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Discussions between members

Feb-Mars 2005: Do mycotoxins cause atherosclerosis? 

Also: Comments about acrylamide and risks

Melchior Meijer
Uffe Ravnskov
Sally Fallon
Melchior Meijer
Bogdan Sikorski
Malcolm Kendrick
Bogdan Sikorski
Malcolm Kendrick
Melchior Meijer
Herbert Nehrlich
Bogdan Sikorski
Jacqueline Walker
Morley Sutter
Melchior Meijer
Uffe Ravnskov
Melchior Meijer
Dag Viljen Poleszynski
Björn Hammarskjöld
Uffe Ravnskov
Herbert Nehrlich
Malcolm Kendrick
Morley Sutter
Shane Ellison
Herbert Nehrlich

Melchior Meijer
Hi Uffe, I hope I'm not annoying you, but the following arguments - I can't find out who wrote them down, they paint the picture pretty well however - keep haunting me form time to time. Could CHD be a manifestation of overexposion to (or the result of a weekened defense against) fungi and their mycotoxins? I fail to shoot holes in the concept.

Article: Atherosclerosis Is A Stored Food-Related Disease

Atherosclerosis is the leading cause of death. Despite intensive research, its etiology remains unknown but there is no question that the etiology of atherosclerosis is in some way related to food. However, and quite obviously, it is not the food itself which is poisonous but rather something which man has done to food in his development and management of his food chain as a part of the creation of a complex urban industrialization.

Man had to store food to make that social machine function and in so-doing, he created food storage and food fermentation.

It was this manipulation of food which brought into the food equation the increased presence of the toxicogenic fungi whose toxins (mycotoxins) now permeate our food and our bodies and has given rise to the mycotoxin-induced diseases.

Atherosclerosis may be one of those diseases. Atherosclerosis is apparently food-related but not to the natural fresh food itself but possibly rather to the mycotoxins related to food storage. The techniques include the creation of toxicogenic fungal growth promoters such as concentrated oil and sugar products; grain fermentation such as making bread and beer; fermenting (curing) tobacco leaves; fermenting milk to make cheeses; etc. To make matters even worse, the Western diet lacks sufficient vegetables and fish, both of which are protective against toxicogenic fungi, and in the case of vegetable fiber, binds mycotoxins.
Atherosclerosis-Linked Risk Factors Are Not Etiologic.

Epidemiological studies have shown an association with such factors as hypertension, diabetes, hyperlipidemia, hyperuricemia, smoking, the "Western diet", and obesity. However, these positive associations are referred to as "risk factors" and not as etiological because, with the exception of what is vaguely described as the Western diet, over half of atherosclerotic patients have none of these risk factors linked to the pathogenesis of their particular arterial lesions.

Cholesterol/Lipids Are Not The Cause Of Atherosclerosis.

Atherosclerosis and hyperlipidemia are clinical entities generally accepted to be of unknown etiology. The postulated causative role of cholesterol and lipids has failed to be proven and, as Steinberg and Witztum (1990) point out, there is increasing movement away from viewing atherosclerosis as a primary lipid/metabolic process and towards finding a nonlipid etiology for its complex cellular nature.

It is a long overdue conclusion for as pointed out by Keys (1963), dietary cholesterol has absolutely no adverse effect in humans. Furthermore, cholesterol is a normal constituent of every living cell; cells can not be injured by their normal components.

The Atherosclerotic Lesion Is Granulomatous-Not Metabolic.

What Steinberg and Witzum see in their contemporary research, and Keys reported 30 years ago, is that lipids, cholesterol, and metabolic processes do not explain the complex inflammatory nature of the atherosclerotic lesion and there has to be something else to account for the "complex cellular nature of the atherosclerotic plaque".

As Virchow did over a hundred years ago, one must look at the underlying cellular pathology of the atherosclerotic lesion in order to climb out of the state of absolute metabolic confusion which now exists regarding the true nature of atherosclerosis.

The underlying cellular pattern of atherosclerotic lesions is one of delayed hypersensitivity. The cardinal finding of delayed hypersensitivity is the immunological granuloma, a type of host response which occurs only against microbes or microbial products such as Freund's adjuvant (dead mycobacteria). No such response has ever been encountered or induced in metabolic entities.

What the atherosclerotic plaque actually constitutes is a granuloma-like lesion flattened by the effect of the intraluminal arterial pressure exerted upon a soft tissue lesion located in the tight confines of the vascular wall.

There is a zone of central necrosis surrounded by macrophages many of which become foam cells, lymphocytes, plasma cells, mast cells, proliferated smooth muscle cells producing collagen which becomes the fibrous tissue encasement complexed with calcific deposition.

Plaque rupture with discharge of the necrotic centrum into the vascular lumen is complicated by thrombus formation with the dire consequence of obstruction of blood flow with resulting infarction of the tissue supplied by the particular artery.

Virchow's view that atherosclerosis is an inflammatory disease is in retrospect obviously quite correct. He perceived in his microscope that cholesterol deposits were secondary phenomena and not the cause of the inflammation.

Lipid/Cholesterol-Oriented Research Proves That Neither Lipids Nor Cholesterol Causes Hyperlipidemia or Atherosclerosis

The hyperlipidemic risk factor dominates atherosclerosis research which has been directed towards attempting to prove that excessive dietary intake of cholesterol and/or lipids causes the disease.

None of this research effort has provided proof that either cholesterol or lipids, or any other particular food, consistently causes atherosclerosis either in animals or in humans. Conversely, severe atherosclerosis occurs in cholesterol-free/fat-free dietary experiments in animals. Also, African tribes whose adults characteristically consume up to 8 liters of whole milk direct from the udder of their cows have the lowest blood lipids in the world and no atherosclerosis.

What the sum total results of the dietary experiments actually prove is that dietary cholesterol and/or dietary fats per se are not the causes of atherosclerosis.

The Fungal/Mycotoxin Nature of The Atherogenic Western Diet

However, there is something in the Western diet which is absent from the "Far East" and the "native" diets and which is the cause of atherosclerosis. The missing link is some items which has been overlooked even in the face of their obvious presence in the Western diet and relative absence in the Far East/native diets. These exogenous atherogenic factors present in the Western diet, which have been documented to cause hyperlipidemia, hyperuricemia and atherosclerosis both in humans and animals, are the various fungi and their unique toxic metabolites, the mycotoxins.

Fungi and mycotoxins are present in variable amounts in the food products of Western civilization such as the stored grains, particularly corn, fat-laddened meat of stored grain-fed animals, yeast-fermented beer, wine, bread, cheeses, and cured (fermented) meats and tobacco leaf.

The recent Harvard study of the dietary habits of 90,000 American nurses followed for 5 years revealed increased atherosclerosis occurred in those nurses who were heavy consumers of two items characteristic of the Western diet, cookies and bread (yeast bread) (Lancet 1993).

The so called native diets and the wartime restricted diets, which are known not to be atherogenic, lack these specific types of fungal/mycotoxic connections. The missing items of the diet are bread, beer, cheese and other fermented foods. Similarly, successfully employed anti-atherosclerosis dietary measures significantly reduce the degree of exposure to these fungal/mycotoxic factors.

The Protective Aspects of Hyperlipidemia

The fungal/mycotoxin observations also may contribute a different meaning of the relationship of hyperlipidemia to atherosclerosis; it is protective mechanism which binds mycotoxins and thereby greatly reduces the degree of their cytotoxicity. Hyperlipidemia also provides an effective degree of antimicrobial activity.

Hyperlipidemia is actually a protective host response to microbial invasion, particularly if associated with microbial toxins. The indiscriminate lowering of one's lipoproteins without understanding their purpose may be a disadvantage such as seen in the several major medical reports (WHO and Finland Long Term Study) which have documented that some lipid-lowering measures may actually result in increased atherosclerosis.

Hyperlipidemia Is A Signal Of An Impending Disaster:

Quickly Find The Cause and Quickly Remove It.

Hyperlipidemia is indeed an ominous finding and needs to be properly investigated as to its specific cause in each individual patient. If it is of fungal/mycotoxin etiology, eliminate that cause and not only do the plasma lipids return to their normal levels, regression of active atherosclerotic lesions will occur. (End stage fibrosis and calcification will not regress any more than they regress in the other immunological granulomatous diseases such as mycoses and tuberculosis).

The Antifungal/Anti-Mycotoxicity Nature Of Effective Anti-Atherosclerosis Agents

Critical to the documentation of the validity of a fungal/mycotoxin etiology of hyperlipidemia/atherosclerosis is the authors' finding that every single one of the quite heterogenous non-surgical measures proven to be effective in treating patients with hyperlipidemia and/or atherosclerosis share nothing in common except antifungal and/or antimycotoxin activity.

The Antifungal/Anti-Mycotoxicity Nature Of Effective Anti-Atherosclerosis Dietary Measures

Lastly, rather paradoxically for it is actually of prime importance, the atherogenic dietary factors to be avoided can now be clearly defined as those which contain mycotoxins, toxicogenic fungi, and fungal growth promoters such as cholesterol, lipids, yeasts, and sugars. The anti-atherogenic foods can be similarly defined in terms of their being antifungal and/or anti-mycotoxic such as green vegetables, beans-particularly soya, garlic, fiber, herbs, spices, fish, fatty acids, proteins and vitamins.

A Unified Etiologic and Therapeutic Concept Leads to more Effective Treatment and Cost Containment.

This unifying concept of etiology. preventive dietary measures and pharmacotherapeutics, provides both the patients and their physicians with a logical approach for both the prevention and the treatment of atherosclerosis as well as significant cost-reduction for those who are charged with paying the bill for the treatment of this common disease.

Uffe Ravnskov
The idea that mycotoxins should play a role in the causation of atherosclerosis is just as good as many other similar ideas. What we need is direct evidence. For instance, does mycotoxins produce atherosclerosis experimentally? Do atherosclerotic lesions contain mycotoxin? 
Most of us agree that inflammatory reactions are key events; the question is, what is starting them? It is also highly likely that a suboptimal diet lacking essential components or mixed up with toxic substances may play a role, as it probably does in most other diseases.
However, as I am not familiar with the literature on this subject, I have submitted your quest to the group.

Sally Fallon
On the subject of mycotoxins, this is where the proper preparation of grains and nuts is so important, because the traditional processes (soaking, sprouting, sour leavening, etc) get rid of the mycotoxins.  Also the new GMO grains are more prone to mycotoxins.

Mycotoxins are potent liver poisons so it would be no surprise that they can contribute to heart disease.  Anything the depletes the body of nutrients is a potential cause.

Melchior Meijer
In that case I post some more data provided by the same unknown author. It might be Constantini, a former WHO scientist who wrote a book on the subject. Since fungi are everywhere, I suggest that if their toxins play a role in the pathogenesis of CHD, the host must have a weakened defense against them. I find it striking that most medications that seem to have some anti-atherogenic effect were originally discovered/designed as potent fungicides (aspirin, the statins, and even folic acid, retinol and beta carotene kill fungi). Once again, I wonder if a statin would show the same 'cardioprotective' effect if administered IV (thus bypassing the gut, where fungi make their toxins).

Just a thought: if this is a fit concept, CHD might be one of the diseases associated with a too sterile environment. Let us assume that an optimal gut flora is able to keep 'unfriendly' fungi in check. Let us assume that our guts were used to get a lot of 'probiotic' help in the old days, for example from bacteria in foods. Then only such a thing as the introduction of Pasteurization (around 1910?) might already have had adverse consequences for the 'milieu interieure'.

Pure and utter speculation. I hope someone in this forum has a substantial arguments. Are mycotoxins found in atheroma? Would not finding them there make them 'not guilty'?


A number of studies have indicated that there are unknown factors present in hyperlipidemia, attached to the low density lipoproteins, that are responsible for the smooth muscle cell proliferation/production of new connective tissue which is characteristic of atherosclerosis (Wissler 1979).

Mycotoxins, which characteristically bind to lipoproteins, are documented not only to cause these changes but to cause atherosclerosis in humans and animals.

Cyclosporin-Induced Atherosclerosis In Humans 

Betina (1989) points out what is well known to mycologists, cyclosporin is actually a mycotoxin, a fungal-derived secondary metabolite, which is toxic to the immune system. Its extensive use in preventing organ rejection in transplantation has given us an unexpected somber side benefit of discovering that it causes accelerated atherosclerosis in almost all long-term survival organ transplantation patients.

Fyfe (1992) has compiled the published findings to date of transplant atherosclerosis. Based upon analysis of clinical risk factors, pathological features of endothelium, macrophages, lipoproteins and vascular smooth muscle cells, and the known pathophysiological mechanisms, Fyfe concluded that transplant atherosclerosis appears to result from a "response to injury" of the endothelium, similar to naturally occurring atherosclerosis.

Ergot-Induced Atherosclerosis-Type Clinical Manifestations

In humans, ergots induce spasm, stenosis and/or thrombosis of the coronary, carotid, aortic, renal, and peripheral arteries. Ergotinduced entities include angina, myocardial infarction, arrhythmia, carotid artery occlusion, stroke, intermittent claudication & gangrene.

Fumonisin-Induced Hyperlipidemia and Atherosclerosis in Primates

Fincham et al (1992) fed primates a low fat diet containing the mycotoxin fumonisin and induced hyperlipidemia and related blood lipid findings characteristic of those found in human atherosclerosis.

In a personal communication with Fincham, he has indicated that autopsy of one of the fumonisin-dosed primates which died during the experiment demonstrated severe generalized atherosclerosis identical in appearance to human atherosclerosis.

Haschek et al (1992) in their characterization of fumonisin toxicity in orally and intravenously dosed swine, found that blood levels of cholesterol were increased.

Fumonisin is a recently discovered Fusarium mycotoxin which is present in high concentrations in all corn kernels thus far examined. Corn is the principle grain used in the Western diet and is also a major part of feed for animals fed for the marketplace. Corn is generally not found in native diets except for that of Indians of the Americas. Data relative to the incidence of atherosclerosis in Indians is limited and confusing in that most now eat a Western-type diet rather than traditional Indian food.

Sporidesmin-Induced Hyperlipidemia/Vascular Disease.

Lipid deposition-type vascular lesions associated with very high levels of LDL occurs in New Zealand sheep exposed naturally or experimentally to the mycotoxin sporidesmin produced by a fungus common in the pasture lands of that country (Taylor 1971). As in human atherosclerosis, cholestyramine provides therapeutic benefit. Zinc is also of benefit.

T-2 Toxin-Induced Cardiovascular Lesions and Hypertension

Wilson et al (1982) found that rats given T2 toxin developed hypertension associated with microscopically severe cardiovascular abnormalities. The pattern of the findings were such that it appeared that T-2 Toxin, which often does significantly contaminate foodstuffs, may represent an important etiology of hypertension and its cardiovascular lesions in both animals and man. The relationship of hypertension to atherosclerosis is well known; the fact that both share an etiologic group of agents explains the relationship.

T-2 Toxin-Induced Coronary Artery Disease

Yarom et al (1982) studied the nature of the T2 toxininduced pathology in the hearts of rats and reported that the lesions consisted of interstitial edema, focal cellularity and damage to single or groups of myocytes. The small intramural coronaries were constricted, swollen and sometimes disrupted. After 7 days, most of the changes subsided. In rats killed 1 or 2 months after the last of 10 daily injections of T2 toxin, cardiomyopathylike changes were seen with hypertrophy, focal fibrosis and abundant cellularity especially in the subendocardial regions of the left ventricle. These findings, although nonspecific, indicate that T2 toxin is cardiotoxic and are quite provocative since subendocardial fibrotic changes are commonly encountered in human atherosclerotic hearts.

T-2 Induces Coronary Artery Damage and Increased Mast Cells.

Yarom and Yagen (1986) reported the effect of T2 toxin on the ultrastructure of coronary microvasculature. The capillaries were most severely damaged and were often disrupted. The plasma membrane of endothelial cells seemed to be the first structure affected. A direct cytotoxicity of T2 toxin to the myocardial capillary lining cells seems to be the pathogenic mechanism of injury. The abundance of mast cells in several of the hearts examined suggests a role for their vasoactive products in the genesis of the capillary lesions.

The presence of mast cells in atherosclerotic lesions in humans has been had no previous explanation; here then is proof of a mycotoxic etiology for this unique finding. Lipids and cholesterol do not induce the recruitment of mast cells.

T-2 Toxin-Induced Microvasculitis and Mast Cells

Yarom et al (1987) in their study of cutaneous injury by topical T2 toxin found that a microvasculitis was produced with involvement of microvessels and mast cells. Damage to the microvasculature was characterized by mononuclear cell infiltration, with many degranulating mast cells.

Ultrastructurally, as is the case in atherosclerosis, the endothelial cells were the earliest sites of change. Another early effect of topical T2 toxin was an increase in number and degranulation of mast cells.

The fact that a micovasculitis occurs in the pathogeneisis of atherosclerosis is not generally appreciated since once the pathologists sees atherosclerotic lesions, little attention is paid to the condition of the microcirculation.

T-2 Toxin-Induced Endothelial Damage and Smooth Muscle Cell Proliferation

Yarom et al (1987) studied the effect of T2 toxin on rat aorta and found that T2 toxin showed endothelial cell damage, accumulation of basement membranelike material in the intima, and activation with proliferation of smooth muscle cells.

Interestingly, three or more weeks after the last injection of 0.3 mg/kg T2 toxin the endothelial cells were normal but an excess of fragmented intimal basement membranelike

material persisted and smooth muscle cells were still activated. Note the presence of the "membrane-like material in the intima for it is what Virchow also saw in human lesions.

These changes are characteristic of the early changes of atherosclerosis.

Aflatoxin-Induced Small Vessel Disease

Jaskiewicz et al (1988) in their preliminary studies on the toxic effects of Aspergillus-produced cyclopiazonic acid alone and in combination with aflatoxin B1 in nonhuman primates found that the mycotoxin caused significant damage to the small blood vessels.

Cyclopiazonic Acid-Induced Small Vessel Disease

The Aspergillus flavus mycotoxin cyclopiazonic acid (CPA), induces in nonhuman primates significant damage to the small blood vessels (Jaskiewicz et al 1988).

Citreoviridin-Induced Myocardial Ischemia.

Nishie et al (1988) reported that citreoviridin, a mycotoxin isolated from Penicillium citreoviride administered to animals, had dramatic cardiac ischemic effects with initial lowering followed by flattening and finally inversion of the T wave of ECG. These are the type of changes seen in humans with coronary atherosclerotic disease.

The interesting human application of the Nishie report is that there are clinical entities in humans of silent myocardial ischemia, myocardial infarction without coronary artery obstruction, long term angina pectoris without myocardial infarction, etc., which are etiologically entirely unexplained. The burden of proof would appear to have to shift towards proving that mycotoxins are not the cause of these functional cardiovascular problems. The nature of the ergot-induced vascular occlusive phenomena appears to backup this new understanding of the role of mycotoxins in cardiovascular disease.


Mushrooms (Edible) Induce Vascular Smooth Muscle Cell Proliferation, a Characterisitic Finding in Atherosclerosis

Toth and her co-workers (1985) reported that phydrazinobenzoic acid, a metabolite produced by the edible and commonly consumed mushroom, Agaricus bisporus, causes severe atherosclerosis-like smooth muscle cell proliferation in mice. The mice were fed the mushroom metabolite for a period of 20 weeks which is consistent with the concept that it is the long term dietary pattern in the Western diet which correlates with the incidence of atherosclerosis. In the case of humans with atherosclerosis, there is no published data relative to the effects of chronic mushroom consumption on human health. It is also important for the mushroom-consuming public to understand that the mushroom is not a vegetable but rather the fruiting body of a fungus whose major form of existance is hidden in the soil layer upon which it erupts to cast out its spores.


Baker's/Brewer's Yeast (Bread, Beer, Wine, Yeast Tablets)

The recent Harvard study of the dietary habits of 90.000 American nurses followed for 5 years revealed increased atherosclerosis occurred in those nurses who were heavy consumers of two items characteristic of the Western diet, cookies and bread (Lancet 1993). The bread is of course a Baker's yeast fermentation product and many cookies have yeast added either for raising the dough or flavor or both. The sugar and fruit (fructose) in cookies are well known to elevate human blood cholesterol levels and to contribute to obesity problems, a well known risk factor for atherosclerosis.

The grains used in cookies and bread not unusually contain toxicogenic fungi and mycotoxins and the moisture content of these finished food products tend to promote further growth of these fungi (stored bread and cookies get moldy).

Baker's Yeast Inhibits Liver Detoxicating Function

Double stranded RNAs are present in Baker's yeast, S. cerevisiae. When Masycheva et al (1988) administered these yeast-derived RNAs to mice, they observed that they had an inhibitory effect on the liver detoxicating function.

This ability of Baker's yeast to decrease the efficiency of the liver to detoxify toxins points to an enhancing effect of Saccharomyces on the toxicity of mycotoxins in general, a situation which hardly can be considered desirable in the dietary intake.

Baker's Yeast is Itself Atherogenic.

Zhikhar et al (1990) investigated the metabolic efficiency of baker's yeast fed to rats. Atherosclerotic-type morphologic changes were observed in the aorta and did not depend on the amount of the yeasts fed to the animals. The kidney became infiltraed with lipids and cholesterol.


Candida-Induced Coronary Arteritis

Murata and Naoe (1984) found that they could induce coronary arteritis and thrombotic occlusive aneurysms in mice by injecting an extract of Candida albicans isolated from a typical patient with Kawasaki disease. It was interesting that five daily injections of the Candida extract produced no lesions but a second round of five injections 5 weeks later induced severe vascular lesions of the coronary arteries as well as to a lesser extent, the renal and mesenteric arteries. The pattern was similar to the distribution found in humans with Kawasaki's disease.

One can only speculate what might be the appearance of such Candida extract-induced vascular lesions in humans exposed to long term interrmittant Candida colonizations over a period of many decades. There is another possibility suggested by the experiment. Could the fungal overgrowth which occurs as a result of penicillin therapy be related to the well known fact that penicllin is the most common known cause of vasculitis.

When one pursues this lead further, one finds that there are a number of reports correlating fungi as the etiology of microvascultitis. This correlates quite well with the fact that all of the diseases postulated by the author to be of fungal/mycotoxin etiology have the finding of microvascultis as an important part of the pathology.

Bogdan Sikorski
May I suggest that you have somewhat confused at least two families from one Kingdom, i.e. fungi.

"Fungi belongs to the kingdom of heterotrophic single-celled, multinucleated, or multicellular organisms, including yeasts, molds, and mushrooms. Previously classified in the plant kingdom, fungi are nonmotile, like plants, but lack the vascular tissues that form the true roots, stems, and leaves of plants. Unlike algae or plants, fungi lack the chlorophyll necessary for photosynthesis and must therefore live as parasites or saprobes. Typically they release digestive enzymes onto a food source, partially dissolving it to make the necessary organic or inorganic nutrients available. Some fungi are pathogenic to humans and other animals. Some molds, in particular, release toxic chemicals called mycotoxins that can result in poisoning or death."

OK, with the help of the above info lets concentrate on the baddies - moulds.  In contrast, mushrooms are mostly beneficial to humans as a source of nutrients and as complementary medicines, although clearly they also can be toxic!

Yes, moulds indeed produce some very nasty toxins, most notably aflatoxin, but they also produce a huge range of compounds which include: a statin, carotenes, and of course a range of so-called antibiotics, i.e. penicillins, as well as those digestive enzymes which are widely used in food processing and fermentation.
Most of those toxins are produce to protect themselves from the attack by other microorganisms. Humans have managed to harvest few of those for our use in a similar endeavor, with some success, particularly in terms of antibiotics, although as we know even those weapons are not very user friendly.

As you suggest, the trick is in keeping the balance, and Sally has shown in her book how to go about it using simple foods humans have enjoyed for .....Most people with normal, healthy bacterial flora have nothing to fear from a range of pathogens to which we are exposed on a daily basis, including in food.

Malcolm Kendrick
I'd better get off to France and tell them to stop eating all those damned mushrooms. I know they have a very low rate of CHD, especially in Southern France where they eat mushrooms and truffles all the time, but just imagine how low their rate of CHD would be if they could avoid fungi altogether.

Bogdan Sikorski
You "poor", malnourished English - you would not know a good mushroom if it fell on you.
It is a constant amazement to me and my family, when we are looked at strangely by concerned "original ozzies", when we are walking with bags full of mushrooms. Once, when we were having a barbie with freshly picked (no name in English for that one) someone protested that I am about to poison my (then little) girls.
C'mon, about time you joined those in the know!
Not that it will make any diff to your health, unless we consider a bucket of butter that normally is used to fry them!

Malcolm Kendrick
Bogdan, Are you a New Zealander?..... I am Scottish, not English, and so you have mortally insulted me. You can take my life, but you can never take my freedom, remember Bannockburn. William Wallace and all that.

We don' t eat mushrooms in Scotland, because the Scottish diet has been scientifically designed to contain no healthy nutrients vitamins, or anything that does not have a high GI index or has not been stuffed with e-numbers. We are Gonzo nutritionalists - existentially attracted to suicidal behaviour. Long-live the deep fried Mars Bar and - almost incredibly - the deep fried Pizza.

If you ever visit Scotland, bring your own food.

Melchior Meijer
Dear Malcolm and Bogdan, Thanks. Some mycotoxins, whether produced by molds, yeast of mushrooms, are clearly atherogenic (f.e. cyclosporin), while others maybe are not (like statins, although they do complicate atheroma). The wonderful mycotoxin ethanol does clearly not harm the French, nor do their mushrooms, nor do their wonderful moldy cheeses. But such observations do not invalidate a possible role for myctoxins in the etiology of CHD. Maybe the french do something that gives them an extremely vivid gut flora (I had a french girlfriend who definitely fitted this picture), which protects them. Maybe 'their' mycotoxins happen to be non-atherogenic.

And how about frequent over exposion? Scottish, mold laden rye versus largely mold free wheat on Crete? For me it's too early to dismiss this item.

Herbert Nehrlich
Bogdan, Malcolm and Skeptics: Don't forget that the poor malnourished English were the ones that "invented" the breakfast fit for kings, all Humpty-Dumpties, all the king's men, women, children.....Bacon and Eggs. Only the horses might not benefit.
Mushrooms are a favourite in my household, sadly no wild ones can be found. I used to worry about "mushroom clouds". Are mushrooms under a cloud now? Rumours have it that butyrated mushrooms are healthful.

Bogdan Sikorski
But in AUS, New Zealanders are equally regarded along with Poms or Scots! Better stop now.
Surely, the Pizza must be with farmed mushrooms?! In a very unlikely event of me visiting Scotland, I will show you how one can live of land, without eating a single plant produce.
Oh, by the way, I know what happened to that poor WW. Never trust ......, be it malnourished or otherwise!

Jacqueline Walker
Hi, A few comments on this burgeoning controversy!

Of the potent properties of some other mycotoxins e.g. aflatoxin, ergot and fusarium there is certainly no doubt. However, note that these effects are quite large and obvious.

In the original piece put forward by Melchior, I also thought there were quite a few 'wild assumptions' e.g.
[Re: Atherosclerosis is the leading cause of death. Despite intensive research, its etiology remains unknown but there is no question that the etiology of atherosclerosis is in some way related to food.]

Is there no question? Why should it be related to food? Has this really been conclusively demonstrated? If we doubt the 'cholesterol hypothesis' then aren't we really doubting the 'it's all down to the Western diet hypothesis' since that is, according to the orthodoxy, one and the same hypothesis?

[Re: The techniques include the creation of toxicogenic fungal growth promoters such as concentrated oil and sugar products; grain fermentation such as making bread and beer; fermenting (curing) tobacco leaves; fermenting milk to make cheeses; etc.]

Here there are confusions between 'harmful fermentation' (spoiling) and other kinds e.g. 'fermenting milk' which could be beneficial lacto-fermentation and likewise so could grain fermentation if done properly as Sally pointed out.

[Re: Fungi and mycotoxins are present in variable amounts in the food products of Western civilization such as the stored grains, particularly corn, fat-laddened meat of stored grain-fed animals, yeast-fermented beer, wine, bread, cheeses, and cured (fermented) meats and tobacco leaf. ]

These are assertions really and can be contradicted e.g. if yeast-fermented wine is so bad, why does it correlate with a heart-protective effect? Why should fat-laden meat be full of mould? Surely cured meats are 'cured' with chemicals and er, salt, which rather inhibits the spread of mould and so on.

[Re: The recent Harvard study of the dietary habits of 90,000 American nurses followed for 5 years revealed increased atherosclerosis occurred in those nurses who were heavy consumers of two items characteristic of the Western diet, cookies and bread (yeast bread) (Lancet 1993).]

Let us not forget that the Nurses' study is a well-known 'data dredge' (see John Brignell's site ) and a guaranteed paper factory. With that many nurses and that many different food stuffs there are bound to be some associations cropping up!

Attempts are often made to link yeast in foods such as bread to human illnesses particularly those caused by candida. However, my problem with this has always been - surely the high temperature baking of the bread (200C +) kills the yeast stone dead? It must do, since our home experience of making pizza and brioche shows that it is pefectly possible to kill the yeast and thus have a heavy unappetising product simply by incubating the rising dough at just ever so slightly too high a temperature.

No, the candida is already in us - in our gut say - at the lower end, having arrived there from the outside via spores - and it is the refined carbohydrates providing the excess sugars which then nourish the yeasts and enable them to grow.

[Re: The so called native diets and the wartime restricted diets, which are known not to be atherogenic, lack these specific types of fungal/mycotoxic connections. The missing items of the diet are bread, beer, cheese and other fermented foods. Similarly, successfully employed anti-atherosclerosis dietary measures significantly reduce the degree of exposure to these fungal/mycotoxic factors.]

I'm afraid I'm not old enough to know through direct experience what people did and did not eat during the war (WWII) but from what I've heard about they were often most deprived (in the UK say) of eggs, bananas and other tropical fruit, butter and sugar and were restricted in the amount of meat they were allowed. On the other hand they did have bread because my father seems to have spent the war eating bread and dripping and (presumably less often) bread and jam.

Morley Sutter
Jacueline: Beautifully analysed and stated.  How refreshing to read a critique rather than a promotion.

Melchior Meijer
Hi Jacqueline, I completely agree with everything you say (I'm sorry). There are a lot of 'wild assumptions' in this texts, but also some clever things that come back at three in the night. So far it was the 'best' I could find on the subject. I still think the idea needs proper investigation. If, for example, it is true that one can induce human like atherosclerosis in chimpansees by feeding them corn contaminated with 'normal concentrations' of a 'normal mold' for a few months, then I get nervous. Maybe it's bullshit, maybe not. So I keep searching and I hope to find some real data. By the way, it was Constantini. Parts of his book are published here: 
Unfortunately it reads like a mixture of astrology and science.

Uffe Ravnskov
I would like to supply Jacqueline´s critical comments to the unknown author. His ideas remind me of the acrylamide scare. The crucial question is the dose. Most of the toxic substances that we are exposed to by eating plants, moulds and fungi are present in very small amounts. All mammals have a liver and two kidneys and they are are very effective in neutralising, metabolising or eliminating such molecules. For instance, a single dose of a poisonous substance that is secreted by the proximal tubules is practically eliminated after less than 24 hours. To study the effects of such substances by feeding rats and other innocent creatures in amounts that are thousand times greater than in their natural food, or by putting them into cell substrates in similar doses, is therefore senseless (but an easy way to increase one´s list of scientific publications).

It reminds me also about the warnings against mushrooms a couple of years ago. In a remote laboratory researchers found that these fungi, if they grew too near a highway, contained a lot of mercury and we were therefore advised not to eat mushrooms more often than a couple of times per year. However, a wise German researcher measured the intake of mercury from mushrooms in test individuals and found that nothing was taken up; all of it was recovered from the faeces.

Your suggestion that the paper was written by a WHO researcher is likely. In the offices of WHO they have just come up with a warning against acrylamide. I haven´t read their report but I guess it goes something like:

2 mg acrylamide per kilogram bw per day and a mouse will die from cancer
An average human being will therefore die from cancer by eating 140 mg acrylamide per day
The average citizen of Scareland eats 50 microgram acrylamide per day
Thus, the total acrylamide consumption in Scareland (10 million inhabitants) is 500 g  per day, or 500000 mg. Therefore 3571 Scarelanders (500 000/140) may die from cancer every year because of eating acrylamide.

But you are of course right – we should not discard any new theory without looking at the evidence. The problem is that he does not give references to his claims. Do you know them and if so, could somebody send these papers?

Melchior Meijer
Very good idea. I will try to trace and contact Constantini and ask him for solid references. 

Dag Viljen Poleszynski
If you buy The garden of Eden longevity diet by Costantini, Wieland and Qvick, you'll find 46 pages of references. There is undoubtedly more than that (my version is from 1998), but it's a good start! Interestingly, the diet is very close to a paleo diet plus herbs and nutritional supplements...

Björn Hammarskjöld
The acrylamide business in Sweden 2002 was a not very well presented dubious research that got a lot of media exposure.

They found, among other things, that coffee contained 20µg acrylamide per liter of coffee. Mice has an LD50-dose of acrylamide of 100 mg/kg bodyweight (rats 150 g/kg). Neither of these species are used to grilled or roasted food so humans probably have a higher LD50. But 70 kg person needs to drink 7 g/20 µg/L = 350 000 L (= to 350 cubic meters) of coffee to ingest a LD50 dose of acrylamide.
Different fried food (Stekt mat, blandade ingredienser) had a median value of 40 µg/kg according to Livsmedelsverket. When I checked their figures the median turned out to be just 30 µg/kg as they had used Excel spread sheed as a median calculator. Included in the list were four values of <30 µg/kg of a total of nine values. The Excel spread sheet does not include the four <30 as numerical values so the rest of the five values (30, 39, 39, 42 and 64) had a mean of 39 which they (wrongly) rounded up to 40. All of their mean values were wrong when I checked them. 

Still, the LD50 of mice is 100 mg/kg, humans probably has a higher LD50 than 100 mg/kg, the acrylamide values are low, usually less than 1 mg/kg. Acrylamide is rapidly decomposed in water. 

I am not impressed by the Livsmedelsverket and as WHO now
goes out with similar information it is unfortunate.

But one thing is good, acrylamide is made from carbohydrates and asparagine at high temperature, this means that if you eat less carbohydates you can avoid acrylamide. In other words, eat more fat and protein and eat much less carbohydrates! I.e. Hunter's diet again!

Uffe Ravnskov
How come that our so-called authorities are so vigilant about acrylamide, the carcinogenic dose of which is about 3000 times the average human consumption (and this amount should probably be eaten every day for 20 years to produce cancer), whereas no one care about the cancer risk associated with statin use, although all animal tests have resulted in cancer after doses similar to those used in clinical practice?*

Newman TB, Hulley SB. Carcinogenicity of lipid-lowering drugs. JAMA 1996; 275: 55-60. 
See also:

Herbert Nehrlich
Well, I have said it before and many others have, most notably a patient of mine many years ago. It all comes down to money. Reminds me of the speed camera debate in the BMJ right now. Talk about saving lives. Just keep talking.

Malcolm Kendrick
It is not just money. The concept of risk, and what people can be made frightened of, or are frightened of, is something that I have been interested for some time.
Friends, that we go skiing with, always insist on their children wearing crash helmets whilst skiing. I do not. These same friends were happily driving along the German autobahn at around 200kph to get to the ski resort. I kept to a much more sedate 160 kph at all times

The risk of serious injury, or death, is hugely greater in a car crash than in a skiing accident, but when I attempt to point this out a 'barrier' of some kind springs up. They just don't' want to know.
The reality is that they are perfectly happy to expose their children to a car crash risk which must be hundreds, or thousands of times more likely than a skiing injury. Why?

It is because our perception of fear is wildly out of step with the actuarial risk. This is why people play the Lottery. They see a huge win, at a small cost, and never really figure the odds. Ask them to take risk is the other direction i.e. they might lose a lot of money (very small chance) to gain a moderate amount of money (very good chance) and they won't take it.

Equally, once people feel comfortable with something e.g. statins - widely used, widely prescribed - their perception of risk diminishes to the 'don't want to know' level. This has nothing to do with actual risk. When HIV first came along, people were terrified of this 'unknown' killer. Now that everyone knows what it is, the levels of fear have reduced to almost zero - whilst the chances of catching HIV have steadily increased.

Acrylamide fits into the 'never heard of it, thus must be scary,' category of human thought. It is always easy to get people to fear things they don't understand - haven't heard of - seem alien, or different e.g. GM crops, nuclear power, the 'Ozone hole' (where did that go, by the way). Trying to get people to be frightened of familiar, trusted, things (or people) is much more difficult. People like things to be 'good' or 'bad' - 'safe' or 'scary.' Once something has been filed in the human mind as 'good and safe' - you will always find it extraordinarily difficult to evince a change of thinking. Statins are, for most people, safe and good. Safe enough to put in the water, good enough for us to think of doing so.

It's not all about money. It's about the way our brains are wired up. Helpful in the past, but not much use in our complex, abstract, world when it comes to determining risk.

Morley Sutter
You are right: people’s perception of risk is not well correlated with actual risk.  I have been interested in risk for quite a few years.  One of the best analyses of the problem was published in Science,1969, 165: 1232-8, Starr, C.  Social benefit versus technological risk.  He made several fascinating points.  First was how one expresses risk is important.  He says that we live in time and that since we all must die and live aproximately 1 million hours, the risk of dying is 1 per million man-hours (it probably should be person-hours but we were less politically correct in1969).  He further argues that unless the risk is ten times that inherent in mere existence, we don’t  pay too much attention too it.  He also points out that the risk of flying, if expressed per man-hours is very similar to that of driving a car except that we spend a lot less time flying than driving.
He also points out that people accept more risk when they initiate the activity compared to when the activity is imposed on them. The whole area is fascinating.

Shane Ellison
You stated: "However... I would contend that it has never been proven that raised glucose levels in the blood are independently damaging."

Could high glucose lead to advanced glycated end (AGE) products?  High glucose levels might initiate reactions between glucose and biological amines.  This non-enzymatic reaction, discovered by Maillard in the early 1900's, could prove damaging.  It is hypothesized that AGE products are showing to bind to collagen, thereby increasing vascular and myocardial stiffness, endothelial dysfunction, altered vascular injury responses and atherosclerotic plaque formation.  If this is true it would help explain why diabetics have an increased risk of suffering from heart disease.  It would also explain the rise in heart disease worldwide - sugar (sucrose) consumption.  And it might explain why plaque buildup occurs in the coronary arteries 90% of the time...Collagen exposure due to mechanical stress, thereby increasing AGE/collagen crosslinking??  Just a guess..I think they even pinpointed and named an AGE receptor - RAGE.  Apparently it is found on collagen??  Just thinking out loud here...

Herbert Nehrlich
[Re: How come that our so-called authorities are so vigilant about acrylamide, the carcinogenic dose of which is 3000 times the average human consumption, whereas no one care about the cancer risk associated with statin use, although all animal tests resulted in cancer after doses similar to those used in clinical practice? Uffe ]

Because the public is begging for statins - not acrylamide.  Though, if we ran a few commercials and sent some good-looking acrylamide sales reps to the office's of medical doctors then acrylamide would be in business.  We could ensure sales with statistical contortionists and spokesmen like statin worshipper Steve
Nissen in Cleveland.




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Published on January 7, 2003