Hemochromatosis is a genetic disease of abnormal iron metabolism. A person who has hemochromatosis absorbs too much iron from an ordinary diet. Consequently, this condition is sometimes called "iron overload" or "iron storage overload." If untreated, hemochromatosis can damage major organs in the body (Roeckel et al. 1998). Iron is a catalyst for the generation of free radical activity that has been identified as an underlying cause of cancer, atherosclerosis, liver cirrhosis, neurological disease, and other aging-related disorders. Approximately 32 million Americans are carriers for hemochromatosis, but only a minority of these carriers actually manifests the disease.
SYMPTOMS AND DIAGNOSIS
Although incidence by this means is rare, hemochromatosis can be acquired from massive doses of iron supplements or from blood transfusions. Far more common is the genetic form of the disease. Genetic hemochromatosis (GH) is also known as hereditary hemochromatosis (HH) and can be detected through screening (Ramrakhiani et al. 1998).
The following are symptoms of hereditary hemochromatosis (HH):
Screening for HH involves multiple tests. It is important to know that a person can be anemic and still have this iron overload condition. Hemochromatosis can be a "silent carrier" as well as a silent killer. "Low iron" cannot be relied upon to determine if a person has HH.
However, the following tests can help screen for HH:
Additionally, a relatively new DNA test called HLA-H, or more commonly HFE or Hfe, is available (Piperno 1998; Piperno et al. 1998). A patient's physician may also want to test liver enzymes and investigate the family history in order to confirm a diagnosis of the genetic disorder. A liver biopsy can also show exactly how much excessive iron the liver is storing. However, with the advent of the DNA test for HH, liver biopsies are not taken as frequently. A study in the 1998 issue of Gastroenterology examined 197 French HH patients with the C282Y homozygous gene. The aim of the study was to define noninvasive predictors of severe fibrosis (a complication usually involving cirrhosis). Ultimately, simple biochemical and clinical variables such as serum aspartate aminotransferase, serum ferritin, and hepatomegaly were just as predictive as liver biopsies except for the diagnosis of severe fibrosis (Guyader et al. 1998).
Traditionally, the fastest and most efficient way to rid the body of excessive iron is through phlebotomy (similar to donating blood at a blood bank): the person "gives" blood (sometimes weekly) until measures of iron stores are reduced to a safe level. If anemia is also present, however, drugs in the form of iron chelators may be prescribed. The number of phlebotomies necessary to "de-iron" the body varies, depending on the severity of the disease at diagnosis. Phlebotomies are usually needed periodically throughout life as well (Borch-Iohnsen 1997).
In addition to phlebotomies, in conventional treatment, the patient may be told to avoid alcohol, vitamin C with meals, cast-iron cookware, breakfast cereals containing 100% of the recommended daily allowance of iron, and raw shellfish. The person may also be told to drink coffee or tea with meals in order to help block iron in the foods eaten.
Using Calcium to Block Iron Absorption
A practical way of lowering iron is to interfere with its absorption from food. The American Journal of Clinical Nutrition stated that if 300 mg of calcium were taken with a meal, the amount of iron absorbed would be reduced by 40%. That is a simple and inexpensive way to reduce iron in the blood (Hallberg 1998). To obtain 300 mg of calcium, it is necessary to take a calcium supplement that supplies 300 mg of elemental calcium. The best way of doing this is to take one or two 1000-mg capsules of calcium citrate with every meal that contains iron.
Each 1000-mg calcium citrate capsule provides 220 mg of elemental calcium. Another calcium supplement called Bone Assure would provide 333 mg of elemental calcium (and other important minerals) for every 2-capsule dose. According to published studies, the maximum amount of calcium that will inhibit iron absorption is 300 mg with each meal. Amounts of calcium greater than 300 mg do not cause any additional interference with iron absorption.
It is important to note that some people become tolerant to calcium-induced, iron-absorption blockage after several months, so if calcium provides a sudden reduction in serum iron levels, be certain it continues to work by having regular blood tests. Soluble fibers such as psyllium seed husks (Metamucil), guar gum, and the pectins also help to block iron (and other mineral) absorption.
A study in the United Kingdom journal Gut indicates that drinking black tea rich in tannin with meals can reduce iron absorption. The control group drank water with meals; the study group drank tea with meals. Intestinal iron absorption was measured by studying serum iron binding capacity and serum ferritin. Results showed a significant reduction in the study group as opposed to the control group. The goal then is to use the drinking of black tea to reduce phlebotomy frequency in the management of patients with hemochromatosis (Kaltwasser et al. 1998).
Green tea extract is a potent iron-chelating agent. Green tea is an antioxidant that helps to remove excess iron from the liver. Hemochromatosis patients should take 4-10 green tea extract capsules with at least 300 mg of active polyphenols per capsule.
A Norwegian study examined the effects of diet on primary hemochromatosis. Health professionals as well as patients have indicated a strong desire to try to reduce the number of phlebotomies necessary a year through following a specialized diet. This study indicated the following items should be avoided:
Recommendations included following a diet rich in the following:
A Swedish study reported in the European Journal of Clinical Nutrition also recommended following a diet in which foods were not fortified with iron. Sweden formerly had the highest iron fortification of its food in the world. In January 1995, the iron fortification program was withdrawn because of the uncertain effects and benefits of such fortification. Sixteen men with hemochromatosis were then studied as to the effects of the fortification withdrawal. The study indicated iron absorption was significantly reduced; these effects were measured through quantitative phlebotomy. The study further concluded that those persons with hemochromatosis will have a slower rate of clinical disease progression when their food is not iron fortified (Olsson et al. 1997).
Iron is a catalyst for many enzymatic reactions as well as for massive free-radical damage to cells. Because hemochromatosis patients have chronic high iron levels, they are at risk for a host of free-radical-generated diseases, including cancer and heart disease. Therefore, it is crucial to inhibit these free radicals by consuming large amounts of antioxidants on a regular basis (Last 1991).
One problem that hemochromatosis patients must face is that the potent antioxidant vitamin C, when taken in the presence of iron-containing foods, can increase the absorption of iron from the digestive tract into the bloodstream. Therefore, hemochromatosis patients should take one 500-mg buffered vitamin C capsule 3 times a day between meals. Published findings demonstrate that in iron-overloaded plasma, vitamin C acts as a potent antioxidant against lipid peroxidation. On the other hand, some doctors suggest that hemochromatosis patients should avoid vitamin C altogether.
To combat liver damage, vitamin E is an important weapon. Vitamin E is a vital lipid-soluble antioxidant that has been shown to be decreased in patients with hereditary hemochromatosis and in experimental iron overload. Iron loading has been shown to significantly decrease hepatic and plasma vitamin E which can be overcome by vitamin E supplementation. Free-radical index markers increase three- to fivefold in the iron-loaded livers, but supplementation with vitamin E has been shown to reduce these levels of free-radical activity by at least 50% (Brown et al. 1997).
Iron-overload disease causes severe depletion of liver glutathione. Glutathione is an important antioxidant, and its depletion in iron overload causes additional free-radical damage. (It should be noted that copper overload induces free radical-induced damage that is similar to iron overload.)
We therefore recommend that hemochromatosis patients take the following in divided doses 2 or 3 times a day with meals:
In addition, patients should take 300 mcg-3 mg of melatonin at bedtime.
Hemochromatosis patients may also consider intravenous (IV) chelation therapy administered by a knowledgeable physician. Chelation therapy refers to a treatment in which certain synthetic chemicals and body proteins bind metal molecules, extracting them from the system. Literally, chelation therapy is derived from the Greek word chele, which alludes to a claw-like action imposed upon unwanted materials accumulating in the body. Chelation is currently best associated with the clearance of plaque from the arteries, establishing normal blood flow to the vasculature. However, it is also an effective tool in treating heavy metal toxicity.
As early as 1941, Providence Hospital (Detroit) used chelation, employing intravenously administered ethylenediaminetetraacetic acid (EDTA), a synthetic amino acid, to extract lead. EDTA, a nontoxic chelator, also clears cadmium, nickel, copper, calcium, and some other metals from the body.
An individual wishing to obtain chelation therapy may want to contact a physician who follows the standard chelation protocol of the American College of Advancement in Medicine. The number of sessions required to enact a change cannot be presupposed, but the recommended maximum dosage is currently about 3 grams of EDTA (dosage usually calculated by body weight) given by IV infusion 1-3 times weekly, as a 3- to 4-hour drip. Initially, the dosage may be as small as 1/2-1 gram of EDTA.
Desferal (deferoxamine) is the preferred agent for iron chelation in cases of secondary iron overload from transfusion-dependent anemias or as an adjunct in acute iron intoxication. Desferal is not administered for primary hemochromatosis because phlebotomy is the current standard procedure. Desferal is given by intramuscular or subcutaneous infusion.
One interesting antiaging and immune-boosting therapy involves freezing one's phlebotomized blood and storing it for future administration during a debilitated state. Having access to one's own youthful blood during a state of disease or severe aging could be of benefit.
Nutritionist Carmen Fusco has successfully helped patients with the most severe form of hemochromatosis. Her regimen includes tea with every meal (for the tannins that bind iron) and extra calcium because calcium competes with iron and prevents some of its absorption. If a glass of wine is desired once the condition of the liver improves, red wine with the tannins and chromium found in the grape skins is preferable to white wine.
The most important step is locating a physician with specialized knowledge of hemochromatosis who will treat the disease as a life-threatening disorder. In too many cases, patients are not aggressively treated with phlebotomies, and liver iron overload reaches lethal levels.
In addition to conventional treatment, the following lifestyle changes and supplements are suggested:
If liver damage has occurred, refer to the Liver Cirrhosis and Liver Degenerative Disease protocols in this book. Refer to Appendix A below for additional suggestions.
For more informatiON
Calcium citrate, green tea extract, buffered vitamin C capsules, vitamin E, selenium, lecithin granules, melatonin, Life Flora, ginkgo biloba, magnesium, Vitamin B complex, zinc, folic acid, grape seed extract, aged garlic extract capsules, alpha-lipoic acid, Gamma E Tocopherol/Tocotrienols, NAC, Silibinin Plus, and Fiber Food caps and powder can be ordered by calling (800) 544-4440 or by ordering online.
Hemochromatosis: A Novel Case Study by WALTER LAST
This unorthodox case study is presented for the interest of our readers. The hemochromatosis patient who wishes to follow Mr. Last's high antioxidant recommendations, especially in regard to vitamin C intake, should first discuss it with his or her physician.
I had two patients with hemochromatosis. Both had normal ferritin levels within weeks of starting nutritional therapy, without any further need for phlebotomies. I was able to monitor one of these patients for 12 years as described in the following case history.
My patient was a 51-year-old male. He had collapsed at work 3 years earlier. His main symptoms were dizziness, tachycardia, profuse sweating, difficulty breathing, and extreme weakness. He was discharged from an Intensive Care Unit without diagnosis and his weight loss and weakness continued. The diagnosis of hemochromatosis was made 15 months later with a serum ferritin level of 3200 ng/mL and a liver biopsy that showed extremely high iron levels. With weekly phlebotomies, this was reduced to 1585 ng/mL before using fortnightly and later monthly phlebotomies, each time removing 1 liter of blood.
Phlebotomies continued for 20 months without reducing the ferritin to normal levels. The lowest level reached was 440 ng/mL. During all of this time, the patient was very weak, and as an additional complication, a specialist diagnosed Meniere's disease. In December 1990, he stopped having phlebotomies and started nutritional therapy. His liver was very hard and enlarged, he was grossly underweight, and his doctor had given him 5 weeks to live. The ferritin level at this time was still at 458 ng/mL. Normal ferritin levels for males are under 400 ng/mL.
Three weeks after starting nutritional therapy, his ferritin was 393 ng/mL (within the normal range for the first time since diagnosis). At the same time, he started gaining weight, his strength rapidly improved, and the symptoms of Meniere's disease (progressive deafness, dizziness, ringing in the ears, headache, and nausea) disappeared as well.
The red blood cell count, which had remained below normal during the period of phlebotomies, became normal and hemoglobin improved to the middle of the normal range. He continued to have blood tests, initially monthly, then at 3 months, and later at 6 months. On two occasions during the first year the ferritin level went slightly above the normal range.
The main aspects of the initial therapy were a vegetarian raw-food diet, combined with 20 g of vitamin C in divided doses before meals and at bedtime, in addition to 1000 mg of natural vitamin E, vitamin A, and vitamin B complex, sublingual vitamin B12, Kyolic garlic, lecithin, acidophilus culture, and trace minerals except iron. After 3 weeks, when the ferritin level had normalized, dietary restrictions were eased by adding cooked food, including fish and white meat. Vitamin C was reduced to 10 grams and later to a maintenance amount of 5 grams in divided doses. However, whenever a ferritin test was slightly above normal, vitamin C was increased to 10 grams until the next test, which then showed a normal ferritin level. Because he could not tolerate ascorbic acid, vitamin C was used in the form of sodium ascorbate.
For about 10 years, his ferritin remained within the normal range without any further phlebotomies. However, in the year 2000, he adopted the high-protein Zone Diet and his next test was 429 ng/mL. After increasing vitamin C to 10 grams and returning to his previous diet, the next ferritin test 6 weeks later was down to 300 ng/mL and again in the normal range. Subsequent tests remained normal up to the present time.
Genetic tests confirmed that his hemochromatosis is the hereditary form. A recent liver scan did not show any abnormalities. His overall health is above average for his age. In comparison, several other patients with advanced hemochromatosis--but in a less serious condition--who were diagnosed at about the same time as my patient and treated in the medically accepted way, have all since died of liver-related diseases. Another indication of the very advanced original condition of my patient is the fact that his ferritin level could not be normalized after 20 months of phlebotomies (generally regarded as a very poor prognosis).
This case was first published over 10 years ago in the International Clinical Nutrition Review (Last 1991), but has been completely ignored by hemochromatosis specialists and researchers. The reason for this may be the prevailing dogma that 90 mg of vitamin C is sufficient for everyone to remain healthy (slightly more for smokers) and that vitamin C supplements may be dangerous, especially with hemochromatosis. I do not need to discuss here the merits of vitamin C supplementation as William Faloon has covered this subject extensively in his article A Critical Analysis of The National Academy of Sciences' Attack on Dietary Supplements at www.lef.org.
The main reasons for the common advice to avoid vitamin C with hemochromatosis are twofold. It is generally acknowledged that vitamin C can improve the absorption of iron, especially in iron-deficient individuals and from vegetarian diets. However, I believe that the body does not normally absorb more than it needs, and the increased absorption by hemochromatosis patients from meals high in vitamin C is mainly the result of an internal deficiency of bivalent iron.
The second reason is that small amounts of vitamin C supplements, in the order of 500 mg, may mobilize stored iron, and this may cause oxidative tissue damage to membrane lipids. This is really not surprising, as it is well known that high concentrations of ferric ions oxidize protective antioxidants, notably the vitamins C and E. This means that with low antioxidant intakes, we can expect pronounced antioxidant tissue deficiencies in iron overload diseases. In this case, low levels of supplemented vitamin C are likely to be present mainly in oxidized form as reversible dehydroascorbate or as irreversible oxidation products. Similarly, any liberated iron would be in the form of ferric dehydroascorbate and other oxidized products, and it is these that cause the peroxidative membrane damage.
Also, vitamin A is important for iron metabolism. Supplementation improves the iron status (serum iron, hemoglobin, as well as transferrin saturation) without at the same time increasing ferritin levels, while iron supplements without sufficient vitamin A just increase ferritin levels. Also, vitamin A-deficient subjects may develop anemia despite sufficient dietary iron (Bloem et al. 1990). These effects may be interpreted as a normalizing function of vitamin A in the transport and usage of iron, while iron alone in the presence of vitamin A deficiency will mainly increase iron stores.
A similar normalizing role in iron metabolism may be exhibited by the other antioxidants. Vitamin C not only improves the absorption of iron, but it is also required to move iron in and out of ferritin tissue stores. Without adequate antioxidants, ferric iron stores may build up because iron cannot be liberated from ferritin tissue and transferred onto transferrin plasma, a step that requires a temporary reduction of ferric to ferrous iron.
There are two sites or steps at which antioxidant deficiency might cause or contribute to hemochromatosis. The synthesis of heme requires the reduction of ferric to ferrous ions. While this reduction proceeds enzymatically through ferrochelatase, it is ultimately dependent on the overall redox potential within the cells. In the case of a generalized antioxidant deficiency, the function of this enzyme is likely to be impeded. This then leads to low hemoglobin levels and increased ferritin stores because a cellular deficiency of ferrous ions for the synthesis of heme will stimulate increased absorption of iron.
However, the second possibility appears to be the decisive defect in hemochromatosis. This is a difficulty in recycling iron from the continual breakdown of hemoglobin from old erythrocytes in the spleen and liver. About 25 mg of iron are recycled daily in this way, but this requires a reduction-oxidation step to transfer ferritin iron in the tissue onto plasma transferrin. With antioxidant deficiency there will be only a partial recycling. Most of the unusable iron stores will build up in the liver.
Very high ferric iron stores in the liver also make this organ more antioxidant deficient than other tissue. The highest antioxidant activity can be expected to be in the intestinal mucosa because these have first call on the antioxidants absorbed from food. Therefore, transferrin will preferentially pick up iron from the intestinal mucosa and avoid the liver stores as they are too difficult to convert. Another piece of evidence for this proposed mechanism may be seen in the rapid normalization of ferritin levels in the reported case without any abnormal loss of iron in the urine being detected.
The initial use of very high amounts of vitamin C was designed to rapidly change the total oxidation-reduction or redox potential of the body from one high in oxidizing to one high in reducing abilities. This allowed the rapid mobilization and normalization of excessive iron stores without any danger of tissue damage that might result from mobilizing iron slowly with low-level antioxidant supplements.
The initial defect in hereditary hemochromatosis (HH) may simply be a higher-than-normal antioxidant requirement to maintain healthy liver functions. Any period of increased antioxidant requirement, such as prolonged or severe stress, infections, or chemical exposure, may lead to a deficiency and thus start the accumulation of ferric iron in the liver. This will then make it increasingly more difficult for a low level of antioxidants to penetrate the strongly oxidative liver environment to reduce ferric iron, and additional iron will be absorbed from the intestines instead. The strongly oxidative liver environment may also be seen as the main cause of the commonly developing liver cirrhosis and liver cancer. Conversely, I attribute the normalization of the liver damage of my patient to his high antioxidant intake.
If there would be a fundamental defect that causes genetically predisposed individuals to automatically absorb increased amounts of iron, then nearly everyone would be affected. However, this is not so. Only a small percentage of genetically predisposed individuals accumulate dangerous amounts of iron. Therefore, the main factor clearly is not genetic and must be something else. From the provided case report, it is clear that this decisive factor is antioxidant deficiency.
This discussion shows that in effect at the cellular level, hemochromatosis may be regarded as a bivalent iron deficiency disease due to chronically low antioxidant levels. Unfortunately, I cannot offer any references from the medical literature to support my case history because a therapy with very high vitamin C levels has not been tried before. However, my theoretical assessment should be obvious to any biochemist. If you, as a hemochromatosis patient, are interested in proof for the efficacy of the proposed vitamin C treatment, then I suggest that you lobby for a clinical trial.
The diet should be high in organic or unsprayed fruits and vegetables with an emphasis on sprouted seeds and fresh vegetable juices. Initially, a vegetarian raw-food diet is recommended, lasting for several days with mild conditions and for several weeks in advanced conditions and suspected liver damage. After this cleansing period, reintroduce other foods individually and with self-observation. Avoid any food that causes an unpleasant reaction or that increases the pulse rate more than most other foods. Check your pulse before and 30-60 minutes after meals.
Highly recommended are the so-called "purple foods" for their high antioxidant value. These produce a purple juice when pressed and include red beets, black and purple grapes, blackberries, black currants, and blueberries. You may use a moderate amount of white meat, such as poultry, fish, and other seafood. However, with a damaged liver, try to obtain organic meat and low-mercury fish. Use extra-virgin olive oil as the main oil or fat.
Initially, avoid and later minimize red meat, gluten-grains (mainly wheat and oats, to a lesser degree rye and barley), cow's milk products, nonfermented soy products, sugar and sweetened food, processed food, and food with added non-biological chemicals. Continue to avoid iron-fortified food, alcohol, nicotine, and other recreational drugs. Moderate amounts of coffee or tea and also a glass of red wine with meals, except with apparent liver damage, are acceptable.
The mainstay of this therapy is a high vitamin C intake. With high ferritin levels and suspected high iron stores in the liver, start with 10 grams in four to six divided doses and if that is well tolerated, increase to 20 grams the next day. If high vitamin C intake causes problems, such as diarrhea, cut back to the amount that can be tolerated. Otherwise stay with 20 grams until ferritin drops to the normal range. Then continue with 10 grams until general health and any liver problems have sufficiently improved. Finally, continue with a maintenance intake of about 5 grams daily. However, whenever a ferritin test is higher than normal, temporarily increase vitamin C again to 10 grams until ferritin returns to the normal range.
With these high intakes, sodium ascorbate or mixed ascorbates (buffered vitamin C powder) are generally easiest to tolerate, but with high blood pressure, additional ascorbic acid is beneficial as well. For a maintenance program, use buffered vitamin C powder, but if your blood pressure is elevated, use ascorbic acid instead. Try to take the vitamin C in liquid form about 30 minutes before meals and at bedtime. However, if that causes digestive problems, then take it with food that is low in iron. With impaired kidney functions, high doses of vitamin C can cause edema. In this case, greatly increase the intake of water and other fluids and reduce vitamin C intake to a level that does not cause problems; also avoid salt.
As the basis of the supplement program, take 4 capsules (or 3 tablets) of the Life Extension Mix 3 times daily. This is free of iron and contains high but balanced amounts of all vitamins, minerals, and other essential nutrients. It is also high in antioxidants with about 2.5 grams of vitamin C, so that for the maintenance program, only an additional 2.5 grams are needed to obtain a total of 5 grams a day of vitamin C. However, initially, until ferritin is in the normal range or if you have continuing difficulty controlling ferritin levels, you may take the capsules half an hour before meals with some fruit or juice.
Until the iron metabolism appears to be normalized, take 10,000 or 20,000 IU of liquid emulsified vitamin A once a day. Many individuals find it difficult to absorb beta-carotene and convert it into vitamin A. As a maintenance dose, the vitamin A in 12 capsules of Life Extension Mix (approximately 4300 IU) should be sufficient.
If weakness remains in advanced conditions try vitamin B12 by injection or 1000-mcg (10-mg) tablets (methylcobalamin) absorbed under the tongue once a day.
To normalize the intestinal tract, take cultures with acidophilus and bifido bacteria, such as high-potency Life Flora capsules. Initially take 2 or 3 capsules before each meal. After sufficient improvement, reduce that to 1 capsule per meal and later 1 a day. Generally, take 1 tsp of lecithin granules mixed with meals.
With indications of liver damage, remain on a program high in antioxidants for an extended period. Also see the other protocols on Liver Cirrhosis and Liver Degenerative Disease for further treatment suggestions.
Combining Nutritional with Conventional Therapy
With a moderately high ferritin level, there is no problem in combining this antioxidant therapy with a series of phlebotomies. On the contrary, repeated phlebotomies are often less than successful because patients deficient in antioxidants have difficulty mobilizing iron stores. With concomitant antioxidant therapy, more iron may be removed with each unit of blood.
However, we do not yet know if antioxidant therapy with very high ferritin levels would pose any problems. Therefore, if the initial ferritin level is very high, it may be advisable to have a series of weekly phlebotomies until ferritin is in the moderately high range or starts leveling off before starting antioxidant therapy. Phlebotomies may then be continued together with antioxidant therapy until ferritin is in the middle of the normal range. From this point on, antioxidant therapy alone should be sufficient to prevent a relapse. However, if you are so inclined, you may make periodic or occasional blood donations even after full recovery.
The main beneficiaries of antioxidant therapy are patients with advanced hemochromatosis and liver damage who until now had a very poor prognosis. These individuals should now have a normal life expectancy by combining nutritional with conventional therapy. Furthermore, individuals who are genetically predisposed to developing hemochromatosis can now easily protect themselves with antioxidant supplements. I assume that 2-5 grams of vitamin C a day will be sufficient, especially if other antioxidants, and especially vitamin E, are used in addition or if the diet is high in antioxidant nutrients. However, during stressful periods, including infections, these amounts may be doubled.
Present nutritional therapies focus on reducing the absorption of iron with special supplements and foods. Commonly used sources are calcium, tea, and soluble fiber. High-dose fiber is not recommended if you choose to follow the high antioxidant therapy proposed above because along with iron, essential trace minerals and even vitamins may be reduced. These alternatives are recommended if you choose conventional treatment with phlebotomies.
In summary, it is postulated that the basic biochemical defect that leads to the development of hemochromatosis is a tissue deficiency of antioxidants. This has two effects. One effect is that it inhibits the recycling of iron from old erythrocytes in the liver and leads to a gradual accumulation of ferritin. The second effect is a deficiency of bivalent iron. This in turn induces increased intestinal iron absorption for the necessary synthesis of heme. Accordingly, hemochromatosis can be successfully treated or prevented with high levels of vitamin C and other antioxidants. The obvious advantages of antioxidant therapy as compared to the traditional management of hemochromatosis will hopefully stimulate more research in this area.
Walter Last studied chemistry and biochemistry at a German university (Greifswald) from 1952 to 1959 and acquired a degree comparable to a master of science degree in the United States. He worked in medical departments of several German universities and at Bio-Science Laboratories in Los Angeles. After 1975 he worked as a health writer and nutritionist in New Zealand and Australia.