What is Hashimoto’s thyroiditis? Symptoms, causes and a functional medicine approach

Hashimoto’s thyroiditis is an autoimmune condition in which the immune system produces antibodies that attack the thyroid gland. White blood cells can infiltrate the gland, further damaging thyroid tissue and reducing its ability to produce thyroid hormones.

It is the most common cause of an underactive thyroid in Australia, but Hashimoto’s and hypothyroidism are not the same thing. Hypothyroidism describes insufficient thyroid hormone production. Hashimoto’s is the autoimmune process responsible for damaging thyroid tissues. Treating the hormone deficit without addressing the immune activity leaves the underlying condition unresolved.

Symptoms of Hashimoto’s thyroiditis

Hashimoto’s symptoms fall into two broad patterns: a temporary hyperthyroid phase in earlier stages, and progressive hypothyroid symptoms as the gland loses function. Because the thyroid influences metabolism and nearly every organ system, these symptoms can appear across the body and are frequently attributed to other causes.

The condition is often silent in its early stages. When the gland is actively inflamed, it can release stored hormones into the bloodstream, producing a temporary hyperthyroid phase sometimes called hashitoxicosis. Unlike true hyperthyroidism, this is not caused by the thyroid overproducing hormones. It happens because inflamed thyroid cells release stored hormone into the bloodstream all at once, rather than the thyroid overproducing it. This can present as anxiety, heart palpitations, or irritability and is frequently mistaken for a panic or anxiety disorder. As the gland loses function, hypothyroid symptoms become more consistent.

One of the first physical signs people notice is swelling at the front of the neck from an enlarged thyroid known as Goitre. This can cause a feeling of fullness, pressure, or difficulty swallowing.

Early or fluctuating symptoms:

• Fatigue and low energy
• Anxiety, irritability, or heart palpitations
• Hair thinning or shedding
• Difficulty with concentration or memory
• Swelling at the front of the neck
• Fluctuating bowel motions

Symptoms as thyroid function declines:

• Weight gain despite no change in diet or activity
• Sensitivity to cold
• Dry skin and brittle nails
• Hoarse voice
• Constipation
• Puffy face, particularly around the eyes
• Joint and muscle pain
• Low mood or depression
• Slow heart rate
• Irregular or heavy periods

If Hashimoto’s is not identified and managed, more systemic complications can develop, including elevated cholesterol, high blood pressure, impaired fertility, insulin resistance, and cardiometabolic changes. It is also associated with a higher likelihood of developing other autoimmune conditions, including type 1 diabetes, rheumatoid arthritis, and Addison’s disease. In pregnancy, untreated hypothyroidism carries risks for both mother and baby, which is why thyroid monitoring before and during pregnancy matters.

In rare cases, severely untreated hypothyroidism can progress to myxedema, a life-threatening state involving profound lethargy and loss of consciousness that requires emergency treatment.

What causes Hashimoto’s thyroiditis?

Hashimoto’s develops when a person with a genetic susceptibility encounters one or more environmental triggers that tip the immune system towards an autoimmune response against the thyroid tissues. Hashimoto’s runs in families, and the risk is highest when a close relative has thyroid disease or another autoimmune condition. Genetics alone does not determine who develops it. Environmental triggers play an important part, and in most cases it is the combination of the two that causes the immune system to have an inappropriate response towards the body’s own tissues.

Around 25% of people with one autoimmune condition go on to develop additional autoimmune conditions over their lifetime.

Beyond genetics, several contributing areas are commonly involved:

• Gut dysfunction: The intestinal lining acts as a selective barrier. When that barrier is compromised, partially digested proteins and microbial fragments can pass into the bloodstream. The immune system responds to these as foreign material, and in some people, that response can extend to thyroid tissue. Reduced diversity in the gut microbiome and sensitivities to certain foods can both add to this immune load.
• Infections: Certain viral and bacterial infections appear to initiate or amplify autoimmune thyroid activity in some people. Lingering or reactivated infections may keep the immune response active
• Chronic stress: High cortisol alters how the immune system communicates and suppresses the part of it that acts as a brake on autoimmune activity.
• Hormonal changes: Hashimoto’s is around ten times more common in women than men, and often surfaces or worsens around pregnancy, postpartum, perimenopause, or other periods of hormonal change
• Environmental exposures: Heavy metals, mould, certain chemicals, and excess iodine have all been associated with increased autoimmune thyroid activity. Many people supplement with iodine, believing it supports thyroid health, but in Hashimoto’s, excess iodine without adequate selenium can accelerate immune thyroid activity rather than support it. Total iodine intake above 200mcg per day (including food sources such as seafood, seaweed, dairy, and iodised salt) can become a problem without adequate selenium, so supplementation is best guided by testing rather than general advice

Those with any of the following carry a notably higher risk of developing Hashimoto’s, and vice versa:

• Coeliac disease
• Type 1 diabetes
• Rheumatoid arthritis
• Lupus
• Addison’s disease
• Sjögren’s syndrome
• Pernicious anaemia
• Autoimmune hepatitis
• Vitiligo
• Inflammatory bowel disease

How is Hashimoto’s diagnosed and assessed?

Hashimoto’s is diagnosed through a combination of blood tests, antibody testing, and, in some cases, thyroid ultrasound. Standard testing is a useful starting point, but the full picture often requires looking further.

Thyroid-stimulating hormone (TSH) is the most commonly ordered marker in routine testing, but it can appear normal even when antibody levels are already elevated and immune activity is underway.

Antibody testing is needed to confirm the autoimmune component. A small number of people with Hashimoto’s will test antibody-negative despite having the condition. This can happen because antibody levels fluctuate, or because in later-stage Hashimoto’s the immune system has been active for long enough that antibody production starts to wind down. In these cases, ultrasound findings showing characteristic changes in gland texture, alongside clinical presentation, can still support a diagnosis.

Standard markers include:

• TSH
• Free T4 (tetraiodothyronine )and free T3 (Triiodothyronine )
• Thyroid peroxidase antibodies (TPO-Ab)
• Thyroglobulin antibodies (TgAb)
• Thyroid-stimulating hormone receptor antibodies (TRAb)

An ultrasound of the thyroid can also be useful. It can show changes in gland texture, size, and the presence of nodules that may not be apparent from blood tests alone.

A broader functional assessment looks beyond thyroid markers to examine:

• Nutrient status (selenium, zinc, iron, vitamin D, B12)
• Gut function and intestinal permeability markers
• Inflammatory markers (CRP, ferritin)
• Evidence of past or active infections
• Sex hormone levels, particularly in women experiencing hormonal transitions
• Cortisol patterns and adrenal function
• Other autoimmune markers (ANA, ENA)

Why you can be on thyroid medication and still not feel well

Hashimoto’s often persists after standard treatment because thyroid hormone replacement addresses the hormonal deficit but does not reduce the immuno-inflammatory response towards the thyroid tissue.

Standard treatment involves supplementing thyroid hormones, most commonly with synthetic thyroxine (levothyroxine). This can improve energy, mood, and metabolism by restoring hormone levels in the blood. What it does not do is slow or stop the immune activity that is damaging the gland.

Antibody levels often remain elevated throughout treatment. The immune system continues producing the same response that damaged the gland in the first place, and the original trigger, whether an infection, gut dysfunction, nutritional deficit, or chronic stressor, remains unaddressed.

Many people on thyroid medication still feel unwell for this reason. The hormones are being replaced, but the immune activity continues in the background. As more tissue is damaged, the dose typically needs to increase. If medication is stopped, symptoms often return because nothing has addressed the root cause of the immune response.

Treating Hashimoto’s: a functional medicine approach

A functional medicine approach to Hashimoto’s begins with the person, their clinical history, symptom patterns, how they have responded to previous treatment, and the factors that may have contributed to the condition developing. Testing builds on that foundation rather than replacing it.

Depending on your presentation, care may include:

• Dietary change: gluten is commonly removed first, as it can increase gut permeability and increase immune activity in people with Hashimoto’s; an anti-inflammatory whole food diet emphasising selenium, zinc, iron, and B vitamins supports both thyroid hormone production and conversion
• Gut restoration: targeted probiotics, prebiotic-rich foods, and gut lining support can reduce the immune stimulation that originates in the gut, which often persists beyond dietary change alone
• Nutritional support: selenium plays a direct role in reducing TPO and thyroglobulin antibodies and supporting T4 to T3 conversion; vitamin D, zinc, magnesium, and iron are commonly deficient and assessed through functional testing rather than supplemented broadly
• Addressing infections and exposures: where testing identifies a past or active infection, mould exposure, or heavy metal accumulation, addressing it directly can reduce the immune stimulation it is generating
• Stress and nervous system support: chronic stress keeps the immune system in an activated state; improving sleep, regular movement, and practices such as breathwork or mindfulness are as important as dietary or supplementation changes
• Ongoing monitoring: as immune activity reduces, thyroid function can improve, and hormone requirements may change; monitoring and adaptation are built into the approach from the start

When to seek support

See your GP or a practitioner if you have:

• Persistent fatigue or low energy without a clear cause
• Unexplained weight changes
• Symptoms that don’t fit neatly into a single explanation
• Already on thyroid medication but continuing to feel unwell
• Antibody levels that remain elevated despite treatment
• Profound lethargy, confusion, or loss of consciousness, which requires immediate medical attention at the emergency department

Frequently asked questions

Does Hashimoto’s cause brain fog?

Yes. Brain fog is one of the most common cognitive complaints in Hashimoto’s. Low thyroid hormone affects brain tissue directly, and even mild insufficiency can impair concentration, memory, and mental clarity. Ongoing immune activity generates inflammatory signalling that compounds this, meaning cognitive symptoms can persist even when hormone levels appear adequate on standard testing.

Why might I still feel unwell on thyroid medication?

Persistent symptoms on thyroid medication are common because levothyroxine replaces T4 but does not address the underlying immune activity or impaired T4 conversion. Conversion into active T3 depends on adequate selenium and zinc, which are commonly depleted in Hashimoto’s. When conversion is impaired, cognitive and physical symptoms can persist regardless of how much T4 is being supplied.

Is Hashimoto’s the same as hypothyroidism?

No. Hypothyroidism describes low thyroid hormone output and can have several causes. Hashimoto’s is the autoimmune condition most commonly responsible for it, in which the immune system progressively destroys thyroid tissue. Treating only the hormone deficit does not address the autoimmune activity.

Can you have Hashimoto’s with normal TSH levels?

Yes. TSH can remain within the standard reference range while thyroid antibody levels are significantly elevated. This is particularly common in earlier stages of the condition. Testing for thyroid antibodies is needed to identify Hashimoto’s when TSH appears normal.

Does Hashimoto’s ever go into remission?

Hashimoto’s can improve significantly when the underlying contributors, including gut dysfunction, nutritional deficiencies, chronic stress, or identifiable infections, are identified and addressed. Antibody levels can reduce substantially and thyroid function can improve as a result. The extent of recovery depends partly on how much thyroid tissue has already been damaged.

How does Hashimoto’s affect pregnancy?

With appropriate monitoring and management, pregnancy is achievable for most people with Hashimoto’s. Thyroid hormone requirements increase during pregnancy, and unmanaged hypothyroidism carries risks for both mother and baby, including miscarriage, premature birth, and developmental effects. Thyroid function is monitored more closely before conception and throughout pregnancy, and medication may need to be adjusted or initiated.

Why do symptoms vary so much day to day?

During active Hashimoto’s, damaged thyroid follicles can release stored hormone into the bloodstream, temporarily raising levels and producing hyperthyroid-like symptoms such as anxiety, palpitations, and irritability. As these bursts ease, fatigue and other hypothyroid symptoms return. This fluctuation is a recognised feature of the condition, not a sign that something else is wrong.

Can diet really make a difference with Hashimoto’s?

Diet can reduce the immune stimulation that originates in the gut, and for many people this also reduces symptoms. Gluten is a particular consideration because it can increase intestinal permeability and amplify immune activation. Removing it alongside other inflammatory foods is associated with reduced symptoms and, in some cases, lower antibody levels.