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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.
Iron is needed for bacterial growth making its bioavailability an important factor in controlling infection. Blood plasma as a result carries iron tightly bound to transferrin, which is taken up by cells by endocytosing transferrin, thus preventing its access to bacteria. Between 15 and 20 percent of the protein content in human milk consists of lactoferrin that binds iron. As a comparison, in cow's milk, this is only 2 percent. As a result, breast fed babies have fewer infections. Lactoferrin is also concentrated in tears, saliva and at wounds to bind iron to limit bacterial growth. Egg white contains 12% conalbumin to withhold it from bacteria that get through the egg shell (for this reason, prior to antibiotics, egg white was used to treat infections).
To reduce bacterial growth, plasma concentrations of iron are lowered in a variety of systemic inflammatory states due to increased production of hepcidin which is mainly released by the liver in response to increased production of pro-inflammatory cytokines such as Interleukin-6. This functional iron deficiency will resolve once the source of inflammation is rectified; however, if not resolved, it can progress to Anaemia of Chronic Inflammation. The underlying inflammation can be caused by fever, inflammatory bowel disease, infections, Chronic Heart Failure (CHF), carcinomas, or following surgery.
Reflecting this link between iron bioavailability and bacterial growth, the taking of oral iron supplements in excess of 200 mg/day causes a relative overabundance of iron that can alter the types of bacteria that are present within the gut. There have been concerns regarding parenteral iron being administered whilst bacteremia is present, although this has not been borne out in clinical practice. A moderate iron deficiency, in contrast, can provide protection against acute infection, especially against organisms that reside within hepatocytes and macrophages, such as malaria and tuberculosis. This is mainly beneficial in regions with a high prevalence of these diseases and where standard treatment is unavailable.
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.
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.
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.
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.
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.
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.
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.
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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.
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.
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.
Micronutrient deficiencies affect more than two billion people of all ages in both developing and industrialized countries. They are the cause of some diseases, exacerbate others and are recognized as having an important impact on worldwide health. Important micronutrients include iodine, iron, zinc, calcium, selenium, fluorine, and vitamins A, B, B, B, B, B, and C.
Micronutrient deficiencies are associated with 10% of all children's deaths, and are therefore of special concern to those involved with child welfare. Deficiencies of essential vitamins or minerals such as Vitamin A, iron, and zinc may be caused by long-term shortages of nutritious food or by infections such as intestinal worms. They may also be caused or exacerbated when illnesses (such as diarrhoea or malaria) cause rapid loss of nutrients through feces or vomit.
Hypochromic anemia may be caused by vitamin B6 deficiency from a low iron intake, diminished iron absorption, or excessive iron loss. It can also be caused by infections (e.g. hookworms) or other diseases (i.e. anemia of chronic disease), therapeutic drugs, copper toxicity, and lead poisoning. One acquired form of anemia is also known as Faber's syndrome. It may also occur from severe stomach or intestinal bleeding caused by ulcers or medications such as aspirin or bleeding from hemorrhoids.
Hypochromic anemia occurs in patients with hypochromic microcytic anemia with iron overload. The condition is autosomal recessive and is caused by mutations in the SLC11A2 gene. The condition prevents red blood cells from accessing iron in the blood, which causes anemia that is apparent at birth. It can lead to pallor, fatigue, and slow growth. The iron overload aspect of the disorder means that the iron accumulates in the liver and can cause liver impairment in adolescence or early adulthood.
It also occurs in patients with hereditary iron refractory iron-deficiency anemia (IRIDA). Patients with IRIDA have very low serum iron and transferrin saturation, but their serum ferritin is normal or high. The anemia is usually moderate in severity and presents later in childhood.
Hypochromic anemia is also caused by thalassemia and congenital disorders like Benjamin anemia.
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.
Mineral deficiency is a lack of dietary minerals, the micronutrients that are needed for an organism's proper health. The cause may be a poor diet, impaired uptake of the minerals that are consumed or a dysfunction in the organism's use of the mineral after it is absorbed. These deficiencies can result in many disorders including anemia and goitre. Examples of mineral deficiency include, zinc deficiency, iron deficiency, and magnesium deficiency.
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.
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.
1- Secondary anaemias
- Chronic infection/inflammation
- Malignancy
2- Thalassaemia
3- Sideroblastic anaemia
Certain gastrointestinal disorders can cause anemia. The mechanisms involved are multifactorial and not limited to malabsorption but mainly related to chronic intestinal inflammation, which causes dysregulation of hepcidin that leads to decreased access of iron to the circulation.
- "Helicobacter pylori" infection.
- Gluten-related disorders: untreated celiac disease and non-celiac gluten sensitivity. Anemia can be the only manifestation of celiac disease, in absence of gastrointestinal or any other symptoms.
- Inflammatory bowel disease.
Heinz bodies form in the cytoplasm of RBCs and appear as small dark dots under the microscope. In animals, Heinz body anemia has many causes. It may be drug-induced, for example in cats and dogs by acetaminophen (paracetamol), or may be caused by eating various plants or other substances:
- In cats and dogs after eating either raw or cooked plants from the "Alium" genus, for example, onions or garlic.
- In dogs after ingestion of zinc, for example, after eating U.S. pennies minted after 1982.
- In horses which eat dry or wilted red maple leaves.
Symptoms include leaves turning yellow or brown in the margins between the veins which may remain green, while young leaves may appear to be bleached. Fruit would be of poor quality and quantity. Any plant may be affected, but raspberries and pears are particularly susceptible, as well as most acid-loving plants such as azaleas and camellias.