Post by Dr. Hildegarde Staninger on Jul 6, 2006 19:24:54 GMT -5
(Mold 101)
Mycotoxins and Their Effect On the Human Body (Part 1)
© October 7, 2003
Dr. Hildegarde Staninger, RIET-1
Industrial Toxicologist/IH,
Doctor of Integrative Medicine
Integrative Health Systems, LLC
415 3/4th N. Larchmont Blvd.,
Los Angeles, CA 90004
Tel: 323-466-2599 Fax: 323-466-2774
Dr. Hildegarde Staninger - (Under Construction)
www.1cellonelight.com/store
Dr. Hildegarde Staninger
www.staningerreport.com
Presented to:
World Safety Organization
17th International Environmental Safety & Health Conference
& Exposition
November 3 - 5, 2003
Conference Theme: “Safety & Health In the Changing Environment.”
Request for Copies of Paper from the WSO International Journal
Ms. Debbie Burgess, Administrative Manager
World Safety Organization – World Management Center
106 West Young Avenue, Suite G
P.O. Box 518
Warrensburg, Missouri 64093
Phone: (660) 747-3132
Fax: (660) 747-2647
E-mail: wsowmc@socket.net
==
Conference Agenda Coordinator
Mr. Skip Chandler
2003 WSO Conference
===================
(Mold 101)
Mycotoxins and Their Effect On the Human Body
Hildegarde Staninger, Ph.D. & Doctor of Integrative Medicine
140 Wigwam Place, Maitland, Florida U.S.A. 32751
Phone: 407-695-1033 Fax: 407-628-1551
ABSTRACT
A mycotoxin is a highly toxic principle produced by molds or fungi. One type, the aflatoxins, is a member of the tricothecene group produced by the fusarium fungus. This has been identified in samples of the so-called “yellow rain” in Southeast Asia, where it is said to have been the cause of many deaths among war refugees. Its presence there is subject to some conjecture, since the Fusarium fungus cannot germinate in the humid environment of that area. There is substantial evidence (blood tests, autopsies, and contaminated gas masks) that the former U.S.S.R. have used such lethal agents in Afghanistan, just as many other countries have used these lethal agents throughout the dawn of history. The human body once exposed to a mycotoxin runs a triple risk to its toxic effects. The triple risk factors are direct toxic effect of the mycotoxin, acquisition of mutated RNAi
from the mycotoxin’s parent fungus and creation of an internal biofilm, which will harbor a toxic soup of disease.
INTRODUCTION
Mycotoxins represent an important class of xenobiotics (in terms of morbidity), which cause renal injury in humans and food animals.1 They are not the indigenous microorganisms of man. The flora and fauna indigenous to man are often referred to simply as normal flora. In this context, “flora” denotes all microscopic life forms and “normal” becomes a statistical term. One must not equate normal with nonpathogenic, for many organisms found on and in the body can pose problems under conditions such as the following:
1. Deterioration of the host’s defense mechanisms.
2. Relocation of microorganisms, when an organism finds its way to another area of the body previously uninhabited by it.
3. A disturbance of the “normal flora.”
Normal floras are commonly referred to as amphibionts, ranging from commensals to pathogens. The amphibionts are obligately parasitic on man and other animals but are not obligately pathogenic. They are encountered at least as often in the absence of disease as in its presence. The indigenous microorganisms may flourish in the general region of tissue damage and contribute to the disease state as opportunists, rather than primary etiological agents. Thus, these organisms may be implicated although Koch’s postulates would not necessarily hold true.2
Amphibiont Sites
As a rule, few or no microorganisms are found in the following anatomical locations: blood, larynx, trachea, nasal sinuses, bronchi, esophagus, stomach, upper intestinal tract, upper urinary tract (including the posterior urethra), and posterior genital tract (passage above cervix included). However, in studies with animals, notably dogs and rabbits, microorganisms from the mouth and throat regions and from the lower intestine were found in the blood and other tissues after these animals were subjected to various types of physical or mental stress and trauma. In particular, Clostridium perfringes (one of the causative agents of gas gangrene) has been isolated from the “healthy” tissues of these animals.
The regions of the body that constitute the major habitats for indigenous microorganisms include the skin and contiguous mucous membranes, conjunctivae, upper respiratory tract (oral-pharynx included), mouth, lower intestine, external genitalia, anterior urethra, and girl thingy. It will become apparent that each habitat has certain characteristics, which allow a different overall range of microorganisms to thrive. These differences can be categorized into the following three types of environment:
1. Extremely high levels of both moisture and nutrients, as in the lower intestines and the mouth.
2. A high level of moisture and a low level of nutrients, as with mucous membranes.
3. A low level of moisture and a moderate level of nutrients, as on the skin.
Other variables include availability of oxygen, pH, temperature, and relative exposures to contaminants and ventilation.
Numbers of total aerobic and anaerobic bacteria in certain anatomical regions:
Lower intestine – approximately 100 billion microorganisms per gram of fecal matter.
Mouth – approximately 1 billion microorganisms per ml of saliva.
Nose – approximately 20,000 microorganisms per ml of nasal washing.
Skin – approximately 1 million microorganisms per cm2; this value is dependent upon the skin surface tested.
Development of the Indigenous Flora
Development of the indigenous flora begins with the normal birth process, since the infant has been bathed during the ingestion period in a sterile amniotic fluid. As the baby passes through the birth canal it begins to pick up organisms, many of which may remain with it for its lifetime. Additional microorganisms are acquired by the infant as a consequence of coming into contact with the air of the environment and with hospital personnel. Such organisms may be transient in nature, or may become permanent members of the flora.
Appreciable numbers of bacteria have been cultured from the mouths of infants within 6 to 10 hours of birth and in the feces within 10 to 20 hours.
The human body has various anatomical organ areas, each anatomical area varies in relation to pH, oxygen content, nutrients, and moisture as well as bactericidal factors, thus different organisms will predominate. While the amphibionts persist in their respective locations, saprophytic as well as many parasitic microorganisms are destroyed or excreted. These locations can change as a consequence of changes brought about by the maturation process of the individual, e.g., hormonal regulation, alteration in dietary habits, chemical exposure, IAQ buildings, AIDS and chemotherapy.
The indigenous fungi are primarily saprophytes of soil, which show preference for a parasitic habitat. Because of their primary saprophytic role, it may appear questionable to call them amphibionts. However, according to Rosenbury, an amphibiont may be considered to be any organism, which is
“. . . encountered in one or more typical indigenous locations frequently, and distinctly more frequently, than in the adjacent environment.” On this basis, and according to the propositions that an organism routinely isolated from the body in the absence of disease may be indigenous, fungi are included, even though they rarely are indigenous to the human body.2, 3
WHAT ARE FUNGI?
Fungi are single cell living forms of life, which inhabit the land, air, and waters of our planet, earth. They are everywhere in our environment, soil and home.
They are more highly developed than bacteria and viruses. They are composed of many more species than are found in other microorganisms. It is estimated that there are over 500,000 different species.
Fungi have been on earth several billion years and, quite remarkably, have had little genetic change over that period of time. They are survivalists. They can change their form from rapidly growing to no growth for thousands of years, such as seen in their living spores which have been found in Egyptian tombs. They secrete and make a poisonous toxin called a mycotoxin.
Single fungi cells can only be seen under the microscope but a colony of these cells makes a visible presence in the form of mushrooms, toad stools and molds on food and other habitats.
While plants, animals and humans are alive and well, the fungi around us are unable to overcome the natural defense mechanisms which higher forms of life possess. But once death overtakes the living, the fungi are the principle undertakers and managers: they reduce all that have ever lived into the
molecules from which they were assembled. Biologists call this the carbon cycle while theologist call it “from dust to dust.”4,5
However, there is one exception to this simple balanced equation of life and death and that is that the fungi can attack the living while they are alive.
At its most simplistic perspective, one has many fungi entering the intestinal tract, the nose and lungs, and organs exposed to the world at large. We generally do not develop an infection from these intruders. However, a person might contract a fungal infection such as “athlete’s foot” or a “ring worm” on the skin.
At the opposite extreme is the patient with AIDS who faces death-threatening major fungal infections because that person’s immune system has lost its effectiveness against fungi. In between the extremes are fungal infections associated with diseases such as diabetes, cancer and other conditions including cross infections amongst humans.
Forturnately, the average person does not succumb to a serious fungal infection such as Candida albicans (yeast) and average life into the 70’s.
All humans are colonized by Candida albicans and normal healthy persons do not die from this organism. This organism plays a very little role in causing human diseases. It has been known to have tremendous elevated growth patterns in individuals who have been diagnosed as being multichemical sensitive or acutely poisoned from exposure to hazardous materials, such as urethane, carbamates, nitrogen mustards and other compounds. It is interesting to note that these same chemicals are known to be extrinsic mutagenic agents in both fungi and human genes.6 This type of extrinsic mutagenic activity by chemicals is also known as a “directed mutation.”7 (See Table 1-1.)
Mycotoxins may be friends or foe. There are as many as 1,000 compounds, classifiable as mycotoxins, where studied by the pharmaceutical industry as potential antibiotics in the 1930’s and 1940’s only to be discarded as being too toxic for higher life forms to be of value in treating bacterial diseases in humans. Little, if any of the discarded data was published. Yet, what these
toxicity studies actually documented was the existence of a large number of fungal-derived toxins, which caused serious, target organ injury in various animal models.
Obviously, in retrospect, what was being seen was the pathology produced by the mycotoxins, in order to understand this toxicity, one only has to look at what some of these mycotoxins, used as medications, causes in humans:
The mycotoxin cyclosporin used for transplantation causes cancer and atherosclerosis, complete with hyperlipidemia in ALL humans who have received it. Many others develop gout and other diseases.
As a friend, the study of such fungal metabolites gave us penicillin at the beginning, which was replaced by a chemical cyanamide man made compound from 1945 to present day. Quite later on cyclosporin, the most potent immuno-suppressant transplantation drug, lovastatin, and the other “statins”, which have revolutionized the treatment of hyperlipidemia and atherosclerosis. The latter group is quite interesting in that they were initially developed as anti-fungal agents which just happened to have an effect in lowering blood levels of low density lipoproteins (commonly refereed to as “bad cholesterol”).
The members of this group of drugs are joined by another anti-fungal antibiotic, griseofulvin, which is also a remarkably efficient anti-atherosclerosis drug. All of this goes a long way to confirm the fungal etiology of atherosclerosis. This appears to be a quite valid conclusion since all of the other effective anti-cholesterol and/or anti-atherosclerotic therapeutic modalities share nothing in common except that they possess anti-fungal and/or anti-mycotoxin activity. Diseases of unknown etiology, which respond to anti-fungal-effective drugs, suggest the probability that they have a fungal origin, particularly when there is no other proven explanation as to how the drug is working. Table 2-2 provides a number of human diseases, which so respond and suggest a fungal or mycotoxin origin.
ENVIRONMENT, FOOD CHAIN and STORED FOOD
Fungi grow all over this planet. They are found in the soil, on trees and in water. Their spores travel throughout the lands by the winds from the four corners of our world. Biosensor testing conducted by the U.S. military has resulted in an increase population of Aspergillus niger on homes, trees and other materials in various areas of the United States of America.8
Over the last decade, starting in the 1990’s, research has implicated many toxin-producing fungi, such as Stachybotrys, Penicillim, Aspergillus and Fusarium species, to indoor air quality problems and building related illnesses. Inhalation of mycotoxin producing fungi in contaminated buildings is the most significant exposure, however, dermal contact form handling contaminated materials and the chance of ingesting toxin containing spores through eating, drinking and smoking is likely to increase exposure in a contaminated environment. Recent advances in technology have given laboratories the ability to test for specific mycotoxins without employing cost-prohibitive gas chromatography or high performance liquid chromatography techniques. Currently, surface, bulk, food and feeds, and air samples can be analyzed relatively inexpensively for mycotoxins.
Homes that have been damaged by water or have had improper construction of ventilations systems have become infected with fungal overgrowth and biofilms, which resulted in bacteria, algae and fungi growing together as a communal colony with microtubules connecting to each other to exchange nutrients. Thus, creating the most toxic forms of mycotoxins, endotoxins, and exotoxins with the potential of forming DNA plasmids in mycoplasma, with mutated RNAi sub-mutated forms of fungi genes.9, 10
The most toxic forms of fungi, mycotoxin is coming from our food itself, which is characteristically present in stored and fermented food. Pesticides used on cereals as a fungicide, such as benomyl have potentated the mycotoxin in selective genes. In 1987 at Yale University, Karl Hager and Mike Plamann performed a very important study, which was based on the plasmid pH303 and its derivatives integrated at his-3 by a single crossover. When introduced to benomyl, the mutant allele of his-3(1-234-723) was present in the genome, and its mutation was mapped to be somewhere downstream of the Sall restriction site. A cloning will occur at a higher transformation frequency using linear than using circular DNA, and the transformation frequencies are independent of the mating type of the host.11
If food is loaded with fungi, then the myctoxin concept is fully operative and the disease-producing potential is more than obvious.
This important question of how much fungal colonization of food exists is answered by the most recent reported mycological study of some quite representative foods; corn kernels, peanuts, cashew nuts and copra (dried coconut). Table 3-3 demonstrates the remarkable degree of fungal colonization of the interior of corn kernels and peanuts.12
Humans who eat these foods are ingesting both the toxicogenic fungi and their mycotoxins. These fungi are capable of surviving in the intestinal stream where they may continue to produce their toxins.
Similarly, animals fed fungal colonized/mycotoxic feed are not only at risk of developing mycotoxicoses, their meat and their fat, constitute another vehicle for human exposure to excessive mycotoxin intake. Animal fat is increasingly being documented to be a major risk factor for a number of human cancers and atherosclerosis. It must be noted that fat, stores polycyclic organic xenobiotics and they are highly lipid soluble. They concentrate in fat depots, which results in low plasma levels and extended half-lives. These same compounds are known to cause distinct mutations. When cattle were accidentally fed contaminated feed in Michigan by PBB’s in 1973, these compounds became stored first in fat deposits of the cows and then, via milk fat, bioaccumulated in fat stores of the people of Michigan, where PBB’s can still be detected. While there is no known effect of PBB’s at the storage site, this store is a potential hazard since mobilization during starvation or other stress could lead to efflux into the bloodstream with subsequent redistribution and toxicity. Similarly, patients treated for acute exposure to organophosporous pesticides may be released from the hospital and later suffer a relapse due to mobilization of the insecticide from fat stores.13
Mycotoxins have been documented to cause a number of specific types of diseases and very specific organ lesions both in animals and in humans. Table 4-4 provides a summary of some of this documentation.
(GO TO PART 2)
Mycotoxins and Their Effect On the Human Body (Part 1)
© October 7, 2003
Dr. Hildegarde Staninger, RIET-1
Industrial Toxicologist/IH,
Doctor of Integrative Medicine
Integrative Health Systems, LLC
415 3/4th N. Larchmont Blvd.,
Los Angeles, CA 90004
Tel: 323-466-2599 Fax: 323-466-2774
Dr. Hildegarde Staninger - (Under Construction)
www.1cellonelight.com/store
Dr. Hildegarde Staninger
www.staningerreport.com
Presented to:
World Safety Organization
17th International Environmental Safety & Health Conference
& Exposition
November 3 - 5, 2003
Conference Theme: “Safety & Health In the Changing Environment.”
Request for Copies of Paper from the WSO International Journal
Ms. Debbie Burgess, Administrative Manager
World Safety Organization – World Management Center
106 West Young Avenue, Suite G
P.O. Box 518
Warrensburg, Missouri 64093
Phone: (660) 747-3132
Fax: (660) 747-2647
E-mail: wsowmc@socket.net
==
Conference Agenda Coordinator
Mr. Skip Chandler
2003 WSO Conference
===================
(Mold 101)
Mycotoxins and Their Effect On the Human Body
Hildegarde Staninger, Ph.D. & Doctor of Integrative Medicine
140 Wigwam Place, Maitland, Florida U.S.A. 32751
Phone: 407-695-1033 Fax: 407-628-1551
ABSTRACT
A mycotoxin is a highly toxic principle produced by molds or fungi. One type, the aflatoxins, is a member of the tricothecene group produced by the fusarium fungus. This has been identified in samples of the so-called “yellow rain” in Southeast Asia, where it is said to have been the cause of many deaths among war refugees. Its presence there is subject to some conjecture, since the Fusarium fungus cannot germinate in the humid environment of that area. There is substantial evidence (blood tests, autopsies, and contaminated gas masks) that the former U.S.S.R. have used such lethal agents in Afghanistan, just as many other countries have used these lethal agents throughout the dawn of history. The human body once exposed to a mycotoxin runs a triple risk to its toxic effects. The triple risk factors are direct toxic effect of the mycotoxin, acquisition of mutated RNAi
from the mycotoxin’s parent fungus and creation of an internal biofilm, which will harbor a toxic soup of disease.
INTRODUCTION
Mycotoxins represent an important class of xenobiotics (in terms of morbidity), which cause renal injury in humans and food animals.1 They are not the indigenous microorganisms of man. The flora and fauna indigenous to man are often referred to simply as normal flora. In this context, “flora” denotes all microscopic life forms and “normal” becomes a statistical term. One must not equate normal with nonpathogenic, for many organisms found on and in the body can pose problems under conditions such as the following:
1. Deterioration of the host’s defense mechanisms.
2. Relocation of microorganisms, when an organism finds its way to another area of the body previously uninhabited by it.
3. A disturbance of the “normal flora.”
Normal floras are commonly referred to as amphibionts, ranging from commensals to pathogens. The amphibionts are obligately parasitic on man and other animals but are not obligately pathogenic. They are encountered at least as often in the absence of disease as in its presence. The indigenous microorganisms may flourish in the general region of tissue damage and contribute to the disease state as opportunists, rather than primary etiological agents. Thus, these organisms may be implicated although Koch’s postulates would not necessarily hold true.2
Amphibiont Sites
As a rule, few or no microorganisms are found in the following anatomical locations: blood, larynx, trachea, nasal sinuses, bronchi, esophagus, stomach, upper intestinal tract, upper urinary tract (including the posterior urethra), and posterior genital tract (passage above cervix included). However, in studies with animals, notably dogs and rabbits, microorganisms from the mouth and throat regions and from the lower intestine were found in the blood and other tissues after these animals were subjected to various types of physical or mental stress and trauma. In particular, Clostridium perfringes (one of the causative agents of gas gangrene) has been isolated from the “healthy” tissues of these animals.
The regions of the body that constitute the major habitats for indigenous microorganisms include the skin and contiguous mucous membranes, conjunctivae, upper respiratory tract (oral-pharynx included), mouth, lower intestine, external genitalia, anterior urethra, and girl thingy. It will become apparent that each habitat has certain characteristics, which allow a different overall range of microorganisms to thrive. These differences can be categorized into the following three types of environment:
1. Extremely high levels of both moisture and nutrients, as in the lower intestines and the mouth.
2. A high level of moisture and a low level of nutrients, as with mucous membranes.
3. A low level of moisture and a moderate level of nutrients, as on the skin.
Other variables include availability of oxygen, pH, temperature, and relative exposures to contaminants and ventilation.
Numbers of total aerobic and anaerobic bacteria in certain anatomical regions:
Lower intestine – approximately 100 billion microorganisms per gram of fecal matter.
Mouth – approximately 1 billion microorganisms per ml of saliva.
Nose – approximately 20,000 microorganisms per ml of nasal washing.
Skin – approximately 1 million microorganisms per cm2; this value is dependent upon the skin surface tested.
Development of the Indigenous Flora
Development of the indigenous flora begins with the normal birth process, since the infant has been bathed during the ingestion period in a sterile amniotic fluid. As the baby passes through the birth canal it begins to pick up organisms, many of which may remain with it for its lifetime. Additional microorganisms are acquired by the infant as a consequence of coming into contact with the air of the environment and with hospital personnel. Such organisms may be transient in nature, or may become permanent members of the flora.
Appreciable numbers of bacteria have been cultured from the mouths of infants within 6 to 10 hours of birth and in the feces within 10 to 20 hours.
The human body has various anatomical organ areas, each anatomical area varies in relation to pH, oxygen content, nutrients, and moisture as well as bactericidal factors, thus different organisms will predominate. While the amphibionts persist in their respective locations, saprophytic as well as many parasitic microorganisms are destroyed or excreted. These locations can change as a consequence of changes brought about by the maturation process of the individual, e.g., hormonal regulation, alteration in dietary habits, chemical exposure, IAQ buildings, AIDS and chemotherapy.
The indigenous fungi are primarily saprophytes of soil, which show preference for a parasitic habitat. Because of their primary saprophytic role, it may appear questionable to call them amphibionts. However, according to Rosenbury, an amphibiont may be considered to be any organism, which is
“. . . encountered in one or more typical indigenous locations frequently, and distinctly more frequently, than in the adjacent environment.” On this basis, and according to the propositions that an organism routinely isolated from the body in the absence of disease may be indigenous, fungi are included, even though they rarely are indigenous to the human body.2, 3
WHAT ARE FUNGI?
Fungi are single cell living forms of life, which inhabit the land, air, and waters of our planet, earth. They are everywhere in our environment, soil and home.
They are more highly developed than bacteria and viruses. They are composed of many more species than are found in other microorganisms. It is estimated that there are over 500,000 different species.
Fungi have been on earth several billion years and, quite remarkably, have had little genetic change over that period of time. They are survivalists. They can change their form from rapidly growing to no growth for thousands of years, such as seen in their living spores which have been found in Egyptian tombs. They secrete and make a poisonous toxin called a mycotoxin.
Single fungi cells can only be seen under the microscope but a colony of these cells makes a visible presence in the form of mushrooms, toad stools and molds on food and other habitats.
While plants, animals and humans are alive and well, the fungi around us are unable to overcome the natural defense mechanisms which higher forms of life possess. But once death overtakes the living, the fungi are the principle undertakers and managers: they reduce all that have ever lived into the
molecules from which they were assembled. Biologists call this the carbon cycle while theologist call it “from dust to dust.”4,5
However, there is one exception to this simple balanced equation of life and death and that is that the fungi can attack the living while they are alive.
At its most simplistic perspective, one has many fungi entering the intestinal tract, the nose and lungs, and organs exposed to the world at large. We generally do not develop an infection from these intruders. However, a person might contract a fungal infection such as “athlete’s foot” or a “ring worm” on the skin.
At the opposite extreme is the patient with AIDS who faces death-threatening major fungal infections because that person’s immune system has lost its effectiveness against fungi. In between the extremes are fungal infections associated with diseases such as diabetes, cancer and other conditions including cross infections amongst humans.
Forturnately, the average person does not succumb to a serious fungal infection such as Candida albicans (yeast) and average life into the 70’s.
All humans are colonized by Candida albicans and normal healthy persons do not die from this organism. This organism plays a very little role in causing human diseases. It has been known to have tremendous elevated growth patterns in individuals who have been diagnosed as being multichemical sensitive or acutely poisoned from exposure to hazardous materials, such as urethane, carbamates, nitrogen mustards and other compounds. It is interesting to note that these same chemicals are known to be extrinsic mutagenic agents in both fungi and human genes.6 This type of extrinsic mutagenic activity by chemicals is also known as a “directed mutation.”7 (See Table 1-1.)
Mycotoxins may be friends or foe. There are as many as 1,000 compounds, classifiable as mycotoxins, where studied by the pharmaceutical industry as potential antibiotics in the 1930’s and 1940’s only to be discarded as being too toxic for higher life forms to be of value in treating bacterial diseases in humans. Little, if any of the discarded data was published. Yet, what these
toxicity studies actually documented was the existence of a large number of fungal-derived toxins, which caused serious, target organ injury in various animal models.
Obviously, in retrospect, what was being seen was the pathology produced by the mycotoxins, in order to understand this toxicity, one only has to look at what some of these mycotoxins, used as medications, causes in humans:
The mycotoxin cyclosporin used for transplantation causes cancer and atherosclerosis, complete with hyperlipidemia in ALL humans who have received it. Many others develop gout and other diseases.
As a friend, the study of such fungal metabolites gave us penicillin at the beginning, which was replaced by a chemical cyanamide man made compound from 1945 to present day. Quite later on cyclosporin, the most potent immuno-suppressant transplantation drug, lovastatin, and the other “statins”, which have revolutionized the treatment of hyperlipidemia and atherosclerosis. The latter group is quite interesting in that they were initially developed as anti-fungal agents which just happened to have an effect in lowering blood levels of low density lipoproteins (commonly refereed to as “bad cholesterol”).
The members of this group of drugs are joined by another anti-fungal antibiotic, griseofulvin, which is also a remarkably efficient anti-atherosclerosis drug. All of this goes a long way to confirm the fungal etiology of atherosclerosis. This appears to be a quite valid conclusion since all of the other effective anti-cholesterol and/or anti-atherosclerotic therapeutic modalities share nothing in common except that they possess anti-fungal and/or anti-mycotoxin activity. Diseases of unknown etiology, which respond to anti-fungal-effective drugs, suggest the probability that they have a fungal origin, particularly when there is no other proven explanation as to how the drug is working. Table 2-2 provides a number of human diseases, which so respond and suggest a fungal or mycotoxin origin.
ENVIRONMENT, FOOD CHAIN and STORED FOOD
Fungi grow all over this planet. They are found in the soil, on trees and in water. Their spores travel throughout the lands by the winds from the four corners of our world. Biosensor testing conducted by the U.S. military has resulted in an increase population of Aspergillus niger on homes, trees and other materials in various areas of the United States of America.8
Over the last decade, starting in the 1990’s, research has implicated many toxin-producing fungi, such as Stachybotrys, Penicillim, Aspergillus and Fusarium species, to indoor air quality problems and building related illnesses. Inhalation of mycotoxin producing fungi in contaminated buildings is the most significant exposure, however, dermal contact form handling contaminated materials and the chance of ingesting toxin containing spores through eating, drinking and smoking is likely to increase exposure in a contaminated environment. Recent advances in technology have given laboratories the ability to test for specific mycotoxins without employing cost-prohibitive gas chromatography or high performance liquid chromatography techniques. Currently, surface, bulk, food and feeds, and air samples can be analyzed relatively inexpensively for mycotoxins.
Homes that have been damaged by water or have had improper construction of ventilations systems have become infected with fungal overgrowth and biofilms, which resulted in bacteria, algae and fungi growing together as a communal colony with microtubules connecting to each other to exchange nutrients. Thus, creating the most toxic forms of mycotoxins, endotoxins, and exotoxins with the potential of forming DNA plasmids in mycoplasma, with mutated RNAi sub-mutated forms of fungi genes.9, 10
The most toxic forms of fungi, mycotoxin is coming from our food itself, which is characteristically present in stored and fermented food. Pesticides used on cereals as a fungicide, such as benomyl have potentated the mycotoxin in selective genes. In 1987 at Yale University, Karl Hager and Mike Plamann performed a very important study, which was based on the plasmid pH303 and its derivatives integrated at his-3 by a single crossover. When introduced to benomyl, the mutant allele of his-3(1-234-723) was present in the genome, and its mutation was mapped to be somewhere downstream of the Sall restriction site. A cloning will occur at a higher transformation frequency using linear than using circular DNA, and the transformation frequencies are independent of the mating type of the host.11
If food is loaded with fungi, then the myctoxin concept is fully operative and the disease-producing potential is more than obvious.
This important question of how much fungal colonization of food exists is answered by the most recent reported mycological study of some quite representative foods; corn kernels, peanuts, cashew nuts and copra (dried coconut). Table 3-3 demonstrates the remarkable degree of fungal colonization of the interior of corn kernels and peanuts.12
Humans who eat these foods are ingesting both the toxicogenic fungi and their mycotoxins. These fungi are capable of surviving in the intestinal stream where they may continue to produce their toxins.
Similarly, animals fed fungal colonized/mycotoxic feed are not only at risk of developing mycotoxicoses, their meat and their fat, constitute another vehicle for human exposure to excessive mycotoxin intake. Animal fat is increasingly being documented to be a major risk factor for a number of human cancers and atherosclerosis. It must be noted that fat, stores polycyclic organic xenobiotics and they are highly lipid soluble. They concentrate in fat depots, which results in low plasma levels and extended half-lives. These same compounds are known to cause distinct mutations. When cattle were accidentally fed contaminated feed in Michigan by PBB’s in 1973, these compounds became stored first in fat deposits of the cows and then, via milk fat, bioaccumulated in fat stores of the people of Michigan, where PBB’s can still be detected. While there is no known effect of PBB’s at the storage site, this store is a potential hazard since mobilization during starvation or other stress could lead to efflux into the bloodstream with subsequent redistribution and toxicity. Similarly, patients treated for acute exposure to organophosporous pesticides may be released from the hospital and later suffer a relapse due to mobilization of the insecticide from fat stores.13
Mycotoxins have been documented to cause a number of specific types of diseases and very specific organ lesions both in animals and in humans. Table 4-4 provides a summary of some of this documentation.
(GO TO PART 2)