I tested out of range high for THYROGLOBULIN ANTIBODIES & THYROID PEROXIDASE ANTIBODIES. I have been told by a doctor I do not have Hashimoto's Thyroiditis as the rest of my thyroid results are in range, however I may develop the thyroiditis in the future. Follow up testing is the plan as other test in range. It seems to me if you know you have antibodies you should try to lower them to prevent further damage to your thyroid. I have started LDN .25mg hoping my antibodies will decrease (thru a functional doctor). Can someone comment on what I have been told based on the figures provided.
Hello and welcome! You have come to the right place for the best shared experiences and wisdom of all things thyroid!
First, how are you feeling? Do you have any symptoms?
What led to you getting a thyroid panel one year ago?
Based on the information you provided, there are a few inaccuracies. High antibodies do indeed confirm autoimmune hypothyroidism - ie Hashimotos. It’s possible your doctor should have said that, but followed it with “you may develop hypothyroid SYMPTOMS in the future. “ Also, antibodies are NOT the cause of anything nor should they ever be something you try to “treat.”
Your free Ts are low enough where I’d be surprised if you didn’t have some hashis symptoms, but you haven’t mentioned any yet.
Most people here on this forum are in the UK. I happen to be in the US so I’d love to know how you found your way to the doctor you have. It’s more typical for doctors to not understand anything about thyroid. Shocking but true, and it looks like yours falls into that category. I just can’t figure out why they would say you don’t have hashis, nor what they think they will achieve giving you LDN. That’s just a little more out there than the usual well-intentioned but incorrect treatments I’d expect.
LDN is definitely a thing in autoimmune circles, but it’s a very strange first option given what you’ve said. Maybe if you can tell us how you feel it might make more sense. But it’s very out of the ordinary and unproven, especially given your bloods.
But we just don’t know enough about you to say. Please let us know how you feel and any additional background on your care history.
Others will likely come along with other opinions or clarifications.
FallingInReverse : Thank you for responding. Regarding how I feel and symptoms: Currently I believe I do not have symptoms of Hashimoto's Hypothyroidism. The only symptom I can relate Hashis Hypo with is fatigue, and unfortunately that is very common symptom of a B12 Deficiency (B12D), which I treat w/ injections. Some background: I requested my 1st thyroid panel from Dr S on 11/2022 & 2nd panel 9/2023 in support of yearly follow ups due to having a B12D caused by malabsorption from pernicious anemia(PA)/autoimmune gastritis (AIG). I understand 35% of patients with autoimmune thyroiditis have PA/AIG. Dr S position after both panels were follow up testing; basically wait & watch if progression happens. I agree the 1st doctor (which was not Dr S) should have said you may develop symptoms in the future. I further gather from what you shared I "do" have Hashimoto's Hypothyroidism; although, I believe currently asymptomatic. . I should clarify one thing: When the second panel was run by Dr S , I was alarmed to see the increase in TPO/TGA antibodies. I did some research & found that if you have those antibodies, you have Hashis. l did ask Dr S after the 2nd panel was run if I had Hashis and she confirmed I did. I thought why not communicated after the 1st panel? Then I thought why wait until the antibodies destroy my thyroid, should I not act on trying to prevent the destruction if there is a way. (I am new to this). Please know prior doctors would only test my TSH as they believed that was a sufficient test. I learnt that not to be the case via B12 deficiency/PA support group I belong to. I decided to advocate for myself went to a functional doctor and her 1st recommendation was Ashwagandha supplement. I asked for the LDN as it appears it does reduce Hashi antibodies, based on the current users of LDN. The functional Dr did not push back on my request for LDN. Maybe I should have gone with the Ashwagandha. I do want to clarify prior to the 2 thyroid panels run I went to a rheumatologist who requested TGA/TPO and he was the one who advised I had Hashis antibodies but not Hashimoto's thyroiditis. He only ran as I share w/ him the relationship between PA and thyroiditis. I do not have arthritis. It was the early days of my B12D/PA diagnosis and did not know most all of my symptoms were B12 related. I am in the US .
So, keep in mind that most people on this board are in the U.K. or otherwise not in the US.
In the U.K., there is a very very high threshold for diagnosing and treating hypothyroid, and the majority of people on this board spend as much time figuring out what they need (a huge challenge as you are experiencing!) as they do fighting to get it. (which we don’t really struggle with as much.)
This forum is like a collection of ivy educated doctors at the best practices. No one is actually a doctor… but it is really nuts how doctors all over the world know so little about thyroid. Many are well intentioned, but they have never really been trained. That’s why all of them only test TSH. Based on what you said about yours - they seem pretty typical. Helpful, sort of informed, but not exactly.
So, we can help you figure it out!
As I noted below, referencing radd ’s comments, linking to a post from Jaydee1507 and I know I’ve read similar from greygoose …
The question I too would love consensus on is this;
why wait until the antibodies destroy my thyroid, should I not act on trying to prevent the destruction if there is a way.
So autoimmune hashis is a one-way street for sure, with lots of twists and turns along the way. Your immune system will indeed continue to attack your thyroid. You will continue to have antibodies in response. It’s autoimmune and there is no cure.
But here you are having caught the very early stages of it. While still asymptotic. Which is awesome and amazing. Well done seeing the PA connection.
So it’s rare to have someone who has found this early, asymptomatic, while also having a good chance of asking your doctors for the treatment you need whether that’s Levo, other thyroid replacement, or LDN, etc.
My thoughts:
1) I’ve heard conflicting comments on here as to whether one should try to reduce antibodies. Do the admins have any consensus?
2) In ANY scenario you should begin testing these 4: B12, folate, ferritin, and D3. As SlowDragon notes, Hashis interferes with absorption of those 4 and those 4 are essential for your thyroid to work its best. Get those tested and come back with a new post and we can tell you how you might supplement and optimize them.
3) I don’t think anyone would recco Levo with your bloods and no symptoms… even though you could get it. I’m not sure anyone would recco LDN either though. It might just be a wait and see. But I would love the input of those on this board - knowing you can get what you ask for - are there any meds anyone thinks you should be on.
4) I also wonder if there are any lifestyle changes that would help. Like, I ran 3 marathons while my hashis simmered unknown to me. I wonder if I sped it up or made it worse.
FallingInReverse .. I just recently responded to SlowDragon. My response to SlowDragon: Having a B12D due to malabsorption from Pernicious Anemia (PA)/Autoimmune Gastritis (AIG) I have my vitamin D check 2-3 times a year, B12 & Folate 2-4 times year along w/ an iron panel which includes ferritin. Those are at solid levels, w/ iron saturation & total iron sometimes dipping. I will then supplement w/ iron and levels correct.. Not sure any doctors will treat w/ Levo if TSH normal and no symptoms.. I would love to know the reason why one would not want to lower antibodies to “undetectable" levels to prevent attacks on your thyroid, knowing there is no cure for autoimmunity, but maybe lowering antibodies stop the invasion., hence prevents progression to symptoms.
A note on iron - as you probably know but an important reminder - too much iron is toxic and causes permanent organ damage . Just take care to monitor closely if you are taking iron supplements.
So when you think of the cause and effect - it’s the autoimmune disease that is the cause.
I know there are some things that say you should try to control you antibodies. I mean maybe it’s just poorly worded and they really mean you should control your autoimmune response in the first place.
Dietary and lifestyle changes would be good for everyone to be healthy overall, reduce stress, and all that stuff.
One could also look at the role of inflammation in the autoimmune process ( gluten free for example) and that certainly can lessen the impact of the disease.
But that’s why I’m looking forward to the smarter folks on this board to weigh in.
ps. The most important thing is that you have no symptoms. Your TSH is ambivalently ok… it’s in range but “in range” does not mean ok any more than wearing a size 7 shoe is “in range” and average/normal, when your shoe size is a 10. Your free Ts are only 20-30% through range … again “in range” but actually if any of us hypo folks on the board had those numbers we’d most likely suggest an increase in Levo. And I’d even say IF you did have symptoms, there would be a clear path to asking for Levo as your antibodies support your Hashis diagnosis.
I would love to know the reason why one would not want to lower antibodies to “undetectable" levels to prevent attacks on your thyroid, knowing there is no cure for autoimmunity, but maybe lowering antibodies stop the invasion., hence prevents progression to symptoms.
But, it's not the antibodies attacking your thyroid. That is the most important thing to know.
Yes opinions vary on whether you should try and reduce them or not - and opinions vary on whether this is even possible and how you would prove it, given that antibodies levels fluctuate all the time. And certainly taking levo would not do it.
But, TPO and Tg antibodies are there for a reason. When the immune system attacks the thyroid, as I'm sure you know, the dying cells deposit their stock of hormone into the blood causing the false-hyper swing of thyroid hormone levels. At the same time, small quantities of TPO (Thyroid Peroxidase) and Tg (Thyroglobulin) - proteins necessary to produce thyroid hormone - leak into the blood where they should not be. So, the antibodies come along to clear them away. Why would you want to stop that happening?
There are those that say the antibodies, whilst they are not responsible for destroying the thyroid, do cause inflammation. But, if that were true, when you look at peoples lab results you would always that when people have high levels of antibodies, they would also have high levels of CRP. But that is not the case. Inflammation can be caused by so many things.
I have been told by a doctor I do not have Hashimoto's Thyroiditis as the rest of my thyroid results are in range
I think your doctor is a bit confused. I don't think he meant you don't have Hashi's, because you obviously do - high antibodies - but that you don't have hypothyroidism. Yet. But, even that I would contest.
TSH 2.03 (0.50 - 5.00)
T4, Free 1.0 (0.75 - 1.54) 31.65%
T3, Free 2.5 (2.3-4.2) 10.53%
With Frees that low, I would say you are hypo. They don't have to be under-range. They should both be around 50% through the range, with the FT3 slightly lower than the FT4. But I expect your doctor is only looking at the TSH and as that is in-range, considers that there can't be anything wrong. But your TSH is saying that your thyroid is struggling to make even meager amounts of hormone. They just don't know enough about thyroid - or blood test results - to understand the ins and outs and how the different levels interact, etc. etc. etc. Basically, they're just ignorant.
When you say you have no symptoms, I wonder if you've read many lists of hypo symptoms - and they are hypo symptoms, Hashi's doesn't have any specific symptoms, it's just the reason for you hypo. Do you not have rough skin on your heels or elbows? Bags under your eyes? Dental problems? An aversion to meat? Wild as that may seem, those are all hypos symptoms. And doctors know nothing about symptoms, anyway. They might quote fatigue, hair-loss, depression, at you but there are many, many more. And, given that T3 is essential for every single cell in your body to function correctly, symptoms can appear anywhere and everywhere.
So, what can you do next? Well, you could get your early morning cortisol tested, see how that is. There's a close connection between cortisol and thyroid hormones.
But, in any case, forget the antibodies, they are not worth focussing on because they are not the main problem. They are just an indication that the cause of your hypothyroidism is autoimmune.
greygoose What you communicated abt TPO and Tg antibodies being there for a reason makes sense to me. In the back of my mind, I remember thinking antibodies in some circumstances help protect the body from foreign invaders. I will stop focusing on how to lower my antibodies associated to Hashis. Yes the very 1st doctor did say you may go on to develop hypo in the future. Can you clarify how to calculate 50% through the range w/ numbers or how you came up with the percentages you shared. I tried to google the calculations but could not make it work. Early morning cortisol on 3/21/2022 was 15ug/dL / AM Range (6-10 AM) 6.0 - 18.4 ug/dL. I do have bags (dark circles) under my eyes. I do not have an aversion to meat , but it is not my favorite thing to consume. I cannot thank you enough for sharing your knowledge as it makes so much more sense now in correlation to what others have shared. 3 different doctors I went to (they are not the doctors who ran the thyroid panel) kept telling me my TSH is good , hence no treatment. They do feel the thyroid glands under my neck as well. Is there any otc thyroid supplements I can take ? Waiting for my thyroid to be destroyed seems wrong. I will watch my diet, gluten & dairy. I eat very little of either one. Thank you for your input.
What you communicated abt TPO and Tg antibodies being there for a reason makes sense to me.
It's the only thing that makes sense to me. Antibodies are there to protect us in one way or another. Why would they suddenly start attacking us in any way?
Early morning cortisol on 3/21/2022 was 15ug/dL / AM Range (6-10 AM) 6.0 - 18.4 ug/dL.
OK, so cortisol not a problem at the moment. But, for that reason alone it would be wise to start thyroid hormone replacement to stop adrenal problems developing. But trying to talk adrenals with your average doctor is like speaking a foreign language. They have no idea what you're talking about!
kept telling me my TSH is good
No, over 2 is not good. It's too high. I euthyroid TSH would be around 1. Over 2 means that the thyroid has been damaged and is struggling to make its quota of hormone, and needs extra stimulation to do so. They should be looking at the thyroid hormone levels - TSH is a pituitary hormone, and pituitaries aren't always reliable any more than thyroids are.
s there any otc thyroid supplements I can take ?
Absolutely not! Avoid like the plague anything that calls itself 'thyroid support'. In no way will it help your thyroid, and for 'support' read 'stimulate'. And, stimulating a sick gland will just hasten its demise.
You do need good levels of the basic nutrients, as I think you know: vit D, vit B12, folate, ferritin, selenium, zinc or copper. But not everybody needs all of them. So, they should be tested before supplementing. But any type of multi-vit - and thyroid 'support' supplements are just glorified multi-vits - contain things you don't need and shouldn't be taking, such as calcium and iodine.
But no supplement is going to have any effect on the Hashi's itself. That will just continue towards its ultimate goal whatever you do. The supplements will just keep you as well as possible during that journey.
Waiting for my thyroid to be destroyed seems wrong.
Well, it would be wrong if there was anything you could do about it. But there isn't. Taking thyroid hormone replacement, whilst essential eventually, is not going to halt the progress of the disease. And, although some levo would do you good at the moment, there's nothing else a doctor can prescribe.
I will watch my diet, gluten & dairy. I eat very little of either one.
Just watching gluten and dairy won't do anything. If you are intolerant to gluten, you have to cut it out 100%. Which means always reading labels because - like soy - they slip in in everywhere! And Hashi's people are very often gluten-intolerant even if they don't have Coeliac. And therefore eating even a small amount of gluten will cause symptoms. It's not like cutting out gluten - or dairy - is going to make any difference to your thyroid, but it will make you feel better if you are intolerant. But, as you say that you are 100% symptom free, maybe you're not intolerant to either of them. Still, worth a try.
greygoose I have had a EGD and blood work to test for celiac. Both came back negative. I do understand cutting out gluten is always recommended. The gluten I do consume, which is very little and never has given me symptoms. But I know you can be sensitive to gluten even if you test negative. My most current TSH was 1.46 mIU/L, so improvement there. I just wish I knew what I did to bring it down. I will stay away from thyroid supplements. Thanks for bring that to my attention.
I do understand cutting out gluten is always recommended
No, it's always recommended to try going gluten-free to see if it helps. If it doesn't then there's no point in staying gluten-free. But my point was, if you're going to try it, it has to be 100%, not just cutting down on gluten. It could very well be that you're not gluten-sensitive and that gluten-free wouldn't be of any advantage to you. But you never know until you try. A lot of people are surprised by how much better they feel. It didn't do anything at all for me, though, nor did sugar-freee, dairy-free or anything else-free, except for soy-free. I react badly to soy.
My most current TSH was 1.46 mIU/L, so improvement there. I just wish I knew what I did to bring it down.
I don't suppose you did anything. TSH does vary a lot, especially when you have Hashi's. But, in any case, it's pretty much irrelevant because it's not high TSH that makes you hypo, it's low thyroid hormones. So, unless they increased in level, the slight difference in the TSH is meaningless.
greygoose When you saw my TSH @ 2.03 you explained over 2 means the thyroid has been damaged and is struggling to make its quota of hormone and needs extra stimulation to do so. Euthyroid TSH would be around 1. They should be looking at the thyroid hormone levels. Although my TSH dropped to 1.46 in 2023 perhaps it will drop to 1 on next test, regardless it's the T3 & T4 levels that count when determining hypo. Thank you for the explanation as to what tests really determine hypo. In 2018 my TSH was 2.779 and based on range the GP thought that was fine. Who knows how long my thyroid has been struggling. Eventually some thyroid test should trigger an alert or maybe some symptoms will. I am still in the learning gathering knowledge phase.
Diagnosing and dosing by the TSH, as most doctors do, assumes that everyone always has a perfectly funcitoning pituitary. But that's not true. Pituitaries can malfunction just as thyroids can, so whilst TSH can give us an indication of thyroid status it is not 100% reliable.
And another terrible problem is that doctors have no idea what euthyroid is. Because of these stupid ranges, they think that any result that falls within them has to be ok because it's in-range. And that is not true at all. Ranges are, at best, just a rough guide, and there are so many other things to take into consideration. Like symptoms, but most doctors don't even know what the symptoms are...
I could go on, but I won't.
So, yes, you could have been hypo for a long, long time. Symptoms tend to start to make themselves felt before any anomelies show up in the blood tests. And you don't really feel the symptoms anyway, to begin with, because the adrenals take up the slack, and mask them. So, by the time the symptoms get bad enough to drive you to the doctors, and the doctor makes up his mind to test, and then test again - and possibly a third/fourth time - you can have been hypo for years.
greygoose I am really going to have to monitor this condition, as the only symptom I can related to hypo is fatigue, however that is also a MAJOR symptom of B12D, which I constantly monitor. What fun this is. Thank you for all your support...
helvella I know very well there in no point to testing B12 while on injections. I let the doctors test as it makes them confident, I am getting enough B12. I know that means nothing regarding symptoms. I treat to my symptoms, never to B12 levels. Thank you for the response.
Have you also had vitamin D, folate, B12 and ferritin levels tested
If not get these included at next test
Was test done early morning?
Free T4 (fT4) 1.0 pmol/L (0.8 - 1.8) 20.0%
Free T3 (fT3) 2.9 pmol/L (2.3 - 4.2) 31.6%
Your Ft4 is already on lower side
Look at trialing gluten free diet too
Hashimoto's affects the gut and leads to low stomach acid and then low vitamin levels
Low vitamin levels affect Thyroid hormone working
Poor gut function can lead leaky gut (literally holes in gut wall) this can cause food intolerances.
Most common by far is gluten.
Dairy is second most common.
A trial of strictly gluten free diet is always worth doing
Only 5% of Hashimoto’s patients test positive for coeliac but a further 81% of Hashimoto’s patients who try gluten free diet find noticeable or significant improvement or find it’s essential
A strictly gluten free diet helps or is essential due to gluten intolerance (no test available) or due to leaky gut and gluten causing molecular mimicry (see Amy Myers link)
Changing to a strictly gluten free diet may help reduce symptoms, help gut heal and may slowly lower TPO antibodies
While still eating high gluten diet ask GP for coeliac blood test first or buy test online for under £20, just to rule it out first
Assuming test is negative you can immediately go on strictly gluten free diet
(If test is positive you will need to remain on high gluten diet until endoscopy, maximum 6 weeks wait officially)
Trying gluten free diet for 3-6 months. If no noticeable improvement then reintroduce gluten and see if symptoms get worse
The predominance of Hashimoto thyroiditis represents an interesting finding, since it has been indirectly confirmed by an Italian study, showing that autoimmune thyroid disease is a risk factor for the evolution towards NCGS in a group of patients with minimal duodenal inflammation. On these bases, an autoimmune stigma in NCGS is strongly supported
In summary, whereas it is not yet clear whether a gluten free diet can prevent autoimmune diseases, it is worth mentioning that HT patients with or without CD benefit from a diet low in gluten as far as the progression and the potential disease complications are concerned
Despite the fact that 5-10% of patients have Celiac disease, in my experience and in the experience of many other physicians, at least 80% + of patients with Hashimoto's who go gluten-free notice a reduction in their symptoms almost immediately.
Similarly few months later consider trying dairy free too. Approx 50-60% find dairy free beneficial
With loads of vegan dairy alternatives these days it’s not as difficult as in the past
SlowDragon Thank you for responding.. Having a B12D due to malabsorption from Pernicious Anemia (PA)/Autoimmune Gastritis (AIG) I have my vitamin D check 2-3 times a year, B12 & Folate 2-4 times year along w/ an iron panel which includes ferritin. Those are at solid levels, w/ iron saturation & total iron sometimes dipping. I will then supplement w/ iron and levels correct. I believe the thyroid tests were run in the AM but I cannot be certain. Should they have been run in the AM ? I have been tested for celiac via blood tests and an EGD. Both results were negative. I have cut down on my gluten consumption drastically since being diagnosed with B12D, however eating gluten does not cause any negative reaction I am aware of. I do understand the reactions can be asymptomatic, so I need to be very careful w/ consumption. I was GF for 10 months and did not feel different (good or bad), however that was in the early days of my B12D, which was undertreated until I took control of my injections. I do not consume much dairy although I enjoy cheese but consume sparingly. Thank you for all the links, I am sure they I will eventually look at them.
Elevated thyroid antibodies can suppress the HPT axis (hypothalamus-pituitary-thyroid), decrease both the number & sensitivity of thyroid hormone receptors and impair conversion of T4-T3. It is always important if symptomatic to try reducing them.
Knowing you have such elevated thyroid antibodies places you in a good position to try reducing them and delay the onset of thyroid gland destruction, and hopefully raise thyroid hormone levels a little without the need to medicate replacement meds as yet.
I agree with FallingInReverse that LDN is strange option to start with. Most find some relief from dietary and lifestyle changes and OTC supplements proven to contain anti-inflammatory properties such as selenium, Vit D and fish oils.
Great advice regarding autoimmune thyroid condition protocols already given by SlowDragon.
Hi radd , I read admin posts all time here saying antibodies fluctuate, come along after an autoimmune attack to clean up, don’t cause symptoms, and aren’t to be treated.
But I am pretty sure greygoose has repeated the same thing frequently.
You are all smarter than me, so just asking if there is disagreement on whether antibodies should be monitored and treated.
With high antibodies and free Ts scraping the floor, why delay Levo (esp if symptomatic) ? Huge caveat - OP has not indicated how they feel yet. Will also say that it’s important to know more about OPs doctor. Possible their functional doctor is trained to complement a traditional doctor, and there is a missing step that’s happened.
But I think we can all agree hashis is hashis and the treatment is hormone replacement, and not LDN as a first step. It’s a red flag to me, which could maybe make sense if we knew context, but we don’t yet.
A competent & healthy immune system is where certain cells and antibodies are equal, to produce a balanced response. For example - balance between killer T Cells & antibody producing B cells, balance between T helpers & T regulators to turn on & off immune system, etc, but auto-immunity will elevate one side of the scales.
Antibodies are molecules made by the immune cells to attack and destroy foreign invaders. They are inflammation by their very nature. Auto-antibodies are unwanted inflammation resulting from an unwanted dysregulating immune system when the body’s defences turn on self and attack own healthy tissue.
When Hashimotos is heightened, large numbers of lymphocytes (WBC’s) accumulate in the thyroid gland with increased levels of immunoglobulins driving the auto-immune process that attacks TPO (key enzyme) &/or thyroglobulin (protein) causing gradual thyroid gland follicle destruction. The auto-antibodies are created to clear debris created by thyroid gland destruction but they also negatively influence other parts of the immune system unbalancing those scales further and creating more (unwanted) inflammation, hence we get fatigue, aches, joint pains, puffiness, flu-like symptoms, etc.
Unaddressed elevated auto-inflammation evolves into chronic (long term), and is well documented for damaging further unconnected healthy cells, tissues, organs, even tissue death and damage to DNA in previously healthy cells. This is when people never seem to ‘get better’ but just keep accumulating more conditions. In addition research evidences those same specific areas of the immune system that become dysregulated in Hashi, also appear in other autoimmune conditions such as PA, RA, sjogrens, celiac, etc. Hence why we become sususpectable to multi auto-immune conditions after gaining one.
These cytokines (chemical messengers) can also affect the working of thyroid hormones. For example TNF-a is a well known pro-inflammatory cytokine involved in systemic inflammation made chiefly of macrophages (type of white blood cell). Its primary role is in the regulation of immune cells but will elevate in the presence of high levels of (auto)antibodies, and when elevated has been shown to reduce blood levels of T4 and T3.
If you are familiar with deiodinase behaviours (enzymes that dictate activation/deactivation of thyroid hormone) you will know that D1 increases cellular thyroid activity by converting T4-T3. This can be suppressed & down regulated by autoimmune inflammation (except conversion in pituitary which acts differently) when cytokines IL-1, Il-6, and TNF-alpha significantly reduce D1 activity and so tissue T3 levels.
CRP is a standardised acute inflammatory measure. This is not supposed to remain high long term (as in chronic) but in autoimmunity it may do so, and there is direct inverse correlation between high CRP and reduced tissue T3 levels. D3 creates RT3 and is stimulated by inflammation, so produces higher than healthy levels of RT3, reducing both FT4 & FT3 levels further.
The level of thyroid antibodies doesn’t always correlate with the level of severity the immune system has been compromised, evidenced by some people living healthy lives with elevated thyroid antibodies, whilst others become extremely unwell with very low. Thyroid antibodies can also become low together with low WBC’s after years of being unwell. Conventional medicine does not understand these labs and can offer no explanation, whereas function medicine will say the immune system is simply worn out as not designed to work at the extended capacity long term that elevated thyroid antibodies demands. .
It is possible to have one type of thyroid antibody or multiple but we are rarely tested for both Hashi & Graves antibodies: Hashi (goitrous) - TPOAb or TGAb; Atrophic - TRAb’s (TSH receptor-blocking); Graves (TSI’s). Yet many of us Hashi sufferers have thyroid gland atrophy indicating the blocking variety of TSI’s. Yes, I agree Hashi is Hashi (in that is never goes) and thyroid antibody levels may fluctuate but symptoms come in varying degrees and by identifying and managing the triggers (such as the removal of gluten) we can make ourselves work a little better and possibly even delay the onset of thyroid destruction.
With knowledge a new era is evolving. My son is managing his own previously elevated thyroid antibodies and autoimmune symptoms with dietary and lifestyle changes, and living a healthy life without the need for thyroid hormone replacement meds (as yet ) by keeping inflammation at bay.
If you read Datis Kharrizian, Isabella Wentz, Chris Kressler and many others with knowledge of autoimmune conditions they all identify how damaging Hashi chronic inflammation is and suggest ways to reduce symptomatic elevated thyroid antibodies with some very effective remedies backed by research. You need a bottomless wallet but I wish I had known all this at the start of my thyroid journey as my thyroid gland is gone, now less than a shovelled up pea.
I have previously written about thyroid antibodies and haven’t seen ‘older’ admins say anything to the contrary to my statements, but have read a ‘relative newbie’’ say antibodies are harmless 🤷♀️. Remember we are all patients simply sharing self-taught knowledge and opinions. Admins also perform a superb job ensuring forum rules are adhered to and discourage trolling, etc but are not necessarily more knowledge than a member. I used to be an admin myself on this forum.
Radd Thank you for the detailed summary. One thing that is confusing me is the terms antibody & autoantibody. I understand antibody being made by the immune cells to attack and destroy foreign invaders (beneficial to us). Autoantibody, unwanted antibodies as they attack our healthy tissue (not beneficial). TPO & TGA test speak to antibodies, but why are they not considered autoantibodies, as we do not want elevated levels. I just would like to understand in testing terms the difference. I will purchase one of the books by the people you mention addressing ways to reduce symptomatic elevated thyroid antibodies, although I am asymptomatic.
TPOAb and TGAb are known as autoantibodies because they are the result of an autoimmune condition. In case of Hashi the self-antigens are TPO (enzyme) and TG (protein) attacked by lymphocytes (type of white blood cell) within the thyroid gland.
Autoantibodies are markers for many autoimmune conditions such as Graves, rheumatoid arthritis, Sjogrens, multiple sclerosis, celiac disease, lupus. When symptomatic the level of autoantibodies may follow the extent of the attack on healthy tissue but this rule doesn't always follow through as many asymptomatic people live well with a degree of autoantibodies.
Think of 'antibodies' as a normal response to maintaining a healthy body whereas 'autoantibodies' are undesirable as a response to a wholly unhealthy and damaging condition.
radd Your last sentence is how I understand antibodies vs autoantibodies. Autoantibodies being unhealthy, hence if a there is means to lower them then that should/could be a good outcome as long as the antibodies (maintains healthy body) are not effected?. Just my thoughts after gathering knowledge from all the many caring & detailed posts & trying to piece it together. Very grateful !
greygoose SlowDragon radd Thank you as always for the master class.
Other than expressing my gratitude for the wisdom and deep appreciation for all of your willingness to share is so precisely and in such a custom 1-to-1 manner…
The big takeaway for today’s lesson is how “words matter.” It is said “the immune system attacks the thyroid.” But this statement can lead to 100 different interpretations. What constitutes the “immune system” what does “attack” mean and … is it really doing that to “the thyroid.”
And when developing a plan of action/treatment plan - words matter. TGab and TPOab are part of the immune system… but they are not attacking the thyroid (I mean it’s right there by definition they target TG and TPO!) But of course they are part of a complex immune response that over time does damage the thyroid.
There is so much misinformation out there - either accidentally because of imprecise language and different interpretations, and then misinformation from people trying to sell us a “cure.”
Radd after your last response above, and Greygoose’s expansion of her reply, I can glimpse how there are no contradictions in the pathological mechanisms you both detail. And it all begins with being precise about the subjects and verbs of the sentences we use and being clear about what is actually happening in our bodies with Hashis.
You are so right! And I'm so happy that someone is finally agreeing with me! lol Words do matter. Which is why I'm always correcting people and telling them they must use the right terminology - especially when talking to doctors - and generally being a pain in the you-know-what! People talking about results being in a good range make me break out in spots! I don't even know what that means. I'm part of the grammar police and proud of it! And using the right word for the right thing is of utmost importance to me. I may make some mistakes myself, but it's not for want of trying.
OK, so yes, Tg and TPO antibodies are part of the immune system. But antibodies are very specific to the job. You won't find them attacking other parts of the body, as some people believe. TPO antibodies are only 'interested/attracted to TPO, Tg antibodies in Tg. And, for that reason can sometimes be found within the thyroid itself. How they get in there is not explained, not that I've seen, anyway, but that is not their main objective. Mainly they exist to clean up the blood. And Graves' has its own antibodies, just as Hashi's does and they don't touch anything else. Same with all other autoimmune diseases.
what does “attack” mean and … is it really doing that to “the thyroid.”
Good question. What does 'attack' mean? According to Dictionary. com it means:
to set upon in a forceful, violent, hostile, or aggressive way, with or without a weapon; begin fighting with
Is the immune system really doing that to the thyroid? It would appear so, or else why would the thyroid stop working?
So very many people do all they can to reduce TPO/Tg antibody levels in their blood, but I've never heard that, in the end, it did anybody any good. Surely if it were possible to do that, and doing it had any beneficial effect, we would know. No?
So, the million dollar question - what’s doing the attacking of what.
Immune system, antibodies… think - antibodies don’t attack, they target and bind. In our situation, they mistakenly target and bind.
But that triggers inflammation. And inflammation is the killer too. But ab’s and inflammation are all part of the immune system.
So yes, the immune system is (mistakenly) attacking in a way that leads to the destruction of the thyroid.
The immune system recognizes the TG and TPO thyroid proteins as abnormal, triggering the production of antibodies against them. These antibodies then bind to the proteins, marking them for destruction by other components of the immune system, such as immune cells and inflammatory molecules. This continuous attack on the thyroid tissue eventually impairs its function, leading to symptoms associated with hypothyroidism.
So, the place people get confused I think is not understanding what part in the chain they are trying to “treat”. Trying to address antibodies is not a root cause of the disease AND not a root cause of symptoms.
We have an incurable autoimmune dysfunction. So there’s that. We have low Ts that cause symptoms. So we can manage that.
Then, as radd noted, there are complex surrounding factors that interplay with all of it. But dissecting that - and even Radd (seems to be) talking about inflammation. But for a casual layman thinker to separate out the role of antibodies from the inflammation … makes your head hurt !
But this whole thread has opened my eyes to the role of inflammation. Why gluten free reducing inflammation is huge. Why stress management for hypos isnt just a feel-good thing, it’s as important as our medicine.
Immune system, antibodies… think - antibodies don’t attack, they target and bind. In our situation, they mistakenly target and bind.
No, they don't mistakenly target. Not for the most part, anyway. They should be inside the thyroid but their job is to get rid of the traces of TPO and Tg in the blood, and that's what they do.
But that triggers inflammation. And inflammation is the killer too. But ab’s and inflammation are all part of the immune system.
What triggers inflammation? You're not being clear, there. But inflammation also has its job. It is necessary sometimes, not always a bad thing.
The immune system recognizes the TG and TPO thyroid proteins as abnormal,
In the blood it does. Not so sure about within the thyroid. Come to think of it, I'm not sure at all why the immune system suddenly sees the thyroid as the enemy. But, I doubt it's due to the presence of Tg and TPO. It's just that once it leaks into the blood, and the antibodies are released, the system becomes sensitised to the Tg and TPO (I think) and the antibodies go 'oh, look, there's some more in there!' Although, actually, I've read that it's only the TPOab that do that, not the TgAB. So, I don't really know.
So, the place people get confused I think is not understanding what part in the chain they are trying to “treat”. Trying to address antibodies is not a root cause of the disease AND not a root cause of symptoms.
True. But, so many so-called 'authorities' tell us that it is the TPOab and TgAB that attack the thyroid. I even read that on the TUK site!!!
And, as things stand today - knowledge, science, research, basic understanding - there is nothing to 'treat' except the lack of thyroid hormones.
greygoose Is it possible because antibodies to TGA/TPO are generated to remove TGA/TPO from blood, once the antibodies are made, they can no longer distinguish between the TGA/TPO in the thyroid, hence they in error attack via auto immune antibodies (those antibodies that attack healthy cells) . I have so much on my brain right now due to the learning curve I just want to get the thought out.
greygoose Sorry - Let me try again. If the body produces antibodies to TPO/TGA in order to remove from "blood", it is possible the body can no longer differentiate the TPO/TGA in the thyroid, hence attack them there as well.
But TPO and Tg antibodies don't do any attacking. What they do is seek out the traces of TPO/Tg in the blood and mark them for lymphocytes to come along and bundle them up and take them away to be destroyed.
From what I've read, TPO antibodies can sometimes be found in the thyroid itself - but not the Tg antibodies - but they don't actually do any damage.
How much of this if fact and how much speculation is difficult to say because not enough research has been done on the thyroid. It isn't considered a priority.
It is widely thought that vitamin D plays an important role in the modulation of the inflammation system by regulating the production of inflammatory cytokines and immune cells, which are crucial for the pathogenesis of many immune-related diseases.
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