The Eleventh International Symposium on Man and His Environment in Health and Di

[Guest guest]

The Eleventh International Symposium on Man and His Environment in

Health and Disease

Special Focus: Human Physiological Effects of Mycotoxins and

Environmental Influences on the Autonomic Nervous System

February 25-28, 1993

http://www.aehf.com/articles/1993symp.html

AThe Fungal/Mycotoxin Etiology of Atherosclerosis and Hyperlipidemia@

A.V. Costantini, MD Clinical Faculty (retired)

University of California School of Medicine San Francisco

San Francisco, California

Atherosclerosis and hyperlipidemia are clinical entities of

previously unknown etiology. Fungi and their toxins have been

ignored as documented etiology of both entities. Hyperlipidemia is

induced by a number of mycotoxins. Seasonal variations in

hyperlipidemia correlate to seasons of maximal fungal growth and

mycotoxin production. It will be shown in this presentation that

hyperlipidemia is a protective-toxin binding mechanism that is seen

in a number of complex infections and it returns 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/calcifications. All of these lesions

are induced in animals and humans by fungi/mycotoxins. Cyclosporine,

a mycotoxin (an immuno-toxic fungal antibiotic), causes accelerated

atherosclerosis and hyperlipidemia in the vast majority of

transplant patients. Primates developed hyperlipidemia and

atherosclerosis when fed Fusarium toxins (corn). Hyperlipidemia

associated with lipid-containing vascular lesions is found in sheep

ingesting 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 infarctions, arrhythmia, carotid artery occlusion,

stroke, intermittent claudication and gangrene. All drugs and

dietary measures effective in treating atherosclerosis and/or

hyperlipidemia share only antifungal or antitoxicity activity

(lovastatin, griseofulvin, ketoconazole, neomycin, fibrates, etc.).

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 proved the validity of the

auto-immune concept with the presence of auto-antibodies against

ubiquitin, which is present in many species including fungi.

Scleroderma responds well to the antifungal agent griseofuvlin.

Against whose ubiquitin is the host raising antibodies to its own or

fungal-derived in a disease state that responds to an antifungal

drug? The auto-immune diseases appearin gto have a fungal/mycotoxin

origin are scleroderma diabetes mellitus, HLA-related disease,

rheumatoid arthritis, Sjogren=s syndrome, psoriasis, and systemic

lupus erythematosus. All of the drugs effective in the treatment of

these diseases possess antifungal or anti-mycotoxin activity. This

includes all NSAIDS.

GOALS AND OBJECTIVES:

The purpose of presenting the three papers relative to the role of

fungi/mycotoxins in the etiology of atherosclerosis/hyperlipidemia,

gout/hyperuricemia, and auto-immune diseases and malignancies is to

introduce the medical and medical-allied profession to a rapidly

evolving data base documenting this etiological relationship.

The Surgeon General has indicated that the leading nine causes of

death (and morbidity) are all diet-related. Yet commonly consumed

natural food is not poisonous, per seCa fact adequately supported by

the lack of published data that natural food itself is toxic.

It is not the food itself but the mycotoxins present on the

foodCparticularly those stored and/or fermented by fungiCthat are

injurious to one=s health.

Animal fat is dangerous in that it contains sequestered/stored

mycotoxins.

Tobacco is actually a fermented leaf that contains fungi plus a

significant amount of known cancer-producing and atherosclerosis-

producing mycotoxins. Passive smoking is causing disease because the

smoke particles are coated with mycotoxins.

Even yeast-fermented bread falls outside the definition of natural

food, which probably accounts for its recent documentation as an

etiological agent of breast cancer in Japan.

The same yeast used to leaven bread caused severe lipid vascular

deposits in ratsCthe pattern mimicking human vascular lipid deposits.

Beer causes cancer of the kidney and breast.

CONCLUSION OF WHAT IS TO BE LEARNED

The dietary connection to environmental health is increasingly being

made clear in that the causation of the major diseases related to

diet are not due to the food but rather to the fungi and mycotoxins

present in the food chain.

While manmade chemicals used in agriculture, industry and homes,

also play a role in human health the data supporting a

fungal/mycotoxin etiology of each of the major diseases is

overwhelming while manmade toxicity studies do not show a similar

connection to these diseases.

However, the two types of environmnetal toxic exposures do come

together at various junctions, such as the increased incidence of

gout and hypertension in persons exposed to lead; the lead injuries

the immune system, which predisposes the person to increased risk of

infections, in general, and, more specifically, in host fungal

colonization/toxin production. On the other hand, the extensive use

of antifungal agents to limit mycotoxin production in stored grains

over the past three decades has probably resulted in the side

benefit of a 50% reduction in heart attacks and gastric cancer over

the same period of time.................