The Copper Revolution: Ch 10: Copper at 10 mg to 20 mg does not harm the liver (Olivares)

Studies on taking 10 mg copper to 20 mg copper, show zero harm, specifically, no liver damage:

Supplementing Copper at the Upper Level of the Adult Dietary Recommended Intake Induces Detectable but Transient Changes in Healthy Adults  (Olivares, 2005)
Note, they call copper at 10-20 mg “mild copper excess”.

The health consequences of “mild copper excess” in humans are unknown. In a previous study, 2 mo of supplementation with up to 6 mg Cu/L in drinking water did not induce detectable changes. Here we assessed a copper supplement at the upper level of dietary recommendations for “healthy” adults. The study was a prospective controlled trial; participants (women and men, 18-50 y old), represented the upper and lower 5% of the ceruloplasmin distribution curve obtained froma community-based sample of 800 healthy adults (n = 41/group, each approximately 50% men). Individuals received a single daily dose of 10 mg Cu for 60 d. Before and after supplementation, blood [copper, ceruloplasmin protein, homocysteine, liver aminotranferases, Cu-Zn -superoxide dismutase activity in erythrocytes (eSOD), and glutathione in peripheral mononuclear cells] and urine [copper excretion after a 5-h administration of a chelator 2,3-dimercapto-1-propano-sodium sulfonate (DMPS)] analyses were performed. After 2 mo, liver enzyme activities remained below the clinical cutoff value used to diagnose liver dysfunction, but had increased significantly in both groups and genders. These increases were no longer present 12 mo after the copper loading period was completed. Glutathione in mononuclear cells (mmol/g of protein) also increased after the 2-mo copper loading in both groups and in both genders (P = 0.01). eSOD activity, serum homocysteine concentration, and urinary copper excretion 5 h after DMPS administration were not affected. We conclude that copper administered as described induced a transient, mild, but significant elevation of aminotransferases.”

“In a previous study, 2 mo of supplementation with up to 6 mg Cu/L in drinking water did not induce detectable changes. Here we assessed a copper supplement at the upper level of dietary recommendations for “healthy” adults.

I pulled that quote out, quoting it twice, and mention it here for greater effect.  6 mg of copper for 2 months did not induce detectable changes.  In other words, 6 mg is not dangerous.  It’s also probably not enough to get you healthy, either.  If you are taking copper you are going to want “positive changes”, not “no detectable changes”.  In other words, 6 mg of copper “does nothing”. 

Again, 2.6 mg of copper does not fix deficiency.  6 mg of copper “does nothing”.  Therefore, for me, this confirms that people need higher levels to get good results from taking copper.

“Individuals received a single daily dose of 10 mg Cu for 60 d.”

“There is scant knowledge of the early effects of chronic exposure to higher levels of copper.”

“There is an anecdotal report of a 26-y-old man who required liver transplantation after self-administering 30 mg of copper daily for 30 mo and then increasing the dose to 60 mg/d for 1 y as a “performance enhancer” (7).”  (I cover this “report” in detail in chapters 40-41 in this book on the “upper limit”.)

“In a previous randomized, controlled, double-blind study, we exposed apparently healthy adults to up to 6 mg Cu/L of water for 2 mo; based on the daily consumption of water, this represented exposures of up to 20 mg Cu/d (1). Copper was ingested at home during the day as plain water or taken as tea, herbal infusions, or soup.”

“Under these conditions, traditional copper biomarkers, including serum copper, serum ceruloplasmin (Cp; protein), and erythrocyte Cu-Zn superoxide dismutase total activity (eSOD) were not affected.”

“DISCUSSION Presently, the WHO/FAO/International Atomic Energy Agency and the National Academy of Science/Food and Nutrition Board DRIs for trace elements and metals are 9 and 10 mg copper/d as the tolerable UL of intake from food, water, and supplements, respectively (17). 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.”

“The main effect was a significant increase in the activities of 3 liver aminotransferases after 2 mo of controlled copper exposure with the specified dose and regimen. This increase was significant, but all enzyme activities were below the corresponding clinical cutoff values used to diagnose liver dysfunction, and participants did not exhibit symptoms or positive findings on physical examination suggestive of liver disease.”

“DMPS, given at a dose that induced a dramatic difference in urinary copper excretion between the patients with Wilson’s disease and normal volunteers in the preliminary protocol, did not significantly increase urinary copper in the study participants (data not shown). The 300 mg of DMPS as a single dose is sufficient to chelate the metal when tissue concentrations are elevated, as observed in patients with Wilson’s disease (24). This dose is currently recommended for individuals suspected of suffering from chronic metal toxicity (25), e.g., individuals with potential mercury toxicity due to mercury from dental fillings (26–28). In our case, we chose an oral DMPS dose that was documented to be well tolerated by individuals suspected of mercury toxicity. The low dose in addition to the rather moderate copper load given to our subjects may explain the lack of an effect of DMPS on urinary copper excretion. Alternatively, the chronic exposure to copper may have led to copper sequestration in body pools that were less accessible to the chelator.”

Gastrointestinal symptoms and blood indicators of copper load in apparently healthy adults undergoing controlled copper exposure  (Olivares, 2003)

“Conclusions: Gastrointestinal symptoms increased significantly in response to 6 mg Cu/L water. No detectable changes were observed in indicators of copper status, which suggests competent homeostatic regulation. The results of liver function tests remained normal in all subjects.”

Title: “Nausea threshold in apparently healthy individuals who drink fluids containing graded concentrations of copper” (Olivares, 2001 Jun)

“Abstract Ingestion of drinking water with a high copper content may induce acute gastrointestinal effects, mainly nausea and vomiting, rarely diarrhea and abdominal pain. The objectives of this study were to define nausea threshold in apparently healthy adult volunteers who received graded concentrations of copper and to explore how individual thresholds were modified by delivering copper in an orange-flavored drink. Sixty-one healthy subjects received 200 mL of a copper-containing solution in purified water, at concentrations 0, 2, 4, 6, 8, 10, and 12 mg/L, as copper sulfate, in random order. Nausea threshold concentration for first response was established and then this threshold was confirmed. Subsequently, following the same design, subjects received the same copper concentrations (up to 12 mg/L), delivered in an orange-flavored drink, starting at the confirmed threshold concentration found in water. Mild nausea shortly after ingestion of copper-containing water was the most frequent finding (33/61 subjects), starting at 4 mg/L; vomiting was observed in 7 individuals, starting at 6 mg/L. The NOEL for copper in purified water was 2 and 4 mg/L for nausea and vomiting, respectively. When copper was provided as an orange-flavored drink, 11 subjects (18%) reported nausea, starting at 8 mg Cu/L, and no subjects vomited up to 12 mg Cu/L. It is concluded that after consumption of copper in purified water, the NOEL is 2 mg Cu/L and the LOAEL 4 mg Cu/L for nausea, while tolerable intake is between 2 and 4 mg Cu/L in water depending on whether apparent or confirmed nausea is used as the criterion to define critical effects.”

“tolerable intake is between 2 and 4 mg Cu/L in water depending on whether apparent or confirmed nausea is used as the criterion to define critical effects.” And 5-15 mg copper is safe:

Copper exposure and potential biomarkers of copper metabolism (Olivares, 2003)

“In adult healthy volunteers that had an estimated daily intake of 0.9 mg Cu/day (approximately 15 microg/kg/d), exposure to additional 50-60 microg of copper/kg/day for three months or up to 150 microg/kg/d for two months resulted in no significant changes of SOD activity in erythrocytes, of copper concentration (in serum, erythrocytes and mononuclear cells) and of serum ceruloplasmin (ANOVA).”

5-15 mg of copper supplements a day, for a healthy 100kg person, (220 pounds) does nothing:

50 mcg x 100 kg = 5 mg,
150 mcg x 100 kg = 15 mg.