Hashimoto’s thyroiditis is an autoimmune disease in which the immune system attacks the thyroid gland, eventually reducing its ability to produce thyroid hormones.
Standard treatment usually involves replacing deficient thyroid hormone with levothyroxine. This works well for many people, but it does not directly address why the autoimmune process developed.
Researchers are studying the possible roles of genetics, nutrition, nutrient deficiencies, infections, the gut microbiome, and other environmental factors. Functional-medicine physicians are particularly interested in whether addressing some of these factors may improve symptoms or markers of thyroid autoimmunity.
Hashimoto’s disease is the most common cause of hypothyroidism in the United States. The immune system produces antibodies—most commonly thyroid peroxidase (TPO) antibodies—that target components of the thyroid gland.
The disease often develops gradually. As thyroid tissue becomes damaged, the gland may no longer produce enough thyroid hormone. Symptoms can include fatigue, feeling cold, weight gain, constipation, dry skin, muscle weakness, and difficulty concentrating, although symptoms vary widely.
Diagnosis usually includes blood tests measuring TSH and thyroid hormone levels, and often thyroid antibodies. Some people have elevated thyroid antibodies for years while their thyroid hormone levels remain normal.
This makes Hashimoto’s unusual among autoimmune diseases: physicians can often measure both thyroid function and evidence of the autoimmune response with relatively simple blood tests.
When Hashimoto’s causes hypothyroidism, standard treatment is thyroid hormone replacement, most commonly levothyroxine, a synthetic form of the thyroid hormone T4. The dose is adjusted primarily by monitoring TSH and thyroid hormone levels.
For many people, this treatment restores normal thyroid hormone levels and relieves symptoms. It is well studied, inexpensive, and generally effective.
Thyroid hormone replacement does not, however, directly stop the autoimmune process that caused the thyroid damage. Researchers are therefore studying whether diet, nutrient status, gut health, metabolic health, or other environmental factors can influence thyroid autoimmunity itself.
Functional-medicine physicians tend to place greater emphasis on identifying and modifying these possible contributors, while conventional endocrinology generally requires stronger clinical evidence before incorporating such approaches into routine treatment.
Diet is one of the most debated aspects of Hashimoto’s disease. People with autoimmune thyroid disease have a higher prevalence of celiac disease, and anyone with both conditions needs to follow a strict gluten-free diet.
The more difficult question is whether people with Hashimoto’s without celiac disease benefit from avoiding gluten. Some small studies have reported reductions in thyroid antibodies or changes in thyroid function after a gluten-free diet, but the evidence remains limited and inconsistent.
Functional-medicine physicians such as Datis Kharrazian, Mark Hyman, and Susan Blum often recommend eliminating gluten as part of a broader dietary approach. They report that some patients experience improvements in symptoms and thyroid antibody levels.
Other dietary approaches—including elimination diets, Mediterranean-style diets, and low-carbohydrate diets—are also being investigated. At present, there is no single diet that has been proven best for everyone with Hashimoto’s, but diet is a legitimate and active area of research.
Several nutrients are being studied for their possible effects on thyroid autoimmunity.
Selenium is required for normal thyroid function and antioxidant defenses. Clinical trials and meta-analyses suggest that selenium supplementation can reduce thyroid antibody levels in some people with Hashimoto’s, although it is not yet clear whether this consistently improves symptoms or prevents progression to hypothyroidism. Excess selenium can also be harmful.
Vitamin D deficiency is more common in people with Hashimoto’s in many studies. Some trials suggest that correcting deficiency may reduce thyroid antibody levels, but evidence that supplementation changes the long-term course of the disease remains limited.
Iodine is essential for thyroid hormone production, but both too little and too much can cause problems. In susceptible people, excessive iodine intake may worsen thyroid autoimmunity.
These findings illustrate an important principle: nutrient status may matter, but more is not necessarily better. Testing for deficiencies and correcting them is different from taking large doses of supplements without evidence of need.
Functional medicine takes a broader approach to autoimmune disease. Rather than focusing only on treating symptoms or replacing hormones, it asks what factors might be contributing to the autoimmune response. These may include diet, nutrient deficiencies, intestinal permeability, the gut microbiome, infections, stress, environmental exposures, and metabolic health.
Datis Kharrazian has been particularly influential in applying this approach to Hashimoto’s disease. Susan Blum and Mark Hyman use similar strategies within broader programs for autoimmune disease.
Their goal is not simply to normalize thyroid hormone levels, but to reduce autoimmune activity, improve symptoms, and, when possible, achieve remission. Some patients and physicians report substantial improvement, including reductions in thyroid antibodies.
One practical approach is to make reasonable dietary or lifestyle changes and see whether measurable improvements occur. Symptoms can be followed along with TSH and thyroid hormone levels and, in some circumstances, thyroid antibodies. Changes in antibody levels need to be interpreted cautiously, but objective measurements can make this more informative than relying on symptoms alone.
Many individual components of the functional-medicine approach have scientific support, although evidence for the complete program remains limited. Carefully monitored individual experimentation may therefore be reasonable while the research continues to develop.
Hashimoto’s is an autoimmune disease, not simply a problem of low thyroid hormone.
Thyroid hormone replacement is effective for treating hypothyroidism, but it does not directly address the autoimmune process that caused the thyroid damage.
Diet, gluten, selenium, vitamin D, gut health, and other environmental factors are legitimate areas of research, although the strength of the evidence varies.
Functional-medicine physicians place greater emphasis on identifying and modifying possible contributors to thyroid autoimmunity and report substantial improvement in some patients.
Because thyroid function and antibodies can be measured, Hashimoto’s offers an opportunity for carefully monitored individual experimentation with reasonable diet and lifestyle changes.
Remission is an intriguing possibility, but improvements in symptoms or antibody levels should not automatically be interpreted as a cure.
A clear medical overview of Hashimoto’s disease, including its causes, diagnosis, thyroid antibodies, & standard treatment with thyroid hormone replacement.
A 2024 review of 35 studies found that selenium supplementation reduced TPO antibody levels and, in some patients, TSH, although not all measures of thyroid function improved
Kharrazian explains his functional-medicine approach to Hashimoto’s, including possible roles of diet, gut health, immune regulation, & environmental factors.
A practical guide to identifying and addressing potential contributors to Hashimoto’s symptoms, including nutrition, stress, gut health, infections, and environmental exposures.
Explores the possible relationship between gluten sensitivity, intestinal health, and Hashimoto’s disease, and discusses why some people with Hashimoto’s may benefit from investigating whether gluten contributes to their symptoms or autoimmune activity.
Dr. Hyman and colleagues discuss Hashimoto’s and other thyroid disorders, including thyroid antibodies, gluten, nutrient deficiencies, gut health, environmental factors, and the functional-medicine approach to finding underlying causes.