Hair Mineral Analysis – Trace Minerals & Toxic Minerals in your Body
Trace Minerals in our Body
TOXIC METALS – Lead, cadmium, mercury, aluminum, arsenic, nickel.
The consensus of most workers in the field is that if hair samples for toxic metals are collected properly, cleaned and prepared for analysis correctly, and analyzed by the best analytical methods using standards and blanks, in a clean and reliable laboratory by experienced personnel, the data are reliable. This has been documented in a recent careful report by the Environmental Protection Agency.1
CALCIUM – Despite detailed calcium balance studies measuring intake and excretion using radio labelled isotopes, it has been shown by Dr. Anthony Albanese2 that it is extremely difficult to determine calcium balance in an outpatient setting. Assessment of dietary intake of calcium is confounded by multiple factors including the quantity of fiber and other natural chelators in the diet, amount of gastric acidity, ratio of dietary calcium to phosphorous, as well as dietary magnesium, gut transit time, etc. All of these factors combined make multivariate analysis not possible with so many unknowns. Serum calcium, like other electrolytes, is subjected to such close homeostatic regulation that its measurement does not reflect body calcium status. (Ionized calcium is being examined in more detail lately and may play a partial role in evaluation of calcium status in the future.)
At present, the most useful screening test for calcium balance is hair. Dr. Jeffrey Bland, Ph.D.3 conducted careful studies of two groups of patients with different calcium/phosphorous intake ratio. Those patients with high phosphorous diets and low intake of calcium consistently showed hair calcium as much as three times higher than normal. Hair calcium then returned to normal with proper supplementation and dietary changes.
MAGNESIUM – Magnesium is an intracellular mineral. It can be considered a macro-mineral as there are approximately 25 grams stored in the body. In the past few years our appreciation for this extraordinary mineral has abundantly grown, as deficiencies are becoming more recognized. Magnesium is a cofactor in nearly all enzyme reactions requiring ATP in the body, it also serves the important functions of protein formation, DNA production, nerve conduction and relaxation of heart and artery muscle walls. Magnesium has been found to slow the release of both adrenaline and noradrenaline, and to partially block adrenergic receptors. Mildred Selig, M.D.4 documents several hundred cases of infant ischemic heart disease related to magnesium deficiency. More recently Dr. Sherman Bloom at the annual meeting of American College of Cardiology (1982) stated that magnesium is “natures own calcium channel blocker.” Magnesium by injection can replace calcium channel blockers for angina and cardiac arrhythmias. Other clinical uses responsive to magnesium include esophageal spasm, some cases of high blood pressure, menstrual and leg cramps, seizure disorders, and urinary stones. Measurement of magnesium status, like other minerals has many problems.4 One of the foremost experts on this mineral states that the magnesium retention test is probably the most accurate method of assessment. An injection of two ml of 50% MGS04 and a 24 hour pre and post urine magnesium and creatinine is collected. Retention of greater than 25% indicates magnesium deficiency. However, this is a cumbersome procedure.
Many factors influence serum magnesium. The degree of binding, complexing or chelating of magnesium and protein bound factions are subject to multiple variables. Thus, serum magnesium is of no value. A value as low as 1.2 mEq/L. has been shown without a depletion of total body magnesium.
It has also been shown that RBC magnesium may vary by a factor of five depending on the age of the red blood cells, making this a very unreliable measurement. Selig and others4 have examined WBC magnesium. The evidence indicates this may be nearly as accurate as the magnesium retention test.
IRON – Iron is first in abundance of essential trace elements. Besides its major function of oxygen transport, iron is necessary for electron transport, peroxide metabolism, DNA synthesis, and catecholamine metabolism. Total body iron is between 4,000 to 5,000 mg.
Breakdown and release of iron from food requires the acidity of the stomach. Absorption occurs in the small intestine and is generally regulated by the amount of iron in the epithelial cells of the intestinal mucosa as well as in plasma transferrin. Gastric hypochlorhydria, inflammatory bowel disorders and infections can severely inhibit iron absorption. Only a minimal amount of iron is excreted daily, between 0.6 and 1.2 mg.
For years serum iron has been used as an indicator of iron deficiency. By itself it is not of much value unless combined with serum transferrin or ferritin measurement. It has been shown that there is considerable variation in serum iron when samples are taken from the same person at the same time each day. There is also considerable diurnal variation in serum iron.
FERRITIN – Ferritin is an iron storage protein accounting for 20% of the total body iron in normal adults. It is principally found in the cytoplasm of reticulo-endothelial cells, liver cells and to some degree in developing red cell precursors in bone marrow. It is responsible not only for iron absorption but for recycling it for hemoglobin synthesis.
When iron overload is associated with hemochromatosis, hemosiderosis, or thalassemia, serum ferritin is elevated in most cases. Other cases where serum ferritin is elevated inappropriately for the level of the body iron stores are in malignancy, inflammatory disease, acute and chronic liver disease. Overall serum ferritin is a convenient and usually reliable measurement of total body iron storage.5,6
ZINC – Zinc is the second most abundant trace element. Its essentiality has been well documented in several deficiency states including growth retardation, hypogonadism, decreased taste perception, alopecia, skin scaling, ulceration and eczema, poor wound healing, reproductive failure and immune system dysfunction. In recent years, zinc has become even more important clinically, being one of the most commonly deficient minerals in North America.
Absorption of zinc (like iron), is homeostatically controlled, ranging from 25% to 100% depending on body zinc status. Absorption occurs in the small intestine by a saturable carrier mediated process facilitated greatly by picolinic acid, a metabolic by-product of pyridoxine, dependent tryptophan metabolism. High protein diets facilitate zinc absorption while copper, cadmium, iron and strict vegetarian diets inhibit zinc absorption. Excretion is generally via bile and feces with less than 10% urine and sweat excretion. Because zinc is an intracellular ion, plasma and serum zinc are not sensitive indicators of depletion. Erythrocyte zinc is even less sensitive as an indicator of zinc status than plasma. Urine zinc as well is not a good indicator. Low hair zinc levels indicate depletion, but normal values do not rule out low body store.8,9 Recently WBC zinc has been investigated and found to be an accurate index of body store.’
COPPER – This element is third in abundance of essential trace elements. Approximately 75 mg is found in the body. One third distributed between liver and brain, one third in muscle and one third in other tissues. Copper, like zinc, takes part in a vast array of metabolic processes. It is essential for iron metabolism, melanin synthesis, catecholamine metabolism, cellular respiration, superoxide free radical detoxification, and connective tissue formation to name a few. Microcytic hypochromic anemia, neutropenia, skeletal demineralization, arterial aneurysms, hypercholesterolemia, and immune system dysfunction, as well as degeneration of the nervous system have all been linked to copper deficiency.
Copper is principally absorbed in the stomach under an acidic environment. Far more copper is absorbed than needed by the body. Nearly all dietary copper is initially stored in the liver leaving only a small percentage in thc blood. 95% of plasma is bound to the protein ceruloplasmin with almost no ionic copper. Thus urinary output is nil. The principal homeostatic mechanism for controlling copper is by excretion through the biliary system.
Absorption of copper is antagonized primarily by zinc but also by high calcium diets, high fiber phytates, vitamin C, iron, cadmium and molybdenum. Gastric hypochlorhydria will significantly inhibit copper absorption as well. As one may imagine with such large turnover of dietary copper, assessing copper status is not easy. Noel Solomons M.D., expert on copper metabolism at Massachusetts Institute of Technology, states there is no best test for subclinical copper deficiency, but at present serum copper may be the best indicator if certain clinical conditions are kept in mind as enumerated in his recent article.11 Perhaps functional studies may be the most reliable in the end. Superoxide dismutase function has been measured as an assessment of copper status. But this enzyme also requires zinc and manganese thus conpounding the picture. More work needs to be done here.
CHROMIUM – Chromium is an ultra-trace mineral in the body. The most well known clinical effect of chromium deficiency is impaired glucose tolerance. Experimentally developed deficiency of chromium indueed a 40% reduction in glucose removal in rats which was corrected by chromium. This effect is mediated by the ability of chromium to form intrachain disulfide bonds of insulin and sulphydyl groups at insulin receptor sites. This has been shown to be stoichiometric with the formation of a characteristic dose-response curve. In addition to altering glucose metabolism, chromium deficiency in animals and humans causes elevated serum cholesterol, impaired growth, increased aortic plaque formation and decreased fertility and longevity.12
Absorption of inorganic chromium is approximately 1%, independent of body status or dose administered. The mechanism of transport across the intestinal membrane is unclear. In contrast, organic chromium complexes extracted from Brewer’s yeast are absorbed 10-25%. Thus, a factor of approximately 20 would be considered when switching from one type of chromium to another. Once chromium is absorbed into the blood it is rapidly cleared and does not appear to be in equilibium with tissue chromium. Only when chromium is complexed with nicotinic acid, glycine, glutamic acid and cysteine (GTF chromium) does it have any biological activity. Inorganic chromium must first be converted to GTF (probably in the liver) before it can be used.
Establishment of reliable laboratory assays for the assessment of chromium status has been a subject of much attention. Only recently have analytical instrument of sufficient sensitivity been developed to allow accurate quantitative analysis for this ultra-trace mineral. Plasma chromium is probably not a valid indicator of body status since it is not in equilibrium with tissue chromium. Plasma levels may be less than 1 ng. per ml making measurement very difficult. Since 80% of chromium is excreted in the urine this may become a valid source of management. Glucose has been known to increase plasma and subsequently urine chromium. Pre and post urine chromium after a glucose load has been measured but so far results are variable. Substantial GTF biological activity has been found in hair follicles suggesting hair chromium may be an indicator of body status.13 This mineral is concentrated over 100 times that found in the blood, making hair chromium a more reliable measurement. Conditions particularly prone to chromium deficiency are diabetes mellitus, multiple pregnancies, low birth weight in infants and the elderly.
MANGANESE – Manganese is an essential trace element for many biologic functions including glucose metabolism, bone, mucopolysaccharide and catecholamine metabolism. Exact biochemical pathways have not been identified, but activity has been associated with pyruvate carboxylase, arginase, glutamine synthetase, various enzymes of the TCA cycle and oxidative phosphorylation as well as being essential for vitamin K function.
Some of the most interesting chemistry of manganese is its ability to displace magnesium for ATP, particularly releasing stored catecholamines in the chromatin granules of the adrenal medulla. This also occurs in the extrapyramidal system inducing a depletion of catechoamines, particularly dopamine.
Chronic manganese poisoning leads to “Manganic Madness”, an initial psychotic period of hallucinations, delusions and compulsions followed by hypokinesia, akinesis, rigidity, tremor, masked facies and dementia. This has been treated with L-dopa as for Parkinson’s disease. Manganese is also known to interfere with iron metabolism, having very similar chemistry.
Manganese deficiency in animals leads to altered reproductive hormones, sterility, ataxia, failure in development of bones and connective tissue, and otoliths of inner ear. In man, manganese deficiency presents as weight loss, nausea and vomiting, changes in hair and beard color and hypocholesterolemia. In some children, with convulsive disorders of unknown etiology manganese has been shown to be significantly below normal (p > 0.001).14
Manganese is absorbed by the small intestine by unknown mechanism. Only 3% of a daily intake is actually absorbed and 1 % retained. Half life in the body is only 10 days, indicating a rapid tumover. Excretion is almost entirely by the biliary tract. Absorption is enhanced by lecithin, alcohol and choline; inhibited by phytates, iron, high calcium diets and magnesium.
Assessment of body status for manganese is difficult due to its low levels, one hundred times lower than copper or zinc in the blood. Proper analytical technique is essential in the collection procedure as well as actual analysis. According to “New England Journal of Medicine,” 308,1230 (1983), “Whole blood manganese is a valid indicator of body manganese and soft tissue levels.”15 Hair manganese may be a rough indicator especially in chronic toxicity, but not as reliable as whole blood.
POTASSIUM – Potassium is the major intracellular ion of the body. Electrical balance at the cellular membrane level is critically dependent on the intracellular/extracellular concentration gradient. Changes in this ratio lead to clinical manifestations ranging from diminished tendon reflexes, muscular paralysis, and pH disturbances to cardiac arrhythmias and cardiac standstill. Potassium is also essential for several enzymatic processes within the cell and depletion will lead to failure of anabolic metabolism.
Potassium is present in nearly all food. The ratio of sodium to potassium in the diet significantly alters potassium homeostasis. Particularly a high sodium/potassium ratio will lead to increased renal clearance of potassium. Modern canning of foods and the addition of salt to many packaged goods exacerbates this problem. The body conserves potassium much less efficiently than it controls sodium and a modest reduction in dietary potassium may contribute significantly to potassium deficiency.
Since potassium is an intracellular ion, serum measurements do not reflect body stores. A low serum potassium usually indicates an intracellular deficit. However, an intracellular deficit may occur with normal or high serum potassium. Studies have been carried out by several researchers on red blood cells.16,17 Most important in these studies is the confirmation that red blood cells reflect the potassium content of other tissue cells. Although red blood cells do not have nuclei, the sodium-potassium membrane pump is intact, maintaining the proper influx and eflux of these ions. Whole blood potassium is as accurate as RBC potassium since 98% of the potassium is intracellular.
An example of the validity of measuring intracellular potassium was demonstrated in a study measuring the alterations of the repolarization phase electrocardiography in the elderly. Alterations of repolarization correlated with intracellular potassium levels but no correlation occurred with serum levels.18
SELENIUM – Selenium is an ultra trace element necessary for growth, fertility and prevention of various disease conditions which show a variable response to vitamin E. Its major function lies in protection from lipid oxidative degradation by detoxifying peroxides. Selenium accomplishes this by its association with glutathione peroxidase in the cytosol, while vitamin C acts on lipid membranes themselves.
Evidence indicates that selenium has an inhibiting effect on carcinogenesis, from both experimental and epidemiological studies. Dr. Gerhard Schrauzer at UC San Diego studies a strain of mice that spontaneously develop breast cancer. Of these 83% on a selenium deficient diet developed breast cancer, contrasted with 10% on selenium supplemented diet.19 In epidemiologic studies, the 1968 55-64 age specific cancer death rates in 19 high selenium states was 429.8 + 12.8. In the low selenium states it was 516 + 10.7 (P less than 0.001).20
Selenium deficiency has also been implicated in heart disease. Keshan disease is a congestive cardiomyopathy with high mortality secondary to very low soil selenium levels in the Keshan region of China. Incidence is 1.35% in selenium deficient individuals, contrasted with 0.22% in those supplemented.21 The “WHO” epidemiologic study in 1973 examine dietary trace minerals in 25 countries determined that selenium appears to prevent breakdown of heart muscle resulting in lower incidence of heart disease deaths.
The immune system is also significantly affected. Conclusions of several experimenters showed dietary selenium enhances both primary and secondary immune response increasing IgG and IgM.22 Selenium is efficiently absorbed, between 40-70%, by unknown mechanism. Reports are variable on types of selenium best absorbed. Both selenite forms and those bound to amino acids have biological effects. After absorption, distribution is throughout the tissues but does not seem to be in equilibrium in the blood. Research so far indicates blood selenium levels do not correlate with selenium intake, except at extremes.23 Hair selenium does correlate well.24 As with chromium and manganese, special analytical techniques must be used to insure accuracy of measurement with this element.
REFERENCES
1. Dale W. Jenkins, Toxic Minerals in Mammalian Hair and Nails, EFA report 600/4-79-049, August 1979. (Available through National Technical Information Service).
2. AnthonyA.Albanese Ph.D.,Bone loss:Causes, Detection and Therapy.AlanR.Liss,lnc.NewYork,1977.
3. Jeffrey Bland, Ph.D., “Dietary calciun phosphorus and their relationship to bone formation and parathyroid activity.” Journal of John Bastyr School for Naturopathic Medicine, Vol. No.1,1979.
4. Mildred S. Seling, M.D., M.P.H., FACN, Magnesium de,ficiency in the Pathogenesis of Disease. Plenum Medical Books, New York, 1980.
5. J.D.Cook ,M.D.Et al.”Serum Ferritin as a measure of iron in Normal Subjects.”American Journal of Clinical Nutrition, 27 July l974, 9681-87.
6. Peter Frank, Stephen Wang, “Serum iron and total iron binding capacity compared with serum ferritin in assessment of iron deficiency. ” Clinical Chemistry, 27/2, 1981, p.276- 269.
7. Stephen Davies, M.A., B.M., B.CH., “Assessment of Zinc Status.” Intl. Clin. Nutr. Rev. July 1984, Vol. 4, No. 3.
8. Hambridge, K.M, ET.AL Low levels of zinc in hair, anorexia, poor growth and hypogeusia in children. Pediatric res., 868-874, 172.
9. Pekarez,R.S.ET.AL. “Abnormal cellular immune response during acquired zinc deficiency.”Am.J.Clin.Nutr.32,1466-lnl.
10. Jones, R.B. ET.AL, “The relationship between leukocyte and muscle zinc in health and disease, 237-239, 1981.
11. Noel Solomons, M.D., FACN., “Biochemical, metabolic, and clinical role of copper in human nutrition.” J. of Am. Coll. Nutr. 4:83-105 (1985).
12. StanleyWallach,M.D., “Clinical and Biochemical Aspects of Chromium Deficiency.” J. of Am.Coll.Nutr.4:107-120(1985).
13. Hamoridge,K.M “Chromium Nutrition in Man,”Am.J.Clinic.Nutr.27:505-514(1974).
14. C.C. Dupont, Y. Tanaka , “Blood Manganese Levels in Children with Convulsive Disorders.” Biochem. Med. 33, 245-255 (1985).
15. CarlL.Keen,Ph.D,,ELAl. “Whole Blood Manganese as an Indicator of Body Manganese.”N.Eng.J.Med.308,1230,(1983).
16. M.Bahemuka,H.M.Hodinsoo,”Red Blood Cell potassium as a practical index of Potassium status in Elderly patients.”Age and Aging,5, 24-29 (1976).
17. Hyman S. Lans, M.D., Et. AI. “The relation of serum potassium to erythrocyte potassium and alernations of the Repolarization phase of Electrocardiography in Old Subjects.” Age and Aging 13, 309-312 (1984)
18.G.BarbagalloSangiorgi,Et.Al”Serum Potassium Levels, Red Blood Cell potassium and alternations of the Repolarzation phase of Electrocardiography in Old Subjects.”Ageand Aging 13, 309-312 (1984).
19. G. Schrauzer, Et. Al., “Bioinorganic Chemistry,” 2, 329-340, (1973).
20. Raymond Schamberger, Ph.D., “Selenium in Health and Disease. ” Symposium on selenium-tellurium in the environment, Univ. of Notre Dame, Indiana. May 11-13, 1976, 253-267.
21. Chinese Medic l Journal 92 (7): 471476 (1979).
22. Spallholz, J. Et Al., “Proceedings of the Society of Experimental Biological Medicine.” 143,, 685-698 (1973).
23. H.W. Lane, Et. Al., “Blood Selenium and Glutathione Peroxidase levels and dietary selenium of Free Living and Institutionalized Elderly Subjects,” Proc. Soc. Exp. Biol. Med. 173 (1):87-95, 1985
24. Jane L., Valentine, Et.AI “Selenium Levels in Human Blood, Urine and Hair in Response to Exposure via Drinking Water,” Environ. Res. 17, 347 355 (1978).
Like us on Facebook