We break down everything you need to know about this disease, which is the most common cause of hypothyroidism.
- What is Hashimoto's disease?
- What causes Hashimoto's disease?
- What are the treatments for Hashimoto's disease?
What is Hashimoto’s disease?
Hashimoto’s thyroiditis (also known as chronic lymphocytic thyroiditis) is the most common cause of hypothyroidism in the UK.
The condition was first described by the Japanese doctor Hashimoto in 1912. The condition is 7 times more common in women than in men, and tends to occur in middle age, though it can be observed at any age.
Hashimoto’s is an autoimmune disease caused by the production of anti-thyroid peroxidase antibodies (TPOAb) and anti-thyroglobulin antibodies (TgAb) by the immune system.
This disease can also be accompanied by normal thyroid function test results, and the presence of antibodies may be enough to diagnose the condition. This is because the antibodies correlate well with the inflammation in the thyroid gland even if the thyroid gland is still producing hormones normally.
Hashimoto’s can also cause a ‘goitre’ or abnormal swelling of the thyroid gland which may be so large that it is visible.
Hashimoto’s thyroiditis is associated with a number of other autoimmune diseases, including:
- Type 1 diabetes
- Pernicious Anaemia
- Addison’s disease
- Coeliac disease
Those who are diagnosed with Hashimoto’s disease should be screened for Coeliac disease.
What causes Hashimoto’s?
The cause of Hashimoto’s disease is considered to be a combination of genetic susceptibility and environmental triggers.
We know that there is a strong genetic component as the disease tends to run in families. One is 20 times more likely to have the condition if a sibling is already affected.
Factors that can trigger Hashimoto's disease include:
- Iodine intake
- Certain medications
Molecular mimicry theory & Hashimoto’s
There have been several theories proposed to explain how the body’s immune system is activated to attack its own thyroid gland. One explanation centres around a concept known as ‘molecular mimicry’.
Our immune system is designed to defend the body against potentially dangerous invaders, such as viruses or bacteria. When the body encounters such foreign antigens (molecules not normally found in the body), it prompts an immune response. The body produces antibodies against the foreign antigen, which attach to it. The attachment is very specific, like a key that only fits only one lock.
Antibodies stay in the body even after the antigen has gone, so they allow the immune system to remember what the antigen looks like. If the same antigen is encountered again, antibodies are able to recognise them immediately and mount a much faster and stronger defence against the foreign molecule.
Unfortunately, the immune system’s recognition may go wrong. If a molecule on the surface of our normal body cells, very closely resembles a foreign antigen, the antibody might incorrectly lock onto it. This would then trigger the immune system to attack our own body’s cells rather than the foreign ones that the antibody was originally designed for.
The idea that a foreign antigen can ‘mimic’ a native antigen is where the term ‘molecular mimicry’ comes from.
In the case of Hashimoto’s there are theories suggesting that a preceding bacterial infection can cause the body to produce antibodies that go on to attack the thyroid incorrectly.
Others believe that molecular mimicry between gliadin, (a component of gluten) and structures on the surface of thyroid cells may lead to an autoimmune reaction.
Leaky gut theory and thyroid disease
Gluten plays a role in another theory used to explain autoimmune thyroid disease. The ‘leaky gut’ syndrome theory was originally developed as an explanation for the abnormal processes underlying coeliac disease. The suggested mechanism is as follows:
- Gluten, which is present inside the gut, provokes an abnormal immune response
- The patient has an underlying genetic predisposition to be susceptible to this kind of disease
- The abnormal immune process results in a ‘leaky gut’ or an increase in the space between the cells that make up the gut lining, such that the lining becomes abnormally permeable
- This then allows particles of gluten to leak through into the underlying tissue, provoking a further immune response and persistent inflammation throughout the body
This leaky gut theory is used as an explanation for an increasing number of diseases, including thyroid dysfunction.
Suggested triggers for this immune response now include undigested food particles, bacterial toxins or other germs.
Some practitioners may suggest nutritional supplementation, probiotics or dietary restriction as a way to address gut ‘leakiness’ or ‘increased intestinal wall permeability’, as it would be called within conventional medicine.
The NHS takes a skeptical view of this as there is a lack of large scale, high-quality evidence to support this approach, though small research studies and anecdotes do exist.
Hashimoto’s and pregnancy
Untreated hypothyroidism can result in poorer outcomes in pregnancy including miscarriage, maternal complications and abnormal brain development in the foetus. For this reason, a pregnant woman with known thyroid disease requires close monitoring throughout pregnancy and should take their levothyroxine as prescribed.
Thyroid dysfunction can also occur after pregnancy in a condition known as ‘postpartum thyroiditis’. This usually involves an initial hyperthyroid phase after which the patient becomes hypothyroid. In a proportion of women this hypothyroidism will become permanent and they will require long-term treatment.
What are the treatments for Hashimoto's disease?
Treatment for Hashimoto’s involves replacing the thyroid hormone that is lacking using medication.
The most commonly available drug is levothyroxine (LT4). Levothyroxine is a synthetic form of thyroxine (or ‘T4’) and does not include any T3. Levothyroxine is converted to T3 as happens with thyroxine.
There are other drugs used in treatment of Hashimoto’s that include T3 and T4 so are known as ‘combination therapy’. These drugs are not generally available on the NHS as there is insufficient evidence from large-scale studies to suggest that they are superior to thyroxine alone.
T3 supplementation can cause long-term problems including atrial fibrillation (irregular heart rhythms) and osteoporosis (thinning of the bones). This concern is compounded by the fact that many combination products usually contain high doses of T3 making long-term problems more likely.
It is important to note that up to 10% of people with hypothyroidism complain about symptoms, despite being treated with levothyroxine, and having normal levels of TSH.
One reason for this, amongst others, could be because levothyroxine is not restoring the body’s T4 and T3 levels to normal (physiological) levels.
The European Thyroid Association (ETA) recommends that levothyroxine should be the standard therapy for hypothyroidism, however, they suggest that combination LT3+LT4 therapy can be used on an experimental basis in patients who still have symptoms despite normal TSH levels.
Combination therapy should only be prescribed by a specialist (endocrinologist) with experience in its use.