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.

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.

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.

Increased consumption of zinc is another cause of copper deficiency. Zinc is often used for the prevention or treatment of common colds and sinusitis (inflammation of sinuses due to an infection), ulcers, sickle cell disease, celiac disease, memory impairment and acne. Zinc is found in many common vitamin supplements and is also found in denture creams. Recently, several cases of copper deficiency myeloneuropathy were found to be caused by prolonged use of denture creams containing high quantities of zinc.

Metallic zinc is the core of all United States currency coins, including copper coated pennies. People who ingest a large number of coins will have elevated zinc levels, leading to zinc-toxicity-induced copper deficiency and the associated neurological symptoms. This was the case for a 57-year-old woman diagnosed with schizophrenia. The woman consumed over 600 coins, and started to show neurological symptoms such as unsteady gait and mild ataxia.

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.

It is rarely suggested that excess iron supplementation causes copper deficiency myelopathy.

Another rarer cause of copper deficiency is Coeliac disease, probably due to malabsorption in the intestines.

Still, a large percentage, around 20%, of cases have unknown causes.

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.

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.

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.

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.

Standard diagnostic measures for haemochromatosis, transferrin saturation and ferritin tests, are not a part of routine medical testing. Screening for haemochromatosis is recommended if the patient has a parent, child or sibling with the disease.

Routine screening of the general population for hereditary haemochromatosis is generally not done. Mass genetic screening has been evaluated by the U.S. Preventive Services Task Force (USPSTF), among other groups. The USPSTF recommended against genetic screening of the general population for hereditary haemochromatosis because the likelihood of discovering an undiagnosed patient with clinically relevant iron overload is less than 1 in 1,000. Although there is strong evidence that treatment of iron overload can save lives in patients with transfusional iron overload, no clinical study has shown that for asymptomatic carriers of hereditary haemochromatosis treatment with venesection (phlebotomy) provides any clinical benefit. Recently, it has been suggested that patients be screened for iron overload using serum ferritin as a marker: If serum ferritin exceeds 1000 ng/mL, iron overload is very likely the cause.

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

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 plants a micronutrient deficiency (or trace mineral deficiency) is a physiological plant disorder which occurs when a micronutrient is deficient in the soil in which a plant grows. Micronutrients are distinguished from macronutrients (nitrogen, phosphorus, sulfur, potassium, calcium and magnesium) by the relatively low quantities needed by the plant.

A number of elements are known to be needed in these small amounts for proper plant growth and development. Nutrient deficiencies in these areas can adversely affect plant growth and development. Some of the best known trace mineral deficiencies include: zinc deficiency, boron deficiency, iron deficiency, and manganese deficiency.

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

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 deficiency can be avoided by choosing appropriate soil for the growing conditions (e.g., avoid growing acid loving plants on lime soils), or by adding well-rotted manure or compost. If iron deficit chlorosis is suspected then check the pH of the soil with an appropriate test kit or instrument. Take a soil sample at surface and at depth. If the pH is over seven then consider soil remediation that will lower the pH toward the 6.5 - 7 range. Remediation includes: i) adding compost, manure, peat or similar organic matter (warning. Some retail blends of manure and compost have pH in the range 7 - 8 because of added lime. Read the MSDS if available. Beware of herbicide residues in manure. Source manure from a certified organic source.) ii) applying Ammonium Sulphate as a Nitrogen fertilizer (acidifying fertilizer due to decomposition of ammonium ion to nitrate in the soil and root zone) iii) applying elemental Sulphur to the soil (oxidizes over the course of months to produce sulphate/sulphite and lower pH). Note: adding acid directly e.g. sulphuric/hydrochloric/citric acid is dangerous as you may mobilize metal ions in the soil that are toxic and otherwise bound. Iron can be made available immediately to the plant by the use of iron sulphate or iron chelate compounds. Two common iron chelates are Fe EDTA and Fe EDDHA. Iron sulphate (Iron(II)_sulfate) and iron EDTA are only useful in soil up to PH 7.1 but they can be used as a foliar spray (Foliar_feeding). Iron EDDHA is useful up to PH 9 (highly alkaline) but must be applied to the soil and in the evening to avoid photodegradation. EDTA in the soil may mobilize Lead, EDDHA does not appear to.

The term fatty acid oxidation disorder (FAOD) is sometimes used, especially when there is an emphasis on the oxidation of the fatty acid.

In addition to the fetal complications, they can also cause complications for the mother during pregnancy.

Examples include:

- trifunctional protein deficiency

- MCADD, LCHADD, and VLCADD

1- Red cell indices and blood film appearances suggest iron deficiency, although peripheral blood changes are not usually as marked as in moderate or severe iron deficiency.

2- Erythropoiesis is abnormal because of ineffective iron utilisation with poor haemoglobinisation of red cell precursors and

3- Bone marrow iron stores are normal or increased and sideroblasts may be frequent and abnormal.

Manganese deficiency in humans results in a number of medical problems. Manganese is a vital element of nutrition in very small quantities (adult male daily intake 2.3 milligrams). However, in greater amounts manganese, like most metals, is poisonous when eaten or inhaled.

Nutritional anemia refers to the low concentration of hemoglobin due to poor diet. According to the World Health Organization, a hemoglobin concentration below 7.5 mmol/L and 8. mmol/L for women and men, respectively, is considered to be anemic. Thus, anemia can be diagnosed with blood tests. Hemoglobin is used to transport and deliver oxygen in the body. Without oxygen, the human body cannot undergo respiration and create ATP, thereby depriving cells of energy.

Nutritional anemia is caused by a lack of iron, protein, B12, and other vitamins and minerals that needed for the formation of hemoglobin. Folic acid deficiency is a common association of nutritional anemia and iron deficiency anemia is the most common nutritional disorder.

Signs of anemia include cyanosis, jaundice, and easy bruising. In addition, anemic patients may experience difficulties with memory and concentration, fatigue, lightheadedness, sensitivity to temperature, low energy levels, shortness of breath, and pale skin. Symptoms of severe or rapid-onset anemia are very dangerous as the body is unable to adjust to the lack of hemoglobin. This may result in shock and death. Mild and moderate anemia have symptoms that develop slowly over time.[5] If patients believe that they are at risk for or experience symptoms of anemia, they should contact their doctor.

Treatments for nutritional anemia includes replacement therapy is used to elevate the low levels of nutrients.[1] Diet improvement is a way to combat nutritional anemia and this can be done by taking dietary supplements such as iron, folate, and Vitamin B12.[2] These supplements are available over-the-counter however, a doctor may prescribe prescription medicine as needed, depending on the patient’s health needs.

Internationally, anemia caused by iron deficiencies is the most common nutritional disorder. It is the only significantly prevalent nutritional deficiency disorder in industrialized countries. In poorer areas, anemia is worsened by infectious diseases such as HIV/AIDS, tuberculosis, hookworm infestation, and Malaria. In developing countries, about 40% of preschool children and 50% of pregnant women are estimated to be anemic. 20% of maternal deaths can be contributed to anemia. Health consequences of anemia include low pregnancy outcome, impaired cognitive and physical development, increased rate of morbidity, and reduced rate of work in adults.

'

Nutritional Anemia has many different causes, each either nutritional or non-nutritional. Nutritional causes are vitamin and mineral deficiencies and non-nutritional causes can be infections. The number one cause of this type of anemia however is iron deficiency.

An insufficient intake of iron, Vitamin B12, and folic acid impairs the bone marrow function.

The lack of iron within a person’s body can also stem from ulcer bacteria. These microbes live in the digestive track and after many years cause ulcer’s in the lining of your stomach or small intestine. Therefore, a high percentage of patients with nutritional anemia may have potential gastrointestinal disorder that causes chronic blood loss. This is common in immunocompromised, elderly, and diabetic people. High blood loss can also come from increases loss of blood during menstruation, childbirth, cancers of the intestines, and a disorder that hinders blood’s ability to coagulate.

Medications can have adverse effects and cause nutritional anemia as well. Medications that stop the absorption of iron in the gut and cause bleeding from the gut (NSAIDs and Aspirin) can be culprits in the development of this condition. Hydrocortisones and valproic acid are also two drugs that cause moderate bleeding from the gut. Amoxicillin and phenytoin are the ability to cause a vitamin B12 deficiency.

Other common causes are thyroid disorders, lead toxcities, infectious diseases (e.g Malaria), Alcoholism, and Vitamin E deficiency.

Symptoms

Symptoms of nutritional anemia can include fatigue and lack of energy. However if symptoms progress, one may experience shortness of breath, rapid pulse, paleness --especially in the hands, eyelids and fingernails---, swelling of ankles, hair loss, lightheadedness, compulsive and atypical cravings, constipation, depression, muscle twitching, numbness, or burning and chest pain.

Those who have nutritional anemia often show little to no symptoms. Often, symptoms can go undetected as mild forms of the anemia have only minor symptoms.

----[1] “Micronutrient deficiencies” World Health Organization. Accessed March 31, 2017. http://www.who.int/nutrition/topics/ida/en/

[2] "Ibid."

[3] "Ibid."

[4] "Ibid"

[5] "Ibid"

[6] "Ibid"

----[1] "Ibid".

[2] “Treatments for Nutritional anemia.” Right Diagnosis. Assessed March 31, 2017. http://www.rightdiagnosis.com/n/nutritional_anemia/treatments.htm

----[1] "Ibid".

[2] “What are the symptoms of anemia?” Health Grades, INC. Accessed March 31, 2017. https://www.healthgrades.com/conditions/anemia--symptoms.

[3] "Ibid."

[4] "Ibid."

[5] "Ibid."

[6] "Ibid"

----[1] "Ibid".

[2] "Ibid".

----[1] "Nutritional Anemia." The Free Dictionary. Accessed March 31, 2017. http://medical-dictionary.thefreedictionary.com/nutritionalanemia.

[2] "Ibid".

[3] "Ibid".

[4] "Ibid".

Nutritional anemia refers to types of anemia that can be directly attributed to nutritional disorders.

Examples include Iron deficiency anemia and pernicious anemia.

It is often discussed in a pediatric context.