Fungal diseases are common place in plants and animals. In such diseases, the fungi are actively growing on and invading the body of their hosts. There is another means by which fungi can cause harm without invading our bodies. When fungi grow on a living organism or on stored food material that we consume, they may produce harmful metabolites that diffuses into their food. It is believed that fungi evolved these metabolites as a means of protecting their food supply by preventing other organisms from eating it. These metabolites are referred to as mycotoxins, which literally means "fungus poisons". Fungi that produce mycotoxins do not have to be present to do harm. If a fungus was growing in, say a grain storage silo, the environment may have become unsuitable for the fungus and it dies. Even though the fungus is no longer alive, while it was growing, if it produced a mycotoxin, it will have poisoned the grains. So for those of you who are always looking to save a little money by buying cheese that has been contaminated with a fungus and cutting out the part where the fungus is growing, perhaps this is not such a good idea. It is possible that the fungus growing on your cheese has produced a mycotoxin that has diffused throughout the cheese, even though the fungus itself has not. The effects of poisoning by mycotoxin is referred to as mycotoxicoses. The knowledge that mycotoxicoses is the result of fungal actions was a relatively, recent discovery. This is understandable since illnesses in this case is due to consumption of mycotoxins that has been released by the fungus and is not directly caused by the fungus. So demonstrating this would not have been an easy task.
We now know that many species of fungi produce mycotoxins, but why? It is thought fungi have evolved production of various mycotoxins in order to prevent other fungi or animals from consuming "their" food. By secreting their mycotoxin into their food the fungus will inhibit growth of other fungi and discourage rotten or other small animals from eating their food.

We will have several lectures on mycotoxins. Today, we will cover some of the more common mycotoxins that are produced by by molds growing in food and describe their symptoms.  The following two lectures will be concerned with a number of different toxins that are all derived from Claviceps purpurea, the fungus responsible for the disease on rye, commonly referred to as Ergot, and later in the semester we will talk about mushroom toxins.

Early Attempts to Demonstrate the Existence of Mycotoxin

The existence of mycotoxins was not documented until 1960. However, just as in the case of diseases, the concept that moldy food could lead to illness in people or domestic animals was long suspected before their existence was demonstrated by science. It is a greater problem, presently, than it was in the distant past. Long ago, before there was adequate means of long term storage for perishable goods, food was normally consumed a short time after it was acquired, but as the world has become more industrialized and technological advanced, storage of food has become more of an issue. Food is now commonly stored for long periods of time, giving fungi a greater opportunity to contaminate our food.

Before 1900, in Italy, researchers there believed consumption of moldy corn by children led to the development of illness (Christensen, 1975). Some experiments, done at that time, included the isolation, and growth of the suspected fungus in pure culture, and isolation of toxic compounds from the fungus that the researchers believed to be the cause of the illness. However, since the compound was not identified and was not actually isolated from the moldy corn, it could not be concluded that this compound was the cause of the illness or that the compound in question was even present on the moldy corn. Nevertheless, it appeared that there was a correlation between the illness and consumption of moldy corn, but this did not eliminate the possibility that it was the fungus, itself, that caused the disease, which most people believed to be the case. It was also possible that there were other reasons for the illnesses that were observed.

Burnside, et al (1957) studied an extensive outbreak of moldy corn disease in the southeastern United States in the early 1950's where hundreds of wild pigs foraging in cultivated corn fields became ill, and many died. Teams of veterinarians and mycologists collaborated to determine the cause of the deaths of these pigs. They isolated a number of different fungi from the moldy corn and inoculated each fungus on moist corn that had been sterilized and then fed them to pigs. The consumption of corn inoculated with Aspergillus flavus caused outward signs and inward lesions found in other cases of the so-called moldy corn disease. However, since there was no toxin(s) isolated, there was little attention paid to the article since it still seemed like old news, i.e. domestic animals poisoned by eating moldy corn.

It would not be until 1960, when approximately 100,000 turkeys and a lesser number of other domestic birds died in England, causing losses of approximately several hundred thousand dollars, before the first mycotoxin was isolated and identified. As you might guess, this did not happen immediately. Initially, the disease was thought to be caused by a virus and the syndrome was named "turkey-X disease". The "X" here indicated that the cause of the disease was unknown. However, with a great deal of detective work, on the parts of the researchers, soon the cause of the disease was traced to feed that was produced by Oil Cake Mills, Ltd. (research always seems to get done more quickly and receive more priority when loss of large sums of money is involved). The oil cake feed was composed mostly of peanuts. However, it seemed unlikely that the peanut meal itself was toxic, since peanut meal had long been used as a feed ingredient and was known to be an excellent source of protein. Thus, it was reasoned that something must have been added to the peanut meal to make it toxic, and one possibility that was investigated was that peanuts had been made toxic by fungi growing in them. From their isolations, the investigators identified Aspergillus flavus, the same fungus that was isolated by Burnside and his research teams. The isolated fungus was again inoculated into the feed and fed to the turkeys. Shortly after feeding, the turkeys died with external signs and internal lesions identical to those observed in the birds that had previously died in the field.

Unlike Burnside, however, chemists were also employed in this investigation, and they were able to isolate and identify the toxin from the oil cake feed. The mycotoxin isolated was named aflatoxin, the "a" from Aspergillus and "fla" from flavus. Feeding test of food containing aflatoxin, with various laboratory animals, demonstrated that to varying degrees, all animals tested were sensitive to aflatoxin. Even consumption of extremely small amounts of aflatoxin damaged various internal organs and could induce development of cancer to the liver.

This was of great concern among the nutritionists and those concerned with problems of pubic health, e.g. The Food and Drug Administration. There was great concerned domestically since peanuts and peanut products were/are of economic importance. It was also of international significance, since peanuts at that time was being lauded as an excellent source of protein, for developing countries, by UNICEF (United Nations International Children's Emergency Fund) and other such organizations. Deficiency in protein often results in "kwashiorkor".

Kwashiorkor (kwä´shê-ôr´kôr´), protein deficiency disorder of children, prevalent in overpopulated parts of the world where the diet consists mainly of starchy vegetables, particularly Africa, Central and South America, and S Asia. Such a diet is deficient in certain amino acids, which make up proteins vital for growth. Depending on the extent, onset, and duration of the deficiency, manifestations include skin changes, edema, severely bloated abdomen, diarrhea, and generally retarded development. The Concise Columbia Encyclopedia is licensed from Columbia University Press. Copyright © 1995 by Columbia University Press. All rights reserved.

Other characteristics include anemia, depigmentation of the skin, and loss of hair or change in hair color. Usually, occurring in children, shortly after weaning. Peanut products were developed in various forms, especially in tropical and subtropical countries, for general distribution. Were these people now exchanging kwashiorkor for potential risk of liver damage and cancer from consuming aflatoxins? Thus, there was a great deal at stake, which provided an impetus to act on this matter, immediately. In the United States, as soon as awareness of aflatoxins surfaced in the 1960s, programs were established by peanut growers, aided by concentrated research, to reduce the possibility of aflatoxin occurring in edible peanuts and peanut products. That they have been successful is indicated through random sampling, by the FDA, of only an occasional batch of peanut products that contains aflatoxin. What has been discovered have almost never been found in sufficient amount to be of any real concern. However, in other countries, in which there are no such regulatory bodies, the people undoubtedly consume an appreciable amount of aflatoxins.

The Fungus

Aspergillus flavus is actually not a single species, but a "species complex", made up of eleven species that are known to occur in many kinds of plant materials, including stored grains. One of the species in the complex, A. oryzae has long been used in the Orient to prepare various kinds of food products, such as sake, tofu and soy sauce, which in turn is used in the United States. Were aflatoxins present in these products as well? This was a question that needed to be answered. Research began to take place at a rapid pace and continues to do so. The number of papers published that have to do with aflatoxins number in the hundreds annually.

What was determined in early research of aflatoxins is that the conditions which allows for growth of A. flavus and aflatoxins is very narrow. Aspergillus flavus seldom invades stored grains alone, i.e. as a pure culture. Various other species of fungi will normally grow on a substrate prior to invasion by A. flavus, e.g. A. glaucus and Candida pseudotropicalis. In a preinvaded substrate, regardless of how dense the A. flavus invasion may be, aflatoxin will not form. This was demonstrated at the University of Minnesota where A. flavus as well as other fungi were grown on grain at moisture content and temperature range that were optimal for aflatoxin production. Although, there was a very dense mycelial growth of A. flavus, the grain that was fed to the various kinds of experimental animals, ducklings, white rats and baby chicks, for as long as eight months, there was not a single case of death from consumption of the feed. In fact, weight gain was the same as that of those animals not fed the with grain containing the fungal growth. Thus, the amount of mycelial growth that occurs in animal feed, with several species of fungi involved, even if one is known to be an aflatoxin producer, was apparently safe to consume. Thus, in order for aflatoxin formation to occur in say a storage bin full of peanuts, A. flavus must be growing alone and the peanuts cannot have been previously or simultaneously invaded by other fungi, an occurrence that is rare. In the case of the Turkey-X disease, the peanuts that were responsible for the aflatoxin poisoning were from South America, where the process used to harvest and dry the peanuts was responsible for providing an environment that allowed for growth of A. flavus and aflatoxin. Aspergillus flavus does not normally contaminate grains and other crops while they are still in the field. It is only after the grains are harvested and stored does A. flavus, as well as other so-called "storage fungi" that have a low moisture requirement, can the grain be invaded. Although conditions favorable for growth of the A. flavus and production of aflatoxin is narrow, the fungus is common and widespread in nature. It can be found growing on various decaying vegetation where it may heat up the substrate to as high as 113-122°F as it consumes the material.

The amount of aflatoxin formed differs as to the substrate on which it is growing. Although the mycelial mass may be the same in each substrate, the aflatoxin produced would be far greater in peanuts than in say soybeans, where relatively very little would be produced. Other seeds of cereal crops, wheat, corn, barley, oats and sorghum are also generally of low-aflatoxin-risk. Weather and climate were also contributing factors. Finally, the amount of toxin produced will vary with the isolate of A. flavus. That is different sources of A. flavus will produce different amounts of aflatoxins. Some isolates of A. flavus may not even form aflatoxin.

Strange as this may sound, in some cultures, fungi are encouraged to grow on certain foods in order to give them the desired taste. For example, the Bantu tribes in Africa prefer the sour flavor of partly spoiled corn to that of fresh corn and fungus is purposely allowed to grow on the corn for this reason (Christensen, 1975). However, this may only be a coincident, but they also have a very high incident of primary liver cancer.

How much aflatoxin is too much?

Christensen (1972), over a period of several years, examined 100 different samples of black pepper from all over the world. In dilution cultures of these samples, the number of fungus colonies in whole or ground black pepper averaged 52,000 per gram/black pepper and the upper range was over half a million per gram. These colonies were mostly of A. flavus, A. ochraceus and A. versicolor. All three species are known to be aflatoxin producers. Some samples of ground pepper were caked lightly with fungus mycelium when first opened in the laboratory and with time, a number of these became solidly caked with mycelium.

How heavily contaminated is 52,000 to 500,000 colonies of fungi, per gram? Lets make a comparison for what is acceptable levels of fungal colonies isolated in other food products at the time Christensen published his results. Wheat, for example, that is intended for milling into flour seldom contains no more than a few thousand colonies of fungi per gram of grain. If barley has as many as 10,000 colonies of the same kind of fungi per gram as in black pepper, it would be rejected for malting in beer making. If breakfast cereals or bread were as contaminated as black peppers, they would have so musty an odor and taste that they would be too revolting to eat. Apparently, the natural spicy odor and flavor of black, as well as white pepper are potent enough to conceal the taste and odor of these fungi. This is also true with many other spices.

One sample of black pepper was even found to contain a rodent dropping and a piece of stone about the same size as the pepper. Most samples contained peppers partly eaten by insects and partly or mostly decayed by fungi and bacteria. However, you should keep in mind that at the time Christensen carried out his little study, quality control was not as much of an issue as it is today. With the quality standards that are being enforced, presently, food products with the type of contaminations described above would not be allowed on the market.

What about the processed food prepared with A. flavus? At least, in the commercial strains that have been utilized to prepare food in the United States, the strains that have been tested have not been found to produce aflatoxins. However, where these products are prepared in a household or village industry, and the fungus is just carried from one batch to the next, wild strains capable of producing aflatoxin may contaminate them. In an investigation, in the Philippines, not a single sample was found that was free of aflatoxin. In such communities probably everyone was suffering to some extent from chronic aflatoxin poisoning.

Mycotoxins in Other Species of Aspergillus, Penicillium and Fusarium

Aspergillus ochraceus and ochratoxin

Aspergillus ochraceus is also a species complex, and consist of nine species. These species are common in soil, decaying vegetation, and in stored seeds and grains undergoing microbial deterioration. However, this fungus is seldom isolated from more than a small percentage of seeds or grains that are undergoing microbiological deterioration in storage because it is evidently not a good competitor, as is also the case with A. flavus. This is a general rule, but at the University of Minnesota, A. ochraceus sometimes has been isolated from 40% or more of surface-disinfected kernels of corns from bins in which deterioration was in progress. It has also been the major organism in some lots of whole black pepper. Also, samples of macaroni and spaghetti were found to be heavily invaded by this species.

Production of ochratoxin, by A. ochraceus, was first described in South Africa by Theron, et al. (1966), where it was isolated along with a number of other fungi. In experiments done with this isolate, the LD50 (the single dose that will kill 50 percent of the individual animals tested) of ochratoxin for rats is 22mg/kg (= 22 milligrams of the toxin per kilogram of body weight of the rat), but a lesser amount will result in severe liver damage. A single dose of 12.5 mg/kg (=12.5 milligrams of the toxin per kilogram of body weight of the rat) was administered to pregnant rats on the tenth day of gestation, and of the 88 fetuses involved, 72, or 81.8% died or were resorbed. Ducklings seem to be equally sensitive to ochratoxin as they are to aflatoxin.

Another fungus, Penicillium viridicatum, can also produce ochratoxin, and is relatively common in stored corn and is a more common producer of ochratoxin than A. ochraceus.

Aspergillus versicolor and sterigmatocystin

This species is another storage fungus. However, it is never found as the only fungus or as the predominating fungus in deteriorating cereals. Normally, by the time a grain sample has become very moldy, A. versicolor, along with other Aspergillus species and usually other filamentous fungi and yeasts as well. Some of the black pepper mentioned earlier, as being decayed by fungi, was very heavily invaded by A. versicolor, but not by this fungus exclusively.

One rather interesting case concerning this species took place, on germinating barley, in a malthouse, in Scotland. The growth of A. versicolor was so luxuriant on the germinating barley and produced so many spores, that the workers who turned the malts with shovels could not see one another because of the spore-filled air. The owners and managers of the malthouse hired a mycologist to determine how the fungus was getting in. They had assumed that the contamination must have been due to the incoming barley. What the mycologist concluded, however, was that there was a lack of sanitary conditions, in the malthouse, and that everything in and around that malthouse must have been thoroughly and heavily contaminated by A. versicolor spores (and probably a lot of other fungi as well). So, when conditions were favorable, i.e. when the barley was brought in, the growth of fungi grew to spectacular quantities. Can you imagine working in such an environment and having to inhale those spores?

This species, under the right conditions, produces sterigmatocystin, a toxic compound given the name because the fungus once was called Sterigmatocystis. The toxin is known to cause lung, liver and kidney tumors in laboratory animals and has been implicated as the cause of disease in calves that have consumed feed heavily invaded by A. versicolor. Experiments carried out in which the fungus were grown, on feed that was fed to calves, produced symptoms of the disease in the calves. However, tests were not done to detect the toxin in the calves. The toxin has also been detected in moldy coffee beans in Africa, but no evidence indicates that even if these beans were used to brew coffee that the toxin would be in the drink.

Aspergillus fumigatus and fumagillin

This particular species is known to be an animal pathogen. Infection occurs through inhalation of spores and affects the lungs. Infection may also occur in eggs and the fetuses of cows.  However, it also produces a metabolic product that may be considered a toxin or an antibiotic. This species differs from the others that we have discussed in that it is said to be thermophilic, that is, it is found in substrate where there are extremely high temperatures, up to 122ºF (=50ºC). This species is usually found on material that is in the advanced stages of decomposition in which the substrate temperature has been significantly raised by microbial decomposition.

Under the proper conditions, A. fumigatus produces fumagillin. This compound is used as an amoebicide, that is, as a means to rid the body of amoebae that are human pathogens and has been used effectively in honey bees as well. However, the correct dosage of this compound is critical. A little bit more than you need to get rid of the amoebae and you will be getting rid of the patient as well.

The Genus Fusarium

Species of Fusarium are widespread in nature as saprobes in decaying vegetation and as parasites on all parts of plants. Many cause diseases of economically important plants. For this reason, there has been a great deal of research carried out in this genus by both plant pathologist and mycologist. However, there are a number of species that produce mycotoxins, mostly trichothecenes and zearalenone. We will discuss a few common examples.

Fusarium tricinctum

The effects of the first trichothecene toxin, T-2, documented was in the 1940s where it was associated with an outbreak of alimentary toxic aleukia (ATA). At its peak, in 1944, the population in the Orenbury District and other districts of the then USSR suffered enormous casualties, more than 10 percent of the population was affected and many fatalities occurred. The term alimentary toxic refers to the toxin being consumed in foods and aleukia refers to the reduced number of leucocytes or white blood cells in the affected person. Other symptoms included bleeding from nose and throat, multiple, subcutaneous hemorrhages.

The infected food in this case was millet, which made up a great part of the diet of the people in the region, and at times, during WWII, it was not uncommon to allow the millet to be left standing in the fields over winter because bad weather in the fall prevented its harvest at the proper time. During the late winter and early spring the millet would become infected with a variety of fungi, including F. tricinctum, and when the people gathered and ate this fungus, many came down with what was diagnosed as ATA. Thousands were affected, and many died. Locally, Joffe, a plant pathologist determined the outbreak of ATA was caused by consumption of a toxin, present in the millet, which had been contaminated by F. tricinctum. This was a remarkable conclusion since this was 20 years before aflatoxin was discovered. However, Joffe did not isolate or identify the toxin involved and as a result his work remained unknown until about 1965 when he presented a summary of his research at a symposium on mycotoxins. The mycotoxin involved was later given the common name T-2, and classified as one of several trichothecenes. Fed orally to rats, it has an LD50 of 3.8mg/kg, which is lower than that of aflatoxin, but still toxic enough.

Fusarium graminearum

Corn is a stable in many countries and is used as a major ingredient in preparation of food for pigs and other domestic animals. Like many other grains, the kernels can be infected with fungi before and after harvest, and can affect the nutritional value of corn as food or feed.

If the weather is rainy and the ears of corn are maturing in late summer and early fall, F. graminearum may infect only a few to a third of the kernels. Whatever amount of the ear is infected, all the kernels in that portion becomes heavily infected and decayed by the fungus. This fungus-infected corn is unattractive to pigs, as well as other animals, and they refuse to it. For this reason, this phenomenon has been called a refusal factor. Regardless of what the composition of the rest of the feed, if it contains more than 5 percent of kernels with this refusal factor, the pigs will not eat it and weight loss will occur. They will starve rather than consume it. The infected corn contains an emetic compound produced by the fungus, and if this corn is consumed by pigs, they suffer prolonged vomiting, after which they sensibly refuse to eat more of the corn (who said pigs were stupid?). The toxin involved is deoxynivalenol (DON), also known as vomitoxin. The isolation and identification of this toxin has occurred only within the last 25 years.

This is a serious problem if you look at it through the eyes of the farmer. If you are a farmer and you have 800-1000 pigs and several tons of feed mixed with corn, contaminated with vomitoxin, was delivered to the farmer's feed bin on a Friday, and it is later determined that the pigs will not eat it, then the farmer has a serious problem. What are the pigs going to eat between Friday and Monday?

Various methods have been tried to make the vomitoxin contaminated corn more acceptable to pigs. Among some of the means that have been tried are adding molasses to the feed to conceal whatever flavor or odor makes it unacceptable to the pigs, heating the feed, in hopes of destroying or inactivating whatever it is that is making the pig refuse to eat it, and composting it so that the heat will break down the toxin. However, none of these treatments have made the corn acceptable to pigs and are impractical, anyway.

The detection of infected corn or feed is also a problem. Since we are talking about mycotoxin here, the inability to isolate the causal agent, F. graminearum, is not evidence that the mycotoxin is absent. Long after a fungus has died off, mycotoxin secreted into the substrate, will still be present. The refusal of pigs to eat feed or corn is an indication that the refusal factor is present, but not necessarily conclusive. There are a number of reasons as to why pigs will refuse to eat. Pigs may be traumatized by being moved to a new pen, strange surroundings or even being offered different food. The only way that the toxin can be detected is to isolate, purify and identify it by spectrographic or other analysis.

Use of Trichothecenes as a Biological Weapon

Yellow Rain

During the mid 1970s, when Vietnam was invading Laos, there were stories of "yellow rain" in areas where entire villages were killed. One eye witness account of such an event was told by a Hmong refugee, in Thailand. While tending his poppies, outside of his village, he and his family witnessed the bombing of their village by the Vietnamese, in MIGS, with a yellow powder that came down like yellow rain. Returning to the village, he found all of the animals and most of the people were dead. The bodies were bleeding from the nose and ears and their skin were blistered and yellowed. The few people left alive, when he arrived, were "jerking like fish when you take them out of the water". These people also eventually died. The witness took his family away from the village, but as they left they felt shortness of breath and sick to their stomach. This story is similar to other stories that were heard concerning yellow rain.

It was believed by the United States at that time that the Soviet Union was somehow involved in what occurred in the Hmong village, and medical teams were sent to investigate. However, because of the remoteness of these villages, news of such attacks normally took 4 to 6 weeks to reach someone who could notify the medical teams. By the time investigators reached a village, there was no evidence as to what happened. It would not be until 1980 that a Defense Department chemist recognized the symptoms described by victims of the bombing as similar to trichothecene mycotoxicosis. Samples from victims and from vegetation in the areas were tested and some were found to contain trichothecenes. With this information, President Ronald Reagan accused the Soviet Union of violating the Geneva Convention and Biological Weapons Convention, which of course they denied. However, these accusations would continue for three more years.

While the accusations and denials were aired, the media and scientific community gave a more critical examination of the yellow rain story. The analysis that demonstrated Trichothecenes were being used was initially based on a single leaf, collected where one of the chemical attacks occurred. Subsequent specimens were collected later that also showed Trichothecenes were present, but the ratio of trichothecenes differed where it was found and was entirely absent in some samples. In addition, little fanfare was given to the over one hundred samples analyzed by the United States Army, which did not find any indication of trichothecenes. The eye witness accounts also came into question. Although it was implied that many villages were attacked with yellow rain, all of the witnesses were from a single refugee camp in Thailand, and even these accounts were thought to be unreliable. For example in relating a story of the bombing, one villager had initially said that 213 villagers were killed, but in a later retelling, there were only thirteen people killed and then forty. Further erosion of the government's yellow rain story came about when a Yale University entomologist, whose expertise was in Southeast Asian bees, examined yellow rain samples and observed that they contained pollen from the native plants in the area. Based on the appearance of these samples, it was concluded that they were feces of bees. In one species of bees, present in the area, there is a tendency for the bees to swarm when they defecated, as a cleansing ritual, which could give the appearance of yellow rain falling. News of such chemical attacks soon stopped and many civilian scientists were convinced that the entire yellow rain incident was a hoax that was carried out by the military to increase funding for defensive chemical and biological weapons.

While a plausible alternative was given as to the cause of the yellow rain, the eye witness accounts while questionable, contradicted this theory.  To date, the question as to what caused the yellow rain has still not been satisfactorily resolved and may never be.

Trichothecenes and the Lack of Population Increase in Europe

Something very interesting concerning mycotoxins in fungi has recently come to light. Historical demographers, that is people that study populations, their distribution, density and other such vital statistics, have shown that long life and good health are a recent phenomenon. Before 1750, in England for example, the life expectancy of a member of the British peerage, that is one who has borne of noble birth, was only 36.7 years, a hundred years later it had risen to 58.4 years. Conditions were worse, and improvement slower among the common folks. However, between 1750 and 1850, the population of Europe almost doubled.

Before 1750 good health was a privilege of wealth, and not even then did all the rich enjoy it. A commoner was often underweight, stunted, sickly and occasionally deranged. They could not even imagine the feeling of well being that we have today. There was a constant battle with death, with results generally coming out in a draw. There were great fluctuations in populations because of mortality crises. After a mortality crisis, more people in a community would marry and they would marry younger and would eventually give rise to more children; so that if things were "normal", a community would tend to produce more babies than corpses. But then pretty soon another crisis would come, e.g., disease, famine, natural disasters, etc., and the gain in population would be wiped out.

The way in which populations were generally explained was in Malthusian terms. That is populations were self regulating; increases and decreases in birth rates were due to the availability of resources, i.e. food, so if there was a lot of available food there would be less death and more people would live to reproduce to increase the population while if there was not enough available food, there would be more deaths and fewer people would be around to reproduce and the population would decrease. This is very sensible, but in recent years it has been demonstrated, statistically, that this is usually not the case.

What has been suggested, more recently, was that it was an increase in fertility that was responsible for an increase in population, and a decline in mortality, between 1750-1850. There have been several reasons that have been proposed for the increase in fertility. One reason that I became interested was the idea that changes in the food supply was responsible for the increase in fertility. In a recent book, by Mary Matossian, Poisons of the Past, she puts forth the theory that it was the change in diet of Europe that was responsible for the tremendous increase in population.

During the 18th century, French adult peasants ate two to three pounds of dark bread a day, when they could afford it. The rich and affluent, which was less than 5 percent of the population, preferred white bread. In the Mediterranean Basin, the diet of the poor consisted of barley, buckwheat, wheat and after the 16th century also included corn. North of the Alps and Pyrenees the poor made their bread from rye or a mixture of rye and other grains, such as barley, oats and buckwheat.

LSD: As you should now know cereal stables such as these come from plants that are seldom free of molds, and it is Matossian's theory that it was the consumption of such contaminated grains that had damaged the immune system of the population of Europe that had relied on grain as their staple and was probably largely responsible for a short life span. T-2 and related trichothecenes are known to compromise an individual's immune system. It would be a change of diet that would begin to give individuals a longer life span. In addition, the change in diet, which included potatoes also affected the birth rate  For example, recall that there was an increase in the Irish population between 1750 and 1850. The reduced fertility in European was believed to be due to the consumption of Rye that had been contaminated with Ergot of Rye, a disease of Rye. (created st. Vitus dance as it's the precursor of LSD, identical to LSD, it IS ORGANIC LSD. . Villagers tripped for hours on end.)  This will be another one of our topics on mycotoxins. The change to a diet which consisted almost solely of potatoes rather than grains was responsible for the increase in population. Matossian presented a number of case studies to demonstrate that this had occurred, but unfortunately, we don't have time to cover all of these cases. SEE PURPLE MOLD

Mycological Terms

Aflatoxins: First mycotoxins discovered, in 1960, produced by Aspergillus flavus.

Aleukia Toxic Aleukia (ATA): Condition associated with consumption of trichothecenes mycotoxin, T-2, produced by Fusarium tricinctum. Some symptoms of condition include low white blood cell count, multiple subcutaneous hemorrhages and bleeding from nose and throat.

Aspergillus flavus: Species complex in which first mycotoxins, aflatoxins, were discovered.

Aspergillus fumigatus: Species of fungi producing mycotoxin/antibiotic fumagillin.

Fumagillin: Compound produced by Aspergillus fumigatus, an example of the fine line between something that is medicinal and a poisonous. Although classified as a mycotoxin, it is also effectively used as an antibiotic for amoebic parasites, in human as well as honeybees. However, dosage is very important here, if too much is used, it can be fatal.

Fusarium graminearum: Species associated with production of mycotoxin, vomitoxin, which causes pigs and other animals not to consume food when present. Pigs would initially eat food, containing toxin, but after a prolonged period of vomiting, refused to consume more food with toxin. Refusal to eat leads to weigh loss in animals.

Fusarium tricinctum: Species producing trichothecenes associated with alimentary toxic aleukia (ATA). First documented in 1940s, of USSR.

Kwashiorkor: Protein deficiency disorder of children in various overpopulated countries in the world.

Mary Matossian: Historian and author of Poisons of the Past. Believed that the population depression (meaning less births, not that everybody was SAD,) that occurred in Europe before 1750 was due to consumption of moldy grains that contained mycotoxins. It was believed that such mycotoxins reduced fertility and life span of individuals, and that it was not until a change in diet from grains to potato did the situation improve. Between 1750 and 1850, population of   Europe doubled as a result of change in diet.

ROTTEN GRAINS? HUH? But we cook all grains, cook them well.  You can't exactly wash the grain with bleach. But many molds grow in our homes, around sinks, toilets, on toothpaste tube, on the glass, the toothbrush. THOSE we can bleach.

Now, read up on the HARM THAT BLEACH DOES when inhaled! (Live link so click on it, come back.)  So ventilate the room, open window and door so there is a strong cross current! Wear gloves and have the kids and dog elsewhere! If you are washing with bleach, hang the clean garment on line, do not use dryer as that puts chlorine in your home's atmosphere. Bleach dissipates into air, leaving those articles when dry. Easy to do on a sunny day!

*  "There is a fungus amongus," is a hilarious phrase I heard at the Picwood Theatre on Pico Blvd in L.A. Calif back in the 50s when they screened "THE BLOB" starring Steve Mc Queen. Some boy behind me called it out and the entire audience laughed. Never forgot it.