Chapter 40: (USA) Upper Limit for copper: 10 mg – another scam

This is the official U.S. Government’s recommendation on RDA and upper limits for copper, and a wide array of nutrients, it’s the same 773-page book.
https://www.nap.edu/read/10026/chapter/9#248
You can download a FREE pdf! (Not that their recommendations are worth anything.)

There are a few ostensible “reasons” why they set the tolerable upper human limit for copper at 10 mg. Some other writers, like myself, see it as totally arbitrary, and due to a lack of reasonable evidence. What they do have is conflicting data, and only one possible dangerous data point. This case study:

“At higher doses, acute liver failure was reported in one subject, who had no known genetic defect in copper homeostasis, after consuming 30 mg/day of copper from supplements for 2 years, followed by 60 mg/day for an additional but unspecified period of time (O’Donohue et al., 1993).”

In other words, they have ONE CASE STUDY. There is no large body of studies showing liver damage in humans who take copper supplements within a certain range. There is no large body of studies showing liver damage in humans who take copper at high doses with all of the other co-nutrients that I’m taking that work to lower copper. There is nothing. In other words, the scientific method has never been applied to determine a tolerable upper human limit for copper.

This case study was never repeated. It is unscientific and unconfirmed.

In fact, since 1993, 28 years ago now, they have not followed up on their own recommendation on p. 252:

“Define the adverse effects of chronic high copper consumption for establishing upper intake levels and to evaluate the health risks of copper supplements.”

This is utterly shocking. No follow-up now in 28 years! We live in the age of information. No follow-up? The government has nearly unlimited funding. They can’t hire anyone to keep up with nearly 110,000 studies on copper published since 1993, nearly three times as many studies as they had back in 1993, of only 31,547 studies in PubMed? Was the internet even available back in 1993? Hardly. It was the age of bulletin boards, AOL, and slow dial-up speeds! Netscape was released in 1994. Even Google was not created until 1998!

No further studies since 1993 is an example of “willful ignorance”. In legal terms, wilfulness carries with it extra penalties.

So this one case study must be extremely important. It is simply unavailable, except the abstract, as follows:

A case of adult chronic copper self-intoxication resulting in cirrhosis
https://pubmed.ncbi.nlm.nih.gov/10383882/

Abstract: “Copper “supplements” taken in a dose of 30-60 mg/day during 3 years caused severe liver cirrhosis necessitating orthotopic liver transplantation.”

As nearly every scientist knows, causation is extremely difficult to determine. And you generally need a large population, interventions, and placebos, and the researchers and participants must be blind to know who gets the placebo, and even then, causality is still difficult to determine. It is impossible to determine causality from a single case study. Therefore, the phrase “caused severe liver cirrhosis” in the one-line case study is another lie.

So, there is no other information on this case study.
No information on what drugs he took. Many drugs can cause liver disease.
No information on whether he was an alcoholic. Alcohol can cause liver disease.
No information on what diseases he had.
No information on what other supplements he took, or did not take.
No information on whether he had pre-existing liver disease, and was trying to cure it with copper.

When I was in college, I heard several stories of young men who died from liver disease. It was all alcohol-induced and happened to the guys who chronically drank 20-40 beers a day or more every day of the week.

Where are the thousands of reports of damage from copper supplements? There are none.

As it turns out, I have been taking over 10 mg of copper, on average 20-30 mg for the past four years now.

I have been taking over 70 mg copper every few days, for the past year now, as my studies encourage me to take more copper, and as I take more, the better I feel.

I AM ALIVE! My wife has done the same. My WIFE IS ALIVE. We are a counter case study. We can actually testify.

My wife HAD liver damage. I was an alcoholic, associated with liver damage, (now nearly 10 years sober).

Neither of us has any signs of liver damage.
Neither of us drinks any alcohol.
Neither of us takes any pharmaceutical drugs.
The whites of our eyes are very white, not yellow, and not bloodshot.
We take plenty of other supplements, and here is a list:
https://revealingfraud.com/2020/08/health/minerals-and-vitamins-im-actually-taking/

We take Iodine, Selenium, Boron, Sea Salt, MSM Sulfur, Potassium, Copper, Magnesium, Vitamin C, B complex, B12, Zinc.

Occasionally, we take iron, molybdenum, chromium, potassium iodide (stronger iodine), calcium, colloidal gold, vanadyl sulfate, colloidal silver, Diatomaceous Earth (Silica), Pantothenic Acid, Niacin.

Our “test” of taking copper in the range that the “case study” did, 30 mg/day, invalidates their conclusion. That is the nature of science. You repeat the experiment, and if you get different results, then you disproved the prior assertion.

The case study is a lie, then, for two reasons. You cannot determine causality from a case study. And our experience invalidates the claim.

It appears possible that this case study claim (that copper causes liver damage) is entirely fabricated. Maybe there was no man at all.

Copper actually cures liver problems. Copper is found in the liver, and copper has a wide array of healing properties and no plausible toxic mechanisms of action. See the chapters on liver disease and the section on copper toxicity.

There were two copper intervention studies in humans, mentioned by the government; one at 7 mg/day the other at 10 mg/day. Neither study noted any liver damage.

From Olivares, 2005, who did further intervention studies, giving 10 mg copper and 20 mg copper in healthy subjects over 60 days:
https://academic.oup.com/jn/article/135/10/2367/4669830

“The UL is not a precise estimate of safe, chronic copper doses in humans; rather, it is based on estimates derived from usual dietary exposure multiplied by a factor of 10, considered a reasonable default value in the absence of specific dose-response evaluations.”

I will go further. The UL of 10 mg showed no adverse events. The government had never studied any amount over that. This does not imply that 11 is dangerous, nor 15 mg, nor 20 mg, nor 30 mg, nor 40 mg, nor 50 mg, nor 60 mg all way up to amounts that real toxicologists have determined cause poisoning, which is around 10,000 to 20,000 mg. The only evidence of an adverse event above 10 mg, before we get to 10,000 mg, is this one famous case study. And as every student who takes statistics in college knows, you cannot draw conclusions about causality from a single case study.

Oh, there is a second case study. One man took 2000 mg copper per day for 4 months. He developed a blood disorder, but no liver damage. If copper caused liver damage, surely it would have shown up in the man taking nearly 100 times more copper than the first guy. So it doesn’t. That second case study is below this other study.

(Olivares, 2011) also went further:

Risks and benefits of copper in light of new insights of copper homeostasis (2011) Olivares
https://pubmed.ncbi.nlm.nih.gov/21342755/

Abstract
Copper is an essential micronutrient involved in a variety of biological processes indispensable to sustain life. At the same time, it can be toxic when present in excess, the most noticeable chronic effect being liver damage. Potent, efficient regulatory mechanisms control copper absorption in the digestive tract and copper biliary excretion; absorption ranges between 12 and 60% in humans, depending on Cu intake, presence of other factors in the diet that may promote or inhibit its absorption and on the copper status of the individual. Current evidence suggests that copper deficiency may be more prevalent than previously thought, while copper toxicity is uncommon under customary daily life conditions. Menkes syndrome and Wilson disease are genetic conditions associated with severe copper deficiency and severe copper toxicity, respectively. Effects of milder degrees of copper deficiency and excess copper exposure are not well described, mainly due to lack of sensitive and specific indicators; serum copper concentration and ceruloplasmin are the most frequently used indicators, but they only detect rather intense changes of copper status. Of the many proteins assessed as potential markers of copper status the chaperone of Zn-Cu superoxide dismutase (CCS1) has yielded promising results; data on its performance under different conditions are needed to confirm its use as an indicator of early copper deficiency. Defining copper requirements and upper safe limits of consumption (UL) is a complex process since there are adverse health consequences from both copper deficiency and copper excess (U shape curve). The regulatory framework for risk assessment of essential trace elements introduced by the International Programme on Chemical Safety (IPCS) has proposed a homeostatic model to determine the Adequate Range of Oral Intake (AROI) of essential trace elements; the nadir of the resulting U shape curve serves to define the AROI. At this range of intake physiological mechanisms allow for normal homeostasis and basically, there are no detectable adverse effects. At present, Recommended Dietary Intakes (DRIs) and Adequate Intakes (AIs) are used to recommend copper intakes at different ages and life situations. Evidence obtained in humans and non-human primates presented here suggest that current copper UL should be re evaluated. Developing the scientific basis for a copper UL and evaluating the relevance of copper deficiency globally are future key challenges for copper researchers.

“Evidence obtained in humans and non-human primates presented here suggest that current copper UL should be re evaluated. Developing the scientific basis for a copper UL and evaluating the relevance of copper deficiency globally are future key challenges for copper researchers.”

So, I’m not the only one saying the government’s upper limit on copper is worthless. Thank you Olivares!

So, “Homeostasis” means “no change”. In other words, they are saying that if you excrete as much copper as you take in, then you are in balance, and you should be good. In my opinion, there are way too many assumptions with that approach. If most of the excess copper is helping to excrete other toxins, then the excess copper might not be available for body processes. We might need more copper just to detox fluoride.

In a series of case reports on copper toxicity, one man took 2,000 mg of copper per day for 4 months, and lived. The adverse outcome was that his red blood cells started dying faster than they could be made (hemolytic anemia).

Source: https://www.ncbi.nlm.nih.gov/books/NBK225400/table/ttt00001/
“≈ 400 g of CuSO4 in water over a 4-mo period (≈ 2 g Cu per day) (2000 mg / day) Resulted in: Abdominal pain, hemolytic anemia”
Note: There was no mention of any liver damage!

So. How can 30 to 60 mg of copper “cause” liver damage if 2,000 mg of copper per day, over 4 months, did not? Again, this is evidence that the case study of the 30-60 mg of copper is a lie.

Here is another case of high copper intake, and no liver damage.

“Mittal 1972 M, 22 yr, 1 Oral ingestion of ≈ 175 g of CuSO4 (≈ 70 g Cu) Severe abdominal pain, vomiting, diarrhea starting 1.5 hr post- ingestion; renal damage with hemoglobinuria; eventual recovery”

The amounts are huge. 175 g of copper sulfate, containing 70 grams of copper is a single 70,000 mg dose! No liver damage. Just kidney damage.

The biggest single copper sulfate intake level I could find:

“Jantsch et al. 1985 M, 42 yr, 1 Ingestion of ≈ 250 g of CuSO4 (≈ 100 g Cu) in attempted suicide Protracted vomiting, hepatic failure, response to chelation therapy, eventual recovery” Finally, we get to a liver problem. At 100,000 mg of contained copper in a single dose! How did he even survive if copper is toxic? I have to do the calculations if that were in pill form: 2 mg copper pills would be 50,000 pills / 90 per bottle = 555 bottles of copper supplements.

Oh my God, not even that much copper contained in 555 bottles of copper supplements killed this guy!? How safe is copper, anyway?

All three cases from the same list, linked above:
https://www.ncbi.nlm.nih.gov/books/NBK225400/table/ttt00001/

So, 20,000 mg is not the lethal dose, but a lethal dose, but only about 13% die at that dose.

The tolerable upper limit of 10 mg is said to be arbitrary. And it is said that it is the level at which we see “no liver damage”. This, too is evidence of a lie. We do not limit pain killers to a level that creates “no liver damage”. With pain killers, some liver damage is allowed! We do not set limits on alcohol to a level that creates “no liver damage”. With alcohol, you can drink whatever you want. And many other drugs would have to be banned for causing liver damage. Copper is not even a drug. They cannot ban it. So, I guess they slander it, right?

As far as 10 mg of copper “causing no liver damage” goes, you could similarly claim, “one drop of alcohol” causes no liver damage. True. But it is totally useless information. People can usually have at least hundreds of thousands, if not hundreds of millions of times more alcohol than one drop before liver damage begins to take place.

Some may object to my complaint about the UL and reason, “Well, Jason, copper is available, and you are taking over the limit, so there really is no limit, right, so why complain about it?”

In one sense, yes. In other ways, no. For example, we live in lawsuit prone society. So organizations would be afraid to recommend copper above the limit. And many people trust government, so they would be afraid to go over the limit, or in many cases, afraid to approach the limit. People inherently think limits are dangerous. And scientific studies appear to be rare in studying above the limit, even though the government itself said it should explore the area above the limit, but did not follow up. And I get banned and blocked on Facebook routinely, for posting that I took above the government limit because what I am posting is “dangerous”. As if neuropathy and copper deficiency, and diabetes, and brain damage from low copper, and heart disease from low copper are not dangerous?

A false claim of a “tolerable upper limit” of a super low, and totally unscientifically backed 10 mg is dangerous to people.

Even the name itself is a lie. “tolerable upper human limit”. People have tolerated well above that limit. We know what a limit is.

Limits are arbitrary dictates, and this one has been proven incorrect, in multiple ways. In sum, it makes no sense. It’s just the RDA “times ten”. It’s not based on evidence. The one case study was a lie, as case studies cannot prove causality. Other case studies, including my own experience, invalidate the case study. The case study was never repeated and is thus not scientifically supported. A limit of 1000 times less than a level of “no liver damage” makes no sense in light of many other things that knowingly cause liver damage and are legal.

Why isn’t the upper limit “what babies get” “times ten”? Or “what babies get, times 15”? Babies get the equivalent of 5 mg. Times 15 is 75 mg.
I am NOT establishing any limits. I expose lies, and I advocate freedom. Limits are, by nature, whimsical, arbitrary, and tyrannical. Limits are the opposite of freedom.

People, when asked why they climb Mt. Everest, retort, “because it was there”. Why did I go above the limit of copper? Because I was confident that I easily could ignore lies, and be far healthier. I was right.

2001 UL version:

Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc.
https://www.ncbi.nlm.nih.gov/books/NBK222312/

The new definition of the UL, and when it’s ok to exceed it:

“TOLERABLE UPPER INTAKE LEVELS
The Tolerable Upper Intake Level (UL) is the highest level of daily nutrient intake that is likely to pose no risk of adverse health effects for almost all individuals. Although members of the general population should be advised not to routinely exceed the UL, intake above the UL may be appropriate for investigation within well-controlled clinical trials. Clinical trials of doses above the UL should not be discouraged, as long as subjects participating in these trials have signed informed consent documents regarding possible toxicity and as long as these trials employ appropriate safety monitoring of trial subjects. In addition, the UL is not meant to apply to individuals who are receiving copper under medical supervision.”

Note, in a copper deficiency forum, doctors have recommended levels up to 30 mg/copper/day!

“Finally, animal species vary markedly in their sensitivity to copper (Davis and Mertz, 1987); thus it is difficult to determine the most appropriate model in which to assess human toxicity to copper.”

I agree, and for another reason. Most animals can make their own Vitamin C, which, at 1500 mg, has been shown to reduce ceruloplasmin, a key copper transport protein in the blood. Many animals make the equivalent of 8000 mg of Vitamin C, which could demonstrate a significantly increased tolerance to copper. However, many animal studies show that animals can tolerate thousands of times more copper than the RDA.

“Copper homeostasis is affected by the interaction among zinc, copper, iron, and molybdenum.” I agree. And over 40 other substances, as we already went over in section 2.

“It is difficult to determine the most appropriate model in which to assess human toxicity to copper.”

I agree. I also propose that since copper helps to detox the body, people will vary greatly in the amounts of copper they can tolerate. How else can we explain why one man survived up to 250,000 mg of copper, yet many people begin to feel nausea at 2-4 mg of copper, that, in my experience, goes away after about 6 months to a year, presumably, once the initial detox effects of fluoride removal are no longer happening. They concur that people adapt.

“However, individuals may be able to adapt to even higher concentrations of copper in drinking water. No adverse gastrointestinal effects were reported in U.S. adults who consumed water containing approximately 8.5 to 8.8 mg/L of copper for over 20 years beginning in childhood (aged 0 through 5 years) (Scheinberg and Sternlieb, 1996).”

The following statement sounds like the government scientists are making thoughtful progress, but they fail to change their UL.

“In view of the weight of evidence supporting a genetic basis for the liver damage in Wilson’s disease, ICC, and ICT, it is not appropriate to use data from such populations to develop a UL for copper in populations with normal copper homeostatic mechanisms.”

Next, they continue to trot out the “one case study”, that was likely all just made up:

The government’s UL is the same as their NOAEL, or “No-Observed-Adverse-Effect Level” In other words, zero harm from 10 mg copper per day.

Once again, they did not study 11 mg, and this does not imply that harm takes place at 11 mg, or even higher.

And once again, studies are showing no harm at 20 mg copper per day.

And I have found no harm in myself and my wife taking 30 mg – 70 mg of copper per day.

There are no intervention studies where they gave people copper, who then later developed liver disease, despite their many claims that this is the main harm they are trying to prevent with their low UL. There is just one case study.

“The Tolerable Upper Intake Level (UL) for adults is 10,000 μg/day (10 mg/day), a value based on protection from liver damage as the critical adverse effect.”

“a value based on protection from liver damage”?

Those are just words on paper with nothing backing them up.

“Other Systemic Effects. Little evidence indicates that chronic exposure to copper results in systemic effects other than liver damage.”

This is interesting. So it’s all about the liver damage, and they have no other adverse claims?

“On the basis of considerations of causality, relevance, and the quality and completeness of the database, liver damage was selected as the critical endpoint on which to base a UL. The selection of gastrointestinal effects as a critical endpoint was considered because of the data involving acute ingestion of soluble (highly ionized) copper salts in drinking water. However, in the United States and Canada, liver damage is a much more relevant endpoint because of the potential for excess intake from food and supplements. Furthermore, extensive evidence from studies in humans and experimental animals indicates that liver damage is the critical endpoint resulting from daily intake of high levels of copper salts (IPCS, 1998).”

Ok. Now we have another source of liver damage from “high” copper, whatever that means: (IPCS, 1998) Great, lets go to the source!

IPCS, 1998 is a 398 page document, from the World Health Organization, here are two links:
https://inchem.org/documents/ehc/ehc/ehc200.htm
https://wedocs.unep.org/bitstream/handle/20.500.11822/29476/EHC200Copper.pdf?sequence=1&isAllowed=y

What is “high” enough copper to cause liver problems, according to the WHO?

“Rats given up to 305 mg Cu/kg per day orally in the diet as copper(II) sulfate for 15 days showed alterations in blood biochemistry and haematology (particularly anaemia) and adverse effects on the liver, kidney and lungs.”

For a 100 kilo man, that would be 30,500 mg copper per day for 15 days. One such dose in one day is lethal about 15% of the time in humans.

And what was the NOEL?

“Effects were qualitatively similar with other copper compounds and in other species. The no-observed-effect level (NOEL) in this study was 23 mg Cu/kg body weight per day.”

For a 100 kilo man, that would be 2,300 mg of copper per day which is the highest “no observed effect” level. In other words, that does nothing, no harm, no liver damage!

So, the US is claiming to rely on these studies to come up with a UL of 10 mg copper? What a trick!

I just love looking up references, listed by the US government, that refute the US government. Both of those values are far, far higher than the 10 mg of copper per day. The lowest is 230 times more! To take 2,300 mg, in 2 mg tablets, would take consuming 1150 tablets. Bottles of copper tablets can contain 90 tablets per bottle. A person would have to consume 12.7 bottles of copper tablets with 90 tablets at 2 mg each to get to 2,300 mg copper in a day. This would give the “no observed effect”, not liver damage! COPPER IS SAFE!

Listed elsewhere, a man took 2000 mg of copper daily for 4 months. No liver disease.

They conclude they need to do more work. This is admirable, but being honest in one point by admitting their total ignorance, does not validate the UL they pronounce, it actually invalidates it, because they have done zero work to determine when bad things might happen at ever higher copper intake levels in a range over 10 mg, nor have they determined if good things happen at higher copper intake levels!

“RESEARCH RECOMMENDATIONS FOR COPPER
Determine the specific health risks associated with marginal copper deficiency.
Define the adverse effects of chronic high copper consumption for establishing upper intake levels and to evaluate the health effects of copper supplements.
Determine the involvement of low and high copper intakes on neurological and cognitive function.”

Earlier, the government or someone had no trouble causing illness by inducing copper deficiency. But they have never given more and more copper until disease hit, or until people got vastly healthier. This is evidence of their anti-copper bias.

I have a chapter on Wilson’s Disease. In sum, Wilson’s Disease is better characterized as a low copper disease.

I will examine liver disease in its chapter, too. In sum, copper deficiency, not copper excess, causes almost all cases of liver disease, which is mostly all hepatitis, because there are almost no cases of high copper causing liver disease except in the 20,000 mg/copper intentional suicide cases.

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