Re: Re: Coconut oil (lectins/celiac)

[Guest guest]

Emma,

> For some, not for others. They're proteins, so some are heat labile

> too. Soy lectins are virtually impossible to destroy by any method

> other than v. long fermentation. Wheat lectins, I believe some types

> of fermentation inactivate them. Also, if a fermentation results in

> the production of some essential sugars out of the starches - as

> mannose can be from (I think, need to check) the maltitol, mannitol

> and maltodextrin found in wheat - the mannose can then bind to the

> mannose binding lectin in wheat, and deactivate it rather nicely. The

> same goes for glucose binders, glucosamine binders, etc.

This is highly interesting, because there have been several studies on

the ability of typcial sourdough cultures to break down gliadin in

wheat. One of them fed them to celiacs for two days, and found that

the celiacs developed alterations in intestinal permeability after

eating regular wheat for two days, but not after eating sourdough

wheat (it was actually a mix of wheat and other grains) for two days.

They implied they were going to begin a long-term study of the safety

of this bread for celiacs, as the 2-day data and the endpoint used is

of ambiguous relevance.

In any case, I was speculating that the fermentation process could

also produce compounds that *prevent* the damage done by the wheat,

only I was assuming the damage was mediated by gliadin-derived

peptides. But the mannose binding the lectins is similar.

> I wonder if there is a vit A/D connection to the ability to

> manufacture essential sugars and/or protect against lectins?

Perhaps. The mechanism currently being considered is their ability to

shift differentiation of Th0 cells to Th2 rather than Th1 cells, and

the high vitamin D group had a quadrupled risk of asthma, supporting

this idea. However, I would like to see what the effect of vitamins A

and D together is, because although some people advocate the idea that

vitamin A induces Th2 differentiation, this depends on the cell being

used and by which CD receptor the costimulation is mediated. Also,

vitamin A is responsible for M2R muscarinic receptors that help

regulate bronchial constriction, diverts bone marrow cells away from

eosinophil/basophil differentiation and into neutrophil

differentiation, and depresses IL-5 levels, which are Th2 associated

and strongly related to allergic and asthmatic reactions, and children

with asthma have low serum levels of vitamin A in proportion to the

severity of their asthma. Thus, I suspect that vitamins A and D

together might help prevent diabetes and asthma rather than one or the

other.

Finally, I found a double-blind placebo-controlled study from the

1970s using vitamin K2 as a highly successful treatment for asthma.

So I suspect that a proper balance of nutrients during infancy would

give us the best of both worlds.

In any case, it would not surprise me if the fat-soluble vitamins were

involved in the production of essential sugars, though I don't think

anyone is investigating this angle of the issue. Most researchers

like to think of a vitamin doing one thing or another, and do not look

at how they interact with each other or other things in the diet.

> > Is it also true, then, that someone with limited salt would use that

> > salt up in excreting them, and thus require more salt? Does my

> > life-long need to drink large amounts of water, urinate frequently,

> > and eat very salty food suggest these chemical sensitivities?

> To me, yes. Urinary urgency/frequency is a common symptom. And I spent

> a year doing something like this - it happened to be the " good health

> year " I had when I started doing Atkins. I was worried about

> electrolyte loss as I was dieting, so I started adding large amounts

> of salt to large amounts of water every day, and felt much better,

> though still not quite right. My eczema cleared up at this same time.

> About a month after I stopped doing it I developed eczema again. Lots

> of other variables involved, I know, but salt does help.

I think that in addition to food chemicals, there is probably a

similar thing with fermentation byproducts. I believe I have probably

always had an ecological imbalance in my gut, so I might have to

excrete large amounts of fungal byproducts.

A couple of months ago, I was overcome by severe fatigue for several

days such that I could barely walk around. I read about salt for

adrenal fatigue, and I took a teaspoon of salt with water and felt

better immediately, as soon as I *tasted* the salt. I suspect that I

was seriously depleted of sodium and rapidly absorbed it into my blood

stream straight from my mouth.

It also seemed to contribute to a canker sore problem though, and I

eventually lowered my salt intake back down. I usually get canker

sores in response to a low-calcium diet, but recently I got them on a

high-calcium diet. Rinsing with coconut oil made them go away

rapidly, which I did on suspicion that enzymes in my saliva would

derive monolaurin and laurate that would be toxic for whatever virus

might potentially be contributing to the canker sores.

>Bicarbonate

> is still better. In fact, all base-forming minerals help to excrete

> through the kidneys: sodium, potassium, magnesium, calcium.

I don't understand why you call these base-forming. My understanding

is that any positively charged metal would at best act as a very mild

acid by binding up water molecules and liberating a hydrogen ion from

one of them. Alternatively, those that have the capability of

precipitating would bind up hydroxide ions or other bases that could

have the capacity to either bind hydrogen ions or release hyroxide

ions. Or do you mean that these minerals are usually complexed with

bases before they are consumed and therefore yield those bases after

they are consumed?

> The other

> behavioural reaction with regards salt is to hate it violently, and

> not use it on anything at all because it gives one a raging thirst.

That is definitely not me.

Although, recently I experimented to see if a teaspoon of salt before

bed would prevent me from having to get up at 4:00 am to go to the

bathroom. Instead, I woke up at 11:00 pm to go to the bathroom. It

could have been coincidence though as I only tried it once.

I essentially have perpetual thirst.

> I don't doubt they mean something, I just want to see definite proof

> that their presence makes one feel physically bad. A lot of immune

> stuff happens fairly passively without giving any physical symptoms.

I empathize with your desire to see more evidence. I am quite

frustrated, in fact, that Dr. Fine has had the assertion that IgA

levels in the stool are associated with gut damage on his web site

since 2003 and still has not, as far as I know, published any data

demonstrating this.

> And IgA/IgG immunodeficiency is associated with worse physical

> symptoms, here their absence makes asthma worse:

> http://content.karger.com/ProdukteDB/produkte.asp?Doi=92252

I doubt this has very much relevance here. If 65% of people do not

have IgA to gliadin and 35% do, it seems unlikely that the 65% all do

not have IgA to gliadin because of a general deficiency in IgA. And

the inverse association with asthma could result from a protective

effect, or it could reflect other processes. Asthma and autoimmune

diseases are generally considered to be polar opposites in the sense

that they are a result of opposite Th cell differentiation. So the

fact that IgA is inversely associated with asthma would, if anything,

suggest that IgA is positively assocaited with autoimmune diseases,

though not necessarily a cause of them.

> As far as I can tell their job is to go around quietly mopping up the

> many antigens that intrude into the body every day, by binding to

> them. IgG is the most common antibody, and high IgG indicates past

> infection and quietly prevents infection from occurring again. IgA is

> present in mucus as a first line of defence. Unlike quietly mopping

> things up, IgE antibodies explode on contact with antigens and release

> massive amounts of histamine.

I think IgG is just the most common in the blood. If you counted all

the antibodies in all the tissues and secretions, I would think IgA

would rival IgG.

Anyway, my impression is similar to yours. The question is: why do

some people have a lot of gliadin to mop up and others who are eating

gliadin do not?

> > In retrospect, I think you were trying to say that the IgG/IgA issues

> > should not be classified as " allergies " and they are probably mediated

> > by other factors such as lectins. Something like that?

> I'm happy for IgG/IgA to be classified as allergy if it causes

> quantifiable physical symptoms of ill health. So far, we just know

> it's an immune response.

I'm rethinking the allergy definition, and I think maybe it is

productive to limit allergy to IgE, because when someone says

" allergy " everyone automatically thinks of IgE-related symptoms

anyway. I don't know: you are right that there isn't enough data to

define an IgG/IgA disorder.

> I'm not convinced that IgG/IgA responses are the determining or

> initial causative factor in celiac disease. Mannose binding lectins

> attack and attach to any cell that has an exposed mannose sugar.

> There's evidence that other binding lectins are involved too -

> glucosamine and galactosamine, with glucosamine actually being the

> primary one involved in wheat (hence the wheat/arthritis connection

> and the reason glucosamine sulphate is good for arthritis).

You mean wheat has glucosamine, or you mean it has lectins that bind

glucosamine? (I'm assuming you mean the latter).

> I think

> probably the initial step is a food lectin or a GI pathogen that

> produces sialic acid binding lectins to strip away the sialic acid

> coating of intestinal cells, followed by the wheat gliadin lectin or

> another GI pathogen that attaches to the exposed mannose sugars, other

> lectins being involved too. The damaged cells are then recognised by

> the immune system as invaders, and are attacked.

In order for this to happen, there would be, as I understand it, some

type of costimulus to activate T cells. What would provide the

costimulus?

I think intestinal damage is likely to precede binding of the

33-residue gliadin fraction to MHC proteins in antigen-presenting

cells, which I think is consistent with your idea. I think this

because tissue transglutaminase dramatically increases the

immunogenicity of the gliadin peptide by deaminating its glutamine

residues, and tissue transglutaminase just isn't there unless there is

tissue damage. (Or maybe I am wrong in this and there is always some

tissue transglutaminase doing day-to-day repair processes?)

> Gluten proteins are not the only thing to which the body becomes

> sensitised in celiac, for example, the immune system has shown to

> become sensitised to the usually harmless baker's yeast saccharomyces

> cerevisiae:

>

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Retrieve & dopt=Abstra\

ctPlus & list_uids=16357623 & query_hl=2 & itool=pubmed_DocSum

>

> And to milk and soy proteins:

>

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Retrieve & dopt=Abstra\

ctPlus & list_uids=8488125 & query_hl=24 & itool=pubmed_docsum

This is a great point, because if only gluten reactions are looked

for, one could mistake a situation where reactions to a large number

of foods is prevalent but only find the reaction to gluten.

> When the mucosa is normalised, these antibodies disappear. This may

> explain the contradictory information on oats - papers report immune

> sensitivity to oats before a gluten free diet, and other papers report

> no such immune sensitivity when patients are on a gluten free diet.

> Is this because the diet is gluten free, or lectin free?

Right. Although even if celiac is initiated by lectins this does not

mean it isn't aggravated by the immunogenicity of gliadin.

> So the theory I subscribe to is that the IgG and IgA mopping up

> responses to gluten and to other foods are simply a secondary response

> to the damage and permeability caused by the lectin-induced autoimmune

> attack on the cells where they have attached.

Even in this scenario, though, the IgG and IgA could have some

diagnostic value as a marker for the process.

> The lectins get in in

> the first place due to genetics, level of exposure, immune failure,

> viral or bacterial infection, or gut permeability caused by infection

> or medication. At this point I have to mention that NSAIDs including

> salicylate are particularly known for increasing gut permeability and

> allowing lectins into the bloodstream, which is why the failsafe site

> has a number of reader's testimonies who have been cured by what are

> thought to be lectin-induced autoimmune diseases - like arthritis and MS.

I have heard that omega-3 fatty acids also increase gut permeability.

I was speaking with someone else recently who was wondering if EPA

could aggravate this problem in the absence of sufficient AA, even

though the concern is universally for the opposite imbalance these

days.

> > Nevertheless, why would the majority of people not have IgA to gliadin

> > in the stool?

> I guess because while IgA is a first line of defence in the mucus,

> it's formed in the bone marrow with the other white blood cells. I

> think IgD is the antibody responsible for recognising the difference

> between the self and foreign material, so it's a line of communication

> rather than localised response. If the body thinks something is

> getting through that shouldn't, IgA is its first line of defence in

> the mucus.

This isn't fully answering the question, though. Are you proposing

that a good majority of people have a deficiency in this line of

communciation, and that people with IgA in the stool are the people

who best tolerate gluten? Or, alternatively, does the IgA indicate a

failure to properly digest gluten and thus the need for something to

be mopped up?

> > Ok. But what are your thoughts on the connection between celiac and

> > anti-tissue transglutaminase antibodies?

> This is my stupid: tissue transglutaminase is where the lectins bind,

> that's why they get attacked. Rather than being a direct attack on the

> intestinal wall, it's an attack on the enzyme that is designed to keep

> the cell wall matrix knitted together.

Is there evidence that lectins can bind to this enzyme that you know

of? This is an interesting idea.

> > I have heard it advocated that tissue transglutaminase crosslinks

> > gliadin to intestinal cells. I don't know whether this is shown

> > experimentally or not, but regardless, what do you think of its

> > plausibility?

> I suppose as wheat gliadin is where the lectin lies and it binds to

> the tissue transglutaminase, and the tissue transglutaminase is what

> binds the cell wall together, the whole mass is going to get stuck

> together...

What a sticky situation to be in. :-\

Chris

--

The Truth About Cholesterol

Find Out What Your Doctor Isn't Telling You:

http://www.cholesterol-and-health.com

[Guest guest]

Emma-

>Incidentally, Elaine Gottschall of SCD fame is

>opposed to use of bifidus supplementation because they overgrow.

Actually, I think her primary reason was that bifidus persisting into

adulthood is epidemiologically associated with colon cancer.

-

[Guest guest]

>

>

>> Anyway, my impression is similar to yours. The question is: why do

>> some people have a lot of gliadin to mop up and others who are eating

>> gliadin do not?

>

>

>Because the gut permeability preceeds the presence of gliadin in the

>blood. Or do you mean why some people with celiac have IgG or IgA to

>gliadin and others don't? That I can't answer - I guess why do some

>people in general have IgG or IgA to their favourite foods? They eat

>more of it, or too often? I don't know.

I don't think so because Enterolab gets a lot of anti-gliadin antibodies

showing up in folks who've gone of gluten for serveral months, even

sometimes up to a year, IIRC. They might be getting trace amounts in

processed foods, but they're eating such small amounts and yet have elevated

AGA. I have no idea why, I'm just thinking it's not due to them eating

*more* gliadin.

>

>

>> > There's evidence that other binding lectins are involved too -

>> > glucosamine and galactosamine, with glucosamine actually being the

>> > primary one involved in wheat (hence the wheat/arthritis connection

>> > and the reason glucosamine sulphate is good for arthritis).

>>

>> You mean wheat has glucosamine, or you mean it has lectins that bind

>> glucosamine? (I'm assuming you mean the latter).

>

>Yeah, the latter.

>The damaged cells are then recognised by

>> > the immune system as invaders, and are attacked.

Which damaged cells?

Suze Fisher

Web Design and Development

http://www.allurecreative.com

Weston A. Price Foundation Chapter Leader, Mid Coast Maine

http://www.westonaprice.org

----------------------------

“The diet-heart idea (the idea that saturated fats and cholesterol cause

heart disease) is the greatest scientific deception of our times.” --

Mann, MD, former Professor of Medicine and Biochemistry at Vanderbilt

University, Tennessee; heart disease researcher.

The International Network of Cholesterol Skeptics

<http://www.thincs.org>

----------------------------

[Guest guest]

>

>> >Because the gut permeability preceeds the presence of gliadin in the

>> >blood. Or do you mean why some people with celiac have IgG or IgA to

>> >gliadin and others don't? That I can't answer - I guess why do some

>> >people in general have IgG or IgA to their favourite foods? They eat

>> >more of it, or too often? I don't know.

>>

>> I don't think so because Enterolab gets a lot of anti-gliadin antibodies

>> showing up in folks who've gone of gluten for serveral months, even

>> sometimes up to a year, IIRC. They might be getting trace amounts in

>> processed foods, but they're eating such small amounts and yet have

>elevated

>> AGA. I have no idea why, I'm just thinking it's not due to them eating

>> *more* gliadin.

>

>I guess firstly with regards enterolab's tests I have to refer back to

>Taty's recent comment on how two years ago most IgG tests were only

>50% accurate, and my reply posting a paper from a laboratory that

>admitted how inaccurate their tests were.

Right, but the stool test is not an IgG test and is not a *blood* test,

which can be very inaccurate. IIRC, Dr. Fine has reported that the stool

test has picked up gliadin IgA in the stool in something like 50-70% of

folks who tested negative on the blood tests, or some remarkable number like

that. The stool test is supposed to be *much* more accurate than any blood

test because most IgA is produced in the intestines and that's the first

place where the reaction occurs. There can be reactions in a gut that is not

leaky, so the antibodies wouldn't be getting into the blood. So, in terms of

accuracy, the stool test *should* be much more accurate than a blood test.

I suppose a counter argument might be that if the body is reacting to

gliadin in some way or another, it's probably producing zonulin, which in

turn would cause the gut to become permeable. But perhaps zonulin is not

stimulated 100% of the time and/or not stimulated in every individual.

>

>If we assume that enterolab is actually seeing what is there instead

>of what they want to see,

How do you propose they can see what they want to see?

and we also assume that those people are

>genuinely gluten-free (i.e. they have not eaten some of the common

>gluten-free products on the market that actually contain gluten, or

>have not eaten hidden, undeclared gluten in other foods),

That's why I mentioned that they might be getting small amounts hidden in

various processed foods, but it's still not *a lot* for many of them, I

think, and I was responding to your point that they might be producing the

AGA because they were still eating a lot of gluten.

and we also

>find out and compare responses to soy, saccharomyces cerevisiae, milk,

>and other foods that have been found to generate IgG antibodies in

>celiac disease and THEN we find that the antigliadin antibodies are

>high when antibodies to other reactive foods are low, then we have a

>problem and we are seeing something specific to gliadin.

Are you suggesting that if one is reacting to casein, for instance, that

that would not only increase one's antibodies to casein but also to gliadin?

I'm not following...

>

>Which might have something to do with the zonulin/calreticulin/gliadin

>connection - which because of its nature appears to have both

>pharmacological effects *and* result in an autoantibody cross-reaction

What for instance, would a pharacological effect of zonulin be?

>We never really sorted out exactly what the lectin was binding to, and

>it may bind to more than one thing since so many different

>autoantbodies and antibodies become involved in the process, but I

>think this paper has an answer for the primary reaction that starts

>the cascade off:

>

>This paper presents a new hypothesis for the etiology and pathogenesis

>of celiac disease (CD). It is our contention that CD is triggered by

>the binding of one or more gliadin peptides to CD-associated HLA class

>II molecules. Furthermore, we propose that these putative CD peptides

>bind to oligosaccharide residues on HLA class II molecules distal to

>the peptide-binding groove invoking recognition and binding by

>specialized subsets of gamma delta T cell receptor-bearing

>lymphocytes. The binding of these gamma delta T cells serves as a

>signal for abrogation of oral tolerance to ingested proteins setting

>in motion a series of immune responses directed against the small

>intestinal epithelium of CD patients. CD patients are victimized by

>this self-distructed immune response because of inheritance of certain

>combinations of HLA-DQ and DR haplotypes. Dimers encoded by HLA-DR

>haplotypes may be the primary restriction elements for lectin-like,

>gliadin peptides while the degree of immune suppression (or lack

>thereof) to ingested gliadins is governed by inherited HLA-DQ

>haplotypes. Finally, we speculate that molecular mimicry between one

>or more gliadin peptides and some, as yet unidentified, bacterial or

>viral superantigen plays a role in disease pathogenesis.

>

>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Retriev

e & dopt=AbstractPlus & list_uids=9364219

But why do the gliadin peptides bind to the HLA genes in the first place?

For many of us, this seems to happen later in life, as adults. What trigged

it? Molecular mimicry as they contend? But what triggered the molecular

mimicry? I know there's a theory out there that some sort of stressor

triggers this reaction. I don't think the binding of gliadin peptides to

certain HLA genes is the *primary* reaction, or, maybe it IS, but the big

mystery, to me, is *what* initial *action* causes this reaction?

Also, re dimers, I don't understand what they mean by " dimers encoded by

HLA-DR haplotypes " . Isn't the term dimer most often used to refer to

disaccharides? I wonder what type of dimer the authors are referring to? The

way it's written I thought they meant some type of *unique* molecule?

Suze

[Guest guest]

On 9/19/06, Suze Fisher <s.fisher22@...> wrote:

> Right, but the stool test is not an IgG test and is not a *blood* test,

> which can be very inaccurate. IIRC, Dr. Fine has reported that the stool

> test has picked up gliadin IgA in the stool in something like 50-70% of

> folks who tested negative on the blood tests, or some remarkable number like

> that. The stool test is supposed to be *much* more accurate than any blood

> test because most IgA is produced in the intestines and that's the first

> place where the reaction occurs. There can be reactions in a gut that is not

> leaky, so the antibodies wouldn't be getting into the blood. So, in terms of

> accuracy, the stool test *should* be much more accurate than a blood test.

I don't think I'll have time to post this tonight, but the fact that

more people have IgA to gliadin in the stool than people who have it

in the blood doesn't mean it's more accurate. If there's nothing

wrong with those people, it would mean it's much less accurate. I

will post research suggesting it is meaningless probably tomorrow, at

least with respect to celiac-like intestinal damage. It also appears

to appear and disappear randomly without respect to diet.

> Also, re dimers, I don't understand what they mean by " dimers encoded by

> HLA-DR haplotypes " . Isn't the term dimer most often used to refer to

> disaccharides? I wonder what type of dimer the authors are referring to? The

> way it's written I thought they meant some type of *unique* molecule?

Dimers and disacharides have nothing to do with each other. A dimer

is a protein made of two interfacing subunits. HLA-DR molecules

produce a subset of the MHC Class II proteins which are responsible

for recognition of antigens by T cells.

Chris

--

The Truth About Cholesterol

Find Out What Your Doctor Isn't Telling You:

http://www.cholesterol-and-health.com

[Guest guest]

>On 9/19/06, Suze Fisher <s.fisher22@...> wrote:

>

>> Right, but the stool test is not an IgG test and is not a *blood* test,

>> which can be very inaccurate. IIRC, Dr. Fine has reported that the stool

>> test has picked up gliadin IgA in the stool in something like 50-70% of

>> folks who tested negative on the blood tests, or some remarkable

>number like

>> that. The stool test is supposed to be *much* more accurate than

>any blood

>> test because most IgA is produced in the intestines and that's the first

>> place where the reaction occurs. There can be reactions in a gut

>that is not

>> leaky, so the antibodies wouldn't be getting into the blood. So,

>in terms of

>> accuracy, the stool test *should* be much more accurate than a

>blood test.

>

>I don't think I'll have time to post this tonight, but the fact that

>more people have IgA to gliadin in the stool than people who have it

>in the blood doesn't mean it's more accurate. If there's nothing

>wrong with those people, it would mean it's much less accurate.

I meant it was a more accurate measure of the presence of AGAs according to

Dr. Fine. Is that not the case? If not, how could it not be more accurate a

test for AGAs if it's picking up a significant percent of AGAs that are not

picked up in a blood test?

I agree that if " accuracy " is in reference to *pathology*, then it would be

a lot less accurate. I'm sorry I wasn't clear on what I meant when I said

" accurate " .

I

>will post research suggesting it is meaningless probably tomorrow, at

>least with respect to celiac-like intestinal damage. It also appears

>to appear and disappear randomly without respect to diet.

Sounds very interesting! I'd sure like to know why the immune system would

produce AGAs randomly...

>

>> Also, re dimers, I don't understand what they mean by " dimers encoded by

>> HLA-DR haplotypes " . Isn't the term dimer most often used to refer to

>> disaccharides? I wonder what type of dimer the authors are

>referring to? The

>> way it's written I thought they meant some type of *unique* molecule?

>

>Dimers and disacharides have nothing to do with each other.

I misunderstood the Wikipedia definition. Or rather, I might've forgotten

which sugars are disaccharides. Wiki says of dimers:

" In chemistry, a dimer refers to a molecule composed of two similar subunits

or monomers linked together. It is a special case of a polymer. It can refer

to halide chemistry, involving halogen bonding. Its more common usage refers

to dimers as certain types of sugar: sucrose, for example, is a dimer of a

glucose molecule and a fructose molecule. "

http://en.wikipedia.org/wiki/Dimer

A dimer

>is a protein made of two interfacing subunits. HLA-DR molecules

>produce a subset of the MHC Class II proteins which are responsible

>for recognition of antigens by T cells.

Gotcha.

Suze

[Guest guest]

On 9/19/06, Suze Fisher <s.fisher22@...> wrote:

> I meant it was a more accurate measure of the presence of AGAs according to

> Dr. Fine. Is that not the case? If not, how could it not be more accurate a

> test for AGAs if it's picking up a significant percent of AGAs that are not

> picked up in a blood test?

I don't think anyone does a serum test for AGAs and intends to measure

the total amount of AGAs in the body. If they did, then measuring the

stool and blood together would be more accurate.

In any case, measuring AGAs is pointless unless doing so yields

meaningful diagnostic information. It is pointless to have a " more

accurate " measurement of AGAs if it yields less accurate diagnostic

information.

> I agree that if " accuracy " is in reference to *pathology*, then it would be

> a lot less accurate. I'm sorry I wasn't clear on what I meant when I said

> " accurate " .

Usually when people run diagnostic tests, its for the purpose of

assessing pathology.

> Sounds very interesting! I'd sure like to know why the immune system would

> produce AGAs randomly...

No idea, but there is a study that seemed to suggest it, of which I've

only read the abstract.

> I misunderstood the Wikipedia definition. Or rather, I might've forgotten

> which sugars are disaccharides. Wiki says of dimers:

> " In chemistry, a dimer refers to a molecule composed of two similar subunits

> or monomers linked together. It is a special case of a polymer. It can refer

> to halide chemistry, involving halogen bonding. Its more common usage refers

> to dimers as certain types of sugar: sucrose, for example, is a dimer of a

> glucose molecule and a fructose molecule. "

Well ok, I guess that isn't inaccurate but I dispute " common. " I

mean, over 99% of the time someone is going to say " disacharide "

instead of " sugar dimer, " whereas the term will almost always be used

for proteins.

Chris

--

The Truth About Cholesterol

Find Out What Your Doctor Isn't Telling You:

http://www.cholesterol-and-health.com

[Guest guest]

>> I meant it was a more accurate measure of the presence of AGAs

>according to

>> Dr. Fine. Is that not the case? If not, how could it not be more

>accurate a

>> test for AGAs if it's picking up a significant percent of AGAs

>that are not

>> picked up in a blood test?

>

>I don't think anyone does a serum test for AGAs and intends to measure

>the total amount of AGAs in the body. If they did, then measuring the

>stool and blood together would be more accurate.

Sure, but I was responding to what Emma said about *serum* IgG and IgA tests

being an extremely inaccurate measures for these antibodies. Unless I

misunderstood her. I can't find that post now.

>

>In any case, measuring AGAs is pointless unless doing so yields

>meaningful diagnostic information. It is pointless to have a " more

>accurate " measurement of AGAs if it yields less accurate diagnostic

>information.

Of course! And I wasn't arguing that finding more AGA in the stool is

meaningful diagnostic info, only that, according to Dr. Fine, AGA is often

detected in stool in people who do not have detectable levels in the blood.

Nothing more nothing less.

>

>> I agree that if " accuracy " is in reference to *pathology*, then

>it would be

>> a lot less accurate. I'm sorry I wasn't clear on what I meant when I said

>> " accurate " .

>

>Usually when people run diagnostic tests, its for the purpose of

>assessing pathology.

Gee, and I thought it was just to squeeze wads of dough out of patients so

docs can send their kids to college. :-)

My alternate answer was... " well, duh! " But it just sounds so sophomoric.

>> I misunderstood the Wikipedia definition. Or rather, I might've forgotten

>> which sugars are disaccharides. Wiki says of dimers:

>> " In chemistry, a dimer refers to a molecule composed of two

>similar subunits

>> or monomers linked together. It is a special case of a polymer.

>It can refer

>> to halide chemistry, involving halogen bonding. Its more common

>usage refers

>> to dimers as certain types of sugar: sucrose, for example, is a

>dimer of a

>> glucose molecule and a fructose molecule. "

>

>Well ok, I guess that isn't inaccurate but I dispute " common. " I

>mean, over 99% of the time someone is going to say " disacharide "

>instead of " sugar dimer, " whereas the term will almost always be used

>for proteins.

OK. Well, I don't take Wiki info as gospel. Thaks for the clarification.

Suze

[Guest guest]

Suze,

> Sure, but I was responding to what Emma said about *serum* IgG and IgA tests

> being an extremely inaccurate measures for these antibodies. Unless I

> misunderstood her. I can't find that post now.

Ah, the wonders of gmail:

============

>I guess firstly with regards enterolab's tests I have to refer back to

>Taty's recent comment on how two years ago most IgG tests were only

>50% accurate, and my reply posting a paper from a laboratory that

>admitted how inaccurate their tests were.

=============

I'm pretty sure she's referring to the accuracy of the measurement,

wherever it is. That is, serum IgG was an inaccurate measure of the

serum IgG, and stool IgG would presumably be an inaccurate measure of

the stool IgG. I think the accuracy would depend on the specificity

of whatever they are using to bind the antibody for the antibody. But

I don't know the tests very well so I'll wait for Emma to explain what

she meant.

If the tests are inaccurate, it shouldn't really matter where they are

measured, I would think. Nor would it matter whether more people

tested positive on a stool test than a blood test. If the tests are

inaccurate, there could be many false positives, so a higher positive

rate is not a measure of accuracy. Also, it could be true that more

people have IgA in the stool than in the blood and that the stool

tests are *underestimating* this with false negatives. Worse, if the

tests are inaccurate there could be a tendency for false positives and

false negatives both!

> >Usually when people run diagnostic tests, its for the purpose of

> >assessing pathology.

> Gee, and I thought it was just to squeeze wads of dough out of patients so

> docs can send their kids to college. :-)

They're probably donating whatever is left over to global warming

propagandists so their friends who are members of the cabal of climate

scientists can get billions of dollars of government money to buy

weather balloons.

> My alternate answer was... " well, duh! " But it just sounds so sophomoric.

Sounds freshman to me.

> OK. Well, I don't take Wiki info as gospel. Thaks for the clarification.

If you did, I think the Lord would get jealous.

Chris

--

The Truth About Cholesterol

Find Out What Your Doctor Isn't Telling You:

http://www.cholesterol-and-health.com