Cobalt: Essential Core of Vitamin B12 — and Its Toxic Side
Table of Contents
- Overview
- Biological Functions
- Dietary Sources
- Deficiency
- Recommended Intake
- Supplementation & Forms
- Toxicity & Upper Limit
- Special Considerations
- Key Research Papers
- Connections
- Featured Videos
1. Overview
Cobalt is a hard, silvery-grey metal — element number 27 on the periodic table, sitting right between iron and nickel. It has a curious double life in human health. On one hand, cobalt is genuinely essential: it forms the chemical heart of vitamin B12 (cobalamin), a vitamin without which we cannot make red blood cells or maintain a healthy nervous system. On the other hand, cobalt in its loose, inorganic form is a recognized toxin that has caused outbreaks of heart failure, thyroid disease, and nerve damage. Understanding cobalt means holding both of these truths at once.
The single most important fact about cobalt nutrition is this: the only established role for cobalt in the human body is as the central metal atom of vitamin B12. There is no recognized dietary requirement for free or inorganic cobalt. Crucially, humans cannot build a B12 molecule from raw cobalt — only certain bacteria and archaea (single-celled microorganisms) possess the enzymatic machinery to wrap cobalt inside the elaborate corrin ring that makes cobalamin. For us, "cobalt nutrition" is really just another way of saying vitamin B12 nutrition. Swallowing cobalt metal or a cobalt salt does nothing useful for B12 status; it simply delivers a potentially toxic metal.
This page therefore covers cobalt from both directions. The essential side is short and points you toward our detailed Vitamin B12 page, because that is where the real human requirement lives. The toxic side is longer and more cautionary, because cobalt's dark history — from cobalt-beer cardiomyopathy in the 1960s to systemic poisoning from worn metal-on-metal hip implants today — is exactly the kind of practical, real-world danger an ordinary reader benefits from knowing about. Cobalt is a textbook example of a metal that is indispensable in microgram amounts locked inside a vitamin, and harmful in milligram amounts running free.
Cobalt versus cobalamin: keeping the terms straight
It helps to separate three things. Elemental (inorganic) cobalt is the free metal and its simple salts — cobalt chloride, cobalt sulfate, cobalt gluconate. Cobalamin (vitamin B12) is the large organic molecule in which a single cobalt atom is held in place by a corrin ring and a series of attached groups. "Cobalt" in nutrition labels and soil-science reports usually means inorganic cobalt, which is not the same as usable B12. When a soil is called "cobalt-deficient," it matters to cattle and sheep — whose gut bacteria need that cobalt to make B12 for the animal — but it tells you nothing about whether a person eating those animals is getting enough B12.
2. Biological Functions
Every biological function of cobalt in humans runs through vitamin B12. There is no known cobalt-dependent enzyme or pathway in people that operates on free cobalt the way, say, iron operates in hemoglobin or zinc operates in hundreds of metalloenzymes. Inside the cobalamin molecule, the cobalt atom is the reactive center — it is where the chemistry actually happens, swinging between oxidation states and forming and breaking a carbon-cobalt bond that few other systems in biology can manage. Strip the cobalt out and the vitamin is inert.
The two human B12-dependent enzymes
Humans use vitamin B12 — and therefore cobalt — in exactly two enzymatic reactions, but both are vital:
- Methylmalonyl-CoA mutase uses adenosylcobalamin (a form of B12) inside mitochondria. It converts methylmalonyl-CoA into succinyl-CoA, a step that lets the body extract energy from certain fatty acids and amino acids by feeding them into the Krebs (citric-acid) cycle. When this enzyme stalls for lack of B12, methylmalonic acid backs up in the blood and urine — which is why doctors measure methylmalonic acid (MMA) as a sensitive marker of B12 deficiency.
- Methionine synthase uses methylcobalamin in the cytoplasm. It transfers a methyl (CH3) group from folate (as 5-methyltetrahydrofolate) onto homocysteine, regenerating the amino acid methionine and freeing up folate for DNA synthesis. This reaction sits at the crossroads of B12 and folate metabolism, which is why a B12 deficiency raises blood homocysteine and can mimic — and mask — a folate deficiency.
What those reactions accomplish for the body
Through these two enzymes, cobalt (as B12) supports three big, easily understood outcomes:
- DNA synthesis and red blood cell formation. By keeping folate cycling, methionine synthase allows rapidly dividing cells — especially the precursors of red blood cells in bone marrow — to copy their DNA properly. Without it, red cells are produced large, fragile, and immature, the hallmark of megaloblastic anemia.
- Nervous-system and myelin health. Adequate B12 is required to build and maintain myelin, the insulating sheath around nerves. Prolonged deficiency damages the spinal cord and peripheral nerves, producing numbness, tingling, unsteady walking, and in severe cases the classic syndrome called subacute combined degeneration.
- Energy metabolism. By feeding odd-chain fatty acids and branched-chain amino acids into the Krebs cycle, methylmalonyl-CoA mutase contributes to the body's energy supply.
In short, the entire human "need" for cobalt is the need to have a few micrograms of it pre-packaged inside cobalamin. For the full mechanistic and clinical picture, see our dedicated Vitamin B12 page.
3. Dietary Sources
Because usable cobalt reaches us only inside vitamin B12, the meaningful dietary sources of "cobalt" are simply the dietary sources of B12 — and B12 is made by microorganisms, not plants or animals. Animals accumulate B12 in their tissues because their gut bacteria (or the bacteria in the soil and feed they consume) synthesize it. That is why bioavailable cobalt-as-B12 comes overwhelmingly from animal-derived foods and from fortified foods, and essentially not at all from unfortified plants.
Foods that supply cobalt as usable vitamin B12
- Shellfish and fish: clams and oysters are among the richest natural sources of B12 on the planet; fish such as salmon, sardines, tuna, and trout are also strong sources.
- Organ and muscle meats: liver is extraordinarily B12-dense; beef, lamb, pork, and poultry all contribute.
- Eggs and dairy: milk, yogurt, cheese, and eggs provide moderate, reliable amounts.
- Fortified foods: many breakfast cereals, plant milks, and nutritional yeasts have synthetic B12 (usually cyanocobalamin) added. These are the main practical source for people who eat little or no animal food.
The plant-cobalt trap
Here is a point that trips up many people. Some leafy greens, nuts, and legumes do contain measurable inorganic cobalt, drawn up from the soil. But this cobalt is not convertible to vitamin B12 by the human body — we lack the bacterial enzymes to do it. So a spinach leaf or a handful of almonds may show "cobalt" on a mineral analysis while delivering zero usable B12. This is the single biggest reason that strict vegans and vegetarians who avoid fortified foods are at real risk of B12 deficiency despite eating plenty of cobalt-containing plants. The cobalt is there; the vitamin is not.
A related caution applies to certain fermented foods, mushrooms, algae, and spirulina that are sometimes marketed as plant B12 sources. Many contain B12 analogues (pseudovitamin B12) that look like B12 on some tests but do not work as the vitamin in humans and may even interfere with true B12. For dependable B12 without animal foods, fortified foods or a supplement are the safe route — see the Supplementation & Forms section below and our Vitamin B12 page.
4. Deficiency
There is no such thing as a distinct human "cobalt deficiency" in the way there is an iron or zinc deficiency. Because cobalt's only job in people is to be the core of B12, a shortage of cobalt-as-B12 simply is vitamin B12 deficiency. The two conditions are one and the same, and they produce the well-known consequences of running short on cobalamin.
What B12 (cobalt) deficiency looks like in people
- Megaloblastic anemia: fatigue, pallor, shortness of breath, and a fast heartbeat caused by large, ineffective red blood cells. See our page on anemia.
- Neurological injury: numbness and tingling in the hands and feet, balance problems, muscle weakness, and — if untreated for long — memory loss, mood changes, and difficulty walking from spinal-cord damage. Importantly, nerve damage can appear before the anemia and can become permanent.
- Other signs: a sore, smooth, red tongue (glossitis), mouth ulcers, and elevated blood markers (high homocysteine and methylmalonic acid) that doctors use to confirm the diagnosis.
The usual causes are not a lack of cobalt in the diet but problems getting B12 out of food or absorbing it: pernicious anemia (an autoimmune loss of intrinsic factor, the protein needed to absorb B12), older age, stomach or intestinal surgery, certain medications (metformin, long-term acid-suppressing drugs), and diets that exclude animal and fortified foods.
Cobalt deficiency in grazing animals — a veterinary story, not a human one
The phrase "cobalt deficiency" is real and important — but in livestock, not people. Cattle, sheep, and goats rely on the bacteria in their rumen (the large fermentation chamber of their stomach) to synthesize B12, and those bacteria need cobalt from the soil and pasture to do it. In regions where soil cobalt is naturally low — parts of Australia, New Zealand, Britain, and the northern United States — grazing animals develop B12 deficiency that farmers historically called "wasting," "pine," or "coast disease." Affected animals lose appetite, fail to thrive, waste away, and can die. The fix is to supplement the soil, pasture, or animals with small amounts of cobalt so their gut microbes can make B12.
This veterinary problem is genuinely a cobalt-deficiency problem, and it is the historical reason cobalt was ever called a "dietary essential" at all. But it does not translate into a human dietary need for cobalt, because we obtain finished B12 directly from our food rather than asking our gut bacteria to build it for us from raw cobalt.
5. Recommended Intake
There is no Recommended Dietary Allowance (RDA) for elemental cobalt, and no official "adequate intake" figure for the inorganic metal. This is a direct consequence of everything above: since the human requirement is for cobalt locked inside vitamin B12, intake guidance is given entirely through the B12 recommendation. National nutrition bodies set a B12 target, not a cobalt target.
Intake expressed as vitamin B12
- The U.S. RDA for vitamin B12 is about 2.4 micrograms (µg) per day for most adults.
- It rises modestly in pregnancy (about 2.6 µg/day) and breastfeeding (about 2.8 µg/day).
- Because absorption efficiency falls as the dose rises (intrinsic-factor-mediated uptake saturates at roughly 1.5–2 µg per meal), people who get B12 from supplements often take far larger amounts so that a small fraction is absorbed by simple diffusion.
For context, the cobalt atom is a tiny fraction of the B12 molecule by weight, so 2.4 µg of B12 contains only a few tenths of a microgram of cobalt as the vitamin. This vanishingly small "cobalt requirement" underscores why no one sets an intake target for the metal itself.
How much inorganic cobalt do we actually eat?
Separately from B12, ordinary diets contain some inorganic cobalt — from plant foods, water, and trace contamination — typically on the order of a few micrograms up to a couple of milligrams per day, with most estimates landing somewhere between about 5 and 40 µg/day in Western diets. This inorganic cobalt is not nutritionally useful to humans (we cannot turn it into B12), and at these everyday levels it is not considered harmful. It only becomes a concern at the far higher exposures discussed in the next two sections — from cobalt supplements, industrial dust, contaminated drinks, or wearing metal implants. In short: aim for adequate B12; ignore "cobalt" as a separate intake goal.
6. Supplementation & Forms
The right way to "supplement cobalt" is to supplement vitamin B12 — never inorganic cobalt salts. Any cobalt your body can actually use must arrive already built into the cobalamin molecule. A B12 supplement delivers exactly that; a cobalt-salt supplement delivers a toxic metal with no nutritional benefit.
The useful forms — all are vitamin B12
- Cyanocobalamin: the most common, most stable, and cheapest form, used in most supplements and fortified foods. The body removes the cyanide group (a trivial amount, harmless at these doses) and converts it to the active forms.
- Methylcobalamin: a naturally occurring active form (the one used by methionine synthase), popular in supplements.
- Hydroxocobalamin: a form often given by injection, valued for its long retention in the body; it is also used (in much larger doses) as an antidote for cyanide poisoning.
- Adenosylcobalamin (dibencozide): the mitochondrial active form, sometimes sold in supplements.
All of these are appropriate ways to obtain cobalt-as-B12, whether by mouth (tablets, sublingual lozenges, fortified foods) or by injection when absorption is impaired. Doses for correcting deficiency are far larger than the 2.4 µg RDA — oral regimens of 500–1,000 µg/day and injection schedules are common — because B12 has an enormous safety margin and poor absorption at low doses.
Do not take inorganic cobalt supplements
Cobalt salts (cobalt chloride, cobalt sulfate, cobalt gluconate) have occasionally been sold or promoted to "boost energy," "build red blood cells," or enhance athletic performance. Avoid them. They cannot be converted into B12, they provide no genuine benefit, and — as the next section details — they are clearly toxic. The idea that cobalt salts raise red-cell counts is technically true (cobalt stimulates erythropoietin) but is exactly the mechanism behind their danger, and it is now classed as blood doping. Historically, cobalt chloride was even used as a medical treatment for stubborn anemias in the 1950s, until the cardiac and thyroid toxicity made the risk plainly unacceptable. There is no modern, legitimate role for swallowing cobalt as a nutrient. If you want the benefits of cobalt, eat B12-containing foods or take a B12 supplement.
7. Toxicity & Upper Limit
This is where cobalt's dual nature comes fully into view. There is no nutritional Tolerable Upper Intake Level (UL) for cobalt, simply because there is no nutritional requirement to bound — but make no mistake, inorganic cobalt is unambiguously toxic in excess. Cobalt poisoning is not a theoretical worry; it has caused real epidemics of heart failure, disabling thyroid and nerve disease, and occupational lung damage. The dose and the route matter enormously: micrograms of cobalt inside B12 are essential, while milligrams of free cobalt circulating in the blood are dangerous.
Cobalt-beer cardiomyopathy: a man-made epidemic
The most dramatic chapter in cobalt's history unfolded in the 1960s. To keep the foamy "head" on draft beer, several breweries began adding small amounts of cobalt sulfate as a foam stabilizer. Within a few years, clusters of severe, often fatal heart failure appeared among heavy beer drinkers in Quebec City, Omaha, Minneapolis, and Leuven (Belgium) — the condition became known as cobalt-beer cardiomyopathy or "Quebec beer-drinkers' cardiomyopathy." Patients developed a rapidly progressive congestive cardiomyopathy (a failing, enlarged heart) often accompanied by pericardial effusion (fluid around the heart) and polycythemia (an elevated red-blood-cell count). Mortality was high. The outbreaks vanished once cobalt was removed from beer, and the episode became a permanent cautionary tale.
What made it so striking is that the cobalt doses involved were not astronomical — heavy drinkers were taking in only a few milligrams of cobalt per day — yet the combination of cobalt with heavy alcohol use, often poor diet, and protein/thiamine deficiency proved cardiotoxic. The lesson stands: chronic exposure to milligram quantities of inorganic cobalt can poison the heart.
Metal-on-metal hip implants and "arthroprosthetic cobaltosis"
The modern face of cobalt toxicity comes from orthopedic surgery. Some hip-replacement designs used a metal-on-metal bearing in which a cobalt-chromium alloy ball rubs against a cobalt-chromium socket. As the surfaces wear, microscopic cobalt particles and ions are released and absorbed into the bloodstream. In a subset of patients this produces systemic cobalt poisoning, sometimes called arthroprosthetic cobaltosis or arthroprosthetic cobaltism. The syndrome can include:
- Cardiomyopathy — the same failing-heart picture seen with cobalt beer, now arising from a worn implant.
- Hypothyroidism and goiter — cobalt blocks the thyroid's uptake of iodine, so the gland can enlarge and underperform. See hypothyroidism.
- Neuro-ocular-auditory toxicity — a distinctive cluster of vision loss (optic-nerve and retinal injury), hearing loss and ringing in the ears, peripheral neuropathy, tremor, and cognitive or mood changes.
Because the symptoms are diverse and can be mistaken for many other illnesses, regulators have issued guidance on monitoring patients with these implants. Health authorities (such as the UK's MHRA and the U.S. FDA) flag blood or serum cobalt thresholds as a trigger for closer investigation — a level around 7 µg/L (about 119 nmol/L) is commonly cited as a point of concern that may warrant imaging and specialist review. These numbers should be interpreted cautiously and always in clinical context: a single value does not diagnose poisoning, but rising levels combined with new heart, thyroid, vision, hearing, or nerve symptoms in someone with a metal-on-metal hip should prompt a careful workup. For normal, healthy people without implants or industrial exposure, blood cobalt is typically well under 1 µg/L.
Polycythemia, erythropoietin, and blood doping
Cobalt has a peculiar ability to fool the body into thinking it is short of oxygen. It does this by stabilizing HIF (hypoxia-inducible factor), the master switch cells use to sense low oxygen. With HIF artificially propped up, the kidneys ramp up production of erythropoietin (EPO), the hormone that drives red-blood-cell manufacture — so cobalt raises the red-cell count and hematocrit. This is exactly why cobalt chloride was once used to treat anemia, why polycythemia appeared in cobalt-beer victims, and why cobalt has been abused as a cheap, oral doping agent by athletes seeking more oxygen-carrying capacity. Cobalt is now on the World Anti-Doping Agency's prohibited list. The "benefit" of more red cells is inseparable from cobalt's toxicity, and the doses needed to boost performance overlap with those that injure the heart and thyroid.
Hard-metal lung disease and occupational exposure
In industry, the danger is mostly inhaled rather than swallowed. "Hard metal" is an extremely tough material made by cementing tungsten carbide with cobalt, used for cutting tools, drill bits, and grinding wheels. Workers who grind or machine hard metal inhale cobalt-containing dust, which can cause hard-metal lung disease — a form of giant-cell interstitial pneumonitis that scars the lungs (pulmonary fibrosis) — as well as occupational asthma. Cobalt is also one of the more common causes of allergic contact dermatitis: it sensitizes the skin, producing itchy, eczema-like rashes on contact with cobalt-containing metals, cement, leather, or pigments, often alongside nickel allergy. See related entries on nickel and heavy metals.
High oral doses
Swallowing large amounts of cobalt salts — whether from misguided supplements, contaminated drinks, or industrial accidents — first irritates the gut, causing nausea, vomiting, and diarrhea, and can then deliver the systemic effects above: cardiac, thyroid, and neurological injury, plus polycythemia. There is no safe rationale for ingesting inorganic cobalt.
How cobalt poisons cells: the mechanism
Cobalt's toxicity comes from several overlapping actions:
- Binding sulfhydryl (thiol) groups and choking cellular respiration. Cobalt latches onto the sulfur-containing parts of key enzymes, notably the lipoic-acid cofactors of pyruvate dehydrogenase and α-ketoglutarate dehydrogenase. By inhibiting these gatekeeper enzymes, cobalt partly "starves" the Krebs cycle of fuel, impairing the heart and other energy-hungry tissues — a plausible explanation for the cardiomyopathy.
- Stabilizing HIF → excess EPO → polycythemia. As described above, cobalt mimics low oxygen and drives red-cell overproduction.
- Blocking thyroidal iodine uptake. Cobalt interferes with the thyroid's ability to trap iodine, producing goiter and hypothyroidism.
- Generating oxidative stress. Cobalt ions catalyze the formation of reactive oxygen species and can damage DNA, contributing to its classification as a possible human carcinogen in certain exposure settings.
Diagnosing cobalt toxicity
When cobalt poisoning is suspected, clinicians typically combine: blood/serum and urine cobalt measurements (reported in µg/L); echocardiography to look for a weakened, enlarged heart and pericardial fluid; thyroid function tests (TSH, free T4) to detect hypothyroidism; and, for implant patients, imaging of the prosthesis and sometimes aspiration of joint fluid to assess metal wear. A complete blood count may reveal the tell-tale polycythemia. Treatment centers on removing the source — taking cobalt out of the diet or environment, or surgically revising a failing metal-on-metal implant — after which blood cobalt falls and many (though not always all) symptoms improve. Chelation therapy has been tried in severe cases with mixed results.
8. Special Considerations
The honest, practical bottom line on cobalt is short and worth repeating: get your cobalt as vitamin B12, and never supplement the inorganic metal. Everything good cobalt does for you, it does from inside the cobalamin molecule; everything dangerous it does, it does when it runs free. Holding those two facts together is the whole story.
Who should pay extra attention
- Vegans, strict vegetarians, and people who avoid fortified foods. Their risk is B12 deficiency, not cobalt deficiency. The plant cobalt they eat cannot be converted to B12, so a reliable B12 source (fortified foods or a supplement) is important. See Vitamin B12.
- Older adults and people with absorption problems. Pernicious anemia, gastric or bowel surgery, and long-term use of metformin or acid-suppressing drugs all impair B12 absorption and may call for higher-dose oral B12 or injections.
- People with metal-on-metal hip implants. Anyone with such an implant who develops unexplained heart failure, an enlarging thyroid or new hypothyroidism, vision or hearing loss, or numbness, tremor, memory, or mood changes should ask a clinician to check blood cobalt and review the implant. Catching arthroprosthetic cobaltosis early — and revising the implant if needed — can halt or reverse the damage.
- Workers in hard-metal, grinding, pigment, and battery industries. Inhaled cobalt dust and skin contact are the main hazards; dust controls, ventilation, and avoiding skin exposure matter, and a cobalt-allergic rash should prompt evaluation.
- Athletes. Cobalt is a banned doping agent and a genuine poison at performance-"enhancing" doses — there is no safe way to use it for an edge.
Putting the dual nature in perspective
Cobalt is one of the clearest examples in all of nutrition of a substance whose value depends entirely on its chemical packaging and dose. Sealed inside vitamin B12 at the level of a few micrograms, it is irreplaceable — the literal core of the molecule that keeps our blood and nerves healthy. Set loose as a salt or worn off a metal implant at the level of milligrams in the bloodstream, it can damage the heart, thyroid, nerves, eyes, ears, and lungs. The site's broader pages on minerals and toxic minerals place cobalt alongside other elements that share this Jekyll-and-Hyde quality, and the lab tests section covers the blood and urine measurements used to tell the difference between safe and harmful exposure. When in doubt, the rule is simple: cobalt belongs in your B12, not in a supplement bottle.
9. Key Research Papers
- Green R, Allen LH, Bjørke-Monsen AL, et al. Vitamin B12 deficiency. Nature Reviews Disease Primers. 2017;3:17040. doi:10.1038/nrdp.2017.40
- Stabler SP. Vitamin B12 Deficiency. New England Journal of Medicine. 2013;368(2):149–160. doi:10.1056/NEJMcp1113996
- Froese DS, Banerjee R. Human B12-dependent enzymes: Methionine synthase and Methylmalonyl-CoA mutase. Methods in Enzymology. 2022;668:309–326. doi:10.1016/bs.mie.2021.12.012
- Yamada K. Cobalt: Its Role in Health and Disease. In: Metal Ions in Life Sciences, vol. 13. 2013:295–320. doi:10.1007/978-94-007-7500-8_9
- Leyssens L, Vinck B, Van Der Straeten C, Wuyts F, Maes L. Cobalt toxicity in humans — A review of the potential sources and systemic health effects. Toxicology. 2017;387:43–56. doi:10.1016/j.tox.2017.05.015
- Morin Y, Daniel P. Quebec Beer-Drinkers' Cardiomyopathy: Etiological Considerations. JAMA. 1967;202(13):1145–1146. doi:10.1001/jama.1967.03130260067015
- Alexander CS. Cobalt-beer cardiomyopathy: A clinical and pathologic study of twenty-eight cases. The American Journal of Medicine. 1972;53(4):395–417. doi:10.1016/0002-9343(72)90136-2
- Packer M. Cobalt Cardiomyopathy: A Critical Reappraisal in Light of a Recent Resurgence. Circulation: Heart Failure. 2016;9(12):e003604. doi:10.1161/CIRCHEARTFAILURE.116.003604
- Tower SS. Arthroprosthetic cobaltism: neurological and cardiac manifestations in two patients with metal-on-metal arthroplasty. Journal of Bone and Joint Surgery. 2010;92(17):2847–2851. doi:10.2106/JBJS.J.00125
- Nemery B, Verbeken EK, Demedts M. Giant cell interstitial pneumonia (hard metal lung disease, cobalt lung). Seminars in Respiratory and Critical Care Medicine. 2001;22(4):435–448. doi:10.1055/s-2001-17386
- Hindsén M. Allergic contact dermatitis from cobalt in jewellery. Contact Dermatitis. 2005;53(6):350. doi:10.1111/j.0105-1873.2005.0592a.x
- Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for Cobalt. U.S. Department of Health and Human Services, Public Health Service. atsdr.cdc.gov/toxprofiles/tp33.pdf
- National Institutes of Health, Office of Dietary Supplements. Vitamin B12 — Health Professional Fact Sheet. ods.od.nih.gov/factsheets/VitaminB12-HealthProfessional
- Medicines and Healthcare products Regulatory Agency (MHRA). Medical Device Alert: All metal-on-metal (MoM) hip replacements — updated advice for follow-up of patients. gov.uk — MoM hip replacement guidance
Connections
- Vitamin B12 (Cobalamin)
- All Minerals
- Toxic Minerals
- Iron
- Copper
- Manganese
- Zinc
- Nickel
- Heavy Metals
- Cardiomyopathy
- Hypothyroidism
- Anemia
- Lab Tests