Iron and Chelation

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Iron and Chelation

 

 

From The June 2000 Issue of Nutrition Science News

Too Much of a Good Thing

by Bill Sardi

 

Recent studies reveal that blood donors exhibit lower rates of many diseases and

experience better than average health. Additionally, the centuries-old practice

of bloodletting is being revived as a treatment for disorders such as heart

disease, cancer and Alzheimer's.1 Why would blood reduction improve health

parameters? In part, because blood removal helps to control circulating iron

levels.

Iron is an essential component of hemoglobin in red blood cells, is associated

with strength, and is required for oxygen transport, DNA synthesis and other

processes. But it also has a destructive nature. In its free form, unbound from

hemoglobin or other binding proteins, it accelerates oxidation or " rusting " of

body tissues. Since iron-induced oxidation worsens the course of virtually every

disease, iron control could be a universal approach to disease prevention and

therapy.2

Whereas poor iron intake, or impaired absorption, may lead to anemia, too much

iron--iron overload--is even more problematic.3 After full growth is achieved,

at about age 18 or so, excess iron accumulates in the blood of all humans at the

rate of 1 mg per day.2 About 80 percent of the body's iron stores are in the

blood. Women are less at risk for iron buildup than men because of the blood

they lose monthly during menstruation. As a result, women have somewhere around

half the circulating iron levels as men. Their rates for heart disease, cancer

and diabetes are also about half those of males. Because men have no direct

outlet for iron, by age 40 their iron levels are similar to those of a

postmenopausal 70-year-old woman. This amount of iron can lead to premature

aging and diseases such as arthritis, cancer, cataracts, diabetes, osteoporosis,

and retinal, liver and brain disorders.4 Postmenopausal women, or women who have

undergone early hysterectomy in their 20s, 30s and early 40s,

may experience similar problems.5

Recognizing the Problem

Iron overload hasn't gone completely unnoticed. There are a number of books on

the topic, but most are written for health professionals, leaving the public

largely unaware of the problem. Also, some confusion exists regarding the role

of iron in health and disease. First, there is a mistaken idea that the majority

of the people affected by iron overload diseases have the genetic form, called

hemochromatosis, which affects only about 1 million of the estimated 275 million

Americans. In fact, the potential threat of iron overload is universal. It comes

with advancing age and regardless of genetic factors. Second, the emphasis on

preventing anemia in children and menstruating women has detracted attention

from progressive iron buildup in adult men and postmenopausal women.6

Upon closer inspection, many health-promoting practices inadvertently control

iron. For example, taking an aspirin a day to prevent heart attacks and strokes

causes blood loss via the digestive tract on the order of about a tablespoon per

day. This results in iron loss.7 Raymond Hohl, M.D., an assistant professor of

internal medicine and pharmacology at the University of Iowa in Iowa City, says

even chronic use of a baby aspirin may help to control iron and in some cases

can induce iron-deficiency anemia.8 Aspirin also appears to increase the

production of ferritin, an iron-binding protein that prevents iron from inducing

oxidation.9 By exercising, a person loses about 1 mg of iron through sweat.10

Fasting and vegetarian diets, both of which promote longevity in animals and

humans, limit iron consumption because red meat contains the highly absorbable

heme iron. Whether or not related to iron consumption, restricting red meat

consumption has been shown in various studies to reduce

the risk of colon cancer.11

Normal Iron Regulation

In healthy individuals there is little if any unbound iron circulating in the

blood. In all disease states, however, unbound iron (also called free iron) is

released at sites of inflammation and can spark uncontrolled oxidation.12

Fortunately, there are numerous automatic mechanisms in the body that help to

control iron, many by chelation--compounds that bind to a toxic substance (such

as iron) and render it nontoxic or nonactive. Albumin, a simple protein found in

blood, acts as a chelator by loosely binding to iron.13 Ferritin, produced in

the liver, is another iron-binding protein.14 Transferrin is a protein that

chelates iron and totes it back to the liver, where it is metabolized and

excreted.15 The liver produces lactoferrin, another iron chelator, when

challenged by infectious agents.16 This is important because pathogenic

organisms such as viruses, bacteria and fungi require iron for growth.

Furthermore, as iron stores increase, the gastric absorption of iron decreases.

So

the body employs numerous mechanisms to control iron that are activated when

threatened by disease. However, these defensive mechanisms can be overwhelmed.

Blood tests for iron levels (i.e., hemoglobin and ferritin levels are checked

for transferrin saturation percentages) are often useful, but the results of

these tests are confounded in states of prolonged inflammation or disease.17 A

skilled hematologist is often the best professional from whom to obtain personal

information concerning blood iron levels.

Differentiating between anemia and iron overload can be difficult because both

conditions cause fatigue. One study at the Department of Medicine, University of

Western Ontario in Canada, found that iron overload can produce a wide range of

symptoms, such as joint pain (particularly hip), unexplained gastric pain,

frequent infections, skin bronzing, elevated liver enzymes, cessation of

menstruation, hair loss and heart flutters (fibrillation). Yet, of 410

iron-overload patients, 27 percent experienced no symptoms whatsoever.18 Common

symptoms of iron-deficiency anemia are lowered resistance to infections,

fainting, breath holding, mental fatigue, sleepiness, cold hands and feet, and

cravings for ice, meat or tomatoes, all which are more likely to occur among

women.19

Dietary Iron Control

Various dietary practices can help control iron levels. In a relatively short

period of time, dietary changes can result in anemia, iron overload or an ideal

state of iron control. Anemia can be induced in about 120 days, while symptoms

of iron overload can come on in just 60 days.

Humans absorb only a fraction of the iron they consume, but there are many

controlling factors.20 Iron absorption rates from food vary widely, from less

than 1 percent to nearly 100 percent.21 Cooks who use iron or stainless steel

pots increase the amount of iron they consume.22 Generally, iron in plant foods

is not as well absorbed as iron from meat: Only 5 percent of iron in plant foods

is available, vs. 30 to 50 percent of iron from meat.23 Olive oil and spices

such as anise, caraway, cumin, licorice and mint promote iron absorption,24

while antacids, eggs and soy reduce availability.25 Since dairy products contain

lactoferrin, milk also inhibits the absorption of iron.26 Moderate alcohol

consumption is unlikely to pose a problem with iron absorption, but excessive

amounts of alcohol is associated with iron overload, particularly in adult

males.27

Vitamin C also increases iron absorption.28 However, there is no evidence that

vitamin C leads to iron overload. Thus vitamin C should not be avoided by

meat-eaters for this reason, since studies show high-dose vitamin C supplements

are associated with a decreased risk for heart disease, cancer, cataracts and

other disorders.29 A vegetarian diet does not generally cause iron-deficiency

anemia because there is more vitamin C in plant-food diets, which enhances

absorption.30

A 1982 human study was conducted to assess the effect of various drinks on iron

absorption. A subject ate a standard meal of a hamburger, string beans, mashed

potatoes and water. When green tea was drunk instead of water, iron absorption

was reduced by 62 percent. Coffee reduced iron absorption by 35 percent, whereas

orange juice (as a source of vitamin C) increased absorption by 85 percent.

Contrary to other studies, milk and beer had no significant effect.31

Bioflavonoids (found in berries, coffee, green tea, pine bark, quercetin and the

rind of citrus fruits, particularly blueberry, cranberry, elderberry and grape

seed) and phytic acid (a component of whole grains and seeds such as sesame)

bind to iron and other minerals in the gastric tract and help to limit iron

availability. If bioflavonoids and phytic acid haven't bound to minerals in the

digestive tract they will get into the bloodstream, where they can bind to free

iron, acting as blood-cleansing iron chelators. Therefore, maximum iron

chelation in the blood circulation is achieved when these iron binders are

consumed apart from meals.

Phytic acid--also called inositol hexaphosphate, or IP6--is comprised of six

phosphorus molecules and one molecule of inositol. It has been mistakenly

described for decades as an " anti-nutrient " because it impairs mineral

absorption. However, in the 1980s food biochemist Ernst Graf, Ph.D., began to

tout phytic acid for its beneficial antioxidant properties achieved through

mineral chelation.32

Phytic acid in foods or bran should be distinguished from supplemental phytic

acid, which is derived from rice bran extract. In foods, phytic acid binds to

iron and other minerals in the digestive tract and may interfere with mineral

absorption. As a purified extract of rice bran, taken between meals so it will

not bind to minerals in the digestive tract, phytic acid is readily absorbed

into the bloodstream, where it acts as a potent mineral chelator.33 Phytic acid

binds to any free iron or other minerals (even heavy metals such as mercury,

lead and cadmium) in the blood, which are then eliminated through the kidneys.

Phytic acid removes only excess or unbound minerals, not mineral ions already

attached to proteins.

Phytic acid is such a potent--but safe--iron and mineral chelator that it may

someday replace intravenous chelation therapy such as the mineral-chelator EDTA

or iron-binding drugs such as desferrioxamine (Desferal). Because of its ability

to bind to iron and block iron-driven hydroxyl radical generation (water-based)

as well as suppress lipid peroxidation (fat-based), phytic acid has been used

successfully as an antioxidant food preservative.34

Phytic acid supplements should not be taken during pregnancy since the

developing fetus requires minerals for proper development. Because aspirin

causes a small loss of blood and consequently helps to control iron levels, the

simultaneous use of phytic acid with a daily aspirin tablet is not advised. A

three-month course of phytic acid should achieve adequate iron chelation, and

prolonged daily supplementation may lead to iron-deficiency anemia. Anemic

individuals who take phytic acid as a food supplement are likely to feel weak

shortly after consumption, whereas iron-overloaded individuals are likely to

feel increased energy.

For those at risk for iron overload, it may be wise to avoid iron in

multivitamins and shun fortified foods that provide more than 25 percent of the

recommended daily intake for iron. No doctor should prescribe iron tablets for

patients who complain of fatigue without blood tests and a thorough health

history. Iron-rich foods such as red meat and molasses may prevent anemia and

build strength during the growing years but in adulthood may lead to iron

overload among men and postmenopausal women. Those individuals who learn how to

achieve iron balance will maintain the most desirable state of health throughout

life.

 

 

 

Bill Sardi is a health journalist and consumer advocate in Diamond Bar, Calif.

He recently published The Iron Time Bomb (Bill Sardi, 1999).

 

References

 

1.Bonkovsky HL, et al. Iron in liver diseases other than hemochromatosis. Semin

Liver Dis 1996;16:65-82.

 

2. Gutteridge JMC, Halliwell B. Antioxidants in nutrition, health and disease.

New York: Oxford University Press; 1994. p 24-39.

 

3. McCord JM. Iron, free radicals, and oxidative injury. Sem in Hem

1998;35:5-12.

 

4. Crawford RD. Proposed role for a combination of citric acid and ascorbic acid

in the production of dietary iron overload: a fundamental cause of disease.

Biochem Mol Med 1995;54:1-11.

 

5. Emery TF. Iron and your health. Boca Raton (FL): CRC Press; 1991. p 1-13.

 

6.Arthur CK, Isbister JP. Iron deficiency. Drugs 1987;33:171-82.

 

7. Rider JA, et al. Double-blind comparison of effects of aspirin and namoxyrate

on pH of gastric secretions, fecal blood loss, serum iron and iron-binding

capacity in normal volunteers. Curr Ther Res 1965;7:633-8.

 

8. Bankhead C. In assessing anemia, doctors must decipher role of iron

deficiency. Med Tribune Clin Focus 1997 Mar; 20:24.

 

9. Oberle S, et al. Aspirin increases ferritin synthesis in endothelial cells: a

novel antioxidant pathway. Circ Res 1998;82:1016-20.

 

10. Vellar OD. Studies on sweat losses of nutrients. Scand J Clin Lab Invest

1968;21:157-67.

 

11. Kampman E, et al. Meat consumption, genetic susceptibility, and colon cancer

risk. Cancer Epid Biomarker Prev 1999;8:15-24.

 

12. Griffiths, E. Iron and infection. New York: John Wiley & Sons;1987. p 1-25.

 

13. Goldwasser P, Feldman J. Association of serum albumin and mortality risk. J

Clin Epid 1997;50:693-703.

 

14. Aust SD. Ferritin as a source of iron and protection from iron-induced

toxicities. Toxicol Lett 1995;82:941-4.

 

15. Aisen P, Brown EB. The iron-binding function of transferrin in iron

metabolism. Sem Hematol 1977;14:31-46.

 

16. Baker EN, et al. Three-dimensional structure of lactoferrin. Adv Exp Med

Biol 1998;443:1-14.

 

17. Hulten L, et al. Iron absorption from the whole diet in men: how effective

is the regulation of iron absorption? Am J Clin Nut 1997;66:347-56.

 

18. Adams PC, et al. The relationship between iron overload, clinical symptoms

and age in 410 persons with genetic hemochromatosis. Hepatology 1997;25:162-6.

 

19. Marinella MA. Tomatophagia and iron-deficiency anemia. N Eng J Med

1999;341:60-1.

 

20. Monsen ER. The ironies of iron. Am J Clin Nutr 1999;69:831-2.

 

21. Hurrell RF. Preventing iron deficiency through food fortification. Nut Rev

1997;55:210-22.

 

22. Park J, Brittin HC. Increased iron content of food due to stainless steel

cookware. J Am Diet Assoc 1997;97:659-61.

 

23. U.S. Agricultural Research Service, USDA Bulletin. 1998 Dec 23.

 

24. El-Shobaki FA, et al. The effect of some beverage extracts on intestinal

iron absorption. Z Ernahrungswiss 1990;29:264-9.

 

25. Morris ER. An overview of current information on bioavailability of dietary

iron to humans. Fed Proc 1983;42:1716-20.

 

26. Davidsson L, et al. Influence of ascorbic acid on iron absorption from an

iron-fortified chocolate-flavored milk drink in Jamaican children. Am J Clin Nut

1998:67:873-7.

 

27. Fletcher LM. Alcohol and iron: one glass of red or more? J Gastro Hepatol

1996;11:1039-41.

 

28. Derman DP, et al. Importance of ascorbic acid in the absorption of iron from

infant foods. Scand J Haematol 1980;25: 193-201.

 

29. Gerster H. High-dose vitamin C: a risk for persons with high iron stores?

Int J Vitam Nutr Res 1999;69:67-82.

 

30. Craig WJ. Iron status of vegetarians. Am J Clin Nut 1994 May; 59(5

Suppl):12335-7.

 

31. Hallberg L, Rossander L. Effect of different drinks on the absorption of

non-heme iron from composite meals. Hum Nutr Appl Nutr 1982;36:116-23.

 

32. Graf E, et al. Phytic acid--a natural antioxidant. J Biol Chem

1987;262:11647-50.

 

33. [No authors listed] Phytic acid: new doors open for a chelator. Lancet 1987

Sept 19:2;2(8560):664-6.

 

34. Lee BJ, Hendricks DG. Phytic acid protective effect against beef round

muscle lipid peroxidation. J Food Sci 1995;60:241-4.

 

 

 

Copyright 2003 Knowledge of Health. .

 

 

 

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