Understanding How Hashimoto’s Thyroiditis Affects Your Body

How Does Hashimoto’s Thyroiditis HAPPEN

Hashimoto’s thyroiditis is the most common cause of hypothyroidism (an underactive thyroid) in the U.S. Hashimoto’s is an autoimmune disease—which means your immune system mistakenly attacks your own healthy tissue. It commonly co-exists with other autoimmune diseases like Type 1 Diabetes,  RA, SLE, liver conditions, Sjogren’s and Celiac.


The Triggers for hashimoto’s thyroiditis

Thyroid level changes can be transient, due to infection or medications.  Aging individuals probably have different ‘normals’ for their levels which haven’t been worked out. So, the diagnosis cannot always be rushed. Obesity and adrenal stress alters your levels and not necessarily he cause or the diagnosis of Hashimoto’s. Low iodine, b vitamin anemias, toxins, heavy metals, nutrient deficiencies and food intolerances are implicated in the cause.  A Essential elements including selenium, zinc, copper, iron or fluorine are critical for normal thyroid hormone producti or exposure to toxic (cadmium or lead) or potentially toxic elements (manganese or chromium) interacts with thyroid hormone synthesis

The Immune System Turns on the Thyroid

In Hashimoto’s, the immune system targets the thyroid gland, a small, butterfly-shaped gland at the base of your neck. Thyroid hormones control metabolism and energy. Specifically the metabolism of all fats, carbohydrates, proteins, minerals, and electrolytes and for regulating body temperature.

The first step in this autoimmune process is infiltration of the thyroid by lymphocytes, a type of white blood cell. T-cell lymphocytes are part of your body’s natural defense system.  In Hashimoto’s, they invade the thyroid as if an infection or threat.

This infiltration is potentiated or worsened by antibodies—specifically anti-thyroid peroxidase antibodies (TPOAbs). These antibodies mistakenly bind to an enzyme in thyroid cells called thyroid peroxidase (TPO). TPO plays a key role in thyroid hormone production.


Destruction of Thyroid Cells

TPO is targeted by TPOAbs marks those cells for destruction. A cascade of inflammation and damage ensues, leading to the destruction of thyrocytes (the hormone-producing cells of the thyroid).

More and more thyrocytes are damaged or destroyed. The gland becomes less and less able to make thyroid hormones. Resulting in hypothyroidism your metabolism slows and symptoms like fatigue, weight gain, cold sensitivity, dry skin, and depression begin to appear.


Early Testing Matters

The earliest and most specific sign of Hashimoto’s is the presence of TPO antibodies, detectable before thyroid hormone levels drop. That’s why checking for TPOAb levels, especially in those with a family history or symptoms of thyroid disease, is a critical part of early diagnosis. Watching TPO Antibody levels over time is less helpful for ongoing thyroid medicine management.


Bottom Line

Hashimoto’s isn’t “just” low thyroid—it’s an active autoimmune condition progressively damaging the thyroid gland through a misdirected immune response. Recognizing and treating it early slows the cascade of symptoms. Treating with thyroid will lower total body inflammation including help normalize your CRP.

If you’re experiencing signs of thyroid imbalance or have a personal or family history of autoimmune disease, ask your provider about a full thyroid panel—including TPO antibody testing.