|
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
Source: http://members.aol.com/jfoverlag/fungalbionics/blue2.htm
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'?
|
MYCOTOXIN-INDUCED
ATHEROSCLEROSIS
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.
THE
DIETARY MUSHROOM CONNECTION TO ATHEROSCLEROSIS
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.
THE
YEAST CONNECTION TO ATHEROSCLEROSIS
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.
FUNGAL/MYCOTOXIN-INDUCED
CORONARY ARTERITIS
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." www.totalwellness.com/definitions.htm |
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
OOOps! Ney!
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 http://www.numberwatch.co.uk/data_dredge.htm
) 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:
http://members.aol.com/jfoverlag/fungalbionics/excerpt2.htm
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. http://www.slv.se/templates/SLV_Page____2372.aspx
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. http://www.rense.com/general30/food.htm
I am not impressed by the Livsmedelsverket and as WHO now http://www.who.int/mediacentre/news/notes/2005/np06/en/index.html
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: www.thincs.org/unpublic.UR3.htm
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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