Copper

Copper (Cu) is a trace mineral needed for cytochrome oxidase, connective tissue, and pigment formation. Copper–Iron balance is central in Ray Peat's framework: deficiency lets tissues retain excess iron; excess iron blocks copper uptake.

Copper
Chemical formula	Cu
Solubility
Bioavailability
Dietary sources	Oysters, shrimp, liver, mushrooms, cocoa
RDA (adults 19–50 y)	900 µg/day (US adult)
Upper limit	10 mg/day (US adult)
Ray's verdict

Copper is the crucial element for producing the color in hair and skin, for maintaining the elasticity of skin and blood vessels, for protecting against certain types of free radical, and especially for allowing us to use oxygen properly for the production of biological energy.

— Ray Peat

Dosing

No fixed supplement dose given. Regular shellfish and balanced meals with limited fortification iron support the copper side of the iron–copper axis. See Harm reduction.

History

Etymology

The English name traces through Latin cuprum, shortened from aes Cyprium ("metal of Cyprus"), since the island of Cyprus was a major Roman-era copper source.

Copper is one of the first metals humans worked, mined and smelted since roughly 9000 BCE; its use gives the Copper Age (Chalcolithic) its name.

Structure/Chemical properties

Copper cycles between Cu⁺ and Cu²⁺ in enzymes including cytochrome c oxidase (complex IV of respiration). Copper loss with age tracks with rising tissue iron and greater Vitamin E need.

Function/Mechanism of Action

Beyond serving as a cofactor of metabolic enzymes, copper takes part in cell signaling, autophagy, cell motility, differentiation, and a copper-dependent form of regulated cell death called cuproptosis.

Adequate copper supports mitochondrial oxygen use and elastic tissues. Low copper impairs substantia nigra function in Parkinson's disease. Thyroid activity increases copper absorption in osteoporosis.

Stress of any kind on energy production, including high estrogen, nitric oxide, low thyroid or too much darkness, makes the respiratory system lose copper, and iron tends to take its place. Thyroid hormone is probably the major regulator of copper absorption and use, because the copper enzyme cytochrome c oxidase is the one it activates.

During aging the body's iron load rises, especially when copper is deficient, while copper content falls; copper is part of cytochrome oxidase and of the cytoplasmic SOD enzyme, and ceruloplasmin helps keep iron in check.

Elastin units are probably bound together by copper atoms, and in old age elastin is among the first substances to calcify, for example in the elastic layers of arteries.

Medical uses/Effects

Shellfish (oysters, shrimp) are Peat's preferred copper sources to prevent iron overload patterns. Pairing Liver with oysters balances zinc-to-copper ratios per community mineral notes on Zinc.

I made it myself, soaking a piece of pure copper with aspirin in water, until a very pale blue color developed. Later, the solution became a deeper blue color, and at a certain concentration I think it's toxic.

— Ray Peat

Side/Adverse effects

Excess supplemental zinc induces copper deficiency via metallothionein (standard nutrition; see Zinc). High-dose isolated copper supplements risk imbalance; Peat favored food sources.

Trace minerals

Boron is a trace element in plant and animal tissues. Mainstream nutrition treats it as possibly essential for bone and hormone metabolism.

Asked whether boron supplements regulate the calcium-to-phosphate ratio and parathyroid hormone, Ray Peat put diet first:

It affects them, but the essential thing is to have adequate calcium in the diet relative to phosphate.

— Ray Peat

History (Boron)

Etymology (Boron)

The name derives from "borax," the mineral sodium borate long used in glazes and preservation since antiquity, with the "-on" suffix modeled on carbon.

Boron was isolated in 1808, independently, by Humphry Davy in England and by Joseph Louis Gay-Lussac and Louis Jacques Thénard in France.

Structure/Chemical properties (Boron)

Boron has no stable monatomic gas chemistry in biology. Food and supplements supply boron as boric acid, borate salts, or chelated forms.

Function/Mechanism of Action (Boron)

Animal and human studies report boron affects steroid hormone metabolism and inflammatory markers.

Daily boron supplementation (10 mg) raised free testosterone and lowered CRP in a human male cohort. A review summarized boron effects on bone, hormones, and inflammation.

Medical uses/Effects (Boron)

Boron supplements are used experimentally for bone and hormone support. Evidence is thinner than for Zinc or Magnesium. See Testosterone and Harm reduction.

In one boron advocate's account, bones from patients who took boron were harder to cut. This rests on informal observation and was never measured.

Side/Adverse effects (Boron)

Excess boron can cause nausea and dermatitis. Asked about borax baths for arthritic joints:

I think enough can be absorbed to be toxic.

— Ray Peat

High doses are toxic to infants and pregnant women in animal data.

Chromium is a trace mineral. Mainstream nutrition links trivalent chromium to insulin signaling through chromodulin (low-molecular-weight chromium-binding substance).

Peat cited McCarty's chromium-picolinate bone hypothesis in his bone-density article, then added:

I think chromium is too toxic to use as a supplement.

— Ray Peat

His blood-sugar writing centers on Glucose oxidation, Thyroid, and lowering PUFA stress chemistry.

History (Chromium)

Etymology (Chromium)

The name comes from Greek chroma ("color"), chosen because chromium compounds are strikingly and variably colored (the basis of chrome pigments and chrome plating).

Louis Nicolas Vauquelin discovered chromium in 1797 and isolated the metal the following year.

Structure/Chemical properties (Chromium)

Biologically relevant form is Cr(III). Hexavalent chromium is an industrial toxin, not a nutrient.

Function/Mechanism of Action (Chromium)

Chromodulin may amplify insulin receptor kinase activity in cell models. Human supplementation trials show mixed results.

Insulin itself has been found to account for only about 8% of the "insulin-like activity" of the blood, with potassium being probably the largest factor.

— Ray Peat

There probably isn't any process in the body that doesn't potentially affect blood sugar.

— Ray Peat

Supplemental chromium picolinate improved glucose and insulin variables in a human type 2 diabetes trial. Meta-analyses remain mixed on clinical benefit. See Glucose, Insulin, Thyroid, Harm reduction.

Medical uses/Effects (Chromium)

Chromium picolinate is sold for glycemic support. Peat opposed chromium supplementation on toxicity grounds (quote above). Community practice usually addresses thyroid, diet, and stress hormones first.

Side/Adverse effects (Chromium)

High-dose chromium supplements can cause GI upset. Renal patients need medical supervision. Occupational hexavalent chromium is carcinogenic (distinct from Cr III supplements).

Manganese is a trace mineral in enzymes including mitochondrial superoxide dismutase and many metalloenzymes. Mainstream nutrition treats deficiency as rare in adults but possible with parenteral nutrition.

Dietary manganese is a nutrient removed or imbalanced by industrial food processing and depleted soils, not as a focus supplement.

Dosing (Manganese)

No Peat supplement protocol. Leafy greens, nuts, and whole grains supply manganese in mainstream nutrition tables; Peat cautioned leafy greens can carry environmental toxins in his calcium writing, so source quality matters. See Harm reduction.

History (Manganese)

Etymology (Manganese)

The name traces to Latin/Italian magnesia nigra ("black magnesia"), referring to the mineral pyrolusite (manganese dioxide), which was historically confused with magnetic lodestone and true magnesium ore before the three were chemically distinguished.

Manganese ores were used in glassmaking since antiquity, but the pure metal wasn't isolated until 1774, by Swedish chemist Johan Gottlieb Gahn.

Structure/Chemical properties (Manganese)

Manganese (atomic number 25) cycles between oxidation states in enzymes. Excess manganese accumulates in brain in occupational overexposure (manganism), distinct from dietary trace intake in mainstream toxicology.

Function/Mechanism of Action (Manganese)

Peat listed manganese among B-vitamin cofactors and minerals removed when grains are refined for shelf life. Soils lacking zinc, copper, manganese, molybdenum, and Selenium produce less nutritious crops in sugar-issues writing he cited.

He grouped mineral balance (copper, zinc, iron, manganese, calcium, magnesium) with thyroid and stress chemistry in the same article's wider mineral discussion. Community mineral practice usually addresses manganese through whole foods and lower refined-grain intake rather than high-dose pills.

Medical uses/Effects (Manganese)

Mainstream medicine uses manganese only in deficiency states. Peat did not promote manganese supplements; his emphasis is adequate whole-food mineral matrix with limited iron fortification and refined oils. See Magnesium, Copper, Zinc.

Side/Adverse effects (Manganese)

High-dose manganese supplements risk neurotoxicity and interact with Iron absorption. Inhalation exposure in welding and mining is the main occupational hazard in standard toxicology.

Molybdenum is a trace mineral at the active site of sulfite oxidase and xanthine oxidase. Mainstream nutrition treats deficiency as rare.

Ray Peat cited purified sucrose feeding studies where animals lacked zinc, copper, manganese, molybdenum, and selenium alongside phosphorus shifts, illustrating mineral-poor refined diets.

Dosing (Molybdenum)

No Peat fixed dose. Varied whole foods and shellfish/organ meats in moderation match his mineral pattern.

History (Molybdenum)

Etymology (Molybdenum)

The name comes from Greek molybdos ("lead"), since molybdenite ore was long mistaken for lead ore (galena) or graphite due to their visual similarity.

Carl Wilhelm Scheele identified molybdenum as a distinct element in 1778; the pure metal wasn't isolated until 1781, by Peter Jacob Hjelm.

Structure/Chemical properties (Molybdenum)

Molybdenum (Mo, atomic number 42) is used biologically as molybdopterin cofactor in oxidase enzymes.

Function/Mechanism of Action (Molybdenum)

Sulfite oxidase detoxifies sulfites to sulfate; xanthine oxidase handles purine catabolism in mainstream biochemistry. The cited reference points out that trace minerals including molybdenum must accompany carbohydrate-heavy refined diets to avoid silent deficiencies.

Medical uses/Effects (Molybdenum)

Mainstream medicine addresses inherited molybdenum cofactor deficiency. Peat did not emphasize molybdenum supplementation; whole foods with minerals accompany Sugar and fruit in his dietary writing.

Side/Adverse effects (Molybdenum)

High molybdenum intake can increase copper excretion in mainstream nutrition texts. See Harm reduction.

Selenium is a trace mineral incorporated into selenoproteins including glutathione peroxidase. Mainstream nutrition treats deficiency as a cause of Keshan cardiomyopathy and immune impairment.

Ray Peat listed selenium among chain-breaking antioxidants that support respiration when oxygen delivery fails, alongside thyroxine, uric acid, vitamin A, Sodium, and Magnesium. Seafood eaters get more selenium than land-only diets in his cholesterol writing.

Dosing (Selenium)

Selenium, I think a hundred micrograms is a ... safe supplement, and selenium is essential for the local production in the tissue

— Ray Peat

Shellfish and varied whole foods match his seafood emphasis in cholesterol and iron articles. Pair with adequate Vitamin E and thyroid support when addressing stored PUFA per his wider writing.

History (Selenium)

Etymology (Selenium)

The name comes from Selene, the Greek moon goddess, chosen because selenium was found alongside tellurium (named for tellus, "earth") and shares some of its chemical properties.

Jöns Jacob Berzelius discovered selenium in 1817 as a byproduct of sulfuric acid production.

Structure/Chemical properties (Selenium)

Selenium (Se, atomic number 34) sits below sulfur in the periodic table. Biological activity is mainly through selenocysteine at enzyme active sites. Inorganic selenite and selenomethionine differ in metabolism but both can replete deficiency in mainstream nutrition.

The thyroid gland holds the highest selenium concentration per gram of any organ. Selenium is built into the iodothyronine deiodinases (DIO1, DIO2, DIO3) that activate and inactivate thyroid hormone, along with glutathione peroxidases and thioredoxin reductases that protect the gland from the hydrogen peroxide generated during hormone synthesis.

Function/Mechanism of Action (Selenium)

Many antioxidant nutrients act like a thyroid supplement did in the 1934 rabbit experiments, preventing atherosclerosis even when extra toxic cholesterol is given to the animals.

— Ray Peat

Peat grouped selenium with Vitamin E and saturated fats as defenses against PUFA-driven lipid peroxidation in heart-disease discussion; the medical establishment long opposed selenium and vitamin E for cardiovascular use while many physicians took vitamin E themselves in his account.

Peat repeated the same glucose-selenium dependency in later interviews: every tissue that converts T4 into locally active T3 needs both glucose and selenium to run the deiodinase reaction, not just the liver. Glucose and selenium support T4-to-T3 conversion enzymes in Peat's thyroid article. Riboflavin, coenzyme Q10, vitamin K, niacinamide, thiamine, and selenium support mitochondrial respiration in FPS compilations Peat endorsed.

In animal models Peat cited, selenium supplementation protected against high-fat-diet atherogenic changes. On mad-cow and amyloid topics selenium and vitamin E limit oxidant damage when PUFA and iron are high.

Selenium activates the thyroid, and thyroid works as an antioxidant by letting cells use oxygen and consume harmful electrons, which prevents random oxidative damage.

Seafood once or twice a week supplies selenium and iodine, along with copper and other trace minerals that land-grown food can lack.

Medical uses/Effects (Selenium)

Exercise raised systemic selenium delivery to the hippocampus, activating neural stem cells and improving learning in aged mice; selenium supplementation alone replicated exercise-level neurogenesis and cognition gains.

Low selenium status is associated with hypothyroidism, subclinical hypothyroidism, and autoimmune thyroid disease (Hashimoto's thyroiditis, Graves' disease); trials of selenium supplementation (commonly 100-200 µg/day) have reduced thyroid antibody levels in autoimmune thyroiditis and improved mild Graves' orbitopathy in some studies, though clinical outcomes vary by baseline selenium status. In a three-arm trial (n=102), 200 µg/day sodium selenite lowered TPO-Ab within-group over three months similarly to 500 mg/day vitamin C, without a significant between-group edge over placebo. In euthyroid men with Hashimoto's and testosterone deficiency, 200 µg/day selenomethionine for six months reduced TPO and thyroglobulin antibodies, more strongly when combined with intramuscular testosterone.

Mainstream medicine uses selenium repletion in deficiency. Dietary seafood and antioxidant context with lower PUFA and iron come before megadose selenium pills as a primary strategy. Rosacea writing names selenium among mitochondrial-support nutrients with riboflavin and thiamine.

Mercury and cadmium antagonism

Selenium lessens methylmercury toxicity in animals: tuna selenium helped Japanese quail survive dietary methylmercury, and comparable selenium intake protected rats. Selenium–mercury and selenium–cadmium interactions include direct chemical complexation and metabolic antagonism. Seabirds convert methylmercury into HgSe nanoparticles and Hg–selenocysteinate complexes in liver and other tissues. See Mercury and Heavy metals.

Side/Adverse effects (Selenium)

Selenium toxicity (selenosis) causes garlic breath, nail changes, and neurologic symptoms at chronic high intake. Brazil nuts vary widely in selenium content. See Harm reduction before high-dose supplements.

Silica (silicon) supports connective tissue and bone in mainstream nutrition. Orthosilicic acid is the usual absorbable species.

Ray Peat did not center silica supplementation in his published articles searched for this page. His collagen and mineral writing emphasizes Gelatin, protein adequacy, and Thyroid before isolated trace supplements.

History (Silica)

Etymology (Silica)

"Silica" (silicon dioxide) comes from Latin silex/silicis, meaning flint or hard stone. Silicon itself was named in 1817 by Thomas Thomson, adding the "-on" suffix (as with boron and carbon) to "silica."

Jöns Jacob Berzelius isolated pure silicon in 1824.

Structure/Chemical properties (Silica)

Silicon sits below carbon in the periodic table. In biology it appears mainly as silicic acid and in plant phytoliths.

Function/Mechanism of Action (Silica)

Silicon may support collagen cross-linking and bone mineralization in animal models.

Inhaled crystalline silica activates inflammatory and oxidative pathways in lung tissue. Aspirin inhibited silica-induced lipid peroxidation and TNF-α in experimental models Peat cited in his aspirin bibliography. That concerns occupational dust, not dietary silica supplements.

Aluminum absorption

Oligomeric soluble silica, but not monomeric silica, reduced gastrointestinal aluminum availability by 67% in healthy volunteers given a <suAl tracer; the oligomer itself was not detectably absorbed. Dissolved silicon at about 100 μmol/L cut peak plasma <suAl to 15% of the silicon-free value in five volunteers. Silicon-rich mineral water can raise urinary aluminum excretion without raising iron or copper loss in Alzheimer patients and carers. See Aluminum.

Medical uses/Effects (Silica)

Silica supplements are marketed for hair, skin, and nails. Evidence is weaker than for dietary protein and Collagen precursors on this wiki.

Side/Adverse effects (Silica)

Inhaled silica dust causes silicosis. Oral horsetail or silica supplements can interact with kidney disease protocols; medical supervision applies.