What are the consequences of not consuming much or any copper? Surprisingly, no one really seems to know.
Here are some quotes by EFSA (European Food Safety Authority) on copper:
I am pretty shocked to see what kind of data is used to tell billions of people how their diet should look like.
How difficult is it to take 10,000 people, divide them into 10 groups, and feed everyone a nutritious whole foods diet with varying levels of copper (like 3mg, 2mg, 1mg, 0.9 mg, 0.8mg, down to 0mg) and look whether actual health issues appear at lower levels.
But the following study gives at least an idea:
You would expect that when the young men only received 0.4mg per day for 42 days, they suffered from debilitating copper deficiency symptoms. Actually, no symptoms at all appeared. Only some lab values were used to consider the diet inadequate in copper. Ceruloplasmin, SOD and plasma copper were a bit lowered (by around 20% or so).
Plasma copper fell from 14.8 to 12.6 umol/L, ceruloplasmin from 302 to 258 mg/L and SOD from 410 to 354 U/g. Interestingly, neither ceruloplasmin or SOD recovered to pre-study levels but stayed lower afterwards.
"The results of our current study clearly suggest that 0.4 mg Cu/d is not sufficient to maintain copper status. A number of indexes declined during the low-copper diet, then increased during repletion. Although clinical symptoms of copper deficiency were not observed in any of the subjects, this is not surprising given the short time period of the depletion. Indexes did not reach deficient ranges, but differences between treatments were significant for the group and the trends suggest that, with time, a pronounced copper deficiency syndrome could have resulted."
Also, "Plasma copper had fallen significantly by the midpoint of depletion, but did not change significantly after that.", implying that there was no trend for copper to fall to zero at all.
These are the kind of studies that are used to tell billions of people what to eat.
Who knows what ideal blood values are when they are not matched against real world symptoms and data? "A pronounced copper deficiency syndrome could have resulted" - it would be nice to see this mythical syndrome in the real world and not just in theories.
Here are some quotes by EFSA (European Food Safety Authority) on copper:
"Clinical symptoms are not common in humans, and generally are seen as a consequence of mutations in the genes involved in copper metabolism."
"The Panel noted that there are no biomarkers of copper status that are sufficiently robust, sensitive and specific to be used for deriving requirements for copper. The Panel also considered whether health outcomes can be used to derive DRVs for copper. However, it was concluded that the limited evidence available on copper intake and cardiovascular disease-related outcomes and cancer cannot be used for setting DRVs for copper."
"The Panel decided to derive Adequate Intakes based on observed intakes in several EU countries."
"Furthermore, there is evidence that copper deficiency is associated with alterations in immune function (Kelley et al., 1995; Turnlund et al., 2004) and possibly bone function (Baker et al. ), although, in a further study, Baker et al. failed to confirm their earlier results. However, all these symptoms can occur in other diseases, making it very difficult to identify copper deficiency from the phenotype."
"According to IOM (2001), the study by Turnlund et al. (1990) showed that a copper intake in 11 young men above 0.38 mg/day is needed to prevent a decrease in relevant biochemical indicators (SOD activity, serum copper and ceruloplasmin concentration), whereas the study by Turnlund et al. (1997) showed that no decline in these biomarkers was observed in 11 young men at an intake of 0.79 mg/day."
I am pretty shocked to see what kind of data is used to tell billions of people how their diet should look like.
How difficult is it to take 10,000 people, divide them into 10 groups, and feed everyone a nutritious whole foods diet with varying levels of copper (like 3mg, 2mg, 1mg, 0.9 mg, 0.8mg, down to 0mg) and look whether actual health issues appear at lower levels.
But the following study gives at least an idea:
The results suggest that these indexes are sensitive to copper depletion; that 0.38 mg Cu/d is not sufficient to maintain copper status in normal, healthy young men; and that the minimum dietary copper requirement is between 0.4 and 0.8 mg/d.
You would expect that when the young men only received 0.4mg per day for 42 days, they suffered from debilitating copper deficiency symptoms. Actually, no symptoms at all appeared. Only some lab values were used to consider the diet inadequate in copper. Ceruloplasmin, SOD and plasma copper were a bit lowered (by around 20% or so).
Plasma copper fell from 14.8 to 12.6 umol/L, ceruloplasmin from 302 to 258 mg/L and SOD from 410 to 354 U/g. Interestingly, neither ceruloplasmin or SOD recovered to pre-study levels but stayed lower afterwards.
"The results of our current study clearly suggest that 0.4 mg Cu/d is not sufficient to maintain copper status. A number of indexes declined during the low-copper diet, then increased during repletion. Although clinical symptoms of copper deficiency were not observed in any of the subjects, this is not surprising given the short time period of the depletion. Indexes did not reach deficient ranges, but differences between treatments were significant for the group and the trends suggest that, with time, a pronounced copper deficiency syndrome could have resulted."
Also, "Plasma copper had fallen significantly by the midpoint of depletion, but did not change significantly after that.", implying that there was no trend for copper to fall to zero at all.
These are the kind of studies that are used to tell billions of people what to eat.
Who knows what ideal blood values are when they are not matched against real world symptoms and data? "A pronounced copper deficiency syndrome could have resulted" - it would be nice to see this mythical syndrome in the real world and not just in theories.
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