I have had 3 miscarriages in the last couple of years. 1 spontaneous 2 mmc. Always around 6 to 7 weeks. I was given aspirin and progesterone on the last pregnancy but it didn't work. After my 3rd mc I had lots of investigations done and it showed I had high TPO antibodies. Everything else was normal. My TSH or TFTS are all normal so im not on any medication but to help lower the antibodies Im on a gluten free diet. We have been told we can try again but I am terrified of having another loss. It really takes me months to get back to normal. I suffered so much insomnia, stress and ill health after each one. Im also now 40 and although we are trying to conceive, nothing has happened in the last few cycles. Previously all my babies were conceived within 3 cycles. The doctor suggests i try a higher dose of aspirin if i get pregnant and clexane injections(heparin) and progesterone again if i conceive. And im on 5mg of folic acid now.
My question is has anyone been through this and gone on to have a healthy child with tpo antibodies/hashimoto's? If so was the child normal and how are you now?
I think it was pregnancy that triggered my hashimoto's or antibodies and a virus but im not sure. Im so terrified im setting myself up for more pain. Would love to hear your stories if you have a similar history. Thank you, Sue
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I'm afraid I don't have any stories for you, success or otherwise, but I would like to ask a question: When you say My TSH or TFTS are all normal, what exactly does that mean? And who told you they are 'normal'? Because if it was a doctor, they could be wrong. When a doctor says 'normal' all he means is that the results fall somewhere within the ranges. But that doesn't make them 'normal' nor optimal. So, maybe if you gave us the actual numbers - results and ranges - we might see something your doctor can't.
Lowering the antibodies probably won't help, because the antibodies aren't the problem. They are just an indication that you have Autoimmune Thyroiditis - aka Hashi's. They don't do any harm, but the Hashi's itself can cause thyroid hormone and TSH levels to fluctuate, so you cannot rule out hypothyroidism - often the cause of miscarriages - on the basis of one isolated blood test. They need to be done frequently, I'm afraid, to see if they are fluctuating and by how much.
hello fellow stevienicksfangirl, whilst I can’t share the kind of story I understand you wanting to hear, I am sorry to read of your miscarriages and your inevitable associated distress.
High TPO antibodies are said to be correlated to negative pregnancy outcomes even in the presence of normal thyroid function. Perhaps there is an association that is yet to be explained/understood. Yet most of us on this forum have grown wary of the term ‘normal’ when it comes to doctors’ understanding of thyroid function. It’s always worth having a full thyroid blood panel (usually only available privately) - and posting the results here for advice.
I suffered increasingly problematic symptoms of low thyroid function for thirteen years after the birth of my daughter before finally being diagnosed with autoimmune thyroid disease. During those years I miscarried all my subsequent pregnancies with no investigations. On diagnosis my TPO antibodies were >3000.
I like to think had I known then what I know now, thanks to this forum, things could have been different. And I hope they still can be for you.
I don’t I’m afraid - but have come across the claim often (it has obviously resonated each time). A cursory google search will no doubt yield such results
Problem is, TPO/Tg antibodies are vilified all the time, with no actual scientific proof. They are said to do all sorts of things that they don't actually do. So, when I hear that they cause miscarriages - as I have heard - I take it with a pinch of salt!
Myself, I have Hashi's, and I have three children. I have no idea when the Hashi's started because I was never tested. Could have been after my first pregnancy, I just don't know, but I went on to have two more so, either it started with the third one, or the antibodies didn't make any difference to my conceiving.
I have reason to believe the Hashi's started with the first one, because I lost soooo much weight. But who really knows. I don't.
If as much money as has been put towards research into erectile dysfunction were to be put into research into thyroid disease, I suspect we’d all be a lot clearer 🤗
Interesting to hear you lost so much weight. Before my first pregnancy I was super skinny & couldn’t gain weight for love nor money. I came out the other side of that pregnancy a uk dress size 20 🥴
Well, that's why I said I think the Hashi's started with the first pregnancy, because it starts with a 'hyper' phase, and I have always lost a lot of weight with the 'hyper' phases.
I was always a bit chubby before the first pregnancy and put on 2 stone during it! Got continually told off about it as if is were my fault! But I wasn't eating for two, or anything like that, and couldn't keep much down anyway. But, they tried to scare me by telling me I'd never be able to lose the baby-weight. Well, I did! And then some! So ya-boo-sucks to them!
If you explore there are many research papers showing elevated TPOAb to risk adverse pregnancy outcomes. I’m in hairdressers atm and so on my phone but here’s one link I found first try … ncbi.nlm.nih.gov/pmc/articl....
I have previously written about the risks of elevated TPOAb complete with references, not just in pregnancy but other conditions such as breast cancer as risks causing dangerous chronic inflammation. In pregnancy TPOAb crosses the placenta and babies are born with elevated levels ☹️
TGAb on the other hand is isolated to the thyroid gland.
Yes, I think it’s because the ‘why’ is so poorly understood, and as Hashi doesn’t warrant immunosuppressive drug treatment, it is none profit making for Big Pharma and simply ignored.
But it is criminal and cruel to allow women to unknowingly risk their pregnancies (even if at this time the risk hasn't been wholly proven but just indicated), just as it is criminal and cruel to tell Hashi sufferers there is no treatment but to wait until the thyroid gland is destroyed enough for thyroid hormone replacement meds, when clear studies have shown both selenium and Vitamin D to reduce TPOAb levels and patients conditions to improve. Layering on to this treatment would be the gluten/dairy free suggestion, good regulation of sex hormones (oestrogen is heavily implicated with immune system regulation) and a healthy life style.
The breast cancer is interesting. We know that thyroid hormones can activate oestrogen receptors and breast cells possess thyroid hormone receptors which has given thought that elevated thyroid hormones can activate breast cancer. Although TPOAb have not yet been proven to engage in interaction with cancerous breast tissue, they have been proven to be inductors of oxidative stress which is a large contributory factor towards cancers.
Therefore, on one hand you have studies showing elevated TPOAb to be a contributory factor by means of chronic inflammation (oxidative radicals and apoptosis), and also possibly cross-reactivity with lactoperoxidase and myeloperoxidase (these are more peroxide enzymes), whilst on the other hand there are studies showing TPOAb to be beneficial in manifest breast cancer.
However, the research is sketchy as all appear to include many different groups with different outcomes and clearly more is required but my own experience has been to benefit from reduced TPOAb and my son having reduced his has delayed/eliminated? the need for thyroid hormone replacement meds.
Hey radd Was also thinking upon my cursory review of info - is it accurate to say that most adverse effects of thyroid abs is largely in context of pre-conception and pregnancy viability; where as adverse effects of actual thyroid hormone levels (T4/T3) is largely in context of fetal outcomes.
Just noticing that the OP asked about fetal outcomes, and without going back to what I read to validate - I think my takeaway was that high T abs are not typically discussed in relation to fetal outcomes (once conception and pregnancy carries to term.)
What I’ve gleaned is both inadequate thyroid hormones and elevated TPOAb may enhance the risk of infertility and adverse pregnancy outcomes including miscarriage, preterm birth, placental abruption, premature rupture of membranes and fetal neurodevelopmental delay.
The difference is adequate thyroid hormones are an essential biological requirement for a healthy pregnancy, whereas elevated TPOAb are only an indication of raised risk of negative outcome. The main concern seems to be that raised TPOAb may affect placental morphology and function.
However, raised TPOAb can also influence in a other ways - Decreasing the thyroid glands ability to adapt to essential pregnancy hormone level changes, or developing Hashi attacks creating unstable thyroid hormones levels. TPOAb also attacks thyroid gland cells to a small extent through cytotoxic mechanisms (unlike TGAb), increasing probability and extend of autoimmune attacks.
Chronic inflammation is known to breed further inflammation. As I understand it the effect of TPOAb inflammation directly on thyroid hormones is relatively minor but the accompanying induced raised levels of inflammatory cytokines such as TNF, certain interleukins, etc are not and can influence by suppressing the HPT axis and impairing conversion so lowering ‘active’ thyroid hormones to possibly below a threshold required to prevent fetal loss or psychomotor/IQ deficits. (For example studies show a direct inverse correlation between raised CRP and reduced tissue T3 levels).
As said above, babies may be born with elevated TPOAb from mothers with elevated levels but also other accompanying damaging inflammatory cytokines such as TNF, IL-6, IL-8, CRP, and many others I am not familiar with. Raised TPOAb and these inflammatory cytokines have also been found in amniotic fluid, and placenta with a decreased length, width, volume, etc. Imagine your new born baby being born with raised CRP!
Any autoantibodies are generated as a result of disrupted central and peripheral tolerance systems which results in autoantibody-generating B lymphocytes (& T cells) that in the case of Hashi infiltrate the autoantibody-releasing plasma thyroid cells to cause thyroid fibrosis. B lymphocytes producing high-affinity autoantibodies to self-antigen are either eliminated or functionally inactivated but B lymphocytes producing low-affinity autoantibodies escape the selection process and continue the maturation process meaning the process is self driven unless TPOAb are reduced through whatever means of reducing chronic inflammation.
As greygoose says - it’s critically important to know your Free Ts - not just that someone said they are “normal.”
A fetus gets all thyroid hormones from the mother through mid-gestation. More important, sufficient thyroid hormones are required for fetal brain development that occurs at 5-6 weeks, which is well before anyone knows they are pregnant.
So it’s critical for you to know and maintain your free Ts while TTC and well before you conceive.
Welcome to our forum and sorry to hear about your miscarriages.
Ovarian problems are common in hypothyroidism induced by high prolactin, low FSH & LH levels which lead to ovulation issues and abnormal luteal phase progesterone levels. Also a decreases in hormones lead to a decrease in receptor sensitivity. Conception and pregnancy retention is dependant upon adequate thyroid hormone levels.
"My TSH or TFTS are all normal' There is normal and there is 'normal'. If you supply your TFT results, members will comment.
Studies on the effect of elevated thyroid antibodies in pregnancy all appear to be fairly old, probably because not a lot outside of functional medicine has evolved in the management of autoimmune disease. Thyroid hormone levels will influence pregnancy hormones and vice versa but the response can be altered in women with elevated TPOAb.
If you read books such as "Your Healthy Pregnancy With Thyroid Disease" by Dana Trentini and Mary Shomon, and view websites such as ‘hypothyroidmom's' the general consensus appears to be to keep antibodies as low as possible through means such as eliminating cross-reactive foods, avoiding sugar spikes, supplementing selenium, fish oils, Vit D, etc. This helps calm an over active immune response and reduces the risk of further self-attacks on thyroid peroxidase which is an enzyme found in the thyroid gland (TPO), & a key protein called thyroglobulin (TG). It is these self-attacks that will keep thyroid antibodies TPOAb & TGAb raised.
Many immune changes take place in the body to accommodate acceptance of the foetus. The immune system having many parts & subdivisions is immensely complicated and way beyond my comprehension but I read the two most relevant in Hashi sufferers are T-Helpers;
- (TH-1) Non -specific immunity macrophages & Killer T cells is our immediate attack response to kill pathogens, subdivided into messenger proteins each having their own job, such as the Interleukin groups.
- (TH-2) Specific Immunity - slowly produces antibodies & identifies invaders so killer cells can attach to prevent them from entering our cells, also broken down into interleukins.
We are usually slightly dominant in one or the other although a balance is required for good immunity. Over activity of TH-1 will suppress activity of TH-2 & vice versa. This can be problematic in autoimmune disease as can further self-attacks on healthy tissue, worsening the condition. Pregnancy can shift the immune system temporarily to TH-2, which is why a lot of women find out they have Hashimoto’s after they give birth and their immune system then returns to TH-1 dominance.
Thyroid antibodies aren’t unusual and many people live healthily with raised levels but in those whose antibodies have caused autoimmune conditions it is thought that raised levels can either risk further disruption of thyroid hormone levels through various methods and encourage other autoimmune conditions to develop.
TSH must be kept low to discourage high prolactin and will also lessen the chance thyroid gland attacks. You might even need thyroid meds before/after? conception to ensure good development of baby. If Hashi is allowed to progress, attacks may cause variations in thyroid hormone levels that can disrupt the pregnancy.
There is also research into thyroid antibodies crossing the placenta and the origin of the TPOAb in those babies born is thought to be from the mother. Don’t expect your consultant or even a fertility clinic to realise the extent of Hashimotos.
I have already supplied two research papers below to FIR. Here are further (although I haven't read these throughly) that give further samples of what is available if you research. .
TPO antibody positivity and adverse pregnancy outcomes
As you have high thyroid antibodies you need coeliac blood test BEFORE considering starting on strictly gluten free diet
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 as per NICE Guidelines
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
Hi, I'm so sorry for your losses. I lost a baby late in pregnancy (details on my profile) and that is how I was diagnosed with Hashimoto's. I had an appointment with Dr Heazell from the Tommy's baby loss clinic (you meet the criteria for referral, which is 3 miscarriages or a late term loss). In my case, my body attacked the placenta and there was a lot of inflammation present. Dr Heazell explained that TPO antibodies cross the placenta. But for some women, the autoimmune issues happen earlier i.e. preventing conception/implantation/earlier miscarriage.
For any future pregnancy (I am TTC now), I will have to suppress my immune system with prednisolone from about 6 or 7 and then be weaned off later. Prednisolone seems to be a key part of any immune system protocol - has this ever been suggested to you? Or not because all the other tests seemed normal?
There is a good Facebook group Reproductive Immunology Support and they great advice about testing/protocols etc.
Another point is that I did a gut healing protocol/ elimination diet/food intolerance testing. So I avoid eggs and Soy as well as dairy and gluten. Also, I am now on LDN and I feel less inflammation since being on it.
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