Michigan Cancer Doctor Isn’t First Oncologist to Mistreat Patients
Oxidative Telomere Attrition, Nutritional Antioxidants And Biological Aging
Dr. Wallach’s Cystic Fibrosis Research
Dr. Wallach’s views on the longevity of physicians
Cardiomyopathy and selenium deficiency
Low back pain and osteoporosis
Wallach on Alzheimer’s disease
Premenstrual Syndrome (PMS) and calcium
Male pattern baldness and tin deficiency
Wrinkles, gray hair and copper deficiency
Copper deficiency – a cause of aneurysms?
How minerals are stored in the body
Diabetes, chromium and vanadium
Concerning “Colloidal Minerals”
Following his discovery of a nutritionally-caused cystic fibrosis (CF)-like syndrome in Rhesus monkeys in 1979, Wallach conducted a survey of 120 families with one or more CF children. The patient profiles obtained were consistent with CF as an acquired environmental disease caused by a prenatal deficiency of selenium, zinc and riboflavin, and/or exacerbated by diets low in vitamin E and rich in polyunsaturated fatty acids. Based on these findings, Wallach proposed a diet for the prevention and treatment of CF. To demonstrate that CF -like pancreatic lesions develop in populations living in regions naturally low in selenium, Wallach and his wife, Ma Lan, in collaboration with researchers at Harbin Medical University, showed that hitherto unrecognized pancreatic lesions occurred in 35% of 1700 documented cases of Keshan disease (KSD), which is a cardiomyopathy occurring in low-selenium regions of China[1]. Other researchers have since drawn attention to the aberrant oxygen-free radical activity and the low selenium and antioxidant status in cystic fibrosis patients[2-4]. It is now also agreed that selenium deficiency may develop in CF children because of digestive malabsorption or after prolonged total parenteral nutrition [5-7]. In addition, a case of cardiomyopathy in a CF patient caused by selenium deficiency has also been described[8]. The therapy of CF patients with selenium and antioxidant vitamins has also been tested in a clinical trial. One German group[9] concluded:
“In cystic fibrosis (CF) patients the antioxidative-oxidative balance is chronically disturbed. Free radicals were generated by bronchialpulmonal infection and additionally (there) exists a deficiency of antioxidative substances by enteral malabsorption especially (of) vitamin E and selenium. For CF patients there-fore we recommend a sodium selenite substitution therapy, best in combination with vitamin E.”
While research is now under way to introduce the missing cystic fibrosis trans-membrane regulator (CFTR-) gene by means of a retroviral transferring agent, it is still not known if this treatment will actually work. Nutritional therapeutic approaches such as were first proposed by Wallach instead hold promise if not as a cure at least to alleviate symptoms and increase the survival of CF patients.
Dr. Wallach’s views on the longevity of physicians
Wallach claims that American medical doctors have an average life-span of only 58.5 years and hence are poor role models of longevity. His critics argue that doctors in reality have a greater life-expectancy than the general population[10]. Wallach calculated the average age of physician death from some of the obituary listings that are regularly published in the Journal of the American Medical Association. From this data, Wallach’s result is indeed obtained. In contrast, the National Center for Health Statistics lists 69.7 years as the average life-span of an American physician. In order to explain this discrepancy, it should be noted that this figure applies to physicians of all specialties and includes nonpracticing physicians. The life-expectancy of General Practitioners (G.P’s) is pertinent because they would most likely be approached by patients for counsel in regard to achieving longevity. According to Goodman [11], G.P’s have the shortest life-span of all medical specialties. The standard mortality rate of G.P’s below age 55 for the years 1969-1973 was 140.4%, at above 55 years, 111.4% above the average mortality of all physicians. The shorter life span of G.P’s was attributed to the fact that they begin their careers at an earlier age and thus are subjected to the stress of practice for longer periods than specializing physicians[11]. While stress undoubtedly is a major factor which shortens the life span of G.P’s, the neglect of their own health and unhealthful habits also contribute. According to a survey published in 1984, no less than 59% of the physicians questioned considered themselves overweight, 73% felt they were not exercising enough, 24% admitted to frequent drinking and 15% were smokers[12]. The same report concludes that “there may be a far larger group of subclinically impaired physicians whose health habits may not only affect their own longevity but their practice of medicine as well”, which in essence proves Wallach’s point. There are, of course, physicians who reach long life-spans by living healthily or by making appropriate life-style changes when necessary. So as far as G.P’s are concerned, however, Wallach is right.
Glacier water and longevity
Dr. Wallach mentions 5 cultures whose populations attain unusually long life-spans. The best known of these cultures are the Hunzas of Kashmir, about whom numerous books have been written. Physicians such as Sir Robert McCarrison established that the Hunzas remain remarkably free of disease during their long lives. This has been attributed to lifestyle, diet, agricultural practices and the mineral-rich glacier milk used for irrigation and as drinking water[13]. Other researchers have ascribed the longevity of the Hunzas, inter alia, to the consumption of glacier water. Dr. Wallach thus is only quoting what can be found in the literature.
Cardiomyopathy and selenium deficiency
Dr. Wallach states that cardiomyopathy is caused by a selenium deficiency, his critics counter that cardiomyopathy is really an entire group of heart muscle diseases with several different causes. He uses a more precise definition of cardiomyopathy, based on the detection of oxygen radical damage of the heart muscle. Oxygen radical damage of the myocardium can occur in many diseases. Since selenium prevents the generation of oxygen radicals, cardiomyopathy is caused by primary selenium deficiency in regions naturally low in selenium, as was first shown to be the case in the Keshan-Disease regions of China[14]. Cardiomyopathies due to selenium deficiency were at first considered unlikely to develop in the Western industrialized nations until they were shown to occur in patients after prolonged total parenteral nutrition, in subjects with destructive lifestyles (such as alcoholics), in patients suffering from intestinal malabsorption or from diseases resulting in decreased Se-retention such as AIDS, and in cancer patients treated with certain cytotoxic drugs. Selenium deficiency also plays a role in the causation of Coxsackie B-virus (CBV) induced cardiomyopathies[15]. Selenium deficiency is, indeed, the major cause of cardiomyopathy, although classical textbooks of cardiology, even the newest editions, still often fail to mention selenium at all. However, M.R.Werbach, in his up-to-date reference book on “Nutritional Influences on Illness” [2nd Edition 1993, Third Line Press, Tarzana, Calif., p. 189], states that selenium deficiency is associated with the development of cardiomyopathy, while deficiencies of other agents, e.g. magnesium, L-carnitine, coenzyme Q only may be factors in the development of the condition.
Low back pain and osteoporosis
Wallach was accused of expressing the “absurd idea” that all low back pain is due to osteoporosis. However, Wallach only mentions osteoporosis as a contributing cause of low back pain. He is (correctly) linking calcium and copper deficiency with the initiation of osteoporosis, which then initiates disk degeneration and back pain. In his book “Let’s Play Doctor”, he writes: “Backache is usually a muscle strain from overwork and/or a subluxation resulting from a fall, auto accident or improper lifting technique. On occasion, a serious case of constipation will cause a ‘backache’ from impacted stool or pressure from gas…. Prevention includes proper lifting technique, strengthening exercises, proper nutrition including calcium (2000 mg) and magnesium (800 mg), high fiber diets and eight glasses of water per day.”
Wallach on Alzheimer’s disease
Wallach was criticized for suggesting that 50% of 70-year old Americans have Alzheimer’s disease when the actual prevalence of the disease in people between the ages of 65-75 years is only about 3.9%. Dr. Wallach did not say “one out of two people who reach the age of 70 years has the disease”, what he actually said was that “one out of two people who reach the age of 70 years gets the disease”, meaning that they have a 50% chance of getting the disease in their remaining life-span. In this he is on realistic grounds if it is considered that senile dementia to-day is often diagnosed as Alzheimer’s disease.
Premenstrual Syndrome (PMS) and calcium
Wallach recommends supplemental calcium, along with essential fatty acids, vitamin B6, Vitamin A, vitamin E, mistletoe, black and blue cohosh, for treatment of premenstrual syndrome. A randomized crossover trial published in 1989[16] has proven the efficacy of calcium supplementation. The authors of this study summarized their findings as follows: 33 patients randomly received calcium carbonate, 1,000 mg daily and placebo for 3 mo. each in either order. On prospective daily ratings, there was a reduction in symptoms while on calcium supplementation during both their luteal (p=0.011) and menstrual (p=0.032) phases, but not during their intermenstrual phase. On retrospective assessment, 73% reported fewer symptoms during calcium treatment, 15% preferred placebo and 12% had no clear preference. 3 premenstrual factors: negative affect (p=0.045), water retention (p=0.003) and pain (p=0.036); and 1 menstrual factor: pain (p=0.02) were significantly alleviated by calcium.
Bell’s Palsy
In his book, Lets Play Doctor , Wallach correctly states that Bell’s Palsy is caused by an inflammation, swelling or squeezing of the facial nerve. He recommends a treatment that involves not only the administration of calcium, but also of magnesium, essential fatty acids, American ginseng, colloidal minerals and vitamin B12. This is a naturopathic treatment which Dr. Wallach in his practice has found to be effective when conventional medical treatments failed.
Male pattern baldness and tin deficiency
Wallach claims that significant hair regrowth can be stimulated following tin supplementation. The stimulation of hair growth by tin at high dilutions is not an unfounded idea. The basis for this claim was originally reported by Schwarz et al.[17] who observed hair loss resembling male-pattern baldness in tin deficient rats. These findings were subsequently confirmed in a 1990 study by Yokoi et al.[18] of Kyoto University.
Wrinkles, gray hair and copper deficiency
That copper influences the pigmentation of hair is well supported by observations with copper-deficient animals. Experiments conducted in the early 1930s showed that the fur of black-coated rats turned gray when they were placed on a copper deficient diet[19,20]. Depigmentation of hair has been described in other species deficient in copper: rabbits, dogs and sheep. Copper is known to be required for the transformation of tyrosine to melanin. In copper deficiency, the physical nature of hair is also affected, it becomes brittle and crinkled because oxidative processes which give hair its normal elasticity require copper[20]. Other factors contribute to the graying of hair, a deficiency of pantothenic acid, for example. Clinical studies of the effects of copper supplementation on hair color in humans appear to be lacking. However, in Rare Earths and Forbidden Cures, Wallach does report the case of a woman whose gray hair regained pigmentation after supplementing with copper. Since copper is required for elastin and collagen biosynthesis, changes of elastic connective tissues are expected occur in copper deficiency. Studies have shown that 75% of the typical diets in the United States furnish less than the current daily requirement of 2 mg of copper per day[21]. Accordingly, chronic copper deficiency could indeed contribute to hair depigmentation and skin wrinkling, especially in women. In a recent study with 20 pregnant women on self-selected diets, positive balance was observed only if a copper supplement was consumed[22].
Copper deficiency – a cause of aneurysms?
Wallach should be given credit for drawing attention to the important role of copper deficiency in the pathogenesis of aneurysms. Wallach has not said that all aneurysms are caused by a copper deficiency. He only claims that aneurysms are most frequently caused by a copper deficiency, which has been shown in studies of many animal species (pigs, guinea pigs, rabbits, cattle, chicks, turkeys, etc.)[19,20]. Copper is needed for elastin synthesis, specifically for the oxidative deamination of lysine. Diminished deamination of this amino acid causes less lysine to be converted to desmosine, the cross-linking group of elastin[21,22]. This results in fewer cross-linkages in this protein, which, in return, results in less elasticity of the aorta. Copper deficiency in humans was considered rare but is now becoming a concern primarily in pregnancy. In a recent study with 20 pregnant women on self-selected diets, positive balance was observed only if a copper supplement was consumed[23]. Copper deficiency need not be caused solely by low dietary copper intakes; copper deficiency may be induced by dietary components, notably fructose and ascorbic acid; some also consider excessive zinc as a possible risk factor.
How minerals are stored in the body
Dr. Wallach’s claim that minerals are stored and used in the body in the colloidal state depends on the definition of “colloids”. Some minerals are bound to proteins which do not pass through dialysis membranes and so do behave as “colloids”. Iron is stored in the body mainly in the form of ferritin. Ferritin contains in its core up to 4500 molecules of iron oxide/phosphate, the core is covered by a protein shell whose molecular weight is 445,000. Because of their large molecular weight, ferritin suspension in water may well be described as colloidal. The claim that minerals are stored in the form of salts or “ions” is wrong inasmuch as salts or ions thereof are mobile forms of the minerals, not storage forms.
Diabetes, chromium and vanadium
Dr. Wallach’s claim that diabetes and hypoglycemia are due to vanadium and chromium deficiency was said to be unsupported by clinical research. However, published evidence is available that indicates a role of chromium and vanadium on the insulin system and in human diabetes[25-27]. According to USDA’s Richard Anderson[25], …suboptimal intakes of chromium by people consuming average diets may lead to signs and symptoms of chromium deficiency that include elevated blood glucose, insulin, cholesterol and triglyceride concentration and decreased insulin binding and receptor number.
Extreme signs of Cr deficiency were observed in TPN patients and were corrected by Cr supplementation. Vanadium is being considered as a therapeutic agent for the treatment of diabetes mellitus. Khandelweal and Pugazhenti at University of Saskatchewan, Canada, state[28]: “Several studies have clearly demonstrated that vanadium has the potential to be used as a therapeutic agent for the treatment of diabetes. In a recent study[29], vanadate was found to enhance insulin sensitivity in diabetic patients.”
Iron in supplements
When Dr. Wallach refers to “rust” or iron oxide in iron preparations he is referring to products such as “saccharated iron oxide” or products such as “Niferex” (Center Pharmaceuticals), containing iron oxide as a polysaccharide complex. Other iron compounds in supplements hydrolyze in the stomach to produce iron hydroxide, which is chemically closely equivalent to iron oxide and has low bioavailability.
Concerning “Colloidal Minerals”
“Colloidal minerals” comprise a group of liquid mineral supplements that are produced by leaching deposits of humic shales with water. The extracts were originally thought to contain the minerals predominantly in colloidal forms. It is now known that they contain the minerals in ionic as well as in colloidal forms. Because the term “colloidal” may give rise to misunderstandings, the products are now referred to as “liquid-” or “plant-derived minerals”. In terms of their composition and efficacy, the extracts resemble certain natural mineral waters that were used in the past against anemias arising from iron deficiency as well as other conditions[30]. As to the superior bioavailability of liquid minerals as compared to minerals in their elemental state, this claim is correct because liquid minerals solutions are acidic which facilitates their absorption in the duodenum.
References
[1] a: J.D.Wallach, Ma Lan, Wei Han Yu, Bo-Qi Gu, Feng Teng Yu and Roy F. Goddard (1990): Common denominators in the etiology and pathology of visceral lesions of cystic fibrosis and Keshan Disease. Biol. Trace El. Res. 24: 189-205. b: J.D.Wallach B. Garmaise (1979): Cystic fibrosis – A perinatal manifestation of selenium deficiency. In: Hemphill D.D. ed., Trace Substances in Environmental Health XIII, pp. 469 – 476.
[2] P.Foucaud, P. Therond, M.Marchand, F.Brion, J.F. Demelier, J.Navarro (1988: Selenium et vitamin E au cours de la mucoviscidose. Arch. Fr. Pediatr. 45(6), 383-6.
[3] A.G.Thomas, V.Miller, A.Shenkin, G.S.Fell, F.Taylor(1994):. Selenium and glutathione peroxidase status in pediatric health and gastrointestinal disease. J. Pediatr Gastroent Nutr 19, 2: 213-219.
[4] B. Salh, K.Webb, P.M.Guyan, J.P.Day, D.Wickens, J.Griffin, J.M.Braganza, T.L.Dormand (1989): Clin. Chim. Acta 181(1) 65-74.
[5] B.M.Winklhofer-Roob (1994): Oxygen free radicals and antioxidants in cystic fibro-sis: the concept of an oxidant-antioxidant imbalance. Acta Paediatr Suppl. 395: 49 – 57.
[6] R.D.Watson, R.A.Cannon, G.S.Kurland, K.L.Cox, F.C. Frates (1985):, Selenium responsive myositis during prolonged home total parenteral nutrition in cystic fibrosis. JPEN J Parenteral Enteral Nutr. 9(1) 58 – 60.
[7] C.Dominguez, M.Llovera, E. Ruiz, V.Araujo, S.Linan, S.Gartner, N.Cobos, Anti-oxidant trace elements, glutathione and glutathione peroxidase in cystic fibrosis patients: relation to lipid peroxidation status. In: Proc. Conf.
Metal Ions in Biology and Medicine, Vol. 4; Ph. Collery, J.Corbello, J.L.Domingo, J.C.Etienne, J.M.Llobet eds., John Libbey Eurotext, Paris, 1996, pp. 592-595.
[8] B.Dworkin, L.J.Newman, S.Berezin, W.S.Rosenthal, S.M.Schwarz, L.Weiss (1987): Low blood selenium levels in patients with cystic fibrosis compared to controls and healthy adults. JPEN J. Parenteral and Enteral Nutr. 11(1), 38 – 41.
[9] D.M.Volk, S.A. Cutliff (1986): Selenium deficiency and cardiomyopathy in a patient with cystic fibrosis. J.Ky. Med. Assoc. 84 5) 222-4.
[10] E.Kauf, E.Janitzky, L.Vogt, K.Winnefeld, H.Dawczynski, M.Forberger, G.Jahreis, H.Vogel (1995): The significance of a selenotherapy in cystic fibrosis patients. Med. Klin. 90, Suppl. I, 41 – 45.
[11] L.J.Goodman (1975): Longevity and mortality of American Physicians, 1969-1973. Milbank Memorial Fund Quarterly; Health and Society 53(3): 353 – 375.
[12]K.B. Wells, C.E.Lewis, B.Leake, J.E.Ware, Jr. (1984): Do Physicians Preach what they Practice? JAMA 252: 2846 – 2848.
[13] J.I.Rodale (1949), “The Healthy Hunzas”. Rodale Press, Emmaus, PA, 1949.
[14] G.Q. Yang (1985), “Keshan disease: an endemic selenium-related deficiency disease. In: Trace Elements in Nutrition and Children.” R.K.Chandra, ed. Raven, New York, pp. 273-290.
[15] O.A.Levander and M.A.Beck (1997): Insights from Coxsackie B Virus induced myocarditis in mice deficient in selenium and vitamin E. Biol. Trace El. Res. 56 (1) 5 – 21.
[16] Thys-Jacobs S. et al “Calcium supplementation in premenstrual syndrome: a randomized crossover trial. J. Gen. Intern. Med. 4(3) 183-9 (1989):
[17] K.Schwarz, D.B. Milne, and E. Vinyard (1970), Growth effect of tin compounds in rats maintained in a trace element-controlled environment. Biochim Biophys Res. Comm. 40, 22-29.
[18] K.Yokoi, M.Kimura and Y. Itokawa (1990), Effect of dietary tin deficiency on growth and mineral status in rats. Biol. Trace El. Res. 24: 223.
[19] H.L.Keil and V.E.Nelson (1931). The role of copper in hemoglobin regeneration and reproduction. J. Biol. Chem. 93: 49.
[20] E.J.Underwood: Trace Elements in Human and Animal Nutrition, 3rd. Ed., Academic Press, New York and London, 1971, pp 53 – 115.
[21] D.M.Danks, B.J.Stevens, P.E.Campbell,, J.M.Gillespie, J.Walker-Smith, J.Blom-field and B. Turner (1972), Menke’s kinky hair syndrome. Lancet, 1: 1100-1102.
[22] L.M.Klevay and D.M.Medeiros (1996), Deliberations and Evaluations of the Approaches, Endpoints and Paradigms for dietary recommendations about copper. J.Nutr. 126: 2419S-2419S.
[23] Taper L.J., et al. (1981), Zinc and copper retention in pregnant women. Fed. Proc. 40: 855.
[24] O.A.Levander and M.A.Beck (1997): Insights from Coxsackie B Virus induced myocarditis in mice deficient in selenium and vitamin E. Biol. Trace El. Res. 56 (1) 5 – 21.
[25] R.A.Anderson (1997): “Nutritional factors influencing the glucose/insulin system: Chromium. J. Am. Coll. Clin. Nutr. 16: 404 – 410.
[26] S.Verma, M.C.Cam and J.H.McNeill (1998). Nutritional factors that can favorably influence the glucose/insulin system: Vanadium. J.Am.Coll. Nutr. 17 (1) 11 – 18.
[27] H.G.Preuss, T.Jarrell, R.Scheckenbach, S.Lieberman, R.A.Anderson (1998). Comparative effects of chromium, vanadium and Gymnema Sylvestre on sugar-induced blood pressure elevations in SHR. J.Amer. Coll. Nutr. 17 (2), 116-123.
[28] R.L. Khandelwal, S. Pugazhenti (1996) Vanadium as a potential therapeutic agent for the treatment of diabetes mellitus. In: Proc. Conf. Metal Ions in Biology and Medicine, Vol. 4; Ph. Collery, J.Corbello, J.L.Domingo, J.C.Etienne, J.M.Llobet eds., John Libbey Eurotext, Paris, 1996, pp.673-675.
[29] A.B. Goldfine, D.C. Simonson et al.(1995) In vivo and in vitro studies in human and rodent diabetes mellitus. Mol. Cell. Biochem. 153: 217-231.
[30] G.N.Schrauzer (1999) An evaluation of liquid vitamin-mineral supplement technology. J. Medic. Food 1(3) 207-216.
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[1] Address for correspondence:
Biological Trace Element Research Institute,
11526 Sorrento Valley Road, Suite A, San Diego, California 92121.