From Cholesterol to Arthritis
I have had to retract nothing from my 1980 book, Mega Nutrition. The most controversial position that I took was in favor of individualizing intake of dietary fat and carbohydrate according to my innovative OrthoCarbohydrate Diet ™. Some people feel and function best on a high fat intake and, contrary to current medical dogma, many do poorly on a high carbohydrate diet, even the best of the complex carbohydrates.
Clinical experience with thousands of patients in my practice plus systematic observations in my initial group of about 100 patients made it clear that for many people, the only authority that they can trust for accurate and sensible advice is their own body. Eventually I renamed my program, "The Listen To Your Body Diet™." It is not my intent to describe all of this here and now, I already have done so at length in my two books, Mega Nutrition and Mega Nutrition for Women.
I am just trying to put forth my sense of perspective as I review my experience and realize that where I came closest to error was in over-emphasizing the dangers of copper and thus putting aside the greater importance of copper deficiency.
Science has learned much about copper in the past four decades; however an RDA had not been determined by the National Research Council until 2001. Instead the "estimated safe and adequate dietary intake" was set at 1.5 to 3 mg daily. Oysters are the richest food source but the more staple supply is found in fish, shellfish, nuts, seeds and whole wheat. Cocoa is a good source of copper and so is blackstrap molasses. Liver is one of the very best food sources and though some may warn that it is also high in cholesterol, the copper more than makes up for it--because we now know that copper deficiency is a prime cause of high blood cholesterol! In a previous article, I highlighted the finding that a diet high in fructose and corn sweeteners (in excess) is incriminated as a cause of copper deficiency. A high starch diet is safe, even when copper is in short supply; but a high fructose diet can be fatal with the same marginal intake of copper. Fructose, a component of sucrose, causes copper deficiency and it was fructose that Dr. Linus Pauling identified as a prime cause of coronary heart disease back in 1977! Pauling was impressed by the work of Dr. John Yudkin, professor of physiology and nutrition at London College. Yudkin marshalled convincing evidence that the incidence of heart attacks correlates with dietary sugar, not fat. The American study at Framingham, Massachusetts, confirmed this as did a major study of Yemenite Jews: found that after they moved to Israel, exchanging their traditional high animal fat diet for a high sugar diet, the incidence of coronary artery disease increased dramatically.
Yudkin reported his 1957 study of heart attack deaths in relation to sucrose consumption in 15 countries. At 20 pounds per year of sucrose intake, there were 60 coronary deaths per 100,000 people. At 120 pounds per year, which is about what we eat here, the death rate increased five-fold to 300. At 150 pounds of sucrose per year the death rate was 750 per 100,000! Pauling thought that was due to the fact that sucrose is made of equal parts glucose and fructose. Glucose is used directly for the production of energy but fructose produces acetate, the start-up material for fat and cholesterol synthesis. Dr. Milton Winitz demonstrated that this was more than theory: dietary glucose did not raise blood cholesterol in his subjects; but even small amounts of fructose led to a prompt increase.
Information about the copper-cholesterol connection has become available in the 1980’s thanks to the work of Dr. Leslie Klevay*. He highlighted the clinical picture of copper deficiency heart disease: high blood cholesterol and low HDL, high triglyceride and uric acid, abnormal EKG and irregular heart rhythm due to damage and fibrosis of the heart muscle, all adding up to high risk for sudden death. This tragically familiar set of symptoms is identical to atherosclerotic coronary heart disease except it is not caused by dietary fat or cholesterol but by deficiency of dietary copper.
If it is so important and so well researched, why is copper deficiency not diagnosed more often? There are at least three reasons. First, doctors are not yet alerted to the problem because they are still off on a wild goose chase after cholesterol. Second, copper deficiency is not easy to identify in office practice: there is no definitive single test. Third, because of the common use of copper plumbing most authorities have been wrongly convinced, as I was ten years ago, that copper excess, not deficiency, is the problem.
Nutrition-oriented physicians, like myself, were thrown off-course since 1970 by the strong anti-copper teachings of Dr. Carl Pfeiffer, a pioneer researcher into minerals and health. His work emphasized the danger of copper in causing cancer, high blood pressure, insomnia, anxiety, obsessive thinking, depression and a low blood histamine type schizophrenia His views on copper were certainly one-sided, especially since he claimed that deficiency was a negligible risk. Out of 25,000 patients tested at his clinic, only 3 were identified with low blood copper. This conflicts with more recent large nutrition surveys that find dietary copper deficiency in over 2 out of 3 Americans! This news is especially important for those of you who regularly take extra amounts of vitamin C, which is known to lower tissue levels of copper. In animal research vitamin C actually increased the incidence of sudden death due to rupture of aortic aneurysm.
Equally startling is the recent demonstration by Dr. Mary Johnson of the University of Georgia that the combination of vitamin C plus iron is even worse, in her research the extra iron competes with copper for absorption, causing copper deficiency and deficiency of ceruloplasmin, which then fails to oxidize iron into its transportable valence state. The net result is iron deficiency in the bone marrow and anemia due to inadequate production of hemoglobin. (https://pubmed.ncbi.nlm.nih.gov/3337044/) Copper is known to be essential for over a dozen adaptive enzymes that increase cell energy output (cytochrome C oxidase), protect cell membranes from oxidative damage (superoxide dismutase), regulate the amino acid levels in stress adaptation (tryptophan di-oxygenase), induce synthesis of neurotransmitters (dopamine hydroxylase), adjust metabolic rate (thyroid oxidase), and promote the production of melanin pigment in skin and hair (tyrosinase), Copper is also involved in peptide amidation, producing powerful regulators of neural and hormonal activity. This may explain why injection of copper evokes prompt release of an ovum in research animals and how copper deficiency causes infertility.
Copper is a powerful anti-aging factor because it activates lysyl oxidase, the enzyme that cross-links lysine into elastin. As its name implies, elastin contributes to elasticity and durability of skin and blood vessels. Inadequate copper is associated with weakening of the wall of large arteries, leading to dissecting aneurysm. Sudden death can occur if this should rupture. Elastin is also vital for healthy lung tissue and we now know that copper deficiency is a cause of emphysema even in non-smokers, Copper induces production of its own storage protein, ceruloplasmin, which also functions as an iron oxidase. Oxidation, the removal of an electron, renders iron transportable from liver to bone marrow. Thus copper is often required in order to recover from iron deficiency anemia. The earliest sign of copper deficiency is usually anemia of a type almost identical with iron deficiency.
Ceruloplasmin and copper, as catalysts of amine oxidases, also control the oxidation of serotonin and noradrenaline, hormones which otherwise would accumulate and overstimulate the intestine and heart muscle.. Thus copper deficiency aggravates irritable bowel disorders and also causes acute disturbances of heart rhythm. This has resulted in a number of cases of sudden death in otherwise healthy people, eg. over 2 dozen people who stayed too long on a copper-deficient liquid protein diet product some years ago died this way.
The total adult body content of copper is about a tenth of a gram, not very much, however it increases with aging by about 15 % in blood and 100 % in the brain and Dr. Pfeiffer theorized about the role of excess copper in high blood pressure and mental illness. He focused on the role of copper as activator of histaminase, which inactivates histamine, in the brain and he found low histamine and high copper together in about half the cases of schizophrenia seen at his clinic He named this condition "histapenia." and these patients are usually paranoid and suffer from insomnia. In these patients high copper also activates dopamine hydroxylase to increase production of noradrenalin and adrenalin in the brain with an over-all stimulating effect. In fact a 5 mg dose of copper duplicated the brain wave (EEG) activation of an equal dose of amphetamine ! Dr. Pfeiffer also described a low copper, high histamine type of mental illness, which he called Histadelia and found this condition in almost a quarter of his schizophrenic patients. Histadelics typically suffer with severe depression, lethargy and obsessive thoughts without the paranoia and hallucinations that are common in the low histamine cases.
The fact that copper and ceruloplasmin are anti-histamine suggests that copper might have anti-inflammatory activity. This has been confirmed and there is little doubt that copper is the active ingredient in most of the anti-inflammatory drugs marketed for relief of arthritis. Aspirin, for example, binds to copper in the stomach and carries it along to various points of inflammation in the body, where copper probably acts by inhibiting enzymes that release PGE2, a prostaglandin hormone, which controls inflammatory activity at the level of the cell membrane.
It is intriguing to consider that theoretically a 300 mg aspirin tablet is capable of binding to the entire 100 mg supply of copper stored in the body. This does not happen in reality; however in case of copper shortage, it is likely that aspirin, ibuprofen and most other nonsteroid anti-inflammatory drugs do remove a substantial amount of copper from the stomach lining, thus disrupting the crucial role of copper in limiting acid production. This is at least a partial explanation for the tendency of these drugs to cause gastric ulcers.
Dr. John Sorensen's research in over 1500 cases found copper in combination with aspirin or sebacic acid (an 8 carbon double acid) to be more effective than cortisone in relieving inflammatory arthritic pain. The wearing of copper bracelets now begins to make sense. Does metallic copper dissolve in the acid medium of sweat and absorb with the undecylenic acid of sweat (the same fatty substance that clears athlete's foot) and travel into the deeper layers of the skin? Dr. Ray Walker of Australia found that 31 of 40 arthritis patients gained positive relief from copper bracelets. On average, their bracelets lost 13 mg of copper per month.
How does it work? Superoxide dismutase (SOD) is believed to be the key to copper's direct anti-inflammatory effect. Injectable SOD has been used by physician's all over the world except in the US, where it was developed. Research reports have demonstrated benefits for almost all inflammatory disorders, including arthritis, migraine, stroke and myocardial infarcts but the patents have expired here without ever getting past the FDA! One consolation: it has been available to veterinarians, who have saved a few sick race horses. Complexes of copper and fatty acids are not only anti-inflammatory, they are also anti-biotic, active against bacteria, viruses, fungi, mycoplasma, protozoa and even flatworm parasites! Copper sebacate has turned out to be the most effective complex and is the one that I prefer in treating my low copper patients. Copper gluconate, an amino acid complex and the most commonly available supplement, has been found less effective in raising serum copper levels in healthy individuals with normal copper levels but effective with those that are deficient.
Anti-convulsant drugs, such as Dilantin, Valproic acid, Phenobarbital and Lorazepam all bind with copper to form complexes that are more powerful than the parent drugs at controlling seizures! The copper superoxide dismutase function may be responsible. it is also possible that copper stabilizes membrane phospholipids as well. One hint is that copper deficiency is often found in multiple sclerosis and other disorders involving breakdown of myelin, the fatty phospholipid sheath that protects nerve fibers.
Immune function is very much responsive to changes in copper. Even a marginal deficiency causes loss of neutrophils and also of antibody-producing B lymphocytes. Unlike the case of zinc deficiency, there is no atrophy of thymus or spleen. The drop in neutrophils is a tip off to copper deficiency and an indication for the doctor to measure ceruloplasmin and SOD levels.
Diagnosis of copper status is seldom attempted in general medical practice. Blood levels are hard to interpret. Hair copper levels would be better as they do correlate with liver stores; however external copper sources, found in swimming pools and in hair products, can cause a false high reading Measurement of ceruloplasmin has proved helpful. It has a half-life of about a week and is a good indicator of short term status. Superoxide dismutase within the red blood cells has a half life of about 60 days and this is a good test of mid-term levels. Taken together these tests offer a good perspective on copper status.
There is much more to the copper story. Copper deficiency is definitely involved in rheumatoid arthritis. Multiple sclerosis and other demyelinating diseases are often copper related. Scoliosis, hernia, varicose veins, hemorrhoids, premature graying of hair, thinning of the bones and chronic fatigue syndrome all are influenced by copper and deserve to be evaluated from the perspective of this maligned mineral.
*https://pubmed.ncbi.nlm.nih.gov/2697136/
Copyright @ Dr. Richard A. Kunin, 2020
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