Complete Thyroid Protocol (Including Hashimoto’s)

The Body’s Thermostat

The thyroid gland weighs 20 grams and sits at the base of your throat like a butterfly draped over the trachea. It is the body’s thermostat — but that metaphor undersells it. Every cell in your body has nuclear thyroid hormone receptors (TRalpha and TRbeta). T3 binds these receptors and directly activates gene transcription — turning on mitochondrial biogenesis, regulating basal metabolic rate, driving protein synthesis, controlling cholesterol metabolism, modulating neurotransmitter production, governing heart rate, maintaining gut motility, regulating body temperature, influencing fertility, and affecting mood, cognition, and energy at every level.

When thyroid function is suboptimal, everything slows. Not dramatically enough to alarm a conventional physician reviewing a TSH result, but enough that the patient feels like they are living life through wet concrete. The hair thins. The skin dries. The brain fogs. The bowels stop. The mood sinks. The weight climbs despite eating less and exercising more. And they’re told their labs are “normal.”

The Full Picture Most Doctors Miss

Here is the central problem with conventional thyroid care: most physicians check only TSH. Some add Free T4. This is like checking the thermostat on the wall and declaring the heating system functional — without ever looking at the furnace, the ductwork, the fuel supply, or whether the rooms are actually warm.

TSH (thyroid-stimulating hormone) is a pituitary hormone, not a thyroid hormone. It tells you what the pituitary thinks about thyroid status, filtered through the hypothalamic-pituitary feedback loop. It does not tell you what is happening at the cellular level. A TSH of 3.0 can represent a person with excellent thyroid function or a person who is functionally hypothyroid with poor T4-to-T3 conversion, elevated Reverse T3, and thyroid antibodies slowly destroying the gland.

The Complete Thyroid Panel

Every thyroid evaluation should include ALL of the following:

TSH: The pituitary’s signal to the thyroid. Conventional reference range: 0.45-4.5 mIU/L. This range was established using population data that included people with undiagnosed thyroid disease — contaminating the “normal” range upward. The National Academy of Clinical Biochemistry has suggested the upper limit should be 2.5 mIU/L.

Free T4 (thyroxine): The unbound, bioavailable form of T4. T4 is a prohormone — a storage form with minimal direct metabolic activity. It must be converted to T3 to be active.

Free T3 (triiodothyronine): The active hormone. This is what matters at the cellular level. Free T3 binds nuclear thyroid receptors and activates gene transcription. You can have adequate T4 and TSH with low Free T3 and be symptomatic.

Reverse T3 (rT3): The metabolic brake. Produced from T4 by the type 3 deiodinase enzyme (D3). Reverse T3 occupies thyroid receptors WITHOUT activating them — functioning as a competitive inhibitor. The body increases rT3 production during starvation, severe illness, chronic stress, inflammation, and caloric restriction as a survival mechanism to conserve energy. Elevated rT3 creates functional hypothyroidism even when TSH and T4 look normal.

TPO antibodies (thyroid peroxidase antibodies): The autoimmune marker. Elevated in approximately 90% of Hashimoto’s thyroiditis cases. TPO antibodies attack thyroid peroxidase, the enzyme responsible for incorporating iodine into thyroglobulin to produce T4 and T3. Can be elevated for years or decades before TSH becomes abnormal — this is the earliest detectable marker of thyroid autoimmunity.

Thyroglobulin antibodies (TgAb): Antibodies against thyroglobulin, the protein scaffold on which thyroid hormones are synthesized. Elevated in 50-80% of Hashimoto’s cases. Some patients have elevated TgAb with normal TPO — BOTH must be checked. Elevated in isolation, TgAb can also indicate thyroid cancer risk.

T3 uptake: Measures thyroid-binding globulin (TBG) indirectly. High TBG (from oral estrogen, pregnancy, liver disease) binds more T3 and T4, reducing free hormone availability. Low TBG (from androgens, nephrotic syndrome, liver failure) increases free hormones. Contextualizes Free T4 and Free T3 results.

Optimal Ranges (Functional, Not Just “Normal”)

Marker	Optimal Range	Conventional Range	Notes
TSH	1.0-2.0 mIU/L	0.45-4.5	Above 2.5 warrants full investigation. 3.0-4.5 with symptoms is subclinical hypothyroidism.
Free T4	1.1-1.5 ng/dL	0.82-1.77	Mid-range to upper-mid-range is optimal
Free T3	3.0-4.0 pg/mL	2.0-4.4	Upper third of range. Below 3.0 with symptoms suggests conversion problem
Reverse T3	<15 ng/dL	<24	Lower is better. Above 15 with low Free T3 is a red flag
RT3 ratio	Free T3/RT3 >0.2	Not conventionally used	Below 0.2 = functional hypothyroidism regardless of TSH
TPO Antibodies	<2 IU/mL (ideally undetectable)	<34	Any elevation indicates autoimmune process
Thyroglobulin Ab	<2 IU/mL	<4	Same principle — lower is better

Conversion Factors: T4 to T3

Only about 7% of thyroid output is T3. The remaining 93% is T4, which must be converted to T3 by selenium-dependent deiodinase enzymes — primarily D1 (in liver, kidney, thyroid) and D2 (in brain, pituitary, brown adipose tissue, skeletal muscle). Approximately 60% of this conversion occurs in the liver, 20% in the gut (via bacterial sulfatase activity), and 20% in other peripheral tissues.

Key conversion factors:

Selenium: 200mcg daily. Selenium is the mineral at the catalytic center of all three deiodinase enzymes (D1, D2, D3). Without adequate selenium, T4 cannot be efficiently converted to T3. Selenium also protects thyroid cells from hydrogen peroxide damage (via glutathione peroxidase) and reduces thyroid antibodies. The single most evidence-based nutrient for thyroid health.

Zinc: 30mg daily (as zinc picolinate or bisglycinate). Required for deiodinase activity, thyroid hormone receptor binding, and TRH synthesis in the hypothalamus. Zinc deficiency impairs both thyroid hormone production and peripheral conversion.

Iron: Ferritin must be 70-90 ng/mL for optimal conversion (many functional practitioners consider 50 ng/mL the minimum, but 70-90 is where conversion works best). Iron is a cofactor for thyroid peroxidase (the enzyme that synthesizes T4 and T3 from iodine and tyrosine). Low iron = impaired synthesis AND impaired conversion. Check ferritin — serum iron and TIBC alone are insufficient. Iron deficiency is the most common nutritional deficiency worldwide and one of the most common correctable causes of hypothyroid symptoms.

Vitamin A (retinol): 5,000-10,000 IU daily from retinol (preformed vitamin A), not beta-carotene. Vitamin A is required for thyroid hormone receptor activation — T3 binds its nuclear receptor as a heterodimer with the retinoid X receptor (RXR). Without adequate retinol, T3 literally cannot activate its target genes, regardless of blood levels. Many people poorly convert beta-carotene to retinol due to BCO1 gene variants (affecting up to 45% of the population). Cod liver oil provides both vitamin A and vitamin D.

Cortisol: Both high and low cortisol impair T4 to T3 conversion. High cortisol increases D3 deiodinase (producing Reverse T3 instead of T3). Low cortisol impairs cellular responsiveness to thyroid hormones — cells need cortisol to utilize T3. The adrenal-thyroid connection is bidirectional and non-optional. Always assess adrenal function alongside thyroid (see HPA Axis Protocol).

Root Causes of Thyroid Dysfunction

Hashimoto’s Thyroiditis

Hashimoto’s is the autoimmune destruction of the thyroid gland and accounts for approximately 90% of hypothyroidism in the developed world. The immune system generates antibodies (TPO-Ab, TgAb) that attack thyroid tissue, causing gradual gland destruction with intermittent hormone release (as cells are destroyed, stored hormone spills into blood, causing transient hyperthyroid symptoms — the “Hashitoxicosis” phenomenon).

Triggers and perpetuators:

Gluten — molecular mimicry: This is the most important dietary connection. Gliadin (the prolamin fraction of gluten) shares amino acid sequences with thyroid tissue, specifically thyroid peroxidase and thyroglobulin. When gliadin enters the bloodstream through a permeable intestinal barrier, the immune system generates antibodies against it. These antibodies cross-react with thyroid tissue because the molecular structures are similar enough to confuse the immune system. Additionally, tissue transglutaminase (the enzyme targeted in celiac disease) is also expressed in the thyroid gland, providing another cross-reactivity pathway. This has been demonstrated in multiple studies (Valentino et al., 1999; Sategna-Guidetti et al., 2001; Naiyer et al., 2008).

Gut permeability: Alessio Fasano’s research established that intestinal permeability (“leaky gut”) is a prerequisite for autoimmune disease — not just a consequence. Zonulin, the protein that regulates tight junctions, is upregulated by gliadin, dysbiosis, and infections. When the gut barrier is compromised, dietary proteins, bacterial endotoxins (LPS), and other antigens access the bloodstream, triggering immune activation and molecular mimicry.

Infections: Epstein-Barr virus (EBV) reactivation is strongly associated with Hashimoto’s — EBV-infected B cells can produce thyroid-cross-reactive antibodies. Yersinia enterocolitica has molecular mimicry with TSH receptors. H. pylori alters immune tolerance. Hepatitis C is associated with thyroid autoimmunity.

Iodine excess: Paradoxically, excessive iodine can trigger or worsen Hashimoto’s. Iodine incorporation into thyroglobulin by thyroid peroxidase generates hydrogen peroxide (H2O2) as a byproduct. Excessive H2O2 damages thyroid cells, exposing intracellular antigens to the immune system. This is why selenium (which powers glutathione peroxidase to neutralize H2O2) must accompany iodine supplementation — and why megadose iodine protocols (12.5-50mg, Brownstein/Abraham protocol) are risky in Hashimoto’s patients.

Stress: Chronic stress suppresses immune tolerance (regulatory T-cells) while activating Th1 and Th17 inflammatory pathways. Every autoimmune patient can identify a period of severe stress preceding or worsening their condition.

Nutrient Deficiencies

Beyond selenium, zinc, and iron already discussed:

Iodine: The raw material — T4 has 4 iodine atoms, T3 has 3. RDA is 150mcg. Many populations are mildly deficient, especially those avoiding iodized salt, dairy, and seafood. Test urinary iodine before supplementing. Deficient (<100 mcg/L): supplement 150-300mcg daily, ALWAYS with selenium 200mcg. Never megadose in Hashimoto’s without close monitoring.

Vitamin D: Maintain 60-80 ng/mL. Vitamin D is a powerful immunomodulator — deficiency is consistently associated with higher TPO antibodies and increased autoimmune risk. Meta-analyses confirm that vitamin D supplementation reduces thyroid antibodies. Dose: 5,000-10,000 IU daily with K2 (MK-7, 100-200mcg) to prevent vascular calcification. Check 25-OH vitamin D every 3 months until stable in target range.

Vitamin B12: Hypothyroidism impairs B12 absorption (low stomach acid, slow gut motility). B12 deficiency mimics and compounds hypothyroid symptoms: fatigue, brain fog, depression, neuropathy. Check methylmalonic acid (MMA) — more sensitive than serum B12. Supplement methylcobalamin 1000-5000mcg sublingual if deficient.

High Reverse T3

Elevated Reverse T3 with low Free T3 creates functional hypothyroidism — T3 receptors are blocked by the inactive rT3, preventing active T3 from binding. Common causes:

• Chronic stress (cortisol drives D3 deiodinase, producing rT3)
• Chronic inflammation (IL-6, TNF-alpha increase D3 activity)
• Caloric restriction and dieting (the body conserves energy by braking metabolism)
• Liver dysfunction (impaired T4 to T3 conversion in hepatocytes)
• Iron deficiency (impaired deiodinase function)
• Selenium deficiency
• Acute illness (sick euthyroid syndrome / non-thyroidal illness syndrome)

Treatment: address the root cause. If stress-driven, treat the HPA axis. If inflammation-driven, find and treat the inflammatory source. If caloric-restriction-driven, eat more (this is the “reverse dieting” concept). Iron and selenium repletion. Liver support.

Environmental Thyroid Disruptors

The thyroid is exquisitely vulnerable to environmental chemicals because of competitive halide chemistry. Iodine is a halogen. Other halogens — fluorine, bromine, chlorine — compete for the same transport and binding sites.

Fluoride: Was historically used as an antithyroid drug for hyperthyroidism — at doses lower than what many Americans ingest daily from fluoridated water (0.7-1.2 ppm), dental products, tea (Camellia sinensis accumulates fluoride), and pharmaceuticals (fluoride is in Prozac/fluoxetine, Cipro/ciprofloxacin, and many others). Fluoride inhibits the sodium-iodide symporter (NIS) and competes with iodine at TPO. Filter drinking water (reverse osmosis removes fluoride; carbon filters do not).

Bromide: Found in brominated flour (potassium bromate — banned in Europe and Canada, still legal in the US), brominated vegetable oil (some citrus sodas), flame retardants (polybrominated diphenyl ethers — PBDEs — in furniture, mattresses, electronics, children’s clothing). Bromide displaces iodine from the NIS and from thyroid tissue itself.

Perchlorate: A rocket fuel oxidizer that contaminates groundwater. One of the most potent known inhibitors of the sodium-iodide symporter. Found in drinking water in many US regions.

BPA and phthalates: Endocrine disruptors that interfere with thyroid receptor binding and T3 intracellular signaling. Ubiquitous in plastics, food packaging, receipts, and personal care products.

Mercury: Binds to selenium, depleting the cofactor needed for deiodinase enzymes. Dental amalgams are a chronic source. See Heavy Metal Detox Protocol.

Pesticides: Organochlorine compounds (DDT, DDE, dieldrin) and organophosphates disrupt thyroid function at multiple levels.

Hashimoto’s Protocol

1. Gluten-Free (Non-Negotiable)

100% elimination. Not reduction. Not “mostly gluten-free.” The immune response is binary — even small exposures (a crouton, a shared fryer, a lick of an envelope with wheat-based glue) maintain the antibody cascade for weeks to months. A 2019 study in Experimental and Clinical Endocrinology & Diabetes found that 6 months of strict gluten-free diet reduced TPO antibodies by 46% and TgAb by 30% in Hashimoto’s patients WITHOUT celiac disease.

Many patients also benefit from eliminating dairy (casein has structural similarities to gluten — molecular mimicry via casomorphin and cross-reactive antibodies). Trial 90 days dairy-free alongside gluten-free. Some tolerate A2 dairy (goat, sheep, some heritage cow breeds) while reacting to A1 casein (most commercial cow dairy).

2. Selenium: 200mcg Daily

The single most evidence-based nutrient intervention for Hashimoto’s. The Toulis et al. meta-analysis (2010, Thyroid journal) pooling multiple RCTs demonstrated that selenium supplementation (200mcg daily as selenomethionine) reduces TPO antibodies by approximately 21% over 3-12 months. Individual studies show even more dramatic reductions:

• Gartner et al. (2002): 36% reduction at 3 months
• Turker et al. (2006): 42.5% reduction at 9 months
• Mazokopakis et al. (2007): Sustained reduction at 12 months

Selenomethionine is preferred over sodium selenite for long-term use (better tissue retention). Do not exceed 400mcg daily (selenosis: brittle nails, hair loss, garlic breath, GI distress, peripheral neuropathy). Two Brazil nuts daily provide approximately 100-180mcg (highly variable depending on soil selenium content in Brazil’s growing regions).

3. Myo-inositol: 600mg Daily

Emerging evidence shows myo-inositol enhances TSH receptor signaling — it functions as a second messenger in the TSH-receptor pathway within thyroid cells. Combined with selenium (600mg myo-inositol + 83mcg selenium), it reduces TSH and TPO antibodies more effectively than selenium alone. Nordio and Pajalich (2013, European Review for Medical and Pharmacological Sciences) demonstrated significant TSH reduction and antibody improvement. Brands: Jarrow Inositol, compounded formulations.

4. Vitamin D: Maintain 60-80 ng/mL

Vitamin D is not just a vitamin — it is a secosteroid hormone with receptors on virtually every immune cell. Low vitamin D is associated with increased Th17 (inflammatory) T-cell activity and decreased T-regulatory (tolerance) cell activity. Multiple studies demonstrate inverse correlation between vitamin D levels and TPO antibody titers in Hashimoto’s.

Dose: 5,000-10,000 IU daily, always with vitamin K2 (MK-7, 100-200mcg, which directs calcium to bone and away from arteries). Check 25-OH vitamin D every 3 months until consistently in the 60-80 ng/mL range.

5. Low-Dose Naltrexone (LDN): 1.5-4.5mg at Bedtime

LDN is one of the most promising and underutilized interventions for autoimmune thyroid disease. At low doses (1.5-4.5mg, versus the standard 50mg dose used for opioid addiction), naltrexone briefly blocks opioid receptors (for approximately 4-6 hours), triggering a rebound increase in endogenous endorphin and enkephalin production. These endogenous opioids modulate immune function by upregulating T-regulatory cells, reducing inflammatory cytokines (TNF-alpha, IL-6), and modulating the Th1/Th2 balance.

Multiple case series, retrospective analyses, and small trials document TPO antibody reduction, TSH improvement, and symptom resolution in Hashimoto’s patients on LDN. The medication requires a prescription and is prepared by compounding pharmacies (standard naltrexone is 50mg tablets — the low dose must be compounded). Start at 1.5mg at bedtime, increase by 0.5mg weekly to 4.5mg. Side effects are minimal: vivid dreams initially (resolves in 1-2 weeks), occasional transient insomnia or headache.

6. Address EBV Reactivation

Screen for EBV with: VCA IgG (past infection — positive in 95% of adults), EBNA IgG (past infection confirmation), and Early Antigen (EA) IgG or IgM (elevated EA suggests reactivation). If reactivation markers are elevated:

• L-lysine: 1000mg 2-3x daily (competes with arginine, which EBV requires for replication)
• Monolaurin (from lauric acid/coconut): 600-1800mg daily (disrupts viral lipid envelope)
• Humic/fulvic acid: 250-500mg daily (antiviral and immune-modulating)
• Immune support: zinc 30mg, vitamin C 1-2g, vitamin A 10,000 IU, medicinal mushrooms (reishi, turkey tail, cordyceps)

7. Gut Healing (The 5R Protocol)

Gut permeability is both a trigger and perpetuator of Hashimoto’s. The 5R framework: Remove (triggers — gluten, dairy, sugar, alcohol, infections, NSAIDs), Replace (digestive enzymes, HCl if low stomach acid), Reinoculate (probiotics — Lactobacillus rhamnosus GG, Saccharomyces boulardii, spore-based Bacillus coagulans and Bacillus subtilis), Repair (L-glutamine 5g twice daily, zinc carnosine 75mg twice daily, DGL 400mg before meals, colostrum, butyrate 300-600mg, bone broth), Rebalance (stress management, sleep, exercise). See the Gut Healing 5R Protocol for comprehensive details.

8. Manage Stress

See the HPA Axis Protocol. Chronic stress suppresses immune tolerance and directly impairs thyroid function at every level of the axis. Every Hashimoto’s patient needs a stress management strategy — meditation, yoga, nature exposure, therapy for trauma and psychological stressors.

Medication Guidance

Levothyroxine (Synthroid, Levoxyl, Tirosint)

Synthetic T4. The conventional standard of care. Works well for patients who convert T4 to T3 efficiently (adequate selenium, zinc, iron, healthy liver, normal cortisol). Brand matters: Synthroid and generic levothyroxine are not always bioequivalent — the FDA allows a 5% variance between manufacturers, and some patients are sensitive to this difference. Tirosint (liquid gel capsule, by IBSA) contains T4 in gelatin with minimal fillers — best option for patients with absorption issues, celiac disease, or filler sensitivities.

Limitations: levothyroxine provides ONLY T4. If the patient’s conversion is impaired (low selenium, iron deficiency, high cortisol, liver dysfunction, D2 polymorphisms), they receive T4 but cannot make adequate T3. TSH normalizes but symptoms persist.

Natural Desiccated Thyroid (NDT)

Armour Thyroid, NP Thyroid, WP Thyroid — derived from porcine (pig) thyroid glands. Contains T4, T3, T2, T1, and calcitonin in approximately physiological ratios. The T4:T3 ratio in NDT is approximately 4:1, whereas the human thyroid produces approximately 14:1. This means NDT provides relatively more T3 than the body produces, which is why many patients feel better on it (more active hormone reaching cells) but which can cause transient T3 spikes (short-lived elevations in Free T3 after dosing).

NDT is preferred by many functional medicine practitioners and patients. Conventional endocrinology generally opposes it, citing historical potency inconsistencies (valid for older formulations, less relevant for current USP-standardized products) and the “non-physiological” T4:T3 ratio. However, the 4:1 ratio may actually be appropriate for patients with impaired D1/D2 conversion — they need MORE T3 relative to T4 precisely because they can’t make it efficiently from T4 alone.

Dosing: start at 15-30mg (1/4 to 1/2 grain), increase by 15mg every 4-6 weeks based on labs and symptoms. Typical maintenance: 60-120mg (1-2 grains). Monitor Free T3 (may peak 2-4 hours post-dose — draw labs before morning dose for trough level).

Compounded T4/T3

Custom ratios of synthetic T4 and T3 prepared by compounding pharmacies. Allows precise titration of each hormone independently. Sustained-release T3 formulations avoid the peaks and troughs of immediate-release liothyronine. Common starting ratios: 76mcg T4 / 18mcg T3 (approximating 1 grain NDT) or customized based on the patient’s specific conversion pattern and lab results.

Medication Timing (Universal for All Forms)

• Empty stomach — food reduces absorption by 20-40%
• 60 minutes before food or coffee (coffee specifically reduces levothyroxine absorption by 36% in studies)
• 4 hours away from iron supplements (iron chelates thyroid hormone in the gut)
• 4 hours away from calcium supplements (same mechanism)
• 4 hours away from PPIs and antacids (reduced stomach acid impairs dissolution)
• Consistency matters: take at the same time every day for stable levels
• Some patients prefer bedtime dosing (at least 2-3 hours after the last meal) — studies show equivalent or superior absorption compared to morning dosing, and it avoids the morning timing complications

Putting It All Together

A Hashimoto’s patient with fatigue, brain fog, hair loss, weight gain, constipation, and a TSH of 3.5 (conventionally “normal”) deserves the full workup and comprehensive treatment:

1. Complete thyroid panel: TSH, Free T4, Free T3, Reverse T3, TPO-Ab, TgAb
2. 100% gluten elimination, dairy elimination trial for 90 days
3. Selenium 200mcg daily, zinc 30mg daily, vitamin D 5000-10000 IU daily with K2
4. Optimize iron (ferritin target 70-90 ng/mL), vitamin A (retinol), B12
5. Address gut health: rule out SIBO, support barrier integrity (5R protocol)
6. Check adrenal function: DUTCH or 4-point salivary cortisol, DHEA-S
7. Screen for infections: EBV panel, consider H. pylori, Yersinia
8. Myo-inositol 600mg daily
9. Consider LDN 1.5-4.5mg at bedtime
10. Consider NDT or combined T4/T3 if nutrient optimization alone is insufficient
11. Reduce environmental disruptors: filter water (reverse osmosis for fluoride), clean personal care products, avoid BPA/phthalates, address mercury exposure
12. Retest complete panel in 8-12 weeks, adjust accordingly

Thyroid optimization is not about chasing a TSH number. It is about restoring cellular metabolism — the fire that powers every mitochondrion in every cell. When the thyroid is right, energy returns, cognition sharpens, mood lifts, bowels move, hair grows, and the body remembers what it feels like to be alive. The conventional approach of “TSH is in range, you’re fine” leaves millions of people suffering unnecessarily. The functional approach says: we don’t treat lab values — we treat the person sitting in front of us.