|Vibrant Life Home Web
All VL Products
Family Of Three Chelation Formulas
Oral Chelation Ingredient Comparisons
The Wednesday Letter
Karl Loren Viewpoints
Frequently Asked Questions
Central Page For 18 Web Sites
|Vibrant Life Home Page||
Separate Search Page
|Navigation Help||Ingredients Technical||Write To Karl Loren||Table Of Contents|
This article first appeared in the
issues of VRP's Newsletter
by A.S. Gissen
Few dietary components are more misunderstood than copper. Although copper is the third most abundant essential trace mineral in the body, after iron and zinc, most people consider it unimportant. Even worse, many people have actually taken steps to exclude it from their diets and dietary supplements, believing it to be nothing more than a cause of free radical reactions. This is surprising, because copper has been recognized as an essential nutrient since the 1920's.1 In the past seventy years, much has been learned about the important biological roles of copper and the copper-dependent enzymes. In fact, copper is emerging as one of the most important minerals in our diet. While unbound, free copper does generate free radicals in vitro, the relevance of this in the body has been called more imaginary than real.2 In fact, copper has an entirely different role in the body, being a component of two of our most important antioxidant enzymes, copper-zinc superoxide dismutase and ceruloplasmin.3
Return To Top
Unbound, free copper is not found in large quantities in the human body. Instead, almost all of the copper in our bodies is bound to either transport proteins (ceruloplasmin and copper-albumin), storage proteins (metallothioneins), or copper containing enzymes.4 A substantial number of copper metalloenzymes have been found in the human body. Copper is essential for the proper functioning of these copper-dependent enzymes, including cytochrome C oxidase (energy production), superoxide dismutase (antioxidant protection), tyrosinase (pigmentation), dopamine hydroxylase (catecholamine production), lysyl oxidase (collagen and elastin formation), clotting factor V (blood clotting), and ceruloplasmin (antioxidant protection, iron metabolism, and copper transport).5 Most features of severe copper deficiency can be explained by a failure of one or more of these copper-dependent enzymes. For instance, depigmentation can be explained by a tyrosinase deficiency, and the defects of collagen and elastin causing abnormalities in the connective tissue and vascular system can be explained by a lysyl oxidase deficiency.
Unfortunately, most research into copper deficiency has focused on acute, severe deficiency. This is relatively rare in humans and animals on typical, varied diets. Marginal, chronic deficiency, however, is much more common. The determination of copper needs and marginal deficiency is complicated by the fact that while copper deficiency doesn't necessarily lower the level of copper-dependent enzymes, it does significantly lower their activity.6 As an example lets look at lysyl oxidase, one of the most important and best understood roles of copper in the body. This is the main enzyme involved in the necessary cross-linking of connective tissue. Optimal functioning of lysyl oxidase ensures the proper cross-linking of collagen and elastin, vital for the strength and flexibility of our connective tissue. A reduction in lysyl oxidase activity affects the integrity of numerous tissues, including our skin, bones, and blood vessels. In copper deficiency the level of lysyl oxidase isn't altered, but the activity of the enzyme can be reduced by more than fifty percent.7 Not surprisingly, some of the hallmarks of copper deficiency are connective tissue disorders, osteoporosis, and blood vessel damage.
Return To Top
The adult human body contains between 80 and 150 milligrams of copper.8 The liver is the major location of stored copper, containing about 10 percent of the total-body content.9 Maintaining a steady level of copper in the body depends upon a balance between intestinal absorption and biliary excretion. Biliary excretion of copper is capable of substantially increasing when excess copper is ingested.10 The exception to this is in persons with the genetic defect causing Wilson's Disease (hepatolenticular degeneration). This genetic disease, affecting approximately 1500 Americans, is characterized by a lack of circulating ceruloplasmin, low serum copper levels, and copper accumulation in the liver.11 This disease is characterized by an inability of the liver to normally transport copper, leading to copper overload. In most animals and humans, however, copper is essentially non -toxic.
Return To Top
Dietary copper is distributed in many foods. Dried beans and nuts are exceptional sources, while milk and dairy products are poor sources.12 Studies have found a wide range of intake among different population groups. In the United States, intakes range from .76 to 3.36 milligrams daily.13 The National Research Council has established a tentative safe and adequate daily intake for copper, which for adults is 2-3 milligrams daily.13 Numerous studies have shown average copper intake to be well below the recommended allowances, with intakes of less than 1 milligram daily being very common.14
Copper is rapidly absorbed from the stomach and small intestine, and this is influenced little by the form of copper ingested.15 Although the absorption of copper may not sound like an exciting subject, if you take vitamin/mineral supplements containing vitamin C or zinc you should pay close attention. This is because convincing evidence has accumulated suggesting that zinc and vitamin C supplements are strong antagonists of copper status and absorption. In the case of zinc, numerous studies have shown that relatively small increases in dietary zinc significantly lowers copper absorption.16 This antagonism has been utilized as a treatment of Wilson's Disease, with 50 milligrams of zinc taken with each meal being effective in lowering the abnormal accumulation of copper in people afflicted with this genetic disease of copper metabolism. Much lower levels of zinc supplementation, as little as 50 milligrams a day, has also been shown to antagonize copper status in healthy adults.17 Numerous cases of zinc-induced copper deficiency have been reported in scientific journals, usually resulting in anemia and blood lipid abnormalities.18 The use of supplemental vitamin C to lower copper absorption, and hasten copper deficiency, has been well documented in laboratory animals.19 It has subsequently been shown in several human studies that vitamin C supplements of as little as 1500 milligrams can adversely affect markers of copper status, including copper-zinc superoxide dismutase and ceruloplasmin activity.20 While the evidence for benefits from taking megadoses of zinc (>50 milligrams daily) and vitamin C (>1000 milligrams daily) are tentative at best, the negative consequences of poor copper status are well documented and certain. There seems little doubt that these interactions will receive increasing attention in the coming years, due to the documented importance of adequate copper intake and the common practice of consuming supplemental vitamin C and zinc without concern or copper supplements.
The long term effects of marginal, subclinical copper deficiency are not well defined. It has been hypothesized that low copper status is not only common, but plays a substantial role in numerous, common degenerative diseases and conditions. If all this has come as a shock to you, that lowly copper could be so vitally important to your health, don't be. Over the years the importance of copper in nutrition has even escaped many of the "so called" experts in the field of nutrition. In the words of one author who reviewed copper's role in human nutrition, " ...but copper has languished as an orphan among human nutritionists because of the obscurity of clinical copper-deficiency states in man. As medical investigators we may have gone down the long road, missing the forest for the trees...But, the influence of subtle differences in dietary intakes of copper on human health may be more important than frank copper depletion."21 Indeed, in next month's newsletter we will continue our review of copper and nutrition, including copper's role in cardiovascular disease, diabetes, arthritis, osteoporosis, free radical damage, cancer, inflammatory diseases, immune function, blood lipids, and thyroid function. In addition, we will examine the remarkable properties of copper complexes like copper salicylate. These copper complexes have been extensively studied for their anti-inflammatory and antioxidant activity, as well as their ability to mimic the superoxide-radical scavenging activity of superoxide dismutase.
Return To Top
Copper and Cardiovascular Disease
Although the relationship between nutrition and cardiovascular disease is generally accepted by most people, rarely will you hear copper mentioned as a contributing factor in this relationship. Based on the scientific evidence, this is surprising. Almost twenty years ago, it was postulated that there is a direct relationship between the level of copper in the human diet and the incidence of cardiovascular disease.22 Copper has been known to be associated with lipid metabolism since 1973,23 and research in numerous animal models, including humans, has shown that copper deficiency can significantly increase the plasma cholesterol concentration.24 Additionally, this increase in cholesterol results in an increase in LDL-cholesterol and a decrease in HDL -cholesterol, resulting in an increase in cardiovascular disease risk.25
Return To Top
It is well documented that animals with copper deficiency often have abnormal electrocardiograms, and die suddenly.26 In one study that looked at this relationship, it was found that copper deficiency reduced the life -span of rats by almost 75%. People with ischaemic heart disease usually die suddenly, often within one hour of the onset of symptoms. The hearts of people who die of ischaemic heart disease are hypertrophied and fibrotic, with edema, loss of cellular outline, and heart rupture often being found.27 Interestingly, all of these pathological changes are found in animals deficient in copper. In one human study that compared heart copper levels in heart attack victims and controls that died of other causes, it was found that the hearts of people that died of myocardial infarction were low in copper.28 Atherosclerotic arteries in humans have degenerative changes similar to those found in the arteries of copper deficient animals.29 It has also been demonstrated that copper deficiency significantly increases the susceptibility of lipoproteins and cardiovascular tissues to lipid peroxidation, thus increasing the risk of cardiovascular disease.30
While the role of adequate copper levels in maintaining cardiovascular health is well established, it is not entirely surprising that copper's importance has been overlooked. One of the laboratory findings often found in cardiovascular disease is increased serum levels of copper. While this may sound confusing, recent research has helped to explain this paradox. It has been suggested, for instance, that an elevated serum copper level is an independent risk factor for heart disease.29 Many researchers have considered this elevation of serum copper to play a role in the pathogenesis of cardiovascular disease, although other researchers have strongly disagreed with this hypothesis. A recent animal study, however, seems to have explained this relationship between copper levels and cardiovascular disease. This study examined the effects of diet-induced atherosclerosis on the copper levels and status of numerous tissues.30 It was found that serum copper levels increase significantly, while aorta and liver copper levels decrease significantly, in rats with experimental atherosclerosis. Instead of assuming that these elevated copper levels contribute to the formation of atherosclerosis, these researchers examined the effects of increasing the dietary copper levels in these animals. Administration of additional copper resulted in a further increase in serum copper, a significant decrease in serum cholesterol, and an increase and normalization in aorta and liver copper levels. However, instead of increasing the incidence of atherosclerosis, additional copper significantly decreased the incidence of atherosclerosis in the aorta and coronary arteries. Further, it has been shown that excess dietary cholesterol causes cardiovascular disease by lowering the absorption of copper, an effect that is preventable by increasing the copper level in the diet.31
Taken as a whole, the role of copper in maintaining cardiovascular health is well established. Copper is essential both for its role in antioxidant enzymes, like Cu-Zn Superoxide Dismutase and Ceruloplasmin, as well as its role in Lysyl Oxidase, essential for the strength and integrity of the heart and blood vessels. With such a central role in cardiovascular health, it is disappointing that copper has been generally overlooked in the debate over improving our cardiovascular health. Copper deficiency has produced many of the same abnormalities present in cardiovascular disease. It seems almost certain that copper plays a large role in the development of this killer disease, not because of its excess in the diet, but rather its deficiency.
Return To Top
Copper and Free Radicals
The function of copper as an integral component of Cu-Zn Superoxide Dismutase (SOD) and Ceruloplasmin is well established. Cu-Zn SOD, for example, performs antioxidant functions in varied tissues and fluids, and is indispensable to oxygen-metabolizing organisms.32 In addition, it has been demonstrated that most copper containing enzymes, including CuZn-SOD, are produced at a similar rate regardless of copper status, although their function is significantly impaired by copper deficiency.33 Thus, the activity of these enzymes are significantly lessened in spite of no decrease in their production.
Return To Top
Copper deficiency has been shown to result in a 2-fold increase in the level of lipid hydroperoxides in liver mitochondria.34 However, an interesting finding was that while the specific activity of Cu-Zn SOD decreased significantly, so did the activity of catalase and glutathione peroxidase, two other important antioxidant enzymes that don't require copper for their activity. Other research has shown that copper deficiency induces an increase in intracellular and extracellular glutathione levels, which the authors ascribed to a compensatory adaptive response to the negative effect of copper deficiency on glutathione peroxidase and Cu-Zn SOD activity.35 It appears clear that the decrease in antioxidant protection caused by copper deficiency goes beyond a decrease in the activity of copper-dependent antioxidant enzymes by inducing a wide range of disturbances in other antioxidant enzyme systems. Additionally, copper deficiency depresses Cu-Zn SOD activity and prostacyclin synthesis in the aorta,36 as well as increases the susceptibility of lipoproteins and heart tissue to peroxidation, providing strong evidence that copper plays a vital role in the protection of the cardiovascular system from free -radical mediated damage and disease.37 Thus, it appears clear that adequate copper is vital for optimal functioning of many antioxidant enzymes, both copper dependent and otherwise, in varied organs and tissues.
Copper and Osteoporosis
Almost two hundred years ago, the German physician Rademacher empirically established that broken bones healed faster when the patient was given copper supplements.38 In the years that have followed, compelling evidence has established a vital role for copper in the biosynthesis of bone and connective tissues and their maintenance.
Return To Top
Lysyl Oxidase, which is involved in the synthesis of the collagen that constitutes much of bone and connective tissue, is a copper dependent enzyme. Like other copper dependent enzymes, synthesis of Lysyl Oxidase is unaffected by copper deficiency, although its activity is significantly impaired.39 Copper-deficiency induced osteoporosis has been documented in numerous animal species, including humans.40 While this condition has most often been documented in young, growing animals and children, it has been found in young adults and the elderly.41 Copper deficiency has even been implicated in the etiology of idiopathic scoliosis.42 Skeletal abnormalities have often been found concurrently with low copper status, and these have usually been associated with osteoporitic changes and increased susceptibility to fractures.43 Insufficient copper intake has also been shown to lower bone calcium levels during long-term deficiency.44
With the essential role that copper plays in maintaining bone health, it is surprising how little attention has been given to copper's role in bone diseases. Interestingly, estrogens, which have a beneficial effect on preventing post-menopausal bone loss, have been shown to raise the level of ceruloplasmin (the main copper transport protein) two to three fold, providing a possible explanation for how estrogen positively influences bone health, as well as cardiovascular health.45 Prolonged cortisone treatment, well known for promoting the development and accelerating the progression of osteoporosis, has been shown to increase the body's excretion of copper and lower copper status, providing more evidence of a correlation between copper status and osteoporosis.46
Return To Top
Copper and Immune Function
It has been well documented that adequate copper status is essential for normal functioning of the immune system in laboratory and domestic animals.47 For instance, not only has it been shown that the functioning of macrophages were decreased in severely copper deficient rats, but even marginally copper-deficient rats had impaired immune functioning.48 Interestingly, immune function was significantly impaired at dietary copper levels that didn't seem to decrease tissue copper or the activity of red blood cell Cu,Zn-superoxide dismutase (SOD).49 However, neutrophil SOD-activity and neutrophil function was significantly diminished, suggesting that immune function may be more sensitive to diets low in copper than standard measures of copper status. It was also found that immune impairment could be detected as soon as one week after the initiation of a diet low or marginal in copper, and the addition of adequate copper reversed the immune suppression within one week of supplementation. The authors concluded that, "...the adverse effects of inadequate copper intake on neutrophil activity occur rapidly and are readily reversed by dietary copper repletion." Additionally, it has been demonstrated that copper deficiency reversibly impairs DNA synthesis in activated T-cells by limiting interleukin 2 activity up to 50%, and this was reversible with copper supplementation.50 Because of this sensitivity to copper status at levels of intake that have little effect on other indicators of copper status, immune system cells have been suggested to be a readily accessible and copper-status sensitive population of cells for the assessment of copper status.51
Return To Top
Copper, Cancer, and Carcinogenesis
The role of copper in the development of cancer is somewhat similar to copper's role in cardiovascular disease. This is because the serum level of copper is often elevated in animals and humans with cancer.52 Like the elevation of serum copper in cardiovascular disease, it seems that the elevation of serum copper that occurs in conjunction with cancer is part of the bodies biological response to the cancer, rather than its cause. Numerous studies examining varied types of tumors have demonstrated that with remission usually comes a decrease in serum copper levels to normal.53 Patients who responded to therapy or surgery usually had a return to normal serum copper levels, while nonresponders had a persistently elevated serum copper level. Interestingly, most tumor cells have decreased Cu-Zn SOD activity compared to normal cells,54 and it has been suggested that the elevation in serum copper is a physiological response designed to activate SOD or other copper enzymes in cancer cells to inhibit their growth. Indeed, numerous copper complexes that demonstrate SOD-mimetic properties, including copper salicylate, have been shown to possess anticancer, anticarcinogenic, and antimutagenic effects both in vitro and in vivo.55 In fact, there is some experimental evidence that copper complexes can cause established tumor cells to redifferentiate into normal cells,56 and because of this it has been suggested that, "..the future use of copper complexes to treat neoplastic diseases has some exciting possibilities."57
Return To Top
Because copper is an essential component of several endogenous antioxidant enzymes, and free radicals have been proposed to play a role in the process of carcinogenesis, the effects of dietary copper levels on the development of cancer has been investigated. Rats fed low copper diets show a higher incidence of carcinogen -induced colon tumors when compared with rats fed a high copper diet.58 Another study in rats found similar results, but with the additional finding of a decrease in aortic integrity possibly leading to eventual aneurysm.59 These findings are especially interesting for two reasons. To begin with, dietary copper has often been incorrectly suggested to be a cause or promoter of cancer. If this was true increased dietary copper would enhance, rather than inhibit, carcinogen-induced gastrointestinal malignancy. Lastly, it has been shown that there is a relationship between aortic aneurysmal disease and malignancy in humans, and this is likely the result of decreased copper status as demonstrated in the animal study mentioned above.60
Return To Top
Copper, Inflammation, and Arthritis
As long ago as 1000 B.C., foods high in copper and copper bracelets were thought to be beneficial in treating arthritic conditions.61 In 1945, patients with rheumatoid arthritis were shown to exhibit higher than normal serum copper levels.62 Indeed, the copper content of serum is known to be elevated above normal values in various inflammatory diseases in man and laboratory animals.63 Despite this seeming contradiction, copper complexes were successfully used from the 1940's to 1970's in the treatment of numerous conditions characterized by arthritic changes and inflammation.64 Even the time-tested copper bracelet was eventually shown to be an effective anti-inflammatory, due to the absorption of copper through the skin.65 However, the development of anti-inflammatory steroids and aspirin-like nonsteroidal anti-inflammatory drugs quickly replaced copper compounds in the treatment of these conditions. Numerous researchers have examined the paradoxical role of copper in the process of inflammation, and they have determined that the increase in serum copper is a physiological response to inflammation, rather than a promoter of it.66 In fact, the main copper containing enzyme, ceruloplasmin, is significantly elevated in inflammatory conditions and has anti -inflammatory activity.67 Additionally, it has been shown that copper deficiency increases the severity of experimentally-induced inflammation,68 and that dietary copper must be increased to maintain adequate copper status of animals in an inflammatory state.69
With the knowledge that many copper complexes possess anti-inflammatory activity, and the finding that these copper complexes almost always have significantly stronger activity than their parent compounds, it has been hypothesized that the active form of many popular anti-inflammatory drugs are their copper chelates. Interest in copper complexes as anti-inflammatory drugs and antiarthritics is evidenced by the large number of reviews and symposia proceedings published in recent years.70 The sum of this research has shown that copper chelates of most anti-inflammatory compounds, as well as many other compounds, have strong anti-inflammatory activity in numerous models of inflammation. Also, these copper chelates have lower toxicity and stronger anti -inflammatory activity than their parent compounds.
Return To Top
Although most research utilizing copper complexes has been to determine anti-inflammatory activity, copper complexes have shown potential as a physiological approach to the treatment of numerous chronic diseases. This potential has been expanded to include, in addition to inflammatory diseases, gastrointestinal ulcers, cancers, carcinogenesis, and diabetes. In these conditions much of the research interest has centered on the finding that many copper complexes demonstrate superoxide dismutase (SOD) activity. Because of this, many of these compounds have been designated as SOD-mimetics. One of the better recent reviews on this topic of copper complexes is a good example of the breadth of research that has been published on this topic. This review, published in the journal Progress in Medicinal Chemistry, is 110 pages long and contains a bibliography of 736 references.71 Unfortunately, despite the tremendous promise that copper complexes have in many varied diseases and conditions, clinical interest in these compounds has been almost nonexistent. While copper is slowly becoming less misunderstood, one can only hope that it will eventually be properly utilized in its potential for maintaining health and treating disease.
Return To Top
The importance that adequate copper nutriture plays in ensuring health, coupled with the fact that few of us obtain the recommended 2-3 milligrams daily of copper in a normal diet, makes copper supplementation essential if we are to prevent an inadequate copper intake. Most human supplements of copper contain either copper sulfate or copper gluconate, two well utilized forms of copper. However, because copper outside of biological systems can catalyze oxidation, the preferred type for multivitamin/mineral supplements is a coated form of copper, such as coated copper gluconate. This allows for all the important benefits of copper, without having the copper lower the vitamin/mineral supplements shelf-life. For most of us on average diets that contain 1-2 milligrams of copper, and not consuming large amounts of the copper antagonists vitamin C (>1000 milligrams) and zinc (>30 milligrams) daily, a daily supplement of 1-3 milligrams of copper should be adequate. Consumers of larger amount of vitamin C and zinc would be well advised to supplement with 3 milligrams of copper daily. Additionally, some people may wish to supplement with special forms of copper such as copper salicylate. Total copper supplementation should not exceed 5 milligrams daily, except under a physician's supervision.
No information in this article should be taken as a recommendation. If you have any questions about the relationship between copper and your health, seek the advice of a qualified physician.
Return To Top
1) E.B. Hart, H. Steenback, J. Waddell, et al, J Biol Chem 1928; 77: 797-812.
Return To Top
2) J.R.J. Sorenson, Med Bio 1985; 63: 40-43.
3) E.D. Harris, In: "Trace Elements in Health." (ed. J. Rose), 1983, Butterworths. London.
4) C.J. Gubler, M.E. Lahey, M.E. Cartwright, et al, J Clin Invest 1953; 32: 405-414. N.W. Solomons, J Am Coll Nutr 1985; 4: 83-105.
Return To Top
5) N.W. Solomons, J Am Coll Nutr 1985; 4: 83-105.
6) N.W. Solomons and L.H. Allen, Nutr Rev 1983; 41: 33-50. N. Romero-Chapman, J. Lee, D. Tinker, et al, Biochem J 1991; 275: 657-662.
7) S.N. Gacheru, P.C. Trackman, M.A. Shah, et al, J Biol Chem 1990; 265: 19022- 19027. N. Romero-Chapman, J. Lee, D. Tinker, et al, Biochem J 1991; 275: 657-662.
Return To Top
8) G.E. Cartwright and M.M. Wintrobe, Am J Clin Nutr 1964; 14: 224-232.
9) G.V. Iyenger, W.E. Kollmer, H.J.M. Bowen, "The Elemental Composition of Human Tissues and Fluids." 1978, Springer. NY.
10) K.O. Lewis, Gut 1973; 14: 221-232.
11) J. Camakaris, M. Phillips, D.M. Danks, et al, J Inher Metab Dis 1983; 6: 44-50.
Return To Top
12) H. Sandstead, Am J Clin Nutr 1982; 35: 809-814.
13) National Research Council. Copper. In: Recommended Dietary Allowances. Washington, D.C.: Food Nutrition Board, NRC/NAS, 1980: 151-154.
14) L.M. Klevay, S.J. Reck, D.F. Barcome, JAMA 1979; 241: 1916-1918.
15) G.W. Evans, Physiol Rev 1973; 53: 535-570.
16) L.J. Taylor, M.L. Hinners, S.J. Ritchey, Am J Clin Nutr 1980; 33: 1077-1082. Anonymous, Nutr Rev 1985; 43: 148-149. H.N. Hoffman, R.L. Phyliky, C.R. Fleming, Gastroenterology 1988; 94: 508-512. E.J. Gyorffy, H. Chan, Am J Gastroenterology 1992; 87: 1054-1055. M.D. Festa, H.L. Anderson, R.P. Dowdy, Am J Clin Nutr 1985; 41: 285-292.
17) P.W.F. Fischer, A. Giroux, M.R. L'Abbe, Am J Clin Nutr 1984; 40: 743-746.
18) See Reference 16
Return To Top
19) D.B. Milne and S.T. Omaye, Int J Vitam Nutr Res 1980; 50: 301-308. G.J. Van Den Berg, J.P. Van Mouwe, A.C. Beynen, Biol Tr Elem Res 1990; 23: 165-170. D.B. Milne, S.T. Omaye, W.H. Amos Jr., Am J Clin Nutr 1981; 34: 2389 -2393.
20) E.B. Finley and F.L. Cerklewski, Am J Clin Nutr 1983; 37: 553-556.
21) N.W. Solomons, J Am Coll Nutr 1985; 4: 98-99.
22) L.M. Klevay, Am J Clin Nutr 1975; 28: 764-774.
Return To Top
23) L.M. Klevay, Am J Clin Nutr 1973; 26: 1060-1068.
24) L.M. Klevay, L. Inman, L.K. Johnson, et al, Metabolism 1984; 33: 1112-1118. L.M. Klevay, Med Hypothesis 1987; 24: 111-119.
25) L.M. Klevay, Med Hypothesis 1987; 24: 111-119.
26) L.M. Klevay, Atherosclerosis 1985; 54: 213-224.
27) L.M. Klevay, Ann NY Acad Sci 1980; 355: 140-151.
Return To Top
28) B. Chipperfield and J.R. Chipperfield, Am Heart J 1978; 95: 732-737.
29) L.M. Klevay, Ann NY Acad Sci 1980; 355: 140-151.
29b) F.J. Kok, C.M. Van Duijn, A. Hoffman, et al, Am J Epidem 1988; 128: 352-360.
30) Y. Rayssiguier, E. Gueux, L. Bussiere, et al, J Nutr 1993; 123: 1343-1348.
Return To Top
30b) M. Vlad, E. Bordas, R. Tomus, et al. Biol Trace Elem Res 1993; 38: 47-54.
31) L.M. Klevay, Biol Tr Elem Res 1988; 16: 51-57.
32) M.A. Johnson, J.G. Fischer, S.E. Kays, Crit Rev Food Sci Nutr 1992; 32: 1-31. 33) N.W. Solomons, AM J Clin Nutr 1979; 32: 856-871.
34) P.S. Baleuska, E.M. Russanov, T.A. Kassabova, Int J Biochem 1981; 13: 489-493.
Return To Top
35) K.G.D. Allen, J.R. Arthur, P.C. Morrice, et al, Proc Soc for Exp Biol 1988; 187: 38-43.
36) L.L. Mitchell, K.G.D. Allen, M.M. Mathias, Prostaglandins 1988; 35: 977-983.
37) Y. Rayssiguier, E. Gueux, L. Bussiere, et al, J Nutr 1993; 123: 1343-1348.
38) H.H.A. Dollwet and J.R.J. Sorenson, Tr Elem in Med 1985; 2: 80.
Return To Top
39) See Reference 6.
40) H.H.A. Dollwet and J.R.J. Sorenson, Biol Tr Elem Res 1988; 18: 39-48. J.J. Strain, Med Hypothesis 1988; 27: 333-338.
41) See Reference 40
42) V. Worthington and P. Shambaugh, J Manipulative Physiol Ther 1993; 16: 169-173.
Return To Top
43) D.M. Danks. Copper Deficiency in Humans. In: "Biological Roles of Copper." CIBA Foundation Symposium-79. Exerpta Medica, Amsterdam, 1980. p. 209.
44) L.G. Strause, P. Hegenauer, R.C. Saltman, et al, J Nutr 1986; 116: 135.
45) E. Frieden, Caeruloplasm. In: "Biological Roles of Copper." CIBA Foundation Symposium-79. Exerpta Medica. Amsterdam. 1980. p. 93.
46) R.J. Cousins, Physiol Rev 1985; 65: 238-240.
Return To Top
47) S. Bala and M.C. Failla, Proc Natl Acad Sci USA 1992; 89: 6794-6797.
48) U. Babu and M.L. Failla, J Nutr 1990; 120: 1700-1709.
49) U. Babu and M.L. Failla, J Nutr 1990; 120: 1700-1709.
50) S. Bala and M.C. Failla, Proc Natl Acad Sci USA 1992; 89: 6794-6797.
51) U. Babu and M.L. Failla, J Nutr 1990; 120: 1700-1709.
Return To Top
52) S. Inutsuka and S. Araki, Cancer 1978; 42: 626. W.M. Willingham and J.R.J. Sorenson, Tr Elem Med 1986; 3: 139-140.
53) W.M. Willingham and J.R.J. Sorenson, Tr Elem Med 1986; 3: 139-140.
54) L.W. Oberley and G.R. Buettner, Cancer Res 1979; 39: 1141.
55) R.J.R. Sorenson (ed.), Biology of Copper Complexes. Humana Press, Clifton, NJ. 1987.
56) R.J.R. Sorenson, Prog Med Chem 1989; 26: 506-507.
57) R.J.R. Sorenson, Prog Med Chem 1989; 26: 507.
58) R. A. DiSilvestro, J.K. Greenson, Z. Liao, Proc Soc Exp Biol Med 1992; 201: 94-99.
59) F.L. Greene, L.S. Lamb, M. Barwick, et al, J Surg Res 1987; 42: 503-512.
60) F.L. Greene, L.S. Lamb, M. Barwick, et al, J Surg Res 1987; 42: 503-512. Anonymous, Nutr Rev 1985; 43: 213 -215. M.D. Tilson and G. Davis, Surgery 1983; 94: 134-141.
Return To Top
61) M.W. Whitehouse, Agents and Actions 1976; 6: 201-216.
62) A.J. Lewis, Agents and Actions 1984; 15: 513-519.
63) A.J. Lewis, Agents and Actions 1984; 15: 515-519.
64) J.R.J. Sorenson and W. Hangarter, Inflammation 1977; 2: 217-238.
65) W.R. Walker, S.J. Beveridge, M.W. Whitehouse, In: Inflammatory Disease and Copper (ed. J.R.JK. Sorenson), Humana Press, Clifton, NJ. 1982. p. 453-467.
66) J.R.J. Sorenson, J Pharm Pharmac 1977; 2: 450-452.
67) E. Frieden, Clin Physiol Biochem 1986; 4: 11-19.
68) J.R.J. Sorenson and V. Kishore, Tr Elem Med 1984; 1: 93.
69) R. Milanino, A. Conforti, L. Franco, et al, Agents and Actions 1985; 16: 504-513.
70) J.R.J. Sorenson, Prog Med Chem 1989; 26: 437-568.
71) J.R.J. Sorenson, Prog Med Chem 1989; 26: 437-568.
Return To Top
|Special Pages On The Various of Web Sites Authored by Karl Loren|
|OC History||Oral Chelation||Testimonials|
|Family Of Three Oral Chelation Formulas||Life Glow Basic||Life Glow Basic Ingredient List|
|Life Glow Plus||Life Glow Plus
|American Heart Association -- Lies|
|Super Life Glow||Super Life Glow
|All Products||Shopping Cart Order Section||Research|
|Taheebo Life Tea||Witch Doctors Versus Harvard||MSM Sulfur|
|Calcium||How Bones Grow||Colloidal Minerals|
|Jean Ross||Philosophy||The Wednesday Letter|
|Arthritis & James Coburn's Use Of MSM||Karl Loren Viewpoints||News And Announcements|
|Dr. Flanagan's Microhydrin||500 Page Book On Heart Disease||Colostrum & Transfer Factor|
|Germanium||Ultrasound Technology||Bulk MSM|
|Cancer & Biopsy||Diabetes||Heart Disease & Bypass Surgery|
|Karl Loren's Diet||Guarantee||Navigation Help Page|
|The Links Below Jump To Pages On Whatever Web You Are In|
|Table Of Contents||Search This Web||Navigation Help Page|
|Write To Karl Loren -- He Pledges To Answer EVERY Personal Message, Personally. Click here or on his name in the box below.|
|The Links Below Are To Various Web Sites Published By Karl Loren|
|Karl Loren Web||Vibrant Life Web||Karl Loren's Book|
|Super Colostrum||Bulk MSM||Heart Disease|
|Instead Of||Chelation Therapy||Super Colostrum (2)|
|Immune Egg||Central Page For All Web Sites!|
SUBSCRIBE: The Vibrant Life Magazine is a free electronic weekly newsletter written and published by Vibrant life. You can view more than 50 back issues of this publication by clicking here. The newsletter subscription list is maintained on a secure server, no name is ever given or sold to anyone, and it is never used except for this Newsletter. The letter has been changed to product and information news which is sent out regularly each week.
REMOVAL: You can remove yourself from the subscription list in several different ways. Click here to read about this entire newsletter system. Every edition of Product and Information Letter is delivered to your address with YOUR name and address in view on the letter, with a link that allows you to remove THAT name from the subscription list. If you try to send this removal message from an address different from the one you used to send in your original confirmation, then you will get a warning notice first, sent to the subscription address, asking you to confirm that you want to be removed from the list -- by replying to THAT request for confirmation, you will then be automatically removed. Thus, no one else can unsubscribe you, from some other computer, without your knowledge. But, if you send in the unsubscribe notice from the same machine used to receive the Letter, then the removal from the subscription list is automatic.
Personal Message: When you send a personal message to Karl Loren, you will receive a personal reply as per his instructions. Karl pledges that every personal message will get a personal answer. When you provide your mail address, we will send you free information including our free catalog and a cassette tape lecture by Karl Loren about heart disease, no charge, by mail, even if outside the US. You can select particular information you would like to receive, along with the free cassette tape and catalog.
You can reach Vibrant Life in many ways, including by mail to Vibrant Life, PO Box 10666, Burbank, CA 91510-0666. Within the US and Canada, use the toll free number: (800) 523-4521, the local number: (818) 558-7099, eMail to email@example.com or any one of the hundreds of message forms throughout the 60 web sites. Vibrant Life normally ships the same day we get an order. There are message forms on each of the 100,000+ pages on this and other sites where you can communicate with Vibrant Life. Check out our companion site, at: http://www.oralchelation.net where Karl's 2000 page book is published. Karl Loren is the author and webmaster for this BOOK, as well as for another web site about ORAL CHELATION. His personal philosophical articles are at PHILOSOPHY.
Copyright © May 23, 2012 4:52 PM by Karl Loren on behalf of Vibrant Life, ALL RIGHTS RESERVED. Permission is granted for non-commercial downloading, copying, distribution or redistribution on two conditions: One, that some form of copyright notice is included in every copy distributed or copied, showing the copyright belonging to Vibrant Life, Burbank, CA, at www.oralchelation.com . The second condition is that the material is not to be used for any purpose contrary to the purposes and objectives of this site. This permission does not extend to materials on this site which are copyrighted by others.