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Does Bcm7 (A Milk Opiod) Initiate Celiac Disease?
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I've heard lots about gluten and how it triggers the immune system to destroy the lining of the small intestine but only when it is ingested.

I've heard quite a bit about casein lately (and pretty interesting stuff on beta-casomorphin-7 (bcm7) - an opiod-like fragment that gets easily released on digestion from A1 milk. Most of our milk today has a mixture of A1 and A2 beta casein.

A1 milk seems like it might be behind many health problems like initiating type 1 diabetic beta cell destruction by the immune system along with heart disease, autism, schitzophrenia and food allergies.

Lately I've debated to myself whether it may possibly initiate celiac disease too. I've heard that the opiods in casein are more powerful than those in gluten. It seems that countries like Finland and Sweden (where A1 milk consumption is highest in the world due to Ayrshire cow breeds) have the highest incidence of type 1 diabetes.

Celiac seems pretty common over there too!

So here's my question... Does bcm7 possibly initiate celiac disease and/or gluten sensitivity?

I'd be very interested in your thoughts on this insightful topic.

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No, it does not.

Celiac is triggered by gluten, but there must be other factors apart from gluten that can contribute to the development of celiac disease.

From the Celiac Disease Center at Columbia University:

"Some of the factors are the timing of the first ingestion of gluten in childhood and the amount of gluten, whether breast feeding occurs and whether other members of the family have celiac disease. Smoking also influences the onset of celiac disease.

Still, why celiac disease develops in some individuals in childhood and others as adults is unclear. One is not born with the disease. One is born with a genetic tendency to develop the disease. It is considered that gastrointestinal infections may be a factor that can trigger the development of the disease."

You keep saying "I've heard"...where exactly do you hear this?

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Lately I've debated to myself whether it may possibly initiate celiac disease too. I've heard that the opiods in casein are more powerful than those in gluten. It seems that countries like Finland and Sweden (where A1 milk consumption is highest in the world due to Ayrshire cow breeds) have the highest incidence of type 1 diabetes.

Celiac seems pretty common over there too!

So here's my question... Does bcm7 possibly initiate celiac disease and/or gluten sensitivity?

I'd be very interested in your thoughts on this insightful topic.

Very interesting - I've not done any research on milk like you obviously have.

In my opinion, there is so much science that has yet to be discovered. This is only punctuated by the fact that so many who are suffering, find relief with eliminating certain foods (e.g. grains, dairy) from their diet - yet so many people go years, and spend a small fortune trying to get a diagnosis. I too am curious about what triggers the gene to express itself.

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But, the research is clear and I just said it: Gluten.

Gluten ingestion, a genetic predisposition and some type of trauma, such as an accident, an injury, pregnancy, extreme stress, and a viral infection. Possibly environmental factors (research is ongoing)

These are the celiac "triggers", as far as we know.

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Is this where you found your information?

http://www.healthnowmedical.com/blog/2011/10/06/study-reveals-why-dairy-products-are-a-bad-idea/

I would not spend too much time bending your brain on this blog.

From my good friend Joy Baurer:

Lactose intolerance is not a food allergy; it does not involve an immune response to milk or lactose, and it is not dangerous. Lactose intolerance occurs in individuals who do not make adequate amounts of the enzyme “lactase,” which is required to digest “lactose,” a specific type of sugar found in milk and other dairy products. Individuals with lactose intolerance experience gastrointestinal symptoms such as bloating, gas, diarrhea and stomach cramping about 20 minutes to two hours after consuming high-lactose foods like milk, ice cream, puddings and creamy soups.

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I've heard lots about gluten...

I've heard quite a bit about casein lately...

I've heard lots of things, too. I've heard that JFK was assassinated by LBJ to gain access to the White House. I've heard that Kraft Foods put gluten in everything they make, and then lie about it. I've heard that Sarah Palin is sane.

I've heard ain't worth nuthin, unless you have a credible source to back it up.

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I've heard lots about gluten and how it triggers the immune system to destroy the lining of the small intestine but only when it is ingested.

I've heard quite a bit about casein lately (and pretty interesting stuff on beta-casomorphin-7 (bcm7) - an opiod-like fragment that gets easily released on digestion from A1 milk. Most of our milk today has a mixture of A1 and A2 beta casein.

A1 milk seems like it might be behind many health problems like initiating type 1 diabetic beta cell destruction by the immune system along with heart disease, autism, schitzophrenia and food allergies.

Lately I've debated to myself whether it may possibly initiate celiac disease too. I've heard that the opiods in casein are more powerful than those in gluten. It seems that countries like Finland and Sweden (where A1 milk consumption is highest in the world due to Ayrshire cow breeds) have the highest incidence of type 1 diabetes.

Celiac seems pretty common over there too!

So here's my question... Does bcm7 possibly initiate celiac disease and/or gluten sensitivity?

I'd be very interested in your thoughts on this insightful topic.

Seems unlikely. I dislike milk and haven't consumed t since I was a child. Lots of people limit milk, and milk products, and still develop problems with gluten. All over the world. Even in places where they drink primarily goat's milk.

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Type 1 diabetes and celiac are related closely genetically, aren't they? Keith Woodford's book: Devil in the Milk is something I read recently and he and scientific papers say that A1 milk gave diabetes prone mice t1 diabetes and a2 milk didn't. I'm thinking bcm7 might be the possible third factor for celiac disease. That's all.

Btw I'm not saying avoid dairy at all. I think milk products are great. Just not the A1 casein.

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Can you tell us any of the papers he cites so we can look them up for ourselves?

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Um guys, you might want to go do some reading before you keep piling on with the skepticism and unsupportive posts. This is an interesting question and not as far-fetched as everyone seems to believe. There is a enough literature on cows milk and diabetes that I couldn't begin to summarize it. It's pretty clear that feeding cows milk in early infancy increases the incidence of T1. What's not clear is whether it has anything to do with A1 milk or BCM7. Casomorphins do get into the bloodstream, are active on opioid receptors, and can have effects on peripheral blood mononucleocytes.

One paper on A1 milk and a rebuttal that doesn't seem to have industry bias. (There is a lot of trouble with very biased and selectively referenced milk industry papers in the A1 casein literature.)

http://www.ncbi.nlm.nih.gov/pubmed/17666771

http://www.ncbi.nlm.nih.gov/pubmed/15867940

If cows milk has the ability to trigger type 1 diabetes (whether or not the mechanism is BCM7), given the links between the diseases it seems an interesting question as to whether it could predispose to celiac.

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Ahh thank you Skylark, I wanted to comment on the OP's topic looking more trigger-related than post-disease gluten-related but couldn't have said it as well as you.

All I could get was a vague "there's a difference between pulling a trigger & pulling a trigger after the safety is off."

Regarding the OP, the area of celiac disease triggers doesn't seem to get much researcher attention, though maybe I'm looking in the wrong places & gene expression does get attn in auto-immune circles.

If an accident were a celiac's trigger, does that mean they'd never been in an accident before? Of course not because severity is left out.

If a pregnancy triggered celiac disease, is it always her 1st pregnancy? I think I've read otherwise here.

I don't know diddly about A1 milk & BCM7, but I do think there's some biological/genetic characteristic(s) analogous to "setting the safety off" on a firearm.

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Isn't it more a case of bad memory cells being created in the bone marrow that respond to dendritic cells with the celiac genes attached to them? Denise Faustman said something about this in a video on t1 diabetes.

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I think so little is really still known about autoimmune diseases. What triggers them, causes them etc. I don't believe it could be a simple as one thing, thanks for the links skylark, It'll be interesting to read.

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Would epigenetics be relevant to any of this?

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The triggers idea for celiac reminds me of the way they used to talk about stomach ulcers. They (doctors) used to say ulcers were casued by stress, too much spicy foods, alcohol, etc. A whole slew of things that sort of sounded reasonable. But it turned out to be a bacteria causing the ulcers. And that is not the same at all. I don't think anyone really knows right now what causes one person to develop celiac vs another. Maybe that will change some day. The same debate is going on about Crohns' disease. None is really sure what triggers it. There is bacteria that some people think may be involved. But it is not really known for sure as other things seem to trigger it also, lots of ideas, not many answers.

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I did hear somewhere that Lyme disease might be the player in RA and MS in a few places. Wasn't an outbreak of RA the way that Lyme was discovered?

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Though I just looked at http://betacasein.org and heart disease and type 1 diabetes incidence is right in line!

Correct me if I'm wrong but doesn't France have a lower incidence of celiac disease than most European countries? They drink more a2 milk and have less t1 diabetes than other places.

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If an accident were a celiac's trigger, does that mean they'd never been in an accident before? Of course not because severity is left out.

If a pregnancy triggered celiac disease, is it always her 1st pregnancy? I think I've read otherwise here.

I don't know diddly about A1 milk & BCM7, but I do think there's some biological/genetic characteristic(s) analogous to "setting the safety off" on a firearm.

I like this analogy. There is something we are doing in modernized countries that seems to predispose to type 1 and celiac. Researchers think there is a "safety off" sort of situation because the incidences of T1 and celiac are rising at very similar rates, particularly in industrialized countries. The hygiene hypothesis doesn't go very far towards explaining it, though.

Would epigenetics be relevant to any of this?

I'm in the middle of reading Dr. Shanahan's book, Deep Nutrition: Why Your Genes Need Traditional Food. It's an eye-opener about how strong a role epigenetics can play in health, even across generations. The chapter on milk pasteurization was also fascinating. There are microstructural changes in milk after pasteurization and homogenization to the point that pasteurized/homogenized milk is a different food from what comes out of the cow's udder.

I would love to know if there is a difference in the T1 rate when babies are fed raw milk vs. pasteurized but I don't think it's even on researchers' radar. The reason I wonder is becasue milk tends to be pasteurized more in industrial countries where T1 and celiac are on the rise. Don't quote me on this; it is idle armchair speculation.

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T1 was around before milk was pasteurized. The a1 bcm7 opiod would have still been released I suspect.

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Would epigenetics be relevant to any of this?

A while back, I watched a program that explained epigenetics. The first thing that went through my mind was that it might explain why someone with genetic factors for celiac might not present the usual symptoms. Surprisingly, yours is probably the first post I've seen that mentioned epigenetics.

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T1 was around before milk was pasteurized. The a1 bcm7 opiod would have still been released I suspect.

I guess what I was wondering about was kinetics of casomorphin release and absorption in raw vs. pasteurized. I don't know if it would be different.

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Well, to throw a slightly different spin into the mix, it seems there is at least suspicion that a bacterial strain in cow's milk (Mycobacterium para-tuberculosis) is what may at least sometimes be involved in triggering Crohn's Disease.

so it wouldn't be a ridiculous idea that something similar may happen to trigger Celiac Disease?

Especially as I think Type 1 diabetes is also thought to be linked to the same Mycobacteria.

I think what no-one is yet sure of is whether such a Mycobacterial strain could be the causative agent of these illnesses, or whether it is an opportunistic invader when the host body is already weakened.

Food for thought at least!

Carolyn

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Wow, that's interesting! Did you happen to bookmark where you read it? I can probably dig it out but it's faster to have a link.

One of the things that can cause celiac is Campylobacter jejuni food poisoning.

And hey, check this article out on celiac autoimmunity and infections that just popped up with Google. Nothing to do with cows milk but really interesting!

http://www.sciencedirect.com/science/article/pii/S1568997208002012

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Wow I can really learn a lot in this thread.

Codetalker, I think I saw the same show on epigenetics, or at least similar. It was fascinating.

Skylark, that last link had the term "molecular mimicry" in the abstract. I've wondered whether when ppl dismiss "cross-reactivity" as (often rightfully imho) nutty, if a valid "molecular mimicry" possibility gets wrongfully dismissed, a la baby/bathwater.

Not that I expect you to speak for "ppl", but thought you could easily reduce my confusion on the terms. :)

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Wow I can really learn a lot in this thread.

Codetalker, I think I saw the same show on epigenetics, or at least similar. It was fascinating.

Skylark, that last link had the term "molecular mimicry" in the abstract. I've wondered whether when ppl dismiss "cross-reactivity" as (often rightfully imho) nutty, if a valid "molecular mimicry" possibility gets wrongfully dismissed, a la baby/bathwater.

Not that I expect you to speak for "ppl", but thought you could easily reduce my confusion on the terms. :)

I don't generally even dismiss cross-reactivity. It seems to be a very misunderstood term on this board. Your antibodies are not perfect, and it's by design. If you made perfect antibodies, you would have no immune response against a slightly different strain of flu or bacteria. Say you get swine flu. You make antibodies and get well. A certain % of those antibodies will cross-react to the bird flu you might see next season. This is really handy because your immune system can go to work against the bird flu much faster. This happens in allergy too. People who are sensitive to ragweed pollen can cross-react to melons, and people who are sensitive to latex can cross-react to mango.

This is probably also the mechanism of oat-sensitive celiac disease and I put a publication here a while back that corn may be another trigger of villous atrophy in some folks. The corn sensitivity tends to happen in adults who have had time to develop a much wider variety of antibodies and thus have a higher probability of cross-reactivity to corn than children. Cross-reactivity to milk has also been demonstrated, but I've not seen a paper where the milk cross-reactivity lead to TTG and damage.

The confusion on the board is thinking that if someone has multiple intolerances they are all cross-reactions. Thus the ridiculous threads a while back on coffee. For example soy intolerance has never been linked to gluten cross-reactivity. It's just allergenic in its own right and our sensitive bodies tend to have a knack for making antibodies to it.

Molecular mimicry is a completely different idea. This is where a pathogen has proteins in its coat that mimic the host. The bacterium tricks your body into thinking it's a cell rather than an invader. If your immune system figures out the deception and makes antibodies to the mimic protein, they can be autoimmune. Again, this is because of that mild built-in cross reactivity antibodies have by design. Campylobacter is particularly dangerous because one of its mimic proteins resembles one in your nervous system. http://www.ncbi.nlm.nih.gov/pubmed/17374131

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