Morley Robbins Interview: The Mineral Imbalance Behind Fatigue

Table of Contents

1. The Short Version: What Robbins Says to Start and Stop
2. How to Read This Page
3. Stress and the Copper-First Mineral Hierarchy
4. Fetuin-A and Insulin Resistance
5. Iron, Anemia and the Daily Iron Budget
6. Hair Colour, Copper and Cholesterol
7. Food Sources and Glyphosate
8. Magnesium, Drug-Induced Depletion and Zinc
9. Vitamin D Versus Vitamin A
10. Iodine, and “There Is No Disease”
11. The Stops, the Starts and the Adrenal Cocktail
12. Epsom Salt Baths
13. The 86-Year-Old Case and the 362 Tracked Cases
14. “Is Meat Enough?”
15. Key Takeaways
16. Safety
17. Key Research Papers
18. Connections
19. Featured Videos

The Short Version: What Robbins Says to Start and Stop

Boiled down, the interview gives one list of things to start, one list of things to stop, and four ideas that hold the lists together. This is Robbins’s advice as he gives it; each item is tested in the sections below, and the tier tags in the chart say how well each core idea holds up.

Start taking

• Retinol (vitamin A) from foods: beef liver, cod liver oil, egg yolks (deep orange, from pastured hens), grass-fed butter and grass-fed heavy cream.
• Copper — from food, and in his protocol from a whole-food copper supplement he formulated.

Stop taking

• Vitamin D on its own (vitamin D-only supplements).
• Zinc supplements.
• Iron supplements.

Four core ideas

1. Copper regulates iron and oxygen. Established in part: copper enzymes (ceruloplasmin, hephaestin) are required to move iron, and cytochrome c oxidase, a copper enzyme, turns oxygen into water in the mitochondria.
2. The goal is to restore energy production. Partly supported: energy production really does depend on copper, iron and magnesium; that restoring it fixes most chronic illness is his hypothesis.
3. Low ferritin is caused by parasites. Robbins’s claim, and the evidence points elsewhere: a ferritin of 12 ng/mL is absolute iron deficiency. Its common causes are menstrual blood loss, blood loss from the gut, and low iron intake or poor absorption; hookworm is one real cause in some regions. Whatever it is, a cause must be found.
4. Low copper causes iron overload (iron dysregulation). Partly supported: severe copper deficiency, and the rare genetic loss of ceruloplasmin, do trap iron in tissues; that this explains common fatigue is unproven.

Back to Table of Contents

How to Read This Page

Each topic below has two parts. First, Robbins’s claim, stated in his own framing as fairly as we can put it. Second, an Evidence check that says what the research actually shows and labels its strength: established (consistent human evidence, textbook physiology), human observational (associations in people, not proof of cause), animal or cell only (never assume it transfers to people), anecdote or self-report, or unverified (we could not find a published source).

The episode is an interview, not a lecture, so it moves quickly from topic to topic. Robbins mentions that he has done about 8,500 one-to-one consultations and says he has read some 12,000 research articles; his book carries close to 300 footnotes. None of that is in dispute here — what follows tests the specific claims, not the person making them.

Back to Table of Contents

Stress and the Copper-First Mineral Hierarchy

Robbins’s claim

Asked whether a mineral imbalance can make you sick, Robbins starts with stress — marital, dietary, occupational. He names two laboratory stress models, “chronic social defeat” and “repeated restraint”, and says the 2020 lockdowns applied both to whole societies, disturbing the body’s iron-recycling system. Stress, in his model, drains minerals.

He then lays out a hierarchy of minerals. Copper sits at the top, with iron and magnesium on the next line down. His chain runs: if copper is not right, iron recycling is not right; poorly managed iron reacts with oxygen to create oxidative stress (“a fancy term for rust”); that rust “burns up” magnesium; and low magnesium undermines the insulin response and the liver’s production of storage vitamin D. Copper, he says, is unique in managing iron and oxygen together — both making energy in the mitochondria and clearing the “exhaust”. “Copper is the general and iron is the foot soldier.”

Evidence check

The first link is established. Copper is not optional for iron handling. The copper enzyme hephaestin is needed to move iron out of gut cells into the blood — mice lacking working hephaestin become iron-deficient and anemic even with iron in the diet (Vulpe 1999, animal genetics) — and its plasma twin, ceruloplasmin, does the same job for the liver and the macrophages that recycle old red cells. People who are genuinely copper-deficient develop anemia and low white-cell counts that iron does not fix (Halfdanarson 2008, a review of 40 patients at one clinic, most after stomach or weight-loss surgery). The superoxide dismutase enzyme Robbins mentions really does carry copper at its catalytic site, with zinc playing a structural role.

The rest of the chain is plausible but unproven as a sequence. Loose iron does drive free-radical chemistry, and chronic stress is linked with magnesium loss, but nobody has shown in people that copper shortage → iron “rust” → magnesium loss is the usual route to tiredness or insulin resistance. The two stress models he names are rodent experiments; the step from them to the 2020 lockdowns is his interpretation, not a finding. Tier: first link established; the chain as a whole hypothesis.

Back to Table of Contents

Fetuin-A and Insulin Resistance

Robbins’s claim

Robbins says he learned only recently of a liver protein called fetuin-A. In copper deficiency, he says, fetuin-A rises; fetuin-A blocks the activation (phosphorylation) of the insulin receptor, a tyrosine-kinase receptor; the result is glucose intolerance and insulin resistance. That, for him, is the copper link beneath the familiar magnesium–insulin story.

Evidence check

Half of this holds up well. Fetuin-A does inhibit the insulin receptor’s tyrosine kinase in laboratory and rodent studies, and in people higher blood fetuin-A goes with lower insulin sensitivity and more liver fat: in a German study of 106 healthy adults, measured with the gold-standard clamp test, fetuin-A was higher in those with impaired glucose tolerance, and falling liver fat during weight loss brought fetuin-A down with it (Stefan 2006, human observational). The other half — that copper deficiency raises fetuin-A — we could not find in PubMed. Searches combining copper and fetuin-A returned nothing. Until a study is produced, that link is unverified, and the better-documented drivers of high fetuin-A are fatty liver and excess body fat.

Back to Table of Contents

Iron, Anemia and the Daily Iron Budget

Robbins’s claim

Robbins notes that roughly a third of the world is labelled anemic, which he finds implausible for a species living on an iron-rich planet. He says we replace about 2.5 million red blood cells every second — some 200 billion a day — and that this needs only about 25 mg of iron a day. Of that, about 24 mg comes from recycling the iron in dying red cells, a system he says copper runs, and only about 1 mg is supposed to come in through the mouth. Modern advice, in his view, has “flipped the narrative”, with fortified food, supplements and iron infusions pushing far more iron than the body was designed for. He distinguishes functional iron deficiency (iron present but not usable, because copper is short) from absolute iron deficiency.

When the host mentions that his sister has low iron with a ferritin of 12, Robbins says she is very likely functionally iron-deficient rather than absolutely deficient, and suggests parasites.

Evidence check

The budget is right; the conclusion drawn from it needs a correction. Physiology textbooks agree that the bulk of the iron used each day comes from macrophages breaking down old red cells, far exceeding what is absorbed from food (Ganz 2012, established), and roughly 20–25 mg recycled against 1–2 mg absorbed is the standard figure. But “1 mg absorbed” is not “1 mg eaten”. Because only a fraction of dietary iron is absorbed, the US National Academies set the recommended intake at 8 mg a day for adult men and 18 mg for menstruating women (Institute of Medicine 2001). Menstruation, pregnancy, growth and blood donation all raise the need well above the 1 mg a man loses daily.

The ferritin-12 example deserves a plain statement. Ferritin reflects stored iron. A ferritin of 12 is below every standard cut-off — the World Health Organization uses below 15 in adults, and many clinicians use below 30 — and it means iron stores are empty: absolute iron deficiency (Camaschella 2015). Ferritin can be falsely raised by inflammation, never falsely lowered this far, so “functional” deficiency is not the explanation for a ferritin of 12. The right next step is to find the cause — heavy periods, blood loss from the gut (ulcers, polyps, cancer), coeliac disease or another absorption problem, or a diet very low in iron — and to replace iron under medical supervision. Parasites such as hookworm are one real cause worldwide, but a ferritin of 12 is not something to treat by withholding iron.

Where Robbins has a point: copper-deficiency anemia exists and is often mistaken for iron deficiency (Halfdanarson 2008), and anemia that does not respond to iron is a reason to check copper and ceruloplasmin. Tier: established for the budget and the copper–iron link; contradicted for treating a ferritin of 12 as functional deficiency.

Back to Table of Contents

Hair Colour, Copper and Cholesterol

Robbins’s claim: black hair needs more copper

Robbins tells the host, who is of Indian heritage, that people with black hair need more copper to make melanin — he says six times more than he does — citing research from 1960s Japan, and adds that this holds for all black-haired animals.

Evidence check

Copper is genuinely required by tyrosinase, the copper enzyme that starts melanin production, and copper-deficient animals and people can lose pigment (greying fur or hair). But we could not find the Japanese study or any human evidence that dark-haired people have a sixfold higher copper requirement. National dietary standards set one copper requirement for all adults, regardless of hair or skin colour. Tier: unverified.

Robbins’s claim: low copper raises cholesterol

Robbins credits the copper researcher Leslie Klevay with a 1973 finding that copper-deficient animals develop high cholesterol, says more than 30 laboratories have since reproduced it, and explains it this way: making one cholesterol molecule consumes 11 molecules of oxygen, so cholesterol acts as an “oxygen sink” when copper-dependent cytochrome oxidase cannot turn oxygen into water. What matters, he says, is oxidised LDL, and oxidation points to an iron problem; plaque is iron dysregulation that calcium then patches over.

Evidence check

The 1973 paper is real: rats fed a higher ratio of zinc to copper developed raised cholesterol (Klevay 1973, animal), and the effect has been reproduced many times in rats. Human evidence is thinner. In a metabolic-ward study, one young man eating 0.83 mg of copper a day saw his plasma copper, ceruloplasmin and superoxide dismutase fall and his cholesterol rise (Klevay 1984, a single-person human experiment). That supports copper being relevant to lipid metabolism; it does not show that most people with high cholesterol are copper-deficient. The oxygen arithmetic is consistent with biochemistry — cholesterol synthesis does use many oxygen molecules — but the “oxygen sink” purpose is his interpretation. Oxidised LDL is a recognised player in plaque, and iron is one of several oxidants involved. Tier: animal, replicated; human, very limited.

Back to Table of Contents

Food Sources and Glyphosate

Robbins’s claim

The best copper foods, he says, are organ meats (especially beef liver), nuts and seeds, shellfish, and leafy greens such as collard, mustard and beet greens — but food is poorer than it was in 1950 because of 50 years of glyphosate. He cites a retired plant pathologist’s “logarithmic chelation scale”, which rates glyphosate pulling calcium and magnesium at 3, iron and zinc at 9 and copper at 12 — meaning, in his reading, copper is stripped a thousand times faster than iron and zinc and a billion times faster than calcium and magnesium.

Evidence check

The food list is sound: liver, shellfish, nuts, seeds and dark greens are among the richest copper sources (see Whole Food Copper Sources). Glyphosate is a real chelator — it binds metal ions, including copper — and a 2018 review concluded that whether this chelation harms plants, soil life or people “has not been fully elucidated”, and that natural soil chelators are far stronger for most metals (Mertens 2018, review). The “logarithmic chelation scale” with its 3, 9 and 12 values is not a peer-reviewed measurement; we found no published paper behind it, and the “billion times faster” figure should not be repeated as fact. Tier: chelation established in chemistry; effect on human copper status unproven.

Back to Table of Contents

Magnesium, Drug-Induced Depletion and Zinc

Robbins’s claim

Robbins credits the late magnesium researcher Mildred Seelig, a physician who studied how medicines deplete magnesium, and a popular book on drug-induced nutrient loss that lists 15 classes of drugs causing magnesium deficiency. Magnesium, he says, governs how strongly we react to stress — low magnesium is “like wearing night-vision goggles”, so everything feels bigger, which drives still more mineral loss. Taking “a bucket of magnesium” treats symptoms but not the cause, which he places upstream in copper. When magnesium is short, he adds, liver enzymes grab zinc instead, blood zinc looks low, and practitioners prescribe zinc — which the protocol rejects because zinc blocks copper uptake.

Evidence check

Drug-induced magnesium loss is well documented. The clearest example is the acid-blocking proton-pump inhibitors: a meta-analysis of nine observational studies covering 109,798 patients found a 43% higher risk of low blood magnesium in users (pooled risk ratio 1.43; Cheungpasitporn 2015, human observational), and the US Food and Drug Administration added a warning in 2011. Loop and thiazide diuretics and some other drugs also waste magnesium. That magnesium status shapes the stress response is plausible and partly supported; that it is always secondary to copper is unproven. The liver-enzymes-grab-zinc idea is unverified.

The zinc warning is correct. High-dose zinc induces metallothionein in gut cells, which traps copper and causes real, sometimes severe copper-deficiency anemia and low white-cell counts that iron cannot fix (Hoffman 1988, case report; many similar cases since). Long-term zinc above the 40 mg/day upper limit, including from denture creams and high-dose supplements, is the classic cause. Tier: established.

Back to Table of Contents

Vitamin D Versus Vitamin A

Robbins’s claim

Robbins calls vitamin D-only supplements “misapplied”. He recounts visiting the lipid researcher Fred Kummerow, then 98, who had studied vitamin D in pigs and told a conference in the early 1980s not to supplement vitamin D. He cites a Johns Hopkins study (Amer and Qayyum) as finding no benefit to a 25-hydroxyvitamin D level above about 21 ng/mL, against targets of 80–100 that some practitioners use. His central point is that high vitamin D blocks vitamin A, and that the retinol-derived signal retinoic acid switches on the copper pumps ATP7A and ATP7B, which load copper into ceruloplasmin, lysyl oxidase and superoxide dismutase. Without enough retinol, copper cannot be used. He recommends cod liver oil (which has far more vitamin A than D), liver, grass-fed butter and cream, and deep-orange egg yolks.

Evidence check

The Johns Hopkins study is real, but it says less than claimed. Amer and Qayyum analysed 10,170 healthy US adults from a national survey: below the population median of 21 ng/mL, higher vitamin D went with lower death rates from all causes and heart disease; above it, there was no further association (Amer 2013, human observational, median follow-up 3.8 years). That fits the view that levels above roughly 20–30 ng/mL bring little extra, and large randomised trials in people who were not deficient have mostly shown no benefit for major outcomes. It does not show that supplementing a deficient person is useless — the authors suggested trials aimed precisely at people at or below 21. Targets of 80–100 ng/mL are well above what most guidelines consider necessary.

Vitamin A and copper pumps: a cell-line finding, not a human one. One study found that retinoic acid, acting through its receptor, switches on the ATP7A copper pump in neuroblastoma cancer cells (Bohlken 2009, in vitro); we found no human study showing retinol status controls copper loading of ceruloplasmin, and no evidence on ATP7B in that paper. Vitamins A and D do interact at the receptor level, and very high intakes of one can blunt the other in animal studies, but “vitamin D blocks vitamin A uptake” in ordinary doses is unproven. The Kummerow account is a personal anecdote. Egg-yolk colour comes mostly from carotenoid pigments in the hen’s feed, not from retinol. Vitamin A deficiency does contribute to anemia, which is real. Tier: mixed — see Vitamin D Controversy.

Safety: preformed vitamin A (retinol) is the one nutrient in this story with a proven birth-defect risk. In a study of 22,748 pregnancies, women taking more than 10,000 IU a day of supplemental vitamin A had babies with more cranial-neural-crest defects (Rothman 1995). Pregnant women and those trying to conceive should not take high-dose retinol, liver-heavy diets or large amounts of cod liver oil without medical advice.

Back to Table of Contents

Iodine, and “There Is No Disease”

Robbins’s claim: iodine loading blocks copper

Asked whether everyone needs iodine, Robbins says that when he looked into iodine loading he found that it blocks copper uptake. He stresses that iodine is not “bad”; the question to ask a doctor is why you need it.

Evidence check

We found no human study showing that iodine at dietary or ordinary supplemental doses blocks copper absorption. Iodine is essential for thyroid hormone, deficiency remains common in some regions, and very high-dose “loading” carries its own thyroid risks. The question “why do I need this?” is a good one. Tier: copper interaction weak to unverified. See Iodine.

Robbins’s claim: there is no disease

Robbins says “there’s no disease” — only stress-induced mineral loss that causes metabolic dysfunction, then energy loss, then symptoms, which medicine collects and names as a syndrome. He describes cells as packed with mitochondria (thousands per liver, kidney and heart cell; hundreds of thousands in a mature egg) and calls chronic illness a cellular energy deficiency. His protocol’s motto is to ignore the enemies and “ignite the energy”.

Evidence check

Read fairly, this is an energy-and-mineral model of chronic symptoms, set against a diagnosis-first model. There is something real in it: mitochondrial energy production does depend on copper (cytochrome c oxidase), iron and magnesium, and fatigue often has several overlapping nutritional and lifestyle causes that a single diagnosis can miss. But taken literally the claim fails. Infections, cancers, genetic diseases (including Wilson’s disease, where copper itself is the poison), autoimmune diseases and blood loss are specific, testable conditions with specific treatments, and missing one of them is the main danger of any single-cause theory. A sensible use of his model is as a set of extra questions to ask alongside a diagnosis, not instead of one.

Back to Table of Contents

The Stops, the Starts and the Adrenal Cocktail

Robbins’s claim

The protocol begins with stops: stop calcium supplements, zinc supplements, vitamin D-only supplements, iron supplements, synthetic B vitamins and once-a-day multivitamins — and, half in jest, stop going to the internet for answers. Then come the starts, phased in: magnesium, whole-food vitamin C rather than ascorbic acid, organ meat, cod liver oil, animal fats and the adrenal cocktail.

His adrenal cocktail: a glass of fresh orange juice with ¼ teaspoon of sea salt and ¼ teaspoon of a potassium salt (potassium chloride or sulfate), taken mid-morning and mid-afternoon, when he says the adrenals are weakest — instead of a coffee break. A second version uses coconut water with the juice of a lime plus the salt and a whole-food vitamin C. He says adrenals should be walnut-sized but have shrunk to “pinheads” in most people, and that 95% of the body’s vitamin C is in the adrenals.

Evidence check

Several of the stops are reasonable for many people: high-dose zinc taken long term does cause copper deficiency; iron should not be taken without a documented need; calcium supplements have been debated for heart risk. But blanket stops are not safe for everyone — someone with proven iron-deficiency anemia, or vitamin D deficiency with bone disease, needs treatment. “Adrenal fatigue” is not a recognised diagnosis in endocrinology, and normal adrenals do not shrink to pinheads from everyday stress (they do shrink after long-term steroid medication). The adrenal glands hold the body’s highest concentration of vitamin C, not 95% of its total. Ascorbic acid is the vitamin C molecule itself; food is a fine source, but it is not chemically a different vitamin.

The cocktail is essentially an electrolyte drink. A quarter-teaspoon of salt supplies roughly 500–600 mg of sodium. The potassium salt is the part to respect: people with kidney disease, or taking ACE inhibitors, angiotensin-receptor blockers, spironolactone or other potassium-sparing diuretics, can develop dangerously high potassium — check with a doctor first.

Back to Table of Contents

Epsom Salt Baths

Robbins’s claim

Robbins recommends Epsom salt baths — magnesium sulfate dissolved in a warm bath — as deeply relaxing and restorative, especially after hard physical activity, to “restore the mineral status in your muscles”. Magnesium, he says, is “the chill pill”, though on its own it can only do so much. He traces the salt to a spring at Epsom in England, and in passing describes it alongside magnesium chloride “oil”.

Evidence check

A warm bath is relaxing, and that alone is a fair reason to take one. But how much magnesium crosses intact skin is poorly established: the human studies are few, small and inconsistent, and none shows that bathing corrects a magnesium deficiency or raises muscle magnesium in a way that matters. Epsom salt is magnesium sulfate; magnesium “oil” is magnesium chloride — two different salts. Food (nuts, seeds, greens, cocoa, legumes) and, where needed, an oral supplement are the proven ways to raise magnesium. Baths are safe for most people; do not drink Epsom salt casually — by mouth it is a strong laxative and can cause dangerous magnesium levels in people with kidney disease. Tier: relaxation plausible; magnesium absorption through skin poorly established. See Magnesium Sulfate (Epsom Salt).

Back to Table of Contents

The 86-Year-Old Case and the 362 Tracked Cases

Robbins’s claim

His favourite success story is an 86-year-old man with fatigue, muscle aches and poor sleep. Robbins suggested one capsule a day of a whole-food copper supplement he formulated (each capsule supplies 2 mg of copper). The man chose to take six — 12 mg of copper a day. His blood copper came back at about 205 against the roughly 100 Robbins considers typical, and the man reported that all his symptoms were gone. Robbins presents this as people being “in charge” of their own healing.

He then describes 362 formal case studies his group tracks — thyroid, blood-pressure, anemia, brain and heart complaints — with 38% complete resolution, 55% improvement and 7% no change.

Evidence check

The 86-year-old took more copper than the safety limit. The US National Academies set the Tolerable Upper Intake Level for copper at 10 mg a day for adults, from food and supplements combined, to protect against liver damage (Institute of Medicine 2001). Twelve milligrams a day exceeds it, and a serum copper of about 205 µg/dL is well above the usual laboratory range. A high serum copper is not proof of benefit: copper and ceruloplasmin also rise with inflammation, infection, pregnancy and the contraceptive pill. One man feeling better is an anecdote; the risk of a dose above the upper limit is not. Anyone with Wilson’s disease, liver disease or a family history of either must not take copper supplements.

The 362 cases are unpublished, self-reported and uncontrolled. 38% resolved, 55% improved and 7% unchanged sounds impressive, but without a comparison group there is no way to tell how much is due to the protocol, to time, to other changes people made, to the natural ups and downs of symptoms, or to the support of a coach. We do not know how cases were chosen, how “resolution” was defined, or how many people dropped out and were never counted. Tier: self-report, unpublished. It is a reason to run a proper study, not evidence in itself.

Back to Table of Contents

“Is Meat Enough?”

Robbins’s claim

The host’s closing question: is meat enough to fix your health? “No, I don’t” think so, says Robbins. Carnivore and keto diets have value, but soils and food have changed in his lifetime (he was born in 1952), and people need to broaden beyond muscle meat. He tells of his grandfather, born in 1879, out-working him on a hillside at 92. Salt alone is not enough either: it supplies sodium and chloride, not magnesium or copper, and he favours salts from many regions.

Evidence check

The nutrition point is fair. Muscle meat is an excellent source of protein, iron, zinc and B12, but it is low in copper and magnesium; liver, shellfish, nuts, seeds, cocoa, legumes and leafy greens fill those gaps, and a high-zinc, low-copper meat-only diet can tilt the zinc–copper balance the wrong way. Whether mineral content of food has fallen across the 20th century is debated; some crop analyses show declines, partly from higher-yielding varieties. The grandfather story is a family anecdote. Tier: reasonable dietary advice.

Back to Table of Contents

Key Takeaways

• Copper matters for iron. Copper enzymes are required to move iron out of cells; copper deficiency causes anemia that iron does not fix. That part of Robbins’s message is solid and under-taught.
• The full cascade is a hypothesis. Copper → iron “rust” → magnesium loss → insulin resistance and low vitamin D has never been tested as a sequence in people.
• A ferritin of 12 is real iron deficiency. Find the cause (often blood loss) and treat it; do not reinterpret it as a copper problem.
• High-dose zinc can cause copper deficiency, and acid-blocking proton-pump inhibitors can lower magnesium — both well documented.
• Vitamin D above about 21 ng/mL showed no extra survival benefit in one large observational study; that is not a reason for a deficient person to avoid treatment.
• Several claims are unverified: copper raising fetuin-A, black hair needing six times more copper, iodine blocking copper, the glyphosate “chelation scale”.
• Doses matter. 12 mg of copper a day exceeds the 10 mg upper limit; high-dose retinol is dangerous in pregnancy; potassium salts can be dangerous with kidney disease or certain blood-pressure drugs.
• The 38/55/7 outcome figures are self-reported and uncontrolled.

Back to Table of Contents

Safety

• Copper: the adult Tolerable Upper Intake Level is 10 mg a day from all sources (Institute of Medicine 2001). Copper supplements are dangerous for anyone with Wilson’s disease or liver disease. Beef liver is so copper-rich that eating it daily on top of a copper supplement can push intake past the limit.
• Vitamin A (retinol): the adult upper limit is 3,000 µg (10,000 IU) of preformed vitamin A a day; above about 10,000 IU of supplemental vitamin A in early pregnancy, birth-defect risk rose (Rothman 1995). Liver, cod liver oil and retinol supplements all count.
• Iron: true iron-deficiency anemia needs a cause found — especially blood loss from the gut in men and in women after menopause — and treatment, not iron withheld. Anemia that does not respond to iron is a reason to test copper and ceruloplasmin.
• Stopping supplements: do not stop a supplement or medicine prescribed for a diagnosed condition (iron for proven anemia, vitamin D for osteomalacia, thyroid medication) without your prescriber.
• Potassium salts and the adrenal cocktail: avoid without medical advice if you have kidney disease or take ACE inhibitors, angiotensin-receptor blockers or potassium-sparing diuretics.
• Zinc: long-term intake above 40 mg a day can cause copper-deficiency anemia and nerve damage.

Back to Table of Contents

Key Research Papers

1. Vulpe CD, Kuo YM, Murphy TL, et al. (1999). Hephaestin, a ceruloplasmin homologue implicated in intestinal iron transport, is defective in the sla mouse. Nature Genetics, 21(2):195–199. — PubMed PMID: 9988272
2. Ganz T. (2012). Macrophages and systemic iron homeostasis. Journal of Innate Immunity, 4(5–6):446–453. — PubMed PMID: 22441209
3. Camaschella C. (2015). Iron-deficiency anemia. New England Journal of Medicine, 372(19):1832–1843. — PubMed PMID: 25946282
4. Halfdanarson TR, Kumar N, Li CY, Phyliky RL, Hogan WJ. (2008). Hematological manifestations of copper deficiency: a retrospective review. European Journal of Haematology, 80(6):523–531. — PubMed PMID: 18284630
5. Hoffman HN 2nd, Phyliky RL, Fleming CR. (1988). Zinc-induced copper deficiency. Gastroenterology, 94(2):508–512. — PubMed PMID: 3335323
6. Klevay LM. (1973). Hypercholesterolemia in rats produced by an increase in the ratio of zinc to copper ingested. American Journal of Clinical Nutrition, 26(10):1060–1068. — PubMed PMID: 4754665
7. Klevay LM, Inman L, Johnson LK, et al. (1984). Increased cholesterol in plasma in a young man during experimental copper depletion. Metabolism, 33(12):1112–1118. — PubMed PMID: 6503710
8. Stefan N, Hennige AM, Staiger H, et al. (2006). Alpha2-Heremans-Schmid glycoprotein/fetuin-A is associated with insulin resistance and fat accumulation in the liver in humans. Diabetes Care, 29(4):853–857. — PubMed PMID: 16567827
9. Mertens M, Höss S, Neumann G, Afzal J, Reichenbecher W. (2018). Glyphosate, a chelating agent — relevant for ecological risk assessment? Environmental Science and Pollution Research International, 25(6):5298–5317. — PubMed PMID: 29294235
10. Cheungpasitporn W, Thongprayoon C, Kittanamongkolchai W, et al. (2015). Proton pump inhibitors linked to hypomagnesemia: a systematic review and meta-analysis of observational studies. Renal Failure, 37(7):1237–1241. — PubMed PMID: 26108134
11. Amer M, Qayyum R. (2013). Relationship between 25-hydroxyvitamin D and all-cause and cardiovascular disease mortality. American Journal of Medicine, 126(6):509–514. — PubMed PMID: 23601272
12. Bohlken A, Cheung BB, Bell JL, et al. (2009). ATP7A is a novel target of retinoic acid receptor beta2 in neuroblastoma cells. British Journal of Cancer, 100(1):96–105. — PubMed PMID: 19127267
13. Rothman KJ, Moore LL, Singer MR, Nguyen US, Mannino S, Milunsky A. (1995). Teratogenicity of high vitamin A intake. New England Journal of Medicine, 333(21):1369–1373. — PubMed PMID: 7477116
14. Institute of Medicine, Panel on Micronutrients. (2001). Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. National Academies Press. — doi:10.17226/10026

PubMed Topic Searches

1. PubMed: Copper deficiency anemia
2. PubMed: Zinc-induced copper deficiency
3. PubMed: Ceruloplasmin, ferroxidase and iron export

Back to Table of Contents

Connections

• All Notable Doctors
• Morley Robbins
• Root Cause Protocol
• Copper–Iron Dysregulation
• Iron Overload and Hidden Toxicity
• Ceruloplasmin and Bioavailable Copper
• Magnesium Replenishment
• Vitamin D Controversy
• Glyphosate and Copper Chelation
• Whole Food Copper Sources
• Adrenal Cortisol and Mineral Connection
• Cure Your Fatigue
• Copper
• Iron
• Magnesium
• Zinc
• Iodine
• Vitamin A
• Vitamin D3
• Ferritin Test
• Ceruloplasmin Test
• Anemia
• Insulin Resistance
• Wilson’s Disease
• Glyphosate

Back to Table of Contents

Featured Videos