Thyroid Truths – seeking the facts 

Our November 2024 ‘Meet the Experts’ webinar was dedicated to navigating the evidence around thyroid health. Our speaker was retired consultant endocrinologist and BTF patron, Dr Petros Perros. BTF trustee, Anna Reavell, chaired the session.

Dr Perros feels strongly about the often confusing and contradictory information that circulates online about thyroid conditions. He recently published a book ‘Seeking Thyroid Truths – A Guide For The Curious.’ This book aims to help people decide what is trustworthy when faced with persuasive ‘evidence’ that is not always based on scientific fact.

In our webinar, Dr Perros addressed some patients’ questions about their thyroid health. This is a summary of his answers.

Do high antibody levels result in worse symptoms with regard to Thyroid Stimulating Hormone Receptor antibodies (TRAb) and Thyroid Peroxidase antibodies (TPOAb)? 

TRAb antibodies are what people with Graves’ disease, the commonest form of thyroid overactivity, have circulating in the bloodstream. They are what drive the thyroid to become overactive. Actually, there is no information about whether these antibodies correlate with any symptoms independently of thyroid hormone levels. There are two exceptions to this: 

TRAbs are associated with, and probably cause, enlargement of the thyroid gland (goitre) and thyroid eye disease. This is independent of thyroid hormone levels.

TPOAb are antibodies that circulate particularly in patients with Hashimoto’s disease (autoimmune hypothyroidism). About 90% of people with Hashimoto’s disease are positive for these antibodies. 

TPOAb are indicative of underlying inflammation and there is an association between having these antibodies and symptoms. It is not clear whether this relationship is cause and effect.

Several years ago when new drugs were introduced for rheumatoid arthritis that reduced inflammation, it was noted that some patients noticed that their tiredness lifted and the brain fog got better. This was long before these drugs had any effect on joint pain and stiffness. 

There is some evidence that has accumulated over the years that inflammation, rather than antibodies, may be important in causing some symptoms in autoimmune diseases. This has led to the theory of what we call neuroinflammation. So if you have inflammation anywhere in your body, be it from an infection or autoimmune disease, inflammation due to autoimmunity may drive some persistent symptoms despite having normal blood tests.

Should I be trying to reduce my levels? If so, how?

TRAb levels are usually reduced by treatments that are used in Graves’ disease (antithyroid drugs and total thyroidectomy. Radioiodine is associated with an initial increase in TRAb, followed by a slow decline. There some evidence that if you combine antithyroid drugs with selenium this can happen quicker than otherwise. 

With regards to TPO antibodies there is evidence that the levels decline with time anyway, and can be further reduced by selenium supplements and total thyroidectomy.

A recent large study in Denmark in patients with Hashimoto’s thyroiditis treated with selenium supplements or placebo showed that TPOAb fell to a greater extent than placebo, but it made no difference to quality of life or symptoms.

Another study published in 2019, also from Scandinavia, looked at the effects of thyroidectomy (complete removal of the thyroid gland) in people with Hashimoto’s. This showed that TPO antibodies reduced markedly when the thyroid is removed and this was associated with improved symptoms. However, this was not a placebo controlled study and it is uncertain whether the operation itself was the reason why patients felt better. Given that having a thyroid operation carries some risks  (infection, bleeding, voice change, low calcium levels), most experts would not recommend this approach until the evidence is clearer. 

Should treatment for autoimmune thyroid disease be more focused on treating the cause of the autoimmune condition? For example, like treating the leaky gut, removing sugar, gluten and dairy from the diet etc?

About a year ago Professor Marian Ludgate spoke at a BTF webinar on this.  Marian is a leading expert in the microbiome and thyroid autoimmunity (‘microbiome’ refers to all the bugs that we carry in our gut and in other places), and there is good evidence now that it is an important regulator of the immune system and probably of the autoimmune response. Marian’s work has provided evidence in mice, and some in humans, that altering the gut microbiome can have an impact on thyroid antibodies and the evolution of thyroid autoimmune diseases. It is early days yet, but we will hear a lot more about this area of research in future.

With regards to other dietary interventions, I would strongly recommend the review ‘Thyroid, diet and alternative approaches’ by Larsen D et al https://pubmed.ncbi.nlm.nih.gov/35952387/. This article reviewed the effects of diet and supplements. In summary, iodine deficiency and iodine excess can have a detrimental effect on the thyroid. Selenium deficiency can also have negative effects on the function of the thyroid, but it has to be severe to do so. Coeliac disease and lactose intolerance, when diagnosed by a doctor and supported by results of appropriate tests, are relevant as absorption of thyroid hormones is affected. 

With regards to other minerals and supplements, including zinc, magnesium, vitamin B12 etc, the evidence is either against or is not convincing, unless there is objective evidence of deficiency.

As iodine is needed to make thyroid hormones people with hyperthyroidism often suggest in forums that reducing, or removing, dairy, seafood and fish from the diet is helpful. What you are saying is to just eat a normal diet and you don’t necessarily need to remove dairy for hyperthyroidism?

In the UK there is no significant iodine deficiency so keeping to a balanced diet is enough for most people. There may be some exceptions. For example, pregnant women may actually require some iodine supplements especially in the early stages of pregnancy. The evidence for exclusion diets, when not supported by an underlying clinical diagnosis of coeliac disease or lactose intolerance or seafood allergy, is very weak.

What do positive thyroid peroxidase antibodies actually mean?

TPOAb are probably merely markers of autoimmunity. One can think of them as a security alarm system that when it goes off it tells us that something is amiss, but it does not tell you whether anything is missing, or has been stolen. The main utility of the TPO antibody test is that if somebody has been found to be hypothyroid and they have positive TPO antibodies then you have an accurate diagnosis of Hashimoto’s disease. 

If TPO antibodies are positive with a borderline TSH, does this mean that I am hypothyroid?

A slightly raised TSH with normal T4 levels is called ‘subclinical hypothyroidism’. If TPOAb are positive, it is probably caused by thyroid autoimmunity. This means that people who fall in this category have approximately a 50% chance of developing ‘overt’ hypothyroidism (hypothyroidism associated with symptoms) over the next 10 years.
Having just one single slightly raised TSH may not mean very much. This is because in about 50% of people, if the blood test is repeated a few months later, it will be normal. 

If both TRAb and TPO antibodies are positive does this mean I have Graves’ and Hashimoto’s? Will I switch between the two and eventually become hypothyroid?

Up to 80% of people who have typical Graves’ disease will have positive TPO antibodies too. Conversely, 10% of people with Hashimoto’s disease, also have positive TRAb (we think these are what we call TSH receptor ‘blocking’ antibodies that inhibit the receptor rather than stimulate it).

There is a condition that we call ‘Hashitoxicosis’, which is actually quite rare. In this condition, patients oscillate spontaneously between hyper- and hypothyroidism without any intervention. It seems that this happens because they have TSH receptor antibodies that are both stimulatory and blocking. It depends on which predominates at any one time which way the thyroid goes.

What happens long term is interesting. If we follow people with Graves’ disease and don’t destroy their thyroid in the process by radioactive iodine or thyroidectomy, then after about 20 years 10 to 20% will become spontaneously hypothyroid and at that point most are indistinguishable from patients with Hashimoto’s disease. We think of Graves’ disease and Hashimoto’s disease as being two distinct entities or diagnoses but there is overlap and sometimes one can morph into the other. 

I’m sure that my Covid booster triggered Graves’ disease. What evidence is there for this?

When Covid appeared and then vaccines appeared, there were lots of case reports of people developing Graves’ disease, thyroid eye disease or other autoimmune diseases after Covid, or after the vaccine. 

One study from Spain showed that the incidence of Graves’ disease doubled after Covid. The best data that we have has been published recently and showed that the incidence of Graves’ disease was no different in those who had received vaccines compared to those who did not. I think this is reassuring, though not conclusive.

Thyroid eye disease is a devastating condition. What are the new treatments being developed in this area? What difference are they likely to make and how quickly will they be available in the UK?

In 2021, there was a big advance with the arrival of a drug called Teprotumumab (Tepezza). This drug works very differently from anything that we have for thyroid eye disease. It blocks the ‘Insulin-like Growth Factor-1 Receptor’ (IGFR) which is very abundant in the tissues behind the eye. For the first time, we have a medical treatment that actually reduced the protrusion of the eyes to roughly the same extent as a surgical decompression. 

It is not yet licensed in Europe but was a huge financial success in the US. The drug is not cheap. At the moment, it costs a third of a million dollars per patient in the US. However, a significant proportion of people treated have relapses. And some of the side effects, like hearing problems, are a concern.

In the past few years, vast amounts of money have been invested by the pharmaceutical industry into developing new drugs that may work for thyroid eye disease. Some of these  in development are:
•    ICFR1R antagonists – e.g. CRDN-001, VB421 and Linsitinib. They are similar to Teprotumumab and may be more effective and have fewer side effects.  

•    Anti-FCRn

•    Anti-IL17A and Anti-VGF which affect the immune system.

In addition there is a number of other drugs that have been around for a while, are far cheaper than teprotumumab and are being tested in thyroid eye disease`; Tamsulosin, Sirolimus, Hydroxychloroquine, Atorvastatin and Rapamycin.

Betoclimab and Anti-FCRn is a promising drug and this is how it works: in Graves’ disease TSH receptor antibodies circulate in high concentration and hang around for a long time because they get recycled. At any one time, a small amount is degraded. This drug interferes with the recycling process so it shunts more of the TSH receptor antibodies towards degradation. As a result, the levels go down and the patient is no longer hyperthyroid and it also helps the eyes. 

I expect within the next five years we will have one, or maybe more, new treatments that will be really effective both for Graves’ disease and thyroid eye disease at the same time. 

Why won’t doctors test free T4 and free T3. TSH alone doesn’t give the full picture. I’ve done a private blood test and my free T3 is at the bottom of the reference range and my free T4 is at the top of the range. My TSH is 1. Surely this means I am not converting T4 to T3 adequately?

About 15% of people on levothyroxine who have a normal TSH have a low or low/normal  FT3 and often FT4 at the upper end of the range. This has led to the suggestion that they do not convert T4 to T3 and that they may benefit from T3 treatment.
To get the full picture it is important that the doctor takes a detailed history from the patient, performed a thorough examination and then decide if any tests are necessary. 

It is well documented that in 80% of cases a diagnosis can be made from the history. 

So why do we test TSH alone?

If you test many people with untreated hyper-and hypothyroidism and people without thyroid conditions, for TSH and free T4 and plot them on a graph, what you find is there an inverse relationship. A 10% increase in free T4 gives rise to a 50% reduction in serum TSH. So the free T4 signal is amplified as reflected by the TSH. 

Commercial assays that we have available for TSH, actually perform extremely well. In 90% of cases they will correctly identify people with an over- or underactive thyroid and in 92% of cases they will correctly identify people without thyroid disturbance. 

They will miss some very rare cases:

Central hypothyroidism (1 in 20,000 to 1 in 80,000)

Thyroid hormone resistance (1 in 20:2000)

Some TSH-producing adenomas (1 in 1,000,000)

The history and examination will pick up something that raises suspicions that there is something wrong with cases and that the normal serum TSH level may be misleading.

Some labs do test free T3 and T4 automatically with TSH and all labs should offer this if the doctor requests it and can justify it. The interpretation is not a simple matter and requires training and experience needing to know which assay platform is used, what the performance characteristics of the assay are and how the reference is derived etc. 

So if you as a consumer are ordering a blood test, and you are paying for it (which I don’t personally recommend), you should be asking these questions to the provider. There are many factors that feed into interpreting blood tests; the effects of illness, drugs, age, body mass index, pregnancy, race, fasting, time of day. All these can impact on the actual results.

There are two main interpretations of results showing low normal T3, high normal T4 and normal TSH. One is that three different measurements are all within the normal reference range so you have ruled out hypo- or hyperthyroidism. The other interpretation is that maybe there is impairment of T4 to T3 conversion. 

The real important question here is ‘How do hormone levels correlate with symptoms?’ and there is data on this: If you take patients with moderate to severe hypothyroidism, by that I mean a serum TSH of an average of 52 and a low T3, 90% of these patients will have symptoms of hypothyroidism,

In moderate hypothyroidism, with a TSH at 46 on average and with a normal T3, only 40% will have symptoms. Then if you go right over to the other end of the spectrum to people with very mildly deranged TSH of less than 10, several studies have shown no correlation in symptoms or quality of life with any of these three parameters (T3, T4 and TSH). 

So this is an important message that symptoms of hypothyroidism are non-specific and correlate poorly with thyroid blood tests, unless they are grossly abnormal. One needs to exercise caution in interpreting how thyroid blood tests impact on symptoms.

I was diagnosed hypothyroid and don’t feel well on levothyroxine. Should I get tested to see whether I have a variant of the DIO2 gene? Should I do this privately?

The background to this is that T3 is the active hormone and is what the tissues see and respond to.  The enzymes deiodinase 1 (DIO1) and 2 (DIO2) convert T4 to T3. There is a common genetic variant of DIO2 (Thr92Ala) that has attracted a lot of attention.
The relevant question is whether people with hypothyroidism who have the DIO2 variant respond better to combination treatment (LT4 and LT3) than to LT4 alone? 

There are studies that have looked at this. The first one was a Dutch study from 2005 of 141 people with autoimmune hypothyroidism. It showed no correlation between having the variant and response to combination treatment. In 2008 another study was published. This was done in the UK and is the biggest (552 participants) and it did find a difference. So people who had this variant seemed to respond better to combination treatment than to levothyroxine alone. The most recent was a study from Italy published in 2024. This showed no difference.

So what do we make of these conflicting results?  A consensus statement published in 2021, which included as co-authors some of those who generated the evidence in favour of an effect of the deiodinase variant, states: ‘The impact of this variant on the clinical treatment benefits of combination therapy for hypothyroidism in humans is currently unclear.’ 

We have a few questions relating to an article with the title ‘Limiting the use and misuse of liothyronine in hypothyroidism’. The first question relating to this paper is: Why do doctors continue to discuss our symptoms and gaslight us? And in this paper there was a link between hypothyroidism and people with type D and somatic symptom disorder. So, they’re saying this is a case in point, surely we are like this because of our condition and not the other way round? 

I was a co-author of this review. Symptoms should never be dismissed. It is important that doctors pay attention to symptoms and, patients should never be gaslighted. 

The type D personality* and somatic symptom disorder** reference was in relation to some studies we have done which showed associations of these two traits with dissatisfaction, poor reported control of symptoms and poor quality of life. Association does not prove causation but this finding is important. 

*, ** (The definitions of type D personality and somatic symptom disorder are: ‘a personality trait characterised by a predisposition to pessimism, worry, stress, negative emotions and social inhibition’ and ’persistent bodily symptoms associated with significant functional impairment, psychological distress, and high health care resource use’ respectively).
If our goal is to relieve symptoms, we need to understand causes. The question is whether combination treatment is the answer for everybody with persistent symptoms and hypothyroidism. In the last 30 years, 20 randomised controlled trials looking at this have been completed and they have shown no superiority of combination treatment compared to levothyroxine alone.
There have also been a number of patient surveys on combination treatment, that show that between 20-50% of people who are on combination treatment continue to experience symptoms. 30% are dissatisfied with the treatment and 45% report poor quality of life. 
If we wish to understand the causes of persistent symptoms we need to broaden our horizons and cast a wider net. Low levels of T3 in tissues may well be important, but there are other potential causes.
•    For example, we know that at any one time about 50% of people on levothyroxine have TSH levels outside the range and often fluctuate between under- and over-treatment. 
•    People with hypothyroidism on average have other health problems. Up to 80% have some other condition, which may be contributing to people not feeling well.
•    Autoimmunity and the underlying inflammation may also be relevant.

All of the above factors are not mutually exclusive. One can have one or more of these contributing to symptoms.

The evidence about how we perceive symptoms like pain, indicate that besides the severity of the underlying tissue damage, many other factors feed into how we perceive symptoms. Amongst them are personality and somatisation. That is why we decided to look into this and found an association. In fact we also found associations between having persistent symptoms and age, sex, cultural background, socioeconomic status and misinformation.

Another point raised in the paper was ‘if symptom relief is the goal then therapeutic failure and disappointment is assured for this group of patients.’ This statement suggests that we are just supposed to put up with feeling ill and how dare we suggest that our doctors start us on treatment to see if it makes a difference. What are we supposed to do, put up and shut up?
The comment in the review has to do with something very specific: There are four different studies from the UK, USA and Denmark that show between 6 and 54% of people who have been labelled and treated as though they have hypothyroidism actually never had hypothyroidism to start off with. This is a shocking statistic but it seems to be true. 

So, if someone’s symptoms are not due to hypothyroidism is it logical to expect thyroid hormones to fix them? I think there is absolutely no justification for handing out thyroid hormones to people who are not hypothyroid. 

Another statement from the paper is ‘In our experience many patients receiving liothyronine are overtreated and might experience an enhanced sense of wellbeing as a result of overuse and misuse.’ Most of us understand the risks of being overtreated. However, if it enables me to function I would rather face this risk than face life without liothyronine and a return to my debilitating symptoms. I feel patronised and dismissed every time my doctor discusses this with me. Surely if I’m aware of the risks, it’s up to me?

This question is really about the risks of treatment of hypothyroidism. We now have not just one or two or three, but four very large population studies that are in agreement with each other. If we look at the risk of cardiovascular diseases, strokes, even death and how these risks relate to the serum TSH that is achieved with thyroid hormone treatment, it is a U-shaped curve. 
The lowest risk happens to coincide with the TSH being in the normal reference range. 

There are data that suggest that people on combination treatment tend to end up with a low TSH. So how should this information be interpreted and how should it be applied in the treatment of hypothyroidism? The consensus from experts is that a low TSH should be avoided.

With regards to the rhetorical question ‘Surely if I am aware of the risk it’s up to me?’: Firstly there is no question that patients should expect the best possible treatment. Every patient who has capacity also has the right to refuse treatment. The scenario of a patient requesting a treatment from the doctor, when the doctor believes it is not in the patient’s best interest is covered by the General Medical Council in its publication ‘Good Medical Practice. It states:

‘The law does not require doctors to provide treatment or procedures that they have assessed as not being clinically appropriate or not of overall benefit to the patient.’

‘Belief perseverance might prevail when the result is disappointing ‘ – again this is taken from your paper. Despite being given evidence of the clinical trials that have demonstrated this patients feel very patronised by this. I know how I feel and the difference T3 has made to me yet why do I continually fed a narrative that it’s just a placebo? 

I am delighted that this person has found solace in T3 and I agree that placebo is not the sole explanation. Placebos do not last beyond a few months but you also have to keep in mind that there are patients who have gone on T3, found it extremely useful and then, for whatever reason, have come off it and have not felt any worse. This is a complex issue and it goes, I think, far beyond just the T3 and the placebo argument. 

‘If medically not yet explained symptoms is the true elephant in the room then low tissue T3 is the mouse in the corner.’ The response to this point is a great frustration that in the current NHS it is such a struggle to get an appointment. How are we supposed to find an empathetic doctor who will support us and investigate further?

A survey of UK-based endocrinologists was published in 2022. One of the questions that was asked was ‘Would you use combination treatment?’ The result was that 51% of respondents said they would use combination treatment for patients treated with levothyroxine who had persistent symptoms and had a normal TSH. So, I think things may not be as bad as they seem if this is truly representative of the body of endocrinologists in the UK.

Doctors’ attitudes are sometimes problematic. What I would say is that empathy and support require more than 10-minute appointments, which is an average GP appointment time, or 15 minutes with a consultant. 

I have always had low blood sugar until I became hypothyroid. I am now pre-diabetic. The doctor tells me this isn’t connected but do you think it is?

I’m going to put aside the low blood sugar and I would like to answer the connection between pre-diabetes and hypothyroidism, diabetes and thyroid disease. If you think first of all there are two kinds of diabetes: insulin-dependent type 1 and type 2. Type 1 is an autoimmune condition so if you have one autoimmune condition you are a little more likely to develop another so there is a link there. 

There have also been studies that have shown an association between type 2 diabetes or pre-diabetes and autoimmune thyroid disease. There is an association between hypothyroidism and increased body mass index and that predisposes to pre-diabetes so that may be one reason why the two are related.

Also, if you have one condition you are much more likely to tested for another so another possible explanation. 
With regards to low blood sugar, one needs to be cautious about how we define it. Some people have symptoms that they attribute to low sugar but if investigated them properly often the true sugar level is actually not low. So having true hypoglycaemia is quite a rare event and I am not sure that is relevant to this particular question.

Information added subsequent to the webinar

Thank you for answering my question in the webinar. I realised that the question I should have asked was: ‘Is it possible that levothyroxine itself is causing my raised blood sugar?’ It says in the patient information leaflet that it does, although my GP says not.  If it does raise it, how and why does it raise blood sugar, and can anything be done about it? The levothyroxine works brilliantly for me, and reversed all of my symptoms of underactive thyroid.

I am glad you are feeling better on levothyroxine. High levels of thyroid hormones (‘thyrotoxicosis’) whether caused by increased production by the thyroid, or as a result of excessive intake of thyroid hormones, can indeed raise blood sugar. The comment in the levothyroxine packet insert refers to this in the context of taking excessive amounts of levothyroxine. When taking levothyroxine for the treatment of hypothyroidism in an appropriate dose that does not raise thyroid hormone levels above normal, or suppress the serum TSH, there is no risk of inducing a high blood sugar over and above what might happen if you did not have hypothyroidism. 

The ways that excessive amounts of thyroid hormones may raise blood sugar are multiple and complex. Thyroid hormones in excess (a) encourage the liver to make more glucose and to release more glucose into the circulation (b) make tissues less sensitive to insulin and less efficient at removing glucose from the circulation (c) in rare cases a patient may present at the same time with Graves’ disease and insulin-dependent diabetes.

I hope this provides some useful information about the relationship between levothyroxine and glucose.

Why doesn’t NICE recognise the advantages of using desiccated thyroid hormone from, say, pigs? Desiccated thyroid hormone was the go-to remedy many years ago and it has many advantages and includes T1, T2, T3, T4 and calcitonin. So why is it not the NHS go-to?

There is a number of things to talk about here. First of all, we now have two randomised control trials comparing desiccated thyroid extract against thyroxine. On well-defined outcomes about symptoms, quality of life and cognitive ability there is no difference between the two. So, based on these randomised control trials there is no evidence that desiccated thyroid extract is better than levothyroxine. 

The ratio of T3 to T4 is rather high in pigs, much higher than in humans. So one has to be careful and I think it is a lot easier when being treated with desiccated thyroid extract to actually over-treat yourself. So, based on the evidence, you cannot really claim those things. 

Does iodine excess or deficiency cause thyroid nodules?

Yes, iodine deficiency is a very well-established cause of thyroid nodules. What tends to happen if you have iodine deficiency is the thyroid gland needs to work harder and there are some cells in the thyroid gland that seem to have an advantage over others in terms of growth and they start to form nodules. So nodular disease is common in areas of iodine deficiency and it can lead to multinodular goitres and what we call endemic goitres. 

I am not aware that iodine excess causes nodules. It is really rather difficult to sustain iodine because you have to ingest large amounts of iodine consistently to really do that.

How much of an effect can stress have on somebody who’s been diagnosed with Graves’ disease even if it’s well controlled with medication?

Stress is very obviously important. There is good data to show that stress has an effect on the immune system. Some years ago there were some very interesting studies that showed in war zones, where there are the most extreme forms of stress on a large population scale, what happened after the war was a little epidemic of Graves’ disease. The plausible explanation that was given to this was that stress actually just caused this. So it was a kind of trigger for Graves’ disease. The way I think most of us would interpret that is if you already have predisposition to develop Graves’ disease and it is lurking in the background and going to happen any time, then stress may just bring it forward. 

With regard to stress during treatment, I don’t think there is necessarily a direct effect. I think living a stressful life can affect how good we are at taking our treatment for instance and that may have an impact. I am not aware of any studies that have looked at stress and what it does to people with Graves’ disease during treatment. Provided the appropriate treatment has been given and is being followed then you will get a good result out of it regardless.

If my grandmother, mother, sister and brother were all diagnosed with hypothyroidism in their forties and fifties, at what point should my children be tested? Should I be looking out for thyroid problems when there’s such a strong history of it in my family?

There is indeed a tendency for autoimmune conditions to run in families. The probability still is not huge. It is not like in some genetic conditions where if the parent has it, 50%, or even 100%, of the offspring will definitely develop it. It is far less than that. I think the best thing to do is just be aware of it. It is unlikely that it will develop during childhood. The average age of people developing autoimmune thyroid disease is the forties and fifties. So I would say just be aware of it and if you notice some unexpected and unexplained symptoms then that would be a reasonable time to test.

There is no evidence that I know of, or any value, in routine screening. One has to be aware that to routine screen something you have to have good evidence that the overall effect is beneficial because so often when you do tests without the absence of symptoms you can get misled and you can get aberrant blood test results that make you anxious. You then have to investigate this and it usually turns out to be a false alarm.

So I would suggest that if someone has a very strong family history of autoimmune thyroid disease and are concerned about their children to just wait and watch. If symptoms arise, then that is the best time to check.