What's behind ME allergies and sensitivities to foods, odors and chemicals?

[Barry]

In Canada they are finding that food allergies/intolerances have increased significantly over the past 10 years in people 50 and older. In the past it was rare for adults to suddenly develop food allergies and they don't know why this is happening now.

Do they distinguish between allergies and intolerances, because my non-medical undertanding is that they are very different. Allergies are auto-immune reactions, sometimes life threatening; intolerances do not involve the immune system as I understand it.

 

[Robert 1973]

I think it is extremely unlikely that there would be an immunological reaction to a volatile substance of the sort that mediates food odours. These tend to be of molecular mass in the hundreds . T cells can only recognise peptides derived from proteins with mass in the tens to hundreds of thousands. Antibodies do not do anything much, even if they bind, with molecules this small. Small molecules can act as haptens if they bind to proteins but the amounts involved in odours are so minute that it is very hard to see how a symptomatic reaction would occur.

I am not aware of any evidence linking odour intolerance to allergies or asthma.

Sorry, you misunderstood what I was trying to say. The odours that trigger what feel like immunological responses are perfumes and sprayed cleaning products (and some other things). The reactions I get from certain foods are from eating them, not smelling them. Apologies if that wasn’t clear from my wording.

I thought it was well established that perfumes and cleaning products can trigger immune responses. Asthma UK reports that 60% of asthma suffers say that perfume can trigger an attack: https://www.asthma.org.uk/about/med...-that-perfume-should-be-banned-in-hospitals2/

Asthma UK also states that many cleaning products contain volatile organic compounds (VOCs) which can trigger asthma symptoms: https://www.asthma.org.uk/advice/triggers/indoor-environment/:

CLEANING
A lot of the cleaning products we use every day contain VOCs. They are found in furniture polish, air fresheners, carpet cleaners, oven cleaners and in the chemicals used in dry cleaning. Sprays can be more likely to trigger asthma than solid or liquid cleaning products, because you end up inhaling the chemicals. Some people also tell us the smell of cleaning products and air fresheners can trigger their asthma. Professional cleaners and others who use a lot of cleaning products all the time are at more risk of developing asthma.

These steps may help:

• Avoid spray cleaners
. It's better to use solid or liquid cleaning stuffs, rather than sprays, as sprays get into the air, so they can be inhaled more easily and get further down into the airways, causing irritation. If you can, use as little of the product as possible, and open windows when you're cleaning for good ventilation. Even using spray cleaning products now and again can trigger asthma.
• Avoid scented products
. If you think the smell of cleaning products triggers asthma symptoms, go for unscented products.
• Consider other cleaning methods. 
The best way to avoid exposure to the chemicals found in cleaning products is to avoid using them. Use a damp cloth for cleaning instead whenever possible and look for products which are labelled allergy friendly, as these have lower levels of VOCs and are usually fragrance-free.

This paper suggests that artificial scents should be banned in hospitals because of the effect on asthma patients: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4627866/

 

[Tilly]

I think that letter was implying that people with coeliac disease were being misdiagnosed as chronic fatigue syndrome. (There is no mention of ME.) That would be very plausible since coeliac disease often goes undiagnosed and is very likely to make people feel fatigued.

I read it as though there was an increased risk and they needed more info. They did include Coeliac in 2007 NICE guidelines. There is also good evidence that small fibre nephropathy is caused by Coeliac and this can be kicked off by gut infections. Would this then tie in with glial cells. This could be a subgroup and my son would fit this.

 

[Jonathan Edwards]

Asthma UK also states that many cleaning products contain volatile organic compounds (VOCs) which can trigger asthma symptoms:

I suspect there is quite a bit of muddle here. I don't know who asthma UK are but I suspect they are a well meaning charity that is not necessarily on top of the science (like some ME organisations?). Aerosols can trigger bronchospasm if they include alcohols or other direct irritants and I suspect that is what this is about. People with asthma get bronchospasm both from immunological reactions and direct physical reactions - either can trigger mast cells.

What I think is very unlikely is that 'smells' or 'odours' as such can medicate an immune response in the nose of any significance.

 

[Jonathan Edwards]

I read it as though there was an increased risk and they needed more info. They did include Coeliac in 2007 NICE guidelines.

My memory of the NICE guidelines is that coeliac disease is something to exclude before making diagnosis of ME.

I don't think neuropathies have anything to do with glial cells - which are in the brain rather than the ends of nerves.

I am not sure what you mean by subset - of what? I am pretty sure we have no reason to think coeliac is linked to ME other than in the sense that coeliac can produce fatigue.

 

[Robert 1973]

I suspect there is quite a bit of muddle here. I don't know who asthma UK are but I suspect they are a well meaning charity that is not necessarily on top of the science (like some ME organisations?). Aerosols can trigger bronchospasm if they include alcohols or other direct irritants and I suspect that is what this is about. People with asthma get bronchospasm both from immunological reactions and direct physical reactions - either can trigger mast cells.

What I think is very unlikely is that 'smells' or 'odours' as such can medicate an immune response in the nose of any significance.

Whatever happens when perfumes and cleaning products trigger asthma symptoms, I suspect it is similar to what is happening with me. It is interesting to me that the types of things which appear to trigger asthma symptoms are similar to the types of things which make my symptoms worse.

I have very little knowledge of immunology. All I can do is describe my experience and hope that those with greater knowledge can make sense of it. Unfortunately, for most the time I’ve been unwell most experts in immunology have taken little or no time to listen (present company excepted). From what you say, I wonder what role mast cells may play in my symptoms. Is this something which can be reliably tested? There seems to be a lot of confusion/disagreement on MCAS and I’m not up to date on current thinking.

 

[Jonathan Edwards]

From what you say, I wonder what role mast cells may play in my symptoms. Is this something which can be reliably tested?

I don't think this is that easy. There are drugs that inhibit mast cell signalling to a degree but not very cleanly and anyway you would have to challenge under controlled conditions, with and without.

I am not sure what sorts of symptoms you link to the triggers? Mast cell activation will produce wheeze in the chest, runny nose and eyes, urticaria on the skin and stomach cramp with vomiting. Of these the runny nose and eyes and urticaria are perhaps the most specific since other things can produce wheeze and stomach cramps.

I am still not convinced that MCAS is a useful scientific category. People have allergies that are well documented to involve mast cell activation. Mast cell activation can also occur with eating strawberries and seafood I believe. Urticaria also occurs without known cause fairly often. So mast cell activation is a well known but complex phenomenon. Whether it deserves a syndrome, which seems to imply some sort of generalised state of hypersensitivity I am doubtful.

 

[JaneL]

- Problems with medication - I am not sure that the problems people report with different drugs/medications relate to one of the three aspects above or are a different issue.

According to the article you posted earlier, sensitivity to drugs/medications might involve a similar mechanism to food intolerance:

The underlying causes of most food intolerances are unknown, but clinical observations suggest that they are likely to have a pharmacological basis. Reactions are dose-dependent, and it is common to observe withdrawal effects, tachyphylaxis and supersensitivity when intake is modified. The range of symptoms is very similar to those seen as a result of drug side-effects and, indeed, it is common for food-sensitive patients to react adversely to various drugs as well.

https://www.slhd.nsw.gov.au/rpa/allergy/research/RoleOfFoodIntoleranceInCFS.pdf

 

[Robert 1973]

I am not sure what sorts of symptoms you link to the triggers? Mast cell activation will produce wheeze in the chest, runny nose and eyes, urticaria on the skin and stomach cramp with vomiting. Of these the runny nose and eyes and urticaria are perhaps the most specific since other things can produce wheeze and stomach cramps.

Not the symptoms you list as associated with mast cell activation. The main symptom I get is an increase in the discomfort in my face, which has been one of my main symptoms from the beginning. (I spend a lot of time with ice packs on my face to numb the discomfort.) Also, an increase in the discomfort in and under my skin throughout my body (I used to take regular cold baths to try to numb this, and I am constantly resisting the urge the scrape my skin), increased brain fog, fatigue and feeling of being poisoned. These are all symptoms I have all the time to a greater or lesser degree but if I smell freshly sprayed perfume or cleaning products it causes an instant and significant increase.

The only time I ever experienced anything like this before I was unwell was when I was in Italy and I handled a plant before touching my face which caused what felt like an allergic reaction with my face swelling up etc. I can’t remember the name of the plant but the locals I was with knew that it could cause such reactions.

From what you say it seems unlikely to be mast cell activation. I wish someone understood what it is.

 

[JaneL]

There is also this paper:

Allergy and the chronic fatigue syndrome
Stephen E. Straw, MD, Janet K. Dale, RN, Ralph Wright, RN, and Dean D. Metcalfe, MD Bethesda, Md.
Journal of Allergy and Clinical Immunology 1988 May;81(5 Pt 1):791-5.
https://www.jacionline.org/article/0091-6749(88)90933-5/pdf

In their study they performed blinded epicutaneous skin testing on 24 patients who were also entering a placebo-controlled trial of acyclovir for chronic fatigue syndrome. They found significantly higher rates of allergy in the patients with chronic fatigue syndrome (50%) compared to rates of reactivity of 20% to 30% noted in large studies of unselected white adults of the age of the CFS patients. (See paper for references).

In the paper they also speculate on the mechanisms linking allergy and chronic fatigue syndrome.

 

[JaneL]

Also this:

Increased Risk of Chronic Fatigue Syndrome Following Atopy: A Population-Based Study.
Yang TY1, Kuo HT, Chen HJ, Chen CS, Lin WM, Tsai SY, Kuo CN, Kao CH.

Abstract
Several hypotheses have been proposed to explain the etiopathogenesis of chronic fatigue syndrome (CFS), including immune dysregulation. However, few population-based prospective cohort studies have been conducted on CFS and atopy. We investigated the relationship between atopy and CFS by using a population-based cohort study. In this prospective, population-based cohort study of the National Health Insurance Research Database, we identified 42,558 patients with atopy and 170,232 patients without atopy from 2005 to 2007 with follow-up to 2011. The incidence rates and risks for CFS were estimated using Cox proportion hazards regression. The overall incidence rate of CFS was higher in the atopy cohort compared with the nonatopy cohort (1.37 versus 0.87 per 1000 person-year), with an adjusted hazard ratio of 1.48 (95% confidence interval 1.30-1.69). The risk of CFS in the atopy cohort increased 1.47- to 1.50-fold for each nonexisting comorbidity. Patients with numerous atopic symptoms exhibited a biological gradient of increasing risk for CFS, and the risk changed significantly after adjustment for age, sex, and comorbidities, increasing from 1.46- to 2.59-fold. We revealed that atopy is associated with CFS, particularly in patients with numerous atopic syndromes. The actual mechanism for CFS development in patients with atopy remains unclear and requires further investigation. We recommend researching the subsequent fatigue symptom in patients with atopy, particularly those with multiple atopic syndromes.

https://www.ncbi.nlm.nih.gov/pubmed/26200644

 

[boolybooly]

A key concept in CFS / CFIDS is TH2 shift, which has been proposed by clinician Dr Paul Cheney for decades and others e.g.

https://www.ncbi.nlm.nih.gov/pubmed/25824300

Cytokine network analysis of cerebrospinal fluid in myalgic encephalomyelitis/chronic fatigue syndrome.
Hornig M1,2, Gottschalk G3, Peterson DL3, Knox KK4,5, Schultz AF1, Eddy ML1, Che X1, Lipkin WI1,2,6.
Author information

Abstract
Myalgic encephalomyelitis/chronic fatigue syndrome is an unexplained debilitating disorder that is frequently associated with cognitive and motor dysfunction. We analyzed cerebrospinal fluid from 32 cases, 40 subjects with multiple sclerosis and 19 normal subjects frequency-matched for age and sex using a 51-plex cytokine assay. Group-specific differences were found for the majority of analytes with an increase in cases of CCL11 (eotaxin), a chemokine involved in eosinophil recruitment. Network analysis revealed an inverse relationship between interleukin 1 receptor antagonist and colony-stimulating factor 1, colony-stimulating factor 2 and interleukin 17F, without effects on interleukin 1α or interleukin 1β, suggesting a disturbance in interleukin 1 signaling. Our results indicate a markedly disturbed immune signature in the cerebrospinal fluid of cases that is consistent with immune activation in the central nervous system, and a shift toward an allergic or T helper type-2 pattern associated with autoimmunity.

The reason for TH2 shift is not clear but it is likely to be pathogen genes because broadly speaking the immune system has two modes of defence, TH1 and TH2 and TH1 arm deals with viruses whereas TH2 doesnt and deals with extracellular antigens and this can cause allergies. The story goes that the two arms are reciprocally inhibitive, i.e. when one arm is active it inhibits the other arm so it makes sense for pathogens to stimulate the opposite arm from the one which attacks them.

So TH2 shifted individuals are more likely to develope allergic responses. I give this idea credence because when my CFIDS started with recurrent virus and neurological disturbance after previous EBV, the following summer I suddenly had extremely severe asthmatic hayfever reacting to grass pollen (diagnosed by Prof Jonathan Brostoff who also advised me about amines see below) after having previously recovered from asthmatic responses to house dust mite allergens in my youth, so my asthmatic allergy apparently reactivated, shifted antigen and became much more severe after ME CFIDS onset. I also have a tendency for more septic type episodes and oedemas in the grass pollen season and I feel even worse than usual, as is currently the case. So I will try to keep this short.

As I understand it allergy is not considered the same as food intolerance. The latter is also something I have had trouble with as part of ME and I cannot pin it down scientifically. I consider my liver is not functioning as well as it used to. My entire metabolism appears to be underperforming in that regard and is also hypersensitive. I cannot tolerate caffeine or certain high amine foods due to the neurological stimulating effect or nightshades due to the fact they make me feel bad and cause mouth ulcers and more recently have been getting headaches from foods known to be high in lectins which could be acting like antigens and it all seems to get worse if I eat dairy and or coconut oil. I also have an exaggerated sensitivity to bacterial products in my food which tends to give me the squits at the drop of a hat so I have to wash my salad with detergent for example to prevent unfortunate outcomes.

How all this fits together I am not sure, I am still (if you will forgive the pun) digesting it though I recently came across a paper which may indicate a mechanism.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3563838/?report=classic

Dietary medium-chain triglycerides promote oral allergic sensitization and orally induced anaphylaxis to peanut protein in mice

If it is true for humans then it implies that the large amount of MCTs in some diets from sources like dairy, palm oil & coconut oil may be exacerbating allergic responses for some people.

I have tried to make sense of these ideas in my blog but its a bit of a work in progress and my writing tends to ramble on a bit circuitously, for which I am sorry, but its a product of the difficulty I have with concentrating and remembering what I have already written (and writing for an audience with the same difficulties). https://boolyblog.blogspot.com/

 

[Amw66]

A key concept in CFS / CFIDS is TH2 shift, which has been proposed by clinician Dr Paul Cheney for decades and others e.g.

https://www.ncbi.nlm.nih.gov/pubmed/25824300


The reason for TH2 shift is not clear but it is likely to be pathogen genes because broadly speaking the immune system has two modes of defence, TH1 and TH2 and TH1 arm deals with viruses whereas TH2 doesnt and deals with extracellular antigens and this can cause allergies. The story goes that the two arms are reciprocally inhibitive, i.e. when one arm is active it inhibits the other arm so it makes sense for pathogens to stimulate the opposite arm from the one which attacks them.

So TH2 shifted individuals are more likely to develope allergic responses. I give this idea credence because when my CFIDS started with recurrent virus and neurological disturbance after previous EBV, the following summer I suddenly had extremely severe asthmatic hayfever reacting to grass pollen after having previously recovered from asthmatic responses to house dust mite allergens in my youth, so my asthmatic allergy apparently reactivated, shifted antigen and became much more severe after ME CFIDS onset. I also have a tendency for more septic type episodes and oedemas in the grass pollen season and I feel even worse than usual, as is currently the case. So I will try to keep this short.

As I understand it allergy is not considered the same as food intolerance. The latter is also something I have had trouble with as part of ME and I cannot pin it down scientifically. I consider my liver is not functioning as well as it used to. My entire metabolism appears to be underperforming in that regard and is also hypersensitive. I cannot tolerate caffeine or certain high amine foods due to the neurological stimulating effect or nightshades due to the fact they make me feel bad and cause mouth ulcers and more recently have been getting headaches from foods known to be high in lectins which could be acting like antigens and it all seems to get worse if I eat dairy and or coconut oil. I also have an exaggerated sensitivity to bacterial products in my food which tends to give me the squits at the drop of a hat so I have to wash my salad with detergent for example to prevent unfortunate outcomes.

How all this fits together I am not sure, I am still (if you will forgive the pun) digesting it though I recently came across a paper which may indicate a mechanism.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3563838/?report=classic


If it is true for humans then it implies that the large amount of MCTs in some diets from sources like dairy, palm oil & coconut oil may be exacerbating allergic responses for some people.

I have tried to make sense of these ideas in my blog but its a bit of a work in progress and my writing tends to ramble on a bit circuitously, for which I am sorry, but its a product of the difficulty I have with concentrating and remembering what I have already written. https://boolyblog.blogspot.com/

Th2 shift has also been suggested for extended fight or flight mode . In anticipation of an oncoming battle your body anticipates wounds and bacteria .

In mice it seems this prolonged response triggers epigeneric changes ( now a new normal) some of which are heritable. I looked at this years ago trying to understand anxiety mechanisms, but didn't save sources.it could be psychological double speak.

Overactive SNS triggering Th2 ?

 

[arewenearlythereyet]

From my own experiences I have definitely got more sensitive to pollen and animal allergic reactions (stronger and more frequent) since getting ME. I also had IBS develop after onset which I would conclude was a downstream affect in my case. This is now controlled and I only get it when I crash (so not really ibs I suppose ..just the same symptoms over 1-3 days). I know when I’m coming out of a crash since things get back to normal. Despite the ibs being under control, my sensitivity to contact with animals is still pretty severe.....my neck swells/get hives from wearing the cashmere scarf I used to wear fine before I got ME for example.

I take an antihistamine daily and this seems to help take the edge off of symptoms and is sort of mildly helpful (although I would need to do it for a few more years to be sure).
I wonder whether there is something that creates a variable high homocysteine (not necessarily simple deficiencies ...could be knock on effect downstream of something else, or liver?) when we crash and this is what causes high histamine or histamine to wax and wane as environmental and food from normal levels for the healthy become temporarily difficult to handle. If so, the more severe you are, the more likely that this is to be a continuous problem. As I mentioned I don’t think in my case this is a fundamental aspect of my ME, more symptoms as a knock on effect of something else.

I’ve never had an anaphylactic reaction to food and I am yet to see anyone on forums describe anaphylaxis directory relating to their ME. However there are enough PWME reporting digestive and allergic symptoms to suggest that something is going on more than the usual confusion in the general public overstating normal reactions and food preferences to intolerances etc.

Of course this is highly speculative on my part ...so I’m just postulating with very little energy to hunt for papers or references.

I wonder whether there should be a larger study on homocysteine levels in the blood for ME patients and monitor it over a period of time to see whether there are unusual fluctuations? I think there was a small study done that showed there may be high levels in ME patients, but I don’t think anyone tried to take this further or replicate it with something more substantial. This is from memory so just bear in mind it’s not great at the moment. It’s possible this has been thoroughly debunked or dismissed when methylation was on the way out as a theory.

Anyway I promised I wouldn’t post and I’ve already broken my rule...back to lurking.

Edit: I haven’t properly read this but thought I would post here since I think it’s interesting the link with homocysteine and other neurological conditions...don’t know whether it’s any good yet.

https://jamanetwork.com/journals/jamaneurology/fullarticle/777652

 

[boolybooly]

Th2 shift has also been suggested for extended fight or flight mode . In anticipation of an oncoming battle your body anticipates wounds and bacteria .

In mice it seems this prolonged response triggers epigeneric changes ( now a new normal) some of which are heritable. I looked at this years ago trying to understand anxiety mechanisms, but didn't save sources.it could be psychological double speak.

Overactive SNS triggering Th2 ?

Well, I would take the view that some stress models presume a priori that stress causes ME which I dont believe, though stress does undoubtedly have an effect on ME patients and healthy people and experimental animals alike. I feel research into stress explains a lot of complications I had after ME onset, before diagnosis 10 years later but I feel the stress was caused by ME directly and indirectly rather than the other way round. i.e. stress did not cause ME, ME was caused by EBV and other viruses and resulted in stress.

I found a book called "Battle for the Mind" by William Sargant very interesting, about stress in shell shock (now PTSD) with insights on transmarginal inhibition and how it is a part of several phenomena, including trauma, transformative religious practice, political brainwashing and torture and psychological warfare. Understanding this perspective helped me to reflect on my own responses to the impact of ME.
https://en.wikipedia.org/wiki/Transmarginal_inhibition

From this point of view it strikes me as plausible that for the reasons you mention the TH2 arm of the immune response may have evolved to allow fight and flight responses to occur for exactly the reason you mention. So rather than stress causing the condition, the condition may be magnifying stress in this way and others. For example in Sargants book he details how bowel disturbance can have a marked impact on the way animals and people respond to stress by making more severe stress responses appear with less additional stress, i.e. the bowel disturbance is a stress factor in its own right.

PWME commonly describe IBS as a part of their syndrome. In addition I have seen plenty of reports of people with ME having adrenal episodes subsequent to onset which I have also experienced and I wonder if TH2 shift in "leaving the door open" to adrenalin might actually predispose TH2 shifted people to have adrenalin episodes somehow.

 

[boolybooly]

From my own experiences I have definitely got more sensitive to pollen and animal allergic reactions (stronger and more frequent) since getting ME. I also had IBS develop after onset which I would conclude was a downstream affect in my case. This is now controlled and I only get it when I crash (so not really ibs I suppose ..just the same symptoms over 1-3 days). I know when I’m coming out of a crash since things get back to normal. Despite the ibs being under control, my sensitivity to contact with animals is still pretty severe.....my neck swells/get hives from wearing the cashmere scarf I used to wear fine before I got ME for example.

I take an antihistamine daily and this seems to help take the edge off of symptoms and is sort of mildly helpful (although I would need to do it for a few more years to be sure).
I wonder whether there is something that creates a variable high homocysteine (not necessarily simple deficiencies ...could be knock on effect downstream of something else, or liver?) when we crash and this is what causes high histamine or histamine to wax and wane as environmental and food from normal levels for the healthy become temporarily difficult to handle. If so, the more severe you are, the more likely that this is to be a continuous problem. As I mentioned I don’t think in my case this is a fundamental aspect of my ME, more symptoms as a knock on effect of something else.

I’ve never had an anaphylactic reaction to food and I am yet to see anyone on forums describe anaphylaxis directory relating to their ME. However there are enough PWME reporting digestive and allergic symptoms to suggest that something is going on more than the usual confusion in the general public overstating normal reactions and food preferences to intolerances etc.

Of course this is highly speculative on my part ...so I’m just postulating with very little energy to hunt for papers or references.

I wonder whether there should be a larger study on homocysteine levels in the blood for ME patients and monitor it over a period of time to see whether there are unusual fluctuations? I think there was a small study done that showed there may be high levels in ME patients, but I don’t think anyone tried to take this further or replicate it with something more substantial. This is from memory so just bear in mind it’s not great at the moment. It’s possible this has been thoroughly debunked or dismissed when methylation was on the way out as a theory.

Anyway I promised I wouldn’t post and I’ve already broken my rule...back to lurking.

Edit: I haven’t properly read this but thought I would post here since I think it’s interesting the link with homocysteine and other neurological conditions...don’t know whether it’s any good yet.

https://jamanetwork.com/journals/jamaneurology/fullarticle/777652

I should probably have quoted the conclusion of the study on anaphylaxis to show the link with TH2 clearly. Since the anaphylactic mice are in this state because they are TH2 shifted. Anaphylactic responses are severe but there are less severe allergic responses which can nevertheless still result from TH2 shift.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3563838/?report=classic

CONCLUSION
Dietary MCT promote allergic sensitization and anaphylaxis by affecting antigen absorption and availability and by stimulating Th2 responses.

It is also worth mentioning that in theory TH2 shift also creates a vulnerability to yeast infection, which many PWME have a problem with which is probably something improved by lower carb diets, as yeast do best on carb. This is because the TH1 arm of the immune system also deals with yeast cells as well as infected human cells and so does not do as good a job when the body is TH2 shifted and TH1 activity is reduced.

Hope that makes sense, did when I wrote it !!

 

[MSEsperanza]

Just adding this paper from 2019 here:

Fritscher-Ravens A, Pflaum T, Mösinger M, et al. Many Patients With Irritable Bowel Syndrome Have Atypical Food Allergies Not Associated With Immunoglobulin E. Gastroenterology. 2019;157(1):109-118.e5. doi:10.1053/j.gastro.2019.03.046

https://www.gastrojournal.org/article/S0016-5085(19)34636-0/fulltext#articleInformation

 

[PrairieLights]

I have pre-existing allergies and sensitivities, and have been lactose intolerant since becoming hypothyroid.

But I have something I don't know how to label, allergy? Sensitivity? The thing is it's shifting. For a couple months I was allergic to most toothpaste (rash mouth sores), then it was gone. Allergic to plastic water bottles, would leave a rash on the shape of the mouth of that bottle on my lips (don't know if that went away as I just stopped using plastic water bottles), a particular shampoo, or even random itchy spots I don't know that cause of. But it all lasts awhile then is just gone.

 

[MrMagoo]

I got eczema and hay fever for the first times in the 2 years before I became unwell (which is now the “start” of my ME) recently become allergic to my cat, also have the micropor tape irritation, can’t bear it!

 

[PrairieLights]

I got eczema and hay fever for the first times in the 2 years before I became unwell (which is now the “start” of my ME) recently become allergic to my cat, also have the micropor tape irritation, can’t bear it!

Adhesives on things like that is one ofy life long allergies

Not long ago I had a 24 hour heart monitor and made sure they used "hypoallergenic" sticky bits. I spent the entire 24 hours thinking only about not touching them and feeling like it was driving me crazy. Itched a week after.