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CHESSER-NAUGLE International Lectureship Grant:

The Fungal/Mycotoxin Connections:

Autoimmune Diseases, Malignancies, Athero-

sclerosis, Hyperllpldemias, and Gou

October 11, 1993

A.V. Costantini, M.D.

[ Dr. A.V. Costantini, MD is the Director of the World Health

Organization (WHO) Mycotoxin Collaborating Center at the

University of Freiburg, Germany. Prof. Dr. A.V. Costantini, MD

was the keynote speaker at the 1993 conference of the American

Academy of Environmental Medicine held in Reno, Nevada.]

T

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IAGNOSIS

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REATMENT

The Fungal/Mycotoxin Etiology of Malignancies

and

Auto-Immune Diseases

The vast majority of malignancies and all of the auto-im-

mune diseases are of unknown cause. Fungi/mycotoxins have

been for the most part ignored as documented cause of many

malignancies and of auto-immune diseases. The

etiopathogenetic mechanisms are not the usual patterns of the

invasive-type mycoses nor of mycotoxicoses, but incorporate

the occult features of both of these mechanisms. Some of the

mycotoxin-induced malignancies are: hepato-cellular carci-

noma, esophageal cancer, lung cancer, colon cancer, kidney

cancer, breast cancer, colon cancer, endometrial cancer, leuke-

mia, lymphoma, astrocytoma and Kaposi’s Sarcoma.

Auto-immune diseases are characterized by the finding

of so-called auto-antibodies. It is a most popular concept but

biologically fatally defective in that no species of life can make

an antibody against itself; particularly causing fatal disease such

as 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 antibodies

against ubiquitin which is present in many species including

fungi. Scleroderma responds well to the antifungal agent

griseofulvin. Against whose ubiquitin is the host raising anti-

bodies to, its own, or fungal-derived, in a disease state which

responds to an antifungal drug? The auto-immune diseases

appearing 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 diseases

possess antifungal or anti-mycotoxin activity. This includes all

NSAIDs.

Fungal/Mycotoxin Etiology of Gout & Hyperuricemia

Gout and hyperuricemia are clinical entities of previously

unknown etiology. Fungi/mycotoxins have been ignored as

documented cause of both entities. The etiopathogenetic mecha-

nisms are not the usual patterns of invasive-type mycoses nor

of mycotoxicoses, but incorporate occult features of both of

these mechanisms resulting in abnormal biochemical findings

associated with specific granuloma tissue lesions. All of the

biochemical findings in gout/hyperuricemia are explainable by

fungal production of preformed urates/urate crystals, oxalate,

glutamate, glycosaminoglycan, glycoprotein & hormones.

Mycotoxins cause hyperuricemia and hyperlipidemia. The gouty

tophaceous 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 in

both avian & human gouty tophi. Asteroids are fungal cells

coated with fungal antigen+host antibody. Spherules and

branching filaments present in tophi have been mis-identified

as urates on silver stain which also stains fungal forms the same

identical color. Periodic acid Schiff stain has demonstrated

faint-staining fungal spherules in gouty lesions. The clinical

course of an acute attack of gout is that of a fungal infection

with 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 as

colchicine. These clues led to the observation that all drugs

and dietary factors improving gout/hyperuricemia possess an-

tifungal and/or anti-mycotoxin activity. The fungal etiology of

gout/hyperuricemia provides a rational basis for preventive

measures and correct therapy.

The Fungal/Mycotoxin Etiology of Atherosclerosis

and Hyperlipldemia

Atherosclerosis and hyperlipidemia are clinical entities of

previously unknown etiology. Fungi & their toxins have been

ignored as documented etiology of both entities. Hyperlipidemia

is induced by a number of mycotoxins. Seasonal variations in

hyperlipidemia correlates to seasons of maximal fungal growth

and 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-agents

including charcoal. Atherosclerotic lesions are characterized

by lipid deposition, foam cells, endothelial cell damage, smooth

muscle cell proliferation, activation of all of the cellular and

humoral 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 (an

immuno-toxic fungal antibiotic) causes accelerated atheroscle-

rosis & hyperlipidemia in the vast majority of transplant pa-

tients. Primates developed hyperlipidemia and atherosclerosis

when fed Fusarium toxins (corn). Hyperlipidemia associated

with lipid-containing vascular lesions are found in sheep in-

gesting the mycotoxin sporidesmin. In humans, ergots induce

spasm, stenosis and/or thrombosis of the coronary, carotid,

aortic, renal, and peripheral arteries. Ergot-induced entities

include 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.).

FUNGALBIONICS VOLUMES

VOLUME I ATHEROSCLEROSIS

VOLUME II CANCER

Future Volumes

VOLUME III AIDS

VOLUME IV GOUT

VOLUME V CROHN’S DISEASE

VOLUME VI MULTIPLE SCLEROSIS