RE: the cause(s) of gluten sensitivity

[Guest guest]

> Re: the cause(s) of gluten sensitivity (was: antibiotics?)

>

>

>

>>>OK, but why in the world does there have to be a CAUSE for

>>>gluten sensitivity, other than gluten?

>>

>>Because millions of people eat gluten and aren't sensitive to it?

>If it were

>>gluten alone causing gluten sensitivity then everyone who eats

>gluten would

>>be sensitive to it, which is not the case. So there has to be some other

>>factor at play. Further, even among those with the GS genes, 1 out of 4

>>aren't sensitive to it (according to Dr. Fine's research). So

>that rules out

>>

>>1) gluten being the sole cause of gluten sensitivity

>>2) gluten AND having the GS genes together being the sole cause of gluten

>>sensitivity

>>

>>Let's just be sure we're on the same page when we refer to gluten

>>sensitivity so that we know we're discussing the same thing. When

>I refer to

>>GS I mean an IgA reaction to gliadin. I assume you mean the same thing?

>

>Well no, I'd add #3, gluten and the gene and " immune training " . There

>are factors that train the immune system in what to react to and how

>much to react to it. And people do study those things and correlations

>have been shown. It's just that the correlations that HAVE been found

>are never the ones that people keep bringing up here. The really

>BIG factor in training the immune system is breastmilk. The factors

>in breastmilk seem to be there for the very purpose of training the

>immune system, and the exact timing of the first solid foods in

>relation to breastmilk are a huge factor, it seems. This is a great

>survival thing: if the mother survived, say, smallpox, she can teach

>her baby to survive smallpox via her breastmilk.

That's fine, we can add " immune training " to the list. But this doesn't

address what I said about there being more than one causal factor in gluten

sensitivity in response to you asking why there needs to be " a CAUSE for

gluten sensitivity, other than gluten? "

What is your response to my rebuttal that not everyone who consumes gluten

is sensitive to it? If gluten were the ONLY cause of GS, then everyone who

eats gluten would be sensitive (have an IgA reaction) to it (above normal

levels), which is not the case. Which is why I listed other factors

necessary for GS.

>

>But the IgA system exists to recognize microbes, and it does

>that very well. When smallpox decimated the Indian tribes,

>it spared a certain small percentage. Smallpox was endemic

>for the Europeans, but most victims survived it. What was the

>difference? The Europeans carried genes that " recognized " smallpox

>as soon as they were exposed to it, before it made them very

>sick. Having a built-in recognition for smallpox is a very good thing.

>The system for recognizing gliadin is a similar system, probably

>there to recognize something like candida, and if so, it would

>recognize gliadin UNLESS IT IS TURNED OFF. Breast milk might

>be the " turn this off " factor, telling the immune system that

>even though this LOOKS like a microbe, it's really ok.

Exactly! That would be an additional factor in the cause of GS *beyond*

gluten itself.

>

>Or, there could be another gene that tends to mute the

>genes that react. Genes tend to work together ... so if

>you have a gluten reactive gene AND another gene, you'll

>be ok.

OK. Another possible causal factor, but only a theory (albeit a plausible

one from this layman's eye). However, it is NOT a theory that one must have

at least one GS gene to be GS (for all intents and purposes) and it is NOT a

theory that nutritional status and other environmental factors cause genes

to express in different ways or express at all.

>

>

>But the people who talk about mercury being a problem are

>generally talking about gut permeability issues, which primarily

>effect IgG allergies.

Actually, gut permeability is just one amongst many, many others in

relation to Hg toxicity and would only pertain to Hg ingested with food, but

not Hg injected via vaccines or Hg vapor absorbed through the lungs.

But gut permeability can be triggered by IgA

>allergies, and in fact that is the primary link that has been found

>to gut permeability. Maybe mercury can trigger gut permeability

>too, but so far it seems to be mainly a theory: kids with autism

>tend to have gut permeability, and everyone knows autism

>is caused by mercury, so mercury must cause gut permeability.

I'm not sure whether that is said facetiously? Certainly there is no

universal agreement that Hg is the cause of autism. I think it is thought to

be one among several causes.

But

>that is arguing the cause from the result: if autistics have

>higher mercury levels, THAT may be the result of gut permeability,

>not the other way around, or they might both be caused by another

>thing.

Sure, but as I said above, gut permeability is only *one* of the many

problems associated with Hg toxicity.

>

>

>>Now, if you're talking about gluten glomming onto villi, that to my

>>knowledge, does not cause an immune reaction. Does it? Or perhaps there's

>>some other mechanism whereby gluten causes ain immune reaction in_everyone

>>that I've never heard of? Please specify what you mean by " so the immune

>>system reacts to it " . In what way? IgA? Other?

>

>It's one of those things that is still under discussion, but yeah,

>a lot of researchers believe that the fact the villi are coated

>by gliadin makes gliadin somewhat a toxin. Not a really bad toxin,

>for most people, but disruptive in the way that, say, phytates are.

>The immune system might in fact be reacting to it because it's

>trying to clean the villi.

You mean *IgA* antibodies reacting to the villi glomming?

>

>And yeah, I was talking about the IgA reaction, though the

>IgG reaction is common too. Most labs figure everyone has

>an IgA reaction to gluten and only call it a problem if it's

>over a certain level, which is something I haven't figured

>out either, since the IgA itself is known to cause damage.

My understanding is that we have IgA antibodies to many foods, not just

gluten. I think that's what that person (maybe ?) posted to the GFCFNN

list from Enterolabs? Something worth checking into...

>

>

>>And others aren't. So, for those that develop GS later in life (I

>seem to be

>>one of them) something ELSE besides gluten causes the GS genes to express

>>themselves thus causing an IgA reaction to gluten.

>

>Except that you don't know (and neither does anyone else) if in

>fact the genes " just started " to express themselves. The rates of

>intolerance as measured in the blood don't get higher and higher

>for older people, as you would expect if the gene gets " turned on "

>in later age.

Well, I don't say that based on blood tests, which I didn't take anyway. And

I don't say that based on my IgA levels, which were in the normal range

anyway, I say that in regards to my antitissue transglutaminase antibody

(ATTA) levels which were only slightly above the normal range. According to

Enterolabs, the ATTA levels ARE indicative of the length of time one's been

GS. The lab rep I spoke with said my level indicates I've only been GS for

maybe 1-3 years. That fits perfectly within the timeframe of my symptoms and

I was already thinking of that very same timeframe before he mentioned it. I

KNOW one can't go by symptoms alone as many GS folks are asymptomatic. But

since Enterolab told me a timeframe based on my ATTA levels that fit nearly

perfectly with my symptom chronology, I'm going on the theory (at least for

now) that I became GS approx. 2-3 years ago.

The rates of *illness* follow this bumpy curve ... for

>one individual, the usual route is that

>

>1. They get sick before they are 5. And then recover.

>2. They get sick again in their late teens. Then recover.

>3. They get sick again in thier late 30's early 40s. Then recover.

>4. Then get sick in their 60s.

Hunh, for me it seems I skipped steps 1 and 2 and went straight to #3.

>

>If they don't die during any one episode, they get better

>and the disease " goes away " . Some people skip a step.

>But the onset seems so highly age related that people

>tend to think it is hormones that trigger the symptoms (pregnancy

>is also a big trigger). At any rate, I don't think the GENES would

>turn off and on again.

Maybe, maybe not, in these individuals. As I understand it, genes CAN be

turned on and off, but no one really knows how to do it beyond a few basic

experiments with specific genes in rats. Although there's probably a lot

more epigenetic research going on that I'm not aware of, so the stuff I've

read on it could be the tip of the iceberg. But I'm sure we'd have heard

about it if someone figured out a way to turn off the GS genes.

>

>>Right, but that doesn't mean the antibiotic treatment can't lead

>to GS. I'll

>>go back and read that section of the Shaw book cuz I don't recall off the

>>top of my head the mechanism whereby this might be possible or perhaps I

>>mixed it up with something else. There are so many interralations between

>>the gut microflora, the immune system and allergies!

>

>I agree. Usually the allergies they talk about though are IgE and IgG.

Not Shaw, in relation to gluten allergy. He focuses on IgA gluten allergies.

Even has a section on ATTA. He actually theorizes that a by-product of

candida called arabinose (a sugar), cross links gluten molecules to tissue

proteins, rather than transglutaminase doing it, in austitic children. And

he theorizes that this cross linking by arabinose leads to a different

autoimmune reaction and gluten sensitivity. He talks a lot about

cross-linking, btw, which is extremely destructive to human tissue. Autistic

kids, btw, tend to be gluten and casein sensitive, but according to Shaw,

they do not often show typical gut damage when biopsied. They DO tend to

have a big problem with the opiods in both gluten and casein though,

probably due to a lack of DPP IV (which neutralizes the opiod fractions).

Dr. Shaw is to autism kind of like Dr. Fine is to GS and Celiac I think. In

that he has his own lab where he runs several unique tests (I think) for

several chemicals produced from various conditions associated with autism

such as candida overgrowth, ATTA, etc.

>

>>

>>Not JUST gluten though, but gluten and a GS gene that has *expressed*.

>>Without the expressed gene one doesn't get GS, as I understand it. So the

>>other common denominator is a trigger - something that causes the gene to

>>express itself. Now, perhaps in the case of *some* folks that could be

>>simply too much gluten? I don't know. But I find it interesting that my GS

>>genes seemed to have expressed at a time when I was consuming a lot LESS

>>gluten than I previously had and at around age 40.

>

>See, the " age 40 " thing is classic. Mine started at age 40 too. Though I

>was also pregnant at the time!

With your son? Doesn't he have some developmental disabilities? I'm asking

because I'd like to have kids and I'm now 42. I'd like to avoid problems

that others in a similar situation have had. Were you GF and CF when you

were pregnant? I'm now GF and CF and still chelating HG one year after

having my amalgams removed.

>

>As for " just gluten " being the trigger, that does in fact seem to be

>the case in tribal cultures who get wheat for the first time.

What do you mean by this? Price's tribes?

For today's

>tribes you might say they were getting vaccines at the same time, tho

>that is clearly not always the case, but the same seems to have held

>true from historical accounts for earlier times.

Can you explain a bit more? I'm still not clear on what tribes and what time

period and what exact foods and/or other changes were going on at the time.

>

>

>>In any case, there are any number of things that cause genes to express or

>>not express including nutrition, which is a biggie.

>

>Absolutely nutrition makes a difference in how sick people get.

>As for " expression " ... you don't *know* if the gene is expressing

>or not. Just if you get symptoms or not. I got rid of most of my

>symptoms by taking probiotic pills. easy peasy.

I agree that we don't know if a gene is expressing or not UNLESS we get

tested for ATTA and the genes. If both come out positive, according to

Enterolab, then yer outta luck - the gene is expressed!

Having said that, I do wonder if it's possible that ATTA is triggered by

antibodies to candida or other microbes, and if the gene might NOT be

expressed in that case.

>>

>>I don't think you can draw that conclusion based on the food aid

>situation.

>>Food aid is sent to people who don't have enough food, who are

>>undernourished, malnourished, experiencing wars, drought, and/or famine.

>>Since it has been established that our nutritional status can

>cause genes to

>>express differently, this is a variable that must be taken into

>account when

>>looking at the food aid situation. Thus, I don't think we can

>>automatically assume that gluten alone is the sole cause of GS in the food

>>aid recipient population, at minimum, since their nutritional status does

>>not represent that of the entire rest of the world, and may be

>causing their

>>genes to express in a particular way.

>

>Maybe you can't assume that from *one* food aid situation, but really,

>it's a big pattern.

But their nutritional status is also a pattern that *may* cause the genes to

express.

The fact they are poor and malnourished and get MORE

>malnourished on American wheat is a smoking gun, in my book. But

>again, it doesn't say anything about gene expression, just about

>symptoms. You give them wheat, they get sick. You take away the

>wheat, they get better. To figure out gene expression you'd have

>to do a lot of tests, and no one has.

Right, but again, there are a LOT of American who eat American wheat and

aren't GS. So gluten alone cannot be the sole cause of GS. And there are a

lot of people with the GS genes who don't produce abnormal levels of IgA

antibodies to gluten. The numbers of these people are much higher than can

be accounted for by the small percent who are low IgA producers.

>

>As for healthy people getting wheat ... you have Price's natives. And

>the Inuit, who were quite healthy in Stefannson's time.

Right, but they got *processed* devitalized foods all at once - white flour,

white sugar and canned foods. Because of this, we can't really pinpoint

whether it was gluten and/or the devitalized displacing foods that caused

their health issues.

>>

>>Except for the fact that not everyone exposed to gluten is gluten

>sensitive

>>and that it seems to require an *expressed* GS gene in order to be GS.

>

>Again, no one has a test for an " expressed " gene. It's a theory, based

>on IgA levels, which are poorly tested for anyway.

According to Enterolab and Dr. Shaw, ATTA is a far more reliable marker of

GS, IIRC, than IgA levels. If you have one of the genes AND you have

elevated ATTA, it's pretty clear your genes are expressed, as I understand

it.

I've met so many

>people who get really, really sick off gluten, have the gene, but don't

>test high for IgA. I don't know what's going on, but gene expression

>probably isn't it.

Did these people take *Dr. Fine's stool IgA* test? If not, that might

explain a lot. If they took that but didn't take the ATTA and gene tests,

then the IgA levels probably won't tell them much. They could be a low

producer, or not be eating much gluten or whatever. If I went only by my IgA

level, then I'd still be consuming gluten.

>>I think that would be a very informative test. Along with " before

>and after

>>candida overgrowth " , " before and after vaccines " etc! Something,

>something,

>>something is causing these GS genes to express in different people at

>>different stages in their lives. It seems to me that there's more than one

>>potential trigger. But it also seems to me that a trigger is almost always

>>involved, or at least, *often* involved. Maybe, due to the

>pregnant mother's

>>diet, or the infant's diet, an infant's GS genes will be expressed from

>>birth, or shortly thereafter. But for others, this just doesn't seem to be

>>the case, aside from whether or not they have symptoms.

>

>We'll have to agree to disagree about the trigger thing.

I'm still not clear on what you disagree with? That there's any such thing

as a trigger? Do you still hold that gluten alone is the sole cause of

gluten sensitivity? In every situation? Or am I misunderstanding you? If

that IS what you think, then I've presented some facts that dispute it and

would love to hear your rebuttal.

Does this mean I don't get to be a deputy glutenator? ;-)

Suze Fisher

Lapdog Design, Inc.

Web Design & Development

http://members.bellatlantic.net/~vze3shjg

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]

>That's fine, we can add " immune training " to the list. But this doesn't

>address what I said about there being more than one causal factor in gluten

>sensitivity in response to you asking why there needs to be " a CAUSE for

>gluten sensitivity, other than gluten? "

>

>What is your response to my rebuttal that not everyone who consumes gluten

>is sensitive to it? If gluten were the ONLY cause of GS, then everyone who

>eats gluten would be sensitive (have an IgA reaction) to it (above normal

>levels), which is not the case. Which is why I listed other factors

>necessary for GS.

Well basically, my response is what it always is:

1. We don't really *know* how many people with the gene ARE

responsive. All the tests are somewhat inaccurate: even the stool

test. A lot of folks are lacking IgA, and a lot of folks who are

gluten-sensitive instinctively avoid wheat. And a lot of folks who

FINALLY get tested have, in fact, been avoiding gluten for months

before the test. So many of the folks I know that get sick off

gluten fail the IgA test that I figure it's not a terribly accurate indicator

of what is really going on (maybe we need a zonulin test?).

2. The factors that we KNOW influence immunity have to do with

when foods are introduced, and breastfeeding.

3. The immune system is designed to look for microbes. Like,

say, smallpox. Now, how would you react if I said " well, your immune

system will look for smallpox, but ONLY if you happened to be exposed

to mercury, or get a vaccine, or get sick with something else, at the time

you were exposed to smallpox " . You would say I was nuts: the body is

looking for smallpox, it finds it, it goes into high alert and kills it.

Now if there were a food that *looked like* smallpox but was

a food, not a microbe, then there might be an " off " switch for

the immune system, or maybe some level of damage has to happen

besides just the smallpox protein showing up before the immune

system will react. There absolutely do seem to be factors that

attenuate the immune system response (which is why allergy shots

work).

Anyway, the more we talk the more I think the old idea of " the

gene needs to be turned on " is an old theory: if 70% of the people

with the gene have high IgA, then it's more likely that the gene

is turned OFF for some subset of people.

>

>Exactly! That would be an additional factor in the cause of GS *beyond*

>gluten itself.

Except that breast milk is more a " turner offer " . I.e., it tells

the baby " this food is ok " .

I'm not arguing that there *aren't* external factors: I've mentioned

several that DO seem to be external factors. But by far the biggest

factor seems to be gluten itself: when it is introduced, the

form it is in, combined with the immune system and the state

it is in. Sure, nutritional status affects the state of the immune

system (as would vaccines, getting enough sleep, stress in the

family, lead paint ingestion, age of the person, etc.) but in the

overall numbers and history of the disease, it just doesn't seem

to be a big factor.

What bothers me is that some folks lately seem to be arguing

that if a person had great health and a great environment

and properly soaked their grains, that wheat would somehow

still be ok. That seems like a dangerous stance, or maybe it's

just a phase of denial. If a person has great health and a great

environment, chances are they can ingest a lot of mercury

too without feeling any side effects.

>

>

>But gut permeability can be triggered by IgA

>>allergies, and in fact that is the primary link that has been found

>>to gut permeability. Maybe mercury can trigger gut permeability

>>too, but so far it seems to be mainly a theory: kids with autism

>>tend to have gut permeability, and everyone knows autism

>>is caused by mercury, so mercury must cause gut permeability.

>

>I'm not sure whether that is said facetiously? Certainly there is no

>universal agreement that Hg is the cause of autism. I think it is thought to

>be one among several causes.

There isn't universal agreement about *anything* at this

point, nor enough data to get even close! But yeah, a lot of folks

do seem to believe that mercury causes autism.

>You mean *IgA* antibodies reacting to the villi glomming?

No, I mean that if gluten gloms on to the villi, the villi

dont' like it much. It's like lectins and the blood cells ... some

foods, mainly beans, can cause blood cells to clump. There

have been major outbreaks of illness from poorly cooked

kidney beans! And castor beans are REALLY toxic because of

their lectins. Gliadin is a lectin. The body doesn't like it much.

Our bodies can tolerate it, or most of us can, but it isn't benign.

The IgA antibodies cause even *worse* damage.

>My understanding is that we have IgA antibodies to many foods, not just

>gluten. I think that's what that person (maybe ?) posted to the GFCFNN

>list from Enterolabs? Something worth checking into...

I did hear that, and that is just very odd. I should read up

on antibodies ...

>

>Well, I don't say that based on blood tests, which I didn't take anyway. And

>I don't say that based on my IgA levels, which were in the normal range

>anyway, I say that in regards to my antitissue transglutaminase antibody

>(ATTA) levels which were only slightly above the normal range. According to

>Enterolabs, the ATTA levels ARE indicative of the length of time one's been

>GS. The lab rep I spoke with said my level indicates I've only been GS for

>maybe 1-3 years. That fits perfectly within the timeframe of my symptoms and

>I was already thinking of that very same timeframe before he mentioned it. I

>KNOW one can't go by symptoms alone as many GS folks are asymptomatic. But

>since Enterolab told me a timeframe based on my ATTA levels that fit nearly

>perfectly with my symptom chronology, I'm going on the theory (at least for

>now) that I became GS approx. 2-3 years ago.

That's an interesting idea ... my ATTA levels were NOT high, but I'm pretty

sure I've been gluten reactive since I was 17 or so, and probably before then.

How do they account for the numbers that seem to show that

the IgA sensitivity is about the same, as a percentage of the population,

for kids as for adults?

>Hunh, for me it seems I skipped steps 1 and 2 and went straight to #3.

So maybe the earlier hormonal issues didn't do it ... or you

were too healthy to notice ...

>Maybe, maybe not, in these individuals. As I understand it, genes CAN be

>turned on and off, but no one really knows how to do it beyond a few basic

>experiments with specific genes in rats. Although there's probably a lot

>more epigenetic research going on that I'm not aware of, so the stuff I've

>read on it could be the tip of the iceberg. But I'm sure we'd have heard

>about it if someone figured out a way to turn off the GS genes.

Some genes are turned on and off ... the HLA genes I'm not sure. Again,

my understanding is that they are there to test for microbes, that's what

they do. I should do more reading ..

>

>Not Shaw, in relation to gluten allergy. He focuses on IgA gluten allergies.

>Even has a section on ATTA. He actually theorizes that a by-product of

>candida called arabinose (a sugar), cross links gluten molecules to tissue

>proteins, rather than transglutaminase doing it, in austitic children. And

>he theorizes that this cross linking by arabinose leads to a different

>autoimmune reaction and gluten sensitivity. He talks a lot about

>cross-linking, btw, which is extremely destructive to human tissue. Autistic

>kids, btw, tend to be gluten and casein sensitive, but according to Shaw,

>they do not often show typical gut damage when biopsied. They DO tend to

>have a big problem with the opiods in both gluten and casein though,

>probably due to a lack of DPP IV (which neutralizes the opiod fractions).

>

>Dr. Shaw is to autism kind of like Dr. Fine is to GS and Celiac I think. In

>that he has his own lab where he runs several unique tests (I think) for

>several chemicals produced from various conditions associated with autism

>such as candida overgrowth, ATTA, etc.

That is my understanding too, that the autistic kids have something

different going on.

>

>With your son? Doesn't he have some developmental disabilities? I'm asking

>because I'd like to have kids and I'm now 42. I'd like to avoid problems

>that others in a similar situation have had. Were you GF and CF when you

>were pregnant? I'm now GF and CF and still chelating HG one year after

>having my amalgams removed.

I suspect my son has issues with a different gene ... Marfan's, which

runs in both my and my dh's family. Marfan's might be one of those

that expresses " only if " ... it's a dominant gene but doesn't always

affect people. Since I was having major gluten issues while carrying

him, I sure wouldn't rule out a connection! Interestingly though,

as a result of his issues, he has *never* had gluten, and he has

a wide dental arch (unlike anyone else on either side of the family)

and wide nostrils.

>>

>>As for " just gluten " being the trigger, that does in fact seem to be

>>the case in tribal cultures who get wheat for the first time.

>

>What do you mean by this? Price's tribes?

Prices tribes, and modern cultures that get food aid.

>For today's

>>tribes you might say they were getting vaccines at the same time, tho

>>that is clearly not always the case, but the same seems to have held

>>true from historical accounts for earlier times.

>

>Can you explain a bit more? I'm still not clear on what tribes and what time

>period and what exact foods and/or other changes were going on at the time.

Oh sheesh, we've discussed this so much over the years in so many

contexts! I don't have the energy tonight to look it all up again.

>I agree that we don't know if a gene is expressing or not UNLESS we get

>tested for ATTA and the genes. If both come out positive, according to

>Enterolab, then yer outta luck - the gene is expressed!

>

>Having said that, I do wonder if it's possible that ATTA is triggered by

>antibodies to candida or other microbes, and if the gene might NOT be

>expressed in that case.

Technically, you know that ATTA is being produced. You *don't* know

that the gene is expressed. I don't think anyone knows that at

this point. People say a " gene is expressed " when it causes something

to happen, but it's not that simple. I mean, I might have a gene that

is expressed to make my hair brown. But I dye it blonde. If you look

at me, you will say " the blonde gene is being expressed " . I don't know

all the factors that effect ATTA and IgA etc, but a lot of them are

environmental (IgA goes down if you don't eat gluten) not gene

expression per se.

>

>Right, but again, there are a LOT of American who eat American wheat and

>aren't GS. So gluten alone cannot be the sole cause of GS. And there are a

>lot of people with the GS genes who don't produce abnormal levels of IgA

>antibodies to gluten. The numbers of these people are much higher than can

>be accounted for by the small percent who are low IgA producers.

Are there a LOT of Americans who eat wheat and aren't GS AND have the gene?

If 70% of the Americans who have the gene are GS, then that leaves

30% to account for. A lot of those probably didn't get gluten in the first

3 months, or they were breast fed. A lot of the others probably don't

eat gluten much or are low IgA. Some of the others might have another

gene involved. So maybe you are left with %5 of unknown etiology.

Maybe.

And that all hinges on counting " abnormal levels of IgA " as being

the smoking gun, which for folks with dermatitis herpitiformis and

autism, isn't the case. There isn't enough research to really know,

but I'm predicting that when the smoke clears, gluten is going

to be one of those things that is just considered bad news.

> >As for healthy people getting wheat ... you have Price's natives. And

>>the Inuit, who were quite healthy in Stefannson's time.

>

>Right, but they got *processed* devitalized foods all at once - white flour,

>white sugar and canned foods. Because of this, we can't really pinpoint

>whether it was gluten and/or the devitalized displacing foods that caused

>their health issues.

Except that the same problems happen in modern times, when

whole wheat berries are shipped to tribes. Also remember that

in a lot of remote places, though they got " displacing foods of modern

commerce " , the foods were expensive and didn't really displace

a lot of their diet. I was talking to a person who sold stuff to the

Inuit, and said the average family would get 100 lbs of flour for

the year, which isn't very much really. It still ruined their health.

>

>According to Enterolab and Dr. Shaw, ATTA is a far more reliable marker of

>GS, IIRC, than IgA levels. If you have one of the genes AND you have

>elevated ATTA, it's pretty clear your genes are expressed, as I understand

>it.

That's a new area to research ...

>

>I'm still not clear on what you disagree with? That there's any such thing

>as a trigger? Do you still hold that gluten alone is the sole cause of

>gluten sensitivity? In every situation? Or am I misunderstanding you? If

>that IS what you think, then I've presented some facts that dispute it and

>would love to hear your rebuttal.

There is a school of thought that says that basically a person

should be able to eat gluten, but then " something happens " and

suddenly they can't, because a gene gets triggered. Once triggered,

the gene is always " on " and doesn't turn off again. I just don't think

this squares with what is known about gluten sensitivity ... I think

the reactivity depends on the type and amount of gluten, and when

it is introduced, and breastfeeding. And the number of symptoms

produced depends on hormones, probiotics, general health, etc.

Debating it won't change the facts though: the folks doing the

research will come up with more data (as it sounds like Dr. Fine

is doing, and Dr. Fasano).

-- Heidi Jean

[Guest guest]

On 7/17/05, Heidi Schuppenhauer <heidis@...> wrote:

> 3. The immune system is designed to look for microbes. Like,

> say, smallpox. Now, how would you react if I said " well, your immune

> system will look for smallpox, but ONLY if you happened to be exposed

> to mercury, or get a vaccine, or get sick with something else, at the time

> you were exposed to smallpox " . You would say I was nuts: the body is

> looking for smallpox, it finds it, it goes into high alert and kills it.

> Now if there were a food that *looked like* smallpox but was

> a food, not a microbe, then there might be an " off " switch for

> the immune system, or maybe some level of damage has to happen

> besides just the smallpox protein showing up before the immune

> system will react. There absolutely do seem to be factors that

> attenuate the immune system response (which is why allergy shots

> work).

>

> Anyway, the more we talk the more I think the old idea of " the

> gene needs to be turned on " is an old theory: if 70% of the people

> with the gene have high IgA, then it's more likely that the gene

> is turned OFF for some subset of people.

Couldn't it also be a possibility that some people have inherited a

permanent off-switch gene? In other words, in areas where wheat

consumption has been high for a long time, people would survive if

they DIDN'T have the gene for GS _OR_ if they had a gene that

down-regulated its expression sufficiently. Since there are

regulatory genes anyway, it could be that this gene is naturally

present but there could be a mutation in some people that makes it

much more active in suppressing the GS gene.

Not that there's any evidence of it... but it could be a plausible

explanation for the gap between the genotype and the phenotype, if, as

you point out, there actually is one when the smoke clears.

> Technically, you know that ATTA is being produced. You *don't* know

> that the gene is expressed. I don't think anyone knows that at

> this point. People say a " gene is expressed " when it causes something

> to happen, but it's not that simple. I mean, I might have a gene that

> is expressed to make my hair brown. But I dye it blonde. If you look

> at me, you will say " the blonde gene is being expressed " . I don't know

> all the factors that effect ATTA and IgA etc, but a lot of them are

> environmental (IgA goes down if you don't eat gluten) not gene

> expression per se.

Aren't ATTA and all antibodies proteins? If so, they must be produced

by a gene.

Chris

[Guest guest]

>Couldn't it also be a possibility that some people have inherited a

>permanent off-switch gene? In other words, in areas where wheat

>consumption has been high for a long time, people would survive if

>they DIDN'T have the gene for GS _OR_ if they had a gene that

>down-regulated its expression sufficiently. Since there are

>regulatory genes anyway, it could be that this gene is naturally

>present but there could be a mutation in some people that makes it

>much more active in suppressing the GS gene.

I think that is very likely (in addition to all the other

stuff that is going on). Esp. since some population groups

have eaten wheat a long time. Genes rarely act alone!

>Not that there's any evidence of it... but it could be a plausible

>explanation for the gap between the genotype and the phenotype, if, as

>you point out, there actually is one when the smoke clears.

>

>> Technically, you know that ATTA is being produced. You *don't* know

>> that the gene is expressed. I don't think anyone knows that at

>> this point. People say a " gene is expressed " when it causes something

>> to happen, but it's not that simple. I mean, I might have a gene that

>> is expressed to make my hair brown. But I dye it blonde. If you look

>> at me, you will say " the blonde gene is being expressed " . I don't know

>> all the factors that effect ATTA and IgA etc, but a lot of them are

>> environmental (IgA goes down if you don't eat gluten) not gene

>> expression per se.

>

>Aren't ATTA and all antibodies proteins? If so, they must be produced

>by a gene.

>

>Chris

I'm not sure there is a gene for *each* antibody. Some antibodies

are produced purely based on " experience " . The body associates

some protein with some bad event somehow, and starts making

antibodies for that protein. I don't know how the body " decides "

that ... there is this whole tracking mechanism that is supposed

to keep the body from getting confused and attacking your OWN

proteins, but even that gets very confused often and then you

get autoimmune diseases and you get antibodies to YOU, which

certainly wouldn't be created by one gene.

That is the whole theory behind vaccines, and part of what

goes on with mother's milk: if you introduce a protein into

the blood, the body looks at that and somehow decides " this

is bad stuff: need an antibody to it! " and for some length of

time produces antibodies. But HOW LONG it produces antibodies

depends on the thing. For cold viruses, for example, your body

apparently produces the antibody for your whole life, once you've

had that particular virus and survived it. But other viruses you

can catch more than once, or it can coexist with your immune

system (herpes, for example). But then there is this " built in "

recognition system for *some* microbes that some people

are born with, and it's my understanding that the HLA gene

that causes gluten issues is a built-in antibody system.

The ATTA thing is new to me ... I can't see, for the life of me and it's

bugging me like crazy ... how you could tell *how long* a person

has been reacting to gluten by measuring one thing. I mean, take

blood pressure. It tends to go up with age, but you can't tell

how long a person has had high blood pressure based on their age:

my granddad died of high blood pressure at 44, it was 300 over something.

IgA levels go up and down depending on how much gluten a person

has been eating, not by how long they have been eating it (unless

perhaps there is an adrenal fatigue thing going on, but that would

depend on the gluten load too).

And virtually no one has EVER been tracked " before and after " becoming

GS, unless Fine or someone has done some studies no one has been talking about

yet. I mean, if they take a kid with zero antibodies, then follow them

for years and years and see if the kid DOES develop antibodies, and

assuming the diet has the same amount of gluten for that entire

period, then you could get some tracking and it would be a great

experiment: but I haven't heard of anyone doing that yet.

But all the studies to date that I know of are random blood samples,

or more commonly, un-random blood samples from sick people (who go in

for, say, gut problems, or send in to Dr. Fine for a stool test

because they suspect something is wrong). The random blood samples

seem to show that in our current population, the IgA levels are

the same percentage for all age groups, but the *symptoms* tend

to cluster at certain ages. So does ATTA track with symptoms or

onset of symptoms? Are they tracking individuals before and after

onset of symptoms?

Heidi

[Guest guest]

> There is a school of thought that says that basically a person

> should be able to eat gluten, but then " something happens " and

> suddenly they can't, because a gene gets triggered. Once triggered,

> the gene is always " on " and doesn't turn off again. I just don't

think

> this squares with what is known about gluten sensitivity ... I think

> the reactivity depends on the type and amount of gluten, and when

> it is introduced, and breastfeeding. And the number of symptoms

> produced depends on hormones, probiotics, general health, etc.

I understand that researchers who study cattle and CLA production say

that if you even give a cow grain *ONE TIME*, then that cow will

never produce the same amount of CLA as it did before, while on a

diet of just grass. The CLA is produced in the rumen, which is

changed once grain is introduced.

IIRC, DH talked to Dr. Tilak and pinned that point down. And he

called another fellow, one of the cattle authorities that we take

seriously, and asked him if that situation was due to the presence of

fungus in the grain. The fellow said it was. I believe the fellow's

response was couched in a tone that indicated " well duh...yes of

course it's due to the fungus. " I'm sorry I don't know the fellow's

name. I will try to find out, if anyone is interested.

Today I did some reading about gluten, gluten flour, and corn gluten

meal. One thing I saw was that someone had bought a bag of gluten

flour from some nearby Amish farmers. The flour had smelled " funny "

and got really bad before too long, and the person had to discard it.

Another person responded that gluten flour is a " moisture magnet " ,

and they needed to be careful how they stored it, and for how long.

That makes me wonder if breads made with lots of gluten become even

more harmful after they have sat for a while. Breads that can sit on

a shelf for weeks and not become moldy or dry seem unnatural!

Researchers at Iowa State have found that they can use corn gluten

meal as an organic weed-and-feed soil supplement. If you apply it to

your soil a couple of times a year, it can kill around 70% of the

weeds in your yard. It kills the weeds by coating the seeds and

damaging the first tiny rootlets when they first appear. The cells

on the roots are damaged and can't grow properly. There may be some

top growth, but once conditions turn dry, the weeds die because their

roots haven't developed normally.

If you use corn gluten meal as a preemergent weed-and-feed, you don't

want to sow grass seed for around 6 weeks, because grass seed is

susceptible, too.

Isn't that interesting? It's like for plants, which get nutrition by

being in touch with the exterior environment, their ability to take

in nutrients through their roots is irreversibly damaged. And people

and animals, which get nutrition from food that is passed through,

lose their ability to take in nutrition because the villi are damaged.

Corn gluten meal damages tiny rootlets of plants, and

wheat/rye/barley gluten does something similar to people.

Fascinating!

Know where corn gluten meal comes from? HFCS producers. That stuff

is already on our " bad list " , isn't it?

According to Dr. Hamer, colon cancer is associated with " ugly

indigestible conflict " , intestinal cancer is associated with

an " indigestible chunk of anger " , and stomach cancer is associated

with " indigestible anger, swallowed too often " .

I know we're not talking about cancer here, but doesn't celiac often

lead to cancer?

Perhaps part of the trigger for GS/GI/IBS/celiac/sprue is an

experience with especially ugly conflict/anger, and likely one that

remains unresolved for a long time.

[Guest guest]

On 7/16/05, Suze Fisher <s.fisher22@...> wrote:

> But gut permeability can be triggered by IgA

> >allergies, and in fact that is the primary link that has been found

> >to gut permeability. Maybe mercury can trigger gut permeability

> >too, but so far it seems to be mainly a theory: kids with autism

> >tend to have gut permeability, and everyone knows autism

> >is caused by mercury, so mercury must cause gut permeability.

>

> I'm not sure whether that is said facetiously? Certainly there is no

> universal agreement that Hg is the cause of autism. I think it is thought to

> be one among several causes.

>

> But

> >that is arguing the cause from the result: if autistics have

> >higher mercury levels, THAT may be the result of gut permeability,

> >not the other way around, or they might both be caused by another

> >thing.

>

> Sure, but as I said above, gut permeability is only *one* of the many

> problems associated with Hg toxicity.

This is Suze responding to Heidi. Google search for gliadin breakdown

produced this long, worth the read link about commonality between GS

and autism

http://www.vaccinetruth.org/gluten.htm

Wanita