DR. MED. HORST KIEF

Londoner Ring 105, 67069 Ludwigshafen Tel.: 0621-66936-0, Fax: 0621-66936-36

1

Oncological care programme with ozone

Part 1: Ozone therapy in chronic aggressive hepatitis as oncological prophylaxis

Part 2: Redox potential in ozone therapy as oncological screening

Presentation by Dr. Horst Kief, M.D. given on 27th July 1985 at the Hilton Hotel, Philadelphia, PA, USA to the Annual Convention of the Foundation for Alternative Cancer Therapies (FACT) Introduction

It is well known that life on our earth would not be possible without ozone since the ozone layer,

with maximum density at a height of about 30 kilometers, protects the biosphere form ionizing

radiation. Apart from this happy action of ozone, however, there are negative aspects of this

therapeutic gas that have to be taken into account.

The injurious action of smog is due to its ozone content, and the forest death in Europe is largely

attributed to ozone, although on the one hand the harmful effect is considerably intensified by

nitrogen oxides and carbon monoxide, and on the other hand oxygen is a plant excretory product

and so an activated excretory product can by no means contribute to plant life.

Quite different viewpoints apply to the action of ozone in man. Here it is certainly a respiratory

poison, but has no cell toxicity when administered parentally. On the contrary, we know that

correctly dosed ozone administration can even stimulate enzymes that degrade oxygen radicals,

such as glutathione peroxidase, catalase and superoxide dismutase. On the basis of the

chemical reactions that can be induced by ozone, we can now postulate that when mixed with

blood, ozone supplies reaction products that, via an intermediate peroxide stage, represent

ozonides and carbonyl group carriers as end products.

However, due to their strong electrical dipole moment in quinones such as ubiquinone. carbonyl

groups acquire crucial significance in oxygen transport so that it can readily be postulated that

ozone therapy prepares a type of replacement for respiratory enzymes. In my opinion this

explains the wide-ranging action of ozone on the body and the broad range of indications for the

use of ozone.

After ozone therapy, increased amounts of adenosine triphosphate are available in the body for

energy-consuming processes. The metabolism of cholesterol and of uric acid in the fat and purin

pathways involve energy-consuming processes so that it is quite understandable that metabolic

diseases can be treated effectively with ozone. Among other things, the normalization of elevated

cholesterol levels indicates that the hypocholesterolaemic action of ozone is actually based on an

activated metabolic process and not on simple chemical breakdown of the cholesterol molecule.

A reduction of the cholesterol level below normal values is not possible with ozone. The same

applies to uric acid.

2

Two other physiological effects of ozone raise hopes of the successful therapeutic use of the

ozone-oxygen gas mixture:

1. Ozone is bactericidal, fungicidal and virucidal, without any development of resistance.

2. Ozone attacks cancer cells but is largely protective of healthy cells, as is demonstrated by

gassing studies and the injection of ozone gas into tumours. According to our current state

of knowledge we must assume that the specific aggressivity of ozone with regard to

malignant cells rests on their different complement of enzymes that neutralize oxygen

radicals.

Considering that the viral genesis of some tumours in both animals and man is nowadays

incontestable and that chronic aggressive hepatitis can, because of the high incidence of primary

liver carcinoma, be accepted as precancerous and that the hepatitis B virus is therefore to be

seen as an oncogen, I think it is justified to speak to you about chronic aggressive hepatitis within

the context of ozone therapy.

STUDY OF CHRONIC AGGRESSIVE HEPATITIS AND OZONE THERAPY

Chronic aggressive hepatitis is predominantly the result of virus B hepatitis. About 60% of

patients are HBsAg-positive, and in patients with chronic persistent hepatitis the figure is nearly

80%. (1). HBsAg-negative patients present an increased incidence of immunological phenomena

that suggest an autoimmune pathogenesis. This is characterized by a high gamma-globulin

fraction and a clearly inflammatory reaction in the liver tissues (2). Due to the serological

autoimmune reactions and the increased incidence of positive LE phenomena, this disease is

also known as lupoid hepatitis (3).

Indicative of the immunological nature of chronic aggressive hepatitis is the detection of humoral

antibodies and/or cellular immune mechanisms. Whereas humoral autoimmune mechanisms

have no tissue-toxic action, the greatest significance is now attached to cellular immune reactions

in the destruction of liver cells. In this connection it is noteworthy that chronic aggressive hepatitis

can be combined with other immunological diseases (Sjorgren's syndrome, glomerulonephritis,

thyroiditis). The mechanisms that trigger these immune reactions have not yet been clarified.

In terms of pathological anatomy, the two forms of chronic hepatitis can be characterized as

follows: In the chronic persistent form there are inflammatory infiltrations of the periportal fields

without involving the adjacent liver parenchyma. In chronic aggressive hepatitis the inflammatory

reaction is not registered to the periportal fields but extends in wedges into the parenchyma and

is also characterized by connective tissue neoformation. Chronic persistent hepatitis is essentially

characterized by an asymptomatic course or no more than a neurasthenic state similar to that of

acute virus hepatitis, with only a slight elevation of transaminases to a maximal 50 mU/l. A

positive HBsAg result is obtained in almost 80% of cases, but autoimmune phenomena are

absent. The disease often cures spontaneously. There is generally a restitutio ad integrum, but

transition to a chronic aggressive form may be observed in rare cases. The chronic aggressive

form is gradually progressive, with a slowly intensifying icterus or a sudden onset of jaundice. Its

symptoms are similar to those of acute virus hepatitis. It occurs preferentially in persons under

the age of 30 years, with about three-quarters of the patients being women. The symptoms

depend on the disease activity, but there is often an almost normal general state even in the

presence of considerable activity.

3

The most common symptoms are fatigue, asthenia, upper abdominal pain, arthralgias and

pruritus. In women there are also hormonal disturbances, often with secondary amenorrhoea.

Persistent icterus is found in forms with a severe course, but in milder forms it is episodic and

occurs only during periods of necrotic evolution. Transaminase activities of 100 mU/l or more are

observed. The electropherogram is characterized by hyperalbuminaemia and marked

hypergammaglobulinaemia. The serum immunoglobulins are characterized by increased IgG

levels. There are also signs of elevated immune reaction to intestinal tract antigens (4) as well as

indications of disturbance of liver RES clearance functions. Chronic aggressive hepatitis has a

physic course; its mortality is greatest in the first two years (about 25%) and then flattens out (5)

(Figure 1).

The clinical treatment of chronic aggressive hepatitis is limited essentially to two therapeutic

possibilities: cortisone derivatives and immunosuppressive.

The results of controlled studies reveal a marked reduction of mortality with these treatments (6).

Prednisolone is mainly given, often as a long-term treatment with daily doses below 15 mg. This

treatment frequently produces side effects and not rarely has to be interrupted, e.g. due to steroid

ulcer with bleeding, osteoporosis, steroid-induced diabetes or aseptic hip joint necrosis (7).

Azathioprine and 6-mercaptopurine are the most commonly used immunosuppressives, although

this type of treatment involves an additional specific risk since these substances are themselves

hepatotoxic and at doses of 2.5-5 mg/kg lead to icterus, centrilobular necrosis and intrahepatic

cholestasis. Treatment is thus restricted to dose rates of 1-2 mg/kg with monitoring of the

depressive action on the bone marrow. Thrombocytopenia and leucopenia are common. New

and interesting insights are being obtained by the activation of the immune system with

levamisole, but therapeutic success is by no means certain (8). The same basically applies to D-

penicillamine; there have also been reports of favourable responses to D-penicillamine, but its

administration is associated with side effects affecting the bone marrow, kidney and nervous

system (9). General treatment is characterized by physical nursing with prolonged bed-rest and

protection from stress. A specific diet is, according to current clinical teaching, unnecessary (10).

So far the discussion has centred on clinical teaching regarding the treatment of chronic hepatitis.

According to Ehrlich's findings (11), it had been established in 1960 that ozone has a reliable

sterilizing action on hepatitis B virus, and certainly at a concentration of 1.8 mg per 100 ml blood,

so that the use of ozone should help to obviate the need for treatment of chronic hepatitis. Wehrli

reported some statistics regarding 10,000 transfusions with ozonated donor blood, in which not a

single case of transmitted virus hepatitis could be found (12). Wolff also surveyed more than

2,000 transfusions, none of which led to virus hepatitis (13). Since the incidence of transfusional

hepatitis is up to 3%, these results must be considered excellent. In 1981, Konrad reported on a

total of 13 hepatitis cases treated according to a modified HOT procedure (8 cases of hepatitis A,

one of non-A/non-B, four of chronic hepatitis). According to his data, the patients were completely

cured after a maximum of 6 administrations during a period of 16 days (14). The four cases of

chronic hepatitis showed similarly positive results together with the achievement of normal

transaminase values. In 1980, Binder reported on the results of treatment in 17 patients (15). This

author did not classify the cases according to virus types or according to their acute or chronic

course. The treatment was successfully concluded in 9 patients; at the time of publication there

were 8 patients still undergoing treatment, and in 6 of these cases an improvement had already

been achieved according to subjective, clinical and laboratory criteria.

4

In 1981 Dorstewitz reported on 7 cases of hepatitis, including two acute forms and 5 cases of

chronic persistent hepatitis (16). In all cases a considerable improvement of condition could be

achieved, including improvement of laboratory parameters.

A critical evaluation of the literature of that period regarding chronic hepatitis form the

conventional and naturopathic viewpoints revealed the therapeutically refractory role of chronic

aggressive hepatitis. This form of hepatitis seems to have been excluded in Dorstewitz’s

extensive work.

In the following table I present to you a selection of 12 cases of chronic hepatitis, including 10

with the chronic aggressive form confirmed by biopsy. At present in my practice I can review 20

cases of chronic hepatitis, including three cases of non-A-non-B hepatitis with similarly favourable

results. From a German nephrological center I have reports of the treatment of another 20 cases

of chronic hepatitis which confirm my results, particularly with regard to HBsAg seroconversion.

At the University of Innsbruck in Austria a controlled trial is being carried out at present to check

my Statements. In a preliminary personal communication it was confirmed to me that

seroconversion can truly be achieved with hyperbaric ozone therapy.

5

Figure 1 Spontaneous course of chronic aggressive hepatitis*

Mild course

Severe course

n = 47

n = 24

Observation time

6-8 years

6-12 years

Cirrhosis

64%

83%

Of which: fatal

23%

46%

stationary course 19% 4%

healing 17% 13%

*Ammann et al.,1971.

Mean survival rate after 2 years of various treatment for chronic aggressive hepatitis*

Placebo 61% (59-63%)

Prednisolone 92% (86-95%)

Azathioprine 74% (64-87%)

Azathioprine and prednisolone 93%

*The figures were calculated from the data in the following studies: Mackay 1968; Cook et al.

1971; Soloway et al. 1972; Murray-Lyon et al. 1973.

Therapeutic results in severe chronic aggressive hepatitis (glucocorticoid therapy) depending on

the presence or absence of HBsAg (taken from Schalm 1979)

Total patients Comparative Group

HBsAg-pos. HBsAg-neg. HBsAg-pos.

HBsAg-neg.

n = 13 n = 82 n = 13 n = 13

Sex, male

89% 30%

89%

89%

Age (years)

52 35

52

50

LE, ANA, SMA 1:40

6% 76%

6%

13%

Remission

46% 80%

46%

85%

Therapeutic failure

46%

16%

46%

8%

6

Figure 1 - continued

Detection of HBsAg (complement-binding reaction) in chronic liver diseases.

PBC = primary biliary cirrhosis CPH = chronic persistent hepatitis CAH = chronic aggressive hepatitis Ci = cirrhosis of the liver (Taken from Wright et al. 1969 and from Kaboth et al. 1970). Acute hepatitis B: Abbreviations used in connection with hepatitis B infection: HBV Hepatitis B virus

HbsAg Hepatitis B surface antigen (antigen of the HBV coating membrane)

Anti-HBs Antibody against HBsAg

HBcAg Hepatitis B core antigen (antigen of the HBV core)

Anti-HBc Antibody against HBcAg

HbeAg Antigen that also occurs in hepatitis B infection

Anti-Hbe Antibody against HBeAg

DNA polymerase = enzyme in the HBV core

100% 50 %

Dane particle (Hepatitis B virus) Structure (diagrammatic) of the hepatitis B virus

HBsAg DNA

7

Figure 1 - continued

Diagram of hepatitis D infection (Frosner, Reinhardt, Roggendorf 1980)

infection onset of disease

Diagram of hepatitis B infection with representation of the antigens and anti-bodies that can be

detected in the serum during a typical hepatitis B infection. I thank Dr. Frosner (Max-von

Pettenkofer-Institut, Munich) for the diagram.

icterus

8

Figure 2 State of the study in April 1982

Case No.

Initials Chronic Aggress.

GOT, GPT, gamma-GT

Values in reactive

GOT, GPT, gamma-GT

HBsAG test

Histolog. detection

Titre before / after

Duration of treatment

Comments

1 N. Th. + 0 342 259

602 802

167 50

160 267

466 446

44 102

27 62 35 + yes + - 90/120 Relapse

2 Sch. H. + 19 29 15 17 23 14 15 7 10 + yes 82 45 90 No graph

3 Sch. E. + 0 180 331 88 103 153 27 9 10 11 - yes - - 210 - -

4 Z. K. H. + 0 115 248 223 245 265 82 16 22 28 + yes - - 180 - -

5 H. Kl. + 0 73 116 109 464 986 271 67 116 77 +

HBeAg+ yes + - 150

Not yet concluded

6 K. F. + 153 476 133 149 344 129 10 23 19 + yes - - 45 No graph

7 W. K. + 0 34

39 48 94 187 61 66 125 48 + yes - - 120 - -

(+cortisone)

8 G. K. - 52 143 61 71 198 67 13 25 16 - yes - - 60/100 Relapse

9 S. E. + conv. to cirrhosis

47 99 83 63 118 74 15 21 26 + yes + - 150 Relapse

10 R. C. + 320 645 -- -- -- 24 38 30+ + yes - - 120 - -

- 27 40 24 +C

11 H. H. - Chron. Persist.

143 270 27 -- -- -- 16 20 13 + no + - 60 - -

12 M. H. J. - chron. persist.

52 97 22 21 39 36 + yes + + 120 Not yet concluded

Total chronic hep.: Mean 144,4 317 91 153 298 81 24 41 29 106

s 111 258 63 129,5 68 72 20 40 19 56

Chron. aggr. hep.: m 133,5 263 103 163 304 85 15,7 25,2 22

s 116,4 234 64 139 286 77 6 15,7 10

9

10

At the present stage, the results of ozone treatment can be summarized as follows

(cf. figures 2 and 3)

1. With only one ineffective treatment (patient # 7) and with an absence of side effects of

hyperbaric ozone therapy, the treatment of chronic hepatitis with ozone can be attested as

having a very good efficacy, with improvement or cure in 92% of cases.

2. On the basis of a preliminary survey, the following treatment scheme can be recommended.

Hyperbaric ozone therapy once per week with 220 ml of the patient's own blood and an

equal amount of 40-gamma O2-O3 mixture. After about 3 - 4 weeks this interval should be

increased to 14 days or longer in order to allow the body time to develop an immune

reaction. Inbetween the treatments, i.e. after 3 to 4 days during the phase of weekly therapy

and ??? one week during the later phase of treatment, a minor retransfusion with 5 ml of

ozonated autologous blood (Minor Autohaemotherapy according to Windstosser) should be

undertaken. Neural therapy is recommended in all cases presenting post-hepatic upper

abdominal syndrome with distension pressure, etc. I carry out neural therapy in the form of

upper abdominal blistering according to Varro, if possible with weekly interchange with a

high right paravertebral injection of 1% procaine "Roedler".

3. After about 75 to 90 days there is an increase in transaminase values, which roughly falls

within the incubation period of hepatitis B and indicates an active immune process such as I

have previously postulated. The immunoinductive action of ozone which I have, unlike

Wolff, discussed previously can be considered to be confirmed by these present findings.

The observation that HBsAg was no longer detectable in some cases after hyperbaric

ozone therapy and showed 50% reduction in titre in another case seems to support this

hypothesis also. (Further evidence is awaited since the studies have not yet been

concluded.)

4. The particularly favourable effect of a prior treatment with calf blood extract suggests that

his type of product may be included in the course of therapy. 20% Acetohaemyl or

Actovegin infusions in the Intervals between HO treatments can be recommended.

5. With a mean treatment time of 106 days, a relatively low level of effort with 1 to 2 ambulant

treatments per week and an amazingly positive result after about 145 days, with absolute

freedom from side effects and remarkable freedom from relapses, hyperbaric ozone therapy

with 02-03 mixtures can be considered as a very cost-effective treatment.

6. Following an initial reduction of transaminase values to a minimum level after a mean of 31

days, approximately 50% of patients show a reactive rise with a peak after a mean of 78

days, probably as a result of immunological factors. Only after this peak 1s there a definitive

normalization of the enzyme activities. It is best to inform the patients of this reactive

response before starting their treatment.

11

Patient No. 1

12

13

14

15

16

17

Patient No. 9

18

19

20

21

References 1) U. Kaboth et al.: Australia (SH)-antigen findings in liver patients and blood donors (in

German). Dtsch, med. Wachr., 95, 2157. 1970.

2) H.G. Kunkel et al.: Extreme hyperglobulinaemia in young women with liver disease of

unknown etiology. J. Clin. lnvest., 30, 654, 1954.

3) I.R. Mackay: Etiology of chronic hepatitis. In: The liver and its diseases.

Eds. F. Schaffner, Sh. Sherlock, C.M. Leevy. Georg Thieme, Stuttgart 1974.

4) M. Bjorneboe: Anti-salmonella agglutinins in chronic active liver disease. Lancet, 1971/II,

484.

R.I. Protell et al.: Antisalmonella agglutinins in chronic active liver disease. Lancet,

1971/II, 33a.

D.R. Triger, M.H. Alp and R. Wright: Bacterial and dietary antibodies in liver disease.

Lancet 1972/I, 60.

5) S.P. Mistilis and C.R.B. Blackburn: The treatment of active chronic hepatitis with

6-mercaptopurine and azathioprine. Austr. Ann. Med., 16, 305, 1967.

6) G.P. Lewis et al.: Prednisone side-effects and serum protein levels. A collaborative

study. Lancet, 1971/II, 778.

7) I.R. Mackay: Chronic hepatitis: Effect of prolonged suppressive treatment and

comparison of azathioprine with prednisone. Quart. J. Med., 37, 379, 1968.

8) K. Havemanni: Treatment of chronic active hepatitis (CAH) and possible points of

departure leading to new therapeutic procedures (in German). Immunitat und Infection, 3,

199, 1975.

9) H. Gros and K. Zwirner: Treatment of chronic aggressive hepatitis with D-penicillamine

(in German). Med. Klin., 69, 333, 1974.

10) H. Lieber and H. Kasper: Liver diseases (in German). Aesopus Verlag, 1975. p. 170.

11) M. Purvis, S. Miller and R. Ehrlich: J. Infectious Diseases, 109, 238-242, 1961.

12) F. Wehrli Trans. 6th Congress of the European Society of Haematology, Copenhagen 1957.

13) H. Wolff: Medical ozone (in German). Page 538.

14) Konrad: Contribution to the Ozone Congress, Berlin 1981. Literature available from the

company Haensler, Iffezheim,

15) Th. Binder: Contribution to the Baden-Baden Medical Week. Literature available from the

company Haensler, Iffezheim.

16) H. Dorstewitz: Ozone Therapy Meeting, Baden-Baden 1981. Literature available from the

company Haensler, Iffezheim.

22

In so far as a complete cure with elimination of the antigen is possible in the aggressive form of

chronic hepatitis, we may thus speak of a true cancer prophylaxis.

I would now like to approach a topic that derives from the need to undertake not only continued

clinical observations but also laboratory controls for the selection of the correct ozone method in

each individual case. This part of my contribution may be called:

Catalytic effect in the peripheral blood of ozone therapy - possibility of early detection of cancer

Various parameters serve for the laboratory monitoring of the action of parenteral ozone

administration. The first to be mentioned should be the increase in leucocyte count after an

intramuscular ozone injection (1). The depressive effect on cholesterol and uric acid levels also

serve, at first sight, for laboratory monitoring (2, 3). However, as a reservation it should be

mentioned that this effect is concentration-dependent and is to be interpreted only in the sense

of a normalization of pathologically elevated values. Furthermore, so far it has been detected

and statistically confirmed in vivo only with one type of ozone administration, namely hyperbaric

ozone therapy. The detection of the various sites of ozone action (free fatty acids, free amino

acids, formation of peroxides and ozonides) requires special laboratory techniques and is thus

unsuitable for routine laboratory control studies.

Starting from the basic concept that the action of ozone is initially an oxidative process in the

widest sense of the phrase, and building on the need to encompass the oxidative actions of the

various possible methods of parenteral ozone administration, the Author sought to find a

process that would largely fulfil the said requirements, i.e. it should:

1) be practicable and easy to execute;

2) encompass the oxidative effect of ozone in its entirety;

3) be as effective as possible in the monitoring of ozone administration,

4) give an indication of the advisability of repetition of the chosen type of ozone therapy.

The measurement of partial oxygen pressure in arterial and venous blood, or the improvement

of oxygen tension, is known within the context of ozone therapy (4) and has a significance that

should not be underestimated in the monitoring of a course of treatment. However, it requires

special equipment (generally very expansive) and requires painstaking work.

In contrast, Westergren ESR measurement is very simple to execute, is practically free from

operating sources of error and shows significant change when undertaken immediately before

and after ozone therapy (5, 6). Available evidence from personal studies on this topic is still

limited but does suggest that the normalization of ESR values, or at least a tendency towards

normalization, indicates n favourable prognosis for the application of ozone therapy in any

individual case (7, Figures 1 and 2). For example, the ESR is unaffected or virtually unaffected

by ozone therapy alone in patients with malignant tumours.

23

The serum or blood redox potential actually represents the one parameter that completely

encompasses all the oxidative processes of ozone therapy. In his decisive work on “Das

System der Grundregulation" ("The fundamental regulation system"), Pischinger clearly

highlighted the significance of reducing substances (8, 9). He also reported an iodometric

process for their quantitative assay (10). However, because of the amount of work involved, this

method is reserved for scientific laboratories.

Due to its enormous oxidative potency, ozone necessarily leads to a shift in the redox potential

which, being electrically detectable, has been demonstrated by measurement techniques and

allowed Kief to evaluate various types of ozone therapy (11). The monitoring of redox potential

by means of electrical measurement techniques is relatively simple to carry out, although it

requires expensive equipment (12). In addition, it gives not the slightest insight into the actual

concentrations of the redox partners.

The Author was thus concerned with developing a procedure that, with the usual equipment

available in a doctor’s laboratory (i.e. a photometer), could determine the total redox substances

(called the “redox concentration” in the following text) quickly and with the greatest possible

exclusion of any sources of error. Building on Pischinger's basic work and with the cooperation

of a medical chemistry laboratory*, it was possible to develop a process (together with its

reagent) that satisfies all the requirements stated earlier. In addition, the reagent is extremely

cheap and has a long shelf-life.

*(MCP-Labor E. Blees, Pommernstrasse 14, D-67125 Dannstadt/Pfalz, FRG. Telephone: 06231/2444).

Materials and Methods

A stabilized iodine solution is used, being added to 0.005 ml of patient's serum. All the iodine-

reducing substances are assayed together on the basis of the photometrically determined

iodine consumption. In principle, the procedure corresponds to an iodometric titration. A green

filter (wavelength 546 nm) is used. The end result is presented in mEq/l, being, calculated from

the measurement result by means of a simple mathematical formula. Details of this procedure

can be obtained from the instructions enclosed with each pack unit.

The following columns of figures show the redox concentrations in mEq after various ozone

treatments, whereby the figure 049 signifies hyperbaric ozone therapy, 0490 signifies

hyperbaric ozone therapy with the addition of vitamin C to the blood flask before oxygenation

and the administration of vitamins A and E after therapy, 035 signifies minor retransfusion

according to Windestosser, 0350 signifies minor intravascular retransfusion according to Kief,

and 029 signifies the intramuscular injection of 10 ml ozone (distributed in both buttocks). The

concentration was 40 gamma in all administration forms. In the case of hyperbaric ozone

therapy, three values were obtained, namely before treatment, blood redox concentration in the

blood flask, and 10 minutes after treatment (Graph I).

24

The post-treatment values were basically obtained about 10 minutes after the end of treatment.

An initial evaluation of the results from 134 measurements leads to the following conclusions:

1. According to the current state of our redox concentration measurements there is no

ideal value. Pischinger gives 81 mg% as the mean value, which corresponds to 6.4

mEq/1 by our measurements. The higher general mean found in our studies is due to

the inclusion of all reducing substances, i.e. including protein-bound reducing

substances, whereas Pischinger worked with deproteinised serum. The values are

scattered above and below the mean irrespective of diagnosis, i.e. the redox

concentration level allows no quantitative evaluation of the patient's state of health. The

blood redox potential is known to depend on the amounts of reducing substances

present, such as vitamin C, vitamin E, glutathione, etc. A majority of our patients

presented malignant tumours and, as currently common in cancer treatment, were

receiving large doses of vitamin C. For this reason alone the values obtained before

ozone treatment could not be considered as "blank values".

2. Even minor therapeutic measures such as minor retransfusion according to

Windstosser lead to a marked shift of redox concentration.

3. Comparison of the values obtained with hyperbaric ozone therapy (blank value, value

for oxidized blood in the flask and post-treatment value) reveals a surprising effect of

ozone therapy (Graph I, Table 1). In the stated sequence, the redox concentration falls

from 9.5 to 9.4 and then to 9.3 mEq/l. This happens even though it should be

considered that 250 ml of ozonated blood has to be neutralized by the reducing

substances of the circulating blood. In actual fact, however, the oxidative process in the

peripheral blood continues after re-infusion of the patient’s blood. This is logically

possible only if the ozonation of the patient's retransfusion blood initiates a catalytic

process that continues in the blood. To the Author's knowledge this is the first time that

evidence has been obtained to support the previously theoretical hypothesis of a

catalytic effect of ozone on human blood.

4. In contrast to "healthy" subjects, a statistical evaluation of the redox responses in the

blood of patients with malignant tumours shows an increase in redox potential despite

oxidation. This effect is, for example, very clear within the context of hyperbaric ozone

therapy. Here there is an increase of 0.4 mEq, whereas in "healthy" subjects there is

only a reduction by 0.2 mEq (Graphs I and II; Tables 1 and 3). Due to the simplicity and

precision of the measurements, this is adequately significant in statistical terms. The

number of measurement values available at present does not yet allow it to be said

whether or not the degree of redox concentration increase correlates with the size of the

tumour of the propensity to develop metastases. Of particular interest is the observation

that even with supposedly "healthy" objects there was occasionally an increase of redox

concentration, and in these cases a suspicion of precarcinoma could be supported on

the basis of clinical status and further laboratory parameters. From this it can be

concluded that, in combination with ozone therapy, this test is actually suitable for

detecting overt tumours as well as precancerous metabolic states.

5. After several daily treatments with the retransfusion of small volumes of a patient’s own

blood supplemented by 1 g vitamin C after ozonation, in cancer patients there was also

a decrease in reducing potential similar to that in subjects with a "healthy' metabolic

status. From this it can be concluded that minor intravascular retransfusion according to

Kief is, a relatively simple measure, suitable for influencing the metalobic state of

25

malignant tumour patients in the sense of a normalization. This also correlates with the

clinical experience that metastases pain not rarely fades either suddenly or during a few

days after a single application of this form of ozone therapy (Graph III; Tables 2 and 8).

6. If several therapeutic measures are combined, e.g. minor retransfusion according to

Kief plus subcutaneous ozone infusion, there is frequently a reductive shift of metabolic

state in cancer patients due to some summation or even subtraction of the therapeutic

effects (Graph IV; Table 6).

7. With regard to minor intravascular retransfusion, the replacement of vitamin C by two

ampoules of "Roedler" SSR carbonyl groups was tested. No modification of the redox

concentration was obtained in cancer patients with this, but there was a slight increase

in "other diagnose' (Graph V; Table 7). The apparent inefficacy of the product with

regard to redox concentration should, however, not lead to the view that the use of the

product would be useless in minor intravascular retransfusion. In actual fact,

outstanding effects can be obtained in PCP patients. In evaluating the results it should

be borne in mind that the redox potential encompasses only a small sector of the total

biochemical spectrum of a therapeutic effect. In addition, the decrease in redox

concentration 10 minutes after therapy represents only a snapshot at the time of the

onset of action of a therapeutic procedure.

8. Hyperbaric ozone therapy with 500 ml of a patient's own blood and 3 g vitamin C before

oxidation plus 2 g vitamin C in the flask after oxidation leads to the greatest changes in

redox potential in cancer patients, with a shift in the sense of an oxidation. This effect

correlates with the corresponding improvement of clinical state in these patients so that

it may again be concluded that this therapeutic measure represents an optimal

treatment in malignant disease and that a simple monitoring of redox concentration

allows some evaluation of various types of treatment, especially in cancer patients

(Graph VI; Table 5).

9. Ion treatment was also tested, using the inhalation of positive or negative ions. As

expected, negative ions led to an increase in redox concentration (Graphs VII and VIII;

Tables 10 and 11) and positive ions led to a decrease. With combined ozone therapy

and ion treatment there was not rarely a potentiating action of positive ions on the

ozone therapy so that Hieber's recommendation (13) to treat cancer patients with

positive ions seems to be justified, at least from this viewpoint. Nevertheless, this

concept still needs to be confirmed by the counter-test with negative ions plus ozone

therapy and evaluation by means of other laboratory parameters (Graph IX; Table 9).

10. It was not possible to show a standard deviation in the graphs with the scales chosen

for them. This was because the standard deviation were so small, which again relates to

the not inconsiderable significance of the test carried out.

At present I can review about 400 measurements which I have just subjected to

statistical analysis and as a sort of preview to a later publication on this topic, I can now

say that the procedure presents adequated significance as well as being adequated

with regard to other statistical parameters such as variance, probability limits and the

like.

26

Summary

A report is given of a simplified iodometric assay for total reduced substances in peripheral

blood (known as "redox concentration" for short) under the conditions of various ozone therapy

procedures. Much new and important information was obtained in this ways:

1. After reinfusion, ozonated (i.e. oxidized) blood initiates a catalytic process in the circulation

that leads to a further decrease in reducing substances in the bloodstream.

2. Comparison of the responses of cancer patients and "healthy” subjects to ozone therapy

reveals a significant difference which gives rise to the hope that the different redox reactions

in malignant disease can lead to the diagnosis of precancerous and overt or occult tumour

states.

3. The simultaneous addition of large doses of vitamin C during hyperbaric ozone therapy

allows the redox reaction in malignant diseases to be changed to that found in "healthy"

subjects, generally also with a corresponding improvement of clinical status.

4. The monitoring of redox reactions during ion inhalation shows that this nonparenteral

treatment is suitable for controlled shifting of the redox concentration towards the oxidative

or reductive poles.

5. A combination of hyperbaric ozone therapy plus high-dosed vitamin C administration with

the inhalation of positively ionised oxygen shows a marked summation effect on oxidative

shifts of the redox reaction and can thus be recommended as a combination treatment.

27

Table 1 Redox concentration (mEq/l) in venous blood before and after hyperbaric ozone therapy:

250 ml blood + 250 ml of O2 – O3 mixture (40 gamma).

Cancer patients

before therapy in vitro after therapy

8.33 8.81 9.04

9.37 10.02 11.21

9.08 9.08 9.67

9.09 9.55 9.95

12.19 11.42 11.92

8.92 9.48 9.16

9.19 9.35 9.12

10.31 10.39 9.72

M 9.6 9.8 10.0

S 1.2 0.8 1.1

n 8 8 8

Other diagnoses

before therapy in vitro after therapy

8.30 8.47 8.63

9.24 9.48 9.64

9.12 8.86 8.89

11.62 9.67 9.34

9.14 10.10 9.96

9.63 9.63 9.92

9.95 10.06 10.20

8.97 9.68 9.71

9.69 9.69 9.43

9.01 9.16 9.65

10.63 10.34 10.60

10.22 10.14 9.20

9.54 8.07 8.38

8.89 7.92 8.58

7.55 8.72 8.89

9.71 8.83 8.22

11.98 10.49 10.37

8.70 --- 8.47

M 9.5 9.4 9.3

S 1.0 0.8 0.7

n 18 17 18

28

Table 2 Redox concentration (mEq/l) with minor intravascular retransfusion according to Kief

Cancer patients Other diagnoses

before therapy

after therapy

before therapy

after therapy

8.6 8.0 8.9 8.8

8.1 7.6 7.3 7.5

7.2 8.2 7.6 7.4

8.9 7.2 7.5 7.5

7.8 7.5 7.3 6.9

9.1 9.9 7.8 7.6

8.0 7.9 7.9 7.5

6.8 7.7 11.4 11.4

8.3 9.0 8.6 8.3

9.2 9.9 8.1 6.4

14.9 15.0 8.4 8.7

14.2 14.9 9.9 8.7

14.5 14.9 9.2 9.4

8.9 8.2

8.0 8.1

8.6 5.8

13.8 12.6

12.5 12.4

10.0 10.6

9.4 9.3

M 9.7 9.83 9.5 8.6

S 3.0 3.0 1.7 1.9

n 13 20

29

Table 3 Redox concentration (mEq/l) with hyperbaric ozone therapy

Cancer patients Other diagnoses

before therapy after therapy before therapy after therapy

9.0 10.8 8.7 8.5

8.8 9.4 12.7 10.2

8.8 9.7 10.0 10.9

12.9 12.6 10.1 10.4

8.5 8.7 10.2 10.5

8.7 8.7 9.2 10.0

10.0 9.4 10.0 9.7

9.3 9.9

11.2 11.1

10.8 9.8

9.5 8.0

8.4 8.2

7.2 8.4

9.2 7.8

11.6 10.1

13.0 13.3

12.7 13.5

M 9.53 9.9 10.2 10.0

S 1.6 1.4 1.8 1.7

n 7 17

Table 4 Redox concentration (mEq/l) with hyperbaric ozone therapy plus 1 g vitamin C + vitamin A and E (250 ml blood).

Cancer patients

before therapy after therapy

10.1 10.4

12.2 12.1

11.4 10.0

M 11.2 10.8

S 1.0 1.0

n 3

30

Table 5 Redox concentration (mEq/l) with hyperbaric ozone therapy plus 5 g vitamin C + 30,000 gamma O3 (500 ml blood).

Cancer patients

before therapy after therapy

9.3 8.4

9.2 8.9

10.8 8.7

9.2 7.0

9.9 8.8

8.9 10.1

8.0 7.4

M 9.33 8.5

S 0.8 1.0

N 7

Table 6 Redox concentration (mEq/l) with minor intravascular reperfusion according

to Kief + 2 x 50 cm3 O2-O3 mixture as s.c. infusion.

Cancer Patients Other diagnoses

before therapy after therapy before therapy after therapy

7.7 7.7 8.2 8.3

9.7 10.0 9.4 8.8

8.5 9.0 10.7 12.3

12.0 12. 4

12.9 13.0

12.8 13.6

10.6 10.8

M 8.63 8.9 10.9 11.3

S 1.0 1.0 1.7 2.0

n 3 7

31

Table 7 Redox concentration (mEq/l) with minor intravascular reperfusion with "Roedler" SSR carbonyl groups.

Cancer patients Other diagnoses

before therapy after therapy before therapy after therapy

10.1 10.2 9.8 10.7

10.2 10.4 10.5 10.6

11.2 11.5 10.2 10.1

9.8 8.5 8.3 10.0

8.8 9.1 9.2 9.7

13.5 13.7 14.1 14.3

12.8 13.3 12.3 12.2

10.7 10.8 8.2 7.6

10.9 10.8 7.4 7.7

7.5 7.8

7.2 7.7

8.7 8.7

M 10.1 10.9 9.45 9.6

S 1.5 1.7 2.10 2.2

n 9 12

Table 8 Redox concentration (mEq/l) with minor intravascular reinfusion plus 1 g vitamin C in treated cancer patients.

Cancer patients

before therapy after therapy

9.55 8.90

9.00 8.46

8.13 9.08

9.93 7.96

8.63 8.28

9.21 9.96

8.93 8.75

7.53 8.54

M 8.9 8.7

S 0.8 0.6

n 8

32

Table 9 Redox concentration (mEq/l) with hyperbaric ozone therapy plus 5 g vitamin C +

30,000 gamma O3 (500 ml blood) + inhalation of positively ionised O2.

Cancer patients

before therapy after therapy

11.55 11.15

9.76 8.83

9.45 8.41

8.72 5.86

9.08 6.88

M 9.7 8.2

S 1.0 2.0

n 5

Table 10 Redox concentration (mEq/l): negative ions in cancer patients.

Cancer patients

before therapy after therapy

12.1 12.0

10.8 10.9

9.4 12.1

12.2 12.3

12.2 12.7

M 11.3 12.0

S 1.2 0.7

n 5

33

Table 11 Redox concentration (mEq/l): positive ions in cancer patients.

Cancer patients

before therapy after therapy

11.60 11.40

8.89 8.57

9.62 9.18

11.55 11.16

8.72 8.44

M 10.1 9.8

S 1.4 1.4

n 5

34

H y p e rb a r ic o z o n th e ra p y

8

9

1 0

1 1

b e fo re th e ra p y in v it ro a f te r th e ra p y

In c a n c e r p a t ie n ts n = 8

In p a t ie n ts w ith o th e rd ia g n o s e sn = 1 8

H y p e r b a r i c o z o n e th e r a p y

( i n c l u d i n g su sp e c te d p r e c a n c e r o u s c a se s)

8

9

1 0

1 1

n = 7

n = 1 7

M in o r in t r a v a s c u la r r e t r a n s f u s io n a c c o r d in g t o K ie f

8

9

1 0

1 1

n = 1 3

n = 8

n = 2 0

M i n o r i n tr a v a sc u l a r r e tr a n sfu si o n + 2 5 0 c m ³

o f O 2 -O 3 m i x tu r e 8 4 0 g a m m a s. c .

8

9

1 0

1 1

n = 3

n = 7

M i n o r i n tr a v a c u l a r r e tr a n sfu si o n + 2 a m p o u l e s S S R c a r b o n y l

g r o u p s (" R o e d l e r " )

8

9

1 0

1 1

n = 9

n = 1 2

I

II

III

IV

V

35

Redox concentration in venous blood of cancer patients before and after inhaltion of ions

H y p e r b a r i c o z o n e th e r a p y w i th 5 0 0 m l o w n b l o o d + 5 g

v i ta m i n c

8

9

1 0

1 1

VI

VII

-

IX

7

8

9

1 0

1 1

1 2

1 3

in h a la t io n o f n e g a t iv e io n s

b y c a n c e r p a t ie n ts

in h a la t io n o f p o s it iv e io n s

b y c a n c e r p a t ie n ts

H y p e r b a r ic o z o n e th e r a p y

w ith 5 0 0 m l o w n b lo o d

a n d 5 g a s c o r b ic a c id +

in h a la t io n o f p o s it iv e ly

io n is e d o x y g e n ( f lo w = 5

lit r e s / m in u te )

36

References 1. Stuttgen-Kanderske; "The biological action of ozone in the form of oxyon" (in German).

Arztl. Forschung, 12(6), II/49-II/50, 1958.

2. H. Kief: "New possibilities in ozone therapy" (in German).

EHK 12, Dec, 1980.

3. H. Kief: "Biozon Scientific Information” (in German). Issued 2.2.1982.

4. H. Kief: "Biozon Scientific Information” (in German). Issued 3.3.1982.

Report entitled: "Difference between parenteral oxygen and ozone medication and

hyperbaric ozone therapy" (in German). (See ref. 2 also).

5. F. Wenning. Wiener Medizinische Wochenschrift, p/ 1069, 1956.

6. H. Wolff: "Medical ozone" (in German) 1979, Verlag. f. Medizin E. Fischer, Heidelberg, p.

291.

7. H. Kief "Biozon Scientific Information" (in preparation).

"Natural cure treatment of cancer - Pathological biochemistry of tumour cells" (in German);

Figures l and 2.

8. A. Piechinger: "Fundamental regulation System” (in German), Haug, Heidelberg.

9. F. Perger: "The fundamental System according to Pischinger" (in German). Phys. Med. O.

Reh., 20(6), 1979.

10. G. Kellner and E. Klenkarti "Differentiation of serum iodometry according to A. Pischinger

(electrometric titration)" (in German). Oesterr. Zeitschrift f. Erforschung und Bekaempfung

der Krebskrankheit, 2, 1970.

11. H. Kief: "Biozon Scientific Information (in German). Issued 3.3.1982. Report entitled

"Difference between parenteral oxygen and ozone medication and hyperbaric ozone

therapy" (in German).

12. S.-H. v. Kapffs "Redox system and three-dimensional measurement" (in German).

Krebsgeschehen, 6, Nov.-Dec. 1981.

13. O. Hieber "Therapeutic problems of artificially ionised room air - need for selective use of

both positive and negative" (in German). Hippokrates, 28(24), Dec. 1957.

Author’s adress: Dr. Horst Kief, M.D. Londoner Ring 105 67069 Ludwigshafen FRC