HASHIMOTO'S THYROIDITIS SCIENCE

Beyond TSH:
Understanding Your Immune Attack

Standard thyroid testing tells you IF you have Hashimoto's, but not whether the immune attack is still active. IgG subtyping reveals if immune modulation could help—or if your disease has already burned out.

The "Your Labs Are Normal" Problem

If you have Hashimoto's thyroiditis, you're probably familiar with this conversation: "Your TSH is controlled on levothyroxine, so you're fine." Meanwhile, you still feel exhausted, your brain fog continues, and your antibodies keep rising year after year.

What Standard Testing Misses:

  • TSH just measures hormone replacement—not immune activity
  • Anti-TPO and Anti-TG tell you that you have Hashimoto's—not if the attack is still active
  • Rising antibodies are dismissed as "expected with Hashimoto's"
  • No one discusses whether immune modulation could help

Here's the problem: Levothyroxine replaces thyroid hormone but does nothing to stop the immune attack. For some patients, the attack is still raging. For others, it's already subsided. The key is knowing which one you are.

IgG Subtyping: Active vs Burned-Out Disease

The most important test your doctor isn't ordering

ACTIVE INFLAMMATION

IgG1 & IgG3 Dominance

What this means: IgG1 and IgG3 are inflammatory antibody subtypes. When these dominate your Anti-TPO and Anti-TG antibodies, it means your immune system is CURRENTLY attacking your thyroid gland—actively destroying thyroid tissue.

Think of it like this: IgG1/IgG3 antibodies are like soldiers actively shooting at your thyroid. The attack is happening right now. Every day, more thyroid cells are being destroyed.

What we test:

Anti-TPO IgG1, Anti-TPO IgG3, Anti-TG IgG1, Anti-TG IgG3, total IgG subclasses

If this is YOU, consider these interventions:

Low-dose naltrexone (LDN), selenium supplementation, vitamin D optimization, possible immunomodulation therapy. The goal is to calm the active attack.

BURNED-OUT DISEASE

IgG4 Dominance

What this means: IgG4 is a non-inflammatory antibody subtype. When IgG4 dominates your thyroid antibodies, it suggests the active inflammatory phase has ended. Your immune attack has largely "burned out."

Think of it like this: IgG4 antibodies are like retired soldiers standing around after the war is over. They're still there, but they're not causing active damage anymore.

What we test:

Anti-TPO IgG4, Anti-TG IgG4, IgG4 to total IgG ratio

If this is YOU:

Aggressive immune suppression won't help much since the attack has already subsided. Focus on optimizing thyroid hormone replacement and managing remaining symptoms.

Additional Immune Pathways in Hashimoto's

Th1 Pathway (Cell-Mediated Attack)

What's happening: Th1 cells release interferon-gamma (IFN-γ) and activate cytotoxic T-cells that directly attack thyroid tissue. This is a cell-mediated immune response—meaning immune cells themselves are destroying your thyroid, not just antibodies.

Clinical significance: High Th1 activity suggests active cellular destruction. May respond to immune modulation with low-dose naltrexone (LDN), selenium, or vitamin D.

What we test:

IFN-γ, IL-2, TNF-α, IL-12

Th17 Pathway (Inflammatory Component)

What's happening: IL-17 promotes tissue inflammation and recruits neutrophils to the thyroid gland. This pathway is more common in aggressive, inflammatory Hashimoto's with rapid antibody rise and symptomatic disease despite "normal" TSH.

Clinical significance: Elevated IL-17 suggests ongoing inflammation that may benefit from anti-inflammatory interventions beyond just thyroid hormone replacement.

What we test:

IL-17A, IL-23, IL-6, IL-21

Why This Testing Matters

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Know If Immune Therapy Makes Sense

If your disease has burned out (IgG4 dominant), aggressive immune modulation won't help. But if you have active inflammation (IgG1/IgG3), interventions could slow or stop thyroid destruction.

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Guide Treatment Decisions

Understanding your immune profile helps your doctor make informed decisions about LDN, selenium, vitamin D dosing, and whether more aggressive interventions are warranted.

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Monitor Disease Activity

Track whether your immune attack is progressing, stable, or subsiding. This helps you and your doctor adjust your treatment approach over time.

The Research Behind IgG Subtyping

Studies show that IgG1/IgG3-dominant Hashimoto's patients have more active disease, higher inflammatory markers, and greater thyroid destruction. IgG4-dominant patients show less inflammation and more stable disease. This isn't experimental—it's established immunology applied to clinical care.

Supporting Factors We Test

Complete Thyroid Panel

TSH, Free T4, Free T3, Reverse T3, TBG (thyroid binding globulin). Shows if you're converting T4 to active T3 and if you might benefit from T3 supplementation.

Nutrient Deficiencies

Vitamin D, selenium, zinc, iron, B12. All affect thyroid function and immune regulation. Correcting deficiencies can reduce antibodies and improve symptoms.

Regulatory Cytokines

IL-10, TGF-β. These anti-inflammatory cytokines help control autoimmune responses. Low levels mean your immune system lacks proper "brakes."

Celiac Screening

Hashimoto's and celiac disease frequently occur together. Testing for tissue transglutaminase antibodies helps identify this common comorbidity.

Understand Your Thyroid Immune Attack

Know if you have active inflammation or burned-out disease with IgG subtyping.

See Hashimoto's Testing Options →