Thyroid antibodies dropped significantly

msf

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I know Prof. Edwards is an immunologist, but I know of a researcher in the UK who is working of the role of Yersinia Enterocolitica in Graves´s Disease. There is a lot of debate about this it seems, but I don´t think the issue has been settled yet (although I´m sure Prof. Edwards will say it has been).

This is a interesting recent study: http://www.ncbi.nlm.nih.gov/pubmed/21488870

It looks like reasonably good evidence against a causal role, but the other interesting thing about it when you actually study it in detail is the prevalence of Yersinia antibodies in the study population (both cases and controls were related to people with autoimmune disease). They found around 30% were positive for IgA! This significantly higher than in any of the seroprevalence studies of the general population.

The authors go on to suggest an explanation for this fact:

A higher prevalence of YOP IgG and IgA in female relatives of patients with AITD than in controls derived from the general population has been reported previously [13]. The higher rate of persistent YE infection in AITD relatives might be due to susceptibility genes for AITD contributing to the risk for YE infection. The Danish twin study indicated that the genetic contribution in the association with YE is modest, and that it is more likely that environmental exposures to confer to the reported association between and YE and AITD [12].

So, even if Yersinia doesn´t cause thyroid disease, the fact that a person has thyroid disease may mean that they might also have Yersinia infection!
 
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My antibodies have dropped from 250 to 61 in three months. I thought it was due to giving up gluten.

I do not feel any better although I cough less (big deal!)

Am I right in thinking (Jonathan Edwards?) that it really makes no difference if my antibodies are high or low? Even though I feel no better, I still felt a sense of achievement in getting them down as it must be better for my body with lower antibodies. Is this rubbish? Could I have high antibodies and be just as ill?

Perhaps it wasn't the gluten at all. Perhaps antibodies just go up and down on their own accord.

I was holding out a lot of hope that lowering antibodies would bring about a health change but this hasn't seemed the case (although I still have antibodies so perhaps I have to get them lower).

Shall I just start eating gluten again? I feel no better so maybe the lowering of antibodies is a waste of time.

I hope this makes sense and thank you so much for all your answers.

DD
Dear digital dog,

As far as I know there is no causal connection between gluten sensitivity and thyroid disease, so I cannot see why one would want to stop gluten to try to alter thyroid antibodies. Maybe someone has suggested that but I cannot think of any reason to.

The standard line from endocrinologists is that you only feel bad with autoimmune hypothyroidism if your T4 and T3 are low. The situation for autoimmune hyperthyroidism is a bit different because it is recognised that eye problems and swollen fingers occur with normal T4 and T3 and are directly due to antibodies that may not actually be affecting the thyroid itself. However, antibodies tend to get ignored by endocrinologists and I think this may be a mistake. I suspect that quite a lot of symptoms in hypothyroid cases are also due to the antibodies directly.

The problem is that the antibody tests used in the lab do not correlate well with what the antibodies may be doing in the body. You might have 100 units of antibody binding on a test but only 13 of those units might be antibodies of a sort that caused symptoms - we simply have no information on this.

In a sense I do agree that if thyroid antibody levels have halved and then halved again you might expect at least a reasonable chance of that being associated with feeling better - but only if your symptoms are due to thyroid antibodies and so far in this thread I am not sure I can see what symptoms you are talking about and whether there is any particular reason to think they are due to anti-thyroid antibodies. The typical features associated with antibodies in autoimmune hyperthyroidism are protrusion and discomfort of the eyes and sometimes bumpy swelling along the shins and podgy fingers. I am not sure that other symptoms would be expected to change if antibodies went down.

The key thing is that all these things involve very specific mechanisms that need to be considered separately. They do not all go together. So, as I say, I cannot think of any good reason to stop gluten if you are worried about thyroid antibodies, whether or not these are causing any symptoms.
 

Gondwanaland

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As far as I know there is no causal connection between gluten sensitivity and thyroid disease
I am sorry, but there is plenty of evidence linking gluten with each and every autoimmune disorders, inlc linking gluten with Hashimoto's and many celiacs have Hashimoto's and many Hashi's patients develop celiac disorder.

Endos are just criminally pretending there isn't.

The connection might not be causal, but it certainly aggravates the autoimmune response.

Edit-- BTW my thyroid antibodies halved after going gluten free.
 
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I am sorry, but there is plenty of evidence linking gluten with each and every autoimmune disorders, inlc linking gluten with Hashimoto's and many celiacs have Hashimoto's and many Hashi's patients develop celiac disorder.
Those are associations, not causal links. And the association is a weak statistical one. There is no association with most of the autoimmune disorders I have been involved with - the genetic risk factors are known and are different. Muddling up associations with causes is not going to help people understand what's going on.

I don't know what you mean by aggravating the autoimmune response. It sounds like pseudo-immunology to be honest.
 

bertiedog

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@Jonathan Edwards Talking about thyroid antibodies and disease, two years ago an elderly gentleman who I knew had a full private thyroid panel done through Genova. He just wasn't feeling well and felt his thyroid might be something to do with this. He was already on 150 mcg thyroxine. Well it came back with both types of antibodies in the high thousands, I had never seen anything like this and rang Genova who said these antibodies were the highest they had ever seen so high so naturally he went back with the report to his GP who referred him on to several consultants including an Endo in the NHS to try and find out what was going on.

They didn't ever really come up with anything significant but did reduce his thyroxine a bit. He even had a full body scan but he wasn't told anything definite until in March this year when he was told he had lung cancer. Two weeks later he died. Am I wrong in thinking that there must be some connection here with sky high antibodies and the immune system bearing in mind that about 18 months later he was dead?

Pam
 

digital dog

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Gondwanaland,

Did you feel better when your antibodies went down? How long did it take you?
I'm more confused now. I do not find a gluten free diet difficult but I would rather not bother if I am not gaining anything.
It feels good to get my antibodies down (I imagine they will be close to zero in the new year) but I am VERY upset there is no improvement in my health. Surely I should feel SOMETHING!!! Perhaps it will keep other autoimmune conditions at bay (have a family history of autoimmune crap).
In my last post I said my TSH was 14 but it was actually 12 and only for a short while. I don't know why it went so far up and then down so quickly. I don't recall being any more tired than I already am.
My TSH is now around 2.2 and my T4 seems to always be at 14 (have records years ago when it was at 14).
I thought my problem might be thyroid but it now seems this was wishful thinking.
I suppose I should be pleased it is not my thyroid as I cannot tolerate the meds and hypothyroidism without meds would be pretty hellish I imagine...
I have a number of well friends who have hypothyroidism and they are full of energy and enthusiasm on thyroxine.
I just wish something could help me. Just one thing.

:cry::cry::cry::cry::cry::cry::cry::cry:
Getting upset now.
 

Gondwanaland

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1115436/
BMJ. 1999 Apr 17; 318(7190): 1023–1024.

PMCID: PMC1115436
Do dietary lectins cause disease?
The evidence is suggestive—and raises interesting possibilities for treatment 
David L J Freed, Allergist
Author information ► Copyright and License information ►

This article has been cited by other articles in PMC.

In 1988 a hospital launched a “healthy eating day” in its staff canteen at lunchtime. One dish contained red kidney beans, and 31 portions were served. At 3 pm one of the customers, a surgical registrar, vomited in theatre. Over the next four hours 10 more customers suffered profuse vomiting, some with diarrhoea. All had recovered by next day. No pathogens were isolated from the food, but the beans contained an abnormally high concentration of the lectin phytohaemagglutinin.1 Lectins are carbohydrate binding proteins present in most plants, especially seeds and tubers like cereals, potatoes, and beans. Until recently their main use was as histology and blood transfusion reagents, but in the past two decades we have realised that many lectins are (a) toxic, inflammatory, or both; (b) resistant to cooking and digestive enzymes; and (c) present in much of our food.2 It is thus no surprise that they sometimes cause “food poisoning.” But the really disturbing finding came with the discovery in 1989 that some food lectins get past the gut wall and deposit themselves in distant organs.3,4 So do they cause real life diseases?

This is no academic question because diet is one part of the environment that is manipulable and because lectins have excellent antidotes, at least in vitro. Because of their precise carbohydrate specificities, lectins can be blocked by simple sugars and oligosaccharides. Wheat lectin, for example, is blocked by the sugar N-acetyl glucosamine and its polymers.5 These natural compounds are potentially exploitable as drugs should lectin induced diseases be identified.

Read the rest at the following link: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1115436/
 
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There is no research on it conducted by Fasano at least. I was talking about autoimmunity
That was my point really - you seem to be talking about autoimmunity as if it were all mixed up together as one process. Autoimmunity to thyroid proteins is quite separate from autoimmunity to tissue transglutaminase in coeliac disease. Digital dog is interested in knowing if there is any reason to think that cutting out gluten would help symptoms that might be associated with thyroid antibodies. I cannot see any reason to think so.
 
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@Jonathan Edwards Talking about thyroid antibodies and disease, two years ago an elderly gentleman who I knew had a full private thyroid panel done through Genova. He just wasn't feeling well and felt his thyroid might be something to do with this. He was already on 150 mcg thyroxine. Well it came back with both types of antibodies in the high thousands, I had never seen anything like this and rang Genova who said these antibodies were the highest they had ever seen so high so naturally he went back with the report to his GP who referred him on to several consultants including an Endo in the NHS to try and find out what was going on.

They didn't ever really come up with anything significant but did reduce his thyroxine a bit. He even had a full body scan but he wasn't told anything definite until in March this year when he was told he had lung cancer. Two weeks later he died. Am I wrong in thinking that there must be some connection here with sky high antibodies and the immune system bearing in mind that about 18 months later he was dead?

Pam
I am not sure that there need be any connection between the lung cancer and the thyroid antibodies. Thyroid autoantibodies are pretty common in healthy people and lung cancer is pretty common. Autoantibodies do sometimes occur in association with cancers (and obviously autoantibodies come from the immune system) but these tend to be rather rare autoantibodies like the ones seen in dermatomyositis.
 

Gondwanaland

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Autoimmunity to thyroid proteins is quite separate from autoimmunity to tissue transglutaminase in coeliac disease.
I am sorry, but there is plenty of evidence linking gluten with each and every autoimmune disorders, inlc linking gluten with Hashimoto's and many celiacs have Hashimoto's and many Hashi's patients develop celiac disorder.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1115436/
BMJ. 1999 Apr 17; 318(7190): 1023–1024.

PMCID: PMC1115436
Do dietary lectins cause disease?
The evidence is suggestive—and raises interesting possibilities for treatment 
David L J Freed, Allergist
Author information ►Copyright and License information ►

This article has been cited by other articles in PMC.

In 1988 a hospital launched a “healthy eating day” in its staff canteen at lunchtime. One dish contained red kidney beans, and 31 portions were served. At 3 pm one of the customers, a surgical registrar, vomited in theatre. Over the next four hours 10 more customers suffered profuse vomiting, some with diarrhoea. All had recovered by next day. No pathogens were isolated from the food, but the beans contained an abnormally high concentration of the lectin phytohaemagglutinin.1 Lectins are carbohydrate binding proteins present in most plants, especially seeds and tubers like cereals, potatoes, and beans. Until recently their main use was as histology and blood transfusion reagents, but in the past two decades we have realised that many lectins are (a) toxic, inflammatory, or both; (b) resistant to cooking and digestive enzymes; and (c) present in much of our food.2 It is thus no surprise that they sometimes cause “food poisoning.” But the really disturbing finding came with the discovery in 1989 that some food lectins get past the gut wall and deposit themselves in distant organs.3,4 So do they cause real life diseases?

This is no academic question because diet is one part of the environment that is manipulable and because lectins have excellent antidotes, at least in vitro. Because of their precise carbohydrate specificities, lectins can be blocked by simple sugars and oligosaccharides. Wheat lectin, for example, is blocked by the sugar N-acetyl glucosamine and its polymers.5 These natural compounds are potentially exploitable as drugs should lectin induced diseases be identified.

Wheat gliadin, which causes coeliac disease, contains a lectin like substance that binds to human intestinal mucosa,6and this has been debated as the “coeliac disease toxin” for over 20 years.7 But coeliac disease is already managed by gluten avoidance, so nothing would change were the lectin hypothesis proved. On the other hand, wheat lectin also binds to glomerular capillary walls, mesangial cells, and tubules of human kidney and (in rodents) binds IgA and induces IgA mesangial deposits. This suggests that in humans IgA nephropathy might be caused or aggravated by wheat lectin; indeed a trial of gluten avoidance in children with this disease reported reduced proteinuria and immune complex levels.8

Of particular interest is the implication for autoimmune diseases. Lectins stimulate class II HLA antigens on cells that do not normally display them, such as pancreatic islet and thyroid cells.9 The islet cell determinant to which cytotoxic autoantibodies bind in insulin dependent diabetes mellitus is the disaccharide N-acetyl lactosamine,10 which must bind tomato lectin if present and probably also the lectins of wheat, potato, and peanuts. This would result in islet cells expressing both class II HLA antigens and foreign antigen together—a sitting duck for autoimmune attack. Certain foods (wheat, soya) are indeed diabetogenic in genetically susceptible mice.11 Insulin dependent diabetes therefore is another potential lectin disease and could possibly be prevented by prophylactic oligosaccharides.

Another suspect lectin disease is rheumatoid arthritis. The normal human IgG molecule possesses carbohydrate side chains, which terminate with galactose. In rheumatoid arthritis much of the galactose is missing, so that the subterminal sugar—N-acetyl glucosamine—is exposed instead. These deficient IgG molecules feature strongly in the circulating immune complexes that cause fever and symptoms.12 In diet responsive rheumatoid arthritis one of the commonest trigger foods is wheat, and wheat lectin is specific for N-acetyl glucosamine—the sugar that is normally hidden but exposed in rheumatoid arthritis. This suggests that N-acetyl glucosamine oligomers such as chitotetraose (derived from the chitin that forms crustacean shells) might be an effective treatment for diet associated rheumatoid arthritis. Interestingly, the health food trade has already siezed on N-acetyl glucosamine as an antiarthritic supplement.13

Among the effects observed in the small intestine of lectin fed rodents is stripping away of the mucous coat to expose naked mucosa and overgrowth of the mucosa by abnormal bacteria and protozoa.14 Lectins also cause discharge of histamine from gastric mast cells,15 which stimulates acid secretion. So the three main pathogenic factors for peptic ulcer—acid stimulation, failure of the mucous defence layer, and abnormal bacterial proliferation (Helicobacter pylori) are all theoretically linked to lectins. If true, blocking these effects by oligosaccharides would represent an attractive and more physiological treatment for peptic ulcer than suppressing stomach acid. The mucus stripping effect of lectins16 also offers an explanation for the anecdotal finding of many allergists that a “stone age diet,” which eliminates most starchy foods and therefore most lectins, protects against common upper respiratory viral infections: without lectins in the throat the nasopharyngeal mucus lining would be more effective as a barrier to viruses.

But if we all eat lectins, why don’t we all get insulin dependent diabetes, rheumatoid arthritis, IgA nephropathy, and peptic ulcers? Partly because of biological variation in the glycoconjugates that coat our cells and partly because these are protected behind a fine screen of sialic acid molecules, attached to the glycoprotein tips.10 We should be safe. But the sialic acid molecules can be stripped off by the enzyme neuraminidase, present in several micro-organisms such as influenzaviruses and streptococci. This may explain why diabetes and rheumatoid arthritis tend to occur as sequelae of infections. This facilitation of lectins by micro-organisms throws a new light on postinfectious diseases and makes the folklore cure of fasting during a fever seem sensible.

Alternative medicine popularisers are already publishing articles about dietary lectins,17 often with more enthusiasm than caution, so patients are starting to ask about them and doctors need to be armed with facts. The same comment applies to entrepreneurs at the opposite end of the commercial spectrum. Many lectins are powerful allergens, and prohevein, the principal allergen of rubber latex, is one. It has been engineered into transgenic tomatoes for its fungistatic properties,18 so we can expect an outbreak of tomato allergy in the near future among latex sensitive individuals. Dr Arpad Pusztai lost his job for publicising concerns of this type (20 February, p 483).
 

Gondwanaland

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http://www.eurekalert.org/pub_releases/2015-10/sh-rfn102215.php
Zonulin in autoimmune disease

Zonulin is a type of protein (a haptoglobin) that was discovered in 2000 by a team of researchers at Maryland School of Medicine in the USA. The protein is found within intestinal cells and it is the only human protein discovered so far that regulates the permeability of the intestine. Zonulin has been called a "tight junction regulator", as it controls the size of the gaps between the intestinal cells and orchestrates the passage of nutrients, water and cells into and out of the gut.

Scientists have found that zonulin is produced and released by triggers including intestinal bacterial infections and gluten, and a link between zonulin and coeliac disease has already been established. In the presence of zonulin, the normally tight junctions between the intestinal cells remain open, creating bowel "leakiness" and initiating an inflammatory cascade that eventually damages the intestinal wall.

"Increased intestinal permeability has been implicated in a range of autoimmune conditions including coeliac disease, type 1 diabetes, rheumatoid arthritis and multiple sclerosis," explained Prof. Barbara. "Since zonulin is a key regulator of intestinal permeability, it is possible that this protein provides a common link between all these conditions."

Zonulin in NCGS and IBS

In the latest study, the team from Bologna recruited patients with NCGS (n=27), diarrhoea-predominant IBS (IBS-D) (n=15), coeliac disease (n=15) and healthy volunteers (n=15) and they measured their blood levels of zonulin. The highest zonulin levels were found in the patients with coeliac disease (mean 0.033 ng/mg), followed by those with NCGS (mean 0.030 ng/mg) and IBS-D (mean 0.012 ng/mg). The mean level in the healthy volunteers was only 0.007 ng/mg. In the patients with NCGS, blood levels of zonulin fell significantly when they were eating a gluten-free diet.

"This study has increased our understanding of zonulin and how it might contribute to the development of these common and disabling bowel conditions," said Prof. Barbara. "Hopefully, our work will lead to new diagnostic and therapeutic strategies for patients with these and possibly other autoimmune conditions."
 

digital dog

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This will be my last question and I very much appreciate everyones input.
Jonathan you say that thyroid antibodies are not uncommon in healthy people. Would you have a percentage for this?
I thought high antibodies was clearly indicative of thyroid problems but if a section of normal people have high antibodies then I am less concerned.
Many thanks