic condition) occurs
when one or more of the eight enzymatic reactions in heme synthesis
are
blocked,
resulting
in the overproduction of porphyrin compounds and their
precursors. Any of these sideroblastic conditions results in the
ineffective
production and maturation of red blood cells, because the
mitochondria cannot
utilize the iron trapped intracellularly.3 HFE hemochromatosis
gene mutations have been linked with porphyria cutanea
tarda and have been
found in patients with acute inherited variegate porphyria.20
- The
inhibition of enzymatic reactions in the heme biosynthetic pathway
can also cause a mitochondrial buildup of iron.3
This enzymatic pathway
is inhibited by metals such as excess iron (or lead that
damages at least six of the enzymes in the pathway) and
by omega 6
fatty acids
and many chemicals.21,22 The dental metals that accumulate
in our mouths (and then bodies), the man-made chemicals,
fats, and
added iron that
are prevalent in our food, beauty, and personal care
products (and therefore in our tissues) are the most insidious causes
of anemia.21,23
Either too much or too little intracellular iron leads
to heme deficiency, anemia, and oxygen-deprived tissues.4,24
Adequate iron and oxygen are vital
for one's immunity.3,25
The iron-rich soils of East and Central Africa have been associated
with the development of Kaposi's sarcoma in HIV-1 positive cancer
patients.15 Conventional responses to cancer such as chemotherapy,
radiation, and testosterone blockade can cause or worsen an anemia.3,9
Cancer patients with anemia have been shown to have a 65% increase
in mortality. The risk of death from either a stroke or heart attack
sharply increases with the severity of an anemia. Extremely anemic
heart-attack patients have been found to be 78% more likely to die
within 30 days and moderately anemic patients 52%. The elderly develop
anemia more frequently than any other blood disorder.9 Iron deficiency
and iron overload are treatable conditions, especially when they are
diagnosed and treated early on.9,10 The good news is that the majority
of anemic patients have been successfully treated simply by correcting
their production of stomach acid.4
Judy Kitchen
3637 Serra Road
Malibu, CA 90265
310-456-9061
Notes
1 . Ramakrishnan U, Yip R. Experiences and challenges in industrialized
countries:
control of iron deficiency in industrialized countries, supplement:
Forging effective strategies to combat iron deficiency. J Nutr.
2002;132:8205-8245.
2. Whittaker P, Tufaro PR, Rader JI. Iron and folate in fortified cereals.
Journal of the American College of Nutrition.
2001;20(3):247-254.
3 . Harmening DM. Clinical Hematology and Fundamentals of Hemostasis. Third
Edition. Philadelphia: F.A. Davis Company, 1997.
4. Wright JV, Lernard L. Why Stomach Acid Is Good For You.
New York: M. Evans and Company, Inc., 2001.
S. Redmon GL. Minerals What Your Body Really Needs and Why.
New York: Avery,1999.
6. Murray M, Pizzorno J. Encyclopedia of Natural Medicine.
Revised Second Edition. California: Prima Publishing, 1998.
7. Hattersley JC. The nearest thing to a perfect food: Part 2. Townsend
Letter. June 2002;227.
8. Balch PA, Balch JF. Prescription for Nutritional Healing.
Third Edition. New York: Avery, 2000.
9. Disease Prevention and Treatment.
Fourth Edition. Florida: The Life Extension Foundation, 2003:92,95,864.
I0. Casdorph R, Walker M. Toxic Metal Syndrome.
New York: Avery, 1995.
11 , Balch PA. Prescription for Dietary Wellness.
Second Edition. New York: Avery, 2003.
12. Martlew G. Electrolytes, the Spark of Life.
Florida: Nature's
Publishing, Ltd., 1994.
13. Arnold RS, Shi J, Murad E, Whalen AM, Sun CQ, Polavarapu R, Parthasarathy,
Petros JA, Lambeth JD. Hydrogen peroxide mediates the cell growth and
transformation caused by the mitogenic oxidase Nox1. PNAS.
May 2001; 98 (10).
14. Rowen RJ. Action to Take to Make Yourself Heart Attack Proof.
Atlanta, GA: Second Opinion Publishing, Inc., 2002.
15. Wojcicki JM., Newton R, Urban MI, Stein L, Hale M, Patel, Moosa
SP, Bourboulia D, Sitas F. Risk factors for high anti-HHV-8 antibody
titers (> 1:51,200) in black, HIV-positive, South African cancer
patients: a case control study. BMC Infect Dis.
2003;3: 21.
16. Pietrangelo A. Hereditary hemochromatosis: A new look at an old
disease. N Engl J Med. 2004;350:2383-97.
17. McLaren GD, Muir WA, Kellermeyer RW. Iron overload disorders: natural
history, pathogenesis, diagnosis, and therapy. Crit Rev Clin
Lab Sci.
1983;19(3):205-66.
18. Beers MH., Berkow R. Hematology and oncology. Chapter 128. In:
The Merck Manual of Diagnosis and Therapy.
Seventeenth Edition. New York: Merck & Co.,2005.
19. Reichenberger F, Habicht JM, Gratvvohl A, Tamm M, Diagnosis and
treatment of invasive pulmonary aspergillosis in neutropenie patients.
Eur Respir J. 2001; I 9:743-755.
20. de Vilhiers, J, Nico P, Hillermann, R, Loubser L, Kotze, MJ. Spectrum
of
mutations in the HFE gene implicated in haemochromatosis and porphyria.
In: Human Molecular Genetics.
Cambridge: Oxford University Press, 1999:1517-1522.
21 . Marks GS., Exposure to toxic agents: The heme biosynthetic pathway
and hemoproteins as indicator. CRC Critical Reviews in Toxicology.
1985; 15 (2).
22. Hanson JW., Dailey HA. Purification and characterization of chicken
erytlirocyte ferrochelatase. Biochemistry Journal. 1984; 222:695-700.
23. Nick GL. Inflammation and detoxification. Townsend Letter.
April 2006; 273.
24. Atamna H, Killilea DW, Killilea AN, Ames BN. Heme deficiency may
be a factor in the mitochondrial and neuronal decay of aging. PNAS.
2002; 99(23): 14807-14812.
25. Kitchen, J. Why nutritional therapies fail in patients who need
them the most. Townsend Letter.
April 2004; 249.
26. Potter BJ, Wang F. Molecular regulation of iron homeostasis and
resistance to infection in alcoholics. Frontiers in Bioscience 7.
May 1, 2002;1396-1409.
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