Author: Alinda Coleman
The thyroid gland is one of the unsung powerhouses of the body – its crucial roles involve controlling our metabolic rate, body temperature, energy levels, and growth and development. If not enough thyroid hormone is produced by the thyroid gland, our metabolic rate and the systems of the body slow down – this is known as hypothyroidism or an underactive thyroid.1 At the opposite end of the spectrum, too much thyroid hormone can cause a speeding up of metabolic processes resulting in an overactive thyroid, also known as hyperthyroidism.1
As thyroid hormone acts directly on the brain, gastrointestinal system, cardiovascular system, bone metabolism, red blood cell metabolism, gall bladder and liver function, steroid hormone production, glucose metabolism, lipid and cholesterol metabolism, protein metabolism and body temperature regulation, any imbalance in thyroid function - producing either too much or too little thyroid hormone - can have significant and widespread effects throughout the entire body.1 Thyroid conditions are relatively common (more so in women) and are on the rise. It may also be surprising to learn that immune dysfunction has a fundamental role in the development of many thyroid disorders.1
The thyroid gland and autoimmune disease
Did you know that autoimmune thyroid disease is the most common cause of thyroid dysfunction in Australia?2 Hashimoto’s disease, the most common cause of hypothyroidism, occurs when the cells of the immune system mistakenly attack the thyroid gland, causing inflammation and destruction of the thyroid. This destruction greatly reduces the thyroid’s ability to secrete thyroid hormone, and leads to a slowing down of the body’s metabolic processes.3
Grave’s disease, frequently associated with hyperthyroidism, is also an autoimmune condition. In this instance, the immune system produces antibodies that stimulate the thyroid gland to grow, with the follicles inside producing an excessive amount of thyroid hormone, leading to a speeding up of the metabolic processes in the body.3
What triggers an autoimmune reaction?
Autoimmune conditions are complex but can be triggered or caused by a number of factors including physical and emotional stress, environmental triggers (iodine, medications, infection, smoking), genetics, and leaky gut (increased intestinal permeability), to name a few.3,4
What’s the link between gluten, coeliac disease and autoimmune thyroid disease?
Prospective studies have identified an increased prevalence of coeliac disease (CD) in patients with autoimmune thyroid disease4,5 In susceptible individuals with CD, when they eat gluten-containing foods, an autoimmune response can be triggered in the body.5 Treatment of CD with a gluten-free diet may reduce the recognised complications of this disease and provide benefits in general health.5
How can a complementary health practitioner help?
There is no ‘one size fits all’ when it comes to treating thyroid conditions, particularly when the immune system is dysfunctional. An individualised and thorough treatment plan works best for these conditions. A complementary heath care practitioner can provide an individually tailored treatment plan that helps to normalise immune function, reduce inflammation and restore thyroid health through dietary advice, lifestyle advice, and if indicated, herbal and nutritional supplementation.
Speak to your healthcare practitioner for more information about looking after your thyroid health.
To find a healthcare practitioner in your local area, use our Find a Practitioner service.
1. Hechtman L. Clinical naturopathic medicine. Chatswood: Elsevier, 2012.
2. Walsh JP. Managing thyroid disease in general practice. Med J Aust 2016 Aug 15;205(4):179-84.
3. Iddah MA, Macharia BN. Autoimmune thyroid disorders. ISRN Endocrinol 2013 Jun 26;2013:509764.
4. Lin R, Zhou L, Zhang J, et al. Abnormal intestinal permeability and microbiota in patients with autoimmune hepatitis. Int J Clin Exp Pathol 2015;8(5):5153-5160
5. Ch'ng CL, Jones MK, Kingham JG. Celiac disease and autoimmune thyroid disease. Clin Med Res 2007 Oct;5(3):184-92.