It's often said that autoimmune thyroiditis (eg Hashimoto's) is caused by TPO antibodies which inhibit one of the enzymes in the thyroid that is on the pathway to making T4. On the other hand in Graves disease (hyperthyroidism) a different antibody is proposed that sits on the TSH-stimulatory axis to force the thyroid to make too much of both T4 and T3. The separation of the two opposing effects may have led people to assume it's one or the other in any one state of disease. This isn't so. In Hashimoto's it's known that both TPO and TSI antibodies co-exist in some cases. This leads to quite wild fluctuations into the hypo or the hyper state as one antibody level temporarily and at random exceeds the other. It's said this is unusual, but doesn't say it's rare, if that were indeed the case. But of course both antibodies are attacking the thyroid, ultimately leading to its complete loss. I don't think enough research has been done into this to harden the statistics of the likelihood of contracting the antibodies. Even TPO antibodies are not often done as a check in potential or real Hashimoto's, and TSI tests, being more difficult and expensive than TPO are probably done very rarely in the Hashimoto state. This could well account for the large fluctuations felt by some Hashimoto patients.
Some useful information: It's often said that... - Thyroid UK
Some useful information
That would explain some of the fluctuations in symptoms. Although there is crossover of those in both hyper and hypo which is what makes it so difficult to treat with the correct dosage of T4/T3
Are TSI antibodies the same as "TSH Receptor Antibodies"?
I have high TG Ab, TPO Ab and TSH Receptor Antibodies. Endo says I have Graves' and is treating with carbimazole (to be fair for the last 18 months, since diagnosis and starting carbi my TSH has been very low and my FT3 and FT4 varying degrees of high, apart from one episode after higher dose of carbi when FT4 and FT3 dropped below range and TSH went very, very high).
I'm seriously wondering about diagnosis now.
Any comments, guidance welcome. TIA.
"But of course both antibodies are attacking the thyroid, ultimately leading to its complete loss."
Just to clear something up, especially as greygoose is hot on this. I thought that antibodies don't usually directly attack cells, but recognise and tag antigens to signal immune cells to attack.
I did save a good article on the immune system for study, but concentration and memory limits have made it difficult to fully grasp.
Yes, that is fair comment. The end result is the same however.
Thank you
Except that people sometimes go to extreme lengths to try and reduce their antibodies, believing that they will also reduce - or even cure - their Hashi's. And, I think it's unfair to encourage them in that belief.
That's a thought! Lowering antibodies (even if that is possible) might slow down deterioration but in no way is it a cure.
If the antibodies don't do the attacking, it won't even slow down deterioration, will it?
They do stimulate other cells to attack, so there is a connection,
but an indirect one.
Where did you read that? And, if that is true, how come 20% or Hashi's people never have elevated antibodies, but their thyroids are still destroyed?
To be honest I hadn't considered that very much. I'm sure someone on here said that it's because antibodies don't happen to be high when the test is done, not that they don't exist.
So assume they must be produced in spurts, at unpredictable intervals.
But high antibodies (even if not always present on testing) must have some function in destroying the thyroid, even if they don't attack it themselves. And therefore it makes sense that if they can be kept low it may slow the deterioration.
Doesn't it?
Of course, it is impossible to "Cure" Hashis by keeping antibodies low. And when the thyroid is destroyed they will become low anyway because there's no more thyroid tissue to trigger production.
Not being difficult, just trying to make sense of things 
What diogenes said when I asked him the question some time ago was that the appearance of TPO and Tg antibodies was triggered by TPO and Tg leaking into the blood when thyroid cells were damaged by an attack on the thyroid by lymphocytes released by the immune system. That's why they fluctuate, and are highest just after an attack. They clean up the traces of TPO and Tg in the blood, then die down again.
But without lymphocytes being "Told" by antibody tagging that the TPO and Tg were "Enemies", they would surely have no reason to attack?
I'm really confused now!
That cannot be because the attack is already in full swing/over by the time the TPO/Tg antibodies arrive. If the attack hadn't already begun, the TPO and Tg wouldn't have got into the blood, because they are enclosed within the thyroid.
First, our human antibodies see TPO or TSH-receptors etc as foreign substances and therefore bind to them. Then phagocytic cells (eaters of foreign substances) take in the antibody-antigen complexes and destroy them. So the binding of the antibodies to the particular substance sends a signal to the phagocytic cells to come to and eat up the whole complex.
Thank You Diogenes . At last someone understands what Hashimoto thyroiditis is all about . I was experiencing exactly the symptoms that you so very eloquently describe. Yet so many Dr's fail to recognise/diagnose and properly treat patients.
Thank you for bringing to the for front .
Thankyou for the useful information, i'll mention it next time it's inferred that i've increased my LT4, when i've been asked to reduce it.
I've been concerned about you on lock-down inside your barrel , hope its big enough
I have the top on and get things through the open bunghole
I’m speaking to an Endo this week. Not through choice having survived and managed on my own for 10 years on T3 only with adrenal and vitamin supplements.
I was telling GPs for years that I was fluctuating intermittently and erratically, highs and lows could come and go and last for half an hour or days or weeks. Was always told thyroid can’t do that. Always assumed that the unidentified (on record) antibodies from 1982 were Hashi, and even seeing Endo back then, couldn’t make mind up, 'was something wasn’t’ from one appointment to the next -surely should have identified ‘something. Hence when finally got a diagnosis ten years later it was ‘Acquired Hypo’. In other words a guess!
More Hyper and Graves in family. More Graves genetics than Hypo too.
Any antibody testing I have had done throughout the years has always come back negative. Of course what antibodies were tested is not recorded. Would Graves antibodies still show now, 40 years on?
If I have to speak to an Endo I want to get to the bottom of it once and for all. No more fobbing off and I am not going back on T4 for anyone. Certainly not without checking everything else out first - adrenals and pituitary and anything else that might be at play. (AI - Lupus/Sjogrens investigation halted before it started, due to Covid.)
"I was fluctuating intermittently and erratically, highs and lows could come and go and last for half an hour or days or weeks. Was always told thyroid can’t do that."
They forgot to tell the thyroid that it can't!
Could help explain the way my symptoms change too
Glad to know it was not all in my head!
There's more graves in my genetics too, probably including my granny who went a bit bats after 2nd pregnancy in 1935 , so they had her committed and gave her electric shock treatment! turned out ok in the end tho. she did a history degree at oxford in her 50's so that showed em.
Then her daughter got it after being pregnant in 1953 , so they chopped a bit off her thyroid and gave her piggy replacement. She had a fine life.
So treatment was improving,....... Then somebody realised you can't 'patent' a pig.......... and its been downhill ever since.
Then mine broke after my second pregnancy............ My daughter has decided if she wants a kid she'll adopt one !
I've always thought it was a bit odd that mine went the other way, and i've always wondered if our problems are different ends of the same ruler , rather than different diseases.
Yes I tend to agree a spectrum. And about the piggy patent.
I lost weight when carrying my first child. (was just over 10st went to 9.5 st.) Went back to normal weight when I stopped feeding him myself. At this point the goitres had been going about 10 years and conjunctivitis/ulcer in left eye had started around the same time. About a year after 1st birth, was eventually diagnosed as hypo and given t4. By the time I was 3 months pregnant with 2nd child, 2 years later, I’d ballooned. Put 4 st on. Have struggled ever since. Lost 1 stin 4 wks when first on T3, combi, then plateaued, but stress and adrenal issues, - maybe caused partially by failing T4, and maybe swine flu, knocked me sideways. About 3 years after starting on t3 only (with supplements) I felt better than I ever had, Never lost any more weight up to that point. Then feeling ‘good' I joined a slimming club and in 11 months lost 4 stone, without hardly trying. Then family stress kicked in and -all went to pot. 4 -5 Whilst meds more balanced adrenals are definitely at play. So still struggling.
The problems are in the training. There is no real training. It is too simplified, too misunderstood, test TSH give T4 is the extent of most knowledge, and most do not even know what T3 is. Even in secondary in too many cases.
My mother died in 2016 TC, I reckon Mam was hypEr most of the time, she was 7 st when she married at 30 yrs of age. Yet there was a part of her life when she ballooned to a size 18. She ate like a bird. Feeding 7 of us! She had little food with a lot of salt.!!
I have two older sisters one had nodules other partial thyroidectomy Aunt, now 97 still lives independently, diagnosed hypEr in 2010. Another 92 year old uncle who I swear is hypEr too. As are many cousins. Though I can also see Hypo there too.
My maternal GM died when I was about 2 so never knew her. But she went a bit odd, I suspect she could have been hypo from the pictures I saw. I think she was committed at some point, and she died aged about 62. Quite young. Genetics!
I suspect there might be more than a few on here, who's grandmothers went a bit odd.
But the stigma of an asylum in the 30's still hangs on a bit. Apparently they were not easy to get out of once you were in...catch 22 , you cant go home unless you agree you're mad.........
Shame you don't remember your's, mine was brilliantly naughty. I remember sitting in her bay window when i was a tot , looking down the lane at the church where she played the organ. She had a fur coat on and was laughing with my Aunty , that nobody in the respectable village had any idea that their old headmistress had been in the 'Hospital' .
My dad had to take her speedy Ford Anglia off her, and get her a little old Austin Seven instead, because of something to do with the Village Green !
She didn't take any s**t, so if you like , i'll send her along in spirit to cheer you on at your Endo Appointment ......... i'm sure she'd love to get her teeth into some Doctors.
Tat x
LOL your gran sounds like a real card! Lovely memories! I shall look forward to her spirit joining me on Tue when I have my telephone Endo appointment. Cheers.
Her names WOOF xx (from pretending to be a dog to entertain my brother )
LOL I’ll bear that in mind!
Yet there was a part of her life when she ballooned to a size 18. She ate like a bird. Feeding 7 of us! She had little food with a lot of salt!!"
I've read that adrenal problems can cause a craving for salt
Yes. I think adrenal issues deep seated. I certainly struggle as does one of my son’s - both diagnosed by Dr P but not mainstream NHS. But a bit chicken and egg - what was there 1st. I like my salt - but nothing like the amount Mam used to eat.
I was very confused about antibodies but have found Dr Tania Smith’s article makes helpful. It sounds like I had atropic autoimmune thyroiditis which seems to be neither quite Graves nor Hashimotos. Dr Tania Smith did a post about Tsab antibodies which I found very interesting. Do you have any comments about it? I think there are two parts to it.
I linked to it here.
Dr Tania Smith is very good at explaining things.
I spotted this a bit late. We should keep in mind that TSH seems to have two purposes, to stimulate the thyroid and to stimulate deiodinase. We can expect TSI antibodies to have a similar effect which might explain why post thyroidectomy Graves' patients often do well on levothyroxine monotherapy - for a few years.
The opposite may happen wiht TSH blocking antibodies TBI. TBI may block deiodinase which may be compensated by an elevated TSH due to TBI blocking feedback to the pituitary. If however the patient is given thyroid hormone TSH will normalise, the blocking effect on secretion compensated by the exogenous hormone but the now normal TSH will not compensate for TBI effects on deiodinase.
We need to redraw all those diagrams of the hypothalamic pituitary thyroid axis to include TSH action on deiodinase, at the moment they give the false impresssion that TSH has a singe action.
We should keep in mind that TSH seems to have two purposes, to stimulate the thyroid and to stimulate deiodinase.
We also need to bear in mind the various isoforms of TSH. As discussed in this and some other papers:
ncbi.nlm.nih.gov/pmc/articl...
An issue which is marked by being almost 100% ignored by "medicine" and practitioners.
Yes, when reporting TSH results the doctor should say 'your TSH are' not 'your TSH is'. TSH is a group of isoforms. More important TSH bioactivity can vary by up to 4x in potency, less potent isoforms are present during illness, depression etc. Often an inappropriately low TSH is lower that it seems due to reduced activity.
The TSH immunoassay measures presence not activity. As Dr Skinner used to say 'a graveyard and a discotheque have similar levels of presence but different levels of activity'.
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