Autoimmune Thyroid Disease: The Hidden Role of Chronic Infections in Hashimoto’s

Autoimmune thyroid disease is often misunderstood as a problem that begins in the thyroid, when in reality it starts much earlier within the immune system. Hashimoto’s, the most common cause of hypothyroidism, develops when chronic immune activation shifts the body into a state of inflammation and oxidative stress. In this blog, we’ll explore how immune imbalance sets the stage for Hashimoto’s and how chronic infections fuel the autoimmune cascade.

The Immune System’s Role in Hormone Health

The immune system and endocrine (hormone) system are in constant communication. Hormones like cortisol, estrogen, and thyroid hormones help regulate immune function, and in turn, immune activity directly impacts hormone production, signaling, and breakdown. 

When the immune system becomes chronically activated, from persistent infections, toxins, gut dysbiosis, or environmental exposures, it releases pro-inflammatory compounds called cytokines, fueling excess oxidative stress. While short bursts of oxidative stress are completely normal, chronic oxidative stress pushes the immune system into a persistent “high alert” mode.

Over time, this ongoing activation disrupts immune tolerance. Regulatory T-cells, which normally protect against autoimmunity and excessive inflammation, become less effective, cytokine patterns shift toward inflammation, and the body begins to struggle to distinguish “self” from “non-self.” This is the earliest stage of autoimmunity.

Chronic immune activation also drains metabolic resources. The body prioritizes essential survival functions like maintaining blood pressure, heart rate, and stress hormones over reproduction and hormone balance. As a result, hormone production, follicle development for ovulation, and thyroid hormone activation all decline. This can lead to fatigue, irregular cycles, acne, fertility challenges, slowed metabolism, elevated inflammation markers like C-Reactive Protein (CPR), low white blood cell counts, and even flu-like symptoms around your period.

Understanding Hashimoto’s Thyroiditis

Hashimoto’s thyroiditis is an autoimmune condition in which the immune system mistakenly targets cells of the thyroid gland, creating inflammation and gradually damaging thyroid tissue over time. 

Although many people think of Hashimoto’s as a “thyroid hormone problem,” it doesn’t begin that way. Hashimoto’s starts as an immune system imbalance that impacts the thyroid, and only later becomes an issue of thyroid hormone imbalance once enough tissue has been affected. In fact, Hashimoto’s can be present for years, even decades, before hypothyroidism develops. 

The Development of Hashimoto’s

Many individuals have elevated thyroid antibodies – thyroid peroxidase (TPO) antibodies or thyroglobulin (TgAb) antibodies – while thyroid stimulating hormone (TSH), Free T4, and Free T3 remain within normal ranges. This early stage is often missed in conventional care because testing thyroid antibodies is not standard practice and symptoms can be subtle or dismissed, even though immune damage is already underway.

We classify Hashimoto’s according to 6 different stages. These stages reflect its progression from simple genetic predisposition to silent thyroid autoimmunity, where antibodies are present but thyroid function is still normal. Next comes subclinical and then overt hypothyroidism as thyroid hormone output begins to shift and TSH rises. At this stage, symptoms often become much more apparent and you’re more likely to receive a diagnosis accompanied by treatment with thyroid medication.

If untreated, Hashimoto’s can further develop into its most advanced stages, leading to progressive thyroid damage and eventually complete thyroid failure if it continues to go unaddressed.

Early Identification Is Key

This progression happens over many years, if not decades. That’s why identifying Hashimoto’s early, before thyroid hormone levels drop, is one of the best opportunities for slowing, stopping, or even partially reversing Hashimoto’s progression. By addressing immune triggers such as chronic infections, it’s possible to reduce antibody levels and protect remaining thyroid tissue.

How Chronic Infections Fuel Autoimmunity

The immune system is built to handle acute threats, like identifying an infection, neutralizing it, and returning to baseline. However, some viruses can hide within tissues and remain dormant for years, reactivating during times of stress or immune weakness. This keeps the immune system chronically activated and adds to overall viral load. Over time, this persistent activation wears down immune tolerance and increases the risk of developing autoimmune diseases like Hashimoto’s.

The Problem with Persistent Infections

Epstein-Barr virus (EBV) is one of the most researched infectious triggers for Hashimoto’s and other autoimmune conditions. More than 90% of the global population has contracted EBV, with infections ranging from completely asymptomatic to classic infectious mononucleosis (“mono”). It lives inside immune B cells and can reactivate during periods of stress, inflammation, or hormonal shifts. 

Current research links EBV not only to autoimmune disease but also to long-COVID. Interestingly, EBV infections acquired in later adolescence or adulthood are associated with a greater risk of other autoimmune diseases as well, such as multiple sclerosis and lupus, compared to infections contracted in early childhood.

Other persistent infections can similarly disrupt the immune system. Cytomegalovirus (CMV) and Herpes Simplex Virus (HSV) drive chronic immune activation and oxidative stress much like EBV. Lyme disease and its co-infections can mimic human proteins, confusing immune regulation, while parasites and gut infections increase intestinal permeability, inflammation, and immune activation.

The Importance of Total Viral Burden

It’s also important to consider overall viral burden, not just reactivation of a single pathogen. High levels of one or several chronic viral infections place cumulative strain on the immune system, regardless of whether or not specific triggers lead to overt reactivation of these infections. 

Understanding whether chronic immune activation is at play is key for addressing autoimmunity and immune dysregulation. Persistent infections generate significant oxidative stress and continually stimulate immune pathways. Over time, the immune system loses resilience, regulatory T cells lose tolerance, and the stage is set for autoimmunity and Hashimoto’s.

A Functional Approach to Restoring Immune Balance

At the root of every autoimmune condition is some level of immune dysregulation. Whether this imbalance manifests as Hashimoto’s or another immune condition depends on genetics, gut health, hormonal shifts, nutrient deficiencies, environmental triggers, and more. 

Managing Hashimoto’s requires more than thyroid medication, and we must address the underlying problem – an overactivated, dysregulated immune system. A functional approach focuses on restoring immune balance by treating dormant or chronic infections, healing the gut to rebuild immune tolerance, reducing inflammation and oxidative stress, supporting detoxification and energy availability, and optimizing nutrients that modulate immune pathways.

Because every case of Hashimoto’s is unique, a personalized treatment plan is essential. Advanced functional testing can pinpoint the specific drivers, especially chronic infections, behind immune dysregulation. 

In our 1:1 Coaching Program we utilize advanced testing alongside Micro-immunotherapy to help retrain immune responses rather than suppress them. This allows for targeted individualized treatment to address the root causes of your autoimmunity – restoring immune balance, protecting thyroid tissue, and preventing the progression of Hashimoto’s. Book your free discovery call today! 

Written by Romana Brennan, MS, RDN