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  Osteoporosis - Pathogenesis and Treatment
  

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By: Otto Wolff, M.D.
Original title: "Zur Osteoporose - Pathogenese and Therapie" in Merkurstab 1993; 46: 440-447. English by A.R. Meuss, FIL, MTA.

Osteoporosis is the subject of considerable research at present, apart from anything else because it is responsible for numerous bone fractures in older people, requiring expensive treatment. It is estimated that more than 1.3 million fractures, with 500,000 vertebral compression fractures, annually are due to osteoporosis in the USA, and that the expenditure involved is in the range of 10 billion dollars.

Beyond all doubt, osteoporosis is a typical disease of old age. As the average length of human life has been markedly extended in recent decades, an increase in the incidence of diseases of aging is only to be expected. The symptomatology has no doubt existed in earlier times when accurate diagnosis was not possible. Historical records also show that the disease was more common in women than in men. The use of terms like "dowager's hump" and representations of witches as old women with bent backs are evidence of this, quite apart from the question as to how many women were burnt as witches "merely" because they had osteoporosis.

As with all diseases, the incidence shows geographic and social differences. Thus postmenopausal women in Gambia in West Africa used to have more or less the same bone mineral levels as British women but the risk of fractures did not exist for them.1 This suggests that mineral content is not responsible for the fracture risk. Geographic differences can be considerable. Thus fracture of the femur was about 30 times as high in Scandinavia, New Zealand and the USA than among the Bantu of South Africa. These differences are partly ascribed to major differences in nutrition.

Postmenopausal onset of type 1 osteoporosis is, however, clearly apparent. As the menopause is a more incisive event than the changes seen in males, onset of the disease is more clearly evident in this case. It is also easy to see why the condition is thought to be due to hormone deficiency. Cessation of hormone production in menopause has been fully researched. The recommendation of estrogen replacement is the logical conclusion of this. Endocrine forms of osteoporosis, including Cushing's syndrome, hyperthyroidism, hypogonadism, diabetes and others, are classified as type 2. Drug-induced osteoporosis is gaining increasing significance, with corticosteroids and thyroid hormones the most common causes. Alcohol is known to be another causal agent, especially in men.

It is of course possible to ascribe osteoporosis in women to estrogen deficiency. The question is, however, why men are so much less liable to develop it. To make relevant hormones responsible in this case is to follow the reductionism which is so prevalent today, merely shifting the problem to somewhere else. Men connect more strongly with the earth than women do, so that their bones are constitutionally stronger and muscle development is greater. These differences between the sexes become less obvious in old age, but continue to exist in essence, so that men may be said to have a "better" skeletal system throughout life.

Estrogen substitution for women in the climacteric will to some extent restore things to what they were before, with anabolic processes and organic osteogenesis resuming and the risk of fractures reduced. It goes without saying that this does not solve the aging problem. Estrogens are generally recommended for prevention and "treatment" not only of osteoporosis but also of cardiovascular problems, for instance.

Estrogens, and especially estradiol, are undoubtedly responsible for the female habitus. The same applies to testosterone, the hormone with the highest androgenic properties, in the case of men. The biphasic nature of the female cycle is also reflected in the hormones, with the first half of the cycle under the influence of estrogens, the second under that of the gestagens, including progesterone. It is easy to observe that the first half is "lighter", the second "heavier". The weight gain which is not uncommon in the second half may be largely due to water retention, but it nevertheless reveals a more earthy trend, which sometimes also shows itself in depression or, in more general terms, premenstrual syndrome.

Biochemically it is possible to see even from the constitutional formulas that progesterone holds a position between estradiol and testosterone. In fact, estradiol production is never direct, but only via androstenedione, which is clearly a male hormone.

It is evident, therefore, that progesterone and other gestagens are more suitable for hormone therapy than estrogens. They are already being prescribed in the USA, though the practice is not generally accepted. It has been reported that progesterones given on their own increase bone mass and reduce the incidence of fractures.2 For the moment, then, the theory is that estrogens partly suppress osteoclast function, while progesterone stimulates osteoblast function. Reports state that progesterone is also effective in advanced cases, whereas estrogens are said to have only preventive value. In the light of what has been said above this should indeed be the case. Quite generally, then, it may be said that estrogens do indeed have more of an anabolic effect which extends also to the psyche. When synthetic hormones were first introduced they were often given in excessively high doses, resulting in an "estrogen high", as it was called. The action of gestagens, on the other hand, goes in the direction of maturation and maintenance, a more earthy aspect which is physiologic for the second half of the cycle, and a potential pregnancy. Gestagens also do not have the virilizing effect commonly seen with anabolic agents. Although estrogens are generally recommended, it may thus be said that gestagens are more likely to be suitable for hormone therapy.

Bone calcium levels have been shown to be reduced in the menopause; they can be determined with some accuracy. It would seem logical to give calcium in this case, but this is not as straightforward as it may appear. In children, calcium deficiency causes rickets, yet exhibition of calcium has no effect. This being the case, why should exhibition of calcium be effective in older people, except in cases where nutrition is clearly at fault? Vitamin D, as it is called, is known to stimulate calcium deposition, which is wrongly interpreted as bone formation. The vitamin is therefore also recommended for treatment.

Calcitonin, a substance obtained from thyroid glands or salmon, is more effective than vitamin D. It is reported to reduce osteoclasts and promote their conversion to osteoblasts (see below). This reduces serum calcium levels, reversing the aging process to some extent. The use of anabolics is essentially at the same level, but it is difficult to control anabolism accurately, so that virilization is liable to occur.

Fluorine plays a special role in osteogenesis. Substantial amounts are found in bone and particularly in dental enamel, the hardest substance in the organism. It has a special relationship to calcium and is therefore indispensable for adequate hardness of bones and enamel. It is used all over the world to give "better" bone formation, also in osteoporosis. It has to be realized, however, that fluorine blocks practically all enzymes; it therefore cannot have an anabolic action but induces hardening of existing structures. This is wrongly interpreted as osteoblast stimulation, analogous to the action ascribed to Vitamin D, when in fact it is increased mineralization. Fluorine salts have been widely used, but after some decades, questions were raised as to the value of the treatment. A review of the situation has been published.3

The symptomatology of osteoporosis suggests that is it essentially "loss of bone tissue mass." This is in line with the general weakening of organic substance and function which is physiologic for the aging process. All organs are subject to this, particularly at a more advanced age. In quantitative terms, a 90-year-old person simply cannot perform like a 30-year-old, and this applies to all areas. Physiologic aging should however be a harmonious process, ending in death when the whole organism is "used up". Osteoporosis is thus to some degree physiologic; it becomes pathologic when bone mass dissolves away prematurely and in excess.

At this point, a well-established therapeutic principle comes into play, which is, that proper use of an organ will strengthen and maintain it. It is known that even short-term immobilization causes bone tissue to deteriorate. Overexertion, on the other hand, also weakens. The art of using and training organs in exactly the right way lies in finding the right measure. Skilled physiotherapists apply this principle.

Parallels to rickets can help us to understand osteoporosis, though in a way, rickets is the opposite of osteoporosis, despite the fact that "calcium deficiency" exists in either case. The main problem with osteoporosis is the increased fracture risk. To see this as a consequence of calcium deficiency and treat it accordingly is to miss the point. Brittleness goes hand in hand with hardness. Soft or semi-soft materials such as clay or cartilage will not fracture. With rickets, ossification of cartilage is delayed, which is also why the bones do not break. Calcium is gradually deposited in bones which are preformed in hyaline cartilage, making them hard but not brittle. This elasticity, which is retained to some degree, is a feature of certain substances such as bone, some types of wood, and steel. If bones consisted of calcium only, they would be extremely brittle. This is more or less the case with osteogenesis imperfecta. Without calcium, bones would remain flexible.

If osteoporosis were due to calcium deficiency, therefore, the bones ought to grow elastic again, as in the case in osteomalacia, which might also be called an extremely late form of rickets. It is quite evident, however, that the pathologic process giving rise to osteoporosis is not a calcium deficiency, even if the density of bone mass is reduced.

How does it become possible for a hard and therefore essentially brittle substance to be hard and yet not brittle? The answer lies in the bone itself. Osteogenesis is known to be intracartilaginous (endochondral) in skeletal bones, and intramembranous (mesenchymal, dermal) in cranial bones. Osteoporosis develops in the skeleton, not the cranium, so that we are able to say: At the beginning there is cartilage, a purely organic material that is mainly chondroitin sulphate (chrondros = cartilage), a substance characteristic for cartilage. This is an amino sugar called galactosamine. Galactose linked with silica gives tissues elasticity, e.g. in the stems of cereal plants. These organic substances clearly prevent brittleness. The fact that old bones tend to grow brittle indicates that these organic substances withdraw to a greater extent than calcium does. The problem of osteoporosis has nothing to do with calcium and the other minerals, least of all fluorine, which hardens bone tissue. The only exception to this in the mineral world is silica. The problem, then, is one of deficiency in organic substances and silica, which provide elasticity and therefore resistance to fracture.

Silica is actively involved in osteogenesis; connective tissue and cartilage both have a high silica content, as do the perichondrial zones. Silica does not become part of bone mass to any appreciable degree, but is responsible for giving it form. This is particularly important in the perichondrial zones, for it prevents calcium form principles from taking effect. Calcium naturally pro­duces a spherical form (see below). This applies also to the completely differ­ent type of osteogenesis in the cranium, which shows roundness of form.

Calcium and silica are polar opposites. Silica predominates during embryonic development, in childhood and youth, but as life progresses the balance shifts in favor of calcium.4 Brittleness of bones is essentially due to relatively excessive calcification, even if density is reduced. It is not a matter of absolute values but of the ratio between osteogenesis and calcification. This, of course, is the silica:calcium ratio, or silica:fluorine, the latter being the characteristic hardening element. Arteriosclerotic changes in the aorta, for instance, are in inverse proportion to the silica content. In the same way, a negative correlation exists between myocardial infarction and the silica content of drinking water.5 Silica thus has a long tradition as an antisclerotic agent, a fact which is little appreciated today.

The situation is the same even in the almost inorganic sphere. Pure iron (ferrite) is known to be relatively soft and ductile. The addition of carbon, the element which serves as a vehicle for the whole organic sphere, makes it denser but also harder. Suitable heat treatment will produce steel, which is hard but not brittle; it is elastic (e.g. watch spring). In the final instance it is again organic substance which prevents brittleness, which helps us to understand the problems of osteoporosis.

All measures designed merely to increase mineralization of bone are thus in the long run doomed to failure. We are also able to see why exhibition of fluorine gives such contradictory results. It does increase bone mass, above all in the lumbar spine, but not in the shaft of the radius, where the result is that "fluoride therapy increases cancellous bone mass, but decreases cortical bone mass, thus increasing skeletal fragility."6

The reason for this becomes obvious if we consider that fluorine mediates the central forces of the earth, while silica reflects the peripheral forces of the cosmos. Many patients not only fail to respond to fluoride therapy but also develop side effects such as gastrointestinal symptoms, peripheral joint pain, peripheral fractures, intraosseous microfractures that heal spontaneously, and so on. As fluorides also have a narrow therapeutic range, assessment of the results is highly contradictory and further research has been called for — as one would expect. It is interesting to note that warnings coming from the USA have been repeatedly said to be false and ascribed to excessive dosage and/or misinterpretation of results.3

The reported results become meaningful if distinction is made between osteogenesis and ossification. In the embryo, development of the extremities clearly begins in the periphery. The hand develops first, followed by the fore­arm, upper arm and shoulder. The same applies to the lower extremities. This is the generative principle, which by its very nature can only work with a substance capable of being modeled, i.e. cartilage, and not with an organ that is hard or has grown rigid. The polar opposite principle is that of ossification, or calcification. This starts from the center, in the shoulder, and progresses to upper arm, forearm and hand in succession. Ossification of the carpal bones may thus be used for a fairly accurate determination of a child's age.

The primary principle of form genesis is thus the polar opposite of the secondary principle of mineralization. We might also say that the form-giving principle comes from the periphery and is mediated by silica, whilst the mineralizing principle starts from the center and comes to expression in calcium and fluorine.

The same polarity exists between organic substance and mineral "filling". In other words, form is created via the organic connective tissues with their high silica content. It also means that the connective tissue-mediated form-giving powers of silica extend to the collagen. The deposit calcium in effect merely fills up forms which have been created out of organic matter. Osteogenesis certainly does not rest on the powers of the minerals —  calcium, phosphorus, fluoride, etc. — which create the bond with the earth. The form principles of calcium can be seen in the roundness of snails, shellfish and foraminifera. In higher animals and humans this tendency has been overcome in osteogenesis by the radiant principle which is based on silica.

The only conclusion to be drawn is that osteoporosis is not a disorder of calcium, let alone fluorine metabolism. In fact, the brittleness of bones is due to premature degradation of organic substances. The powers of the ego organization are mediated by these organic substances, above all silica. The skeleton is thus "an image of the ego organization,"7 and osteoporosis may seen as a disease of the ego organization.

This calls for a completely different approach to treatment than is customary today. On the one hand, treatment may consist in giving silica, in which case a further question would be in which form it is used. Quartz is of course the most universal form of silica. Its domain is essentially in the neurosensory sphere. For bone, an organic form such as chalcedony would be indicated. As we are, however, also dealing with the metabolic sphere, a vegetable form should be more effective, e.g. Equisetum silicea cultum. A soluble form of silica, e.g. the relatively concentrated form used in Sclerosol® an effective antisclerosis preparation of proven clinical value, might also be considered. It is also generally known that our diet is low in silica. Barley and millet are two grains with high dietary silica. Iodine is another element to be considered; like silica it was widely used to treat older people in the past (KI solution or suitable baths). The role of the thyroid in osteogenesis has only been established in recent years, leading to the discovery of calcitonin in 1961. This polypeptide hormone is produced in the C-cells of the thyroid; its action is independent of thyroxin activity, which is generally catabolic. Iodine acts at a higher level. It would be perfectly possible to activate thyroid function nonspecifically with KI solution (e.g. 5%, 10-15 drops tid) or with Thyreoidea 4-6x, which would achieve the calcitonin action at a much smaller fraction of the cost. Iodine may here be seen as an opponent of fluorine, which is definitely contraindicated, as shown above.

On the other hand, a more causal effect may be achieved with anything that strengthens the ego organization. Apart from medicinal quartz preparations, speech formation may be indicated, and over and above all the right lifestyle.

Gelatin preparations obtained from shark cartilage are important in this field, for obvious reasons. Sharks are cartilaginous fishes, i.e. their skeleton does not calcify. It seems logical, therefore to use this substance in medicine, leaving aside the question as to whether this is substitution therapy or a stimulus to form cartilage. Yet although the use of this gelatin seems perfectly rational, the method is never discussed, let alone practiced by members of the medical profession specializing in this field. The preparation, called Hai (German for shark) is, however freely available as an over-the-counter preparation in Germany and may even be obtained in the USA, not being a registered drug. Chemical analysis has shown a high concentration of specific amino acids, among them proline, a heterocyclic amino acid also found in cereal proteins.

Hydroxyproline is only found in connective tissue proteins and collagen molecules denatured to soluble gelatin by boiling. It is interesting to note that conversion of proline to hydroxyproline depends on molecular oxygen, ascorbic acid and ferrous iron. This means that proline helps to establish a connection with the earth, which inevitably has to be via oxygen and iron, with ascorbic acid also involved. Brawn or meat jelly produced by boiling up bones and joints has a long tradition in popular medicine as helpful in degenerative joint disease.

This is not to say that mineral-based medicines are not indicated. Experience has shown that fluorite, a natural calcium fluoride, given in the 4x or 6x potency has a beneficial effect on bone pain due to osteoporosis.

Another interesting substance used to inhibit bone resorption is sodium pamidronate, a biphosphosphonate with an amino group. It is practically a specific, acting not on mineralization but through osteoclast inhibition, and is also used to treat hypercalcemia with malignancies and Paget's disease.

Pamidronate Molecule           


                    PO3HNa
                           |
H2N—CH2—CH2—C—OH—5H2O
                           |
                    PO3HNa

It is immediately apparent from the formula that this is a partly organic phosphate linked with C–C–N as a basic structure; this is a common structure, found e.g. as the basis of amino acids, in this case beta-alanine. This, however, is clearly not an amino acid (–COON) but a "similar" structure (–OH). It is a characteristic of amino acids that they have anabolic functions. The action of this compound may therefore be said be as follows:  Through phosphorus, the human ego is brought into anabolism. This counteracts the excarnating process of old age.

Interestingly enough, this substance also has an effect on hypercalcemia, a condition commonly seen in malignancies, the highest incidence with lung cancer, at 35%, and as much as 25% with breast cancer. A high degree of hypercalcemia may in turn cause severe problems related to calcium poisoning. If tumor-induced bone resorption is inhibited, the calcium level goes down. Treatment with this phosphorus compound may be seen as substitution therapy; direct stimulation of the ego can be achieved with potentized phosphorus (5x).

Agaricus comp./Phosphorus has proved effective in treating osteoporosis. R. Steiner originally recommended it for a woman with tuberculosis of the bones.8 This is, of course, a different condition, but being a disease which takes people away from the earth involves an excarnating process just as osteoporosis does. The preparation contains phosphorus, the therapeutic use of which has been discussed above, Argentum, which  governs anabolic processes, and Agaricus muscaris. According to R. Steiner Agaricus is indicated when "the ego organization makes excessive demands on the astral body and does not allow it to enter into the ether body."9

Nutrition obviously plays an important role. Generally all that is advised is a "balanced diet", with dairy produce important for its calcium content. It has been known for a long time, however, even if little account is taken of it, that diet influences pH levels, and if these become acid, calcium is withdrawn from bone to act as a buffer. Inordinate metabolic acidity develops if the diet is high in phosphorus and sulphur, i.e. primarily from meat. Fruit on the other hand, including really sour fruit, has an alkalizing effect, being degraded to CO2 and H2O which alkalize the ever present potassium salts. The situation is different with refined sugars. Fructose degradation in particular yields intermediary acids which require buffering. Many soft drinks contain large amounts of phosphates which are acid-producers. This is known but generally disregarded. The subject has been discussed on a previous occasion.10 Diet can be used to stimulate collagen production, as briefly mentioned above.

Summing up it may be said that to some extent osteoporosis is physiologic in old age. How far it may be considered pathologic depends on the time of onset and the symptoms, with fractures the biggest problem. As bones characteristically have a high mineral content, research and treatment are almost exclusively going in this direction. Minerals make bone hard, but also brittle. Brittleness is prevented by the organic constituents of bone and by silica. Bone density determinations do not measure these, however. Treatment should essentially aim to maintain, stimulate or replace the organic constituents, which is a totally different approach. Like all connective tissue, the organic constituents of bone are subject to silica dynamics which, like the skeleton, are an expression of the ego organization. Treatment of the ego organization should thus be our primary concern. A number of suggestions have been made.

Otto Wolff, M.D.
Auf der Hohe 10
CH-4144 Arlesheim
Switzerland

 

References

1. Abstracts of the 6th International Congress on the Menopause 1990.

2. Lee JR. Osteoporosis reversal: The role of progesterone. Intern Clin Nutr Rev 1990; 10: 884.-Lee JR. The Lancet 1990; 336: 1327.-Prior JC. Progesterone as bone-trophic hormone. Endocr Reviews 1990; 11.

3. Wolff O. Merkurstab 1990; 43:197.

4. Stuebler-Woff. Kalk and Kiesel. Quadrivirum: D-56112 Lahnstein 1984.

5. Quote from Kieffer. Spurenelemente. Sandoz Bulletin Nr. 51-53 1979.

6. Riggs. New Engl J Med 1990; 322: 805.

7. Steiner R, Wegman I. Fundamentals of Therapy (GA 27). Transl. by E. Frommer and J. Josephson. London: Rudolf Steiner Press 1983.

8. Walter H. Die Sieben Hauphnetalle Kg. Nr. 48.

9. Steiner R. Curative Education (GA 317). Transl. by M. Adams. London: Rudolf Steiner Press 1981.

10.Wolff O. Das hyperkinetische Syndrom. Merkurstab 1993; 46: 1.





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