Manganese (Mn) – Scientific Paper Abstracts
Manganese Deficiency & Its Role in Structural Balance
Cheryl Hawk, D.C.
The American Chiropractor, March/April 1982
In a certain percentage of patients with low-back pain and other problems related to structural balance, adjustments will not hold. These patients are the ones who are easy to adjust but who say, “I felt fine for a couple of hours and then my back went right out again.” Often these patients have been in car accidents or have otherwise injured their lower backs -lifting heavy objects, etc. They are often the patients who do not respond well to standard chiropractic technique in which manual manipulation of the articulations is done, but who respond better to low-force adjusting like Activator, SOT, or other techniques that do not directly mobilize the joints.
There are, of course, many factors which may contribute to chronicity in structural problems: the patient may not be following instructions properly; there may be metabolic problems like hypothyroidism or hypoglycemia complicating the situation; there may be emotional and mental stress which disturb the patient’s nervous system.
Often, however, with or without complicating factors, there is a simple deficiency present which, when corrected, soon turns the three-adjustments-a- week patient into twice-a-month patients. Manganese is the mineral which often accomplishes this. When a hair analysis is performed on a patient with a chronic structural problem (usually in the lower back), the manganese level is invariably low. This fact alone, however, would not be significant since manganese deficiency is widespread in the general population and since the clinical significance of hair levels of manganese is presently unknown. What is significant is that, when these chronic patients are given manganese, they begin to hold adjustments and their symptoms decrease in frequency and severity.
There are several reasons for this dramatic improvement. Although manganese is most commonly known for its role in bone growth, reproduction, and enzyme synthesis, Its role in maintaining structural balance is not so frequently mentioned. There are three principle functions of manganese to consider in discussing this role: its function in connective tissue, in the thyroid, and in glucose metabolism.
Manganese is needed in the production and repair of connective tissue, which includes bones, ligaments, tendons, and fascia. Its specific role is in the manufacture of mucopolysaccharides, which are one of the main components of all connective tissue. Experimentally it has been found that manganese deficiency may produce structural deformities in animals. The slipped tendon and perosis syndrome in chickens -in which bone deformity and ligamentous laxity are involved -has for some time been used as a rationale for manganese supplementation in humans with ligamentous and osseous problems.
The thyroid gland also requires manganese in order to produce thyroxin. Consequently, correction of a manganese deficiency is necessary for proper thyroid function. This is important in relation to musculoskeletal problems because lowered thyroid function may result in muscle aches, spasms, and weakness; In the case of severe hypothyroidism, the general musculature becomes hypertrophied due to infiltration of mucopolysaccharides. This situation has obvious implications in the patient’s ability to maintain structural corrections.
Manganese is involved, too, in glucose metabolism The enzyme pyruvate carboxylase, which is utilized in gluconeogenesis, contains tightly bound manganese. Patients with hypoglycemia often complain of chronic back pain due to nervous system irritation and muscle imbalances set up by an endocrine disorder. Correction of the hypoglycemia condition is necessary before the patient’s structural problems will subside permanently, and manganese deficiency must be considered to be a factor.
Any form of soluble manganese may be used although preparations with manganese glycerophosphate and Vitamin B12 are specially formulated for maximum benefit. Though manganese is a trace element and only about 4 mg. is required daily, many patients benefit from larger amounts until their deficiency states have been corrected. At least 15 mg. per day is generally recommended for several months, and sometimes, especially in the case of sprains and strains, and disc lesions, more than that may be beneficial. Many manganese supplements contain far more than the minimum. Dr. George Goodheart has recommended up to 140 mg. of manganese six times per day or even as much as 140 mg. hourly
for severe disc lesions. Since manganese is not toxic except when exposure is very great, such as in the mining and manufacturing professions, short-term use of large amounts followed by a maintenance dose of approximately 15 mg. per day should pose no dangers of toxicity. It usually takes several months to correct long-standing ligamentous problems. Manganese deficiencies can’t be expected to be corrected in less than six months. The large doses of manganese, as mentioned previously, should only be used when physical medicine treatment is initiated. After symptoms have been reduced, a small maintenance dose (4-15 mg.) is all that is usually needed. In eight to ten months, a hair analysis may be repeated to determine whether to continue supplementation and to monitor progress. The improving symptoms should, however, be apparent within weeks or two to three months at most.
The following are indications for manganese supplementation (a hair analysis may be performed to verify deficiency):
1 -Sprains and strains which take longer than normal to heal. It is often wise, in fact, to suggest manganese supplementation immediately after an injury to prevent such a delay in healing,
2 -Chronic low back pain which does not readily respond to treatment,
3 -Hypermobilities of the spinal and extra spinal joints. This condition indicates ligamentous laxity and/or previous trauma.
Manganese and Carbohydrate Metabolism
A relationship between manganese and abnormal carbohydrate metabolism was first suggested by Rubenstein and coworkers (1962). They reported the case of a diabetic patient resistant to insulin therapy who responded to oral doses of manganese chloride with decreasing blood glucose levels. Interestingly, these investigators tried manganese supplementation partly because of the patient’s statement that his diabetic condition could be controlled to some extent by an extract of lucerne (alfalfa, Medicago sativa), an old South African folk medicine treatment for diabetes. Upon analysis it was found that the alfalfa contained a high concentration of manganese. In contrast to manganese, oral supplements of zinc, magnesium, cobalt, or iron had no effect on the patient’s blood sugar levels. The authors hypothesized that manganese acted by inhibiting the release or function of glucagon. Consistent with the observation of Rubenstein et al., patients suffering from chronic manganism show a prolonged reactionary hypoglycemia following intravenous glucose tolerance testing (Hassenein et al., 1966). A hypoglycemic effect of manganese has also been reported in rabbits (Pignatari, 1932) and dogs (Bellotti, 1956). Large-scale studies evaluating the therapeutic effect of manganese supplementation in treatment of diabetes have not been reported.
In experimental animals, an essential role of manganese in carbohydrate metabolism was demonstrated by Everson and Shrader (1968). These investigators found that guinea pigs born to manganese-deficient dams and fed manganese-deficient diets to 60 days of age had abnormal glucose tolerance curves and decreased utilization of glucose. Tissue pathology in these animals included hypertrophied pancreatic islet tissue with degranulated beta-cells and an increased number of alpha-cells (Shrader and Everson, 1968). All of these signs of manganese deficiency were reversed following dietary manganese supplementation for 2 months. Interestingly, the pancreatic lesions seen in the manganese-deficient guinea pigs appear to be similar to those of human infants born to diabetic mothers.
Manganese and Brain Function
Manganese is essential for normal function of the brain. Manganese-deficient rats are more susceptible to convulsions than are normal rats and show electroencephalographic recordings similar to those of epileptics (Hurley et al., 1963). The importance of these observations is underscored by the recent report by Papavasiliou and coworkers (1979), who found that whole blood manganese levels were significantly lower in epileptics than in control subjects.
In the human the highest brain manganese concentrations are in the pineal gland, olfactory bulb, median eminence of the hypothalamus, and basal ganglia (Bonilla et al., 1982; Barbeau et al., 1976). In the rat the highest concentrations are in the median eminence, hippocampus, midbrain, and cerebellum (Donaldson et al., 1973). Manganese in the brain accumulates mainly in pigmented structures, such as the melanocytes of the substantia nigra.
OTHER BIOLOGICAL ROLES OF MANGANESE IN HUMANS AND ANIMALS
1. is an integral part of the enzyme, arginase, that facilitates conversion of toxic ammonia into urea –which is a good diuretic and stimulates wound healing.
2. is essential to reproduction and growth of mammals –also is vital to sex functions.
3. activates the enzyme, acetyl-CoA-carboxylase –which operates in conjunction with biotin and adenosinetriphosphate to normalize fat metabolism.
4. participates in acetylase activity in reuniting acetyl and choline in nerve impulse transmission processes.
5. deficiency causes malformation of bones.
6. its lack allows loss of calcium from bone.
7. aids biosynthesis of glucuronic acid –needed for detoxification purposes.
8. improves formation of connective tissues.
9. stimulates hemoglobin formation.
10. tends to prevent hypothyroidism by stimulating thyroxine synthesis.
11. is stored in thyroid for various emergency needs.
12. protects against kidney degeneration.
13. concentration in blood plasma is twice as high as in blood cells.
14. levels rise markedly in fetus during latter part of pregnancy.
15. is excreted largely via bile and colon.
16. aids metabolism of calcium and phosphorus.
17. has unexplained relationship to Vitamin B1 activity.
18. in vitro tests show manganese activates blood and bone phosphatases as well as liver and intestinal phosphatases –also cholinesterase.
19. in mitochondria of the cells; are the principal site of uptake of manganese.
20. in newly hatched chickens, the concentration of manganese is 0. 124 mg/% of whole liver, and this figure is doubled during first week of life. By the 18th day the weight of liver increases sevenfold whereas manganese increases 17 times.
Despite the essentiality of manganese, its metabolism and biochemistry are still poorly understood. Although a deficiency or toxicity of this element has pathological consequences, the underlying biochemical lesions have not been well defined.
Absorption of manganese is not well regulated and is influenced by several dietary factors. Homeostatic regulation of manganese is mainly through excretion of the element into the intestinal tract via bile. Absorbed manganese is transported on alpha-2-macroglobulin and transferrin; retained manganese concentrates in mitochondria-rich tissues. Within a cell, much of the element is localized in the mitochondria. Fluctuations in the intracellular concentration of free Mn, like that of Mg2 + and Ca2+, may be a mechanism of cellular metabolic control. Manganese functions both as an enzyme activator and as a constituent of metalloenzymes. It is the preferred metal cofactor for a number of glycosyltransferases, and much of the connective tissue defects seen with manganese deficiency may be explained by depression in activity of these enzymes. Manganese metalloenzymes that are affected by manganese status include arginase and superoxide dismutase. Some of the membrane abnormalities seen with manganese deficiency may be the result of depressed superoxide dismutase activity, with subsequent increased lipid peroxidation.
Manganese is involved in carbohydrate metabolism, as a deficiency of the element may produce abnormal insulin metabolism and abnormal glucose tolerance. Acute manganese toxicity also perturbs carbohydrate metabolism. The relationship of manganese to lipid metabolism has not been defined, but it appears to have a lipotropic action and is involved in cholesterol and fatty acid synthesis.
Manganese is essential for normal brain function, at least in part through its role in the metabolism of biogenic amines. Manganese toxicity is a serious health hazard in some industries, resulting in a permanently crippling neurological disorder of the extrapyramidal system. The role of manganese in immunocompetence and oncogenesis is poorly defined.
The adequacy of manganese nutrition in man has not been well characterized, in part because of lack of methods for the detection of suboptimal manganese status. Future studies defining manganese status of various population groups at risk, coupled with a greater understanding of the element’s function in metabolism, will further delineate the role of this element in biological systems.