Visiting the GP - What you should know

Who has autoimmune thyroid disease?

Autoimmune thyroid disease (Hashimoto’s thyroiditis and Graves’ disease) is very common and it can affect any age group. Hashimoto’s thyroiditis is more frequently diagnosed in women, but thyroid disease affects men as well. However men often go under the radar and thyroid disease is usually not suspected.

Hypothyroidism can affect people who are overweight and slim. Weight gain can be a symptom of hypothyroidism, but the weight gain is not significant in all patients with hypothyroidism. Hyperthyroidism can cause weight loss, but many patients with hyperthyroidism are overweight and hyperthyroidism or excessive thyroid hormone replacement therapy can even contribute to weight gain.

Could I have Hashimoto’s disease or Graves’ disease?

Autoimmune thyroid disease (Hashimoto’s thyroiditis and Graves’ disease) often runs in families. Other autoimmune diseases like rheumatoid arthritis, type 1 diabetes and coeliac disease can also be seen in people with a family history of autoimmune thyroid disease. If you have a family history of autoimmune disease, you can ask your doctor for a thyroid function test and you should be screened for thyroid antibodies.

Thyroid disease is often misdiagnosed and may be masked by the following conditions:

Thyroid disease can change your personality, but often the changes are very subtle. If you are developing an underactive thyroid then perhaps you don’t have as much energy, or you have become withdrawn socially and your moods might be unstable. These symptoms can be reversed with the right dose of thyroid hormone. Thyroid disease can affect you physically, emotionally and mentally.

I want to get pregnant, should I have a thyroid function test?

YES, whether you have a family history of thyroid disease or not! Pregnant women require on average an additional 40 to 50 per cent of thyroxine for their baby’s brain development, but if you are in the early stages of autoimmune thyroid disease (Hashimoto’s thyroiditis) or if there is a lack or excess of iodine in your diet, then your body may not be able to produce more thyroxine.

In the first trimester the foetus relies 100% on the maternal thyroid hormone production. After 13 weeks the foetus starts to produce thyroid hormone, but still relies on the maternal thyroid hormone production.

Results from human and animal research consistently show that the mother’s thyroid hormone production during pregnancy has a significant long term impact on the behaviour, locomotor ability, speech, hearing and cognition of her children. Lower IQ, difficulties with reading and language, visio-spatial impairments have all been observed when compared with children whose mothers were not hypothyroid during pregnancy.

All newborns in Australia are being screened for hypothyroidism and hyperthyroidism. Usually this is done at the hospital upon birth (test is also known as the ‘heel prick’). Congenital hypothyroidism is relatively rare, but hypothyroxinemia (low or low normal thyroxine levels) is very common! Some authorities have suggested to screen all pregnant women for maternal hypothyroidism.

Studies that looked at the first trimester maternal thyroxine level (free T4), but NOT the maternal TSH, concluded that a low supply of maternal thyroxine was a significant predictor for future neurodevelopmental difficulties.

If a doctor does check for thyroid dysfunction, then generally the TSH is checked (standard test to diagnose and treat hypothyroidism) and therefore the doctor may miss the diagnosis. The GP may also not be familiar with trimester-specific ‘normal’ TSH ranges for pregnant women. Once pregnant the TSH decreases significantly!

The thyroxine level (free T4) should be in the upper third of the normal range!

What do I need to know before I visit the doctor?

Thyroid dysfunction can cause many symptoms and affect every organ in your body. Your thyroid related symptoms also occur in other conditions, so often the doctor might treat your symptoms and the real culprit, your ailing thyroid, is not discovered. If your doctor does check your thyroid function, then the doctor may only check your TSH (thyroid stimulating hormone).

If your TSH level falls anywhere within the ‘normal range’ then your doctor may tell you that the test is normal, but this test does not rule out hypothyroidism. In some people the TSH is very sensitive and reliable, but in others it is not. If you have classic symptoms of hypothyroidism, antibodies present, family history of autoimmune disease and low circulating thyroxine levels (in the normal range or below the normal range) then there is a good chance that you are in the early stages of thyroid disease. You should ask for a thyroid function test and ask for a copy. Blood tests should be used as a guide and should not replace clinical evaluation (classic symptoms and signs).

I was diagnosed with Hashimoto’s thyroiditis and I take thyroxine, but I still feel depressed. The doctor has prescribed antidepressants for me, but I am not sure if I should take it or not.

Depression or dysthymia (mild depression) can be a symptom of hypothyroidism. One of the reasons why some people who take thyroxine (T4) still suffer from depression is that they may not be on the right dose. However some people only feel better on a combination therapy of T4 and T3. Research has shown that people with a commonly inherited variation in the DIO2 gene don’t feel well on T4 alone. DIO2 activates T4 by converting it to T3. People who have this variation are not able to convert T4 to T3 in all tissues including the brain and this may result in depression and their psychological well-being only improves on a combination therapy of T4 and T3 (http://press.endocrine.org/doi/full/10.1210/jc.2008-1301).

If T4 alone is not effective then a GP or an endocrinologist may be able to prescribe a combination therapy of T4 and T3. However it is important to note that the dose of both T4 and T3 needs to be optimal. If the T4 is reduced too much and not replaced with enough T3, then people will not notice any improvements. 

An alarming number of thyroid patients are on antidepressants instead of proper treatment of thyroid disease! Antidepressants can have some serious side effects and these medications can make the depression worse. Once a thyroid patient is on antidepressants it will also become more difficult to monitor the treatment for the thyroid condition, because the symptoms and signs of too little or too much thyroid hormone may be confused with the side effects of the antidepressants. It is always very important to ask your doctor or pharmacist for a list of possible side effects of any prescribed medication before you consider the risks and possible benefits. The aim of antidepressants is to balance the neurotransmitters (brain chemicals) in the brain, but there is no diagnostic test to measure these neurotransmitters. Prescribing antidepressants therefore is based on guess work. What we do know is that T3 plays an important role in the brain and scientists have shown how T3 acts like a neurotransmitter. 

The aim of the thyroid hormone replacement therapy should be to relieve all symptoms and signs of hypothyroidism through clinical evaluation and at the same time patients need to watch out for symptoms of excessive thyroid hormone replacement therapy such as heat intolerance, frequent loose stools, inability to hold fingers still, fast resting pulse etc. 

© 2016 Monique Atkinson

References

Panicker, V. et al. (2009). Common Variation in the DIO2 Gene Predicts Baseline Psychological Well-Being and Response to Combination Thyroxine Plus Triiodothyronine Therapy in Hypothyroid Patients: The Journal of Clinical Endocrinology & Metabolism. Vol 94(5),pp. 1623–1629. [online] Available at:http://press.endocrine.org/doi/full/10.1210/jc.2008-1301

Biondi, B and Wartofsky, L. (2011). Combination Treatment with T4 and T3: Toward Personalized Replacement Therapy in Hypothyroidism? The Journal of Clinical Endocrinology & Metabolism: Vol 97, No 7. The Journal of Clinical Endocrinology & Metabolism. [online] Available at: http://press.endocrine.org/doi/full/10.1210/jc.2011-3399

 Kooistra, L. et al. (2006). Neonatal Effects of Maternal Hypothyroxinemia During Early Pregnancy. Pediatrics. 117(1), pp.161-167. [online] Available at: http://pediatrics.aappublications.org/content/117/1/161

Leung, A. and Braverman, L. (2013). Consequences of excess iodine. Nat Rev Endocrinol, 10(3), pp.136-142.  [online] Available at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3976240/

Morreale de Escobar, M. et al. (2000). Is Neuropsychological Development Related to Maternal Hypothyroidism or to Maternal Hypothyroxinemia? The Journal of Clinical Endocrinology & Metabolism. Vol 85, No 11. (2000. [online] Available at: http://press.endocrine.org/doi/full/10.1210/jcem.85.11.6961

Gallego, G. (2010). Iodine deficiency in Australia: is iodine supplementation for pregnant and lactating women warranted? | Medical Journal of Australia. [online] Available at: https://www.mja.com.au/journal/2010/192/8/iodine-deficiency-australia-iodine-supplementation-pregnant-and-lactating-women

Gullo, D. et al. (2011). Levothyroxine Monotherapy Cannot Guarantee Euthyroidism in All Athyreotic Patients. PLoS ONE, 6(8), p.e22552. [online] Available at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3148220/

Disclaimer The information provided is for educational purposes only and is not intended to be medical advice. The contents must not be relied upon in place of advice and treatment from a qualified medical practitioner. THYROID WA SUPPORT GROUP INC. and the author disclaim any liability whatsoever.