Hopefully you re-educated them on what is allergy and what is not?

> I do have a comment to your assertion that diabetes can be caused by
> toxins…but

I did not say it can be caused by toxins - you did:-))
I said it needed special circumstances to have toxin involvement.

Duncan - I find this argument futile. I feel I stated how I see it
clearly enough, and spent many, many hours doing so in the most
reasonable way I cold.

I have to choose where I spend what time so I can only hope something I
said was useful somewhere.
Namaste,
IRene

Most had "environmental sensitivities", "multiple chemical
sensitivities" or in other words higher sensitivity than normal,
always accompanied by something like allergic and/or cold symptoms,
and they usually also a slack immune reponse due to the toxin load
and were catching every bug that went through the neighbourhood.

Point is, I’m where the rubber meet the road, treating clients who
don’t use the ight terminology,so unless a client tells me they had
been tested and were "found by tests to be allergic" to specific
substances, I don’t believe it any more right off the bat. Even the
clients who come with a list of "allergies" the Vega Testing unit
coughs up, are mistaken, as is the Vega operator.

I do have a comment to your assertion that diabetes can be caused by
toxins…but

> Only if the immune system is already skewed to TH-2.
> Not otherwise. There is more to it than toxin load. It needs that
PLUS
> prior immune system skewing.

I think arsenic exposure might be an exception to the rule.

What I got out of it is that toxin load causes mitochondrial
disorders when the disorders are not of genetic origin. Obviously
this makes a good case for controlling toxin load to cure the vast
majority of mitochondrial disorders, which are earned rather than
inherited, and diabetes and cancer both make the list.

> It’s important to read scientific papers with care to detail, and
not to
> jump to conclusions from what is said.

I’ve cured a case of inclusion body myositis, a wasting disease with
no cure that kills the client in about four years, by jumping to
these same conclusions. Maybe I can increase my effectiveness
generally, but I hit 100% that time
> I have a master’s degree in immunology and imunopharmacology.

Oh, then you’ll love Haltiwanger’s document. I found it fascinating.

We have had technical details in our discussions and that is very
inappropriate if we are not calling a spade a spade.
IMO.

> A lot of people have sensitivity reactions to aflatoxin,
> including anaphylaxis,

Toxic shock is also life threatening but is not anaphylaxis.
It needs to be differentiated (IMO) from a bona fide allergic response
to foreign protein. I have said that before. I stand by it.
The treatment is also different depending which you are seeing.

I’m sorry I can not smear them into one.

Only if the immune system is already skewed to TH-2.
Not otherwise. There is more to it than toxin load. It needs that PLUS
prior immune system skewing.
Sadly most people are skewed as children to TH-2 - by the vaccinations
pumped into them. that is why we mainly see TH-2 chronic illness rather
than TH-1.
But that skewing can be reversed by homeopathy and then you can not
induce illness the same way as is being assumed here.

There is no such thing there as you claim to suggest diabetes is caused
by mitochondrial defect. The words they use are:

"Clinical: Point mutations associated with wide variety of syndromes"
and they include diabetes in a list they have there.
There’s a big difference between "caused by" and "associated with".
Nor does any such association mean all type 1 diabetes is so associated.

It’s important to read scientific papers with care to detail, and not to
jump to conclusions from what is said.

> I do hope you catch the drift of my nonsense now
????

says who

> and I’ve recently
> posted some references for you that links the two.

it failed to link them.
I have a master’s degree in immunology and imunopharmacology. It’s a
very complex subject and a growing one but there is a difference between
cell level inflammation and immune systenm generated inflammation that I
think you have not seen.

Chronic blood coagulation is also at cell level. The fatty acids with
the problematic eicosanoid results (AA) are located in the phospholipid
layer of cell walls. Enzymes split them off, and the eicosanoids so
formed include prostaglandins and thromboxanes (split by cyclo-oxygenase
enzymes) - not just the leukotrienes you listed (split by lipo-oxygenase
enzymes). The prostaglandi 2 series from AA is ALSO inflammatory - while
those from EPA are anti-inflamamtory.
The AA ones *directly* act to inflame by affecting platelet aggregation
and/or constricting blood vessels (Causing high BP) or by affecting
intraglomerular pressure in the kidneys (causing kidney damage from high
pressure and low flow).
YEs it starts with the cell wall, and no it does not involve the immune
system.

No. The skewed immune system is a *prerequisite* to allergic response.
For an immune system response to an *allergen* you also need a specific
antibody to have been developed in the bone marrow - in response to
foreign protein in the blood stream - all at a prior date to allergen
challenge.
The inflamamtory reaction *you* are describing with leukotrienes is
nothing to do with allergens or the immune system. There is no allergen
involved - no pollen or peanut protein or whatever.
There is only an inflamamtory cell level response where leukotriene
directly releases the SAME kind of chemicals that the immune system woul
release IF it was involved.
It’s a short-cut to asthma symptoms that do NOT involve the immune
system or any allergen such as pollen etc.

It’s not a true allergic response - it has the same asthma symptoms but
it is an inflammatory response at cell level.

Namaste,
IRene

No apology needed - you are sending refs that have nothing to do with my
comments (which are missing here, you did not quote them, much less the
context) :-))

> This Pubmed search (linolenic acid conversion to DHA) turned up a
> lot of work; ……………
……….
> So, the research is in agreement that plants don’t supply
> adequate omega-3 fatty acid, ESPECIALLY DHA.

Well yes of course. I did not question that. I have always advocated
fish oil supplements and AVOIDING plant oils other than extra virgin
olive oil :-)))

What you said was that nuts specifically are bad. None of this research
verifies that contention:-)

> Chilton’s book — I have a copy — doesn’t disrespect nuts

But you did in your post and that was my complaint :-))

I disagree. It is included in the word "reasonable" that one is not
going overboard:-))

You presented no anti-nut research……

Namaste,
IRene

I think your first mistake in commenting my dicussion with Liz is
not accepting as a given that when people talk about their
‘allergic reactions’, they nearly always mean they have
sensitivity issues, which are really more like ‘multiple chemical
sensitivities’ and not bona fide allergies. But MCS symptoms are
much like allergic symptoms and they do involve the immune
response. I responded in kind to Liz; with respect Irene, people
who have bona-fide allergies are acutely aware of the difference.

A lot of people have sensitivity reactions to aflatoxin,
including anaphylaxis, the ‘classic’ allergic-type reponse. No,
the aflatoxin is not -simply a poisoning- or the dose required to
produce the effect would be similar for everyone. But we know

that many people don’t react at all to the same dose of aflatoxin
that would close the next guy’s throat. So, sensitivity to this
toxin is individual and that reaction can be improved.

I do hope you catch the drift of my nonsense now
Thank you for your summary of TH1 and Th2 involvement. Because
many or even most people are Th-2 skewed they do indeed have a
chronic low level inflammatory (immune) response. Inflammation
brings the immune system into the picture, and I’ve recently
posted some references for you that links the two. Inflammation
also brings chronic blood coagulation into the picture; this
eventuality isn’t handled well by your contention that it’s only
a cell-wall thing.

I can tell that you’ve at least heard of this relationship by
your quote :

Re: references for my wild statements, I had considered that
you could find them again in a couple of minutes like I did. My
apologies.

This Pubmed search (linolenic acid conversion to DHA) turned up a
lot of work; here follows a passage from a new review in PubMed
titled "Long-chain n-3 PUFA: plant v. marine sources." PMID:
16441943 [PubMed - indexed for MEDLINE]

"An important question is whether dietary intake of the precursor
n-3 fatty acid, alpha-linolenic acid (alphaLNA), can provide
sufficient amounts of tissue EPA and DHA by conversion through
the n-3 PUFA elongation-desaturation pathway. alphaLNA is present

in marked amounts in plant sources, including green leafy
vegetables and commonly-consumed oils such as rape-seed and
soyabean oils, so that increased intake of this fatty acid would
be easier to achieve than via increased fish consumption.
However, alphaLNA-feeding studies and stable-isotope studies
using alphaLNA, which have addressed the question of
bioconversion of alphaLNA to EPA and DHA, have concluded that in
adult men conversion to EPA is limited (approximately 8%) and
conversion to DHA is extremely low (<0.1%). In women fractional
conversion to DHA appears to be greater (9%), which may partly be
a result of a lower rate of utilisation of alphaLNA for beta-
oxidation in women."

So, the research is in agreement that plants don’t supply
adequate omega-3 fatty acid, ESPECIALLY DHA. Further, some work
says much less EPA is converted from LNA than this study does.

Chilton’s book — I have a copy — doesn’t disrespect nuts as you
suggest; it analyses the amount of, and describes a balance of,
specific fatty acids in foods, as I already told you. Lots of
people have commented on the bestselling book. I don’t care if
the reviewer whose comment you chose understood the work or not,
or if he doesn’t see any value of an inflammation index. Using it
much as we do an alkaline ash chart or the glycemic index today
will be commonplace.

Your quote here "EXCESS omega-6 and omega-3 oils such as canola
oil and flax seed - and from animal fatty acids such as
arachidonic acid. Not from the reaonable amounts of
monounsaturated and polyunsaturate fats in nuts which if eaten in
reasonable amounts are beneficial", doesn’t recognise that a
potential for excess and imbalance exists even with ‘reasonable
amounts’ of nuts or any other omega-6 contributing food because
all omega-6 intake for the day is additive.

Duncan

I agree with the comment below fom Dr Cousens; they don’t call
them essential fatty acids for nothing.

Duncan

With no more success then than now:-)))

> Inflammation Nation was published in 2005;

No. That’s a reprint. It was in 2004.

> Chilton is a fatty acid expert

???

I have not read his book as if it contains what you say I have no

interest. Even the cover does not claim he is an expert.

> It’s important to understand that it’s not a blood-type factor

There is that AS WELL - even if Chilton has skipped the research on that.

but
> direct inflammatory messengers as in leukotrienes and prostaglandins
> of the arachidoinic acid reactions that interest Chilton.

Really? Then it is odd you have not mentioned arachidonic acid in all
your speeches on PLANT omega-6 and 3s, allergies and immune system
cytokine stories you have been telling? Arachiodonic acid is animal
fatty acid not plant fatty acid :-)) It’s nowhere in your posts
As for the inflamamtory "messages" as you call them - there are specific
eicosanoid components from EACH fatty acid (prostaglandins, thromboxanes
and prostacyclin) that add together in any specific fatty acid - to
EITHER be net inflamamtory in action (as in arachidonic acid) OR be net
anti-inflammatory (as with DHA and EPA as in fish oil).

I do not know why you call them "messengers". They have direct chemical
action such as dilating blood vessels (which lowers pressure in them so
you will see high BP come down) or which dilates kidney vessels
(improving intraglomerular pressure and flow-through) - or doing the
opposite in the case of arachidonic acid’s NET effect.

Each fatty acid has eicosanoid products that are weaker or stronger.
The fish omega-3’s COMPETE with arachidonic acid for eicosanoid
production causing the inflamamtory effect of arachidonic acid to be
lowered and to become anti-inflamamtory instead. SO you can get the
benefits of BOTH fatty acids. It’s a matter of balance in what you eat!

IT’s the NET inflammation that matters, not only the individual bits.
Antioxidants can also undo inflamamtory responses.

WE need ALL the esential fatty acids for various functions. But AA is
not all enemy - it is essential to some functions and so are omega-6
plant oils that you are so against - but the quantity matters - and the
RATIO of anti-inflamamtory ones matters - so that we can get the
benefits of the inflammatory ones while using anti-inflamamtory ones to
overcome the "side effects" of the inflammation potential.

The REAL problem occurs when doctors get into the mix and tell people to
take NSAIDS like aspirin or cox-2 inhibitoprs to supposedly be
anti-inflamamtory or suposedly prevent heart attacks. They are NOT
anti-inflamamtory - they are blockers - they have no direct effect. They
can somewhat block the inflamamtion from inappropriate fatty acids - but
only if they ALSO block the good effects of ANTI-inflamamtory fatty
acids. They basically close the door to both.

So you/we need to see the WHOLE picture, including ALL the types of
fatty acid, plus all drugs that affect it plus all antioxidants plus the
competition between fatty acids for eicosanoids.
It’s not just about the fatty acid components as you have implied with
your Chilton references.

So the ideal is to have PLENTY of DHA and EPA from fish oil (as humans
have a natural block to its internal production in any decent amounts)
AND SOME of the other fatty acid items to cover their functions - and
ZERO Nsaids and cox-2 inhibitors.

> These
> inflammatory factors involve the whole immune response,

No - you need to study the immune system as you do not understand the
difference between immune response (such as in allergies or macrophage
type engulfing lymphocytes) and inflamamtory response which is at cell
level and involves direct chemical action on cell walls and blood vessel
walls - with no immune system involved at all.

blood
> coagulation, heart attack and stroke risk, and fibrosis of the ogans,
> the leading cause of organ failure.

You are flying off at a tangent again here.
The inflamamtory eicosanids from fatty acids affect ALL the cells of the
body, but they are by no stretch of the imagination the only
inflamamtory aspects that affect cells - adn so they are NOt respnsible
for your entire list of evils.

Eating too many carbohydrates is also inflamamtory at cell level. So is
having a high insulin level.
These do different kinds of inflamamtory damage.
Glycation for example.

Do not confuse glycation damage and consequences with prostaglandin ones!

> It’s also important to stress that the inflammatory effect is not
> type-specific, but extends more or less equally to everyone.

You’re wrong in that there are additional inflamamtory factors involving
blood type.
You have tried to put all the blame for inmflamamtion on fatty acids -
but that’s only ONE of many components in cell level inflammation.
Blood type reactions are another one.

The
> exception is that some people convert LA to GLA less than others and
> that will add to their load.

This is also a separate issue. Anyone on this list will likely be short
of the enzyme for this conversion, and would be wise to get a supplement
of blackcurrant oil or whichever one suits their blood type best.
(Blackcurrant works for type O, evening primrose and borage do not)

It’s not. Fatty acids do NOT involve cytokines!

SO?
There’s no *connection* between fatty acids and cytokines!!!
All that said is that both items are out of whack in some diseases.

To be more specific - when one of the T-2 cytokines such as Il-1 (and
there are many more) is too high, the immune system is "Th-2 skewed".
That predisposes many diseases including the few listed - also diabetes
and fibromyalgia are relevant here since we are on a diabetes list.
LTB4 is also high in some diseases, but it’s a separate issue from
the high Il-1. It will just be one more factor to help to push the
system towards disease.
There is no interaction between the skewed immune system and the fact
that fatty acid inflamamtion is high. They are separate factors, not
interacting ones.

It goes on to say fish oil supplements are good, which they are. But
they will not rebalance the out of balance cytokines:-))
They can only help the cell level inflammation to reduce that aspect in
these diseases.
That is why conventional medicine never cures chronic disease, only
tries to "control" it. They use drugs to block eicosanoids (good or bad
eicosanoids) - basically sweeping some of the symptoms under the carpet.
But there is nothing they do to fix the skewed immune system.

So maybe the book had it right but you misinterpreted it as having a
connection between fatty acids and the immune system?
Your quote showed none here - but your posts to the list have been
consistently very flawed whenever you mention immune system or
allergies. I suspwect you have a very basic misundersttanding or lack of
understanding about the immjuen system.

Whether Chilton also does - is now in question, since it is not muddled
in the part you quoted - only in your interpretations in your own posts.

Namaste,
IRene

Agree.

Not true.
You need to look at the food in total - including not only its fatty
acid ratios but its other nutrients such as minerals and antioxidants -
as these offset the negative fatty acid components.
This is why it is incorrect to call nuts inflamamtory - but it is
correct to call flax oil inflamamtory.
From what you say - Chilton at best has tunnel vision on fatty acids.

For example - walnuts are far more beneficial than Chilton and you claim

due to the high antioxidants included, that are not in other nuts
which don’t need them.

Like it or nut, the nut was not a nutty design:-)

Namaste,
IRene

Duncan, You are with respect talking nonsense.
The response of the body to aflatoxin or any other toxin is NOT an
allergic response - it’s a completely different response and depends on
the individual toxin as to what is poisoned and how the body responds!

Allergic reactions on the other hand are very specific responses to
specific (protein) allergens - and an allergen is usually NOT a toxin
though it might be if protein is involved and other conditions are also
meet: The allergen has to first inadvertently get into the blood at a
time when the immune system is TH-2 skewed and therefore the immune
response to the foreign protein will be to develop antibodies as if the

protein was an infection.
A NON-Th-2 skewed system will instead use TH1 cytokines to develop
macrophages to engulf and eliminate the foreign protein - without ever
involving the TH2 antibody system at all (which is supposed to only be a
backup for for in case the TH1 system is overwhelmed by multiplying
infectious agents.)]

So the reaction to aflatoxin is not an "allergic reaction". Aflatoxin is
a poison - a toxin - the body’s response has nothing to do with
allergies! It is a poisoning response, not an allergic response. These
are VERY different responses.

No way!!! Where do you get these ideas? It bothers me that you come out
and make such wild statements on a list where people are serious about
their health.
Allergies are not a product of toxins generally!
The kidneys and liver are responsible for toxin handling as is the skin
and other eumunctories.
[Where did you study immunology?????]

Toxins can build up and overwhelm the kidneys - and when that happens
the liver steps in to try to help out - not the immune system or
allergic response.

> Although excess omega-6 oils contribute in a major way to
> inflammation, and this involves the immune and allergic respnses,

Definitely not.
Again I dunno where you studied immunology but you have been misled,
and maybe need a refund. Allergies involve proteins not fatty acids.
And inflammation due to fatty acids involves the phospho-lipid layer
cell walls and not the immune system.
You have it all muddled up.

> Repeated exposure to any toxin can eventually cause a bona-fide
> allergic reaction.

Again - Not true.
A "bona fide" allergic reaction involves the body’s TH-2 skewed system
recognizing foreign *protein* in the bloodstream. Period. No other way
can an allergic reaction occur.
TOXIC responses are not allergic reactions.
Allergic response to toxin (in the extremely rare case where it occurs)
depends on the toxin and whether it has protein components, AND gets
in the blood AND the immune system is Th-2 skewed - and only then is an
allergic response even possible to a toxin.

MOST toxin exposures cause direct poisoning damage due to the toxicity
of the item - NOT allergic responses.

Allergic responses are the SAME symptoms regardless of allergen -
whereas toxic responses are all different poisoning responses depending
on what damage the specific toxin does in the body.

That’s why toxins are called toxins (poisons)…
and are *not* called allergens (foreign proteins).

NAmaste,
IRene