Quote from: CMdeux on December 04, 2013, 06:52:20 PM
Adults who have adult-onset food allergies have just always had that be so--  most people with adult-onset, there's this weird opening phase of things where even stuff you ARE NOT allergic to, you react to-- it's like your immune system views everything with some degree of suspicion, and some days, some things... more than others.  But unpredictable.

I'm curious about this because I had a very different experience with shellfish and milk which were very clear cut, no side reactions, no correlative sensitivities at all. And then with almonds, much more wonky and unpredictable with sudden reactions to different stuff (wool, greater sensitivity to pine, etc). Although I do have a lot of food intolerances that predate my allergies. When I was at the allergist I started telling her how I don't eat rice, even minute amounts of powdered rice in medications and vitamin supplements because it gives me a stomach ache and diarrhea and red spots and I was, like, oh, ding, ding, ding, maybe that was actually gearing up to an allergy, or WAS an allergy? She's testing it. Maybe I headed that one off at the pass and the others I just went too far to the breaking point of anaphylaxis? Most of the time I feel like I just overdid it on these foods and caused my own allergies. I has intestinal cramping for a full year and a half before this almond reaction which I thought was something else. Sometimes I think if I were more intuitive like I was with the rice, I could have avoided this?

Yeah-- I wonder, too, if adult-onset allergies are somehow more.... mutable in some ways, and less so in others.  Just-- different.

It seems like the conventional wisdom is that many childhood food allergies are HIGHLY mutable with external pressors of various kinds (which is what immunotherapy is based around) and that the adult versions tend to be less so in terms of MOVING the person's response from intolerant to tolerant... on the other hand, adult threshold doses seem to be more mutable in some cases, and honestly, less predictably so. 

Kids tend to have relatively stable sensitivity to allergens, and as they age into adolescence and young adulthood, something happens that destabilizes that-- which is where you get those very sad and scary anecdotes about teens or young adults being COMPLETELY caught by surprise when they anaphylax out of the blue to something that has "always been fine before."

Adults who have adult-onset food allergies have just always had that be so--  most people with adult-onset, there's this weird opening phase of things where even stuff you ARE NOT allergic to, you react to-- it's like your immune system views everything with some degree of suspicion, and some days, some things... more than others.  But unpredictable.

The allergen itself seems to matter less than the age of onset in some strange way, though the 'persistant' allergens tend to be of the "adult-type" right from the get-go in some people who are likely to have them be life-long.  Peanut, nuts, shellfish... though even there, people with them tend to age into that adult presentation where sensitivity can vary wildly, symptoms can vary wildly, etc.

Quote from: rebekahc on December 04, 2013, 04:29:57 PM

Quote from: CMdeux on December 04, 2013, 03:40:45 PM
Oh, as are we all, really-- just opinions.    Conversation, that's all.  Things to muse upon.

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Interestingly enough, DD's shellfish allergy manifested early and behaves more like a severe peanut/egg/etc. allergy.  Her first exposure to shellfish was when she was 3 years old.  We were out to dinner and DH ordered shrimp.  DD was sitting next to him and ate two french fries from his plate (from the side of the plate furthest from the shrimp) which resulted in hives and vomiting.  When she was 4, she put two fingers in the touch tank at the aquarium and reacted with full-body hives.  At age 6 we attempted the ocean - after about 45 minutes the first hives started to pop up.  Grocery shopping, she gets blotchy and wheezy when we're near the seafood counter.  That's why I was wondering if different proteins might be involved with adult-onset (exposure sensitization) and childhood-onset presentations like DD.

That is really interesting and I wonder? I find my own shellfish allergy extremely fascinating because I share it with my mother. As a kid, I'd assumed she was always allergic since she was a kid but it turns out we developed it at about the same age. Hers is mild, though, and she never ate shellfish growing when given the choice. I ate it all the time and my allergy is much more severe. Who knows? I mean, the people who get paid to figure it out haven't figured it out, so....

Oh, rebekah that's an interesting thought. It never occurred to me to think about pediatric-adult sensitization to different proteins or parts thereof.

Quote from: CMdeux on December 04, 2013, 03:40:45 PM
Oh, as are we all, really-- just opinions.    Conversation, that's all.  Things to muse upon.

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Interestingly enough, DD's shellfish allergy manifested early and behaves more like a severe peanut/egg/etc. allergy.  Her first exposure to shellfish was when she was 3 years old.  We were out to dinner and DH ordered shrimp.  DD was sitting next to him and ate two french fries from his plate (from the side of the plate furthest from the shrimp) which resulted in hives and vomiting.  When she was 4, she put two fingers in the touch tank at the aquarium and reacted with full-body hives.  At age 6 we attempted the ocean - after about 45 minutes the first hives started to pop up.  Grocery shopping, she gets blotchy and wheezy when we're near the seafood counter.  That's why I was wondering if different proteins might be involved with adult-onset (exposure sensitization) and childhood-onset presentations like DD.

Oh, as are we all, really-- just opinions.    Conversation, that's all.  Things to muse upon.

Quote from: rebekahc on December 04, 2013, 09:52:36 AM
I think it's a fallacy to assume most shellfish allergy is adult-onset and therefore different from peanut (though there may be research suggesting such that I'm not aware of).  Personally, I know equal numbers of people with adult-onset peanut allergy as I do adult-onset shellfish allergy.  My kids and I are all childhood-onset shellfish allergy.

However, if it's true that shellfish allergy is statistically likely to be adult-onset, then that could suggest the possibility of sporadic exposure leading to sensitization since shellfish allergy isn't more prevalent in coastal regions or populations who consume higher than average quantities of shellfish.  I'd be curious to know if adult-onset shellfish allergy is caused by different protein sensitization (perhaps one in chitin) than the sensitizing protein(s) of childhood-onset shellfish allergy.

I was really just musing on how I would be thinking about it (and do think about my own kids), not trying to put forth and prove any definitive thesis. Most articles I have read say that shellfish allergy is extremely rare in young children and much more common in teens and adults. I have no idea if it's more prevalent where it is a staple or not. Adult onset shellfish allergy matches my experience in the world, too. I have never met a kid with shellfish allergy, but I know tons of adults. That does not contradict the idea that children AND adults frequently become allergic to other foods equally (like peanuts), just that shellfish seems to need ongoing sensitization to develop through ingestion. It seems rare to have a toddler who reacts on first ingestion of shellfish but not rare at all to have a toddler who reacts on first ingestion of peanuts which gives me the thought that maybe there are different pathways to sensitization. I don't really know at all but those are the kinds of things I consider when I think about whether to expose my kids to foods I am allergic to (they have no food allergies). I was really just saying how I developed my judgement on the subject given the general information available. I am no expert, just a mom trying to think through the same quandary. The only thing I really have done is try to minimize the dust because the suggested link between shellfish allergy and dust mite allergy. Just stabbing in the dark here, really  .

Yeah-- and many such studies have such significant sampling methodology problems to begin with that gross correlation may turn out to be all that they are good for.

Country-sponsored birth cohort studies are the most useful here-- but those are quite rare, and almost never available in mixed-ethnicity nations.

The other big reveal, which has actually been a huge pink elephant in the room the entire time, is that much of the data used in allergic disease has only been correlative because the statistical analysis has not been sophisticated enough to support causal relationships. The mathematicians here can explain it better than myself but to begin to statistically propose causality SEM (structural equation modeling) is required whereas what has been in use is only general linear regression.

In other words no matter how sophisticated the studies have been the math has been primitive, relatively speaking. I'm not saying DH & I are changing the world but we have pestered at least one large circulation allergy journal editor about moving towards SEM in order to study causal relationships. Yeah, when I first heard about that I needed my teddy bear and someone to hold me.

editing to add re: dust mite sensitization for the purposes of climate and regional populations Australia was included in an Australasia geographic boundary. I think what's interesting there is it's a population that has similarities to similar, young immigrant population based protoculture nations like USA, Canada, NZ (sorta, Maori have greater presence than other indigenous people in terms of percentage of population), and with Asian nations.

Think about it this way--

IF this were true, peanut allergy rates should be falling as the North American food supply becomes ever more cross-contaminated with the stuff. 

Right?

But it hasn't. 

It's population correlation, of course--

and I have NO doubt that increasing exposure means increasing opportunity for contact among predisposed members of the population... but it looks (to me) as though increasing exposure through cultural dietary practices is what causes the frequency to reach some kind of saturation point.

It's both children and adults, though I'm not aware of data that pulls that one out specifically.  Just broad population data in incidence studies done in Scandinavia and the Middle East, as well as in SE Asia.

That seems to be what is happening in North America with sesame currently-- that it is attaining a level of ubiquity that means that everyone who will become allergic to it is becoming allergic.  The latency is being realized because of exposure, I mean.  I'm not sure that it supports the idea of "eating the allergen to prevent sensitization to it."

When you look at things that have always been ubiquitous in the diet in North America, though, like wheat, milk, egg, and to some extent some tree nuts like almond or walnut, the rates seem more stable and lower in incidence.

It'd be fascinating to look at rates in coastal versus inland areas and rates of fish consumption. 

In any event, consumption doesn't seem to actually be protective.  At least-- not anymore.  Whatever is causing additional food sensitization isn't playing favorites, it seems, and like everything else, the common wisdom that was perfectly valid for 40+ years about food allergy management doesn't necessarily apply to anyone now. Least of all to those born in the last 20 years.


I agree with the earlier observation that such advice is probably based on understanding of food immunotherapy methodology, and it may not even apply to those without the propensity to develop food allergy... of course, then that begs the question "is that this PARTICULAR child?"  The bottom line is that probably nobody knows-- the possibility probably exists if a genetic sibling already HAS developed food allergy, but beyond that,  it's anyone's guess as to whether it matters or not.

In any case, unless there are OTHER reasons to bring the allergen into the home, I would not necessarily call the evidence for "preventing allergy" to be compelling.  In the least.
 

In your examples, has there been a causal relationship found or could it just be that higher rates of exposure result in higher rates of diagnosis?  Are the rates higher for just adult-onset or is it childhood-onset (perhaps due to earlier exposure in ubiquitous consumption diets)?

Really not trying to argue with anyone...just thinking out loud and asking out of curiosity...I have done no research on any of this.

At least with fish allergy, though-- the demographics DO support a model that suggests that exposure IS the lynchpin for development of the allergy.    It is most common (at least in Caucasian ethnicity) in countries where fish is a regular, even ubiquitous, part of the diet.

Sesame, same thing-- it's most common in cultures where it is pretty ubiquitous in the diet (Middle East), and less so in places where consumption is sporadic (as in N. America).

I think it's a fallacy to assume most shellfish allergy is adult-onset and therefore different from peanut (though there may be research suggesting such that I'm not aware of).  Personally, I know equal numbers of people with adult-onset peanut allergy as I do adult-onset shellfish allergy.  My kids and I are all childhood-onset shellfish allergy.

However, if it's true that shellfish allergy is statistically likely to be adult-onset, then that could suggest the possibility of sporadic exposure leading to sensitization since shellfish allergy isn't more prevalent in coastal regions or populations who consume higher than average quantities of shellfish.  I'd be curious to know if adult-onset shellfish allergy is caused by different protein sensitization (perhaps one in chitin) than the sensitizing protein(s) of childhood-onset shellfish allergy.

As far as I know about mite-crustacean cross reactivity I don't think that exists outside of testing. A component test may reveal what protein fractions are shared but the Asia Pacific region is much harder hit with dust mites, they deal with more species due to temperate/tropical climates. It has not correlated positively to crustacean sensitization. Wheat and milk are significant in East Asia, Singapore is also heavy on milk allergy to a special milk carbohydrate along with peanut. The lengthened pollen seasons do seem to correlate to an increased sensitization to fruits and vegetables beyond OAS.

Mainly though, the allergic march there is epidemically sensitized to heinous dust mites with epidemic levels of asthma and eczema. It's possible that the population in USA in isolation correlates with dust mite-crustacean but this does not present as such globally, even in regions with more species and incidences of dust mite population and sensitization. Open access papers and abstracts available in threads I posted to.