Could your thyroid be ruining your health?
Hypothyroidism (low thyroid function) affects millions of people around the world and is one of the most commonly treated hormone conditions.
The most common signs and symptoms of low thyroid function, that we see in our clinic are;
What does the thyroid gland do?
The thyroid is a butterfly shaped gland that sits at the base of the neck, wrapped around the trachea (windpipe).
It secretes hormones that play critical roles in processes that are influenced by ‘speed’ and every cell in the body can use thyroid hormones.
Thyroid hormones control factors such as;
What hormones is the thyroid responsible for producing?
The thyroid gland secretes a number of different hormones but the primary hormone secreted is thyroxine (T4), the inactive form of thyroid hormone.
T4 can then be converted to the most biologically active form, triiodothyronine (T3), as and when required.
T3 is important as it is this active hormone that regulates metabolism.
The thyroid gland secretes around 80% T4 and around 20% T3 (4) and levels of these hormones are tightly controlled by signals from areas of the brain called the hypothalamus and pituitary gland.
Imbalances in these signals from the hypothalamus or pituitary, or in the ability of the thyroid gland to synthesise thyroid hormones, can cause thyroid function problems.
So what is hypothyroidism?
Hypothyroidism, also referred to as low thyroid function or under-active thyroid, is when the thyroid gland doesn’t produce enough thyroid hormone (or the thyroid hormone isn’t binding to thyroid receptors).
However, there are various potential underlying reasons why someone may be suffering with hypothyroidism.
This is important to understand in order to support optimal thyroid function (and in some cases to avoid medication or help the medication to work more effectively).
How common is hypothyroidism?
Hypothyroidism is ten times more common in women than men (5) and Levothyroxine (a synthetic form of T4), a medication used to treat hypothyroidism, is the third most commonly prescribed drug in the UK – a huge 29 million prescriptions (in 2014) (6).
Why is hypothyroidism a silent epidemic?
The real number of people suffering with hypothyroidism could be (and we’d go as far as to say we’re quite sure it is) much higher than the official figures suggest.
In our clinics, we commonly work with clients who have low thyroid function, who were previously unaware that they had a problem.
Of more importance clinically, low thyroid function can help us to understand why someone may be experiencing certain symptoms.
Overt vs subclinical hypothyroidism
Now just to be clear; there is a significant difference between the incidence of overt (clearly defined) hypothyroidism and subclinical hypothyroidism.
Overt hypothyroidism is clear hypothyroidism, with lab results that show an increased TSH and a decreased T4 level, as per the conventional lab ranges used by doctors.
Subclinical hypothyroidism is where the TSH may be ‘sub-optimally high’ or normal, where the T4 may be ‘sub-optimally low’ or normal, and people are still experiencing signs and symptoms of low thyroid function, due to other thyroid imbalances.
In our clinical experience, additional in-depth thyroid testing can reveal imbalances and therefore the reason(s) for symptomatic, sub-optimal thyroid function (where you suffer from symptoms despite test results being normal, according to conventional lab ranges, or not clinically relevant).
‘Normal’ thyroid test results
At Coho Health, our practitioners frequently discover a ‘subclinical’ state of hypothyroidism during our investigations – even where standard testing has come back ‘normal’.
This is often where the TSH level is within the NHS (UK) ‘normal’ range and a diagnosis of hypothyroidism is not made.
Despite a ‘normal’ test result, and the patient being told there is no thyroid problem, the imbalance can still be significant enough to manifest in low thyroid symptoms, sub-optimal quality of life and sadly, fertility issues.
Why do results come back ‘normal’ when I still have symptoms?
There are several key issues to consider;
Firstly, in conventional medicine, a hypothyroidism diagnosis is fundamentally flawed.
It’s based on TSH and T4 levels only. And the ranges used in this testing are often too broad (if you keep reading you’ll learn why this just doesn’t cut it).
Secondly, subclinical hypothyroidism is both very common and under-diagnosed (due to inadequate test quality and other factors).
One study reported that almost 11% of women may have subclinical hypothyroidism (7) and some hormone experts suggest that, in their opinion, thyroid insufficiency affects 20% to 50% (20 to 50 people in every 100) of a standard population (8).
The lack of comprehensive testing means that thyroid hormone imbalances aren’t always picked up (unless you’re working with a Functional Medicine or Naturopathic practitioner who has access to, and is able to correctly interpret, the most accurate testing).
Thirdly, the underlying cause of thyroid hormone imbalance is not considered – and this can alter the clinical approach taken in helping to restore thyroid hormone balance.
Lastly, for a diagnosed hypothyroid case, the prescribed treatment is the same, levothyroxine (synthetic form of T4) and there are some cases where the underlying issue isn’t a T4 deficiency.
And why don’t I feel any better despite taking thyroid medication?
But what if low thyroid function isn’t due to low T4? There are several other reasons why someone may have low thyroid function, despite producing good levels of T4.
If you’re taking thyroid medication and still don’t feel any better for it, keep reading.
TSH and T4 ‘normal’ ranges
The conventional range used for TSH levels is broad so that most of the population fall within a ‘normal’ range and therefore most patients are informed that their results are ‘normal’ and they do not have a thyroid issue.
However, when applying the same test result to an optimal (functional) range, the interpretation can be different.
In Functional Medicine, optimal ranges are applied to test results, and the question considered in defining these ranges is, how much of a nutrient/hormone etc is required for processes in the body to function at 100%, i.e. to function optimally.
In hypothyroidism, we know that imbalances in metabolism can occur long before a lab test result for TSH is above the standard NHS upper limit.
What does regular thyroid testing cover?
‘Standard’ thyroid testing, which is commonly available in the UK through the NHS and private health insurance is usually limited to:
The TSH is produced by the pituitary (in the brain) and acts as a signal to the thyroid gland.
TSH says ‘hey, my body needs more thyroid hormones, so make some more’.
The lower the perceived level of thyroid hormones, T4 and T3, the louder (higher) this signal is.
So, when the body senses there isn’t enough thyroid hormones, the TSH goes up.
Usually, in subclinical and overt hypothyroidism, the pituitary released TSH is higher, signalling to the thyroid gland to produce more hormones.
TSH ranges: Coho Health vs conventional testing
At Coho Health we consider the upper limit of the optimal range for TSH to be 2.5 mU/l (milliunits per litre).
If your TSH level has been tested, is above 2.5, and you are displaying signs or symptoms of low thyroid function, we recommend you work with a Functional / Naturopathic practitioner to have a full thyroid screen performed.
This way we can begin to understand where the imbalance is coming from – and how to address it.
The NHS upper limit for TSH is usually around 5.0 mU/l
However NHS guidelines currently state ‘‘Consider levothyroxine for adults with subclinical hypothyroidism who have a TSH of 10 mlU/litre or higher on 2 separate occasions 3 months apart.’ (9).
You read that right – treat hypothyroidism when TSH is higher than 10!
But guidelines also state to start treatment where there is;
‘a TSH above the reference range [so above the usual 4 or 5] but lower than 10 mlU/litre on 2 separate occasions 3 months apart, and symptoms of hypothyroidism’ (10).
The ‘Thyroid UK’ organisation states: ‘In America and some other European countries, they have reduced the TSH level to 2.5 which means that anyone above that figure will be treated if they have symptoms of an underactive thyroid.’ (11).
Hypothyroid and other health problems
Recent studies suggest that a TSH greater than 2.5 increases the risk of infertility and miscarriage (12).
There is also a strong correlation between heart disease and sub-clinical hypothyroidism.
A study following 1365 patients with pre-existing heart failure found that a TSH ≥7 and low T3 levels was associated with poor prognosis (various end points were considered including death) (13).
One reason for the increase in cardiovascular risk are the changes in lipids (cholesterol profile) that can be seen in sub-clinical and overt hypothyroidism.
In these cases is it best to treat high LDL cholesterol with statins, or to address the root cause of the high LDL – for example sub-clinical hypothyroidism?
The TSH take-home
We see clients weekly at our clinic who have a TSH over 2.5, and who are displaying symptoms of hypothyroidism.
We also see ‘normal’ TSH results, alongside other thyroid hormone imbalances that we identify through additional testing.
Together with the presentation of symptoms, this makes it necessary to address thyroid hormone balance.
The take home is this – if your TSH is above 2.5 and you’re displaying signs and symptoms of low thyroid, or have a family history of thyroid issues, please go and speak with someone who understands thyroid function.
Someone who can help with ordering comprehensive testing that can pinpoint where the imbalance is, and who can help you to bring your hormones back into balance.
Free T4 testing
The next thyroid hormone that is tested (in some cases along with the TSH, but in other cases only if the TSH is out of range), is free T4.
The thyroid gland makes and releases thyroxine, i.e. T4.
However, not all of the T4 is ‘free’.
Thyroid hormones, like many other hormones, can be bound to proteins (14), this allows the body to carefully regulate the amount of hormone that is ‘free’ to be used by cells.
So, the ‘free’ portion is often tested by doctors to help understand the amount of ‘usable’ thyroid hormone.
The ‘Free T4’ normal range is usually 12 – 22 pmol/L.
What about Free T3?
Conventional testing will include TSH and free T4, but that’s usually it.
In some cases, free T3 may be tested and in our clinical experience, measuring levels of free T3 is very useful as this is the active hormone available to bind to the receptors on all of our cells to control the speed of cellular function.
The conventional ‘Free T3’ ‘normal’ range is usually around 3.1 – 6.8 pmol/L.
Subclinical hypothyroidism: why a full thyroid screen can be life changing
Let’s say TSH and Free T4 levels are within the ‘normal’ range.
But you still suspect hypothyroidism.
Maybe it’s because you have many of the associated symptoms.
Or maybe there’s a family history of hypothyroidism (and therefore you have a higher risk).
What next? Our experience suggests that a full screen is hugely beneficial.
Good thyroid health testing should ideally include:
Why test Free and Total T3?
T3 is the metabolically active thyroid hormone.
It allows us to check your ability to convert T4 to T3.
This conversion is dependant on enzymes called deiodinases, which require the minerals, zinc (15) and selenium (16).
The levels of deiodinase enzymes we produce can be influenced by our microbiome.
A diverse microbiome can also help to create a ‘reservoir’ of thyroid hormones which may reduce fluctuations in thyroid hormone levels and the need for thyroxine medication (17).
So gut health plays a key role in supporting thyroid hormone balance.
Free T3 is the amount of active thyroid hormone ‘free’ to be used by cells.
Low T3 is a hormone imbalance we frequently identify with our clients and is linked to symptoms of low thyroid function, as well as to a significantly increased risk of heart attack (18, 19).
Remember that the conventional treatment for hypothyroidism is synthetic T4.
If your body isn’t converting T4 to T3 then this could be one reason why your medication isn’t working and you’re not feeling better.
What is Reverse T3?
T4 should be converted to T3 as and when the body requires it.
But under some situations, T4 can go down a different path and be converted to the ‘mirror image’ of T3 – Reverse T3.
This can happen when critically unwell or in periods of starvation (20) (including extreme calorie restriction), heart failure, chronic stress and high cortisol (stress hormone) levels.
The increase in Reverse T3 is a consequence of alterations in thyroid hormone metabolism.
It is one reason why chronically restricted calorie intake or carbohydrate restriction can actually slow down metabolism in the long run.
If TSH, T4 and T3 all look fine, but you still suspect low thyroid function, then it’s time to check reverse T3.
When thyroid hormones are not ‘free’, it’s because they are bound to proteins.
The main binding protein is Thyroxine-binding globulin (TBG) (21). Other hormones can also affect TBG levels such as oestrogen and testosterone.
This marker is helpful to understand if there are issues around levels of TBG, causing either higher or lower levels of ‘free’ thyroid hormones (T3 and T4).
In such imbalances, the issue isn’t around how much T4 or T3 the body is making, but how the hormones are being bound to TBG.
Let’s take a look at some test results…
1/ In this test result, we see the elevated levels of thyroglobulin possibly causing the low free T4, and the low iodine, selenium and high mercury…
2/ In this test result, we can see low free and total T4, and sub-optimally low free and total T3, is this nutrient insufficiencies affecting T4 and T3 synthesis…
3/ In this test result, we can see high thyroid peroxidase antibodies – this person doesn’t need more T4, but to reduce the antibodies (remove triggers and address inflammation, immune modulation and intestinal permeability)…
4/ In this test result, we saw over medication of levothyroxine, undiagnosed Hashimoto’s and high reverse T3…
As you can see, each test result shows something different – different root causes and different systems at play.
Based on each individual test result and case presentation, our team would devise an individual plan to address the factors at play.
What’s the root cause of hypothyroidism?
Studies suggest that up to 90% of hypothyroidism may have an autoimmune cause (22) – specifically Hashimoto’s thyroiditis disease.
This is where the body is producing antibodies (an immune response) that are destroying the thyroid gland and therefore reducing thyroid hormone synthesis.
Often these antibody levels are not tested by the doctors, so many people who have a diagnosis of hypothyroidism, may actually have Hashimoto’s but they just don’t know.
On the other hand, thyroid antibodies may be present but the person may not be presenting with symptoms of hypothyroidism.
In this case it’s still relevant to know about the antibodies, as risk for developing hypothyroidism at some point is increased.
For doctors, it’s usually a case of ‘watch and wait’ for the antibodies to cause enough damage to throw the TSH and T4 out of range.
This approach doesn’t sit well with us when we have a body of evidence suggesting that nutrition and lifestyle interventions can reduce antibody levels and prevent or delay the onset of thyroid problems.
An iodine (mineral) deficiency is another common cause for hypothyroidism (23).
The reason for this is that thyroid hormones are synthesised from iodine molecules and the amino acid tyrosine.
In T4, the ‘4’ denotes the four iodine molecules present in the thyroid hormone. So it goes without saying that a deficiency or insufficiency of iodine, influences levels of thyroid hormones.
Iodine deficiency is a worldwide problem – iodine content in soil is low and amounts of fish consumed varies significantly.
Seafood and sea plants, such as nori, kelp, wakame and kombu are the best sources of iodine (but levels can vary significantly, potentially also leading to dangerously high levels of iodine).
Iodine supplementation should be avoided in autoimmune thyroiditis.
Other nutrient deficiencies
Other nutrient deficiencies can also interfere with thyroid function.
Selenium is required for the conversion of T4 to T3 (24). Selenium is needed to produce the deiodinase enzymes that drive this conversion.
Iron a component of the enzyme, thyroid peroxidase, involved in the early stages of thyroid hormone synthesis (25).
It is common to find a low iron status in people with hypothyroidism (26). We consider a ferritin level of 50ug/L as an absolute minimum (27), most conventional lab ranges are set much lower than this.
Zinc has a complex role in thyroid hormone regulation. It plays a role in the metabolism of thyroid hormones by regulating deiodinase enzymes, and also plays a role in the synthesis of thyrotropin releasing hormone (TRH) (28), secreted from the hypothalamus and TSH (in the pituitary gland).
What about thyroid medication?
In Functional Medicine, we’re looking to identify and address the root cause(s) of thyroid signs and symptoms.
Providing medication is not always the answer, because it corrects the end result – the hormone imbalance, rather than the root cause, which is often an autoimmune problem.
Without addressing the ‘autoimmune’ aspect of the condition, it’s difficult to see how there can be long term improvement in thyroid health.
The underlying immune dysregulation can manifest in other ways – in Hashimoto’s disease there is an increased risk of having additional autoimmune conditions, such as coeliac disease (29, 30, 31, 32).
Often with coeliac disease, the symptoms can be so mild that the condition is undiagnosed.
However the damage caused to the intestinal cells can mean that Levothyroxine isn’t well absorbed, and a higher dose is required (or a Functional Medicine approach is required to help improve absorption of medications and food).
And just as an aside – the recommendation in the UK is to screen for coeliac disease at the time of an autoimmune thyroiditis diagnosis.
In our clinical experience, thyroid medication alone, does not always lead to complete resolution of low thyroid symptoms – a root cause, multifactorial, individualised approach is required.
In Hashimoto’s we need to understand what is driving the immune response for each client.
Is it an immune reaction to a food or drink, an environmental factor, a chronic viral infection, a gut bacteria imbalance, increased intestinal permeability or chronic stress, for example?
Low thyroid function can be supported through nutrition, nutritional supplements and lifestyle interventions.
But be aware that medication can be the best option if your condition is more advanced or for your individual circumstances – there is definitely a time and place for medication.
Never change your medication dose or stop taking it without consulting your doctor.
Other reasons for hypothyroidism include (but are not limited to):
Are you taking medication for hypothyroidism but still feeling the symptoms of low thyroid function?
There are multiple causes for low thyroid function as seen above.
To recap, it could be due to:
However, the standard treatment for all cases is usually Levothyroxine.
This may not solve your problem.
Consider for one moment that the prescribed medication Levothyroxine, is simply synthetic T4: inactive thyroid hormone.
What if that T4, being taken as a pill every morning, isn’t being converted to active thyroid hormone, T3?
Well then someone with hypothyroid symptoms is likely to still experience symptoms of hypothyroidism, even when their lab test for free T4 is within the normal range.
This is one reason why you can still feel terrible despite your lab test results being normal.
The conversion of Levothyroxine (T4) to T3 needs to be supported in order for it to be effective.
Additionally, there may be ‘normal’ levels of T4 and/or T3 in the blood, but high levels of Reverse T3, which blocks the action of thyroid hormone, again causing symptoms of low thyroid function.
There are several other reasons too as mentioned above, but you get the picture – comprehensive testing and employing optimal ranges, is a must in order to understand thyroid function.
Concerned about your thyroid health?
Further thyroid health resources
Further information is available over at Thyroid UK; http://www.thyroiduk.org/
Book your free 15 minute Discovery Call with Dee Brereton-Patel now
We hope you found this article useful, if you suffer from some of the problems highlighted here, or know someone who does, please feel free to share this post so we can reach and help more people!
If you’re looking for a Functional Medicine Nutritional Therapist delivering real health transformation, you’re in the right place.
We’d love to help you.
To your optimised, healthy future,
Dee & the Coho Health team
How can we help you? Send us a message below and we’ll come right back to you…
1, 2, 3.
Mullur R, Liu Y.Y., & Brent G.A. (2014). Thyroid Hormone Regulation of Metabolism. Physiol Rev. 94(2) pp.355–382. DOI: 10.1152/physrev.00030.2013. PMID: 24692351. https://www.ncbi.nlm.nih.gov/pubmed/24692351
Kansagra S.M., McCudden C.R., & Willis M.S. (2010). The Challenges and Complexities of Thyroid Hormone Replacement. Laboratory Medicine. V41 (6) pp. 338–348. https://doi.org/10.1309/LMB39TH2FZGNDGIM
Gietka-Czernel M. (2017). The thyroid gland in postmenopausal women: physiology and diseases. Przeglad menopauzalny = Menopause review, 16(2), pp. 33–37. DOI: 10.5114/pm.2017.68588. PMID: 28721126. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5509968/
Rodriguez-Gutierrez R., Maraka S., Ospina N.S., et al. (2016). Levothyroxine overuse: time for an about face? Lancet Diabetes Endocrinol [Online]. Available at: https://www.british-thyroid-association.org/sandbox/bta2016/rodriguez_gutierrez_lancet_diabet_endo_2017__2_.pdf (Accessed on 05 November 2019).
Hak A.E., Pols H.A., Visser T.J., et al. (2000). Subclinical hypothyroidism is an independent risk factor for atherosclerosis and myocardial infarction in elderly women: the Rotterdam Study. Ann Intern Med, 132 pp. 270-8. DOI: 10.7326/0003-4819-132-4-200002150-00004. PMID: 10681281. https://www.ncbi.nlm.nih.gov/pubmed/10681281
Thyroid UK (2019). Hypothyroidism [Online]. Available at:http://www.thyroiduk.org.uk/tuk/about_the_thyroid/hypothyroidism.html (Accessed on 5th November 2019).
National Institute of Health and Care Excellence (2019). Thyroid disease: assessment and management [Online]. Available at: https://www.nice.org.uk/guidance/ng145/chapter/recommendations (Accessed on: 6th November 2019).
Thyroid UK (2019). Hypothyroisim [Online]. Available at:
http://www.thyroiduk.org.uk/tuk/about_the_thyroid/hypothyroidism.html (Accessed on 5th November 2019).
Orouji J.T., Fourman L.T., Lee H., et al. (2018). Higher TSH Levels Within the Normal Range Are Associated With Unexplained Infertility. J Clin Endocrinol Metab. 1;103(2) pp. 632-639. DOI: 10.1210/jc.2017-02120. PMID: 29272395. https://www.ncbi.nlm.nih.gov/pubmed/29272395
Kannan L., Shaw P.A., Morley M.P., et al. (2018). Thyroid Dysfunction in Heart Failure and Cardiovascular Outcomes. Circ Heart Fail. 11(12): e005266. DOI: 10.1161/CIRCHEARTFAILURE.118.005266. PMID: 30562095. https://www.ncbi.nlm.nih.gov/pubmed/30562095
Fröhlich E. & Wahl R. (2019). Microbiota and Thyroid Interaction in Health and Disease. Trends Endocrinol Metab, 30(8) pp.479-490. DOI: 10.1016/j.tem.2019.05.008. PMID: 31257166. https://www.ncbi.nlm.nih.gov/pubmed/?term=Microbiota+and+Thyroid+Interaction+in+Health+and+Disease
Olivieri O., Girelli D., Stanzial A.M., et al. (1996). Selenium, zinc, and thyroid hormones in healthy subjects: low T3/T4 ratio in the elderly is related to impaired selenium status. Biol Trace Elem Res. 51(1) pp.31-41. DOI: 10.1007/BF02790145. PMID: 8834378. https://www.ncbi.nlm.nih.gov/pubmed/8834378
Coceani M. (2013). Heart disease in patients with thyroid dysfunction: hyperthyroidism, hypothyroidism and beyond. Anadolu Kardiyol Derg. 13(1) pp.62-6. DOI: 10.5152/akd.2013.008. PMID: 23086805. https://www.ncbi.nlm.nih.gov/pubmed/23086805
Iervasi G., Pingitore A., Landi P., et al. (2003). Low-T3 syndrome: a strong prognostic predictor of death in patients with heart disease. Circulation.11;107 5 pp.708– 13. DOI: 10.1161/01.cir.0000048124.64204.3f. PMID: 12578873. https://www.ncbi.nlm.nih.gov/pubmed/12578873
Gomes-Lima C. & Burman K.D. (2018). Reverse T3 or perverse T3? Still puzzling after 40 years. Cleveland Clinic Journal of Medicine. 2018 June;85(6):450-455. DOI: 10.3949/ccjm.85a.17079. PMID: 29883303. https://www.ncbi.nlm.nih.gov/pubmed/29883303
Köhrle J. (2018). Thyroid Hormones and Derivatives: Endogenous Thyroid Hormones and Their Targets. Methods Mol Biol. 1801 pp.85-104. DOI: 10.1007/978-1-4939-7902-8_9. PMID:29892819. https://www.ncbi.nlm.nih.gov/pubmed/29892819
Zimmermann M.B., & Boelaert K. (2015). Iodine deficiency and thyroid disorders. Lancet Diabetes Endocrinol. 3(4) pp.286-95. DOI: 10.1016/S2213-8587(14)70225-6. PMID: 25591468. https://www.ncbi.nlm.nih.gov/pubmed/25591468
Zimmermann M.B., & Köhrle J. (2002). The impact of iron and selenium deficiencies on iodine and thyroid metabolism: biochemistry and relevance to public health. Thyroid. 12(10) pp.867-78. DOI: 10.1089/105072502761016494. PMID: 12487769. https://www.ncbi.nlm.nih.gov/pubmed/12487769
Dahiya K., Verma M., Dhankhar R., et al. (2016). Thyroid profile and iron metabolism: mutual relationship in hypothyroidism. Biomedical Research, 27 (4) pp.1212-1215. [Online]. Available at: https://www.alliedacademies.org/articles/thyroid-profile-and-iron-metabolism-mutual-relationship-in-hypothyroidism.pdf (Accessed on 9th November 2019).
Koulaouzidis A., Cottier R., Bhat S., et al. (2009). A ferritin level >50 microg/L is frequently consistent with iron deficiency. Eur J Intern Med. 20(2) pp.168-70. DOI: 10.1016/j.ejim.2007.09.024. PMID: 19327606. https://www.ncbi.nlm.nih.gov/pubmed/19327606
Severo J.S., Morais J.B.S., de Freitas T.E.C., et al. (2019). The Role of Zinc in Thyroid Hormones Metabolism. Int J Vitam Nutr Res. 89(1-2) pp.80-88. DOI: 10.1024/0300-9831/a000262. PMID: 30982439. https://www.ncbi.nlm.nih.gov/pubmed/30982439
Bibbò S., Pes G.M., Usai-Satta P., et al. (2017). Chronic autoimmune disorders are increased in coeliac disease: A case-control study. Medicine (Baltimore). 96(47):e8562. DOI: 10.1097/MD.0000000000008562. PMID: 29381930. https://www.ncbi.nlm.nih.gov/pubmed/29381930
Ruggeri R.M., Trimarchi F., Giuffrida G., et al. (2017). Autoimmune comorbidities in Hashimoto’s thyroiditis: different patterns of association in adulthood and childhood/adolescence. Eur J Endocrinol, 176(2) pp.133-141. DOI: 10.1530/EJE-16-0737. PMID: 27913607. https://www.ncbi.nlm.nih.gov/pubmed/27913607
Farahid O.H., Khawaja N., Shennak M.M., et al. (2014). Prevalence of coeliac disease among adult patients with autoimmune hypothyroidism in Jordan. East Mediterr Health J. 11;20(1) pp.51-5. PMID: 24932934. https://www.ncbi.nlm.nih.gov/pubmed/24932934
Hadithi M., de Boer H., Meijer J.W., et al. (2007). Coeliac disease in Dutch patients with Hashimoto’s thyroiditis and vice versa. World J Gastroenterol. 13(11) pp.1715-22. DOI: 10.3748/wjg.v13.i11.1715. PMID: 17461476. https://www.ncbi.nlm.nih.gov/pubmed/17461476