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Main article Autovaccine therapy

Autovaccine therapy

Leendert Kunst (MD)

  • The back story

    The back story

    Autovaccine therapy is a relatively unknown but effective treatment for chronic inflammatory diseases. Details of autovaccination as a treatment were published back in 1929 in the prestigious Journal of the American Medical Association by Barger, Horgan and Horgan1. In this article they described how they had successfully used a particular method of autovaccine therapy on hundreds of patients suffering from colitis ulcerosa. Their method involved sterilized culture filtrates originating from a culture of a patient’s own gut bacteria which was then injected back into the patient.

    The experiments done by these pioneers faded out of the collective medical conscious as a result of the advent of sulphur drugs and antibiotics that arrived 10 years later. The simplicity of these new pharmacological treatments eclipsed the more complex therapies such as that devised by Barger et al. and stood in the way their further development. These days, almost 100 years later, it seems that antibiotics for colitis ulcerosa and other chronic inflammatory diseases are much less effective than was first hoped and the idea of using the body’s own substances and systems as a treatment is slowly enjoying more scientific interest. 

    In the last few decades this idea has been developed further by different clinics using diverse techniques2,3,4. The object of these treatments is to prevent recidivism following a previously undergone surgical or chemical or radiological treatment directed at eliminating tumor tissue. Either cancer cells or specific blood cells from the cancer patient are used to produce a vaccine for that particular patient. Scientific literature also notes successful use of autovaccines for acute infections, especially in cases where antibiotic resistance is an issue, such as is the case with the MSRA bacteria5,6. Personalized sterile vaccines are made, using pathogens taken from the infected organ or tissue that are subsequently identified by culture in a suitable medium according to the de Vito method. This is a carefully documented combination of incubation, application of formaldehyde and dilution7.

    Even veterinary medical literature reveals cases of the successful use of the blood of a sick animal as an autovaccine when antibiotics and other treatments offered no solution. Repeated injections of fresh own blood in cases of difficult to treat allergies in dogs often had a healing effect, as shown in a study published by Klein in Biologische Tiermedizin8. These and other similar own-blood treatments in humans were frequently used in Germany until the mid-20th century – mainly in general practice – for treating allergies, recurring infections, habitual abortion and all sorts of enigmatic chronic complaints.

    A scientific explanation for the effectiveness of this treatment has not yet been found. These own blood treatments and their popularity in Germany can be traced back to August Bier (1861-1949), in his time a world renown and talented surgeon who was consulted by celebrities from all over the world to be treated or operated on. Bier not only devised all manner of inventions for surgical practice, he also had a name for his many publications in a variety of fields. The concept of self-healing was a central tenet of his vision on medicine. He developed various treatment methods to promote this capacity in patients, including the treatment with own blood of the patient.

    Bier’s treatment involved injecting a few millilitres of a patient’s own fresh blood intramuscularly or intravenously, treatments varying from once every two weeks up to once a month for patient’s suffering from either a chronic ailment or for wounds that were difficult to heal. Bier had apparently very good results with this. He attributed the positive reaction to the treatment to the stimulation of the body’s own healing mechanisms, so that the treatment was called ‘stimulation therapy’. Once antibiotics became available in huge quantities – approximately at the same time as his death – the interest in ‘stimulation therapy’ collapsed9.

  • Autovaccine therapy today

    Autovaccine therapy today

    Based on the results described by Bier, and encouraged by a colleague, in the 1970s I decided to use this ‘stimulation therapy’ as a short-term pilot treatment for a select few patients with chronic illnesses where the normal treatments had not achieved the desired results. According to Bier’s theory, these patients would be suitable candidates for ‘stimulation therapy’, but in my pilot study, the results were ineffective – except for a few patients with hay fever. However, I noted that none of the patients experienced any negative side-effects. After a short time, I stopped using this therapy, not least because I could not find any theoretical basis for the effectiveness of the treatment in any of Bier’s work, nor in the work of any other author. Bier had never published his exact methodology. It could be that my lack of clinical success can be explained by the fact that antibiotic use was then universal and had a severe negative influence on the self-healing capacity of the whole population. 

    My interest in a treatment using own blood returned as a result of a convergence of circumstances. In 2007 I was suddenly confronted with symptoms of neurological disfunction which were attributed to Lyme’s disease after I had been tested for antibodies in the Lyme Clinic in Apeldoorn (the Netherlands). The standard treatment with antibiotics had no effect. Because it was patently clear that I was chronically ill as a result of a bacterial infection, and there was no existing treatment, I began my own thorough and critical study of microbiology. I focused on publications by microbiologists who were involved in fundamental research and also dared to challenge standard ideas current in microbiology circles. Some of these innovative thinkers are named below.

  • The root of the problem

    The root of the problem

    During my study to be a doctor, it was impressed upon me – and all other doctors studying at the time – that the blood of healthy people is sterile by definition; in other words, it does not contain any bacteria. According to the most recent understanding of the topic, it appears only to be true for classical bacterial forms which, can be recognized under a light microscope by their characteristic shapes and growth patterns in a suitable medium. They are often named for their exterior shape, such as staphylococci, streptococci, etc. Various microbiologists have indicated since as early as the end of the 19th century up until now, that there is possibly an even larger number of bacteria that are not able to be determined using the standard methods and that these have been linked to chronic illnesses10. Recent avante garde research done by the Errington Group at Newcastle University have confirmed this link for chronic urinary tract infections, among others11.

    It is now apparent that the blood of people that do not suffer from an infectious disease, can still contain microbiological RNA or DNA as a remnant of previously undergone infection(s)12-15. Most of the bacteria from the previous infection have been eliminated in the battle with the immune system, but thanks to improved testing methods, we know that that does not necessarily apply for the pathological DNA in the cellwall deficient bacterial forms. Depending on the type of bacteria and the effectiveness of the immune system, a portion of the invaders can evade the immune system by “removing their jacket”. In this way, the bacterium assumes an amorphous exterior with a wafer-thin exterior membrane, which makes the micro-organism unrecognizable for the immune system and non-responsive to antibiotics. Not only that, antibiotics can apparently trigger that transformation of a classical bacteria into this Cell Wall Deficient Form - with the development of a chronic inflammation as consequence. Grayston et al. have shown that C. pneumoniae can persist unrecognized in the blood for a long time and in the end can be found in atherosclerotic plaques16,17.

    This development in microbiological science shows that these polyform bacteria do not conform to the strict postulates drawn up by Robert Koch, the founding father of orthodox bacteriology. In his teaching, it is stated that there can be no living bacteria present in a healthy human, animal or plant18. In the era when these principles were established very little was known about the polymorphic properties of bacteria and the influence that might have on molecular biology. Robert Koch’s ideas are still counted as authoritative in the field – especially by doctors who are still taught his principles during their studies. It is quite understandable that the existence of polymorphic bacteria has been overlooked by mainstream medical practice, and that is still the case today. There has been and still is little place for the clinical significance of these Cell Wall Deficient Bacteria (or L-forms) in mainstream medical practice. However, increasing numbers of prominent scientists working in the previous century – more than can be named here – have linked these bacteria to chronic illnesses. Microbiologist, Professor Doctor Lida Mattman10 who was nominated for the 1997 Nobel Prize for Medicine wrote a meta-overview of many research studies into Cell Wall Deficient Bacteria. In Chapter 1 of her book Cell Wall Deficient Forms, she acknowledges many of these scientists and discusses the clinical implications of their work.

    More recently, Professor Jeff Errington, director of the Centre for Bacterial Cell Biology (CBCB) at Newcastle University (UK) and his team have brought CWDB back into focus in scientific circles under the name of L-forms. In his work he explores their role as a logical link in the biological evolutionary process19. The Physics and Mathematics faculty at Leiden University (The Netherlands) has been studying L-form bacteria under the supervision of Professor D. Dennis Claessen and in collaboration with Errington’s group at Newcastle. From Wageningen University (the Netherlands), immunologist Professor H. Savelkoul, has written that “cellwall deficient bacteria have been found in persistent infections and chronic inflammatory diseases, such as rheumatism, endocarditis, other heart and vascular diseases, Crohn’s disease and sarcoidosis.” At the Technical University of Delft, Professor of Physics, Cees Dekker, has connected these bacteria to chronic illnesses. L-form bacteria are not figments of the imagination. they are the victims of ignorance that deserve the renewed attention of medical science20.

  • Connecting the dots

    Connecting the dots

    Chronic illnesses such as atherosclerosis and rheumatism can be understood if previously undergone infections and L-forms are considered. It has been convincingly shown in various publications that bacterial DNA has been found in arteriosclerotic plaques and in pathological joint fluid in rheumatic patients and that there is a relationship between these two things and periodontitis. Martinez et al. showed that periodontal bacterial DNA is present in the serum of patients with both dental problems and arthritis20. Whoever makes the effort to immerse themselves in this material, will inevitably come to the conclusion that scientific literature is literally full of publications that link oral bacteria to all kinds of chronic illnesses22-41. Polyform bacteria are a constant factor, and it is specifically this type of bacteria that is difficult to detect using standard laboratory testing or using a light microscope.

    Rheumatic joint inflammation is called a “sterile” inflammation, but it is easy to find viable L-form bacteria in the fluid as I have found using Fluorescent in situ Hybridization (FISH) testing. The FISH test is an accredited RNA-test which shows viable bacteria in body fluids – including blood. This test is not normally available in hospital laboratories. However, bearing in mind that approximately 50% of the population in the Netherlands suffers some form of chronic disease, the majority of which are caused by infections, it would seem sufficient reason to test for the presence of L-form bacteria using FISH technology. A positive result could provide powerful support for developing and applying a modern own-blood therapy based on the Bier method.

    The recent Q-fever epidemic (2007-2010) in North Brabant (the Netherlands) offered the ideal opportunity to show that the Q-fever pathogen, C. burnetii – in the L-form variant – was still present in patients suffering from Q-fever Fatigue Syndrome (QFS). Using the FISH test it was shown in all the QFS patients tested, that the L-form was present in their blood. Whereas all the healthy control subjects taken from the north of the Netherlands tested negative. This disease was almost unknown in the Netherlands before 2007 and the blood bank, Sanguin, calculated that the epidemic affected between 50,000 and 100,000 people, mostly living in the North Brabant province.

    According to this source – following the acute infectious stage – 20% of these patients developed chronic QFS. Fifteen years later thousands of them still suffer from this condition. Mainstream health care assessed that there was no effective medical treatment as in all the years of PCR testing only in extremely rare cases did the test reveal the presence of C. burnetii in the blood a very few patients.
    The QFS patients were offered emotional support in the form of cognitive behavioural therapy. In 2019, in the absence of any known medical solution, the majority of patients were given €10,000 compensation by the Dutch government. 

    However, using the FISH test instead of PCR, it was simple to determine that C. burnetii could be found in the blood of QFS patients. This was shown in a pilot study done with 10 QFS patients from North Brabant, and published in an international scientific journal42. Although on a very limited scale, this one small study provided, in principle, the evidence that viable L-form C. burnetii bacteria exist and that they are still present in the blood of QFS patients from the region hit by Q-fever. The 10 control patients from the north of the Netherlands were free of this L-form bacterium in their blood. At the time of writing, there are plans by a third party to do a second study underway on a larger scale using the FISH test to check if the results of the small-scale study can be replicated.

    Before embarking on the small-scale study into QFS patients, I had substantiated my experience with the FISH test in one hundred patients suffering from varying chronic ailments. In all cases one or more pathogens in their L-forms were found in the blood, the average being 1.7 per case. These patients were then treated with an autovaccine made with their own blood and later surveyed using an anonymized format. The 114 respondents reported an average improvement in their symptoms of 80% after their autovaccine treatment. (See the Autovaccin Lege Artis Survey results on the website www.artofmedicure.eu.)

  • How does autovaccine therapy work?

    How does autovaccine therapy work?

    A comparison with the treatment of an infection using antibiotics might raise the expectation that a sub-clinical infection of L-form bacteria in the blood would disappear following a successful autovaccine treatment. But this is not the case, as was shown using routine testing. The L-form bacteria were not eliminated by the autovaccine, but their pathogenic effect was at best neutralized or severely reduced. There is, as yet, no cellular or molecular explanation for this effect. However, based on more than 10 years’ experience with administering the autovaccine treatment and monitoring the reaction to it, I have noticed that a large proportion of patients report phenomena that remind them strongly of symptoms they had previously experienced (sometimes many years earlier). This is quite remarkable. It is as if the autovaccine treatment makes the body refer back to the initial illness which, in effect, had never been completely dealt with.

    We generally view infections as being purely threats to our existence, but there is apparently a positive side to them. The brilliant microbiologist Lynn Margulis (1938-2011) was convinced of this. She saw the phenomenon ‘infection’ as being an important fundamental principle of evolution particularly in microbiology. She defended the endosymbiotic hypothesis in her doctoral thesis43 which declares that eukaryotic cells originate in the symbiosis of diverse bacterial strains and that it is precisely the complex cell organelles that form the definitive proof of the theory of evolution.

    Margulis remains to this day associated with the quote, “Life did not take over the globe by combat, but by networking.” This could be seen as a feminine view, in contrast to that of Darwin, who saw evolution as an endless struggle: the ‘survival of the fittest’ with the logical result being ‘natural selection’. But it is, in contrast, all about synthesis, according to Margulis.

    Because – as is mentioned above – L-form bacteria cannot be conquered in a ‘fight’ with antibiotics or the immune system, an alternative way has to be found to allow the undesirable pathological influence of the bacterial DNA in the L-forms to be neutralized. The fact that the autovaccine treatment appears to be effective, could be explained as being a result of a successful benign integration of the pathological DNA into the host.

  • Preparing the Autovaccine™

    Preparing the Autovaccine

    The general criterium for preparing the Autovaccine in a responsible way, is to use strict sterile conditions. It is also recommended that the health professional preparing the Autovaccine has at least a basic understanding of the of the laws of osmosis and physiological properties of blood. 

    The procedure for preparing the Autovaccine begins with the sterile removal of 2 ml of blood [from the patient]. Two millilitres of blood is drawn into a vacutainer and thoroughly mixed with an exact volume of sterile water for injection. (We have a video instruction and a well written instruction of the procedure. We are aiming at a very controlled way of practicing the procedure. If you have the intention of wanting to do the procedure please contact us by e-mail)

    By adding (sterile) water to the extracted blood, hydrolysis causes the osmotic functions of all the cell membranes in the blood sample to disintegrate, including those of any L-form bacteria that may be present. The cell organelles and various types of DNA are released into the solution and come freely into contact with each other. 

    Subsequent injections in a course of treatment for a particular patient should be prepared with more or with less quantities of blood and water depending on the initial reaction of the patient to the Autovaccine. The stronger the reaction, the less strong the Autovaccine needs to be. (1 ml blood with 2 ml water or 3 ml blood with 4 ml water, to a maximum of 4 ml blood and 5 ml water). The physiological salt solution has to be adjusted each time to become 0.9% of the preparation – using a sterile sodium chloride solution of 10%.

    The blood preparation is subjected to a gentle rocking period to intensify the hydrolytic reaction of the water on the blood cells. By adding concentrated NaCl-solution at the end, the physiological osmolarity is restored and the Autovaccine preparation is ready for subcutaneous injection.

    The intracellular proteins which have been freed into the Autovaccine, including any bacterial DNA, is now able to stimulate the patient’s immune system which in turn can trigger a temporary exacerbation of the symptoms of their ailment, slight fever, extra pain, extra fatigue, etc. It is not unusual for the patient to experience these exacerbations as a déjà vu feeling from illnesses they had experienced in the (distant) past. The body, triggered by the Autovaccine, makes a renewed effort to complete the unfinished healing process of previously undergone infections. 

    By repeating the injections several times, the strength of the body’s reactions decrease over time, signaling that the body has arrived at a higher evolutionary level. In the end, it is clear that there is a new balance in the body. This is evident not only because the patient feels significantly better than before the treatment, but because there is no further reaction to an injection; not even when the dosage of the Autovaccine is higher. This means that there is true immunity. The bacterial DNA has been integrated; a previously undesirable invader has been turned into an accepted guest. It could be said that an evolutionary step has been made.

  • No quick fix

    No quick fix

    This self-healing process can cost time, sometimes a long time. This demands patience and understanding on the part of the patient who is used to (or spoiled by) the quick effect of symptom suppressant medication. In my own case, the neurological symptoms of Lyme diminished very slowly over the period of one year. The result of the treatment and the necessary duration of it cannot as yet be predicted. The self-healing capacity of each patient is the determining factor and this becomes apparent during the treatment. That capacity varies widely, and the strength of the Autovaccine dosage also plays a role.

    A medical treatment made of fresh blood which has been hydrolyzed with sterile water seems bizarre, especially when a doctor uses this treatment to stimulate a healing process for patients with “incurable” ailments like chronic arthritis and other autoimmune illnesses. My own practice has shown that the clinical effect of the autovaccine depends on the dosage. A small over-dosage of the autovaccine can trigger a significant reversal by a patient that has clearly been improving. Although this may seem weird to the layman, the same reaction is commonly found when using effective pharmaceutical products.

    I have found that using an autovaccine treatment prepared as explained in the video and in this article, has been successful in 80% of patients with various pathogenic L-form bacteria in their blood and suffering from chronic illnesses. The Autovaccine preparation as described above is the result of significant improvements developed in the 10 years that it has been used in my practice.

    Despite the improvements, it is still possible that healing can be hindered or prevented altogether by a variety of factors, such as the genetic make-up of the patient, severe stress, bowel dysbiosis, dental infections (hidden jaw-bone infections), heavy metal contamination or concurrent use of particular medicines.
    In order to determine possible blockades to the self-healing process, it is recommended that extra tests should be undergone to check if radical dental treatment is required.

    The Autovaccine™ therapy has undergone a long developmental process. 100 years after it was first conceived, the long forgotten “stimulation therapy” conceived by Bier has been given a plausible, scientific hypothesis for its effectiveness based on up-to-date scientific knowledge and it has evolved into a practical and effective form of autovaccination therapy for treating chronic illnesses.

  • REFERENCES

    REFERENCES

    1. Barger J A, Horgan E, Horgan J. De behandeling der chronische ulceratieve colitis met autovaccins en cultuurfiltraten van enterococcen in Referaten A.J.L. Terwen: N Tijdschr Geneesknd 1929;73.II.44.
    2. Foon KA. Immunotherapy for colorectal cancer. Current Oncology Reports 2001;3(2):116-26.
    3. Besser MJ et al. Clinical Responses in a Phase II Study Using Adoptive Transfer of Short-term Cultured Tumor Infiltration Lymphocytes in Metastatic Melanoma Patients. Clin Cancer Res. 2010;16(9):2646-55.
    4. Rosenberg SA et al. Use of tumor-infiltrating lymphocytes and interleukin-2 in the Immunotherapy of patients with metatstatic Melanoma. N Engl J Med 1988;319: 1676-80.
    5. Caterina Rizzoa, Gianluca Brancacciob, Danila De Vitoc and Giovanni Rizzod. Efficacy of autovaccination therapy on post-coronary artery bypass grafting methicillin-resistant Staphylococcus aureus mediastinitis. Interact CardioVasc Thorac Surg 2007;6 :228-29.
    6. Wilczyński K, Koźmińska J, Biliński A. The testing of auto-vaccination of patients with chronic purulent otitis media. Otolaryngol Pol. 1995;49(23):183-185. 
    7. De Vito D, Rizzo G. Il ritorno di una pratica trascurata: la terapia con autovaccini. Igiene Moderna 1999; 112:1245–51. 
    8. Klein, M. Atopische Dermatitis des Hundes: Behandlung mit der Auto-Sanguis-Stufentherapie. Biol Tiermedizin 2009;26 (2): 31-35.
    9. Riet A. van’t. August Bier en de Homeopathie.(1978) Dissertatie V.U.
    10. Mattman LH. Cell Wall Deficient Forms, Stealth Pathogens 2001; 3rd ed; CRC Press Washington DC.
    11. Errington J, Mickiewicz, K.M., Kawai, Y., Drage, L. et al. Possible role of L-form switching in recurrent urinary tract infection. Nat Commun 10, 4379 (2019). 
    12. Haranaga S, Yamaguchi H, Leparc GF, Friedman H, Yamamoto Y; Detection of Chlamydia pneumoniae antigen in PBMNCs of healthy blood donors. Transfusion 2001; 41(9):1114 – 19.
    13. Yamaguchi H, Yamada M, Uruma T, Kanamori M, Goto H, Yamamoto Y, Kamiya S. Prevalence of viable Chlamydia pneumoniae in peripheral blood mononuclear cells of healthy blood donors. Transfusion. 2004; 44(7):1072-8.
    14. Boman J, Söderberg S, Forsberg J, Birgander LS, Allard A, Persson K, Jidell E, Kumlin U, Juto P, Waldenström A, Wadell G. High prevalence of Chlamydia pneumoniae DNA in peripheral blood mononuclear cells in patients with cardiovascular disease and in middle-aged blood donors. J Infect Dis. 1998;178(1):274-7.
    15. Karimi Gh, Samiei Sh, Hatami H, Gharehbahian A, VafaiyanV, Tabrizi Namini M. Detection of Chlamydia pneumoniae in peripheral blood mononuclear cells of healthy blood donors in Tehran Regional Educational Blood Transfusion Centre. Transfusion Medicine Volume 2010; (4): 237-43.
    16. Grayston JT. Background and current knowledge of Chlamydia pneumoniae and atherosclerosis. J. Infect. Dis. 2000; 181 (3): 402-10.
    17. Boman J, Söderberg S, Forsberg J, Birgander LS, Allard A, Persson K, Jidell E, Kumlin U, Juto P, Waldenström A, Wadell G. High prevalence of Chlamydia pneumoniae DNA in peripheral blood mononuclear cells in patients with cardiovascular disease and in middle-aged blood donors. J Infect Dis. 1998;178(1):274-7.
    18. The Four Postulates of Robert Koch: 
      1. The microorganism must be found in abundance in all organisms suffering from the disease, but should not be found in healthy organisms.
      2. The microorganism must be able to be isolated and grown in culture media.
      3. The cultured microorganism should cause the same disease when introduced into a healthy organism.
      4. The microorganism must be re-isolated from the experimental host and identified as being identical to the original specific causative agent.
    1. Errington J, Lysozyme Counteracts b-Lactam Antibiotics by Promoting the Emergence of L-Form Bacteria Yoshikazu Kawai,1,2 Katarzyna Mickiewicz,1,2 and Jeff Errington 1,3, Centre for Bacterial Cell Biology, Institute for Cell and Molecular Biosciences, Newcastle.
    2. Costerus, M. 2019 January 28, updated 2020, January 9, Bacterie zonder jasje verborgen ziekmaker https://www.rd.nl/artikel/820305-bacterie-zonder-jasje-verborgen-ziekmaker Reformatorisch Dagblad
    3. Martinez-Martinez, RE et al. Detection of periodontal bacterial DNA in serum and synovial fluid in refractory rheumatoid arthritis patients. J Clin Periodontol. 2009; 36(12):1004-10.
    4. Témoin, S et al. Identification of oral bacterial DNA in synovial fluid of patients with arthritis with native and failed prosthetic joints. J Clin Rheumatol. 2012;18(3):117-21.
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    8. Seymour, G. J., Ford, P. J., Cullinan, M. P., Leishman, S. and Yamazaki, K. (2007), Relationship between periodontal infections and systemic disease. Clinical Microbiology and Infection 2007, 13: 3–10.
    9. Beck JD, Garcia R, Heiss G, Vokonas PS, Offenbacher S. Periodontal disease and cardiovascular disease. J Periodontol 1996; 67: 1123–1137. 
    10. Hung H-C, Willet W, Merchant A, Rosner BA, Ascherio A, Joshipura KJ. Oral health and peripheral arterial disease. Circulation 2003; 107: 1152–1157. 
    11. Desvarieux M, Demmer RT, Rundek T, et al. Relationship between periodontal disease, tooth loss, and carotid artery plaque. The oral infections and vascular disease epidemiology study (INVEST). Stroke 2003; 34: 2120–2125
    12. Jansson L, Lavstedt S, Frithiof L, Theobald H. Relationship between oral health and mortality in cardiovascular diseases. J Clin Periodontol 2001; 28: 762–768.
    13. Janket S-J, Baird A, Chuang S, Jones JA. Meta-analysis of periodontal disease and risk of coronary heart disease and stroke. Oral Surg Oral Med Oral Pathol 2003; 95: 559–569. 
    14. Khader YS, Albashaireh ZSM, Alomari MA. Periodontal diseases and the risk of coronary heart and cerebrovascular diseases: a meta-analysis. J Periodontol 2004; 75: 1046–1153. 
    15. Hujoel PP, Drangsholt M, Spiekerman C, DeRouen TA. Periodontal disease and risk of coronary heart disease. JAMA 2000; 284: 1406–1410. 
    16. Periodontal disease is associated with brachial artery endothelial dysfunction and systemic inflammation. Arterioscler Thromb Vasc Biol 2003; 23: 1245–1249. 
    17. Mercanoglu F, Oflaz H, Oz O et al. Endothelial dysfunction in patients with chronic periodontitis and its improvement after initial periodontal therapy. J Periodontol 2004; 75: 1694–1700. 
    18. Tonetti MS, D'Aiuto F, Nibali L et al. Treatment of periodontitis and endothelial function. N Engl J Med 2007; 356: 911–920         
    19. Sheu JJ, Lin HC. Association between multiple sclerosis and chronic periodontitis: a population-based pilot study. Eur J Neurol. 2013; 20(7):1053-9. 
    20. Fitzpatrick SG, Katz J. The association between periodontal disease and cancer: a review of the literature. J Dent. 2010; 38(2):83-95       
    21. Li L, Messas E, Batista EL, Levine RA, Amar S. Porphyromonas gingivalis infection accelerates the progression of atherosclerosis in a heterozygous apolipoprotein E-deficient murine model. Circulation 2002; 105: 861–867. 
    22. Lalla E, Lamster IB, Hofmann MA et al. Oral infection with a periodontal pathogen accelerates early atherosclerosis in apolipoprotein E-null mice. Arterioscler Thromb Vasc Biol 2003; 23: 1405–1411   
    23. Ford PJ, Gemmell E, Timms P, Chan A, Preston FM, Seymour GJ. Anti-P gingivalis response correlates with atherosclerosis. J Dent Res 2007; 86: 35–40. Mattman LH. Cell Wall Deficient Forms, Stealth Pathogens 2001; 3rd ed; CRC Press Washington DC
    24. Kunst L. Jansen GJ, de Klyn BR. J Med Microb Diagn 2019, 8:2 The Presence of Intracellular Coxiellae burnetii as Polymorphic Cell Wall Deficient Bacteria in the Blood of Patients with Q-Fever Fatigue Syndrome Determined Using FISH Technology.
    25. Margulis L. 1970. Origin of Eukaryotic cells; Evidence and Research Implications for a Theory of the Origin and Evolution of Microbial, Plant and Animal Cells on the Precambrian Earth. New Haven: Yale University Press. 

L. Kunst MD and the development of a medicine for psoriasis

Dr Kunst's "drive" to help patients with chronic conditions lead to the development of a medicine to help patients with chronic psoriasis. He did this in collaboration with a pharmacist working in Helmond, the Netherlands and by applying knowledge gained and published by W. Schweckendieck.

Dr. Kunst had seen the clinical benefits of dimethylfumarate (DMF), the discovery by Dr W. Schweckendieck. DMF had been brought to the Netherlands by Dr van Dijk, but this version of it had debilitating effects on the patients' digestive system. 

In 1985 together with the pharmacist, Dr Durlinger, Dr Kunst developed a version of a DMF-pill that had a slow release mechanism (in the new terminology now mentioned as extended release), as a result, the irritating substance is slowly be distributed in the whole of the intestinal tract, diminishing it's corrosive effect. This has the advantage that many more patients can withstand the side-effects of DMF.

This version of the medicine was named Psorinovo, and was made and distributed by Mierlo-Hout pharrmacy, currently called Infinity Pharma. It has been in use to treat thousands of patients with an effectivity of around 70%.  More about this medication and its development can be viewed on the website of Psoriasispatiënten Nederland, the official website of  the Psoriasis Patients Support Group in the Netherlands. 

Dr Kunst was recently interviewed by Psoriasis Magazine, the official publication for Psoriasispatiënten Nederland. The resulting article can be downloaded here. [An English version will be added soon]. 

NB Several patients with psoriasis have since been successfully treated with the autovaccine therapy. This fact makes it likely that there is a microbiological causal factor related to this condition.

 

 

 

Autovaccine therapy, summary and Literature

On this site you can find video and text testimonies by a number of patients that show that we can achieve very positive, even spectacular, results using autovaccine therapy. This therapy has a broad application for conditions that regular medical practice does not yet have an answer for. Below you will find a complete - but compact - summary. An extended literature list will show that this therapy, which is still new in the Netherlands, is solidly based on scientific knowledge and research. 

Read more …Autovaccine therapy, summary and Literature

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