THE THYROID–IRON–METABOLISM CONNECTION

Thyroid symptoms often have little to do with the thyroid itself. Instead, they frequently stem from a systemic metabolic bottleneck driven by iron overload. Excess iron disrupts liver function, slows bile flow, creates insulin resistance, promotes estrogen dominance, and primes the immune system for autoimmunity — all of which impair thyroid hormone production and conversion.

Iron is essential for thyroid hormone synthesis and metabolism, but excess iron becomes a

metabolic toxin.

Excess iron accumulates in the liver, pancreas, thyroid, and gut, where it:

• Generates oxidative stress, damaging tissues
• Drives insulin resistance in the liver and peripheral tissues Slows bile flow, impairing detoxification and hormone clearance
• Promotes estrogen dominance through reduced clearance
• Disrupts the microbiome, increases gut inflammation, and allows LPS and other toxins to enter the bloodstream

The result: a metabolic bottleneck that affects the thyroid, hormones, and immune system

simultaneously.

Too much iron = too little energy.

It’s the hidden cause of sluggish thyroid conversion, insulin resistance, poor bile flow, gut

inflammation, and estrogen dominance.

The liver is the control center where thyroid, estrogen, and iron metabolism intersect.

The liver converts T4 → T3 (active thyroid hormone), produces proteins like thyroid-binding

globulin (TBG), clears estrogen, manages bile flow, and regulates iron through hepcidin.

When iron overload inflames the liver:

• Deiodinase enzymes that convert T4 → T3 are impaired → low T3, high reverse T3 (rT3).
• Insulin receptors become resistant → hepatic insulin resistance.
• Bile flow slows as oxidative stress damages hepatocytes and bile canaliculi.
• Estrogen builds up because detox pathways (methylation, sulfation, glucuronidation) stall.

Impaired bile flow, often driven by iron overload, creates multiple layers of metabolic

dysfunction. Sluggish bile slows the conversion of T4 to active T3, resulting in low T3 levels and

elevated reverse T3 (rT3), which blocks thyroid hormone activity at the cellular level. At the

same time, poor bile flow prevents efficient estrogen clearance, leading to estrogen recirculation

and dominance, which raises thyroid-binding globulin (TBG) and lowers free thyroid hormone

availability. Iron-induced liver stress also promotes hepatic insulin resistance, further slowing

metabolic signaling and contributing to overall energy depletion and thyroid dysfunction.xidative

stress → primes thyroid tissue for autoimmune attack

Bile is the central hub linking liver detox, estrogen clearance, iron regulation, and gut health.

The result: sluggish metabolism, hormonal congestion, and “thyroid resistance.”

Healthy insulin signaling tells the liver it’s safe to convert T4 → T3.

But when iron accumulates in hepatocytes:

• Insulin signaling is blocked.
• Glucose piles up in the blood.
• The liver stops converting T4 efficiently.

High insulin + high iron = low metabolic output and fat storage mode.

Iron-driven oxidative stress increases somatostatin, the hormone that inhibits both insulin and

TSH (thyroid-stimulating hormone).

Too much somatostatin → thyroid and pancreas suppression → metabolic slowdown.

When the liver is iron-loaded and bile is stagnant:

• Estrogen can’t be cleared.
• It recirculates through the enterohepatic pathway, feeding estrogen dominance.
• High estrogen increases thyroid-binding globulin (TBG) → less free T3/T4.➢ Estrogen metabolites activate immune pathways → TPO antibody formation.

The combination of iron overload + estrogen dominance + immune activation = thyroid

autoimmunity in motion.

Iron overload alters the microbiome, killing beneficial bacteria that produce short-chain fatty

acids (SCFAs) — the molecules that regulate hepcidin and reduce inflammation. Gut

inflammation and dysbiosis increase toxin production, promote leaky gut, and allow toxins to

enter the bloodstream, which primes the immune system for autoimmunity.

Low SCFAs → high hepcidin → iron trapped in tissues → inflammatory loop.

Leaky gut allows immune cross-reactivity → TPO antibodies rise.

Dysbiosis + iron overload = immune and thyroid chaos.

• TPO (Thyroid Peroxidase): Requires balanced iron to catalyze iodine binding; damaged by excess iron and peroxides.
• TGB (Thyroglobulin): Storage protein for thyroid hormone synthesis; oxidized by iron stress.
• T4 → T3 Conversion: Requires selenium, zinc, glutathione — all depleted by iron overload.
• rT3 (Reverse T3): Rises when the liver is inflamed or stressed, blocking T3 activity.

Iron overload drives oxidative stress, causing:

• Hepatic insulin resistance
• Sluggish bile flow
• Impaired estrogen clearance
• Reduced T4 → T3 conversion
• Increased reverse T3 (rT3) and TPO antibodies
• Slowed metabolism

Dr. Kristy will review your labs and create a personalized plan to restore your thyroid health!