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Saturday, May 9, 2015 10:13 PM | Venöse Multiple Sklerose, CVI & SVI, CCSVI Volg link
Copper (bound on Ceruloplasmin) is an essential mineral for antioxidative enzymes in the human body. While vital, it appears to be sufficient in the human diet and water supply with no known beneficial role for supplementation. Excess [unbound] copper is involved in some cases of Alzheimer's.

Summary
Copper is an essential trace mineral that is used in a variety of processes in the body. The major function for copper is in catalyzing oxidation-reduction (REDOX) reactions important for the activity of a number of enzymes. Although copper is essential to health, most Western diets meet the recommended intake, making supplementation unnecessary in most healthy individuals.
Cases where copper deficiency may occur include patients who have undergone gastric bypass as well as chronic users of proton pump inhibitors, both of which interfere with copper absorption. Also, high levels of zinc intake may increase production of a protein known as metallothionein that can bind copper and reduce its levels in the body.
Although the REDOX chemistry catalyzed by copper is essential for a number of immune functions, copper also may play a role in Alzheimer's disease. Copper levels generally rise in the body with age, but seem to rise more sharply in those with Alzheimer's. Moreover, copper levels have been linked to Alzheimer's symptom severity, leading some to suggest that a lower copper intake may benefit the elderly.

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"...This low dose of copper appears to be associated with increased inflammation following an inflammatory stressor[27] and altered cardiovascular function ranging from altered mitochondrial structure and impaired cardiac function (seen at 50% of the standard copper level) to signs of cardiomyopathy (25% of the standard copper level).[29][28] There also appear to be alterations in blood flow[30] and increases in bleeding with reduced copper intake in rats.[31] One study also noted an upregulation of the pro-inflammatory enzyme COX-2 in rats with low copper intake.[32]
These studies on reduced intake have noted effects that are similar to but less severe than models of true [bound] copper deficiency in rodents, where instances of substantially increased inflammation[33][34] and congestive heart failure have been reported.[35] Alterations in cardiac function prior to cardiomyopathy[36] and cardiac hypertrophy secondary to more drastic copper deficiencies[37] appear to be reversible following copper repletion.
In rodents given a 'marginal' copper deficiency, (50% of the standard copper intake or less) there are negative changes in immune and cardiovascular function. These changes can be normalized when copper is introduced back into the diet at sufficient levels.
True copper deficiency may result in myelopathy,[38][39] which has been noted in instances following gastrointestinal surgery.[25] Such myelopathy is known to occur in ruminants, where it is known as 'swayback'[25] and presents in both ruminants and humans as gait ataxia and sensory symptoms.[38][39] As assessed by MRI, copper deficiency myelopathy appears similar to subacute degeneration of the dorsal column in cases of Vitamin B12deficiency.[38][39][40]
True copper deficiency results in a neurological condition that is, to a degree, clinically similar to Vitamin B12 deficiency. This has only been noted in situations following gastrointestinal surgeries where copper absorption has been significantly impaired, however...."
"...In regard to dietary factors that can interact with copper absorption, high protein diets tend to promote copper absorption while higher than normal intakes of phytic acid may reduce absorption. These alterations in absorption are similar for most other divalent cations including calcium and magnesium...."
"...The majority of copper found in circulation is tightly bound to the primary binding protein known as ceruloplasmin, with the remaining amount of copper, known as free copper, more loosely associated with albumin. Significant increases in free copper are considered a risk factor for toxicity..."
"...Depression - Serum copper levels are consistently higher in patients with unipolar depression, even after successful treatment, thus suggesting that serum copper levels may be a "trait marker" for depression.[75] Copper levels have also been shown to correlate with depression levels in shift nurses[76] and post-partum depression.[77]
Another study found that patients with depression had higher levels of serum copper compared to controls which was treated with a combination of antioxidant therapy and Zinc for 8 weeks; depression did not respond to this treatment, nor did copper serum levels did not change post-treatment.[78]..."
Full paper: http://examine.com/supplements/Copper/


Copper - Scientific Review on Usage, Dosage, Side Effects | Examine.com
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