Thoughts on Wilson’s Disease

The current treatment for Wilson’s Disease is one chemical chelator, and zinc.

In wild controversy that made a Wilson’s Disease Associate resort to censoring my post, and blocking me, I suggest several natural chelators, and a few more minerals. Why not the full list, here:

It is an interesting controversy I’m creating. Should Wilson’s disease patients take copper or not? I think so. I think the evidence is on the weight to take copper. I see no mechanism of action for how copper could cause nerve problems when copper actually restores the myelin sheath and increases neurotransmitters, and detoxes nerve poisons like fluoride that bind to copper. Taking clean copper would be the solution, not the problem. Also, Wilson’s disease is characterized by low serum copper and low cereloplasmin, both markers of copper deficiency. Copper is needed to fix both of those problems, and fluoride causes both of those problems, and copper detoxes fluoride.

Research challenge. Prove that copper is toxic. Not provide a reference where someone expresses that opinion. But prove that copper is toxic, with both reasons and evidence, to a level of proof say, “beyond a reasonable doubt”.

Here is another challenge for my friends who are good at research. Can you find a single example or case study of copper supplements causing Wilsons disease, or a person who had Wilsons disease who took copper supplements that then made it worse?

I could not find either example.

Today, I got another insight from my studies on copper and how it detoxes fluoride, and on how fluoride strips copper…

Posted by Jason Hommel on Saturday, May 16, 2020

Today, I got another insight from my studies on copper and how it detoxes fluoride, and on how fluoride strips copper from pipes. See:

Wilson’s disease is said to be a disease of “high copper”. 1 in about 30,000 people have it. It’s said to be genetic. The solution is said to be a chelator and zinc, which should, in theory lower the copper. But the mystery is that this does not work very well.

I think I have solved this mystery. What if it’s not copper that is the problem? What if it’s copper in the water from copper pipes, and the copper from the pipes only leaches into the water when the water is loaded with fluoride? What if it’s not “high copper”, but high “copper fluoride” that is causing Wilson’s disease? If this is the case, then trying to “lower copper” is the exact wrong solution to the problem. The solution would be to provide clean copper, so the body can let go of the copper/fluoride. And the solution would be to provide other fluoride detoxifiers, such as iodine, boron, copper, calcium, phosphorous, etc.

Here is the far bigger problem. There is nobody in the world to tell this to.

Doctors, you can’t tell them, they are not interested. They want sick people.
I joined a Wilson’s disease online group, and they are not interested. They ban people for even proposing solutions. So, I post here, to my facebook page. Any suggestions?


Updated thought. If copper binds to fluoride, what other metal toxins does copper bind to? Is this why the standard methods ‘chelation’ and zinc, tend to work for Wilson’s, because chelation tends to remove toxic metals other than copper, along with copper?


All of the other problems listed in people with Wilson’s Disease here, appear to be signs of fluoride toxicity. Low bone density, endocrine problems, kidney problems, growth disorders, hypothyroidism (low iodine from high fluoride) liver problems, etc.


Furthermore, Wilson’s is said to be a disease of “high copper”, but they have low copper in the blood. And copper coming out in the urine. This, to me, indicates that the body needs more copper, not less, and that the body is consuming what copper it does have, to detox fluoride. Several other indicators of high fluoride are in the description of the diagnosis of Wilson’s disease: Increased bleeding time, and low phosperous. I had just discovered last week that the molecule more stable than Copper (2) fluoride is one with a phosperous atom added. Wilson’s disease people are also low in cereloplasmin, which, to me, means they need molybdenum. Sure enough, they do use a chelator that has molybdenum in it to try to help eliminate the supposed “high copper”.

I messaged the WDA, Wilson Disease Association: Here is the dialog:

ME: I see that my post was deleted. Was there a reason that you allow posts, but deleted my posts?

WDA: We have the right to delete any posts that we deem necessary to delete.

ME: Well of course you do. It’s your page. I’m not an idiot. I asked you for the reason. The reason why I’m asking for a reason is that I’m wanting and trying to be helpful. And I’m looking for a discussion.

WDA: You don’t know anything about Wilson’s disease and what you posted is just wrong and bad information. We protect our patients

ME: How often do you test wilson’s disease patients for fluoride toxicity?

ME: Do you dispute that copper binds with fluoride?

Copper(II) fluoride – Wikipedia
Copper(II) fluoride is an inorganic compound with the chemical formula CuF2. It is a white crystalline, hygroscopic solid with a rutile-type crystal structure, similar to other fluorides of chemical formulae MF2 (where M is a metal).

ME: So, what specifically is wrong about my information?

Time passes…

ME: The fact that you appear incapable of responding intelligently indicates to me that you are toxic with fluoride yourself.

WDA: I do not have Wilson’s and I am not toxic with flouride

ME: Intelligent people are often capable of responding with what are called reasons. Not accusations. For your information.

ME: Great. Please respond with reasons. What specifically about my information is bad?

ME: Do you dispute that copper binds with fluoride?

ME: Do you dispute that the put fluoride in the national water supply?

WDA: It’s late and I am not going to argue

ME: Do you dispute the fluoride in the water binds with and leeches copper from the pipes?

ME: It is late. I’m excited by my discovery. I do not appreciate being treated badly by you today. That energizes me.

ME: You can try intelligent dialog tomorrow.

Right after I posted that, a dialog began on my facebook. I’ll share some of it:

Marianne Tysinger Collins In Wilson’s Disease, the liver does not produce enough ceruloplasmin or sometimes none at all. Ceruloplasmin binds with copper to remove excess from the body bit without it, there is an excess of free or non protein bound copper. This causes brain damage and liver damage. And yes serum bound copper is low, not high. Nothing to do with flouride. But yes sometimes we use drugs with molybdenum in it as it creates a loose binding with copper so that it isn’t as dangerous. Still it is not enough to prevent oxidative damage.

Jason Hommel Marianne Tysinger Collins Thank you so very much for your wonderfully intelligent reply. I found that molybdenum increases cereloplasmin. Also exercise increases it. And maybe vitamin A, but I was not yet able to confirm Vitamin A with a scientific study like the other two, exercise and moly. Most of the high copper studies I ran across study high copper in people, generally from water. That is from fluoride in the water stripping the copper from the pipes.

Jason Hommel Marianne Tysinger Collins Do you test for fluoride in people with Wilsons disease?

Marianne Tysinger Collins Jason Hommel no we do not

Jason Hommel Marianne Tysinger Collins Then how do you know that fluoride has nothing to do with it, as you say?

Marianne Tysinger Collins Jason Hommel “We are laughing”…

Jason Hommel Marianne Tysinger Collins It would be easy to prove me wrong. Prove that fluoride in the water does not pull copper from the pipes. Prove that fluoride does not attach to copper and would not follow copper into the liver, brain, and bones to cause fluoride damage. I pity you and your scorn for knowledge.

Marianne Tysinger Collins We did not have fluoridated water. I am not asking for pity.

Jason Hommel Marianne Tysinger Collins oh. A dialog. Fluoride is found in chicken dired fruits, grapes, teflon pans, goretex, dental floss, and fluoride treatments at the dentist. Fluoride is everywhere, even fresh cherries.

Jason Hommel Marianne Tysinger Collins fluoride in water is 0.7 ppm. Chicken feed is 135 ppm fluoride.

Note, there were 3 dialogs with Marianne going at once. She blocked me. So she might not have seen my last two comments.

Sally Berry The function of Asea is to normalize intracellular communication. Wilson’s is due to copper homeostasis dysfunction. Returning the cells to balance may be the answer, and that is what redox signaling molecules do. The FDA mandated disclaimer is: Asea does not diagnose, treat, remedy, or cure any medical condition. <- There the muzzle is in place.

Marianne Tysinger Collins Sally Berry we will stick to proven treatments. Wilson’s is ALWAYS fatal if not treated appropriately.

Sally Berry Marianne Tysinger Collins Homeostasis is a proven result of drinking redox signaling molecules. It does not discriminate and treat sliced and diced symptoms , it goes to where the imbalance is and normalizes the function on a system by system basis bar nothing. And of course to each his own.

Marianne Tysinger Collins Sally Berry yes I prefer to stick with information from scientists and doctors who specialize in this very rare liver disease.

Jason Hommel Marianne Tysinger Collins I would be more than happy to offer a free consult to any doctor or scientist you may know who specializes in Wilsons disease.

Jason Hommel The state of the world is so utterly biased against new information. Yet, the world bemoans that nobody has the solutions to major problems.

Marianne Tysinger Collins Jason Hommel there’s nothing wrong with new information but I will not change current proven treatments until new treatments have been investigated and trials been performed.

Jason Hommel Marianne Tysinger Collins . Trials are for criminals and toxic drugs. Copper iodine, etc. Are not toxic, and are available as supplements just like foods, and you do not need a prescription. Do you need a clinical trial before putting salt on eggs? Do you even know how utterly insane that sounds to rational people?

Jason Hommel Marianne Tysinger Collins Im not sure you understand the economics of what you think should happen. Clinical trials cost up to $100 million. Who would spend that so anyone could sell non patentable minerals to a few people with Wilsons, which could hurt sales of drugs to that very same group?

Jason Hommel Marianne Tysinger Collins was the moderator for the online facebook group: She blocked my post there, and she was likely the person who very half heartedly responded there, and finally came here when I posted the dialog exchange, up above. She ended up facebook blocking me last night.

My notes from this morning’s research: Copper deficient diets in rats lead to a situation found in Wilson’s Disease. Compare the following two statements:
The rats were raised in a copper-deficient diet and the vitamin A level was regularly determined. In these conditions serum and liver levels of vitamin A are normal and do not vary, ceruloplasmin level is zero; however apoceruloplasmin is still being synthetized
In Wilson’s from the wiki on Wilson’s:CeruloplasminLevels of ceruloplasmin are abnormally low (<0.2 g/L) in 80–95% of cases.[5]
“Both functions of ATP7B are impaired in Wilson’s disease. Copper accumulates in the liver tissue; ceruloplasmin is still secreted, but in a form that lacks copper (termed apoceruloplasmin) and is rapidly degraded in the bloodstream.[10]”
Furthermore, the wiki confirms Wilson’s patients are low in copper:
Serum and urine copper Serum copper is low, which may seem paradoxical given that Wilson’s disease is a disease of copper excess. However, 95% of plasma copper is carried by ceruloplasmin which is often low in Wilson’s disease.
Furthermore, Wilson’s patients can’t have a “problem” of not excreting copper, because they excrete an excess:
Urine copper is elevated in Wilson’s disease and is collected for 24 hours in a bottle with a copper-free liner. Levels above 100 μg/24h (1.6 μmol/24h) confirm Wilson’s disease, and levels above 40 μg/24h (0.6 μmol/24h) are strongly indicative.[5] High urine copper levels are not unique to Wilson’s disease; they are sometimes observed in autoimmune hepatitis and in cholestasis (any disease obstructing the flow of bile from the liver to the small bowel).[12]
If Wilson’s patients excrete an excess of copper, then how can it be said to “build up” or be a problem of excess?
They are said to have an excess copper in the liver.
Biopsies “confirm”, but not always? If there is not always excess copper in their livers, then how can excess copper be a causal mechanism of action, that makes no sense.
From wiki: “A level of 250 μg of copper per gram of dried liver tissue confirms Wilson’s disease.”
And what are normal copper levels?

“A normal hepatic copper concentration (<50 μg/g) almost always excludes a diagnosis of Wilson’s disease.”
So, the copper excess said to cause all of these problems is 500% greater!
From the wiki again: “A level of 250 μg of copper per gram of dried liver tissue confirms Wilson’s disease. Occasionally, lower levels of copper are found; in that case, the combination of the biopsy findings with all other tests could still lead to a formal diagnosis of Wilson’s.[5]”
I don’t understand how the disease can be genetic from birth, but problems don’t show up until people reach age 20-40. That makes no sense.

COPPER DEFICIENCY IN WILSON’S DISEASE article unavailable to the public.

Serum copper normal range: “a range for normal copper status include serum copper (normal range 0.64-1.56 ug/ml)”
This is a variability of up to nearly 243% from low to high! 1.56/.64 = 2.43.
A 243% variability of copper in the serum is normal.
What is low Wilson’s copper serum level?
Found it: a Wilson’s diagnosis:Serum ceruloplasmin Normal (>0.2 g/L) 0 0.1–0.2 g/L 1 <0.1 g/L 2A similar article copying much of the prior article:
“Serum and urine copperSerum copper is low, which may seem paradoxical given that Wilson’s disease is a disease of copper excess.”
Wow. The liver uses copper to make cereloplasmin!
“Thus the liver utilizes some copper for its metabolic needs, including synthesis and secretion of ceruloplasmin (a copper containing protein) which is also involved in iron metabolism”

Key Questions.
How can copper cause nerve damage or brain damage when copper heals the nerves in several ways: restores the myelin sheath, and increases neurotransmitters.

How can copper cause bone problems, when copper heals the bones in several ways; helps the body make stronger bones, and helps the body convert iron into blood cells in the marrow?

It appears as if these problems are more explained by copper deficiency rather than copper excess.

If Wilson’s patients have a problem of excess copper excretion in the urine, why are they given a chemical chelating agent, Penicillamine, which increases copper excretion in the urine by up to ten times greater values? That is so obviously wrong, and is actually reported as making people worse off, and causes symptoms of copper deficiency, such as lack of collagen formation.

Current therapy for Wilson’s is chemical chelators and one mineral.

Why would natural chelators and many natural minerals be considered worse or crazy or insane, instead of the more rational approach?

Natural chelators: greens, distilled water, coffee, and many minerals are actually copper chelators, specifically, not only zinc, but also, iodine, sulfur, and many others.

Natural minerals: iodine, sulfur, zinc, moybdenum, etc.
The following list of things I have found lower copper:

Vitamin C


having high iron








sweating heavily

drinking distilled water

watermelon (glutithione)

curry chicken

From my article:

Curcumin binds copper:

How would copper even harm the liver in the first place?


“Copper may damage liver cells and other cells in the body by causing the formation of activated chemical intermediates.”

That is exactly what I’m saying. Copper binds to fluoride, a toxin. What other toxins might bind to copper?

If the body is loaded with toxins, and if the body’s available copper is being used to bind those toxins, then the answer is more copper, or other minerals that can detox the body, to flush out and chelate those toxins.

But what is running counter to my theory is the Kayser-Fleischer rings, copper rings in the eyes. Might that be toxin bound copper? Unknown.

Join the conversation


  1. Wow. My thoughts of the danger of the fluoride, not the copper, from the drinking water that contains fluoride that leeches the copper from the pipes, is all echoed in this article here from the very entity that set the limit of 10mg/day on copper, the Food and Drug Board:
    And they mention Wilson’s disease several times!

    Allowable Levels of Copper in Drinking Water Should Not Be Increased Until Studies Are Done
    News Release | March 2, 2000
    WASHINGTON — The federal government should not increase the maximum level of copper allowed in drinking water, because higher levels could lead to liver poisoning in infants and children with certain genetic disorders, according to a new report from the National Academies’ National Research Council. Instead, the government should conduct studies on the health effects of copper in these sensitive populations, the committee that wrote the report urged.

    Under the Safe Drinking Water Act, the Environmental Protection Agency (EPA) is required to establish the concentrations of contaminants that are permitted in public drinking water supplies. EPA has set a goal for copper at a maximum allowable level of 1.3 mg per liter of drinking water, to protect against short-term gastrointestinal tract problems. However, some states, such as Nebraska and Delaware, have difficulty maintaining copper levels below this goal.

    Because some recent population studies have reported no adverse health effects from ingesting copper at higher concentrations, questions have been raised about the validity of the science on which EPA based its goal for drinking water. Some people believe that the goal might be unnecessarily low, and others believe that some individuals might get sick from copper levels at or below EPA’s current goal. In response to these concerns, Congress asked the Research Council for an independent review of the scientific and technical basis for EPA’s goal for copper in drinking water.

    Too much copper can cause several health problems, the committee said. Excessive doses can cause nausea, vomiting, and diarrhea. Long-term exposure can lead to copper poisoning, especially in people whose bodies have trouble regulating copper because of certain genetic disorders or illnesses, such as Wilson’s disease. Severe cases of copper poisoning have led to anemia, liver poisoning, and kidney failure.

    “We reviewed a wide range of data on exposure to copper from both food and water and concluded that EPA’s current level protects sensitive individuals from the acute effects of excess copper,” said committee chair Richard Bull, senior staff scientist, Battelle Pacific Northwest Division, Richland, Wash. “We assume this level is protective to people with chronic disease, as well. But we need more information about the total copper doses received from drinking water, along with a better idea of how many people are sensitive to copper and what happens to them when they are exposed. Once this information has been gathered, the current level should be re-evaluated. We don’t know enough to change it right now, but if it is raised, there may be harm done to children with a defective gene.”

    In the past, people with Wilson’s disease, which is caused by a defect in a gene that is important in eliminating excess copper from the body, were considered such a small and special portion of the population that it was thought best to protect them by limiting their copper intake individually. However, new evidence suggests that brothers and sisters of people with Wilson’s disease also may be at risk, even though they do not have the disease themselves. This in turn suggests that carriers — people with one copy of the defective gene — also could be at risk.

    Children who carry the gene would be at particular risk because their consumption of water is greater than adults in proportion to their size. Although Wilson’s disease is found in only 1 out of 40,000 people in the United States, the committee believes that as much as 1 percent of the population may carry the gene for the disease. But there is no test available yet to identify individuals that could be at risk.

    Copper is an essential mineral nutrient that is found in soil and plants. Most copper contamination in drinking water is the result of corrosion of copper pipes or fittings. Corrosion can occur from water that is high in acidity and high in temperature. Corrosion also can be caused by water that is “soft,” or free of magnesium or calcium salts that create a protective coating inside the pipe.

    In 1989 the Institute of Medicine estimated that adults could safely ingest 1.5 to 3.0 mg of dietary copper per day and infants could consume 0.4 to 0.6 mg per day to maintain good health. Generally, the copper that people ingest through their daily diet falls within this range, and typically only a small fraction of an individual’s copper intake comes from drinking water. However, water characteristics in some states and municipalities are conducive to greater leaching of the mineral into drinking water. The length of time that water sits in copper pipes also can greatly increase the mineral’s concentration to several milligrams per liter of water. The concentration of copper decreases in water that has been running from the tap for a few minutes.

    The committee’s work was funded by the EPA. The National Research Council is the principal operating arm of the National Academy of Sciences and the National Academy of Engineering. It is a private, nonprofit organization that provides advice on science and technology under a congressional charter. A committee roster follows.

    Read the full text of COPPER IN DRINKING WATER for free on the Web, as well as more than 1,800 other publications from the National Academies. Printed copies are available for purchase from the National Academy Press Web site or at the mailing address in the letterhead; tel. (202) 334-3313 or 1-800-624-6242.


    Bill Kearney, Media Relations Associate
    Megan O’Neill, Media Relations Assistant
    (202) 334-2138; e-mail

    Commission on Life Sciences
    Board on Environmental Studies and Toxicology

    Committee on Copper in Drinking Water

    Richard J. Bull, Ph.D. (chair)
    Senior Staff Scientist
    Molecular Biosciences Department
    Battelle Pacific Northwest Laboratory
    Richland, Wash.

    Michael Aschner, Ph.D.
    Professor of Physiology and Pharmacology
    Wake Forest University School of Medicine
    Winston-Salem, N.C.

    George J. Brewer, M.D.
    Departments of Human Genetics and Internal Medicine
    University of Michigan
    Ann Arbor

    Edward D. Harris, Ph.D.
    Department of Biochemistry and Nurtition
    Texas A&M University
    College Station

    Carl L. Keen, Ph.D.
    Department of Nutrition
    University of California

    Karl T. Kelsey, M.D.
    Departments of Cancer Cell Biology and Environmental Health
    Harvard School of Public Health

    F. William Sunderman Jr., M.D.
    Visiting Scholar
    Department of Chemistry and Biochemistry
    Middlebury College
    Whiting, Vt.

    Joyce S. Tsuji, Ph.D.
    Bellevue, Wash.

    Lauren A. Zeise, Ph.D.
    Reproductive and Cancer Hazard Assessment Section
    California Environmental Protection Agency


    Carol A. Maczka, Ph.D.
    Study Director

  2. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc

    p. 229: “Several indicators are used to diagnose copper deficiency. These indicators—serum or plasma copper concentration, ceruloplasmin concentration, and erythrocyte superoxide dismutase activity—are low with copper deficiency and respond to copper supplementation”

    p. 230: “Serum copper concentration is a reliable indicator of copper deficiency, falling to very low concentrations in copper-deficient individuals.”

    “Ceruloplasmin concentration is also a reliable indicator of copper deficiency. Ceruloplasmin carries between 60 and 95 percent of serum copper, and changes in serum copper concentration usually parallel the ceruloplasmin concentration in the blood. Ceruloplasmin, too, falls to low concentrations with copper deficiency, far below the lower end of the normal range of 180 mg/L, and it responds quickly to repletion (Danks, 1988).”

    p. 233 Copper Balance // Balance studies have been used in the past to estimate dietary recommendations. Numerous copper balance studies in humans have been conducted over a wide range of intakes (Mason, 1979). Unfortunately, there are a number of problems with this approach, as reviewed by Mertz (1987). Copper balance, which can be achieved over a broad range of dietary copper intakes, reflects prior dietary intake; thus long adaptation is required for results to be meaningful. Seldom are studies long enough. Such studies are prone to numerous errors, and data from some studies would suggest that an unacceptable amount of copper would accumulate over time if these levels of retention were continued. In addition, miscellaneous losses, while small, are very difficult to quantify. Therefore, balance studies were not used as an indicator of copper status.

    p. 234 Zinc: “This zinc-induced inhibition of copper absorption could be the result of competition for a common, apically oriented transporter or the induction of metallothionein in intestinal cells by zinc. Because this protein has a higher binding affinity for copper than for zinc, copper is retained within enterocytes and its absorption is reduced.”

    “High iron intakes may interfere with copper absorption in infants.”

    p. 237-8: Human milk contains 250 mcg/L of copper. Cows milk contains 60-90 mcg/L. “Copper deficiency has been observed in infants fed cow milk (Cordano et al., 1964; Levy et al., 1985). ”

    p. 240: “Platelet copper concentration, however, declined significantly for eight of ten women fed 570 µg/day and increased with supplementation.”

    “While an EAR based on the first two studies was estimated at 550 µg/day, the latter study suggests that 600 µg/day may be a marginal intake in over half of the population. Therefore, another increment was added to cover half of the population, and the EAR was set at 700 µg/day.
    ” This seems crazy to me. They know 580 is too low, so they arbitrarily move the number to 700??! Where is the science? Where is the testing? Why did they not say what the supplementation level was to fix the deficiencies at 0.57 mg/day

    p. 241: They do something very weird. On either copper restricted diets, or zero copper diets, they try to estimate copper losses. They they imagine this might be a lower minimum. But this fails to take into account that the body might (and actually does) hold on to copper more tightly under such conditions. IE, more copper is absorbed, at a higher percentage, when copper deficient. So, they are measuring copper excretion in copper deficient people.

    “There are no data on obligatory copper losses in healthy people” This is troubling. It’s as if they have avoided looking at normalcy, on purpose.

    p. 242: “Other losses, such as hair, nails, semen, or menstrual, have not been measured, and it is assumed they are similar to surface losses. Therefore the amount of absorbed copper needed to replace obligatory losses is 344 µg/day (240 + 20 + 42 + 42). Copper absorption at this level of intake is approximately 75 percent. Therefore, 460 µg/day of dietary copper would be the minimum amount required to replace obligatory losses. Endogenous fecal copper was 50 µg/day higher at 380 µg/day than at 460 µg/day, and so 50 µg/day was added to endogenous fecal losses to account for the increase that occurs between 380 and 460 µg/day. Thus 510 µg/day (460 + 50) of dietary copper is required to replace copper losses from all sources and to achieve zero balance.”

    My comment: they are specifically trying to come up with a minimum daily intake (EAR Estimated Average Requirement) that will be too low and create deficiencies; and they already know a higher level 580 ug/day or 0.58 mg creates deficiencies in 8/10 women! Problems. Copper comes out in the hair at high concentrations, and hair is not measured. Copper goes into the skin as copper is used to create a tan. Copper is therefore used up more when tanning. They are not measuring copper being used up through exercise, or copper being blocked by other supplements. This is HORRIFIC science. Well, it is government science.

    p 242,243: “The data available to set an EAR are limited for men and women, as well as the number of levels of dietary copper in depletion/repletion studies. Thus, a CV of 15 percent is used. The RDA is defined as equal to the EAR plus twice the CV to cover the needs of 97 to 98
    COPPER 243
    percent of individuals in the group (therefore, for copper the RDA is 130 percent of the EAR). The calculated RDA is rounded to the nearest 100 µg.
    RDA for Men 19–50 years 900 µg/day of copper 51–70 years 900 µg/day of copper > 70 years 900 µg/day of copper
    RDA for Women 19–50 years 900 µg/day of copper 51–70 years 900 µg/day of copper > 70 years 900 µg/day of copper”

  3. I carefully read the reasoning of how the government came up with the RDA for copper. The reasoning is so absurdly flawed in so many ways. They set the minimum based on assuming with many wrong assumptions, that 510 mcg would be a minimum. They tested 570 mcg for women, and 8 out of ten had deficiency symptoms at that level. So they just arbitrarily set the RDA at 900 mcg, with no further testing or reasoning.

    A standard american diet provides 1.1 to 1.6 mg of copper. A pound of liver contains 64 mg of copper.

    An infant typically gets 250 mcg of copper from breastfeeding.

    A 200 pound man might need 20 times as much. Or more during hard exercise. That would be 5 miligrams minimum.

    A far better way to estimate your intake needs would be to look at what copper does. And to keep taking more, slowly, until symptoms related to those things disappear.

    Copper makes skin pigment to tan. Copper makes energy. Copper makes the master hormone DHEA. Copper fixes nerves. Copper boosts neurotransmitters.

    And I think copper detoxes fluoride.

    The government recommendations for copper are less scientific than every pronouncement about the covid. Thats very, very bad.

  4. Another insight. Wilson’s disease sufferers have low to no cereloplasmin.

    The obvious question is formed once on the right track. Hard to know what questions to ask if you are not on the right track.

    Does fluoride lower cereloplasmin? I looked it up. Yes.


    The present study describes the effect of fluoride (10 mg NaF/kg body weight/day) on the total protein-bound sialic acid and ceruloplasmin levels in rabbit serum after receiving sodium fluoride intragastrically for 3, 5, 8 and 10 months. The total protein-bound sialic acid and ceruloplasmin levels in serum were reduced, whereas the fluoride levels were increased showing a cumulative effect. It is suggested that the decreased circulatory sialic acid and ceruloplasmin levels with increased serum fluoride may be used in an early detection of fluorosis.

  5. Found another study. Copper and Moly protect against fluoride being deposited in the bones of rabbits.

    Beneficial Effect of Copper Supplementation on Deposition of Fluoride in Bone in Fluoride- And Molybdenum-Fed Rabbits

    And! Fluoride lowers serum copper!

    “serum Cu was significantly lower in the F and F + Mo than the C and F + Mo + Cu groups”

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