Mineral Health Connection

Selenium (Se)

Selenium (Se)

Mineral Health Connection

Over 200 years ago, Jöns Jacob Berzelius discovered the element selenium, which he named after the goddess of the moon, Selene. Aside from its industrial applications, selenium is an essential trace nutrient that is found in seafood, liver, lean red meat, and grains that are grown in selenium-rich soil. A deficiency in selenium is a severe obstacle in areas of the world where the soil contains little selenium such as the case in the United Kingdom, Australia, New Zealand (source) and some areas of China (source) among others.

Supplementing doses above the RDA (40 to 70 μg) is required to inhibit genetic damage and cancer (>100 μg). The most recent revision of of the RDA for selenium is based on the estimated average requirement (EAR) required to maximize the antioxidant enzyme glutathione peroxidase (GPx) activity in plasma (source) and not necessarily for seleniums anticarcinogenic effects. Excessive doses of selenium may cause oxidative damage leading to genomic instability which raises the question, how much is enough? In this article, I try and find clarity regarding this question and bring transparency to selenium and its supplementation.

Americans have been advised that supplementation is not needed on the basis of the EAR and their serum concentrations being met according to the National Health and Nutrition Examination Survey (NHANES III) (source). However, selenium intake is on the decline in many areas of the world due to the effect of sulphur-based fertilisers on crops such as wheat (source).

Worldwide, up to one in seven people have been estimated to have low dietary selenium intake. Using moderate climate change projections, it has been predicted that future soil selenium losses from 58% (between the year 2080–2099). Predicted losses from croplands were even higher, with 66% of croplands predicted to lose 8.7% selenium. These losses could increase the worldwide prevalence of selenium deficiency (source).

Selenium has a protective effect against some forms of cancer and may enhance male fertility, decrease cardiovascular disease mortality, and regulate inflammatory mediators in asthma (source). It has also been proposed that optimal selenium levels may potentially be useful for decreasing the risk of atherosclerosis, cataracts, emphysema, inflammatory-immune disease, senile dementia, aging, and rheumatoid arthritis.

Selenium prevents cellular and subcellular lipids and fats from being peroxidized, which means it prevents body fats from going rancid (seen externally as “age spots” or “liver spots” called ceroid lipofuscin). Iron chelators such as desferrioxamine and antioxidants such as vitamin E, glutathione, and selenium may slow lipofuscin accumulation (source). An exclusive and indispensable role of selenium noted in that it is required to prevent hydroperoxide-induced ferroptosis, preventing fatal epileptic seizures and protecting the brain (source). A subclinical selenium deficiency seems to be associated with reduced immunocompetence, depression, thyroid imbalances and reproduction difficulties in both sexes.

Mechanism of action:

Selenium is essential for the amino acid Selenocysteine, the 21st essential amino acid (source). Selenium exerts various biological functions which are found in at least 25 selenoproteins. Selenoproteins are involved in diverse roles such as stabilizing the integrity of the sperm flagella and are essential for thyroid hormone metabolism aiding conversion of thyroxine (T4) to the active thyroid hormone, 3,3′5-triiodothyronine (T3). Selenium is a vital component of several significant metabolic pathways such as protection from neurodegeneration, maintaining lens cell viability, and reducing oxidative damage during aging. (source, source).

Selenium is a significant contribution to the anti-oxidant system. As a component of glutathione peroxidase, selenium acts as an antioxidant and has a sparing effect on vitamin E. Glutathione peroxidase blocks the generation of free radicals that destroy polyunsaturated fatty acids in cell membranes. Cellular and plasma glutathione peroxidase is the functional parameter used for the assessment of selenium status in the body, though hair and nails are also valuable and accurate. Selenium enhances the enzyme required for the detoxification of xenobiotic chemicals in the liver, glucuronyl transferase, and is involved in the regulation of prostaglandin synthesis and the degradation of intracellular peroxides.

Selenium is believed to encourage the immune system (source) and has been postulated to reduce the risk of cancer by a variety of mechanisms (source, source). Though the potential benefits of selenium supplementation in tumour patients are undeniable (source). By enhancing the stability of the genome inhibiting carcinogen-induced covalent DNA adduct formation, selenium may also reduce the risk of cancer, retard oxidative damage to DNA, lipids, and proteins, retarding angiogenesis, and modulating cellular events critical in cell growth inhibition. Laboratory studies, that have demonstrated oxidative stress induced by sodium selenite at high concentrations in both acute and chronic treatments of prostate cancer cells, have proposed different mechanisms were involved (source). After acute exposure to selenite, cells presented mitochondrial injury and cell death, mainly by apoptosis. While chronic exposure of selenium exerted its effects on human prostate cancer cells by altering the intracellular redox state, subsequently blocking the cell cycle.

Food sources:

The selenium content of foods is largely dependant on soil levels. It can generally be found in brewers yeast, kelp, seaweed, brazil nuts, seafood (e.g. tuna, herring), garlic, milk, eggs, and kidneys.

Dose:

The RDA for selenium is 55 μg for healthy adult males and 55 to 75 μg for healthy females. The RDA for children starts at 15 μg and increases to 40 μg by the age of 9 years. The therapeutic dose range is 200 to 800 μg/day and does not lead to toxicity (source). Selenium has a narrow safety margin, with clinical toxicity reported on daily doses of 1000 to 2000 μg over a month. The dose for long-term use is believed to range between 100 to 400 μg. Extrapolation from animal experiments suggests that 400 to 700 μg/day may be needed for cancer protection. Since 400 μg daily is probably the upper limit of safety, daily doses of 100 to 200 μg may be more realistic and safe objectives for inhibiting genetic damage and carcinogenesis in humans(source, source). Such recommendations are contrary to the traditional nutritional essentiality paradigm; however, as such advice is consistent with a better health outcome, perhaps it is time that the paradigm is reviewed (source, source).   

One of the safest selenium supplements is selenium organically bound to yeast. Yeast-based selenium is approximately 40% selenomethionine, 20% other amino acid conjugates (e.g., selenocysteine, methylselenocysteine), and 40% unidentified selenopeptides (source). Doses of 500 to 1000 μg have been observed to be well tolerated. Another safe form of organic selenium is selenomethionine at doses of 200mcg (source). Selenomethionine appears more effective at increasing selenium status; while selenite and selenate are more bioavailable than selenomethionine. In one animal study, co-administration of vitamin C suppressed the chemopreventive effect of inorganic selenium (selenite), but not those of selenomethionine.

Animal studies have established that the dose and form of selenium compounds are critical factors in regard to circumscribing cellular responses, inorganic selenium at doses up to 10 μmol, and organic selenium compounds at doses equal to or greater than 10 μmol achieve distinctly different cellular responses (source). Animal studies using multiple different tumorigenesis models have mainly found that selenium has notable chemopreventive activity.

Clinical Uses:

Biochemical changes produced by selenium deficiency predisposes people who experience additional stresses to develop certain illnesses (source). Insufficient selenium intake has been estimated to affect up to 1 billion people worldwide (source). Selenium has cancer-protective effects (source, source, source, source). In a placebo-controlled human trial, supplementation of 200 μg selenium from 0.5 g brewer’s yeast has been determined to decrease the incidence of several types of cancers (source). This prospective study found that a daily supplement of 200 μg selenium over an average of 4.5 years revealed no protective effects against the primary endpoint of squamous and basal cell carcinomas of the skin. However, the selenium-treated group did have substantial reductions in the incidence of prostate cancer and total cancer incidence and mortality(source). This dose is three or four times the RDA. Nevertheless, such findings are supported by epidemiologic studies, which have shown that low selenium status is associated with an increased total cancer incidence, particularly of gastrointestinal, prostate, and lung cancers (source). Surely, epidemiologic, laboratory and serendipitous results of two randomized clinical trials suggest that men with high selenium and vitamin E intake have a lower risk of prostate cancer (source). In addition, a case-control study has also found that low plasma selenium is associated with a four-to-five-fold increased risk of prostate cancer (source).
It should be noted that the reduced levels of prostate-specific antigen (PSA), a commonly used marker for prostate cancer, observed with selenium supplementation are expected due to the effect of selenium on cancer cells and not because of selenium interfering with the production of PSA for any reason other than a decrease in cancer cells. A useful indicator in the disease progression in individuals is the change in serum PSA levels during selenium supplementation (source).

Due to the fact that plasma selenium decreases with age, supplementation may be beneficial to older men. It appears that low selenium serum levels have a correlation with cancer of the head, neck (source) and lung (source). Low selenium serum levels have also been associated with increased risk of thyroid cancer and may play a role in carcinogenesis (source). In addition, serum concentrations of selenium are significantly decreased in patients with malignant tumours (source).

While the protective effect of selenium against cancer and the low serum level of selenium is fairly well documented, there is less clinical evidence to support the anti-inflammatory effect of selenium in arthritis. A clinical trial failed to demonstrate that selenium treatment (200 μg/day) produced any clinical benefit in the case of rheumatoid arthritis. However, when examining the quality of life, there was a significant improvement in arm movements and health feeling in selenium-treated patients (source).

The Human Immunosuppression Virus (HIV) depletes the body stores of selenium, which, in turn, cause the immune system failures manifested as Acquired Immunodeficiency Disease Syndrome (AIDS). Selenium supplementation has been shown to forestall the progression of HIV infection to developing AIDS, to reduce the symptoms of AIDS and to improve the lifespan of AIDS patients. (source, source, source)

Selenium can up-regulate genes related to phase II detoxification enzymes, certain selenium-binding proteins and select apoptotic genes, while down-regulating those related to phase I activating enzymes and cell proliferation. Independent of tissue type, selenium arrests cells in G1 phase of cell cycle, inhibits CYCLIN A, CYCLIN D1, CDC25A, CDK4, PCNA and E2F gene expressions while influencing the expressions of P19, P21, P53, GST, SOD, NQO1, GADD153 and certain CASPASES. In addition to those described above, genes such as OPN (involved in metastasis) has been reported to be down-regulated by selenium (source)

Animal studies suggest other areas for investigation. It is possible that selenium deficiency and vitamin E deficiency can activate latent viruses such as herpes (source). Animal studies have also shown that mice on either selenium or vitamin E deficient diets developed myocarditis when exposed to coxsackievirus infection; those with adequate selenium or vitamin E status did not (source). Viral-induced neuropathy was found to abate once selenium, vitamin E, carotenoid, and riboflavin blood levels were increased. It appears that a normally avirulent viral genome may become pathogenic in a nutritionally deprived host. An experimental animal study has also found that growth retardation induced by selenium deficiency is associated with impaired bone metabolism and a reduction in bone mineral density (source).

It appears that selenium is critical for healthy sperm and may improve fertility and the chance of a successful conception for both men and women. Supplementation in the case of selenium deficiencies in the procreation period of both women and men is of utmost significance to prevent gestational complications, miscarriages and the damaging of the nervous and immune systems of the fetus as well as to promote fertility (source). 56% of subfertile men with low selenium status showed a positive response to selenium supplementation, improving sperm motility and the chance of successful conception. This study highlights the inadequate provision of this essential element in the Scottish diet (source).

Hair Test Notes:

There are moderate correlations between selenium levels in whole blood, serum, toenails and hair and correlate with dietary intake assessed through dietary records and food frequency questionnaires (source, source, source, source). Thus hair mineral analysis (HMA) may be a useful tool in monitoring selenium treatment (source) or occupational exposure (source). There is a good correlation between hair and plasma selenium levels in healthy children (source)

Selenium can protect and antagonise arsenic and has the potential to mitigate arsenic toxicity (source). As well as a mutual antagonism between mercury (source), cadmium (source), silver (source), thallium and selenium (source, source). Excess storage of iron can be produced by deficiencies of selenium, copper, zinc, and is wrongly blamed for liver cirrhosis, fibrosis of the pancreas, hypertrophic cardiomyopathy and diabetes. These diseases are not the direct result of iron excess, but rather a deficit or biounavailability of the elements listed above.

High Hair Selenium

High hair selenium can be due to the use of shampoos containing selenium may indicate a loss of selenium through the hair.

Low Hair Selenium

Low hair selenium may be due to dietary deficiency, which is relatively common, especially among those who eat refined foods.

Toxicity or Drug interactions:

Selenium toxicity is increased in animals with low or depleted stores of vitamin E. Chronic ingestion of more than 0.6 mg/day can cause toxicity.

Possible Symptoms of Selenium Toxicity

  • Garlic breath

  • Paresthesia

  • Rough Hair

  • Hair loss

  • Nausea

  • Gastric disturbances

  • Brittle fingernails

  • Dermatitis

  • Hepatorenal damage

  • A metallic taste

  • Nervous irritability

  • Depression

  • Unusual fatigue

  • Vomiting

  • Lameness

  • Pain

  • Sloughing of skin

  • Erosion of joints

  • Liver cirrhosis

  • Cardiac Atrophy

  • Lowered conception rates

  • Anemia

  • Birth defects

  • Muscle spasms

Clinical Caution:

  • Less than 11mcg selenium daily is considered to unquestionably put people at risk of selenium deficiency and genetic damage (source). An increased risk of cancer is suspected to be associated with selenium deficiency. Clinically, conclusions consistent with selenium deficiency include fingernail and skin changes, cardiomyopathy (source), and skeletal muscle fatigue, tenderness, and weakness.

  • Patients on monoamine inhibitors should avoid yeast-containing selenium products.

  • Although an adequate vitamin C status is necessary for normal selenium metabolism, megadoses of vitamin C may decrease absorption of selenium taken as sodium selenite (source).

  • Selenium deficiency could exacerbate iodine deficiency (source).

  • Smoking tends to lower selenium biomarker concentrations, even though smoking is a source of selenium exposure - a phenomenon that might be related to increased excretion of the metalloid due to interaction with cadmium or other heavy metals (source, source)

Selenium Deficiency Diseases:

  • HIV (AIDS) Anemia (RBC fragility)

  • Age Spots & Liver Spots–ceroid lipofucin

  • Fatigue Muscular weakness

  • Myalgia (Fibromyalgia, muscle pain and soreness)

  • Rhabdomyalisis (breakdown of skeletal muscle cell walls following exercise)

  • Scoliosis

  • Muscular Dystrophy (MD, White Muscle Disease, Stiff Lamb Disease)

  • Cystic Fibrosis Cardiomyopathy (Keshan Disease, “Mulberry heart” disease)

  • Multiple sclerosis (MS) Blindness – cataracts, macular degeneration Heart palpitations Irregular heart beat

  • Liver cirrhosis

  • Pancreatitis

  • Pancreatic atrophy

  • Lou Gehrig’s disease (ALS)

  • Parkinson’s Disease

  • Alzheimer’s Disease

  • Adrenoleukodystrophy (ALD – “Lorenzo’s Oil” Syndrome)

  • Infertility

  • Low birth weight

  • High infant mortality

  • Miscarriages

  • Sudden Infant Death Syndrome (SIDS)

  • Cancer

  • Clinical AIDS (HIV infection)

  • Pathogenic viruses

  • Sickle-cell anemia; thalassemia

  • Wilson’s Syndrome (hypothyroidism)

  • Hyperthyroidism

Practice Tips:

  • Animal studies have shown selenium causes birth defects when given in large doses.

  • Close monitoring of patients on selenium supplementation is necessary.

  • Vitamin E 500 IU enhances the efficacy of selenium.

  • Selenium and vitamin E have closely related mechanisms of action, and deficiency in one often overlaps with a deficiency in the other.

  • Muscular pain associated with selenium deficiency may be corrected with 200 μg daily.

  • Selenium modulates T lymphocyte-mediated immune responses and stimulates peripheral lymphocytes to respond to antigens.

  • Selenium 200 μg daily combined with beta-carotene 15 mg and vitamin E 500 IU may reduce the risk of cancer.

  • Selenium does not protect against skin cancer, whether it be basal or squamous cell cancer.

  • Those with low levels of selenium before selenium supplementation had a significantly lower incidence of lung cancer due to selenium supplementation (source, source)

References:

https://lpi.oregonstate.edu/mic/minerals/selenium

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5432259/

https://www.ncbi.nlm.nih.gov/pubmed/18444146

https://ker.com/equinews/selenium-deficiency-or-toxicity-horses/

http://seleniumfacts.com/dr-schrauzer-selenium-researcher/

https://www.sciencedirect.com/science/article/pii/S0006306100801647?via%3Dihub

https://www.ncbi.nlm.nih.gov/pubmed/19514891

https://www.ncbi.nlm.nih.gov/pubmed/14713754

https://ods.od.nih.gov/factsheets/Selenium-HealthProfessional/#en6

https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD005195.pub4/epdf/standard

http://www.selcote.com.au/selenium-deficient-areas/

https://www.lifeextension.com/magazine/2012/ss/selenium-protect-against-cancer/page-01

http://seleniumresearch.com/

https://www.ncbi.nlm.nih.gov/pubmed/1702669

https://www.ncbi.nlm.nih.gov/pubmed/3552651

https://link.springer.com/article/10.1007/BF01989914

https://www.ncbi.nlm.nih.gov/pubmed/10894365













Chromium (Cr)

JB_MineralHealth_Chromium.jpg

Mineral Health Connection

Chromium is an essential trace mineral. In its trivalent state, it is critical for carbohydrate, lipid and nucleic acid metabolism. Chromium enhances the effects of insulin. Chromium activates phosphoglucosonetase and other enzymes.

Mechanism of action:

Chromium plays an important role in carbohydrate, fat and protein metabolism and has an impact on the expression of genes and nucleic acid synthesis.  
Insulin binding to cells seems to be increased by the presence of chromium as well as the number of insulin receptors. It activates insulin receptor kinase which increases insulin sensitivity (source). Trivalent chromium is an essential component of glucose tolerance factor. Glucose tolerance factor is believed to aid glucose transport across the cell surface as well as mediate the effects of insulin. Glucose tolerance factor also consists of two nicotinic acid molecules and a small oligopeptide, chromodulin. Chromodulin is believed to play a role in the auto-amplification of insulin signalling (source).

Food sources:

Chromium is found in various foods in quantities that correlate to the presence in the soil. It can be found in brewers yeast, cheese, molasses, wheat germ and whole grains, sugar beets, eggs, meat and seafood. Some recommend barley as a good source for chromium. Absorption of chromium is about 10%.

Dose:

A safe and adequate daily intake of chromium is between 50-200mcg. However, the therapeutic dose ranges from 200-2000mcg/day.

Clinical Uses:

Dietary sugar loads increase the natural rate of urinary chromium loss by 300% for 12 hours (source). Those with glucose intolerance such as type-1, type-2, gestational, and steroid-induced diabetes have all shown improved glucose metabolism with supplemental chromium (source). Chromium picolinate at 1,000mcg/day has had notable beneficial effects on hemoglobin A1C, glucose, insulin and cholesterol levels in those with type-2 diabetes in a clinical trial (source). It should be noted that the beneficial effects of chromium appear to only be relevant at levels which are five-fold higher than the upper limit which is supposed to be the estimated safe and adequate daily intake without any documented side-effects.

The overall requirement of chromium is relative to the degree of glucose intolerance, and while a higher intake is more effective, 200mcg of supplemental chromium is adequate to improve mild glucose intolerance in individuals. Daily intake of 8mcg/kg body weight of chromium is more effective than 4mcg/kg in women with gestational diabetes (source) and steroid-induced diabetes can be reversed with doses of 600mcg/day (source). Corticosteroids deplete chromium. A double-blind, crossover trial has confirmed that chromium supplementation improves glucose and lipid levels while decreasing medication dosage in type 2-diabetes. The results found that brewers yeast (consisting of 23.3mcg/day) was more marginally more effective than chromium chloride (200mcg/day) (source).  Preliminary observations suggest that those with a dysthymic disorder may experience symptomatic improvement within three days of treatment with chromium supplementation once or twice daily and it may enhance antidepressant therapy (source). Chromium supplementation may also be helpful for refractory mood disorders with mild side-effects (enhanced dreaming and mild psychomotor activation). The antidepressant effects of chromium have been accounted for due to the enhancement of insulin utilization and the related increases in tryptophan availability in the central nervous system, and/or by the effect of chromiums norepinephrine release (source).

Caloric restriction in athletes seeking to maintain low bodyweight compromises chromium status. Chromium has been praised as a trace element that maintains lean body mass and decreasing body fat (source), though it appears that supplementation does not promote muscle growth, strength or fat-loss in young men and women (source). Sweating from acute yet intense activity induces a short-term loss of chromium in both urine and sweat which may affect recovery days after exercise.

Significant decreases of chromium concentrations of hair, sweat and blood have been reported in age-related diseases (source).

Hair Test Notes:

Chromium concentrations in human hair is ten times greater than that found in blood. For this reason, hair tissue mineral analysis is a much more accurate representation of chromium stores in the human (there is an average of 1.5 mg in the human body under optimal conditions).

Toxicity/ Drug interactions:

At present, there is little information regarding the long-term toxicity of chromium supplements.

Not much chromium is stored in the human body; once chromium is absorbed, it is almost entirely excreted in the urine (and for this reason, urine chromium levels can be used to approximate dietary chromium status). The estimated safe and adequate daily allowance level appears to be safe and non-harmful (source). Trivalent chromium appears to have a broad safety range and no toxic effects have been reported at doses upwards of 1mg/day (source). Chromium intake excess of 100mg/day may lead to retardation of growth, cardiomyopathy, and perhaps hepatic and renal damage.

Iron and chromium compete for binding on transferrin and supplemental chromium picolinate decreases transferrin (but not chromium chloride). Chromium nicotinate or chromium picolinate has a high bioavailability. Oral hypoglycemic agents may be enhanced by chromium while reducing insulin requirements. Those that are consuming hypoglycemic agents may need to modify their dosage (source)

Vitamin C and the B vitamin niacin increase chromium absorption.  

Antacids, corticosteroids, H2 blockers (such as cimetidine, famotidine, nizatidine, and rantidine), Proton-pump inhibitors (such as omeprazole, lansoprazole, rabeprazole, pantoprazole, and esomeprazole) may inhibit chromium absorption due to alterations in stomach acidity. Whereas Beta-blockers (such as atenolol or propanolol), corticosteroids, insulin, nicotinic acid, nonsteroidal anti-inflammatory drugs (NSAIDS), or prostaglandin inhibitors (such as ibuprofen, indomethacin, naproxen, piroxicam, and aspirin) may have their effects enhanced when taken in conjunction with chromium, or increase chromium absorption (source, source, source, source)

Clinical Caution:

Assessment of dietary chromium is often problematic and suboptimal due to the absence of a reliable indicator for chromium status. Suboptimal intake of chromium is associated with risk factors for diabetes and cardiovascular diseases such as impaired glucose tolerance and metabolism, elevated circulating insulin levels, glucosuria and hyperlipidemia. The lowest normal intake of chromium has deleterious effects on glucose tolerance, insulin and glucagon levels in those with mildly impaired glucose tolerance (source). 200 mcg of chromium increased the number of insulin receptors in people with hyperglycemia. Diabetes may intensify chromium deficiency. People with type-2 diabetes lose more chromium in their urine than those who don't have diabetes. Diets with low chromium intake may have negative effects on those with borderline diabetes (source).

Diseases and Symptoms of Chromium Deficiency:

  • Low blood sugar

  • Reactive hypoglycemia

  • Bedwetting

  • Pre-diabetes

  • Diabetes (Type 2)

  • Hyperinsulinemia

  • Hyperactivity

  • Learning disability

  • ADD/ADHD

  • Hyperirritability

  • Depression

  • Manic depression

  • “Bi-polar” disease

  • Dr Jekyll/Mr. Hyde rages (“Bad Seeds”)

  • Impaired growth

  • Peripheral neuropathy

  • Negative nitrogen balance (protein/muscle loss)

  • Elevated blood triglycerides (> 200)

  • Elevated blood cholesterol (> 270)

  • Coronary artery disease

  • Aortic cholesterol plaque

  • Infertility (anovulation and low sperm count)

  • Shortened life span

  • Elevated CRP

Practice Tips:

  • Long-term chromium supplements are generally not recommended in excessive doses because the effects are unknown.

  • People who consume a diet of refined foods and high dietary sugar over prolonged periods are at risk for a chromium deficiency.

Additional Reading:

https://www.ncbi.nlm.nih.gov/pubmed/10565402

https://www.ncbi.nlm.nih.gov/pubmed/29975702

http://www.orthomolecular.org/library/jom/2000/articles/2000-v15n03-p145.shtml

http://articles.latimes.com/1992-10-20/news/mn-637_1_chromium-picolinate

Manganese (Mn)

JB_MineralHealth_Manganese.jpg

Mineral Health Connection

Manganese is an essential trace element to all known living organisms. It is an activator of several metalloenzymes, including arginase, pyruvate carboxylase, glutamine synthetase, and one form of superoxide dismutase (SOD). Manganese also functions as a non-specific enzyme activator and facilitates the synthesis of mucopolysaccharides (such as chondroitin sulfate), lipids and thyroxine. It helps prevent tissue damage caused by lipid oxidation and is an antioxidative transition metal. Manganese is part of the developmental process and the structure of the fragile ear bones.

Deficiency of this element has been induced in several animal species by feeding diets low in manganese. Signs of deficiency in animals include impaired growth, skeletal defects, depressed reproductive functions, ataxia in newborns, and defects in metabolism.

Mechanism of Action:

Manganese is an essential nutrient involved in the formation of bone and in amino acid, cholesterol, and carbohydrate metabolism. It is an enzyme activator and is a component of many metalloenzymes and may play a prominent role in calcium mobilisation. Manganese is part of the enzyme manganese superoxide dismutase and reduces the exposure to free radicals. It generates oxaloacetate, a substrate in the tricarboxylic acid (Krebs) cycle, as a constituent of pyruvate carboxylase and may play a role in glucose homeostasis. Manganese also activates enzymes that are involved in the synthesis of cartilage, facilitate the formation of urea, and activates various kinases, decarboxylases, hydroxylases and transferases.

Food sources:

Sources of manganese include; nuts, seeds and vegetables. It’s found in hazelnut, blackberries, pineapple, lentils, beans and whole grains. Due to milling, manganese content is much lower in milled whole grains. Absorption of manganese varies from 10-40%. The average body content is 0.012 g.

Dose:

Biliary secretion is the main pathway for manganese excretion (source, source). In the liver, Manganese is extracted from the blood, conjugated with bile and excreted into the intestine. A small amount of manganese in the intestine is reabsorbed, establishing an enterohepatic circulation (source) which is critical for maintaining manganese levels. The recommended intake ranges from 2.5-3mg (source). The therapeutic dose range is between 2-50mg/day.

Clinical Uses:

The control of blood sugar in diabetes and a reduction of inflammation in arthritis has been speculated of manganese.

As a component of superoxide dismutase, manganese may be useful to define therapeutic strategies for the clinical management of glioblastomas. High levels of manganese superoxide dismutase is found in patients with glioblastomas have a median survival time lower (6.11months) whereas those with low levels of this enzyme have a median survival time of 12.17 months (source). Two distinct groups of glioblastomas can be distinguished based on the content of manganese superoxide dismutase.

Toxicity/ Drug Interactions:

Oral consumption of manganese is generally non-toxic. Excessive levels of manganese found in certain community water supplies and in some industrial processes can produce a Parkinsonian syndrome or a psychiatric disorder (“locura manganica”) that resembles schizophrenia.

The clinical syndrome associated with excessive manganese and its neurodegenerative effects of manganese toxicity is known as 'Manganism' (source). However, mild inhalation of manganese could impair memory and coordination, weakness, anorexia, fatigue, depression, apathy and disturbed sleep have all been reported, irritability, hallucinations, and poor coordination have all been reported in those with manganism. Manganese in excess amounts can irreversibly damage the nervous system (source). Several clinical neurological disorders of manganism have been described as extrapyramidal motor system dysfunction and in particular idiopathic Parkinson’s disease and dystonia (source). Tremors are a critical sign of excess manganese. Despite having similar effects as the symptoms described in Parkinson's disease, the dopamine transporter activity (source).

Manganese deposits have been found in patients with biliary atresia. Possibly caused by an increase in portsystemic shunt, and latent or subclinical encephalopathy (source).

Clinical Caution:

The signs and effect of human deficiency of manganese have not been clearly established, but some potential cases in adults have shown failure in normal hair pigmentation, dermatitis, and hypocholesterolemia (source). Deficiency may cause growth impairment, tendon and bone disorders in animals but not necessarily in humans. Multiple sclerosis and Amyotrophic lateral sclerosis may have dysfunctional manganese metabolism.

Mineral Relationships

Manganese, iron, vitamin C and/or molybdenum deficiency can lead to an accumulation of copper.

Synergistic Nutrients

  • Zinc, choline, vitamin K

Antagonistic Nutrients

Absorption

  • Calcium, phosphorus, iron, soy protein.

Metabolic

  • Copper, magnesium, iron, vanadium

Practice Tips:

  • The only known reliable indicator of manganese at this time is hair tissue mineral analysis.

  • Deficiency diseases of manganese ranges from severe congenital birth defects (such as congenital ataxia, deafness, chondrodystrophy, Ehlers-danlos Syndrome etc.), allergies, asthma, convulsions, retarded growth, skeletal defects, disruption of fat and carbohydrate metabolism to joint problems (tendon and ligament degeneration, TMJ, repetitive motion syndrome, carpal tunnel syndrome, etc.), hypoglycemia, diabetes myasthenia gravis, dizziness, ringing in the ears, fatigue, muscular weakness, bone fractures or osteoporosis, weak ligaments and tendons.

Additional Reading:

https://www.crnusa.org/sites/default/files/files/resources/29-CRNVMS3-MANGANESE.pdf

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6309959/

https://www.ncbi.nlm.nih.gov/pubmed/25057538

http://www.arltma.com/Mineral_Information/Manganese.html

https://raypeatforum.com/community/threads/manganese-and-its-unimportance-in-health.22375/

http://www.traceelements.com/Docs/The%20Nutritional%20Relationships%20of%20Manganese.pdf

https://www.ncbi.nlm.nih.gov/pubmed/12711814

Iodine (I)

JB_MineralHealth_Iodine.jpg

Mineral Health Connection

Iodine is essential for red and brown algae as well as all invertebrates. The heaviest known essential trace element for humans is iodine (source). Iodine is a member of the halogen family on the periodic table of elements.

A dietary deficiency of iodine is the single most significant cause of preventable brain damage and mental retardation.

A lack of iodine is one of the most common nutritional deficiencies in the world (source).

Mechanism of action

Iodine in combination with the amino acid tyrosine link together to manufacture thyroid hormones. Thyroxine (T4) is much more abundant. However, it is not as biologically active as triiodothyronine (T3). Thyroid hormone speeds up metabolism and increases basal metabolic rate, in addition to controlling the rate of oxygen utilisation and releasing energy from energy-producing nutrients.

When there is inadequate dietary intake, plasma levels of thyroid hormones are reduced and more thyroid stimulating hormones (TSH) is released from the pituitary gland (source). If an iodine deficiency is chronic, the thyroid gland enlarges as an attempt to soak up more iodine to increase thyroid hormones. The glandular response, the stage of disease, and the concentration of thyroid hormones increasing or decreasing is dependant on the amount of iodine present. According to epidemiological studies, the primary consequence of mild to moderate iodine deficiency is hyperthyroidism, which is intricate with symptoms such as cardiac arrhythmia, osteoporosis, and muscle wasting in the elderly (source).

Iodine is a protective antioxidant that can be oxidised to hypoiodite, a potent oxidant involved in the host defence against microorganisms (source).

Food sources

The availability of iodine in foods is different depending on various regions of the world and their soil levels. Good sources for iodine include saltwater fish, seaweed, dairy products, and eggs.

Iodine can be lost during cooking, possibly as much as 70% (source). Thus, iodised salt should be added after cooking and not before or during.

Dose

Absorption of iodine is 100%. The current Recommended Daily Allowance for iodine is 110-150 mcg in adults. The levels are high for those pregnant (220 mcg) and lactating (290 mcg) respectfully (source). Supplementary dosages range between 1,000-10,000 mcg. Prolonged intake of 1,000 mcg may result in toxicosis.

Certain areas of Poland have been classified as being mild to moderately deficient in iodine. Iodine prophylaxis (a preventive protection measure aimed to avoid the health damage of individuals resulting from an accumulation of radioactive iodine in the thyroid in case of nuclear or radiation accident (source)) based only on iodised household table salt that contains 30 mg of potassium iodide per kg of salt has been highly effective (source). If iodised salt is left exposed to the air, that it will slowly lose its iodine content (source).

Many try and mimic the Japanese intake of iodine and depending on their source of information; it could be dangerous. The amount of iodine the Japanese consume daily from seaweeds has previously been estimated as high as 13.5 to 45 mg/day (source, source). Dr Lawrence Wilson suggests that the current RDA is too low and that the ideal dosage of iodine today is much higher, somewhere between 5 and 15 mg daily (source). However, a literature-based analysis estimates that the Japanese iodine intake-- mostly from seaweeds--averages 1,000-3,000 mcg per day or 1-3 mg/day (source). Thus it appears that a daily intake of 2,000 mcg (2 mg) is a safe dosage and non-toxic.

Clinical Uses:

Urinary Iodine test has revived due to the interest and growing realisation of a widespread iodine deficiency (source).

TSH should not be above 3.5, while many physicians use 5 as the upper limit of "normal" (source).

Athletes may require additional iodine as it can be excreted through sweat. Dietary iodine stores could be depleted in an athlete undergoing a regular training regime (source). In one hour of playing soccer, athletes may excrete 52 mcg, and profuse sweating may cause an iodine deficiency. This may suggest that those who have a high workload (such as an athlete), or those which are heat stressed have an increased requirement of iodine (source).

Iodine significantly increased both basal and post-stimulation TSH (source)

Our modern environment is very high in iodine antagonists such as flourine, bromine and chlorine. We quite literally bathe and swim in it! Halogens compete with one another because they look similar at the atomic level and can replace each other (source, source).

Hair Tissue Mineral Analysis Notes:

Hair appears to be a valuable biological indicator tissue for assessing long-term iodine status.

Adequate iodine status corresponds with hair iodine uptake saturation (source).

Thyroid iodine uptake is antagonised by Lead and can inactivate thyroxin (source). Flouride can inhibit thyroid hormone utilisation and interfere with iodine metabolism (source).

Mercury and copper toxicity stimulate hormone synthesis. Thyroxine (T4) requires manganese, iodine, tyrosine, cyclic AMP, vitamin C, B-complex and other micronutrients.

Low hair potassium is associated with reduced sensitivity of the mitochondrial receptors to thyroid hormone (source).

Toxicity / Drug interactions:

Excessive intake of iodine will inhibit the synthesis of thyroid hormone which can result in goitre.

In infants, an enlarged thyroid gland may obstruct their airway. It has been shown that high intakes of iodine may contribute to autoimmune hypothyroidism and that Graves’ disease can manifest at a younger age (source). Foods from the Brassica family, such as broccoli, cabbage, and turnips impair utilisation of iodine and increase dietary intake requirements.

Excessive consumption of brominated vegetable oils will deplete iodine levels. It is commonly found in citrus flavoured soda (source).

Clinical Caution

Nodules are frequently associated with Graves disease in iodine-deficient areas, and the incidence of carcinoma is high in palpable cold nodules. Iodine should be limited for clients that have graves disease. However, they generally need nutrient.

Excessive iodine intake has been linked to both hypothyroid and hyperthyroid (source, source).

It has been noted in literature that an excess of iodine can react with H202 to form free radicals that cause irreversible thyroid tissue damage (source).

Practice Tips

  • Urinary iodine reflects intake while plasma-bound iodine or thyroxine reflects function.

  • Deficiency in dietary iodine can cause low thyroid hormone production, and excess can depress thyroid function as well as cause an overactive thyroid.

Additional Reading:

https://ods.od.nih.gov/factsheets/iodine-healthprofessional/#en1

ARL : Understanding Thyroid Activity - arltma.com.

https://drlwilson.com/Articles/IODINE.htm

Lithium (Li)

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Mineral Health Connection

Lithium gets its name from the Greek word for stone, lithos because it is present in trace amounts in virtually all rocks [4]. In the human body, lithium is a trace mineral and only needed in minute quantities. Initially discovered in 1800, by the Brazilian chemist José Bonifácio de Andrada e Silva in a mine on an island in Sweden.

Major depression is far more disabling than many other diseases, including lung disease, arthritis and diabetes.. Depression is a world-wide phenomenon, happening at young and younger ages.
— Dr. Myra Weissman, psychiatric epidemiologist at Columbia University Presbyterian Medical Center in New York [3]

More than 10 million people in this country suffer from clinical depression in a given year, and two-thirds of them go undiagnosed or untreated, says Dr. Frederick Goodwin, director of the National Institute of Mental Health.

Gerhard Schrauzer, in a study relating violent crime and the drug use rate of Texas counties lithium levels in the counties drinking water:

Using date for 27 countries from 1978 to 1987, it is shown that the incidence rates of suicide, homicide, and rape are significantly higher in counties who drinking water supplies contain little or no lithium than in other counties with water levels ranging from 7-=17 ug/L;
the differences remain statistically significant (p<0.01) after corrections for population density. The corresponding associations with the incidence rates of robbery, burglary, and theft were statistically significant with p<0.05. these results suggest that lithium has moderating effects on suicidal and violent criminal behavior at levels that may be encountered in municipal water supplies. Comparisons of drinking water lithium levels in the respective Texas counties, with the incidence of arrests for possession of opium, cocaine, and their derivatives (morphine, heroin, and codeine) from 1981 to 1986 also produced statistically significant inverse associations.. [1]
— Lithium in Drinking Water and the Incidences of Crimes, Suicides, and Arrests Related to Drug Addictions [1]

Sources Of Lithium

  • Small amounts are found in a wide variety of foods

  • Lubricating grease

  • Batteries

  • Ceramics and glass

  • Used in medication to treat bipolar disorder

Dietary Sources Of Lithium

Neurotonics, functional foods that have been defined as having a nourishing and tonifying effect on the brain and nervous system, are excellent sources of Lithium such as:

  • Cacao, oats, seafood, seaweed, goji berries, various fruits and vegetables (depending on the soil in which they’re grown), and

  • egg yolks are significant sources of lithium, along with other trace minerals such as iron, copper, and manganese, which are known to co-migrate along with lithium from the soil to the plant. [2]

Functions Of Lithium

  • Decreases manic symptoms in manic-depressive patients

  • May modulate the conversion of essential fatty acids into prostaglandins

  • Anti-aggressive action

  • Correlated with the amino acid histidine

  • Stabilizes the neurotransmitter serotonin, activates glucocorticosteroid receptors and affects the production of CAMP.

Roles In The Body

  • Research by Frazier found that those patients who were helped by lithium experienced increased uptake of sodium through their cell membranes.

  • According to Sheard, lithium can replace sodium in the cells, and its structure resembles calcium and magnesium. It appears to have the same stabilising effect on nerve cells as calcium and magnesium.

Symptoms Associated With A Lithium Deficiencies

Deficiency is associated with excessive aggressiveness, manic states, depression alcohol cravings, impotence and increased suppressor cell activity.

  • Mass Murder - Austin, TX, Waco TX, Oklahoma, Columbine, Fort Hood, Virginia Tech, Batman Theater, Sandy Hook, Boston Marathon, Washington Navy Yard)

  • Serial Killers - Jack the Ripper, Boston Strangler, Jeffrey Dahmer, Green River Murderer, Michigan Old Man Stabber, etc.

  • Cannibalism

  • Domestic Violence

  • Violent Crime - Arson, Murder, Rape, Assault, Armed Robbery, etc

  • Suicide - and Suicide Bombers.

  • Signs of possible deficiency include behavioural problems,

Symptoms Associated With A Lithium Toxicity

Signs of possible deficiency include behavioural issues, depression, alcohol cravings, manic depression, impotence and increased suppressor cell activity. Disturbed mineral transport and fluid balance, nausea, vomiting, tremors, thirst, excessive urination, thyroid swelling, weight gain, drowsiness, confusion, disorientation, delirium, skin eruptions, possible kidney damage, and even seizures, coma and death.

Fluorine also has the capacity to bind to lithium in the brain. [3]

 

Hair Analysis Notes

  • Lithium appears to lower sodium levels. This would correlate with the research by A. Frazier.

  • The meaning of hair lithium levels is a topic of research.

Indications For Supplementation

Aggressive behaviour, manic-depression and some cases of depression.

 

[1] Lithium in Drinking Water and the Incidences of Crimes, Suicides, and Arrests Related to Drug Addictions GERHARD N. SCHRAUZER AND KRISHNA P. SHRESTHA

[2] Lithium as a Nutrient Timothy M. Marshall, PhD.

[3] Walters, Charles. Minerals for the Genetic Code: An Exposition & Analysis of the Dr Olree Standard Genetic Periodic Chart & the Physical, Chemical & Biological Connection (p. 10). Acres U.S.A.. Kindle Edition. 

[4] Lithium: occurrence, dietary intakes, nutritional essentiality. Schrauzer GN

 

Aluminium

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Mineral Health Connection

While many have assumed Aluminum (Al) to be a toxic element and have even correlated the metal with Alzheimer's. There remains still a biological function for the element, such as its role in activating the enzyme, succinic dehydrogenase. Which increases the survival rate of newborns.  Leaving the element in a unique position as an essential trace nutrient. 

In animal studies, Aluminum blocks the action potential (electrical discharge) of neurons, reducing nervous system activity. It also blocks essential enzyme expression in the brain such as Na-K-ATPase and hexokinase. Aluminium may also inhibit uptake of important neurotransmitters such as dopamine, norepinephrine, and 5-hydroxytryptamine  (5-HTP) by nerve cells.

Aluminium is known to compete for absorption with Calcium. Thus increased amounts of dietary Aluminum intake can decrease skeletal mineralisation, leading to osteopenia. 

Bauxite

A particularly rich Aluminum clay, named Bauxite was found in Las Baux, France in the early 1700's.

Aluminium itself does not express itself as a free metal in Nature and is only found in combination with oxygen which forms a hard oxide called alumina. When contaminated with other elements alumina differentiates into gems such as rubies and sapphires which have been used for thousands of years in the art of Ayurvedic Medicine. 

Hans Christian Oerstad in 1825, first isolated the metal Aluminum by treating alumina-containing clay with carbon and chlorine amalgams of potassium, resulting in a volatile mixture of Mercury and Aluminum, once the mercury was separated as a vapor by boiling, what remained was a powdery metal that resembling the metal Tin in both colour and luster. Aluminium! A versatile, semiprecious metal!

Aluminium Toxicity?

According to professor Gerhard Schrauzer, Aluminum should be listed as an essential mineral for all vertebrates including humans. 

The Lethal Dose, of Aluminum Sulfate, also called the LD50 is 6207/mg/kg orally for a mouse. To consume this much aluminium, would be the equivalent of 500 grams (more than an lb of coffee) for an 80 kg human per day!

While Aluminum intake does indicate sensitivity to some individuals, resulting in contact dermatitis and digestive disturbances, however toxicology research has concluded that Aluminum is not as toxic as other elements such as mercury, cadmium, or arsenic. 

While I was growing up, there was a rumour correlating Aluminum to Alzheimer's disease, to date I have not come across any literature that suggests exposure could cause any disease, let alone a disease such as Alzheimer's..  [1] Furthermore, on the Alzheimer's Society of Canada website, they state: Studies have not provided strong evidence of aluminum being a risk factor for the development of dementia. [2] 

Sources Of Aluminum Toxicity

  • Aluminium cans (soda pop and beer)

  • Food cooked in aluminium cookware

  • Aluminium-containing antacids

  • Antiperspirants.

  • Water (Aluminum is frequently added to municipal water)

  • Fluoridated water increases leaching of aluminium from aluminium pots and pans.

  • Baking Soda, and Baking powders

  • As a drying agent in salt and other products.

  • Processed cheese

  • Bleached flour

Today children are often born with elevated aluminium, that is passed from mother to fetus through the placenta

Detection Of Aluminum

Blood Tests. There is debate whether blood testing for aluminum has much value. Blood levels do not indicate total body load of aluminium.

Hair Tissue Mineral Analysis. Aluminium levels appear to correlate well with bone levels of Aluminum. Several hair tests may be required before aluminium is revealed, however, most often it is prevalent. Low Aluminum on an HTMA, may indicate that the element is tightly bound within body tissues, and may take several months on a nutritional balancing program to mobilise.

Possible Conditions Associated With Aluminum Toxicity

Early symptoms of aluminium toxicity include flatulence, headaches, colic, dryness of skin and mucous membranes, a tendency for colds, burning pain in head relieved by food, heartburn and an aversion to meat.

Later symptoms include paralytic muscular conditions, loss of memory and mental confusion.

 

[1] Absence of aluminium in neuritic plaque cores in Alzheimer's disease J. P. Landsberg, B. McDonald & F. Watt Nature 360, 65–68 (05 November 1992)

[2] http://www.alzheimer.ca/en/Home/About-dementia/Alzheimer-s-disease/Risk-factors/Aluminum

 

Silver

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Mineral Health Connection

Silver has been entangled with healthcare and the search for immortality among alchemists for over 8,000years. While many feel that Silver (Ag) is an essential micronutrient, this is not because the element is required for any known biological function. Instead, it is believed that Silver is an indispensable tool as a systemic disinfectant, or perhaps for immune system support.  

Thanks to ongoing research, Silver is emerging as a wonder of modern medicine. An antibiotic kills perhaps only a half-dozen different pathogenic organisms, but silver kills 650. Even more surprisingly, resistant strains fail to develop! Moreover, silver is virtually non-toxic. According to a pioneering silver researcher, Dr Harry Margraf of St Louis: "Silver is the best all-around germ-fighter we have." [1] As Humans, we can safely consume 400mg of silver each day. 

In fact, I remember being told by my grandmother that Silver dollars were added to milk to prevent the liquid from spoiling and thus lasting longer without refrigeration. This is due to Silver's ability to block specific enzymes that are required for micro-organism respiration. Some of silvers functions include its uses as an anti-fungal, anti-bacterial, and anti-viral agent. 

According to Dr Robert Becker, in the book Body Electric, "Silver deficiency was responsible for the improper functioning of the immune system, and silver does more than just kill disease causing organisms. It also stimulated major growth and repair of injured tissue" Human fibroblast cells were able to grow at an accelerated rate, producing large amounts of primitive stem cells in wounds. These stem cells are able to differentiate into other cells to drastically increase wound repair.

 

[1] Extract from Science Digest - March 1978 OUR MIGHTIEST GERM FIGHTER By Jim Powell