That link doesn't make a claim quite that strong. I also don't know anyone that has eaten it.
Given that I know dozens of people who demonstrably lost their sensitivity to poison oak via the accidental chronic exposure regimen I outlined above, at the very least it should raise a scientific question. It would be easier to dismiss if it was an isolated case or two. No one exposes themselves like that intentionally.
> lost their sensitivity to poison oak via the accidental chronic exposure regimen
This is not how the immune system is known to work.
Sensitivity does not downregulate. Increased exposure enhances detection and response. Recognition proliferates. Once you're allergic to something, it'll only worsen.
You can become allergic to new things, but you won't lose allergies unless the recognizer population dies off entirely. And even if it did, you're likely close enough to training your immune system to this sensitivity again. (You've already done it at least once.)
> Sensitivity does not downregulate. Increased exposure enhances detection and response. Recognition proliferates. Once you're allergic to something, it'll only worsen.
I don't think that's correct. If it were, then allergy immunotherapy wouldn't work. Which... it does. Not perfectly, and not for everyone, but it does for many.
One is correct in that repeated exposure to an allergen can upregulate IgE production, especially in cases of severe allergies like bee stings or peanuts. This is due to the immune system's sensitization process, where each exposure can lead to more intense reactions, driven by the Th2-mediated immune response that promotes IgE production and allergic inflammation.
However, one is also correct that controlled exposure through allergen immunotherapy (SCIT or SLIT) can downregulate IgE and mitigate allergic responses. This therapy works by gradually introducing the allergen in controlled doses, which shifts the immune response from a Th2-dominated profile to a Th1-dominated or regulatory T cell (Treg) profile. This shift reduces IgE levels and increases the production of blocking antibodies like IgG4, leading to long-term desensitization and reduced allergic reactions.
In particular environmental allergens (pollens, dust mites, animal dander, molds), insect venoms (bee, wasp) may respond well to immunotherapy but we’ve had poor success or disproportionate risk attempting to mitigate food allergens (peanuts, tree nuts, and shellfish), certain medications, and latex .
I don't think that's necessary. I've been doing allergy immunotherapy for the past few years, and it's all subcutaneous. Definitely not into the bloodstream.
Looks like you are giving "Ackshually" technically correct points, when it's clear what others are trying to say. Please engage with what they are trying to convey instead of coming up with technical gotchas.
From personal experience, exposure does not lead to lasting immunity. Quite the opposite. I've had several intense exposure rashes that were debilitating, like not being able to walk properly for a week due to leg swelling. And I still get rashes from poison oak.
Maybe there's a bit of short term immunity from severe exposure. I've never tested that since the discomfort from an intense rash makes me avoid exposure like the plague for a few years.
In fact urushi is the Japanese word for lacquer, the plant is in the genus Toxicodendron.
Like most jobs until recently, making lacquerware was hereditary, and (clearly) the people making it were able to withstand sustained and direct exposure. It's possible that there is a genetic proclivity involved in ability to do the work, but just as clearly, there is hyposensitivity gained in exposure.
Wasnt there some sort of natural selection centuries ago so that only folks tolerant to such chemistry actually performed the job?
I know next to nothing about these topics but there are some wildly opposite claims in this thread. Truth has the tendency, despite being complex, to generqlly favor one direction.
