Autoimmune Thyroid Conditions

Autoimmune thyroid conditions occur when the immune system mistakenly attacks the thyroid gland or its receptors, impeding its optimal function.

This attack is carried out by antibodies — proteins produced by the immune system that are designed to identify and neutralise foreign threats such as bacteria and viruses. In autoimmune conditions, these antibodies mistakenly target the body's own tissues instead.

Autoimmune thyroid conditions are among the most common autoimmune disorders worldwide, affecting an estimated 5% of the general population — with women up to 10 times more likely to be affected than men.

Each of these triggers shares a common pathway — driving chronic immune activation until the immune system loses its ability to distinguish between foreign invaders and the body's own tissues.

The good news? Many of these triggers are modifiable. Part 3 covers our top evidence-based tips for reducing your risk.

One of the most common reasons autoimmune thyroid conditions go undiagnosed for years is that standard testing is often incomplete. A routine GP thyroid panel typically only includes TSH — which, while useful, does not provide a full picture of thyroid function or immune activity.

A comprehensive thyroid panel should include:

TSH (Thyroid Stimulating Hormone) High TSH suggests an underactive thyroid, low TSH suggests overactive. However TSH alone cannot identify the cause, confirm autoimmune activity, or detect subclinical dysfunction in all cases.

Free T4 (fT4) Measures the unbound, biologically available fraction of T4 circulating in the bloodstream. More clinically meaningful than total T4.

Free T3 (fT3) Measures the active, unbound fraction of T3. Critical for assessing conversion — a person can have normal TSH and T4 but insufficient active T3 if conversion is impaired. This marker is frequently omitted from standard panels.

Reverse T3 (rT3) (functional testing) When the body is under chronic stress, T4 is preferentially converted into inactive reverse T3 rather than active T3, blocking T3 receptors and impairing cellular function.

TPO Antibodies (Anti-TPO) The primary antibody marker for Hashimoto's thyroiditis and autoimmune thyroiditis. Elevated levels indicate active immune activity targeting the thyroid, often present years before TSH becomes abnormal.

Thyroglobulin Antibodies (TgAb) A secondary antibody marker for Hashimoto's. Some people with Hashimoto's have elevated TgAb but normal TPO antibodies, making it important to test both.

TSH Receptor Antibodies (TRAb) / Thyroid Stimulating Immunoglobulins (TSI) The key antibody markers for Graves' disease. Elevated TRAb or TSI confirms autoimmune hyperthyroidism and differentiates Graves' from other causes of elevated thyroid hormone.

If you suspect a thyroid condition, request TSH, fT3, fT4, TPO antibodies, and TgAb as a minimum. If Graves' is suspected, add TRAb or TSI.

Hashimoto’s Thyroiditis and Autoimmune Thyroiditis

Hashimoto's thyroiditis is the most common autoimmune thyroid condition. The immune system gradually damages the thyroid by producing antibodies — TPO and/or TgAb — that target the proteins involved in thyroid hormone production, progressively reducing the thyroid's ability to produce T3 and T4. This leads to hypothyroidism (high TSH, low T3/T4).

Autoimmune thyroiditis (AIT) refers to the same underlying disease process with one key distinction — the absence of a goitre. In Hashimoto's, local autoimmune inflammation causes the thyroid gland to swell, producing a visible or palpable mass at the base of the neck. In AIT, this swelling is absent and the gland may instead atrophy over time.

NOTE: As the immune system attacks and damages thyroid tissue, the gland can release a flood of stored hormone into the bloodstream, causing a temporary period of feeling wired, anxious, and hyperthyroid before settling back into its underactive state.

Graves’ Disease (GD)

Graves' disease accounts for 60–80% of hyperthyroidism cases and is most commonly diagnosed in women between the ages of 40–60. Unlike Hashimoto's, where antibodies damage thyroid tissue directly, Graves' involves antibodies — known as thyroid stimulating immunoglobulins (TSI) or TSH receptor antibodies (TRAb) — that mimic TSH and bind to TSH receptors on the thyroid, continuously overstimulating it to produce excess hormone. This results in hyperthyroidism (low TSH, high T3/T4).

Additional manifestations: In approximately 25–30% of cases, the same antibodies responsible for overstimulating the thyroid also trigger inflammation behind the eyes — known as thyroid eye disease (TED). This can cause the eyes to appear bulging or prominent, along with dryness, irritation, light sensitivity, and in more severe cases double vision or changes in eyesight. TED can occur before, during, or even after Graves' disease is treated, making it important to monitor eye health alongside thyroid health.

Postpartum Thyroiditis

Postpartum thyroiditis occurs in approximately 5-10% of women in the year following childbirth. It is thought to be triggered by the dramatic immune system rebound that occurs after delivery, as the immune suppression that protects the baby during pregnancy is lifted. It typically presents in two phases — an initial hyperthyroid phase followed by a hypothyroid phase — before resolving. However, up to 25% of women go on to develop permanent hypothyroidism.

Symptoms are frequently attributed to the demands of new motherhood rather than thyroid dysfunction, making this condition significantly underdiagnosed.

Thyroid function should be monitored for at least 12 months following delivery and annually thereafter, particularly in women with a personal or family history of autoimmune thyroid conditions or those who have experienced postpartum thyroiditis previously.

Silent Thyroiditis

Silent thyroiditis follows a similar pattern to postpartum thyroiditis but occurs independently of pregnancy. It is characterised by painless inflammation of the thyroid and often goes undetected as symptoms can be mild or mistaken for other conditions.

Ords Thyroiditis

Ord's thyroiditis is closely related to Hashimoto's thyroiditis and is often considered a variant of it. The key distinction is that rather than causing the thyroid to enlarge (goitre), Ord's thyroiditis causes the thyroid gland to atrophy and shrink over time. It is thought to be more prevalent in iodine-sufficient regions and may actually account for a significant proportion of cases currently diagnosed as Hashimoto's.

Want to know how to avoid this?

Part 3 —> Tips to reduce your risk