Homeopathy/Herniated Disc L5-S1
Charles Weber wrote at 2012-10-31 07:58:38
COPPER TO TOUGHEN HERNIATED DISCS by Charles Weber
ABSTRACT Copper is part of lysyl oxidase, which is the enzyme that cross links elastin tissue. The strength of elastin depends on its cross links (Sandberg). Upper spinal discs are made of elastin. Therefore it is imperative that copper status be brought up to normal before an operation. Sometimes an operation will not even be necessary if this is done. Copper status must be kept normal thereafter in order to prevent a recurrence by total intake of at least 3 mg per day.
Herniated discs are the most painful, and numerous diseases in modern society. Slipped or herniated discs are estimated to cost more than 200 billion dollars directly and indirectly each year in the USA alone [http://www.futuremedicine.com/doi/pdf/10.2217/14750708.4.1.51
]. I suspect that copper deficiency status is the most important parameter affecting them. Two hundred and eighty patients having back pains were treated with copper salicylate. A majority was believed to have a slipped disc. Improvements were considerable and rapid [Sorenson & Hangarter]. Restoring copper during that disease is imperative.
Therefore increasing copper intake should have a dramatic effect on our collective health. Copper should always be made adequate even when a disc operation is in order. If the copper status is unknown, there should be at least a week of 6 mg total intake per day prior to the operation, or at least high in copper foods such as shellfish or liver, especially sheep liver. There should not be great danger if there is a concurrent bacterial infection because a depleted liver removes free copper from the blood with extreme rapidity, [Peisach, et al], so the danger of bacterial stimulation is probably not acute. Even so, using ceruloplasmin injections might be a safer way during such an infection because copper is tightly bound in ceruloplasmin.
CAUSES of COPPER DEFICIENCY
That copper is below optimum in a large number of people is virtually certain from current evidence. This is caused by the low copper content of dairy products, loss of copper by removal of the germ from grain, and refining of sugar. Fructose (corn syrup) and sucrose sugar in fruit apparently produces a much greater need for copper once in the body [Reiser] [Fields & Lewis]. Treating vegetables with the chelating agent, ethylene diamine tetraacetate, reduces both their copper and their zinc to 20% of original values [Pfeiffer, 1972,p161]. Eating large amounts of vitamin C (ascorbic acid or ascorbate) is thought to interfere with utilization of copper within the body [Harris 1991][Underwood p71] although Evans thinks the problem is that absorption is decreased [Evans 1973b]. Vitamin C does cause greater excretion of copper via the bile and decreased absorption [Van Den Berg], so these may be the main mechanisms for vitamin C’s interfering with copper. Vitamin C causes ruptures of the aorta in copper deficient animals [Owen]. Vitamin C inhibits copper sulfate injection to stimulate lysyl oxidase under a deficiency of copper if given before or at the same time as copper sulfate injection. But, strangely, if given 75 minutes later, accentuates copper’s affect in stimulating lysil oxidase [Di Silvestro, 1981].
WORLD COPPER STATUS
Polish people are said to average 30% below the RDR (recommended daily requirement) from food [Pietruska] and 70% of Japanese are below the MDR (minimum daily requirement) [Otsuki]. Keep in mind that the MDR is designated too low to start with, as is the RDR. Young adult American women average 1.16 mg per day [Murphy] and men about 1.5. The difference between the sexes is no doubt primarily due to women eating less food than men. People in Belgium average 1.5 +/- 0.4 mg per day [http://www.springerlink.com/content/m552011168630u37/
]. Adolescent males, both incarcerated and free, are below the RDA [Gans] which has been set at 2.0 but should be at least 3.0. Porto Rican school lunches are below the federal RDR [Preston]. Hemodialysis patients have low copper and zinc serum levels [Komindr]. Even so, a full blown copper deficiency takes several months to develop in people with an injured digestive system, much longer than for zinc [http://www.nphp.gov.au/enhealth/council/pubs/pdf/copper.pdf
(p68)]. This is because the liver stores large amounts of copper.
SYMPTOMS of COPPER DEFICIENCY
People vary considerably in their genetic makeup, and there are several dozen enzymes and hormones containing or affecting copper, so it should not be surprising that the symptoms of the copper deficiency diseases should vary greatly or that "spontaneous" remissions are possible. Other enzymes than lysyl oxidase require copper to activate them, They include; Two forms of Superoxide dismutase or SOD1 (Breaks down the superoxide free radical), Tyrosinase, Cytochrome c oxidase (Electron transport involved in energy production), Dopamine –hydroxylase, (Converts dopamine to norepinephrine), Clotting Factor IV (Blood clotting), Thio oxidase (Disulfide-bond formation), Protein Kinase (Development of Nervous System), Dopamine mono-oxygenase (Catecholamine Synthesis from Tyrosine), diamine oxidase,histaminase.
Low white blood cell count (neutropenia) is the earliest symptom in copper deficient babies [Cordano, et al]. The immune system is very sensitive to adequate copper [Prohaska & Lukaseqycz ][Percival]. TETA poison reduced IL-2 (interleukin-2) production 50% but not in the presence of copper supplements [Hopkins 1996] and interleukin-2 is reduced by a copper deficiency [Percival p1065]. Neutrophils are reduced in numbers as well as function and superoxide anion production is 60% less. 2.5 milligrams total per day prevented further decline but was not enough to return to normal even though neutrophils turnover every 3-5 days [Percival p1067]. Thus this is a reasonable basis for setting 2.5 milligrams as the minimum daily requirement. ). 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. The standard hospital diet is less than 0.75 mg per day [Owen p13]. When you further consider that other nutrients and circumstances also vary enormously, at least for those eating processed food, it is not safe to assume that copper is not deficient because all the symptoms are not present. Any symptom should trigger consideration of increased intake from some source. Emphysema [Soskel], premature gray hair [Wu], blood clotting [Milne 1896], slow healing bone breaks [Dolwet], diabetes enhancement [Cohen 1982], high cholesterol [Klevay 1978] [Reiser] aneurisms, hemorrhoids [author’s observation], and anemia are such symptoms.
The median layer of the blood vessel (where the elastin is) is thinner from a deficiency but its elastin copper content is the same as normal men. The overall thickness is not different [Senapati, et al].
A copper deficiency halves serum DHEA (dehydroepiandrosterone) in rats [Klevay and Christoferson].
Elastin makes up the vertebrate disks above the sacroiliac, the blood vessels, much of the skin, the lungs, and the bronchial tubes of all vertebrates except the jawless fishes [Sage & Gray]. Elastin is about as flexible as a rubber band and can stretch to two times its length [Carnes 1977]. The 39 or more different kinds of collagen are about 1000 times stiffer. A healthy artery requires about 1000 mm of mercury or 10 times the normal mean blood pressure in order to rupture [Shadwick]. Therefore keeping strength of arteries up would seem to be even more important than keeping blood pressure down so far as arteries are concerned, although not necessarily so far as kidney glomeruli are concerned. However a copper deficiency coupled with high sodium (or high chloride?) causes disruption of the glomeruli basement membrane resulting in acute kidney failure [Moore]. Aneurisms are involved because copper is essential for lysyl oxidase, which enzyme cross links the elastin tissue. Numerous animal experiments have shown that a copper deficiency can cause diseases affected by elastin tissue strength [Harris]. The lysyl oxidase is secreted normally, but its activity is reduced [Kosonen] due, no doubt, to some of the initial enzyme molecules (apo-enzyme) failing to contain copper [Rucker] [Smith-Mungo]. Cross linking is especially crucial for elastin tissue because elastin gets all of its from cross linking [Carnes 1971] [Sandberg]. Elastin probably has a high turnover [Robert] and also may be porous to the enzyme, lysyl oxidase. I feel that improvement in less than a week is reasonable to expect for elastin tissue [Author's experience]. Activation of lysyl oxidase itself is rapid in copper deficient chicks rising greatly 6 hours [Harris 1976]. Elastin has a fairly high turnover rate [Robert] and lysyl oxidase has a half-life of only 16 hours [Siegel]. Restoration of elastin is near normal by 3-4 days after copper has been restored in chicks [Tinker] so cross linking must be rapid even if turnover is not. However strengthening is hardly instantaneous. My own experience as a young man leads me to suspect one must allow at least a week for sure total strengthening of the whole tissue. A normal body contains about 100 mg of copper [Turnlund, 1998], so even someone containing only half of normal should be able to correct a deficiency in a reasonable time with a total intake no more than 10 mg per day (8 mg supplement or so for a junk food diet) because at least 30% should be absorbed, but cutting intake back to no more than 4 or 5 milligrams or so total [Osterberg 1980 pp. 135, 142] upon repletion and making sure that seven times as much zinc is taken with the supplement dose at least when a routine intake is established. I suspect it is preferable if the zinc is imbibed at a different meal than the copper. In animal experiments adequate intake may be 5 to 10 times as high as intakes which cause deficiencies [Klevay & Madeiros 1996 p2422S]. More than 6 mg per day routinely is said not to be effective because per cent absorption becomes very low after that amount [Wapnir 1998 p1055s][Turnlund & Keyes].
Milne found that 2.6 milligrams per day of copper could not recover a deficit in 40 days while 3 to 6 mg per day did it in about 30 days [Milne] so the recommended daily requirement should be at least 3.0 instead of the current 2.0. [Turnlund & Costa].
You may see an extensive review of the chemistry of lysyl oxidase and its action upon elastin and the 39 or more different types of collagen. [http://herkules.oulu.fi/isbn9514267397/isbn9514267397.pdf
The strength of collagen is not as badly affected because of the long length of collagen molecules close order enabling hydrogen bonds to be affective. However inadequately cross linked collagen is subject to creep. The discs below the sacroiliac of the spine are composed of collagen. The strength of pig or chick tendon is little affected by copper deficiency, even though the animals are dying of ruptured aortas and even though the tendons have 70% the cross links of normal [O'Dell] [Chou]. The normal lesser number of cross links are desirable nevertheless, for they permit the tendons to return to their original position after stress is relieved and not to cold flow as polymers held together only by hydrogen bonds do. The number of cross-links is probably optimum, because too many would make the tendon brittle. Too few cross-links would cause the tendon to become slack with time. Thus the body has a tough material which approaches steel in strength weight for weight and bones which are almost as strong as cast iron (I do not know how cross linked bone collagen is although both bone and tendon are type I collagen [O'Dell]). The lesser reliance by tendon collagen on cross-linking for strength may be the reason why the body uses collagen to repair lesions in arteries during a copper deficiency instead of elastin [Waisman, et al]. Such a strategy may be a good immediate expedient for survival, but I suspect it results in an intractable hypertension eventually because collagen is much less rubbery or elastic than elastin. It is conceivable that something like that goes on to a lesser extent in spinal discs. It might be a good idea to find out
Ankylosing spondilitis probably heals slowly because the sacral and ileal joints are made of type I cartilage [Paquin, et al].
COPPER AFFECT on the SPINAL NERVE SHEATH and FLUID
A copper deficiency produces a degeneration of the spinal cord involving the sheath around the nerve fibers, It is similar to the degeneration caused by a vitamin B-12 deficiency. Winston and Jaiser have proposed that the similarity is because of a dysfunction of the methylation cycle, which is dependant on vitamin B-12 catalyzed enzymes and may be dependant on copper catalyzed enzymes also [Winston]. Methionine synthase requires copper and they suggest that s-adenosylhomocysteine may be regulated by copper.
There is raised copper in the cerebrospinal fluid during Parkinson's disease [Beshgetoor]. Perhaps copper should be investigated for Parkinson's disease.
MOVEMENT OF COPPER IN THE BODY
Copper, largely tied up as protein, enters the stomach, and there and in the upper intestine [Sachs, et al] [Underwood p70], the proteins other than those entering from the bile [Owen] are degraded (bile proteins are degraded in infant rats when glucocorticoids are low [Mistillis & Mearrick] ), thus making the bile the means of excretion for adults [Sarkar p246]. Loss in sweat is usually negligible [Underwood p74] as are losses in urine [Evans 1973b p547]. The copper is moved across cell walls possibly associated with certain amino acids [Neumann PZ & Silverberg M] [Sarka p236]. It may be alpha aminoisobuteric acid which is involved since this amino acid behaves the opposite of other amino acids from cortisol [Chambers, et al]. The copper is probably carried to a metallothionein barrier and storage substance by glutathione [Steinebach] and then moves past the metallothionein barrier inside the cells [Cohen, et al] into the serum. Both copper and zinc increase the metallothionein barrier [Oestreicher & Cousins]. The serum carries it, largely complexed to albumin and histidine [Frieden 1980 p104], to the liver. The liver rapidly [Peisach, et al p482] removes it and stores it until such time as unknown hormones (which probably do not include cortisol in any direct way) cause the liver to release ceruloplasmin (which protein contains copper) to bring copper to the target cells [Frieden] for general purposes, as well as unbound copper when under stress. The liver releases no copper to the plasma during a deficiency when the liver copper is below 2.7 milligrams per kilogram [Levenson 1998]. Adrenaline (epinephrine) stimulates ceruloplasmin release 150% [Weiner and Cousins] as well as free copper and may be the stress hormone for copper [Evans 1973b p556, 557]. Cortisol does not directly mobilize copper in stress.
I suspect the immune peptide hormones (one or more of the interleukins) may be used to stimulate copper for immunity but I have no data. The ceruloplasmin transporter is destroyed by the target cells, which includes those that make bile proteins for copper excretion. Ceruloplasmin has a half-life of 130 hours [Sternlieb]. The target cells could include the cells that synthesize tropoelastin (elastin precursor). If these cells synthesize Lysyl oxidase (which cross-links connective tissue), they probably must incorporate the copper into that enzyme inside the cell [Harris, et al, p175]. <a href=http://www.ikp.unibe.ch/lab1/harrison00.pdf
> Copper chaperone proteins move the copper inside the cell cytoplasm into target enzymes, which may be a process to avoid copper toxicity. These chaperones have been identified in cells from bacteria on up to humans.</a> These chaperones and cell membrane transport proteins have been <a href=http://nature.berkeley.edu/departments/nut/undergrad_class/nst-160/Puig.pdf
>elucidated considerably in recent years, and are very complicated.</a> A defect in the gene that makes ATP7A chaperone protein is responsible for causing Menkes syndrome and a defect in the gene responsible for ATP7B chaperone protein causes Wilson’s syndrome. Linder and Hazegh-Azam have written a review of copper movement inside the body [Linder].
Because anemia is the first clinical sign of copper deficiency, the goal of the study was to reduce ceruloplasmin to 20% of baseline value without reducing hematocrit below 80% of baseline. Brewer, et al [Brewer, et al] felt that ceruloplasmin is a reliable and sensitive measure of copper status at 20% and above, and tetrathiomolybdate was nontoxic when ceruloplasmin was reduced to 15-20% of baseline. <a href=http://www.nphp.gov.au/enhealth/council/pubs/pdf/copper.pdf
>However ceruloplasmin is not reliable when there is inflammation, infection or after surgery because ceruloplasmin makes up 80-90% of the blood’s copper or more. Ceruloplasmin content can be correlated with C-reactive protein (p69).</a> C-reactive protein will rise 10 to 100 fold within 48 hours of infection or injury. Most of the enzyme systems other than growth factors were not degraded excessively. No exacerbation of toxicity was obvious by the addition of interferon alpha to the tetrathiomolybdate treatment in one of the patients. This procedure would probably work for other copper toxic conditions also, and was originally used to solve toxicity during Wilson’s syndrome. <a href=http://george-eby-research.com/html/anti_ang.html
>See this site for sources of tetrathiomolybdate, physician’s liability, and discussion with regard to Hodgkin’s syndrome.</a> This may prove to be a good strategy to buy time until interferon, naltrexone, or other low side affect strategies can take hold (see discussion of naltrexone at the end).<P> Supplements or copper rich foods should be used for babies with extreme care, as should be formula made from water out of copper plumbing (which can contribute 0.8 mg per day to adult intake [Delves HT]), or brass pots (which have harmed American Indian children [Bremner p45]), because babies can not excrete copper. Nursing babies would be even a little more at risk from supplements since mother's milk contains five times cow's milk [Delves p7]. Babies have 19 mg total copper at term, half in the liver [Klevay 1996 p2424] or more. New borne babies have 230 PPM (parts per million) in the liver, which compares to 35 PPM in an adult. It must be obvious that even 2 mg per day would overwhelm a baby in a short time if continued. Copper absorption is proportional to intake from breast milk and formula (in rats), which formula is up to 10 times the amount in breast milk [Lonnerdal 1998 p1048s], although babies can tolerate a fairly high oversupply of copper beyond the above (Lonnerdal 1998 p1051s], so they must have a mechanism for retarding absorption through the intestines during excess. Mason says that infants should get 0.05 milligrams/kilogram of body weight per day and premature infants should get 0.09 milligrams/100 Kcal [Mason p1998]. Cordano recommends between 0.42 and 0.135 milligrams [Cordano 1998]. That last may be too high.<P>Two mg per day has been recommended for copper deficient babies, but I suspect this is much too high if maintained. Premature babies are usually born with too small a liver reserve to get safely past the nursing period, but one must use care with supplements. 0.09 mg per 100 Kcal has been recommended [Mason p2028]. I suspect that a seat of the pants criteria for such babies would be little more totally that is known to be absorbed from the particular source than the amount in the liver of normal babies above and beyond the amount they otherwise would receive in their mother's milk. Perhaps half again as much would be reasonably safe. Normal should probably be two or three times as much per body weight as adults require or about 0.08 mg/Kg. and 0.04 for toddlers. Perhaps that ratio should be less for very fat babies. A full term baby has 230 milligrams per kilogram of liver of copper in its liver, or 105 mg per pound of liver [Dorea]. A full term baby goes from 2.5 milligrams to 9.5 milligrams total in its liver during the last 10-12 weeks of pregnancy [Cordano 1998]. I know of no reasonable way to determine clinically how much it actually contains although modern ultra sound devices should be able at least to determine liver size. Mason says that infants should get 0.05 mg/Kg per day and premature infants should get 0.09 mg/100 Kcal [Mason p1998]. I do not know at what age they can start to excrete copper. However they are said to have an adult like liver in two years [Evans 1973b] and their serum levels increase to near adult levels in one month (4-6 months for preterm babies) [Lonnerdal 1996]. All these problems of too much and too little are more arguments for using mother's milk if at all possible. Babies are very important so it would be a good idea to throw as much light on problems of infancy as possible. we dare not give our babies just anything with no thought. We had better know as much as possible. A survey of infant formulas and ready to eat cereals disclosed that 25% contained no copper and non of the ready to eat cereal had copper or manganese even though half of them had more than 25% of the RDR for iron and zinc [Johnson]. They can not all have been correct. We would be wise to perform research to determine the best strategy as soon as possible.<P>Of course it is essential that the mother receive sufficient copper before the baby is born. <a href=http://jn.nutrition.org/cgi/content/abstract/133/5/1477S
>If she does not, birth defects can often materialize, which can persist into adult life.</a> Fructose sugar, alcohol, silver, diarrhea, and diabetes can make the matter worse [Cordano 1998]. Older children probably are similar to adults in their handling of copper and should probably receive an amount about proportional to their weight (but I know of no long-term study). A 2.5-milligram per day supplement was given to a copper deficient child. It took 5 days for serum free copper to return to normal, 2 weeks for ceruloplasmin and neutrophils [Cordeno 1998].
COPPER STATUS TESTS
Red blood cell superoxide dismutase has been proposed as a good criterion of copper status in rats [Feller, et al]. However, blood cells maintain their copper as much as 15 weeks into a deficiency before dropping [Milne 1998]. Platelet cytochrome C oxidase is not sensitive to factors other than copper and blood platelet activity is said to be the most sensitive indicator [Milne 1996].
Plasma diamine oxidase has been proposed as a sensitive marker [Kehoe]. <a href=http://jn.nutrition.org/cgi/content/abstract/130/1/30
>Plasma diamine oxidase (DAO) and liver content have been found to be the only way to distinguish between marginal and deficient copper states.</a> However, <a href=http://www.ajcn.org/content/44/6/907.full.pdf
diamine oxidase is dependant on vitamin B-6,</a> so it would not be a reliable indicator during a vitamine B-6 deficiency. The function of Diamine oxidase is the <a href=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8
>oxidative deaminating of several polyamines, essential substances for cell proliferation, which are found in rapidly proliferating tissues such a bone marrow and intestinal mucosa. DAO is thus a regulating enzyme to down regulate rapidly proliferating tissue</a> and is<a href=http://www.ajcn.org/content/44/6/907.full.pdf
> important during pregnancy.</a>
Liver biopsies are impractical but would be the best way if they were available [Klevay & Madeiros, 196, p2423S]. Kidney biopsies may prove to be just as indicative since their copper turnover is higher than liver (66% in the few weeks measured) [Levenson]. Brain and heart biopsies would be useless since their turnovers were 1% and 3% respectively [Levenson].
Hair analysis is ambiguous, does not change much [Danks p222][Hambridge], and subject to contamination. People with white hair have lower copper content than those with colored hair [Bertazzo] although old people will be often white haired even if their copper is adequate.
Marginal copper deficits do not change serum copper, or tissue copper-zinc superoxide dismutase enzyme even though ultra structural alterations in the heart, reduced copper in the brain, markedly decreased IL-2 production, and reduced immune function appear [Hopkins & Failla]. Serum contents of copper are not a reliable indicator since infections, emotional stress, and possibly potassium deficiency have an overriding effect. If the plasma free copper is less than 12 millionth of a mole, though, a deficiency is highly likely
There are many less lost time accidents in copper producing industries even though the number of accidents is greater [U.S. Department of Labor]. 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. I am convinced that this is because of copper's role as part of the enzyme that cross links connective tissue. So, copper nutrition is important for anyone considering or preventing accidental injury or even treating it after the fact, including herniated discs.
Copper supplements would be infinitely superior to and safer than statin drugs [http://www.health-heart.org/causes.htm
] for lowering cholesterol or eating low cholesterol food [Couzin]. However adding copper without zinc can actually make that situation worse [Festa]. So if a patient is afflicted with high cholesterol it is apparently necessary to supplement with 7 times as much zinc the same day, but preferably at different meals. Copper is also essential for an adequate immune system [Prohaska 1981] [Percival]. Premature babies can have too little copper. However babies should be supplemented with extreme care because they can not excrete copper, which is excreted with the bile in adults. This care includes not making formula out of water from copper pipes.
CONCLUSIONS Copper deficiency is pervasive in our society because of very low copper content of dairy foods, refined grain and sugar, and honey. If copper is made normal by supplements or liver and shellfish for people with herniated discs, any operation will be sure to be more successful. In many cases an operation will even prove to be unnecessary if combined with an inclined bed in such a way as to stretch the spine.
REFERENCES [ http://charles_w.tripod.com/copper4.html
]. The articles starting at; http://charles_w.tripod.com/copper.html
would be useful to you, especially copper from food in http://charles_w.tripod.com/copper3.html
. There is also a copper and zinc table at; http://members.tripod.com/~charles_W/copperzinc.html
expressed as weight per calorie, the most useful designation
Sharifah Rosso wrote at 2013-01-09 17:16:33
In Los Angeles, we have UPPER CERVICAL HEALTH CARE, which can relieve subluxations that often cause pressure and neurological interference. See http://www.youtube.com/user/subluxationskill
for further information.