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CHESSER-NAUGLE International Lectureship Grant:The Fungal/Mycotoxin Connections:

Autoimmune Diseases, Malignancies, Athero-sclerosis, Hyperllpldemias, and Gou

October 11, 1993A.V. Costantini, M.D.

[Dr. A.V. Costantini, MD is the Director of the World HealthOrganization (WHO) Mycotoxin Collaborating Center at the

University of Freiburg, Germany. Prof. Dr. A.V. Costantini, MDwas the keynote speaker at the 1993 conference of the American

Academy of Environmental Medicine held in Reno, Nevada.]TWENTY-EIGHTH ANNUAL MEETING NEW HORIZONS IN

CHEMICAL SENSITIVITIES: STATE OF THE ART DIAGNOSIS AND TREATMENT

The Fungal/Mycotoxin Etiology of Malignanciesand

Auto-Immune DiseasesThe vast majority of malignancies and all of the auto-im-

mune diseases are of unknown cause. Fungi/mycotoxins havebeen for the most part ignored as documented cause of manymalignancies and of auto-immune diseases. Theetiopathogenetic mechanisms are not the usual patterns of theinvasive-type mycoses nor of mycotoxicoses, but incorporatethe occult features of both of these mechanisms. Some of themycotoxin-induced malignancies are: hepato-cellular carci-noma, esophageal cancer, lung cancer, colon cancer, kidneycancer, breast cancer, colon cancer, endometrial cancer, leuke-mia, lymphoma, astrocytoma and Kaposi’s Sarcoma.

Auto-immune diseases are characterized by the findingof so-called auto-antibodies. It is a most popular concept butbiologically fatally defective in that no species of life can makean antibody against itself; particularly causing fatal disease suchas scleroderma. Scleroderma is considered to prove the valid-ity of the auto-immune concept with the presence of auto-anti-bodies. However these are now documented to be antibodiesagainst ubiquitin which is present in many species includingfungi. Scleroderma responds well to the antifungal agentgriseofulvin. Against whose ubiquitin is the host raising anti-bodies to, its own, or fungal-derived, in a disease state whichresponds to an antifungal drug? The auto-immune diseasesappearing to have a fungal/mycotoxin origin are: scleroderma,diabetes mellitus, HLA-related disease, rheumatoid arthritis,Sjogren’s syndrome, psoriasis & systemic lupus erythemato-sus. All of the drugs effective in the treatment of these diseasespossess antifungal or anti-mycotoxin activity. This includes allNSAIDs.

Fungal/Mycotoxin Etiology of Gout & HyperuricemiaGout and hyperuricemia are clinical entities of previously

unknown etiology. Fungi/mycotoxins have been ignored asdocumented cause of both entities. The etiopathogenetic mecha-nisms are not the usual patterns of invasive-type mycoses norof mycotoxicoses, but incorporate occult features of both ofthese mechanisms resulting in abnormal biochemical findings

associated with specific granuloma tissue lesions. All of thebiochemical findings in gout/hyperuricemia are explainable byfungal production of preformed urates/urate crystals, oxalate,glutamate, glycosaminoglycan, glycoprotein & hormones.Mycotoxins cause hyperuricemia and hyperlipidemia. The goutytophaceous lesion is a granuloma of the delayed hypersensitiv-ity type and is identical to fungal granulomas. Asteroid bodies,characteristic of fungal lesions, are found in the giant cells inboth avian & human gouty tophi. Asteroids are fungal cellscoated with fungal antigen+host antibody. Spherules andbranching filaments present in tophi have been mis-identifiedas urates on silver stain which also stains fungal forms the sameidentical color. Periodic acid Schiff stain has demonstratedfaint-staining fungal spherules in gouty lesions. The clinicalcourse of an acute attack of gout is that of a fungal infectionwith prodrome, all the usual signs of infection, ascending lym-phangitis, fever, chills, increase in sedimentation rate, desqua-mation of the overlying skin. Gout responds to griseofulvin,an antifungal antibiotic which has the same mode of action ascolchicine. These clues led to the observation that all drugsand dietary factors improving gout/hyperuricemia possess an-tifungal and/or anti-mycotoxin activity. The fungal etiology ofgout/hyperuricemia provides a rational basis for preventivemeasures and correct therapy.

The Fungal/Mycotoxin Etiology of Atherosclerosisand Hyperlipldemia

Atherosclerosis and hyperlipidemia are clinical entities ofpreviously unknown etiology. Fungi & their toxins have beenignored as documented etiology of both entities. Hyperlipidemiais induced by a number of mycotoxins. Seasonal variations inhyperlipidemia correlates to seasons of maximal fungal growthand mycotoxin production. It will be shown in this presenta-tion that hyperlipidemia is a protective-toxin binding mecha-nism that is seen in a number of complex infections and re-turns to normal with antibiotic therapy and/or toxin bind-agentsincluding charcoal. Atherosclerotic lesions are characterizedby lipid deposition, foam cells, endothelial cell damage, smoothmuscle cell proliferation, activation of all of the cellular andhumoral elements of delayed hypersensitivity, and fibrosis/cal-cifications. All of these lesions are induced in animals and hu-mans by fungi/mycotoxins. Cyclosporine, a mycotoxin (animmuno-toxic fungal antibiotic) causes accelerated atheroscle-rosis & hyperlipidemia in the vast majority of transplant pa-tients. Primates developed hyperlipidemia and atherosclerosiswhen fed Fusarium toxins (corn). Hyperlipidemia associatedwith lipid-containing vascular lesions are found in sheep in-gesting the mycotoxin sporidesmin. In humans, ergots inducespasm, stenosis and/or thrombosis of the coronary, carotid,aortic, renal, and peripheral arteries. Ergot-induced entitiesinclude angina, myocardial infarction, arrhythmia, carotid ar-tery occlusion, stroke, intermittent claudication & gangrene.All drugs and dietary measures effective in treating atheroscle-rosis and/or hyperlipidemia share only antifungal or anti-tox-icity activity (lovastatin, griseofulvin, ketoconazole, neomy-cin, fibrates, etc.).

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