Why no longer getting allergies or even sick as often might not be a good thing. A theory from a top immunologist

General Discussion
#1

Who here feels they dont get sick as often or suffer from allergies like they used to?
As far as the allergy front, if you feel your no longer having allergic type reactions like you used to post Fin, SSRIs, etc,
Consider testing ige antibodies and even getting a skin prick test from an allergist for common airborne allergies. What im saying is for some even though they no longer perceive allergic reactions, they could still be there, the body might just not be generating the appropriate “clearing” response.
I have elevated ige antibodies and my back lit up so much with skin prick tests, the nurse grabbed another nurse to show her.

A controversial theory may explain the real reason humans have allergies

We know that allergens often cause physical damage. They rip open cells, irritate membranes, slice proteins into tatters. Maybe, Medzhitov thought, allergens do so much damage that we need a defense against them. “If you think of all the major symptoms of allergic reactions–runny noses, tears, sneezing, coughing, itching, vomiting and diarrhoea–all of these things have one thing in common,” said Medzhitov. “They all have to do with expulsion.” Suddenly the misery of allergies took on a new look. Allergies weren’t the body going haywire; they were the body’s strategy for getting rid of the allergens.

But understanding the purpose of allergies could lead to dramatic changes in how they’re treated. “One implication of our view is that any attempt to completely block allergic defenses would be a bad idea,” he said. Instead, allergists should be learning why a minority of people turn a protective response into a hypersensitive one. “It’s the same as with pain,” said Medzhitov. “No pain at all is deadly; normal pain is good; too much pain is bad.”

For now, however, Medzhitov would just be happy to get people to stop seeing allergies as a disease, despite the misery they cause. “You’re sneezing to protect yourself. The fact that you don’t like the sneezing, that’s tough luck,” he said, with a slight shrug. “Evolution doesn’t care how you feel.”

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#2

Interesting, indeed, I am not allergic to cats anymore. Prepfs I would suffocate if playing with some cats for long time. Also, I am not getting cold anymore. Prepfs I was getting really bad cold at least once per year. I guess as a lot of people here.

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#3

Here’s a thought that goes with the first post. This is just one study, but here histamine had no effect on an allergic type hyper response. Meaning Histamine might not drive allergies, it might be a reactive response to an allergen.

Disruption of L-Histidine Decarboxylase Reduces Airway Eosinophilia but not Hyperresponsiveness

endogenous histamine depletion had no effect on the allergic reaction-induced airway hyperresponsiveness. Therefore, airway eosinophilia and hyperresponsiveness after allergic reaction seem to be mediated by distinct mechanisms in our present model.

Eosinophils are crucial for combating parasitic infections and inflammatory processes, such as allergic reactions. Other functions include killing cells, anti-bacterial activity, and controlling inflammatory responses.Jan 17, 2019

#4

To add to this, im also keeping the opposite in mind as well, meaning histamine is a problem, but im not sure about that.

Antihistamines are immunosuppressive and increase susceptibility to bacterial and viral infections

Effects of antihistamines on innate immune responses to severe bacterial infection in mice.

Here, we show that oral treatment with first-generation H1R antihistamine diphenhydramine, H2R blocker cimetidine and H3/4R blocker thioperamide impairs optimal innate immune responses

sedating first-generation H1R antihistamines and H2R blockers might impair innate immune responses to bacteria

to link this with SSRIs, I have posted they might have potent antihistamine properties.

Then back to Retinoic acid, (Accutane)

Retinoic acid is a negative regulator for the differentiation of cord blood-derived human mast cell progenitors

RA appears to function as a negative regulator for both the multiplication and intracellular histamine level of human mast cells. Our results may provide a new strategy targeting the production process of mast cells for prophylactic treatment of allergic disorders.

#5

Retinoic acid potentiates inflammatory cytokines in human mast cells: identification of mast cells as prominent constituents of the skin retinoid network

Retinoic acid (RA), the active vitamin-A-metabolite, has well-established functions in skin homeostasis and in the immune system. Skin mast cells (MCs) combine traits of both structures, being of hematopoietic origin, but functional in the skin environment. It remains largely unknown whether mature MCs are targeted by the retinoid network. Here, we demonstrate that human skin MCs display substantial susceptibility to RA by which they are instructed to increase pro-inflammatory mediators (IL-1β, IL-8, TNF-α) but not histamine release. The effects are observed at physiological RA levels, in different microenvironments, and are largely donor-independent. RA susceptibility is owed to the cells’ abundant expression of RARA, the receptor mediating MC cytokine responses. Unexpectedly, bioinformatics calculations on the FANTOM5 expression atlas revealed general enrichment of retinoid network components in MCs against other skin cells, and MCs rapidly upregulated RA responsive genes. In conclusion, MCs are important yet overlooked retinoid targets in the skin.

This one is interesting as well,

You can have too much of a good thingSkin fibroblasts shield mast cells from excess Vitamin A

Excess amounts of Vitamin A wakes a sleeping lion in the skin. In the normal state, Cyp26b1 degrades retinoic acid, a metabolite of vitamin A. In the hyper vitamin A condition, activation of mast cells occurs and subsequently dermatitis is observed.

Dermal fibroblasts are cells within the dermis layer of skin which are responsible for generating connective tissue and allowing the skin to recover from injury.

The accelerating effect of histamine on the cutaneous wound-healing process through the action of basic fibroblast growth factor.

So a few possibilities here.

Also a real simple thought going back to the title of this thread. Its almost too simple it cant be right.
Do people with allergies require more histamine?

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#6

Do most people get dermatitis after accutane?

#7

I had a bad flou, last week. I haven’t any improvment.

#8

ive had skin and scalp irritation since Accutane. Its been rather permanent. I Also sun burn much more easily.

#9

Right. Im not saying getting sick is the be all end all for resolution of symptoms, but a possible correlation to PFS that it seems more then a few have noticed.

#10

Going back to the skin,

Filaggrin in the frontline: role in skin barrier function and disease
Recent human genetic studies strongly suggest that perturbation of skin barrier function as a result of reduction or complete loss of filaggrin expression leads to enhanced percutaneous transfer of allergens. Filaggrin is therefore in the frontline of defence, and protects the body from the entry of foreign environmental substances that can otherwise trigger aberrant immune responses.

Feeding filaggrin: effects of l-histidine supplementation in atopic dermatitis

In mammalian skin, l-histidine is rapidly incorporated into filaggrin. Subsequent filaggrin proteolysis releases l-histidine as an important natural moisturizing factor (NMF). In vitro studies were conducted to investigate the influence of l-histidine on filaggrin processing and barrier function in human skin-equivalent models. Our further aim was to examine the effects of daily oral l-histidine supplementation on disease severity in adult AD patients. We conducted a randomized, double-blind, placebo-controlled, crossover, nutritional supplementation pilot study to explore the effects of oral l-histidine in adult AD patients (n=24). In vitro studies demonstrated that l-histidine significantly increased both filaggrin formation and skin barrier function
Data from the clinical study indicated that once daily oral l-histidine significantly reduced ( P <0.003) AD disease severity by 34% (physician assessment using the SCORingAD tool) and 39% (patient self-assessment using the Patient Oriented Eczema Measure tool) after 4 weeks of treatment.

^So here its almost like they are using histamine (or its precursor) to treat the allergy.

#11

I’m allergic to everything even worse after accutane and anti histamine helps.

Also if I get sick, I am really sick and for a longtime.

Maybe just for myself it’s not so complicated, that’s what I’m thinking anyway.

I really do think this has effected me differently to everyone else.

#12

I think if a person has allergies, controlling them on some level might still be important, maybe even as a way to conserve histamine for more important functions? Unless im wrong of course. Just thinking of the drying effect alone of antihistamines post Accutane, i’m not sure if long term use is the best solution.

To look at one of the more potent versions, this is what could be dangerous like mentioned in the first post. Theory.

Antihistamines suppress upregulation of histidine decarboxylase gene expression with potencies different from their binding affinities for histamine H1 receptor

Antihistamines inhibit histamine signaling by blocking histamine H1 receptor (H1R) or suppressing H1R signaling as inverse agonists. The H1R gene is upregulated in patients with pollinosis, and its expression level is correlated with the severity of nasal symptoms. Here, we show that antihistamine suppressed upregulation of histidine decarboxylase (HDC) mRNA expression in patients with pollinosis, and its expression level was correlated with that of H1R mRNA. Certain antihistamines, including mepyramine and diphenhydramine, suppress toluene-2,4-diisocyanate (TDI)-induced upregulation of HDC gene expression and increase HDC activity in TDI-sensitized rats. However, d -chlorpheniramine did not demonstrate any effect. The potencies of antihistamine suppressive effects on HDC mRNA elevation were different from their H1R receptor binding affinities. In TDI-sensitized rats, the potencies of antihistamine inhibitory effects on sneezing in the early phase were related to H1R binding. In contrast, the potencies of their inhibitory effects on sneezing in the late phase were correlated with those of suppressive effects on HDC mRNA elevation. Data suggest that in addition to the antihistaminic and inverse agonistic activities, certain antihistamines possess additional properties unrelated to receptor binding and alleviate nasal symptoms in the late phase by inhibiting synthesis and release of histamine by suppressing HDC gene transcription.