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Essential Macrominerals and Microminerals

Essential Minerals
Macrominerals Microminerals
Sodium Iron
Potassium Zinc
Chloride Iodine
Calcium Selenium
Phosphorus Copper
Magnesium Fluoride
Sulfur Chromium
Molybdenium
Manganese

Selenium edit

Absorption edit

The primary site of absorption of selenium is in the duodenum, as no absorption takes place in the stomach, but very little occurs in the two segments of the small intestine. Seleniumare organic and inorganic. Selenium in forms of Selenocysteine and Selenomethionine are found in animal and plant respectively as they are ingested into the body system as part of Amino acids. All The absorption of selenium occurs in the small intestine’s lower end. 80 percent of Seleniumsabsorpted as shown in experimental animals and humans.Selenomethionine are absorbed more effectively than the organic forms, especially selenite, where 90 % of selenomethionine and 60 % of selenite are absorbed in the intestinal tract.The retention of it also differs in human due to differences in chemical forms. Humans and experimental animals have shown that selenomethionine is retained more effectively than selenite or selenate, however it is not as efficient in maintaining the selenium status. Selenomethionine is also better retained in tissues than selenocysteine where it is embedded into proteins, for instance in methionine, but not limited to methionine. Evidence has shown the differences in the levels of seleniumabsorption if it is supplied along with food and not as an isolate or in form of other supplement. Absorption of Selenium is affected by a number of dietary factors and also the chemical form of the element. Selenium absorption is enhanced by the presence of vitamin E, vitamin A, and protein, and is decreased by sulphur, arsenic, mercury, guar gum, and vitamin C.[1] Selenium absorbed from the diet is transported in the blood from the intestine to the liver where is it reduced to selenide before been transported into the blood, bound to alpha and gamma globulins to various organs and target tissues. Thereafter, it is incorporated into specific selenoproteins, as selenocysteine, and nonspecifically, as selenomethionine. Furthermore, the highest levels of selenium are deposited in the red blood cells, liver, heart, spleen, nails, and tooth enamel. Absorbed selenium is excreted via urine, while some are also lost in sweat and in hair. However, some very little amount is lost via bilary, pancreatic, and intestinal secretions in faeces.[2]

Transport and Metabolism edit

Transport of Selenium in the Body

Selenium that is absorbed is transported in the blood mainly in bound protein and subsequently undergoing initial reduction in the erythrocytes to selenide.[3] This involves the using reduced glutathione and also involves the enzyme glutathione reductase.[4] Almost all the proteins-bound selenium in human blood has been shown to be in very low density lipoprotein fraction, with smaller amounts bound to other proteins.[5] Distributing this protein is dependant of the diet composition. 50 percent of plasma selenium is associated with albumin in people who consume diets which selenomethione is the main form of selenium.[6] Evidences, has also shown that different proteins acts as carriers of selenium in otherspecies of animals.[7]

Excretion of Selenium in the body

The retention of selenium in the body is estimated to be 100 days. Selenium is excreted from the body through the main channels, that is, via the kidneys, faeces from the gastrointestinal tracts and expired air in the lungs. The amount of excretion from each type of route depends on the level of selenium in the diet.[8]

Urinary Excretion of Selenium

The dominant excretion route for selenium in humans is the urine pathway.[9] Hence, the ratio of intake excreted depends on the level of intake in the diet, that is, when intake is high, consequenty, urinary excretion will be high and at low levels of intake, half or less of selenium would appear in the urine.[10] The chemical forms of selenium found in the urine includes, selenomethionine, selenocysteine, selenite, selenate, and selenocholine. Studies reported that the major form of selenium in the urine is trimethylselenonium and it accounts for 50 percent of the total urine excreted of the chemical and the levels increase with increased intake of selenium, however, it is generally thought that it is produced as a way of eliminating excess and potentially toxic selenium.[11]

Fecal Excretion of Selenium

Fecally excreted selenium is largely composed of unabsorbed dietary selenium, and also bilary, pancreatic, and intestinal secretions.[12] Selenium fecal excretion, also as in urinary excretion is affected by chemical forms and dietary intake.

Pulmonary Excretion of Selenium

Selenuimexcretion via pulmonary route in expired air and via dermal route in sweat are of minor significance at normal level of dietary consumption. It’s excretion via the lungs is usually due to high intake of the chemical. Excess selenium is detoxified bysuccessive methylationto form the volatile dimethyl selenide and other methylated species. An evidence of selenium intoxication in humans is the characteristic garlic like odour in the breath.

Losses of Selenium in Hair and Nails

Selenium is excreted in the hair and nails in a limited extent, as matter of fact, homeostasis view it at of little consequence. Hair and nail excretion of selenium can be used to reflect long-term intake and also provide a convenient and noninvasive assessment method.[13]

Physiological functions edit

Selenium is an integral part of glutathione peroxidase, which is an enzyme that acts as antioxidant in cells and also influences vitamin E functions. Glutathione peroxidase also plays an important function in protecting the skin from ultraviolet radiation.Selenium also helps in the proper functioning of the liver, synthesis of protein and protects the body from minerals, such as cadmium, arsenic, mercury and lead, which are toxic. It has also been shown to play a germane role in the creation of male reproductive system, and maintain a healthy eyes, hair and skin.[14]

Recommendations edit

Nordic recommendations:

Age/Life Stage Males (µg/day) Females (µg/day)
2-5 years 25 25
6-9 years 30 30
10-13 years 40 40
14 years and older 60 50
Recommended Dietary Allowance (RDA) for Selenium in US
Age/Life Stage Males (µg/day) Females (µg/day)
0-6 months 15 15
7-36 months 20 20
4-8 years 30 30
9-13 years 40 40
14 years and older 55 55
Pregnancy - 60
Breast-feeding - 70


Health effects edit

The Role of Selenium in the Development of Cardiomyopathy—Keshan Disease

The first hints about the significance of selenium in the cardiovascular system go back to earlier reports about a rapidly progressive and severe cardiomyopathy (Keshan Disease), which is characterized by myocardial necrosis and calcification. Although selenium deficiency obviously appears to represent the primary pathogenic factor in the development and occurrence of this disease, it was subsequently considered more likely to be a conditional predisposing factor than an etiologic factor for this form of juvenile cardiomyopathy. In this context, previous studies demonstrated that selenium supplementation in deficient mice, reduced the cardiotoxicity of the coxsackie b virus that was previously isolated from patients with Keshan disease. Subsequent studies confirmed these findings and showed an increased susceptibility of mice to the development of viral-induced cardiomyopathy, when fed with a selenium-deficient diet (Carina Benstoem, 2015 ). [15]

Although the exact mechanisms remain vague, more recent studies have demonstrated the protective properties of GPx activity on the disease development and reported an increased sensitivity to this viral infection in mice with 50% of GPx1 knockout, whereas wildtype mice remained resistant.

Zinc edit

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Absorption edit

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Transport and Metabolism edit

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Physiological functions edit

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Recommendations edit

Nordic recommendations:

Age/Life Stage Males (µg/day) Females (µg/day)
0-6 months - -
6-11 months 15 15
12-23 months 20 20
2-5 years 25 25
6-9 years 30 30
10-13 years 40 40
14 years and older 60 50
Pregnancy - 60
Breast-feeding - 60
Recommended Dietary Allowance (RDA) for Selenium in US
Age/Life Stage Males (µg/day) Females (µg/day)
0-6 months 15 15
7-36 months 20 20
4-8 years 30 30
9-13 years 40 40
14 years and older 55 55
Pregnancy - 60
Breast-feeding - 70

Magnesium edit

Nordic recommendation edit

Magnesium mg/d Women Men Children 2-5y Children 6-9y Children 10-13y
Recommended intake RI 280 350 120 200 280
Average requirement AR - -
Lower intake level LI - -
Upper intake level UL - -

[16]

US recommendation edit

In 1997, the Food and Nutrition Board of the Institute of Medicine increased the recommended dietary allowance (RDA) for magnesium, based on the results of recent, tightly controlled balance studies that utilized more accurate methods of measuring magnesium (table below). Balance studies are useful for determining the amount of a nutrient that will prevent deficiency; however, such studies provide little information regarding the amount of a nutrient required for chronic disease prevention or optimum health.

Recommended Dietary Allowances (RDA) for Magnesium
Life stage Age Males (mg/day) Females (mg/day)
Infants 0-6 months 30 (AI) 30 (AI)
Infants 7-12 months 75 (AI) (75 AI)
Children 1-3 years 80 80
Children 4-8 years 130 130
Children 9-13 years 240 240
Adolescents 14-18 years 410 360
Adults 19-30 years 400 310
Adults 31 years and older 420 320
Pregnancy 18 years and younger - 400
Pregnancy 19-30 years - 350
Pregnancy 31 years and older - 360
Breast-feeding 18 years and younger - 360
Breast-feeding 19-30 years - 310
Breast-feeding 31 years and older - 320

[17]

Recommendations elsewhere (UK, France, India, China) edit

Group and source of intake (reference) Magnesium intake, mg/day
Infants; 750 ml liquid or formula as sole food source
Human milk
United Kingdom (21, 22) 21 (20-23)
India (23) 24 +/- 0.9
Formula
United Kingdom (whey based) 30-52
United Kingdom (soya based) 38-60
Adults: conventional diets
France, males (25) 369 +/- 106
France, females (25) 280 +/- 84
United Kingdom, males (26) 323
United Kingdom, females (26) 237
India 300-680
China, females 190 +/- 59
232 +/- 62
333 +/- 103

[18]

Absorption edit

Absorption is complex, depending on the individual’s magnesium status. Magnesium absorption appears to be greatest within the duodenum and ileum and occurs by both passive and active processes. [19]

Magnesium homeostasis is maintained by the intestine, the bone and the kidneys. Magnesium — just like calcium — is absorbed in the gut and stored in bone mineral, and excess magnesium is excreted by the kidneys and the faeces. Magnesium is mainly absorbed in the small intestine although some is also taken up via the large intestine. Two transport systems for magnesium in the gut are known. The majority of magnesium is absorbed in the small intestine by a passive paracellular mechanism, which is driven by an electrochemical gradient and solvent drag. A minor, yet important, regulatory fraction of magnesium is transported via the transcellular transporter transient receptor potential channel melastatin member (TRPM) 6 and TRPM7—members of the long transient receptor potential channel family — which also play an important role in intestinal calcium absorption. Of the total dietary magnesium consumed, only about 24–76 % is absorbed in the gut and the rest is eliminated in the faeces. It is noteworthy that intestinal absorption is not directly proportional to magnesium intake but is dependent mainly on magnesium status. The lower the magnesium level, the more of this element is absorbed in the gut, thus relative magnesium absorption is high when intake is low and vice versa. When intestinal magnesium concentration is low, active transcellular transport prevails, primarily in the distal small intestine and the colon. [20]

Excretion edit

The kidneys are crucial in magnesium homeostasis as serum magnesium concentration is primarily controlled by its excretion in urine. Magnesium excretion follows a circadian rhythm, with maximal excretion occurring at night. Under physiological conditions, ∼2400 mg of magnesium in plasma is filtered by the glomeruli. Of the filtered load, ∼95 % is immediately reabsorbed and only 3–5 % is excreted in the urine, i.e. ∼100 mg. It is noteworthy that magnesium transport differs from that of the most other ions since the major re-absorption site is not the proximal tubule, but the thick ascending limb of the loop of Henle. There, 60–70 % of magnesium is reabsorbed, and another small percentage (∼10 %) is absorbed in the distal tubules. The kidneys, however, may lower or increase magnesium excretion and re-absorption within a sizeable range: renal excretion of the filtered load may vary from 0.5 to 70 %. On one hand, the kidney is able to conserve magnesium during magnesium deprivation by reducing its excretion; on the other hand, magnesium might also be rapidly excreted in cases of excess intake. While reabsorption mainly depends on magnesium levels in plasma, hormones play only a minor role (e.g. parathyroid hormone, anti-diuretic hormone, glucagon, calcitonin), with oestrogen being an exception to this rule.[20]

Transport in the body edit

The rate of magnesium transport through cell membranes is higher in the heart, kidneys and liver and lower in the brain, red cells and skeletal muscle. Rapidly proliferating cells have higher intracellular magnesium, which indicates that the metabolic activity of the cell is linked to the transport of cellular magnesium. [21]

Magnesium is transported across the cell membrane by magnesium transporter proteins. [22]

Physiological functions edit

Magnesium is included in over 300 essential metabolic reactions. Magnesium is very important for humans because of its functional and structural effects in the body. Magnesium is required in energy production, synthesis of essential biomolecules such as nucleic acids, carbohydrates and lipids, ion transport across cell membranes, cell signaling and cell migration as well as in bones, cell membranes and chromosomes as a structural component. [23]

Magnesium is the fourth most abundant cation in vertebrates and the central ion of chlorophyll in plants is magnesium. Most of the total body magnesium is situated in the bones, muscles and non-muscular soft tissue. The content of magnesium in the bones decreases with age. Magnesium stored in the bones is not entirely bioavailable during magnesium deprivation. One third of skeletal magnesium can be exchanged and it serves as a reservoir for the maintenance of physiological extracellular magnesium levels. [20]

Approximately 1-5 % of intracellular magnesium is ionized while the major part is bound to proteins ATP and negatively charged molecules. Only 1 % of total body magnesium is extracellular magnesium, primarily found in red blood cells and serum. The serum magnesium can be ionized/free, bound to a protein or complexed with phosphate, bicarbonate and citrate anions or sulphate. Ionized magnesium in the plasma has the greatest biological activity. [20]

As magnesium functions as a counter ion to ATP, it stabilizes many ATP-generating reactions, thus magnesium is involved in numerous important physiological functions. ATP metabolism, muscle contraction and relaxation, normal neurological function and release of neurotransmitters all require magnesium. Magnesium also has an important role in the regulation of vascular tone, heart rhythm, platelet-activated thrombosis and bone formation. [20]

Emerging data on health effects edit

Magnesium is a cofactor for more than 300 enzyme systems and is involved in both aerobic and anaerobic energy generation and in glycolysis, either directly as an enzyme activator or as part of the Mg-ATP complex. Magnesium is required for mitochondria to carry out oxidative phosphorylation. It plays a role in regulating potassium fluxes and in the metabolism of calcium. The human body contains about 760 mg of magnesium at birth and 25 g in adulthood. Just over half the body's magnesium is found in bone, where it forms a surface constituent of the hydroxyapatite mineral component, and a further third is found in muscles and soft tissues. The intracellular concentration is about ten times that of the extracellular fluid. [23]

Magnesium is widely distributed in the food supply in both plant and animal foods. Most green vegetables, legumes, peas, beans and nuts are rich in magnesium, as are some shellfish and spices. Most unrefined cereals are reasonable sources, but highly refined flours, tubers, fruits, oils and fats contribute little. Between 50 % and 90 % of magnesium in breast milk or infant formula is absorbed. In adults on conventional diets, the efficiency of absorption varies greatly with magnesium content ranging from 25 % on high magnesium diets in one study to 75 % on low magnesium diets. The homeostatic capacity of the body to adapt to a wide range of intakes is thus high. [23]

Magnesium is absorbed in the duodenum and ileum by both active and passive processes. High fibre intakes (40-50 g/day) lower magnesium absorption, probably because of the magnesium-binding action of the phytate phosphorus associated with the fibre. There is no consistent evidence that moderate increases in calcium, iron or manganese affect magnesium balance. However, high intakes of zinc at 142 mg/day reduce absorption. Protein may also influence magnesium absorption. When protein intake is less than 30 g/day, magnesium absorption decreases. When protein intake is greater than 94 g/day, renal magnesium excretion may increase, although adaptation may occur. [23]

The kidney plays a central role in magnesium homeostasis through active reabsorption that is influenced by the sodium load in the tubules and possibly acid-base balance. High dietary calcium intake (about 2,600 mg/day) with high sodium intake enhances magnesium output, contributing to a shift to negative magnesium balance. [23]

Pathological effects of primary nutritional deficiency of magnesium occur only rarely in humans, unless low intakes are accompanied by prolonged diarrhoea or excessive urinary loss. The body is generally protected by the lability of serum magnesium. Most of the early signs of deficiency are neurologic or neuromuscular defects that may develop with time into anorexia, nausea, muscular weakness, lethargy, weight loss, hyper-irritability, hyper-excitability, muscular spasms, tetany and finally convulsions. [23]

Hypocalcaemia also occurs in moderate to severe magnesium deficiency. Some studies have indicated that low magnesium status may be a risk for postmenopausal osteoporosis, however others have not confirmed the link between low magnesium and risk of osteoporosis. Sub-optimal magnesium status may be a factor in the aetiology of coronary heart disease and hypertension, but evidence is relatively sparse. Magnesium depletion has been shown to cause insulin resistance and impaired insulin secretion, and magnesium supplements have been reported to improve glucose tolerance and insulin response in the elderly. [23]

Indicators used for estimating magnesium requirements have included serum magnesium, plasma ionised magnesium, intracellular magnesium, magnesium balance, estimates of tissue accretion in growth, magnesium tolerance tests and epidemiologic studies including meta-analysis. However, serum magnesium has not been properly validated as a reliable indicator of body magnesium status. Plasma ionised magnesium may be an improvement on serum magnesium but requires further evaluation and the validity evidence for intracellular magnesium is limited. Magnesium balance is problematic if not carried out under close supervision, as magnesium in water can confound results, a factor that precluded the use of many early studies conducted in free-living situations or current studies where intakes were calculated, not analysed. [23]

Accurate estimates of tissue accretion during growth throughout childhood are dependent on more extensive information about whole body mineral retention than are currently available, although there is some information for specific ages from cadaver data. The magnesium tolerance test is an invasive procedure based on renal excretion of parenterally administered magnesium load. It is considered accurate for adults but not infants and children. The test requires normal renal handling and may be unreliable in diabetics or drug or alcohol users. It may also be affected by ageing of kidney tissue. Epidemiological studies with meta-analysis may indicate relationships between magnesium intake and health outcomes. [24]

Manganese edit

Nordic recommendation edit

No recommendation given due to lack of sufficient evidence. [16]

US recommendation edit

Because there was insufficient information on manganese requirements to set a Recommended Dietary Allowance (RDA), the Food and Nutrition Board (FNB) of the Institute of Medicine set an adequate intake (AI). Since overt manganese deficiency has not been documented in humans eating natural diets, the FNB based the AI on average dietary intakes of manganese determined by the Total Diet Study — an annual survey of the mineral content of representative American diets. AI values for manganese are listed in table below in milligrams (mg)/day by age and gender. Manganese requirements are increased in pregnancy and lactation.

Life Stage Age Males (mg/day) Females (mg/day)
Infants 0-6 months 0.003 0.003
Infants 7-12 months 0.6 0.6
Children 1-3 years 1.2 1.2
Children 4-8 years 1.5 1.5
Children 9-13 years 1.9 1.6
Adolescents 14-18 years 2.2 1.6
Adults 19 years and older 2.3 1.8
Pregnancy all ages - 2.0
Breast-feeding all ages - 2.6

Due to the severe implications of manganese neurotoxicity, the Food and Nutrition Board (FNB) of the Institute of Medicine set very conservative tolerable upper intake levels (UL) for manganese; the ULs are listed in table below according to age.

Age group UL (mg/day)
Infants 0-12 months Not possible to establish
Children 1-3 years 2
Children 4-8 years 3
Children 9-13 years 6
Adolescents 14-18 years 9
Adults 19 years and older 11

[17]

Recommendations elsewhere (Australia and New Zealand) edit

Recommendations by life stage and gender AI Manganese mg/day
Infants
0-6 months 0.003
7-12 months 0.600
Children and adolescents
All
1-3 years 2.0
4-8 years 2.5
Boys
9-13 years 3.0
14-18 years 3.5
Girls
9-13 years 2.5
14-18 years 3.0
Adults
Men
19-30 years 5.5
31-50 years 5.5
51-70 years 5.5
> 70 years 5.5
Women
19-30 years 5
31-50 years 5
51-70 years 5
> 70 years 5
Pregnancy and lactation
14-18 years 5
19-30 years 5
31-50 years 5

[25]

Absorption edit

The amount of manganese absorbed across the gastrointestinal tract is variable, but typically averages about 3–5 %. Adults maintain stable tissue levels of manganese through the regulation of gastrointestinal absorption and hepatobiliary excretion. Absorbed manganese is widely distributed throughout the body, with higher levels found in the liver, pancreas, and kidney. [26]

Gender differences for Mn absorption have been noted, men absorbing significantly less Mn compared to women. It has been postulated that reduced gastrointestinal Mn absorption in men reflects the iron status and the higher serum ferritin concentrations in men. Within the plasma, Mn is largely bound to gamma-globulin and albumin, and a small fraction of trivalent (3+)Mn is bound to the iron-carrying protein, transferrin. Mn absorption by the gastrointestinal tract is influenced by several factors. For example, the concentration of Mn in the diet is known to influence the amount of Mn absorbed from the gastrointestinal tract as well as its elimination via the bile. Adaptive changes to high dietary Mn intake include reduced gastrointestinal tract absorption, enhanced liver metabolism, and increased biliary and pancreatic excretion of this. Mn absorption from the diet is also influenced by the presence of other trace minerals, phytate, ascorbic acid, and other dietary constituents. Competition between Mn and iron (Fe) at the gastrointestinal tract has been documented, and it is most likely mediated via the divalent metal transporter 1 (DMT-1). Furthermore, absorption of Mn from the gastrointestinal tract is also influenced by the age of an individual. [27]

Excretion edit

The primary route of elimination is fecal elimination via hepatobiliary excretion. [26]

Manganese is excreted primarily via the bile in the feces. Excess absorbed manganese from the diet is quickly excreted by the liver into the bile to maintain homeostasis. Very little manganese is excreted in the urine. Moreover, urinary manganese does not correlate with intake and does not increase even when dietary intake of the mineral is excessive. However, excretion of manganese through sweat and skin desquamation has been shown to contribute to manganese losses. [28]

Transport in the body edit

The specific transport mechanisms for manganese have not been determined, although there is some evidence that iron and manganese may share common transport pathways. [23]

Even though the precise mechanism of manganese transport is unknown, it is suggested that manganese is transported across the blood-brain barrier to the brain via facilitated diffusion, active transport or transferrin-dependent transport. The mechanism most likely consists of more than one route. [29]

Physiological functions edit

Manganese is a controversial mineral element, because as it is nutritionally essential but also potentially toxic for living organisms. Manganese has an important role in many physiological processes as it functions as an element in numerous enzymes and as an activator for some enzymes. Manganese is required in some antioxidant functions, in the metabolism of carbohydrates, amino acids and cholesterol, in the synthesis for proteoglycans that are essential for healthy bone and cartilage and in collagen production to heal wounds. [23]

There have not been reported any cases of manganese toxicity as a result of dietary intake. Manganese is stored in the liver, kidney, pancreas and bones. It has a role in the formation of connective tissue, bones, sex hormones and blood-clotting factors, it is also required for normal rain and nerve function. [30]

Emerging data on health effects edit

Manganese is an essential element involved in formation of bone. It is also involved in the metabolism of carbohydrate, cholesterol and amino acids. Manganese metalloenzymes include manganese superoxide dismutase, arginase, phosphoenolpyruvate decarboxylase and glutamine synthetase. Cereal products provide about one-third of the intake of manganese and beverages (tea) and vegetables are the other major contributors. Less than 5% of dietary manganese is absorbed. In excess, it can interfere with iron absorption. Manganese is taken up from blood by the liver and transported by transferrin and possibly alpha2-macroglobulin or albumin to other tissues. Retention can be affected by immediately prior intakes of manganese, calcium, iron and phosphorus. Low ferritin levels are associated with increased manganese absorption, thus exerting a gender effect on manganese bioavailability. Manganese is excreted rapidly into the gut through bile and lost primarily in faeces. Low bile excretion can therefore increase the potential for manganese toxicity. Urinary excretion is low and not related to diet. Manganese deficiency in animals is associated with impaired growth, reproductive function and glucose tolerance as well as changes in carbohydrate and lipid metabolism. It also interferes with skeletal development. Clinical deficiency in humans has not been associated with poor dietary intake in otherwise healthy individuals. Skin symptoms and lowering of cholesterol were also seen in one experimental depletion study in young men. Accidental overdose has been shown to result in symptoms such as scaly dermatitis, hypocholesterolaemia, hair depigmentation and reduced vitamin K-dependent clotting factors. The indicators for estimating the requirement of manganese include balance and depletion studies, serum, plasma, blood or urinary manganese concentration, arginase activity and manganese superoxide dismutase activity. However, none of these is reliable or sensitive enough to be used for setting recommended intakes. Balance studies are problematic because of the rapid excretion of manganese into bile and because balance studies over short to moderate periods do not appear to give results proportional to manganese intakes. Serum, plasma, blood and urinary manganese measures seem highly variable over the normal range of consumption and largely insensitive to moderate dietary change. Arginase activity is affected by a number of factors, including high protein diet and liver disease. Ethanol and dietary polyunsaturated fats can affect manganese superoxide dismutase. [23]

1 mmol manganese = 55 mg manganese

Manganese (Mn) is an abundant transition metal essential to mammalian physiological processes. [31]

The brain is particularly vulnerable to oxidative damage due to its high rate of oxygen consumption, intense production of reactive radicals and high levels of transition metals, such as iron and manganese [32]. both metals can catalyze the production of the very toxic hydroxyl radical (OH·) through Fenton's reaction. Mitochondria, nucleus and synaptosomes of neuron and astrocytes of globus pallidus are described as the primary sites of Mn accumulation and toxicity in the brain [33]. Additionally, many studies reported that the sub-clinical neurological effects are the decrease of intellectual functions and increased risk of mortality of infants during their first year of life [34].


Iodine edit

Recommendations edit

Nordic recommendations edit

Age/Life Stage Males (µg/day) Females (µg/day)
0-6 months - -
6-11 months 50 50
12-23 months 70 70
2-5 years 90 90
6-9 years 120 120
10-13 years 150 150
14-17 years 150 150
18-30 years 150 150
31-60 years 150 150
61-74 years 150 150
75+ 150 150
Pregnancy - 175
Breast-feeding - 200

[35]

USA recommendations edit

Age/Life Stage Males (µg/day) Females (µg/day)
0-6 months 110 110
7-12 months 130 130
1-3 years 90 90
4-8 years 90 90
9-13 years 120 120
14-18 years 150 150
19-30 years 150 150
31-50 years 150 150
50-70 years 150 150
70+ 150 150
Pregnancy - 220
Breast-feeding - 270

[36]

Japanese recommendations edit

Age/Life Stage Males (µg/day) Females (µg/day)
0-5 months - -
6-11 months - -
1-2 years 60 60
3-5 years 70 70
6-7 years 80 80
8-9 years 100 100
10-11 years 120 120
12-14 years 140 140
15-17 years 140 140
18-29 years 150 150
30-49 years 150 150
50-69 years 150 150
70+ years 150 150
70+ 150 150
Pregnancy - +110
Breast-feeding - +190

[37]

Food sources edit

Sources of iodine include iodinized salt, seafood and dairy products. Iodine content in plants depends on the iodine content in soil. Areas located inland or mountain areas, like Bolivia, are poor in iodine compared to coastal areas[38]. Iodinized salt usage is recommended, because it is the most easiest way to ensure intake of iodine[39].

Iodine in soil can be in the form of NaIO3 and NaIO4. In seaweed or algal phytoplankton iodine can be in the form of KI, NaI, I2 or iodide. Seaweeds, such as wakame, nori and mekabu, are widely used in Asian food. They contain large amounts of iodine that can be in molecular form or bound to amino acids[40] .

Absorption, Transport and Metabolism edit

Molecular iodine is transported from the gastrointestinal tract by facilitated diffusion. Iodide ions are absorbed via sodium-iodide trasporter that is a trasport protein located in the gastric mucosa[40] .

Transportation is classified as active transportation, because iodide ions are transported against the electrochemical gradient across basolateral plasma membrane. In passive transportation, iodide ions translocate across apical membrane. Transportation into the thyroid regulates the synthesis of thyroid hormones[41]

In thyroid tissue, iodide is absorbed through the sodium/iodine symported protein (NIS) that is found in thyroid follicular cells. Activity of NIS can be regulated by thyroid stimulating hormone (TSH). Thyroid peroxidase enzyme oxidises iodine. Oxidised iodine is incorporated into the thyroglobulin molecule[40] .

Thyroid hormones, T3 and T4, are excreted into the bloodstream. Hormone T4 can convert into T3. This reaction is catalyzed by deiodinase enzymes. Two deioidinase enzymes control the amount of iodine that is in breast tissue. Deiodinase enzyme type 1 is produced during pregnancy and lactation whereas type 2 is produced during non-pregnancy and postpartum[40] .

Physiological functions edit

Thyroxine (T4) and triiodothyronine (T3) are hormones produced by the thyroid gland. Formation T3 is the active hormone that has many functions in the body, including regulation of energy metabolism, cell growth, physical and mental development in children. Iodine also plays a role in the formation of blood cells and controls temperature of the body. Most of the body’s iodine is located in mammary tissue, eyes, cervix, gastric mucosa and salivary glands. Human breast milk contains iodine that is needed for growing fetus and infant[41] [40] .

Iodine bound into lipid molecules are iodolipids and they seem to regulate the thyroid cell metabolism and cell proliferation. 6-iodo-5-hydroxy-eico-satrienoic acid (delta-iodolactone) is a potential inhibitor that controls the proliferation of thyroid cells. This compound can also control the proliferation of cells in breast tissue[41] [40] .

Iodine and selenium interaction edit

Both minerals, iodine and selenium, are needed for the proper function of thyroid gland. Selenium is essential in biosynthesis of iodothyronine deiodinases. In New Zealand, there is a little iodine and selenium deficiency. According to one study, there was no synergestic connection between iodine and selenium, but selenium supplement increased activities of selenium and glutathione peroxidase in plasma [42].

Health effects edit

Deficiency edit

Iodine deficiency is common in the developing countries like Africa, Southeast and Central Asia, but it’s also found in Europe, in Germany, France, Italy and Belgium. Iodine defiency is common among adult women in the United States. In Japan, the incidence of iodine deficiency is low due to high consumption of iodine rich food such as seaweed. The average daily intake of iodine varies between 5,280 mcg and 13,800 mcg in Japan, whereas in USA the average daily consumption is 167 mcg[40] . Iodine deficiency is the most easily preventable cause of mental retardation, goitre and primary hypothyroism[41] [40] Iodine deficiency can increase the risk of thyroid cancer. Low iodine intake leads to nodular enlargement, which is a visible symptom of iodine deficiency[43] .

Iodine intake is particularly critical in pregnancy and during lactation. Iodine is concentrated in mammary glands during pregnancy and lactation[40] .

It seems that adequate iodine intake minimizes the risk of fibrocystic breast disease and prostate cancer. Fibrocystic breast disease can increase the risk of breast cancer[40] .

Iodine deficiency can lead to neurological damage, hearing loss, leasing deficits, myelination and even increase the risk of infant mortality. Maternal iodine deficiency can cause IQ deficits in 7–9 years old children[40] It is estimated that more 260 million school age children and 2 billion people worldwide suffer from iodine deficiency[44] .

Goitrins are compounds found in cruciferous plants such as manioc, broccoli, cauliflower. Consuming excessive amounts of these plants can lead into iodine deficiency if there is not enough iodine in the diet.

As an Antioxidant and Antiproliferant edit

Iodine might have antioxidative functions in cells. Iodide can donate an electron in the presence of hydrogen peroxide and peroxidase. Amino acids such as tyrosine and histidine and lipids can be iodinated by the left iodine atom[45] .

Iodine can have a suppressive effect on cancer cell proliferation, benign and cancerous neoplasm. Oxidized iodine can induce the mitochondria-derived cell death, apoptosis [46] .

Iodine and Stomach Cancer edit

Protective role of iodine is based on its antioxidant function. Iodine can acts as an electron donor and free radical scavenger that might protect stomach cells from harmful oxidation and regulate cell proliferation[47] .

Toxicity edit

Elemental iodine (I2) is poisonous if taken orally in larger amounts; 2–3 grams of it is a lethal dose for an adult human. [48]

How to make references? edit

Just some examples

Cite journal [49]

[50]

[51]


Cite book [52]

Cite web [53]


References edit

  1. ↑ Susan J Fairweather-Tait; et al. (1997). "Selenium bioavailability: current knowledge and future research requirements". Journal of Nutrition: 20–23. {{cite journal}}: Explicit use of et al. in: |last= (help)
  2. ↑ Linder, Maria C. (1988). Nutritional biochemistry and metabolism: With clinical applications (2nd expanded ed.). New York: Elsevier. p. 177. ISBN 978-0838570845.
  3. ↑ Dreosti, I (1986). "Selenium". Journal of Food Nutrition: 60–78.
  4. ↑ Jenkins KJ, Hidiroglou M. (1972). "Comparative metabolism of 75 Se-selenite, 75 Se-selenate, and 75 Se-selenomethionine in bovine erythrocytes". Can J Physiol Pharmacol. 10: 927–935.
  5. ↑ Markus Sandholm (1974). "Selenium Carrier Proteins in Mouse Plasma". Nordic Pharmacological Society: 427–431.
  6. ↑ Whanger, P.; Xia, V.; Thomson, C. (1993). "Metabolism of different forms of selenium in humans". Journal of Trace Elements and Electrolytes in Health and Disease. 7: 121.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  7. ↑ Young VR, Nahapetian A, Janghorbani M. (1982). "Selenium bioavailability with reference to human nutrition". American Journal of Clinical Nutrition. 35: 1076–1088.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  8. ↑ O. A. Beath, J. H. Draize, H. F. Eppson, C. S. Gilbert, O. C. McCreary (1934). "Certain poisonous plants of wyoming activated by selenium and their association with respect to soil types". J. Am. Pharmacol.: 94–97.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  9. ↑ Yang G1, Zhou R, Yin S, Gu L, Yan B, Liu Y, Liu Y, Li X. (1989). "Studies of safe maximal daily dietary selenium intake in a seleniferous area in China. I. Selenium intake and tissue selenium levels of the inhabitants". J Trace Elem Electrolytes Health Dis. 3: 77–87.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  10. ↑ Robinson, M.F. McKenzie, J.M. Thomson, C.D. Rij, A.L. van. (1973). "Metabolic balance of zinc, copper, cadmium, iron, molybdenum and selenium in young New Zealand Women". British journal of nutrition: 195–205.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  11. ↑ Kuehnelt, D., Kienzl, N., Traar, P. (2005). "Selenium metabolites in human urine afteringestion of selenite, L-selenomethionine, or DL-selenomethionine: a quantitative casestudy by HPLC/ICPMS". Anal. Bioanal. Chem.: 235–246.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  12. ↑ Levander, O.A. and Baumann, C.A. (1966). "Selenium metabolism VI. Effect of arsenic on excretion of selenium in the bile". Toxicol. Appl. Pharmacol.: 106–115.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  13. ↑ Longnecker, M.P., Stram, D.O., and Taylor, P.R. (1996). "Use of selenium concentrations in whole blood, serum, toenails, or urine as a surrogate measure of selenium intake". Epidemiology: 384–390.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  14. ↑ Mineralvita. "SELENIUM". Retrieved 22 November 2016.
  15. ↑ Carina Benstoem, Andreas Goetzenich, Sandra Kraemer, Sebastian Borosch, William Manzanares, Gil Hardy, and Christian Stoppe. "Selenium and Its Supplementation in Cardiovascular Disease—What do We Know?". Retrieved 22 November 2016.{{cite web}}: CS1 maint: multiple names: authors list (link)
  16. ↑ a b "Nordic Nutrition Recommendations 2012". Integrating nutrition and physical activity 5th edition. 2014.
  17. ↑ a b Food and Nutrition Board, Institute of Medicine (1997). "Dietary Reference Intakes: Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride". National Academy Press: 190–249.
  18. ↑ "FAO/WHO expert consultation on human vitamin and mineral requirements". 2001. {{cite journal}}: Cite journal requires |journal= (help)
  19. ↑ "Human Vitamin and Mineral Requirements". FOOD AND AGRICULTURE ORGANIZATION OF THE UNITED. 2002.
  20. ↑ a b c d e Jahnen-Dechent, Wilhelm (2012). "Magnesium basics". Clinical Kidney Journal. 5 (1): 3–14. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  21. ↑ Swaminathan, R (2003). "Magnesium Metabolism and its Disorders". Clin Biochem Rev. 24 (2): 47–66.
  22. ↑ Roof, SK (1994). "Magnesium transport systems: genetics and protein structure (a review)". J Am Coll Nutr. 13 (5): 424–428. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  23. ↑ a b c d e f g h i j k Higdon, Jane; Drake, Victoria J. (2012). An Evidence-based Approach to Vitamins and Minerals. Stuttgart: Thieme.
  24. ↑ Matias, C (2012). "Magnesium intake mediates the association between bone mineral density and lean soft tissue in elite swimmers". Magnesium Research. 25 (3): 120–125. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  25. ↑ Nutrient Reference Values for Australia and New Zealand Including Recommended Dietary Intakes 2006.
  26. ↑ a b "ToXGuide for Manganese". ATSDR. 2012.
  27. ↑ "Nutritional aspects of manganese homeostasis". Molecular Aspects of Medicine: 353–362. 2005.
  28. ↑ "Advanced Nutrition and Human Metabolism". Cengage Learning. 2008.
  29. ↑ Preedy, Victor R.; Watson, Ronald Ross; Martin, Colin R. (2011). Handbook of Behavior, Food and Nutrition. New York: Springer.
  30. ↑ Mason, Moya K. "Manganese". Retrieved 22 November 2016.
  31. ↑ D. Santos (2014). "Manganese in human parenteral nutrition: considerations for toxicity and biomonitoring". Neurotoxicology. 43: 36–45. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  32. ↑ Ansari, M.A (2008). "Oxidative stress and modification of synaptic proteins in hippocampus after traumatic brain injury". Free Radical Biology & Medicine. 45: 443–452. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  33. ↑ Martinez-Finley, E.J (2013). "Manganese neurotoxicity and the role of reactive oxygen species". Free Radical Biology & Medicine. 62: 65–75. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  34. ↑ Hafeman, D (2007). "Association between manganese exposure through drinking water and infant mortality in Bangladesh". Enviromental Health Perspectives. 115: 1107–1112. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); line feed character in |title= at position 86 (help)
  35. ↑ Nordic Nutrition Recommendations 2012: Integrating nutrition and physical activity. ISBN 978-92-893-2670-4. {{cite book}}: Cite has empty unknown parameter: |subscription= (help)
  36. ↑ DIETARY REFERENCE INTAKES FOR Vitamin A, Vitamin K, Arsenic, Boron, Chrmum, Copper, Iodine, Iron, Mangenese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. ISBN 0-309-07279-4. {{cite book}}: Cite has empty unknown parameter: |subscription= (help)
  37. ↑ "Dietary Reference Intakes (DRIs in Japan)". Asia Pac J Clin Nutr. 17: 420–444. 2008. {{cite journal}}: |first= missing |last= (help); Cite has empty unknown parameter: |coauthors= (help)
  38. ↑ "Iodine in diet".
  39. ↑ Santos, JE. (2015). "Iodine deficiency and thyroid nodular pathology--epidemiological and cancer characteristics in different populations: Portugal and South Africa". BMC Res Notes. 8: 284-. doi:10.1186/s13104-015-1155-3. {{cite journal}}: Check |doi= value (help)
  40. ↑ a b c d e f g h i j k Patrick, Lyn (2008). "Iodine: Deficiency and Therapeutic Considerations". Alternative Medicine. 13: 116–127.
  41. ↑ a b c d Carrasco, Nancy (1993). "Iodide transport in the thyroid gland". Biochimica et Biophysica Acta. 1154: 65–82.
  42. ↑ Thomson, C. (2009). "Selenium and iodine supplementation: effect on thyroid function of older New Zealanders". The Am J Clin Nutr. 90: 1038–1046. doi:10.3945. {{cite journal}}: Check |doi= value (help)
  43. ↑ Santos, JE. (2015). "Iodine deficiency and thyroid nodular pathology--epidemiological and cancer characteristics in different populations: Portugal and South Africa". BMC Res Notes. 8: 284-. doi:10.1186/s13104-015-1155-3. {{cite journal}}: Check |doi= value (help)
  44. ↑ Santos, JE. (2016). "Iodine deficiency a persisting problem: assessment of iodine nutrition and evaluation of thyroid nodular pathology in Portugal". J Endocrinol Invest.: 1–7. doi:10.1007/s40618-016-0545-2.
  45. ↑ Aceveset al. (2007). "The Extrathyronine Actions of Iodine as Antioxidant, Apoptotic, and Differentiation Factor in Various Tissues". REVIEWS and SCHOLARLY DIALOG. 23: 938–946. doi:10.1089/thy.2012.0579.
  46. ↑ Aceveset al. (2007). "The Extrathyronine Actions of Iodine as Antioxidant, Apoptotic, and Differentiation Factor in Various Tissues". REVIEWS and SCHOLARLY DIALOG. 23: 938–946. doi:10.1089/thy.2012.0579. Venturi, S. (2001). "Is there a role for iodine in breast diseases?". The Breast. 10: 379–382. doi:10.1054/brst.2000.0267. Shrivastava et al. (2006). "Is there a role for iodine in breast diseases?". THE JOURNAL OF BIOLOGICAL CHEMISTRY. 10: 19762–19771.
  47. ↑ Gołkowski et al. (2007). "Iodine prophylaxis—the protective factor against stomach cancer in iodine deficient areas". Eur J Nutr. 46: 251–256. doi:10.1007/s00394-007-0657-8. {{cite journal}}: line feed character in |title= at position 41 (help)
  48. ↑ "The National Institute for Occupational Safety and Health (NIOSH): Iodine".
  49. ↑ Mumford, David (1972). "Perfect article on everything". UCLA Law Review. 20: 75–83. doi:10.1007/b62130.
  50. ↑ Keum, NaNa (2014). "Calcium intake and colorectal cancer risk: dose-response meta-analysis of prospective observational studies". International Journal of Cancer. 135 (8): 1940–1948. doi:10.1002/ijc.28840. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  51. ↑ Martinez-Finley EJ; et al. (2013). "Manganese neurotoxicity and the role of reactive oxygen species". Free Radic Biol Med. 62: 65–75. doi:10.1016/j.freeradbiomed.2013.01.032. {{cite journal}}: Explicit use of et al. in: |last= (help)
  52. ↑ Mumford, David (1999). The Red Book. Lecture Notes. Vol. 1358 (2nd expanded ed.). Berlin: Springer Verlag. p. 198. doi:10.1007/b62130. ISBN 354063293X.
  53. ↑ Spiegel, Rachel. "Research: Thalido..." Retrieved 30 April 2006.
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