Affect on Copper of Cortisol, Potassium, Disease
by Charles Weber
Copper nutrition is crucial for slipped discs (herniated, ruptured, prolapsed), hemorrhoids, emphysema, aneurysms, immunity, and maybe preventing gray hair.
Page 1. - copper physiology, elastin tissue, copper enzymes, diabetes, potassium, superoxide, cortisol and corticosterone.Page 2. - cortisol, ceruloplasmin, copper in the diet
Page 3. - copper sources, milk, copper for babies, interfering food, copper toxicity, affect on society.
A site to obtain a book about potassium nutrition and physiology is shown at the end of this article.
A table expressing copper and zinc in food as milligrams per thousand Calories.
A new dictionary is also available at this site.
cortisol works by declining effect, not necessarily declining concentration. Indeed, in most diseases glucocorticoids actually rise. However, at the same time T white blood cells secrete a protein, glucocorticosteroid-response modifying factor (GRMF), and the protein hormone interleukin-1, both of which inhibit the effect of cortisol on white blood cells other than the suppresser cells [Fairchild, et al]. The effect of GRMF on physiological processes is unknown at present. The husband and wife team working on GRMF was almost murdered and this disrupted investigations. I suspect that most of cortisol's effects on copper enzymes will prove to be involved with GRMFs. These two protein factors thus raise the effective set point of cortisol. This system also uses interleukin-1 to stimulate the production of ACTH, and thereby also cortisol, instead of the brain's corticosteroid releasing factor (CRF) which last is used in the absence of infection. The immune cells thus take over their own regulation.
Cortisol
Cortisol, like DOC, also stimulates lysyl oxidase activity [Siegel], and undoubtedly for the same reason, that is to provide extra copper to white blood cells during infection upon decline. Its action on collagen is exactly the opposite of DOC's: [Popsilova & Popisil] for cortisol inhibits collagen formation [Manchester p273]. This is significant because collagen is the most bulk of protein, is inert, and makes relatively non vital structures, the skin being especially targeted by cortisol by ten times [Houck, et al]. This attribute of cortisol would be a desirable attribute if the pathogen were in the serum, because increased synthesis of collagen when cortisol declined would considerably lower free amino acids in the blood stream, and thus slow down bacterial growth. There would be little advantage from this during diarrhea, and this may be why DOC acts in the opposite direction and thus counteracts cortisol's effect when diarrhea is involved.
I submit that potassium would be a lot safer way of increasing cortisol than use of injections. Steroids are hormones, not pharmaceuticals. Their sole purpose is to keep important body functions and concentrations at values optimum for survival. There should be no reason why artificial additions should be necessary under normal conditions and adequate nutrition for anyone free of genetic defects (which is undoubtedly almost everyone). Quite often a steroid is injected with impunity and seemingly no immediate obvious adverse symptoms. But this is usually because other hormones alter in an attempt to adjust the imbalance and because many of the adverse symptoms such as, for instance, negative feedback which causes reduction in secretory cells of the hormone is a long time in materializing. One medical writer summed it up so: "it is remarkable how effective cortisol is in getting a seemingly hopeless patient on his feet again. Sometimes it is so effective, he can walk all the way to the autopsy table".
CERULOPLASMIN
Ceruloplasmin is higher than normal in the blood serum of arthritic people [Aiginger, et al]. The total serum elemental copper concentrations have a bimodal distribution for these rheumatoid arthritic people, with the bottom mode about the same as normal people or people with osteoarthritis [Youssef, et al]. Normal people averaged about 22 millionths of a mole or 1.4 milligrams per liter, but with a fairly wide distribution. It could be that the bottom mode was from misdiagnoses.
Ceruloplasmin is almost certainly used as a transport protein to bring copper from the liver to the target cells [Frieden] in addition to its other transport uses. Ceruloplasmin is a blood protein which contains 6 [Frieden] or 8 [Sekiya, et al] atoms of copper inside the molecule which are not in equilibrium with the serum [Pelsach, et al]. Such a transport mechanism would be extremely useful in case of infection, because, since ceruloplasmin's copper is not in equilibrium with the serum, it is thus not available to pathogens. With that many copper atoms it is conceivable that it can give up its copper in more than one way. It must be destroyed in order to give up all its copper. Ceruloplasmin's half-life is 130 hours [Sekiya] but has a higher turnover in rheumatoid arthritis [Sorenson, 1978 p217]. One of its copper atoms may be exchangeable under reducing (anaerobic) conditions [Peisach], however. The hormone which causes rise of serum copper and ceruloplasmin from the liver because of stress may be epinephrine (adrenaline) [Evans 1973b p556] [Meyer, et al]. Cortisol is not directly part of it, although decline of ACTH, which regulates cortisol, may be for immunity [Evans 1973b p554]. Cortisol does stimulate the formation of the copper storage protein, metallothionein, four or five fold. [Piletz & Herschman]. Thus copper should become more available for ceruloplasmin synthesis inside the liver upon decline of cortisol. The main advantage of this last may be to help drain the intestinal contents of copper to deny copper to diarrhea bacteria, however. It may be cortisol's decline that inhibits bile flow after adrenalectomy (amputation of adrenal glands) [Evans 1973b p556], and is conceivably further indication that a decline of cortisol’s affect due to intestinal disease does the same thing. DOC decline inhibits liver copper uptake and increases free copper secretion from the liver [Gregoriadis & Sourkes]. This is logical since the serum copper can not nourish diarrhea bacteria.
The mortality of chicks from salmonella infections rises significantly from zero if large amounts of copper as copper sulfate is fed, which supports the contention that this is the reason why their bodies increase ceruloplasmin four fold or even as much as six fold [Underwood p58] during infection but not equilibrium copper bound to albumin and histadine [Starcher & Hill]. This concept is reinforced by the fact that chicks in the absence of infection have a very low ceruloplasmin serum content [Starcher & Hill] unlike mammals. The fact that people with Wilson's disease are not susceptible to infection even though they cannot synthesize ceruloplasmin does not refute ceruloplasmin's role proposed above. This is because people with Wilson's disease can not transport copper to the bile using ceruloplasmin, so that their cells are already loaded and even overloaded with copper. The inability to synthesize ceruloplasmin in Wilson’s disease is because of a defect in a gene that synthesizes an inside the cell chaperone protein called ATP7B, which is required to move copper into ceruloplasmin in the liver [Cox]. The high ceruloplasmin content of mammals in the absence of infection may originally have been an adaptation from their immune use to supply extra copper to the embryo by females. Even today human females have a higher ceruloplasmin content than males do [Frieden 1980 p110]. There may be a similar advantage keeping free copper from funguses as well as bacteria if a limited experiment I tried is an indication. Bacteria could not make use of the copper in ceruloplasmin unless they were to evolve an elaborate mechanism for preferentially binding the ceruloplasmin and then degrading it. This would be a very unlikely occurrence. Ceruloplasmin declines in the serum greatly during a deficiency [Gomi]. This would not itself affect immunity except that the ability to increase ceruloplasmin during infection is probably decreased also.
Something about ceruloplasmin may be related to Parkinson's disease [Frieden 1980, p108].
It is possible then, that the best way to relieve a copper deficiency that is concurrent with a bacterial infection would be by ceruloplasmin injections. Such a procedure would bear investigation since it is unlikely that people will change their diets and eat enough copper or delete copper physiology poisons, which may include tobacco (which I suspect because of tobacco's involvement with emphysema). White blood cell count is very sensitive to copper status and is the earliest and most consistent symptom of a deficiency [Cordano, et al]. Even a mild deficiency causes spleen derived immune cells to be significantly less competent as stimulators in general and also to be stimulated by endotoxin, pokeweed, and concavalin A [Lukasewicz & Prohaska]. Such animals took an average of one third as long a time to die as replete animals, and had four times the mortality [Newberne & Gebhardt]. I believe that the efficacy of adequate copper prior to an infection is established beyond any reasonable doubt. Dietary copper during an infection may be disadvantageous however, except during a deficiency, when it probably would be best to spread it out across the day complexed to protein. A depleted liver removes free copper from the blood with extreme rapidity, [Peisach, et al] however, so the danger of bacterial stimulation is probably not acute.
Since ceruloplasmin is probably used to transport copper to the bile for excretion, excretion may inadvertently rise when ceruloplasmin rises during infection (I have no data to establish this). A similar mechanism may account for the higher ceruloplasmin content in the serum of arthritic people. Apparently decline of cortisol is not used for this purpose and the hormones that do are not known for sure. There could therefore be an increased excretion arising from the higher serum ceruloplasmin content of arthritic people. If this is so, arthritic people may need somewhat more copper than others until their potassium deficiency is relieved. This may be why their liver copper is low, why their whole blood copper (which includes the red and white cells) does not rise even though the serum is high [Sorenson 1978, p217] and part of the reason why they are much more likely to die from ruptured blood vessels (aneurysm) and infection than others [Matsuoka, et al]. Thus rheumatoid arthritis could be viewed as often a multiple deficiency, not all of the symptoms of which can be always removed by supplying only potassium.
Arthritic people also have a higher free copper content in their blood serum [May & Williams p294]. This would seem at first glance to be at variance with the concept that arthritis is an inappropriate immune response. However, intestinal diseases should not be affected much by free copper in the serum, so that immune copper responses accentuated by potassium deficiency may have some subtle differences from responses that are involved primarily with serum infections. Free copper may be more useful to an animal when muscle exertion is needed, because when sheep which have been subjected to a copper toxicity hear the bark of a dog, so much free copper can suddenly be released from the liver that it can kill them [Bremner p42]. Therefore this may be additional indication that people who have a serum infection should be guarded from fear. Free serum copper may be useful to someone with intestinal disease so that he can operate optimally. In addition, the vigor of copper's absorption may even be increased in babies in a diarrhea situation because of the decline in cortisol mentioned previously. Thus diarrhea bacteria would have the use of less copper. I have no assurance that this is the case in adults, and indeed corticosterone injections cause greater secretion of bile in baby rats but not in adults [Evans p234]. This may be an adjunct of coticosterone, used to get baby rats out of the non-excretion mode. Rats are poor experimental animals for this concept because they do not secrete cortisol. They probably were able to lose that secretion because they have a marked inhibition of cholera toxin by something in their intestinal fluid [Donowitz & Binder] and because their ascending colon absorbs water under c-AMP stimulation unlike their descending colon and other mammals [Hornyck, et al]. Rodents should not be used for any experiments involving immunity, and perhaps better yet, for no experiments.
Histamine and Inflammation
A copper deficiency will enhance the number of mast cells [Schuschke][Schuschke]. This causes the amount of histamine secreted by these cells which, in turn, accentuates the inflammation called for by immune hormones. These increased mast cells may be the reason why copper supplements seem to have a beneficial immediate affect on rheumatoid arthritis, since inflammation is one of the more distressing symptoms of that disease in its advanced state.
DHEA steroid
A copper deficiency halves serum DHEA (dehydroepiandrosterone) in rats [Klevay and Christoferson]. I do not know how this happens or what the significance of it is.
Copper in the Diet
A copper deficiency is possible even without the inappropriate requirements of a potassium deficiency proposed. Processing food often lowers copper content. The standard hospital diet is less than 0.75 mg per day [Owen p13]. None of 40 ready to eat cereals had copper or manganese supplements although 50% and 25% or more respectively for the MDR of iron and zinc was supplemented. 25% of supplement pills contained no copper [Johnson]. Zinc without copper is very dangerous because zinc interferes with absorption. I lost a relative from a brain hemorrhage because she took zinc supplements but no copper while taking blood thinners. A zinc deficiency during a copper deficiency is even more dangerous for the heart than high zinc so the zinc [*] to copper ratio is important. Diets of free choice are 1 mg of copper per day [Holden, et al]. Western diets usually range between 2 and 4 mg per day and 20 USDA diets contained 1.05 per day [Mason p1998]. This compares to 4.5-5.8 mg per day in the Indies [Peisach p1998]. 0.8 mg of copper per day was found to be the amount for maintenance in young men [Turnlund} but this is undoubtedly much too low for the general population in order to accommodate those who are; under stress, eating interfering food elements, with age deteriorated organs, or afflicted by disease. Intravenous is suggested to be one-third the oral intake [Mason p2036] or 0.3 mg per day normally or 0.4 to 0.5 during diarrhea [Shike]. The unpopularity of the rich source, liver, and the high cost of mollusks reinforce this situation for poor people not in the military (the military provides occasional shellfish). 2 mg per day is thought to be the minimum daily requirement (MDR) [Klevay 1982] and I suspect that 4 mg per day would be the safest intake (RDR) in order to cover everyone or perhaps the 6 mg. or so received in the Indies. Copper intestinal absorption is linear up to about 6 mg per day after which it tapers off (but based on rat experiments) [Marceau], so I would suspect that copper beyond about 6 mg would be superfluous.
Lending some support to this contention is the circumstance that underground Utah copper miners had 15.1 accidents per 200,000 man hours with no lost time Vs 10.9 accidents with lost time to give a ratio of 1.4. The figures for all underground Utah non copper miners were 4.4 and 8.4, giving a ratio of 0.5 [US Dept. Labor] as computed from bureau of mines statistics. There are figures for Arizona [Inzan & Hoyle]. Figures from other states trend in the same direction for underground mines, open pit mines, and processing plants. This would seem to indicate that copper miners are tougher than other miners, since each injury is less likely to cause lost time for copper miners. Also, the greater number of injuries to copper miners suggests that their greater toughness tends to make them more careless. The figures might have been even further apart if injuries not connected to strength such as eye injuries and burns had been removed from the data. New Jersey copper smelter workers Have 8% of injuries as back injuries vs. 20% for all other occupations [*]. Two hundred and eighty patients having severe back pains were treated with copper salicylate. A majority was believed to have a slipped disc. Improvements were considerable and rapid [Sorenson & Hangarter]. Finnish copper miners are said to have much less arthritis and the women miners less anemia then other Finns [Sorenson p223]. Finns have a lower copper intake than Americans, and as little as one half the intake of Africans and Asians, [Mason p1083], probably partly because of a high milk intake. Finns have the highest arthritis rate in the world, [Kellgren JH] possibly partly because of perspiration potassium losses during saunas. Such figures suggest an environmental cause rather than genetic, and probably not climatic because Laplanders not much further north have a lower rate, while Masai people [Best & Taylor p768] join the Finns' high rate probably because of their milk intake also as well as low vegetation in the diet. Males who die from aneurysms have one fourth the tissue copper and two thirds the liver copper contents upon autopsy than normal [Tilson]. Since young women are not as affected by copper deficiency as men generally it must be because of the fact that estrogen enhances absorption [Cohen, et al]. I suspect that this is an adaptation to furnish babies with sufficient copper to surmount the low intake into babies while nursing milk. This is evidence that disruption of copper in arthritis is secondary because women have arthritis much more often than men.
A pervasive copper deficiency would be suggested from the beneficial effects of copper supplements on such diverse diseases as anemia, psoriasis, ulcers, ankylosing spondilitis (Ankylosing spondilitis probably heals slowly because the sacral and ileal joints are made of type I cartilage [Paquin, et al]. The lower ceruloplasmin in that disease may also be implicated in some way [Sorenson 1978, p223, 225, 253] ), infection, cancer [Nriagu], impaired growth of the retina [Danks p211], seizures as discussed by Sorenson, and deficiency creates atherosclerosis of the kidneys [Owen], because some of these diseases are common in our society. Copper supplement has healed slipped discs (in combination with pharmaceuticals). A copper deficiency may be the cause of arrhythmias associated with use of liquid protein diets [Klevay & Viestenz (this reference has EKG data)]. Low thyroid secretion has also been shown to be accentuated by too low a copper status and energy generation by rat BAT fat cells during cold stress is reduced by a copper deficiency which may be partly due to decreased thyroid secretion [Oliver], but I am unaware of the mechanism. If these diseases are related to copper there should be a correlation between them, but I have no information for this. Copper helps in removing abnormal EKGs caused by a copper deficit but is not always on time, and did not prolong life indefinitely [Viestenz & Klevay] which indicates that heart disease is usually a multiple deficiency. In addition, any problem that is a function of strength of elastin tissue has a high probability of being accentuated by a copper deficiency. This may include Marfan's syndrome. Several of these symptoms together would make the probability of a copper deficiency existing very high indeed and anything which would reduce or interfere with copper very dangerous.
Continue to copper sources, milk, interfering food, copper toxicity, and affects on society
Back to copper physiology, elastin, enzymes, potassium, superoxide, and glucocorticosteroids
REFERENCES
SOME HEALTH ARTICLES
VIII.
You may see here the way to acquire a very comprehensive book about potassium nutrition and physiology. It is called “POTASSIUM NUTRITION in Heart Disease, Rheumatoid Arthritis, Gout, Diabetes, Metabolic Shock, and High Blood Pressure”. The table of contents and the introduction are shown.
There is an article discussing anacardic acids in cashew nuts to cure a tooth abscess that might prove useful
There is also an article which proposes some speculation about diabetes amelioration and a possible cause.
See this site (for a summary of potassium and copper nutrition)
V. Electrolyte regulation (sodium and potassium) -- VI. Purpose of cortisol -- Back to; VII. Copper nutrition and physiology, page one -- Copper in Foods -- There is evidence that cell phones can produce tumors. Using remote ear phones would seem to be a good idea.
Fluoride in city water will cause fluorosis discoloration of teeth, weakened bones, damage to the kidneys an immune system, and, worst of all, damage to the nerves resembling Alzheimer’s disease.
The pioneering efforts about potassium for arthritis by Charles de Coti-Marsh enabled him to form a foundation currently active in England that promotes the use of potassium for arthritis and it has helped cure more than 3500 people.
The author, Charles Weber, has a degree in chemistry and a masters degree in soil science. He has researched copper for over 30 years, primarily a library research. He has cured his own slipped disc and other symptoms with copper supplement. He has published articles on allied subjects in; The Journal of Theoretical Biology (1970, 1983), The Journal of Applied Nutrition (1974), Clinical and Experimental Rheumatology (1983), and Medical Hypotheses (1984, 1999, 2007, 2008)
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Updated Marh 2014