Graves’ disease is an unfortunate name for a medical condition, but with appropriate and timely treatment (Read: 8 Things your Doctor won’t tell you about Graves Disease) you can definitely feel optimistic about reversing it.

Treatment is so important for avoiding major health risks down the road (Read: The 4 biggest concerns with Graves Disease you need to know). Let’s discuss what causes Graves’ disease, and what you can do about it today.

Graves’ disease and Hashimoto’s thyroiditis are actually more related than you might think. Some patients even produce antibodies that both stimulate and block the thyroid’s function.

It is also curious to note that both conditions can show up within the same family, the conditions share certain susceptibility genes, and they both result in lymphocytic infiltration of the thyroid and possibly areas of cell death.1

The Role of Genetics

The simplest question to answer, when trying to ascertain the cause of disease, is the role of genetics versus the role of the environment. With Graves’ disease, there is a recognized role for genetics.

Key Insight: If you have Graves’ disease, then your siblings also have a higher risk, especially if they are female. Some of the genes conferring risk for Graves’ disease also give an increased risk to other autoimmune conditions.1

However, there is definitely a role for environmental and lifestyle factors, and this is encouraging because this is an area where you can have control! Let’s look into some of these factors…

Stress and Graves’ Disease

This one might not surprise you! Stress affects your health in so many ways and was noted as a trigger for Graves’ disease years and years ago. An early study in this area compared 70 patients with Graves’ disease to 70 healthy controls.

Each participant was asked a number of questions about life events in either the year prior to disease onset for the patients, or the year prior to the interview for control participants.

These life events could fall under six different categories:

  1. The entrance of a person (such as marriage)
  2. The exit of a person (such as a death)
  3. Desirable event
  4. Undesirable event
  5. Controlled event
  6. Uncontrolled event

The patients with Graves’ disease had a significantly higher rate of both positive and negative events in each of these categories in the year leading up to their disease onset, and this was especially noticeable for “exits.”2

This association held up even when the researchers excluded events that could have been related to early signs of hyperthyroidism, like anxiety or irritable mood and their effects on relationships.2

Stress and the Relapse of Graves’ Disease

You may be someone who can identify a stressful event or events in the year prior to the onset of Graves’ disease. Can developing methods of coping with your stress now still have a positive impact on disease progression or remission? Definitely!

For example, one study looked at patients on antithyroid treatments for Graves’ disease for one year. After being on that treatment for one year, researchers followed the patients for an additional five years.

Key Insight: Patients who had achieved remission at the end of the five years had fewer stressful events than those who experienced relapses or exacerbations. Those who had relapses or exacerbations experienced a stressful event prior to each relapse or exacerbation.3

This study was not perfect, but other studies point us in the same direction. Another fascinating study looked at people with Graves’ disease before and after beginning antithyroid therapy. What they found was that even smaller sources of stress, calculated by a “daily hassles score” were associated with how effective therapy was.

In women with higher daily hassles scores, there was a 3.9 times increased risk for being in a hyperthyroid state after 12 months of treatment.4 If you’re struggling with daily hassles like getting a good night’s sleep or finding time for your hobbies maybe it’s time to give these items a higher priority in your life.

Not all researchers agree on an association between stress and Graves’ disease.5,6 This is partly because different studies use such different methods that they are difficult to compare or do not allow for us to draw more conclusive results.

For example, various studies may evaluate stressful events in different ways and some may take into account the type of stressful event while others do not.

Bottom Line: Although stress levels are an important component of health, there are other factors besides stress that also play into the development or progression of Graves’ disease.


One of these other factors is smoking. There are several ways in which smoking has been proposed to trigger Graves’ disease: through direct damage to the thyroid cells, through increased inflammation, or through epigenetic changes.7,8 Smoking has also been associated with higher rates of relapse.8

Key Insight: If you need yet another reason to quit smoking you can also consider that smoking greatly increases risks and severity of Graves’ eye disease, while at the same time decreasing responsiveness to treatment.9

This may be partly due to poorer blood flow around the eyes of smokers.10 Quitting is associated with decreased risks for Graves’ eye disease.9

Interestingly, new research is suggesting people with Graves’ disease may not be able to clean up cellular debris as well.7 Make it easier for your body to heal by limiting your exposure to toxicants and decreasing levels of inflammation.


We’ve always been quite adamant about the importance of limiting iodine intake for those with thyroid disease. Did you realize that this impacts Graves’ disease as well as Hashimoto’s thyroiditis?

Once countries started iodine supplementation programs, rates of thyrotoxicosis increased.8 Does this mean everyone will end up with thyrotoxicosis with too much iodine? No, many of these cases occurred in people with pre-existing goiters or pre-existing thyroid antibodies.

Sources of iodine include medications like:


There are a handful of infections with links to the later development of Graves’ disease, including yersinia enterocolitica and Hepatitis C.7 In addition, many patients with Graves’ disease report a viral infection prior to onset.8

How is it possible for microbes to cause a problem with your thyroid? There are several mechanisms that are possible. Two of the more straightforward ones are molecular mimicry and the bystander effect.

Molecular mimicry means some part of the infectious agent looks similar enough to a part of your thyroid that your immune system accidentally attacks your thyroid as well as the infectious agent.

The bystander effect means that your immune system tries to attack the infectious agent, but a little bit of your thyroid gets hurt in the process because of its proximity to the offending agent.


During pregnancy, there is some immune suppression to prevent your immune system from attacking the growing child. Once you’ve given birth, your immune system becomes more vigilant, and in some cases might overdo it, leading to autoimmunity.

The Triggers Behind Graves’ Disease

There are many steps you can take to help your treatment become more effective, such as avoiding certain foods and ensuring the right nutrients and avoiding harmful substances (Read: The foods you must avoid with graves disease).

Each person is different, and a single trigger can’t always be isolated or identified. However, this might be a good time to pause and reflect on what was happening in your life when you were first diagnosed with Graves.’

The Good News

The good news is that, as bad as Graves’ can be, it is reversible for 95% of people. By reversible – I mean that the disease can go into remission and you can be free of symptoms.

Most are unnecessarily rushed off to aggressive treatments like radioactive iodine or thyroid removal surgery. At Integrative Health we are able to help the vast majority of those with Graves’ disease return to normal thyroid function without risky treatments.


1. Davies, T. F. Pathogenesis of Graves’ disease. UpToDate (2018). Available at: of graves&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1. (Accessed: 4th October 2018)
2. Sonino, N. et al. Life events in the pathogenesis of Graves’ disease. A controlled study. Acta Endocrinol. (Copenh). 128, 293–6 (1993).
3. Vita, R., Lapa, D., Trimarchi, F. & Benvenga, S. Stress triggers the onset and the recurrences of hyperthyroidism in patients with Graves’ disease. Endocrine 48, 254–263 (2015).
4. Yoshiuchi, K. et al. Psychosocial factors influencing the short-term outcome of antithyroid drug therapy in Graves’ disease. Psychosom. Med. 60, 592–6
5. Conte-Devolx, B. & Vialettes, B. Can stress induce dysimmune dysthyroidism? Ann. Endocrinol. (Paris). 74, 483–486 (2013).
6. Effraimidis, G., Tijssen, J. G. P., Brosschot, J. F. & Wiersinga, W. M. Involvement of stress in the pathogenesis of autoimmune thyroid disease: A prospective study. Psychoneuroendocrinology 37, 1191–1198 (2012).
7. Struja, T. et al. Is Graves’ disease a primary immunodeficiency? New immunological perspectives on an endocrine disease. BMC Med. 15, 174 (2017).
8. Marinò, M., Latrofa, F., Menconi, F., Chiovato, L. & Vitti, P. Role of genetic and non-genetic factors in the etiology of Graves’ disease. J. Endocrinol. Invest. 38, 283–294 (2015).
9. Bartalena, L. & Piantanida, E. Cigarette smoking: number one enemy for Graves ophthalmopathy. Polish Arch. Intern. Med. 126, 725–726 (2016).
10. Sadeghi-Tari, A. et al. Effect of smoking on retrobulbar blood flow in thyroid eye disease. Eye 30, 1573–1578 (2016).