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Updated 7/24/2013   

         Dr. Bernard Presser D.C.

5696 Magnolia Woods Drive

Memphis, TN 38134


If you have any questions, please contact us at 901-417-7905

 More articles coming soon.


Iron is essential to life.  Although concern has usually been about low iron levels, there is new anxiety regarding iron overload.  Iron deficiency is still a reality in the US, particularly affecting toddlers (7%), teenage girls and women of childbearing age (9% to 16%).  Nearly 8 million women are iron deficient and 3.3 million women have clinical iron deficiency anemia.  However, hemochromatosis is the most prevalent inherited disease, expressed by the uptake of excessive iron, the absorption of two to three times as much dietary iron as normal.  It affects mostly men.  Iron deposits develop in major organs, especially the liver, pancreas, and heart, and may eventually lead to widespread organ failure.  Recently alarm has arisen about excessive iron stores in people who do NOT have an inherited disease.  A theory linking high levels of stored iron to cardiovascular disease has gained notoriety.  A Finnish study in 1992 fueled the idea that a high level of iron increases the risk of a heart attack.  Warnings sound about the dangers of getting too much iron.

Every cell in the body contains iron, which plays a vital role in numerous biochemical reactions.  The total amount in an adult body is about 4 grams, enough to make a 3-inch nail.  Of this amount, 2.72 grams are in red blood cells as hemoglobin which carries oxygen in the blood.  About 0.12 gram is in myoglobin which carries oxygen in muscle.  About 1 gram is stored in the liver and spleen, 0.003 gram is in transferrin (a globulin in the blood that binds and transports iron), and 0.0035 gram is in cytochromes (proteins involved in cellular respiration) such as cytochrome-C which is essential in production of cellular energy.  Tiny amounts are stored in bone marrow.  Iron has many roles in life-supporting enzyme actions for energy transformations in the cells and for deactivation of toxic peroxides.  Iron is required in cell division, immune function, and the synthesis and activity of various proteins.

Iron is stored as the soluble protein complex ferritin or as the insoluble protein complex hemosiderin in the liver, spleen, bone marrow and skeletal muscles.  Stored iron is available should the need arise from inadequate diet, blood loss, or increased need (pregnancy, lactation, growth, inflammation, infection, chronic illness, excessive physical activity, etc.).  Iron is tightly regulated by the body.  Only a small portion of dietary iron is absorbed, the amount determined by need.  If there is a deficit, more is absorbed.  If there is a sufficiency or overabundance, less is absorbed and ferritin stores increase.  Absorption is affected, not only by the amount ingested, but also by the source (form) and various bodily determinants.  A healthy man may absorb only 1% of dietary iron whereas a pregnant woman may absorb and retain more than 35%.  Excretion of iron is limited, ‘recycled' as long as possible.  Iron is not readily excreted via usual excretory routes (urine, bile, sweat), but primarily through shedding of cells from the skin or gastrointestinal tract, in hair, or through blood loss.  When iron stores are loaded, ferritin in the feces increases.  Each day, almost 1% of a person's red blood cells are destroyed and 25 milligrams of iron is released from the hemoglobin.  The majority of this iron is conserved and reused.

Iron appears in two primary forms in the body - ferrous and ferric.  Ferrous iron is more active and available for use.  Ferric iron is quite insoluble and tends to be a storage form. Ferric iron must be converted to the ferrous form to become bioavailable.  The intestinal mucosa can reduce dietary ferric sources into a form that can be transported across the gut wall.

There are two forms of food iron: heme and nonheme.  Heme is absorbed more efficiently (about 30%) than nonheme (about 10%).  Heme does not necessarily require other food agents such as vitamin C complex or chelating agents for absorption, whereas nonheme readily uses such agents.  Heme is present in animal tissues, mostly from hemoglobin and myoglobin.  About one-third of the total iron in animal foods is heme; the remaining two-thirds and ALL the iron in vegetable products is nonheme.  Nonheme is present in grains, legumes, fruits, vegetables, and dairy products.  Consumption of a little heme-iron increases absorption of nonheme iron - thus a little red meat enhances iron absorption from plant foods.  Prolonged cooking at high temperatures reduces absorption of iron up to 40%. i


Symptoms of iron deficiency or excess are initially not striking.  Even as more obvious signs develop, they may be attributed to other causes.  It can take months or even years for symptoms to become evident.

People who are iron deficient are often irritable, depressed, easily fatigued, easily chilled, pale, and weak.  They may experience shortness of breath, heart palpitations, emotional lability, muscle weakness and fatigue, impaired immune function, loss of appetite, restless legs, feelings of "pins and needles" in feet and hands, itchy skin, hair loss, ringing in the ears.  Depression may last months after the anemia is resolved.  Chronic inflammatory diseases (recurrent respiratory infections, rheumatoid arthritis, etc.) often lead to anemia.  Iron deficiency may impair memory, concentration, cognitive abilities, endurance, and aerobic adaptation to exercise.  In babies it may cause problems with motor coordination or language.  Iron deficiency, even without clinical anemia, can result in many of these symptoms in some people.  Other people with overt anemia may experience only a few symptoms or several to only a mild degree.  Because an individual is tired does not mean he/she is iron-deficient.  Any of the symptoms can be caused by other factors, deficiencies, or imbalances.

People who experience iron excess may feel profound fatigue; have joint pain; skin that turns gray, bronze, or brown; loss of libido; impotency in men; irregular or no menstrual periods in women; abdominal pain; irregular heartbeat; depression; loss of body hair.  There may be elevated blood sugar or diabetes, chronic intermittent diarrhea, an enlarged liver or spleen, congestive heart failure, hypothyroidism or cirrhosis.  Iron overload due to hemochromatosis is caused, in 95% of cases, by a defective gene.  Major symptoms may be viewed as independent conditions by different doctors rather than as a grouping of problems pointing to iron overload.  Typically, the disorder does not become apparent until middle age.  Hemosiderosis, excess iron deposition especially in the liver and spleen, occurs in diseases in which there is marked red blood cell destruction, such as pernicious anemia, hemolytic anemia, chronic inflammation or infection. ii


It was believed that calcium interfered with iron absorption, so people were advised to take iron and calcium supplements at different times and to avoid eating calcium-rich foods (such as milk products) with iron-rich foods (such as green leafy vegetables and whole grains).  But recent studies using real foods and a normal, varied diet found that calcium intake has no significant influence on iron absorption.  Even consumption of milk with every meal does not reduce nonheme-iron absorption.  However, NONFOOD calcium supplements, such as calcium phosphate, can reduce iron absorption.

Iron absorption from nonheme-iron foods is significantly enhanced - sometimes too much -- by ascorbic acid.  But vitamin C COMPLEX in REAL food (not isolated, synthetic ascorbic acid) is far superior for iron utilization, enhancing proper absorption without causing imbalances.  Excessive iron is not absorbed and other nutrients are present for proper iron utilization.  For example, copper needed for proper iron balance and function is present in vitamin C complex.  Copper (tyrosinase) is depleted when ascorbic acid alone is habitually ingested.  High doses of ascorbic acid deplete calcium, another very important nutrient for iron metabolism.  Vitamin C complex does not disrupt calcium.

Copper deficiency impairs iron metabolism.  The protein ceruloplasmin (Cp) contains most of the copper in blood serum.  Cp stimulates iron uptake by cells.  Individuals lacking this protein accumulate damaging levels of iron in their tissues.  Iron depletion, even without anemia, is associated with low Cp concentrations, low serum copper, and low superoxide dismutase activity.  Copper is necessary for the release of iron from storage sites.  Export of iron by tissues requires oxidation of ferrous iron to the ferric state by plasma Cp.  There are at least three copper oxidases involved in iron metabolism (Cp, FET3, hephaestin).  So, having too little copper can cause anemia even with an ample iron supply.

Concentrations of minerals such as copper and selenium (required as cofactors for numerous enzymes) are diminished in iron deficiency.  These enzymes include catalase, superoxide dismutase, glutathione peroxidase.  Studies indicate there are metabolic interactions among iron, zinc, and vitamin A complex.  Supplementation by a nonfood iron (such as ferrous gluconate) may interfere with zinc absorption and lead to lower plasma vitamin A concentrations.  A beta-carotene enzyme may be iron-dependent and sensitive to copper status.  Coffee and tea inhibit absorption of nonheme iron by about 40% and 70% respectively, but this inhibitory effect may be overcome by consumption of vitamin A-containing foods with the same meal.  Recent research indicates that moderate amounts of oxalates in plant foods (such as spinach, beet greens, chard, etc.) do not block iron uptake.  Oxalase, an enzyme in these vegetables, prevents the oxalates from blocking mineral uptake.  Cooking destroys oxalase.

Phytates (in whole grains, legumes, nuts, and seeds), tannins (in tea and coffee), polyphenols (in some vegetables), and alcohol are believed to inhibit iron absorption - though there is still debate about nutritional relevance.  If grains, beans, nuts, and seeds are soaked to begin the germination process or if flours are allowed to slowly leaven (sourdough or yeast dough), phytates dissipate and additional nutrients are released.  "Modest amounts" of vitamin C complex from fruits and vegetables also counteract the inhibitory effect of phytates on iron absorption.  In fact, phytate intake appears to have little influence on body iron stores.  As for dietary phenols, their large number and complexity make analysis of their influence on iron absorption quite challenging.  Essentially, when effects of whole meals are examined rather than single foods, only minimal difficulties are found.  Consumption of more than 30 grams of alcohol a day is associated with markedly elevated ferritin concentrations, so excess alcohol intake may increase iron absorption.

Ionized minerals, electrolytes, and vitamin complexes are INTERDEPENDENT.  Many nutrients are affected by iron deficiency or iron overload.  Vitamins A, B, and C complexes; zinc; copper; manganese; molybdenum, proteins, polypeptides, and certain amino acids (such as cysteine) are among the nutrients involved in iron absorption and function.  Any tissue injury or toxicity or inflammation, or any chronic infection can result in iron deficits.  Deficiencies of multiple nutrients may prolong iron deficits.  Chronic physical and/or emotional stress cause a greater loss of iron (up to 44%) than any other trace mineral tested.  But overweight and obese people are more likely to have elevated ferritin.

Sufficient hydrochloric acid in the stomach is required to free iron from food and convert it from ferric iron (the most common form in food) to the more absorbable ferrous form.  Anemia can cause decreased gastric activity, making the situation even worse.  Decreased hydrochloric acid and anemia can contribute to damage in the gastrointestinal lining, causing nutritional deficiencies, food sensitivities, and other problems to develop.  Increased intestinal permeability ("leaky gut") may allow excessive amounts of iron to permeate the intestinal lining.

Can vegetarians obtain sufficient iron from their diets since they consume only nonheme iron?  If the diet consists of nutrient-dense whole foods and is well-planned and balanced, the answer is ‘yes'.  Some studies have shown that people (especially young women) following vegetarian diets for some time have reduced iron stores compared to omnivores.  But a number of studies have shown that hemoglobin levels and other indices of iron status in long-term adult vegetarians are similar to those of non-vegetarians.  The incidence of iron-deficiency anemia among vegetarians is not much different from that of omnivores.  Whole grains, legumes, dark-green vegetables, nuts, seeds, and dried fruits are major vegetarian sources of iron.  Leafy greens, for example, often have a higher concentration of iron than animal-flesh foods.  If fresh fruits and vegetables are included with each meal, absorption is better.  However, highly restrictive vegetarian diets or diets high in refined and processed nonfoods may lead to iron deficits.  Vegetarians simply need to consume more iron in their diet (about 33 mg) than meat-eaters (about 18 mg) because of lower absorption.  And people may assimilate iron from various foods differently.  For example, long-time vegetarians may absorb and assimilate iron differently than meat eaters. iii


There are four general causes of iron deficiency anemia:

     1. Excessive blood loss as occurs with heavy menstrual bleeding, gastrointestinal bleeding (e.g., from taking NSAIDs like aspirin or ibuprofen, inflammatory conditions, tumors, ulcers), anti-coagulant drugs like Coumadin, accidents, injuries, etc.  Red blood cells appear normal in size and in hemoglobin content, but their number in circulation is reduced - low red blood cell (RBC) count.

     2. Simple iron deficiency which causes the RBCs to be smaller than normal (microcytic) and have reduced hemoglobin content.

     3. Decreased red blood cell formation which may occur with a deficiency of vitamin B12 and/or folic acid as well as iron or vitamin C complex.  The RBCs may be larger (macrocytic) and the number in circulation reduced (low RBC count).  Elevations of mean corpuscular volume (MCV, volume of RBCs), mean corpuscular hemoglobin (MCH, amount of hemoglobin in a single RBC), and mean corpuscular hemoglobin concentration (MCHC, how much space in the RBC is occupied with hemoglobin) can reflect biochemical compensations for anemia.

     4. Excessive RBC destruction (hemolytic anemia) may arise from several causes such as rare blood diseases, toxic agents, or chemical poisoning.  RBCs break down and spill their hemoglobin into circulating blood plasma.  Some hemoglobin may be recaptured and reused to produce RBCs.  If there is more free hemoglobin in the blood than the body can recycle, the excess is carried off by the kidneys, imparting a reddish color to the urine.  (Other conditions can cause blood in the urine.)

Some types of iron deficiency are related to a reduced capacity to convert ferric iron into the ferrous form, which may indicate the need for vitamins B12 and B6, folic acid, copper, molybdenum, and/or other nutrients.  Even before anemia becomes obvious, iron deficiency may be identified by measuring plasma iron levels (serum iron) and total iron-binding capacity of plasma transferrin. In anemia, the iron concentration of transferrin is low (in iron overload, the concentration is high).  This concentration can be tested by serum ferritin.

People most likely to have some degree of iron deficiency are premenopausal women (especially those who bleed heavily during menstruation); pregnant women (increased needs, increased blood production); infants, children, adolescents (rapid growth increases iron needs); dieters (inadequate consumption); long-distance runners and other high-impact endurance athletes (especially women and vegetarians).  There is still much about iron deficiency that is not known.  Anemia occurs without actual iron deficiency, perhaps indicating the importance of nutrient interrelationships. iv


Excess iron is usually related to hemosiderosis or hemochromatosis.  Hemosiderosis is characterized by the deposition (especially in the liver and spleen) of hemosiderin (an iron-containing pigment derived from the hemoglobin left over from the disintegration of RBCs.  This is one way iron is stored until needed for making more hemoglobin).  It occurs in diseases in which there is marked red blood cell destruction such as hemolytic anemias, pernicious anemia, and chronic inflammation or infection.

Hemochromatosis (usually a hereditary disease) causes the body to absorb and store too much iron.  From 1 in 200 to 1 in 500 Americans are affected.  Less than 1% of those who have the genetic mutation from both parents will go on to develop the full-blown disease.  A person who inherits the gene from only one parent will be a carrier (10% to 15% of Americans) but will not get the disease, although there may be a slight increase in iron storage.  Excessive iron storage results in excessive iron deposited in organs and tissues, principally the liver, pancreas, heart, and pituitary gland.  If not treated early enough, organ damage and failure may result.  Advanced stages are manifest by problems such as cirrhosis, diabetes, arthritis, enlarged heart, heart failure (not heart attack), hypogonadism, other endocrine problems.  Cancer of the colon or liver may develop.  The usual treatment is drawing blood regularly until the excessive iron stores are removed (several months to a year).

A serum iron blood test is not as reliable for assessing iron overload as are serum ferritin (the protein that stores excess iron) and transferrin saturation (transferrin is the protein in blood needed for transferring iron from the intestines to the bloodstream).  However, some scientists argue that high serum ferritin is not identical to high iron stores.  Some disagree with the reliance on transferrin saturation.  Thus, a thorough case history, family history, physical examination, and numerous blood tests are needed to rule out other disorders.  A genetic mutation test can indicate hemochromatosis.

In recent years, concern about excessive iron has occurred as relating to heart attacks, colon cancer, and other health problems in people who do not have hemochromatosis.  A widely quoted study from Finland (1992) suggested that people with the highest levels of iron were also at highest risk for heart attacks.  In a 1999 study from the Netherlands, heme iron intake was associated with heart attacks.  Another study found that elevated serum ferritin concentrations - not serum iron or transferrin or dietary iron - were linked to increased risk of heart attack.

However, other studies have indicated that a LOW level of iron is a risk factor for heart attack.  Iron does facilitate transport of oxygen to tissues, including the heart.  One study found that men with the greatest amount of serum iron were 20% LESS likely to die of heart disease than men with the lowest levels.  Women in the high-iron group had half the risk of heart disease than the low-iron group.  Overall, people with the highest iron levels were about 30% to 40% less likely to die from any cause during the 5-year study.  Other studies have found no association between iron status and cardiovascular disease risk.  Research continues, but to date, results supporting the hypothesis of a high-iron/heart attack connection "are weak and inconsistent."

The idea that iron causes oxidation and thus oxidative damage in the body is essentially unfounded (i.e., not true).  Treatment of iron deficiency by iron supplements has not been associated with oxidative damage.  Studies do not support a relation between iron status and LDL oxidative susceptibility (considered a cardiovascular disease risk factor).  Although iron can participate in oxidative reactions in test tubes, any involvement in free radical formation in humans or in the cause or progression of disease is "questionable."  The reaction required to produce free radicals involving iron as a catalyst is "unlikely to occur under physiologic conditions."

Iron has been accused of causing diabetes, cancer, neurodegenerative diseases (e.g., Parkinson's, Alzheimer's etc.), and other problems, but there has been no convincing evidence of this.  Hemochromatosis can increase the risk for diabetes and some cancers due to iron deposits in organs.  But consumption of iron-rich foods by persons without the genetic defect has not been linked to such problems.  Actually, iron deficiency, not excess, has been linked to some cancers such as prostate and stomach cancers.  Some animal and "in vitro" (in test tubes) studies indicate a role for excess iron in inducing cancer, but iron from foods has not been indicted and human evidence is lacking.  "Even prolonged high dietary intakes are unlikely to result in iron overload..."

Yet there are increasing numbers of people who do not have hemochromatosis developing iron overload.  Primarily a liver-cell iron overload, this is a "new syndrome."  Increased iron retention has been observed in chronic inflammation, obesity, abnormal glucose metabolism, high blood pressure, and elevated cholesterol levels.  But the question is whether excess iron intake causes such disorders OR whether the disorders lead to excessive iron retention.  When the body functions normally, excess or unneeded iron remains in the intestines (not absorbed) and is excreted.  Problems arise only when too much iron somehow "escapes" into the intestines and then the blood.

One might look at iron supplementation and iron fortification of processed foods - rather than iron naturally occurring in foods.  The amount of nonfood iron given for anemia is "often astronomical" though it is believed to be poorly absorbed.  Many people are getting more than the recommended dietary levels of iron - not from natural foods - but from iron supplements (including "multi" vitamins or minerals) AND "enrichment" or "fortification" of processed foods such as refined flours, rice, cereals, and other items.  Consumption of red meat - a naturally rich source of food iron - has been dropping for almost two decades while consumption of processed foods has been rising sharply.  Data indicate that absorption of iron from natural, unadulterated foods does not result in iron overload in healthy iron-replete persons.  Traditional people who were or are meat eaters (some almost carnivores) did and do not have iron overload.  However, inhaled tobacco smoke contains significant amounts of iron; alcohol enhances iron absorption; and unbalanced estrogens (as in hormone replacement therapies) promote iron and copper uptake.

People who develop the new iron-overload syndrome often take nonfood iron supplements.  Iron leaches from cast iron cookware into foods, especially when acidic foods (like tomatoes, wine, or citrus fruits) are included.  Cooking in stainless steel (which account for 43% of cookware sold) can also significantly increase the iron content of some foods.  This has been viewed as an advantage for people with iron deficiency.  But cast iron and stainless steel are NOT foods; the iron they contain is not a food form of iron and may contribute to imbalances. v


"Iron is extensively supplemented," not only voluntarily (choosing to take iron-containing supplements) but also involuntarily through iron "fortification" or "enrichment" in a number of foods.  Such "broadly based supplementation" is supposed to aid iron deficiency, augment hematocrit, and increase energy levels.  Yet it is possible that many people are being "injured".

It is not simply the amount of iron being ingested that can cause problems; it is the form it appears in.  Iron supplements come in various strengths and forms.  Individual needs and capacities for absorption (e.g. age, adequacy of stomach acid output, intestinal flora, intestinal disorders) also vary.  Certain forms of iron are better tolerated than others.  Ferrous forms are better absorbed than ferric forms.  The amount of elemental iron varies depending upon the formulation; elemental iron is less well absorbed than soluble iron compounds. Iron from food is different than the iron in most supplements.  Minerals in food are usually bound to proteins and complexed with organic molecules in food.  After a food is chewed and digested, the minerals generally emerge in the intestine as charged ions.  Real food provides primarily organic forms of iron whereas most supplements provide inorganic forms.  Organic means it is from an animal or vegetable source.  Elemental iron is taken up and acted upon by plants, ‘organizing' the iron into a complex of nutrients and other food factors that the body can use while maintaining "selective absorption" according to its needs.  In other words, iron from real food is more bioavailable and "user friendly" than inorganic, nonfood forms added to processed foods or put in most supplements.

It is highly unlikely that a person would develop iron toxicity from natural food sources alone (unless all foods are prepared in iron cookware).  But nonfood sources may be toxic: the estimated lethal dose is 180 to 300 mg/kg, but doses as low as 60 mg/kg have been lethal and doses of 30 mg/kg have been associated with acute toxicity.  From 1986 to 1996, about 110,000 children accidentally swallowed supplements containing iron, resulting in poisoning with 35 deaths.  As few as 5 high-potency over-the-counter iron pills (1 to 3 g) can be fatal for a small child.  Large doses (over 20 mg) of nonfood iron can cause constipation, dark stools, nausea, vomiting, and diarrhea.  It can worsen peptic ulcers, regional enteritis, and ulcerative colitis.  Ingestion of large quantities can eventually damage the liver, cause tachycardia, vomiting of blood, and peripheral vascular collapse.  It may decrease absorption of zinc, calcium, copper, and other nutrients.

Use of isolated ascorbic acid can greatly increase iron absorption.  Vitamin-C complex rich foods naturally enhance balanced iron absorption, the body choosing the amount it needs at that moment.  The proper use of real food can improve iron status in people with iron deficiency.  Food works!

Nonfood forms of iron in supplements include ferrous sulfate (the most commonly used form of iron is a combination of sulfuric acid and an iron salt.  It is also used as a wood preservative, pesticide, leather dye, and in writing ink), ferrous fumarate (ferrous sulfate + sodium fumarate), ferrous gluconate (gluconic acid + ferrous sulfate), ferrous lactate (lactic acid + iron salt).  Chelated iron - iron combined with a protein or amino acid (such as iron aspartate) is better assimilated and is easier on the intestinal tract than the above forms. The BEST source, of course, is real food!  The BEST supplement is a REAL food concentrate! vi

This website has excellent nutritional protocols for IRON PROBLEMS which are available in conjunction with the Symptom Survey.  Take the Symptom Survey to discover specifically what nutrition you need for your individual health problems.  I want to emphasize that the whole-food nutrition I recommend CANNOT be purchased in any retail store: so-called "health food" store, drug store, super market, etc.  The whole-food nutrition I recommend will help rebuild your body and help restore your health.  Those other products will only give you a pharmaceutical (drug) effect.  They will attempt to deal with your symptoms, which is the ONLY thing any drug can do, while leaving the state of your health unchanged.

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ii C Lammi-Keefe et al, Top Clin Nutr, Jul-Sept 2004, 19(3): 200-14; T Brutsaert et al, Am J Clin Nutr, 2003, 77: 441-8; J Halterman et al, Pediatrics, 2001, 107: 1381-6; A deSilva et al, Am J Clin Nutr, Jan 2003, 77(1): 234-41; K Nesbitt, Veg Times, Oct 2000, 278: 22-3; T Brownlie et al, Am J Clin Nutr, 2002, 75: 734-42; Health News, 5 Jan 1999, 5(1): 4-5.

iii S Harris, Nutr Clin Care, Sept/Oct 2002, 5(5): 231-5; M Reddy & J Cook, Am J Clin Nutr, Jun 1997, 65(6): 1820-5; L Grinder-Pedersen et al, Am J Clin Nutr, Jul 2004, 80: 404-9; J Kitchen, Townsend Lttr D&P, May 2004, 250: 109; B Mulvihill et al, Internat J Food Scienct & Nutr, May 1998, 49: 187-92; C Mukhopadhyay et al, Science, 30 Jan 1998, 279(5351): 714-17; R Eisenstein, Nutr Rev, Jan 2000, 58(1): 22-6; S Gropper et al, J Am Col Nutr, Dec 2002, 21(6): 545-52; Healthline, Jul 1999, 18(7): 10-11; F Troost et al, Am J Clin NutrNov 2003, 78(5): 1018-23; A Puring et al, J Am Col Nutr, Aug 1999, 18(4): 309-15; F Wieringa et al, Am J Clin Nutr, Mar 2003, 77(3): 651-7; JM Liv et al, Am J Clin Nutr, Dec 2003, 78(6): 1160-7; L Allen et al, Am J Clin Nutr, Jun 2000, 71(6): 1485-94; F Staubli et al, Am J Clin Nutr, Dec 2001, 74(6): 776-82; J Cook, Am J Clin Nutr, Apr 1998, 67(4): 593-4; UC Berkeley Wellness Lttr, Jun 2000, 16(9): 7; Health & Healing, Sept 2001, 11(9): 5; G Cousens, Conscious Eating, Berkeley (N Atlantic Books), 2000: 348-50.

iv UC Berkeley Wellness Lttr, Feb 2004, 20(5): 6-7; John R Lee MD Medical Lttr, Aug 2002: 1-3; A Rangan et al, J Am Col Nutr, Aug 1998, 17(4): 351-5; K Hurtado, Am J Clin Nutr, Jan 1999, 61(1): 115-9; C Breymann et al, Lancet, 6 Mar 1999, 353(9155): 841-3; M Roncagliolo et al, Am J Clin Nutr, Sept 1998, 68(3): 683-90; P Hinton et al, J Appl Physiol, 2000, 88: 1103-5; Health News, 25 Jun 1999, 5(8): 7; DJ Unsworth et al, Lancet, 27 Mar 1999, 353(9158): 1100; E Ross, Nutr Clin Care, Sept/Oct 2002, 5(5): 220-4; T Brutsaert, Am J Clin Nutr, Feb 2003, 77(2): 441-8; T Brownlie et al, Am J Clin Nutr, Mar 2004, 79(3): 437-43; N Ahluwalia et al, Am J Clin Nutr, Mar 2004, 79(3): 516-21; L Ritchie, presentation, Amer Soc Nutr Sciences meeting, Apr 17-21, 2004; F Verdin et al, BMJ, 2003, 326: 1124; N Solomons, Nutr Rev, Mar 2002, 60(3): 91-6.

v L Neff, Nutr Rev, Jan 2003, 61(1):38-42; A Gaby, Townsend Lttr D&P, Oct 2000, 207:32-3; C Northrup, Hlth Wisdom for Women, May 2003, 10(5):4-5; UC Berkeley Wellness Lttr, Feb 2004, 20(5):6-7; Health News, Apr 2001, 7(4):7; R Wood, Nutr Rev, May 2002, 60(5):144-8; K Senior, Lancet, 25 Sept 1999, 354(9184):1099; K Klipstein-Grobusch et al, Am J Epidemiol, 1999, 149(5):421-8 & Am J Clin Nutr, Jun 1999, 69(6):1231-6; C Sempos, Am J Clin Nutr, Sept 2002, 76(3):501-3; S Gropper et al, J Nutr Biochem, 2003, 14: 409-15; J Dersteine et al, Am J Clin Nutr, Jan 2003, 77(1):56-62; A Heath et al, Nutr Rev, Feb 2003, 61(2):46-62; Tufts Hlth & Nutr Lttr, Apr 2004, 22(2):2; S Lynch, Nutr Rev, Sept 2001, 59(9):310; R Jiang et al, Am J Clin Nutr, Jan 2004, 79(1):70-5; M Reddy et al, Nutr Rev, Mar 2004, 62(3):120-4; L Hallberg et al, AM J Clin Nutr, Dec 2003, 78(6):1225-5; R Moirand et al, Lancet, 11 Jan 1997, 349(9045):95-7; R Nelson, Nutr Rev, May 2001, 59(5):140-8; J Kaetwasser et al, Gut, 5 Nov 1998, 43:699-704; D Fleming et al, Am J Clin Nutr, Mar 2001, 73(3):638-46; A Patterson et al, Am J Clin Nutr, Nov 2001, 74(5):650-6.

vi R Nelson, Nutr Rev, May 2001, 59(5): 140-8; S Nightingale, JAMA, 7 May 1997, 277(17): 1343; Z Roughead et al, Am J Clin Nutr, Oct 2000, 72(4): 982-9; R Hurrell et al, Nutr Rev, Dec 2002, 60(12): 391-406; M Makrides et al, Am J Clin Nutr, Jul 2003, 78(1): 145-53; J Cook et al, Am J Clin Nutr, Jan 2001, 73(1): 93-8; Alt Med Alert, Sept 2001, 4(9): 51-2; S Lunch, Nutr Rev, Jul 2002, 60(7): 53-56; L Turner, Nutr Rev, Jul 2002, 60(7): S16-7; A Heath et al, J Am Col Nutr, Oct 2001, 20(5): 477-84; A Schauss, Minerals, Trace Elements & Human Health, Tacoma(Life Sciences Press), 1996: 1-15.

Originally published as an issue of Nutrition News and Views, reproduced with permission by the author, Judith A. DeCava, CNC, LNC.