calcium orotate abstracts

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Terry Suttles

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Subject: calcium orotate abstracts

THE CLINICAL EFFECT OF CALCIUM OROTATE1 ON CARTILAGE TISSUE

1 also known as calcium diorotate

A specific function in relation to pentose metabolism of bradytrophic

tissue?

We are presenting here an orientation into the clinical effect of calcium

orotate. Calcium orotate is absolutely free of any side effects and in this

respect, it is far superior to all the conventional calcium salts now being

used. Because calcium orotate can penetrate the complex cell membranes, it

can compensate for a disturbed calcium transport through these cell

membranes. In addition, calcium orotate has a special affinity for

bradytrophic tissue - cartilage, for example - where it is metabolized.

Parallel studies have shown that a defective calcium transport through the

cell membrane is of great pathogenetical significance.

Previous experience, up to now:

We have employed calcium orotate extensively since 1968, hospitalized and

ambulatory, to treat decalcification conditions and even in many cases,

immunological diseases. The results accomplished here are in complete accord

with what we discovered in 1959 concerning the transmembrane transport

complex. Calcium is first released as an ion, on the cytoplasma membrane

level, because orotic acid is chiefly metabolized there, not in the outer

cell membrane. The clinical results that we have seen up to now are very

encouraging, with a minimum of side effects completely unparalleled with

anything that we have seen in the entire field of calcium supplementation.

And what is more, in suitable cases, this substance is a very satisfactory

agent in the recalcification of metastatic defects in the skeletal system

(1), (2). I reported this at the 1970 cancer congress in Houston.

The results of calcium orotate therapy with juvenile decalcification and

with osteoporosis of the aged, are completely satisfactory for the first

time, especially in view of the absence of side effects. This finding was

contrary to all my previous experience with recalcification therapy.

The very remarkable results which we have achieved in hip joint plastic

surgery, (3) are due to a hardening of the bone by preliminary treatment

with calcium orotate. Previously, in this periodical, I reported the

recalcification of bone metastases. Illustration 1. show another patient

(f), in which a severe defect of the acetabular roof was so improved

(recalcified), that hopeless immobilization was replaced by fully normal,

pain-free locomotive ability. This was accomplished after about 2.5g calcium

orotate tgl2 for 10 weeks. A long period of therapy with a conventional

calcium seltzer, had been carried out previously, with no effect.

2tgl=daily (from the German " taglich " )

Calcium Orotate and Liver:

A several year search through many long term treatments with calcium orotate

for side effects was absolutely negative. On the contrary, a whole series of

positive observations came to light, which may be connected with the unique

transmembrane calcium transport. We should mention here, that there is still

quite a bit of clinical interest here. I will discuss this before I dwell on

the main theme of the skeletal effect of calcium orotate.

One noteworthy observation is that patients with chronic cholangitis and

light cases of chronic hepatitis - and also in severe aggressive cases -

show a considerable improvement in their ailments, their state of health,

their gall function, and to some extent, their biochemical and biological

findings. This is especially true under long term therapy. It appears to be

associated with an anti-inflammatory effect on the mesenchymal stroma system

in the liver.

The carrier molecule - orotic acid - has an especially high affinity for

mesenchymal tissue (4). Free orotic acid, magnesium orotate, or other

calcium salts do not show this effect on the liver. We should refer here to

the research of Deborah Doniach (10) on all immunological liver disease -

with and without cirrhosis - concerning antimitochondrial (not anticellular)

antibodies, as sickness motivation. Calcium orotate liberates its calcium

ion - this the classic anti-inflammatory principle - at the level of the

mitochondrial membrane. This explains the anti-inflammatory effect in the

liver.

Four patients who had taken, on the average, 3g of calcium orotate in

stomach acid resistant capsules per day, for more than a year, submitted to

a liver puncture. (For reasons which had nothing to do with the application

of calcium orotate.) In all cases there was no sign of fatty liver

development. Quite the contrary, three of the patients with stage 3 fatty

liver showed a remarkable improvement under long term calcium orotate

therapy.

The first patient was a teamster - very heavy consumption of alcohol. His

condition had been a constant stage III for six years. After one year of

therapy - tgl 2g calcium orotate - not only were the complaints lessened,

but a liver biopsy showed nothing but a normal amount of fat accumulation.

Another patient - U.S. American (f) - came to us for treatment for a severe

case of fatty liver. In just ten days, after tgl 6g calcium orotate therapy,

the complaint was improved and also a mild case of jaundice was cleared up,

which had been with her for three years, following an influenza attack.

After three weeks, a biopsy showed a dramatic improvement. Every possible

liver therapy had been tried earlier, both in the United States, and here in

Germany, with no success whatsoever. A third case of fatty liver III, showed

a similar improvement after hyperalimentation.

It is absolutely necessary that we conduct a very thorough investigation on

this effect of calcium orotate on fatty liver. We must remember that the

lipase enzymes which are necessary for the mobilization of stored fat, are

activated by Ca++. I might assume, in this connection, that the primary

source of fatty liver is a defective calcium transit in the liver cell. A

magnesium washout caused by chronic alcoholism, in the liver cell membrane,

could explain this. Mg++ is necessary in the cell membrane for Ca-transit

into the cell. (6a) Anything which disturbs or injures the cell membrane

function can affect calcium transit through the cell membrane. So there are

possibly some other significant considerations, such as essential hypertonia

or the ingestion of detergents which stick to kitchen utensils after

washing. Also a fare too rich in carbohydrates puts a strain on the P-pools

and likewise interrupts the Ca-transport through the membranes. Free orotic

acid has no effect on the fatty liver condition. Likewise the same is true

for magnesium orotate.

Effect on Heart and Circulation

Another interesting observation is of a moderate, to often marked, dropping

of the blood pressure with fixed hypertonia. This treatment will elevate the

lowered blood pressure both in the chronic, as well as the light form of

renal hypertonia. Normal blood pressure is not affected. What is especially

convincing is the disappearance of angina pains, especially with a

hypertrophied heart. In addition, the improvement is remarkably good with

infarct anamnesis with hypertonia and a distinct sclerosis of the heart.

Digitalis or Strophanthin tolerance appears to be better. With a dosage of

10g calcium diorotate tgl., no incompatibility of Digitalis can be observed,

in the EKG, subjectively, or otherwise. Probably because no membraneous

calcium ions are created. In this connection, I must point out that some

time ago, Kaufmann and coworkers (Kaufmann and Mitarbeit) (11), researched

the problem of defective or insufficient calcium transit in hypertrophia of

the heart muscles. They conclude that this is the reason for contractile

insufficiency, in hypertrophy and other metabolic problems of the

hypertrophic heart. Special reference must be made to the papers of the

Kaufmann group. We have made a series of tests with 14 year old dogs on a 14

percent incline. Our results were a very good confirmation of the pathogenic

mechanism that Kaufmann portrayed. We will give you the details in a later

article.

Rilling (12) has verified the research of Zondek (13) and Kylin (14) with

his comprehensive spectrographic studies. These authors maintain that

essential hypertonia is a cellular calcium-deficient pathognomonic

condition. This interpretation is much the same as Kaufmann's explanation of

heart muscle hypertrophy and would explain the blood pressure-lowering

effect of calcium orotate. At the time that Nieper and Laborit were doing

clinical research on potassium magnesium aspartate, we hoped to be able to

correct disturbances of the heart action regulation system. Except for a

suppression of ventricular and supraventricular extrastole, this hope was

not realized. (15) As you know, the heart action regulation system is

musculature in nature, which consists of a different type of metabolism, the

direct oxygen or " pentose pathway " . The stimulatory regulation of ganglion

tissue provide especially good protection against oxygen deficiency

intrafetally and later. Orotic acid plays an essential role in the pentose

pathway, and so appears to be the electrolyte transporter needed for that

tissue. In view of that, it should not be surprising to learn that we were

able to normalize apparently therapy-resistant tachyarrhythmia with auricle

flutter, in three doses, with a dosage of 5g calcium tgl.

After this excursus, I would like to mention the immune-inhibiting effect

(as already reported) (4), of calcium orotate on a succession of

bradytrophic tissues.

Specific Effect On Cartilage:

It was first reported by White towards the end of 1969, that calcium orotate

showed an astounding curative effect on the Tietze syndrome. These reports

were repeated over and over during 1970 and 1971, so that we were induced to

try calcium orotate in three cases of stubborn Tietze syndrome. The effect

of the calcium orotate was indeed surprising - all details of the White

article were fully verified. Tietze syndrome, according to our information,

is much more common in the US than here in Germany. According to White, the

syndrome is suppressed by very low doses - down to 1g/week, which we could

verify. A dosage of 500mg/day is fully effective. It is highly significant

that there is no effect whatsoever from calcium EAP, calcium-L dl aspartate

(calciretard), calcium gluconate, calcium citrate, magnesium orotate, and

K-MG-aspartate, upon the Tietze syndrome.

On the basis of our knowledge of the effect of calcium orotate on the Tietze

syndrome, we must conclude, that a favorable trophic effect on the

cartilaginous intervertebral substance is the reason for the not

infrequently spectacular improvement of the patient.

This fully specific effect of calcium orotate on cartilage, as evidenced by

the Tietze syndrome experience, appears now to be of tremendous clinical

significance. Unfortunately, we only learned this after the repeated reports

of White. While we were treating patients with spinal column syndrome and

calcification damage, it had been apparent, for a long time, that the

reported and verified improvement of their condition, must be attributed to

more than simply an influence on the bone tissue. For example, we had five

patients (f) and one patient (m) from 26 to 76 years, with symptoms of

weakness and painful sensitivity in the wrists. In three cases, it could be

observed only with a sphygmomanometer, and in three cases observation was

not possible at all. In every case, the complaints disappeared with calcium

orotate therapy. Upon removal of the therapy, or when the dosage was

insufficient (less than about 1.6g/week) the complaints returned.

Especially puzzling are the findings for 18 patients from our files, in

which there were severe dislocating alterations of the spinal column.

Treated with calcium orotate, these patients became exceptionally free of

complaints. Other medications - Butazonderivate, cortisone, indomethacin,

physical therapy, gold medication - had failed. Even intensive treatment

with calcium EAP, and calciretard along with calcium-sandoz and

K-Mg-aspartate were ineffectual.

CASE HISTORY:

NOTE: The illustrations which are x-ray images cannot be reproduced by our

copy machine, so they are omitted here. They are in the German manuscript

however.

Illustration 1, Frau K, 35 years old, before and after therapy with calcium

orotate. Metast. Mamma-carcinoma

Illustration 2a, patient (f) H. Sch. 64 years

Severe complaint complex with LWS syndrome. Every imaginable therapeutic

preventive measure taken to no avail. Infusion treatment with calcium-L-dl

aspartate (calciretard) plus calcium EAP for more than six months. Complete

stationary immobilization for three months 1970/71 to no avail. The pain

associated with the LWS syndrome had forced her almost to the point of

complete immobility. About three to five weeks after starting calcium

orotate therapy - an average of 3g/daily - the patient was complaint free

and remained so for 16 months - practically normal movement and walking

ability. In contrast to calcium orotate, other calcium transporters such as

calcium EAP and calciretard were fully ineffective. Is the improvement to be

sought in a structurally favorable influence of the intervertebral tissue?

Illustration 2b,

Almost complaint free after six weeks intensive treatment with calcium

orotate. reconstruction mainly in the gap between 3 and 4. LWK Both

developments are stabilized. These findings are not the only ones which gave

rise to our questions about the effectiveness of calcium orotate on

cartilage.

In 1968, we started using calcium orotate to treat patients with definite

Bechterewschen disease. There were, in all, five such patients and in all

the cases the very intense pain in the spinal column disappeared for the

most part. All previous treatments - phenylbutazone, cortisone, gold therapy

and healing baths - had been ineffective.

Illustration 3, patient (f) N.N. 56 years

In 1963, the disease has progressed so far in this 56 year old patient, that

she was almost completely immobilized. In spite of standard therapies and

seltzer water cure, the progression continued. By 1968, the face was almost

in a fixed position, movement and sitting were almost impossible. 1.5g

calcium orotate was prescribed daily for 54 months continuously. No more

complaints. The face could be moved normally and the patient resumed her

household duties. The second picture is the patient (f) with Morbus

Bechterew after 54 months continuous treatment with calcium orotate.

Illustration 4, patient (f) M.B. 71 years

Most severe complaints for three years as a result of spondylitic arthrosis

deformation. Treatment with phenylbutazone and also in combination with

cortisone and with pyrazolone showed only slight palliative effect.

Calcium-sandoz forte tgl. 3 tabl. for over four months without any effect.

After 10 days tgl. 5g calcium orotate, the patient was almost complaint

free, and has remained that way.

Illustration 5, patient (f) N.B. 81 years

A sister of Frau M.B. above. 10 years older. Xrays and symptom complex

indicate a very severe case. After being treated with calcium orotate tgl.

5g, she became complaint free, that she again took up vigorous employment

after previous inactivity.

Illustration 6, patient R. 79 years (f)

Frau R., mentally and bodily vigorous. Had an acute attack of a long time

existing osteochondrosis. Quite comfortable lying down, but experienced

immediate unbearable pain in the spinal column upon standing up. After

treatment with 5g calcium orotate daily, the patient became complaint free

within three weeks. The pain had previously worsened under cortisone

therapy. Calcium-gluconate-citrate, phenylbutzone and indomethazine had no

effect whatsoever. The curative effect of calcium orotate was permanent (now

over 14 months).

Illustration 7, patient (m) St. 55 years

Acute monarthritis of the right tibiotarsal joint, forcing him almost to the

point of immobilization. Three tablets realin daily were of very little

effect. Soludecortin H 50mg likewise. Volon 80 brought limited relief for 36

hours. Calcium orotate 8 tabl. each .5g daily brought improvement after 2

days and corrected the condition in 6. There are four similar cases.

Latest findings

By the end of 1972, we had experience with 21 cases of deforming

spondylarthosis - five men, sixteen women, from 58 years up. Clinical and

objective findings were consistent with the cases mentioned previously.

14 out of 16 women and 4 out of 5 men were helped by calcium orotate alone.

They were observed for over a year. The remarkable effect of calcium orotate

(called Ca orotate for short) with Tietze syndrome in the intervertebral

disk (and possibly in the ligamentous apparatus) causes us to again evaluate

the metabolic specificity of cartilage and other bradytrophic tissue. Here

the pentose pathway (so-called direct oxidation) plays a very crucial role -

an extremely old phylogenetic-metabolic pathway, which is not dependent upon

the erythrocyte oxygen donation. In the pentose pathway, the ribose is

activated through orotate coupling. For this reason, orotic acid plays a

very essential role in the pentose pathway.

Here we are concerned with a large variety of tissues. Besides cartilage and

ligamentous tissue, there is the connective tissue, the skin, the walls of

the blood vessels, a specific section of the venules in the blood-brain

barrier, the heart stimulation-regulation tissue and keratin building tissue

(hair, nails, etc.). Also the pentose pathway plays a very important role in

the bone matrix, in the heart muscle and in the liver (both in the liver

cells and in the stroma). The aromatic structure of the orotic acid is

responsible for the high complex stability of the salts, and the already

mentioned highly complex passage through the cell membrane typical of orotic

acid, plainly make the orotate an ideal mineral transporter. (4)

We are indebted to the tireless effort of Laborit (8) and his scholars (7)

who made public the results of their year-long research which disclosed the

vital effect of the pentose pathway in the function and structure of

bradytrophic tissue. Life would not be possible without it. Previously,

cartilage and connective tissue had been considered uninfluencable, for the

most part.

If calcium orotate can bring about a change here, as was demonstrated, then

there is not much value in the geriatric therapeutic concept.

Summary

An orientation is given concerning the clinical effects of calcium orotate

(called Ca orotate for short). Because calcium orotate is free from side

effects, it is superior to conventional calcium salts, which have certain

problems when applied in osteoporosis with concomitant arteriosclerosis of

the abdominal aorta. Calcium orotate, on the other hand, protects the body

from arteriosclerosis.

Calcium, for this reason, is of value as a food supplement when used in the

form of calcium orotate, which can penetrate the cell membranes as a complex

form, compensating for defective calcium transit into the cells. In

addition, calcium orotate has a special affinity for cartilage and other

bradytrophic tissue, where it is metabolized.

Not only is the basic principle of action quite simple, but the long time

therapeutic effects are of considerable interest. A new dimension of therapy

now appears with the improvements in osteochondrosis and disk degeneration

treatment. Far better than the present therapeutic possibilities. Much the

same observations seem to apply to osteoporosis.

Parallel investigations point to the important pathogenetic significance of

a defective calcium transport through the cell membrane. This is the case,

for example, in hypertensions - especially essential hypertension - in fatty

liver, in disturbances of the ductile of the heart, and in contractile and

metabolic insufficiency of the hypertrophic myocardium. In respect to all of

these indications, calcium seems to bring about the most promising

therapeutic results, when combined with the carrier orotic acid for better

transmembrane transport, in the form of calcium orotate.

Literature

1. Nieper, H.A.: Recalcification of Bone Metastases by Calcium Di-orotate,

Agressologie II, 6, 495-502 (1970); 2.Nieper, H.A.: A Clinical Study of the

Calcium Transport Substances Ca-di-aspartate and Ca-2-aminoethanol Phosphate

as Potent Agents Against Autoimmunity and Other Anticytological Aggressions,

Agressologie VIII, 4 (1967); 3.Al Haddad, M.: Pers. Mitteilung; 4.Nieper,

H.A.: The Anti-inflamm. and Immune Inhibiting Effects of Calcium Orotate on

Bradytrophic Tissues, Agressologie X, 3, 349-353 (1969); 5. White, M.D.: In

Preparat. und pers. Mitteilung; 6.Nieper, H.A.: Metabolisme du Calcium et du

Phosphore des patients traites pa l'Orotate de Calcium, Agressologie (Paris)

1971, 12, 6, 401-408; 6a.Nieper, H.A.: Bilanzuntersuchung des Calcium- und

Phosphatstoffwechsels bei Patientin, die mit Calcium-Orotat behandelt

werden, Z. praklin. Geriatrie (1197) 9, 184-191; 7.Sonka, J. (Prag): Voies

de Pentoses-Physiologie et Physiopathogenie, Agressologie VII, 5, 461-477

(1966); 8.Laborit, H.: Regulations metaboliques dans le Tissu Conjonctif,

Agressologie 1969, 10, 1, p.11-26; Silberberg, R.: Gesamtband Act

Rheumatologica, Documenta Geigy, No. 26 (1972), " Wachstum und Alterung des

Skelettes " ; 10.Doniach, D.: Die klinische Bedeutung der antimitochondrialen

Antikorper, Deutch in: Triangel-Sandox, Band 11, 1, 29-34 (1972);

11.Kaufmann, R.I., Homburger, H., und H. Wirth: Disorder in

Excitation-Contraction Coupling of Cardiac Muscle from Cats with Exptl.

Produced Right Ventric, Hypertrophy Circulation Research, Vol. XXVIII,

346-357 (1971); 12.Rilling, S.: Gesamtdokumentation Bayer Spektromat

Laboratorien, Stuttgart, Klagenfurter Str. 4 (1972); 13.Zondek, R.: " Die

Elektrolyte " , Springer, Berlin (1927), p. 299-300; 14.Kylin, E.: Die

Hypertoniekrankheiten, J. Springer, Berlin (1926); 15.Nieper, H.A. und Kj.

Blumberger: Wirkung von Elekrolyutschlepper - Verbindungen

(K-Mg-Asparaginat) auf den Herzstoffwechsel, Beh. von Extrasystolien Verh.

dt. Ges. Kreislaufforsch. 27, 238-242 (1961).