Poisoning of Mankind: Blood Types, Copper Deficiency,
Evolution Theory, Shroud of Turin & Illuminati

 

 

Copper

Defining the Human Requirement
A.S. Gissen

As regular readers of our newsletter already know, coppers importance in our nutrition is a popular topic on these pages. Long ignored by all but a handful of dedicated minimum human nutrition researchers, copper is inexpensive and unglamorous. In animal nutrition, however, where the ill effects of copper deficiency are well established, copper is liberally added to diets, and copper deficiency is a scientific curiosity usually caused by poor animal management. One of the problems of accurately determining the minimum human requirement for dietary copper is the lack of a sensitive test to detect deficiencies of copper which are not severe enough to cause the unmistakable symptoms of anemia, leukopenia, and skeletal demineralization found in severe copper deficiency. Numerous short-term studies of copper deprivation in human subjects have provided evidence to support the belief that copper deficiency may cause long term negative consequences, namely cardiovascular disease. Most of these studies have utilized young men or women over short periods of time. Now a new study has been published that examined the effects in postmenopausal women of a diet low in copper over a four-month period.

This study was designed to test the hypothesis that copper-containing enzymes in blood cells are more sensitive indicators of copper status than plasma copper levels. The women were fed a copper-depleting diet containing .57 milligrams of copper daily for 105 days, followed by a copper-repletion period of 35 days during which the women consumed 2.57 milligrams of copper daily. Plasma copper and ceruloplasmin did not change significantly during copper depletion. This was in spite of significant changes in several enzymes in circulating blood cells that are directly related to oxygen metabolism or antioxidant function, including cytochrome c oxidase, superoxide dismutase, and glutathione peroxidase. In the authors words, These enzymes seem to change before other indicators that have been associated with severe copper deficiency in animals, such as plasma copper, cholesterol, or hemoglobin concentrations. This provides strong evidence that the traditional measures of copper status are not particularly useful at detecting the subclinical deficiency we are most likely to develop. Because most of our understanding of human copper requirements are based on these inaccurate measures, these findings will force a re-evaluation of decades of copper research.

Among the changes found, platelet cytochrome c oxidase activity seems to be a sensitive indicator of changes in human copper status. Low tissue cytochrome c oxidase has already been shown to be an early and consistent finding in copper deficient animals. In this study, platelet cytochrome c oxidase activity dropped by almost one-half after 9 weeks of copper deprivation. During the 35 day repletion phase its activity only partially recovered. As the authors point out, Defects in cytochrome c oxidase activity may cause neurologic, cardiac, and muscle disease when the activity is only about 50% of normal. In many ways this resembles the deficiency symptoms of one of cytochrome c oxidases partners in energy production within cells, coenzyme Q10. Additional research with rats has shown that the cytochrome c oxidase activity in platelets correlates well with liver copper stores, the benchmark measure of copper status. The fact that 35 days of copper repletion with slightly more than the RDI of copper didnt restore cytochrome c oxidase activity to pre-depletion levels is troublesome. This activity didnt drop significantly until after 8 weeks of depletion, and then dropped markedly over the next five weeks. Apparently five weeks of almost 2.6 milligrams of copper daily doesnt provide enough excess copper beyond the bodys actual requirement to significantly replete copper stores. Incidentally, of the 13 women who began the low-copper-intake phase of the study, three were withdrawn and supplemented with copper after the detection of a significant increase over control values in the number of ventricular premature discharges, a heart rhythm abnormality. One could easily speculate that this is only the tip of the iceberg in relation to the relevance of copper deficiency to the incidence of heart rhythm abnormalities.

In the case of erythrocyte superoxide dismutase, a decline in its activity was observed during copper depletion. During the period of copper repletion its activity failed to recover to pre-depletion levels. This lack of recovery of erythrocyte superoxide dismutase activity, coupled with the decrease in cytochrome c oxidase activity, adds evidence to the belief that current copper recommendations for humans may be understated. The researchers write that, It is likely that the response of these enzymes to copper repletion after copper depletion is influenced by the amount of copper fed, the duration of depletion and repletion, and the rates of cell turnover. They then provide evidence from other studies in which superoxide dismutase activities were lowered during copper deprivation. Recoveries of activity were documented when either 3 mg or 4.3-6.4 mg copper per day was fed for greater than 30 days, but not when less than 2.6 mg per day was fed for periods of up to 42 days. Erythrocyte glutathione peroxidase, a selenium-containing antioxidant enzyme, was also sensitive to changes in copper intake. Although it, too, significantly decreased during copper depletion, it was restored to normal levels during the copper repletion phase of the study. Like superoxide dismutase, glutathione peroxidase is an important antioxidant enzyme. While the long-term effects of this are unknown, the importance of these two enzymes in protecting us from free-radical damage cannot be overlooked.

One of the interesting findings from this study was that coagulation factors V and VIII, which contain copper and have structural similarities to ceruloplasmin (the main copper-containing protein in plasma), are sensitive to changes in copper intake. Surprisingly, copper depletion caused factor VIII activity to significantly increase to almost twice the normal range. Factor VIII is a procoagulant, and an elevation of factor VIII activity is often seen in hypercoagulation and thrombotic disease, important risk factors for vascular disease. An increase in factor VIII activity is consistent with the increased incidence of thrombotic events observed in copper-deficient animals. This adds an additional cardiovascular risk factor to go with the electrocardiogram abnormalities, lowering of antioxidant enzymes, and promotion of atherosclerosis already known to be associated with copper deficiency. It seems likely that copper deficiency has relevance to many patients with hypercoagulation and thrombotic disorders, as well as atherosclerosis in general. While taking aspirin to prevent abnormal blood clotting is widely practiced and recommended, adequate copper supplementation seems even more logical, beneficial, and necessary for overall cardiovascular health.

While the work of these and other researchers will eventually result in a better understanding of copper metabolism in humans, their results also force us to take a new look at how we view copper deficiency and requirements in humans. One of the most important discoveries was that, unlike other animal models of copper deficiency, low copper intakes did not induce the changes in serum cholesterol and hematology generally found in copper-deficient animals. Because of this the authors suggest that, These results indicate that a paradigm shift may be needed in evaluating copper status in adult humans. Taken in its entirety, the findings of this research should provide a wake-up call for the nutritionally concerned.

It is already well-documented that most of us get only about 1 milligram of copper daily from our diets, well below the recommendation of up to 3 milligrams daily. In fact, subclinical copper deficiency is believed to be a common cause of illness in this country. The problem, up until now, has been proving the existence of subclinical copper deficiency in otherwise healthy human subjects. It is likely that the finding of several sensitive indicators of copper status, including the functional activities of platelet cytochrome c oxidase, glutathione peroxidase, and clotting factor VIII, will make it possible to more fully quantify the incidence of copper deficiency in the general population. More importantly, it will make it possible for the first time to accurately determine the optimal copper requirement for diverse population groups with different copper needs based on sensitive indicators of copper status. Because of the vital roles copper plays in ensuring our health, this will be an important advancement in human preventive nutrition. It is also one of many examples of how far we have yet to go in determining our optimal dietary requirements.

Reference:
D.B. Milne and F.H. Nielsen, AM J Clin Nutr 1996; 63; 358-364.

 

Poisoning of Mankind: Blood Types, Copper Deficiency,
Evolution Theory, Shroud of Turin & Illuminati