Individuals of sub-Saharan African descent with ferroportin Q248H are more likely to be diagnosed with African iron overload than individual without ferroportin mutation because individuals with ferroportin Q248H have elevated level of serum ferritin concentration. Individuals of African descent should also avoid drinking traditional beer.

Originally, this was blamed on ungalvanised barrels used to store home-made beer, which led to increased oxidation and increased iron levels in the beer. Further investigation has shown that only some people drinking this sort of beer get an iron overload syndrome, and that a similar syndrome occurred in people of African descent who have had no contact with this kind of beer (e.g., African Americans).

This led investigators to the discovery of a gene polymorphism in the gene for ferroportin, which predisposes some people of African descent to iron overload.

It is most common in certain European populations (such as the Irish and Norwegians) and occurs in 0.6% of the population. Men with the disease are 24 times more likely to experience symptoms than affected women.

Affected individuals over age 40 or who have high serum ferritin levels are at risk for developing cirrhosis. Iron overload increases the risk of hepatocellular carcinoma. This risk is greater in those with cirrhosis but is still present in those without cirrhosis. Significant problems occur in around one in ten.

Studies indicate that persons with symptomatic haemochromatosis have somewhat reduced life expectancy compared to the general population. This is mainly due to excess mortality from cirrhosis and liver cancer. Patients who were treated with phlebotomy lived longer than those who weren't. Patients without liver disease or diabetes had similar survival rate to the general population.

Possible reasons that athletics may contribute to lower iron levels includes mechanical hemolysis (destruction of red blood cells from physical impact), loss of iron through sweat and urine, gastrointestinal blood loss, and haematuria (presence of blood in urine). Although small amounts of iron are excreted in sweat and urine, these losses can generally be seen as insignificant even with increased sweat and urine production, especially considering that athletes' bodies appear to become conditioned to retain iron better. Mechanical hemolysis is most likely to occur in high-impact sports, especially among long distance runners who experience "foot-strike hemolysis" from the repeated impact of their feet with the ground. Exercise-induced gastrointestinal bleeding is most likely to occur in endurance athletes. Haematuria in athletes is most likely to occur in those that undergo repetitive impacts on the body, particularly affecting the feet (such as running on a hard road, or Kendo) and hands (e.g. Conga or Candombe drumming). Additionally, athletes in sports that emphasize weight loss (e.g. ballet, gymnastics, marathon running, and wrestling) as well as sports that emphasize high-carbohydrate, low-fat diets, may be at an increased risk for iron deficiency.

Mild iron deficiency can be prevented or corrected by eating iron-rich foods and by cooking in an iron skillet. Because iron is a requirement for most plants and animals, a wide range of foods provide iron. Good sources of dietary iron have heme-iron, as this is most easily absorbed and is not inhibited by medication or other dietary components. Three examples are red meat, poultry, and insects. Non-heme sources do contain iron, though it has reduced bioavailability. Examples are lentils, beans, leafy vegetables, pistachios, tofu, fortified bread, and fortified breakfast cereals.

Iron from different foods is absorbed and processed differently by the body; for instance, iron in meat (heme-iron source) is more easily absorbed than iron in grains and vegetables ("non-heme" iron sources). Minerals and chemicals in one type of food may also inhibit absorption of iron from another type of food eaten at the same time. For example, oxalates and phytic acid form insoluble complexes which bind iron in the gut before it can be absorbed.

Because iron from plant sources is less easily absorbed than the heme-bound iron of animal sources, vegetarians and vegans should have a somewhat higher total daily iron intake than those who eat meat, fish or poultry. Legumes and dark-green leafy vegetables like broccoli, kale and oriental greens are especially good sources of iron for vegetarians and vegans. However, spinach and Swiss chard contain oxalates which bind iron, making it almost entirely unavailable for absorption. Iron from non-heme sources is more readily absorbed if consumed with foods that contain either heme-bound iron or vitamin C. This is due to a hypothesised "meat factor" which enhances iron absorption.

Following are two tables showing the richest foods in heme and non-heme iron.

In both tables, food serving sizes may differ from the usual 100g quantity for relevancy reasons. Arbitrarily, the guideline is set at 18 mg, which is the USDA Recommended Dietary Allowance for women aged between 19 and 50.

Iron deficiency can have serious health consequences that diet may not be able to quickly correct; hence, an iron supplement is often necessary if the iron deficiency has become symptomatic.

Haemochromatosis is one of the most common heritable genetic conditions in people of northern European extraction with a prevalence of 1 in 200. The disease has a variable penetration and about 1 in 10 people of this demographic carry a mutation in one of the genes regulating iron metabolism, the most common allele being the C282Y allele in the "HFE" gene. The prevalence of mutations in iron metabolism genes varies in different populations. A study of 3,011 unrelated white Australians found that 14% were heterozygous carriers of an HFE mutation, 0.5% were homozygous for an "HFE" mutation, and only 0.25% of the study population had clinically relevant iron overload. Most patients who are homozygous for HFE mutations will not manifest clinically relevant haemochromatosis (see Genetics above). Other populations have a lower prevalence of both the genetic mutation and the clinical disease.

Genetic studies suggest the original haemochromatosis mutation arose in a single person, possibly of Celtic ethnicity, who lived 60–70 generations ago. At that time when dietary iron may have been scarcer than today, the presence of the mutant allele may have provided an evolutionary or natural selection reproductive advantage by maintaining higher iron levels in the blood.

There are many studies about LID and the frequency varies according to country of origin, diet, pregnancy status age, gender, etc. Depending on these previous conditions, the frequency can change from 11% in male athletes (Poland) to 44.7% in children less than 1 year old (China):

Frequency of LID in different countries and populations:

- Poland: 14 of LID (11%) in 131 male athletes and 31 of ID (26%) in 121 female athletes

- India: 27.5% of LID amongst student nurses

- Spain: 14.7% of LID in 211 women of child-bearing age in Barcelona

- China: In 3591 pregnant women and 3721 premenopausal from 15 provinces. It was found: LID 42.6% in pregnant women (urban first-trimester 41.9%) (rural 36.1%) while 34.4% of LID in premenopausal non-pregnant women (urban 35.6%)(rural 32.4%). Pediatric samples: In 9118 children from 31 provinces aged 7 months to 7 years, the global incidence of LID in children was 32.5%. Sub-classifying the cases according to age and origin (global/countryside): less than 1 y (7m to 12m) LID 44.7% (35.8% in countryside), 1 – 3 years LID 35.9% (31% in countryside), 4 to 7 years (LID 26.5%) (30.1% in countryside).

There is no consensus on how to treat LID but one of the options is to treat it as an iron-deficiency anemia with ferrous sulfate (Iron(II) sulfate) at a dose of 100 mg x day in two doses (one at breakfast and the other at dinner) or 3 mg x Kg x day in children (also in two doses) during two or three months. The ideal would be to increase the deposits of body iron, measured as levels of ferritin in serum, trying to achieve a ferritin value between 30 and 100 ng/mL. Another clinical study has shown an increase of ferritin levels in those taking iron compared with others receiving a placebo from persons with LID. With ferritin levels higher than 100 ng/mL an increase in infections, etc. has been reported. Another way to treat LID is with an iron rich diet and in addition ascorbic acid or Vitamin C, contained in many types of fruits as oranges, kiwifruits, etc. that will increase 2 to 5-fold iron absorption.

Iron poisoning is an iron overload caused by a large excess of iron intake and usually refers to an acute overload rather than a gradual one. The term has been primarily associated with young children who consumed large quantities of iron supplement pills, which resemble sweets and are widely used, including by pregnant women; approximately 3 grams is lethal for a two-year-old. Targeted packaging restrictions in the US for supplement containers with over 250 mg elemental iron have existed since 1978, and recommendations for unit packaging have reduced the several iron poisoning fatalities per year to almost zero since 1998. No known cases of iron poisoning have been identified that are associated with iron mining.

In nature, iron is usually found in its oxidized form, iron (III) oxide, which is insoluble. Ferrous iron, iron (II), is soluble and its toxicity varies, largely with the integrity of the gastrointestinal lining. Iron supplements are typically used to treat anemia. Modalities include: diet, parasite control, vitamin A, riboflavin (B), vitamin C (for absorption), folate(B), vitamin B and multivitamin-multimineral supplements, with or without iron; potentially avoiding the use of iron only supplements.

In terms of genetics of atransferrinemia researchers have identified mutations in the TF gene as a probable cause of this genetic disorder in affected people.

Transferrin is a serum transport protein that transports iron to the reticuloendothelial system for utilization and erythropoiesis, since there is no transferrin in atransferrinemia, serum free iron cannot reach reticuloendothelial cells and there is microcytic anemia. Also, this excess iron deposits itself in the heart, liver and joints, and causes damage. Ferritin, the storage form of iron gets secreted more into the bloodstream so as to bind with the excessive free iron and hence serum ferritin levels rise in this condition

Hemosiderosis (AmE) or haemosiderosis (BrE) is a form of iron overload disorder resulting in the accumulation of hemosiderin.

Types include:

- Transfusion hemosiderosis

- Idiopathic pulmonary hemosiderosis

- Transfusional diabetes

Hemosiderin deposition in the lungs is often seen after diffuse alveolar hemorrhage, which occurs in diseases such as Goodpasture's syndrome, granulomatosis with polyangiitis, and idiopathic pulmonary hemosiderosis. Mitral stenosis can also lead to pulmonary hemosiderosis. Hemosiderin collects throughout the body in hemochromatosis. Hemosiderin deposition in the liver is a common feature of hemochromatosis and is the cause of liver failure in the disease. Selective iron deposition in the beta cells of pancreatic islets leads to diabetes due to distribution of transferrin receptor on the beta cells of islets and in the skin leads to hyperpigmentation. Hemosiderin deposition in the brain is seen after bleeds from any source, including chronic subdural hemorrhage, cerebral arteriovenous malformations, cavernous hemangiomata. Hemosiderin collects in the skin and is slowly removed after bruising; hemosiderin may remain in some conditions such as stasis dermatitis. Hemosiderin in the kidneys has been associated with marked hemolysis and a rare blood disorder called paroxysmal nocturnal hemoglobinuria.

Hemosiderin may deposit in diseases associated with iron overload. These diseases are typically diseases in which chronic blood loss requires frequent blood transfusions, such as sickle cell anemia and thalassemia, though beta thalassemia minor has been associated with hemosiderin deposits in the liver in those with non-alcoholic fatty liver disease independent of any transfusions.

Treatment for hemosiderin focuses on limiting the effects of the underlying disease leading to continued deposition. In hemochromatosis, this entails frequent phlebotomy granulomatosis, immune suppression is required. Limiting blood transfusions and institution of iron chelation therapy when iron overload is detected are important when managing sickle-cell anemia and other chronic hemolytic anemias.

In terms of treatment of atransferrinemia, iron supplements (oral iron therapy) are the preferred choice, one finds that RBC transfusions are very infrequently needed.

Genes involved in iron metabolism disorders include HFE and TFR2.

Hepcidin is the master regulator of iron metabolism and, therefore, most genetic forms of iron overload can be thought of as relative hepcidin deficiency in one way or another. For instance, a severe form of iron overload, juvenile hemochromatosis, is a result of severe hepcidin deficiency. The majority of cases are caused by mutations in the hemojuvelin gene (HJV or RGMc/repulsive guidance molecule c). The exceptions, people who have mutations in the gene for ferroportin, prove the rule: these people have plenty of hepcidin, but their cells lack the proper response to it. So, in people with ferroportin proteins that transport iron out of cells without responding to hepcidin's signals to stop, they have a deficiency in the action of hepcidin, if not in hepcidin itself.

But the exact mechanisms of most of the various forms of adult hemochromatosis, which make up most of the genetic iron overload disorders, remain unsolved. So while researchers have been able to identify genetic mutations causing several adult variants of hemochromatosis, they now must turn their attention to the normal function of these mutated genes.

These genes represent multiple steps along the pathway of iron regulation, from the body's ability to sense iron, to the body's ability to regulate uptake and storage. Working out the functions of each gene in this pathway will be an important tool for finding new methods of treating genetic disorders, as well as for understanding the basic workings of the pathway.

So though many mysteries of iron metabolism remain, the discovery of hepcidin already allows a much better understanding of the nature of iron regulation, and makes researchers optimistic that many more breakthroughs in this field are soon to come.

Ted DeVita died of transfusional iron overload from too many blood transfusions.

The body normally gets the iron it requires from foods. If a person consumes too little iron, or iron that is poorly absorbed (non-heme iron), they can become iron deficient over time. Examples of iron-rich foods include meat, eggs, leafy green vegetables and iron-fortified foods. For proper growth and development, infants and children need iron from their diet. A high intake of cow’s milk is associated with an increased risk of iron-deficiency anemia. Other risk factors for iron-deficiency anemia include low meat intake and low intake of iron-fortified products.

The leading cause of iron-deficiency anemia worldwide is a parasitic disease known as a helminthiasis caused by infestation with parasitic worms (helminths); specifically, hookworms, which include "Ancylostoma duodenale", "Ancylostoma ceylanicum", and "Necator americanus," are most commonly responsible for causing iron-deficiency anemia. The World Health Organization estimates that "approximately two billion people are infected with soil-transmitted helminths worldwide." Parasitic worms cause both inflammation and chronic blood loss by binding to a human's small-intestinal mucosa, and through their means of feeding and degradation, they can ultimately cause iron-deficiency anemia.

Iron oxide present in welding material, foundries, iron ore mining. It can also be caused by powdered hematite, sometimes used by Egyptians to protect tombs.

Bantu tribes of Africa suffer from Siderosis because they drink beer in iron utensils.

Siderosis is the deposition of iron in tissue.

When used without qualification, it usually refers to an environmental disease of the lung.

Also Siderosis Bulbi, deposition of iron into the eye causing injury as the material chemically reacts with tissues and cells.

Treatment is by phlebotomy, erythrocytapheresis or chelation therapy with iron chelating agents such as deferoxamine, deferiprone or deferasirox.

If iron overload has caused end-organ damage, this is generally irreversible and may require transplantation.

Thalassemia can coexist with other hemoglobinopathies. The most common of these are:

- Hemoglobin E/thalassemia: common in Cambodia, Thailand, and parts of India, it is clinically similar to β thalassemia major or thalassemia intermedia.

- Hemoglobin S/thalassemia: common in African and Mediterranean populations, is clinically similar to sickle-cell anemia, with the additional feature of splenomegaly.

- Hemoglobin C/thalassemia: common in Mediterranean and African populations, hemoglobin C/β thalassemia causes a moderately severe hemolytic anemia with splenomegaly; hemoglobin C/β thalassemia produces a milder disease.

- Hemoglobin D/thalassemia: common in the northwestern parts of India and Pakistan (Punjab region).

Limiting some microbes' access to iron can reduce their virulence, thereby potentially reducing the severity of infection. Blood transfusion to patients with anemia of chronic disease is associated with a higher mortality, supporting the concept.